how to live sucessfully with diabetes! i.e., madhumeha ke sath safal jeevan ! kaisa sambhav ?

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Posted by on जून 19, 2011 in Uncategorized


how to live successfully with diabetes! i.e., madhumeh ke sath safal jeevan ! kaise sambhav ?



Nestled among the Himalayas, in the Holy city of Rishikesh, Uttrakhand, India, is Kanti Diabetic and Heart Care Centre bringing relief to thousands of ailing Diabetics. For successful treatment the patient has to come for initial check up and later on treatment continues by contacting on phone, fax, e-mail etc. Later on the Herbo-Mineral Patent medicines can be sent through registered post also.

The Herbal Medicines are prepared at Kanti Diabetic & Heart Care Pharmacy (Lisenced and GMP approved), situated inside the Centre. The medicines are 100% pure Herbal and are especially prepared for Diabetics (Diabetes and it’s complications). The centre is fully computerized and continuously in touch with the patients who can contact any time and is forever ready for your service.


Dr Deepak Joshi

Senior Diabetalogist

M.B.B.S. M.D. (Medicine) K.G.M.C. (Lucknow)
Dr Joshi’s knowledge of the ancient treatment methods and unrelenting hard work at the Kanti Diabetic center led to making of some anti-diabetic drug formulae by a team of allopathic and ayurvedic physicians and para-medical staff. Their honest use in patients and continuous research led to a highly effective herbal treatment, which has been successfully used on thousands of patients (~23,000).

What is Diabetes?

Diabetes is a disease brought on by either the body’s inability to make insulin (type 1) or by the body not responding to the effects of insulin (type 2). Diabetes can also appear during pregnancy (GDM- which most of the times reverts after termination of the pregnancy). As per Vedotpattik Chikitsa (Ancient therapy) as well as  Modern Therapy i.e., Allopathy, Insulin (Pittagni) is one of the main hormones that regulates blood sugar levels (the other important hormone in balancing blood glucose levels is Glucagon, which is anti-insulin in action) and allows the body to use sugar for energy. Diabetes if not treated effectively leds to several life threatning complications.

Born in 1962 at the holy city of Rishikesh, Dr. Deepak Joshi was awarded the degree of M.D. (medicine) in 1988 from King George’s Medical College, Lucknow. After this he made Rishikesh his working field for serving mankind by his noble profession and found the Kanti Diabetic Centre in 1994. Besides he engrossed himself in extensive research work and study of all ancient writings of the Vedas, Ayurveda, Homeopathy, Chinese, Tibetan, Acupuncture and other Popular therapies. In doing so, he consulted a number of ‘Unani’ and ‘Ayurvedic’ practitioners for the enrichment of his knowledge and practice. He developed keen interest in vedotpattik chikitsa and his faith in holistic treatment strengthened. He also wrote several books on diabetes for patients’ education. His deep knowledge of the ancient treatment methods and unrelenting hard work at the Kanti Diabetic Centre led to making of some ant-diabetic drug formulae by a team of allopathic and ayurvedic physicians and para medical staff. Their honest use in patients and continuous research led to a highly effective herbal treatment, which has been successfully used on thousands of patients.
Freqently asked Questions

Q1. What is the aim of Kanti Diabetic Care Centre, Rishikesh and what are its related activities?
Ans: At present, this centre is dedicated to trying to put a curb on the rapidly increasing number of diabetics in all the developing countries of Asia. Besides, it is steadily engaged in providing relief to thousands of ailing diabetics by Dr. Joshi’s combination therapy and experienced holistic approach towards treatment. Moreover, this centre aims at establishment of a disease free society with the help of natural medical measures, Yoga and Pranayama. Dr. Deepak Joshi and his team at Kanti Diabetic Care Centre is continuously making strides in this field. Apart from Allopathy, with the help of natural treatment and herbal medicines, he has proved diabetes to be a boon and not a bane.

Q2. Why is it beneficial to take treatment by Dr. Joshi?
Ans: The complete answer to this question can be given by the patient himself. It has been seen for the first time that despite attaining master’s degree of medicine in allopathy, a physician has successfully approached and developed a new combination therapy for treatment of diabetes by natural herbal measures. Dr. Joshi is performing great, rare work of acquainting a patient to treatments by all possible methods of treatment from vedotpattik chikitsa to modern therapy.

Q3. What are the prominent specialties of Dr. Joshi’s treatment?
Ans: Dr. Joshi’s style of treatment is totally different and not centralized and does not include only one line of treatment. He preaches simple, day to day practicalities to his patients which alleviate his patients’ suffering, and they start developing faith in him.

Q4. Where is Kanti Clinic located?

Kanti Diabetic & Heart Care Centre

Kanti Clinic

1, Sadanand Marg, Rishikesh



Contact Us

Ph: 91-135-2431305, 2433905 Fax.0135-2431503

Mob.: 9412917264, 9410987715


The blog contains a systematic and chronological description of the concepts of different treatment paties for preserving of human health from vedic (pre-historic) period to the present age.
I have tried to combine treatments and cures of diabetes as described in various medical therapies (especially Ayurvedic treatment) with and modern medical treatment. By doing so I have tried to establish a relation between various medical therapies (since 300 BC) and Modern medicine.
It is my experience that by studying and utilising this procedure a diabetic can become an expert in curing his diabetes. Thereafter one could say ‘Diabetes A Boon Not A Bane’.
The outstanding feature of the blog is a systematic description of diabetic treatments as per Ayurvedic and Allopathic science. It is accmpanied with a vivid and lively description (pictures of Yoga postures) of the usefulness of the Yoga and Pranayama science in curing difficult diseases.
For treading towards Victory over Diabetes or to minimise or avoid of allopathic medicines, how herbo-minerals can be effective (code of cures) is all described in the blog.
My experience is that medicine of this disease i.e., Diabetes & it’s Complications exists in nature as in different foods, herbs, air, sun, water, salts, positive thinking, physical and mental exercises etc., hence it is essential that the patient makes maximum use of all natural means around him and becomes capable of understanding the importance of each measure himself.
It has been clearly explained in the blog as to how the vitiation of the three body humours that is, vata, pitta and kapha leads to diabetes. The effective measures to cure ‘Ama‘ that is immature humours ( in allopathy it is probably sorbitol which is the root cause of diabetic complications) is a distinguished feature of this blog.
Treatment of diabetes with all popular systems of medicine like Homeopathy, Biochemic, Emchi, Chinese, Unani ‘Greek’, Accupuncture, Naturopathy, Magnet therapy, Pranic therapy, Chromo therapy, Hydro therapy, Moon therapy, Vitamin therapy, Treatment with clays, Mechano therapy, treatment with Climates etc. have also been dealt in detail.
Efferots have been made to enable the patient to correctly judge the treatment to be undertaken as different treatments exist for different types of patients.
The lively picturization and detailed description of the rare herbs found in the Himalayas and clarification of the subject with the help of graphs and tables is also worth mentioning.
Dr Deepak Joshi
                      M.B.B.S., M.D.(MEDICINE), K.G.M.C. (Lko)
                                  “DIABETES A BOON! NOT A BANE?”




* Relevant endocrinology in diabetes

Thyroid gland

Suprarenal gland ‘adrenals’

Pituitary gland

* Important organ systems of the human body

Integumentary system

Muscular system

Skeletal system

Digestive system

Circulatory system

Respiratory system

Uro-Genital system

Nervous system

Immune system ‘ body defence against diseases’


* Pancha Mahabhuta and their association with the three Body Humours

* Dosha, Dhatu and Malas i.e.,  Body Humours, Tissues and Excretions in Human Body.

*Dosha, Dhatu and Malas i.e., Body Humours, Tissues and Excretions in the  Diseased Human Body.


* Pre-Clinical Diabetes or Chemical Diabetes

* Prameha or Pre-Diabetes ‘The Precursor of Madhumeha’

* Impaired Glucose Tolerance Test (IGTT)

* Gestational Diabetes Mellitus (GDM)

* Obesity Related Diabetes in Teens

* Malnutrition Related Diabetes Mellitus (MRDM)

* Stress Diabetes

* Diseases of the Endocrinal Glands other than the Pancreas

* Viral Diseases: Coxsackievirus, Mumps, Measles, Hepatitis, Infectious Mononucleosis, and Rubella

* Diabetogenic Drugs

* X-Syndrome

* Other Genetic Syndromes


* Difficulty in the Diagnosis of Diabetes

* Glucose Tolerance Test or ‘GTT’

* Glycosylated Hemoglobin ‘GHb’

* Investigations in Insulin Dependent Type-1 Diabetes

* Diabetes Self Management Education ‘DSME’

* Self-Monitoring Diabetes Control or ‘SMDC’

* Routine Blood and Urine Investigations in Diabetes

   Erythrocyte Sedimentation Rate (ESR)

   General Blood Picture (GHb)

   Routine Urine Examination

* Specialized Blood and Urine Investigations


* Definition of Diabetes

* Diagnosis of Diabetes

* Presenting Features of Diabetes

* Classification of Diabetes according to all Important Therapies

* Modern Classification of Diabetes

   Primary Diabetes

   Secondary diabetes

* Bio-synthesis and Physiology of Insulin (Pittagni)

* The Somogyi Effect and the Dawn Phenomena


* Diabetes as per Ayurveda

* Genetic Factors in Etio-pathogenesis of Diabetes

* ‘Tulya Dosha dushyata’ and Progession of Pre-Diabetes into Diabetes

* Metabolic Disorders during Diabetes

* Pathogenesis of Diabetes as per Ayurveda (madhumeha samprapti)

*  Pathogenesis of Diabetes as per Allopathy

     (a) pathogenesis of type 1 diabetes

     (b) pathogenesis of type 2 diabetes

* Biosynthesis and Physiology of Insulin (pittagni) Hormone

* The Somogyi Effect and The Dawn Phenomena


* Biochemical Background of Food Utilization

* Fuel Supply, Utilization and Balance

* Regulation of Substrate (oxidizable fuels) Mtabolism

* Food Metabolism in Diabetes

* Biochemical Effect of Starvation

* Target Tissues of Insulin

* Insulin Resistance Syndrome


 * As per Ayurveda & As per Allopathy

 * Promoting Weight Gain as a Therapeutic Option


 * Upadrava (complications) of Diabetes As Per Ayurveda

    Madhumeha aur pet-sansthan (Diabetes and the digestive system)

Madhumeha aur mutra-sansthan (Diabetes and the urinary system)

    Madhumeha aur youn (Diabetes and sex)

    Madhumeha aur chakshu (Diabetes and eyes)

    Maduheha aur raqt-parisancharan tantra (Diabetes and the circulatory system)

Madhumeha aur tantrika-tantra (Diabetes and the nervous system)

Madhumeha aur manshik-rog (Mental diseases)

    Madhumeha aur rog-pratirodh tantra ke rog (Diabetes and the diseases of the immune system)

Madumeha aur pad-rog (Diabetes and the feet)

* Diabetic Complications as per Allopathy

1. Acute complications

– Non-ketotic hyper-osmoler hyperglycemic coma

– Ketotic coma

– Hypoglycemia

– Severe acute infections

2. Chronic complications

  – Impotence

  – Diabetic nephropathy ‘DN’

  – Urinary tract infection ‘UTI’

Diabetic neuropathy

  – Cerebro-vascular accident (CVA) ‘stroke syndrome’

  – Diabetes and eyes

  – Diabetes and the feet

Infections in diabetes ‘diabetic sepsis’

Diabetes and pregnancy

Gestational diabetes mellitus ‘GDM’

Diabetes and the heart

** TREATMENT OF DIABETES: Vedotpattik, Allopathic and All Popular Treatment Pathies

* The Four Pillars Of Diabetic Treatments

– The first pillar: Investigation, Examination, Nari Parikshan, Upkshaya

– The second pillar : Disciplines of living in day, night and changing weathers (Day routine ‘dincharya’ & Night routine ‘ratricharya’)

– The third pillar : Appetizing/tasty/healthy diet in diabetes

– The fourth pillar : Medicines- Ayurvedic, Allopathic and other Popular Alternative Treatments

* Understanding Food Constituents as per Modern Science

1. Carbohydrates (sugars and starches)

2. Proteins (amino acid)

3. Fats (fatty acid)

4. Fibres

5. Elements and minerals

6. Vitamins

7. Water

* Classification of Food Items (Caloric value, Food Value), helpful in making Diabetic’s Diet Chart

1. Cereals

2. Lentils and pulses

3. Vegetables

4. Milk

5. Fruits

6. Oils and clarified butter

7. Meats

8. Dry fruits and others

* Procedure for making diet chart

* Diet chart of 2000 calories

* The Vedic Concept ‘iFood s the Best Medicine of Diabetes’

* Relishing and appetising ayur-diet of a diabetic

* Classification of eatable items, Their Rasa-Guna (constituents), Vipaka (digestion and metabolism), Virya and Shakti (Power), and Medicinal value 

  1. ‘Dhaanya’ cereals and pulses

2. ‘Shaak’ vegetables

3. ‘Phal and majja’ fruits and seeds

4. ‘Dugdh’ milk

5. ‘Ghrita and tel’ clarified butter and oil

6. ‘Jal, ambu’ water

7. ‘Meva’ dry fruits

8. ‘Egg and maans’ meat

9. ‘Madhu and sharkara’ honey, sugar

10. ‘Lavan and chhar’ salts and bases

* Qualities of ‘Kratanna varg’ (cooked and ready to eat food)

* ‘Prepared foods’ varieties and useful properties

* Quantity of food in a diabetic’s diet (ayurvedic diet plan)

** DIABETIC TREATMENTS: 1- ‘Vedotpattik chikitsa’ Ayurvedic treatment

‘Santarpan or promotary treatments’ medications, diet and activities

‘Aptarpan processes’ and treatments of diabetes

‘Aptarpan karmas’ or body reducing measures

‘Panch karmas’ or five purification acts

l Prevention of diabetes

l How to prevent seasonal collection of abnormal humours

l Herbo-minerals useful in diabetes ‘madhumeha aushad yog’

l Shuddh shilajit ‘the most effective anti-diabetic natural medicine’

l Major groups of herbal substances used as anti-diabetic drugs

l Useful herbo-minerals for treatment of diabetes and associated illnesses

l Single herbo-mineral substances for treatment of diabetes

l Ojus and power restoring herbo-minerals for regular use in diabetics

l Bhasmas (ashes) useful in diabetes

l Herbo-minerals (medicines) used for treating diabetic complications

l ‘Shastrokta yog’ anti-diabetic formulations sanctioned in religious ‘vedic legal books’

l Herbo-mineral management of diabetic complications

l Hyperglycemia induced earlier symptoms/complications/treatment of diabetes

lHypoglycemia (atilanghan) induced symptoms/complications/treatment of diabetes

** Ayurvedic Treatment of Diseases of Importanat Organ-Systems involved in Diabetes

1. Mutra-sansthan ke rog (Diseases of the urinary system)

2. Hridaya-parisancharan sansthan ke rog (Cardio-vasular system ‘diseases of heart and circulatory system)

3. Tantrika-rog (Diseases of the nervous system and brain)

4. Chakshu rog (Diseases of the eye)

5. Pada rog (Leg diseases in diabetes)

6. Madhumeha aur yaun rog (Diabete and sex disorders)

7. Pait rog (Diseases of gastro-intestinal tract)

8. Sankraman aur pratiraksha sansthan (Infections and diseases of the immune system)

9. Shwas sansthan ke rog (Respiratory diseases)

10. Madhumeha mei Mile-jhulla rog (Miscellaneous diseases in diabetics)

Jwar (Fever ‘clinical features and treatment’ in diabetic patients)

** DIABETIC TREATMENTS- 2: The Philosophy of Yoga and Pranayama and its usefulness in diabetic treatments

* Yoga

* Yoga asanas (postures)

1. Sitting postures

2. Standing postures

3. Topsy-turvy posture (upside down postures)

4. Backward bending postures

5. Spinal twisting postures

6. Elbow balance postures

7. Forward bending postures

8. Additional postures

9. Relaxation postures

10. Mudras and Bandhas

* Pranayama

1. Kapalabhati

2. Suryabheda

3. Ujjayi

4. Sitkari

5. Sitali

6. Bhastrika

7. Bhramari

8. Murchha

9. Plavini

** DIABETIC TREATMENTS-3 : Allopathic treatment of diabetes

l The Ist group patients who have to use insulin lifelong

l The IInd category patients who may require insulin injection temporarily

l The IIIrdcategory patients who maintain good diabetic control just by diet,exercise and oral drugs life long

* Currently available oral hypoglycemic agents

* Insulin, Human Insulin, Doses 

** DIABETIC TREATMENTS- 4 : Popular alternative treatments of diabetes

l Chinese medicine

   Chinese herbo-mineral anti-diabetic medications

Use of hydrotherapy in chinese diabetic treatment

l Homeopathy

   Homeopathic drugs useful in diabetes

l Biochemic Therapy

   The use of 12 ‘cell salts’ 

lEmchi and Diabetes

    Management of ‘Gichin-Nyi’

l Acupuncture and Diabetes

  Treatment of Diabetes & Diabetic complications 

l Unani ‘Greek’ Medicine and Diabetes

   The use of scented oil containing herbs 

l Pranic Therapy and Diabetes

   Pranic Healer, Colour Pransa 

l Chromo Therapy and Diabetes

   Use of Treated water (having medicinal properties) 

l Moon Therapy and Diabetes

   Different dates for treating different diseases 

l Vitamin Therapy and Diabetes

    200 calorie fruits per day for diabetics 

l Magnetic Therapy and Diabetes

    Magnetised water 

l Miscellaneous Therapies

  * Treatment with clays

* Mechano or Massage Therapy

* Treatment with Climates


* Introduction

* Pathogenesis of complications of diabetic nephropathy

* Management of diabetic nephropathy

* General measures

* Specific measures


* Diabetic retinopathy in patients of DN

* Blood Pressure control in patients of DN

* Self care education in patients with DN

* Management of chronic renal failure

* Uremia

* CRF supportive treatment

* When should Renal Replacement Therapy (RRT) be started?

* Dialysis and Transplantation in the treatment of chronic renal failure in diabetes

* Hemodialysis

* Peritoneal dialysis

* The advantages of PD over hemodialysis are

*  Disadvantages of PD 

* Kidney Trasplantation

* Selection of donor

*  Living related donor

* Cadaveric donor

* Other aspects of renal transplantation

      Blood transfusion 

       Immune reaction

       Immunosuppressive treatment

      Clinical course and management of the recipient

It is only knowledge that can teach you to convert diabetes into a Boon rather than a Bane. In my writings I will share   with you the knowledge that I have gained through treating my diabetic patients (till now ~21,000) in last 26 years and by understanding diabetes through several medical books of several therapies. including Allopathy, Ayurveda (vedotapattik Chikitsa), Chinese medicine ‘Yin/Yang’ method of analysis, Homeopathy, Biochemic, Emchi, Acupuncture, Unani ‘Greek’ medicine, Pranic therapy, Chromo therapy, Naturotherapy, Magnetic therapy, Vitamin therapy, Moon therapy, Clay therapy, Traditional therapies and other Miscellaneous therapies.

** Words in italics are of Hindi/Sanskrit/Unani origin. Their most appropriate English meanings, translations and synonymous words are also given.

Aadhaman-Aanah: Pain due to accumulation of wind in stomach and intestines

Aagneya: Fiery and high energy substances

Aakshep: Fits or throwing out

Aalepan: Besmearing

Aapyayana: Increase in body tissues

Aarochak: Loss of interest in food, anorexia

Aarochakta: Dislike for food

Aarogyata: Perfect physical and mental health

Aashu: Swiftness

Abhishyandi: One which collects water and produces swelling over the body, Ponderous

Abhyang: Anointing oil over the body

Acharya: A learned person or a teacher

Acid-peptic disease: amla-pitta

Acne: mukhdushika

Addhaman: Distension of abdomen

Addhyasan: Eating before the previous food has yet not digested

Adhimand or sambal vayu: Glaucoma

Adho mukha Hastasana: Raised arm pose

Adhvasana:Reverse of the savasana

Agantuj rog: Exogenous disease

Agni mandata:Decreased digestion

Agni sweda: Heat diaphoresis

Agni visarp: Septicemia

Agnibal: Digestive power

Ahaar-viharjanya madhumeha: Type II diabetes

Ahiputan: A disease of infants

Ahit ayu: Unblessed age

Ajeerna: Indigestion

Ajjagalika: Painful pimple on face

Ajna chakra: Centre of spiritual enegy situated in he middle of the eyebrows

Akanghat: Monoplegia

Akarnadhanurasana: Karana– ear, Dhanu– bow and Asana– posture

Akash element: Ether or Space element

Akasheeya dravya: Space substances

Akshikoot shoth: Early morning swelling

Alaji: A boil

Alalameha: Albuminuria

Alasya: Laziness, Lethargy

Alchemy: Strengthful medications

Alochak pitta: One of the five pitta (bile) humour which helps in vision

Alsak: Paralytic illeus

Alteratives: Blood purifiers

Ama: Immature humours

Amaras: Immature nutrients in plasma

Amasaar: Essence of digested nutrients

Amatisar: Diarrhoea with mucus

Amavata: Immature vata humour

Ambu: Water, Fluid

Amenohrria: Anatarva

Aml ras: Sour taste

Aml-pitta: Acidity, retrosternal chest burning

Amlodgara: Hyperacidiy

Amyloid: Ama

Anaah:Obstruction of faeces and urine along with pain in abdomen

Anaemia: Raqtalpata

Anatarva: Amenorrhoea

Anayushya ayu: Unblessed age

Angamejayatva: Nervousness

Angina pectoris ‘cardiac pain’:Hriday-shool

Anidra: Less sleep

Anjeera adam: Ficus glomerta

Annavah shrotas: Pore through which food or nutriemts move inside the body

Antahkarana: Internal sense organs

Antaranga yoga: Internal yoga

Antarayama: Kyphosis, forward bending of spine

Anti rachitic activity: Strengthens up joints

Anti worm medication: Krimi-chikitsa

Anti-meda: Anti obesity

Anubhut yog: Herbal drug prepared through self experience over patients

Anuloman: Circulation of air

Anupaan dravyas: Liquids during meals

Anush-virya: Neither hot nor cold

Anuvasan vasti: Enema with strengthful substances including oils

Anva Haldi: Curcuma amada

Apach: Indigestion

Apan vayu:One of the five vata humours that resides in human body

Apathya: Non-regimen diet

Apathyajanya madhumeha:Obese diabetes. Type 2 diabetes

Apathyanimittaja: Dependent on non-regimen diet

Aphara: Distension of stomach

Aphorisms :Neeti vachan

Apripakwam ras: Immature nutrients

Apsamar: Epilepsy

Aptanak: Postpartem eclampsia

Arbud: Benign tumour

Ardha Matsyendrasana: Pose like a half bend fish

Ardha Chandrasana: Half moon pose

Ardha navasana: A Yog posture

Ardit: Facial palsy

Ardra kasa: Wet cough

Aristotle (384-320 B.C.): Father of the Unani medicine

Arochak: Unpleasant

Arsh: Piles

Arthritis: Sandhigat-vata

Aruchi: Disinterest

Arun ‘vatanari’: Nerve

Asadhya: Incurable

Asamyak: Disproportionate

Asavas: Distilled products

Aschyoten: Eye drops

Ashmari: Stones in urinary system, gall blader

Ashwa Sanchalanasana: An equestrian pose

Asthapan vasti: Fixation enema

Asthi: Bones

Asthi dhatu: Bone tissue

Asthi-bhang: Fracture bone

Asthi-bhangur: Osteoporosis

Asthi-ksheenta: Loss of minerals from bones

Asthi-sandhi: Bony joints

Asthi-shool: Pain in bones

Asthi-shoonya: Numbness in the bones

Asthi-shosh: Bone-tuberculosis

Asthi-shoth: Ostitis and periostitis

Asthila: Obstruction of stools, urine and wind

Asthivah shrotas: Pores through which nutrients flow into the bones

Atap: Sunbath

Atidravata: Liquidity

Atisar: Loose motions or dysentery

Aushad upchar: Treatment wih herbs

Aushadhi: Medicinal herb

Avar: Inferior

Avasthapak: Local digestion

Avgahan: Ablution

Avgahan: Immersion in a tub full of oil

Avilamutratha: Turbid urine

Avrita vatajanya madhumeha: Type I diabetes

Ayama: It refers to exercise

Ayamic hrid rog: Dilatation of heart

Ayurvedotpattik: Originated from ayurveda

Ayushya: Increases age

Ayushya ayu: Long life

Baanjhpan: Infertility

Baddha hasta: Closed hand

Baddha purishatva: Stool like hard bullets

Baddhapurishatva: Constipation

Badhirya: Muteness

Badkan: Vata humour or wind in unani medicine

Bahiranga Yoga: External Yoga

Bahumutrata: Excess urination

Bahushosh rog: Frozen shoulder

Bahyayama: Bending of vertebral column outside

Bajikaran: Sex strengthening measures

Bajikar: Anti-impotency herbal dugs

Bajikaran aushad: Sex stimulants

Bal: Strength

Bal samprapti: Intensity of the disease

Bal vardhak: Increasers of the strength

Balgum: Kapha humour

Balgum: Phlegm

Bandhas: Locking of exremities

Bandhyatva: Sterility

Basant ritu: Autumn season

Basic chakra: Centre of spiritual energy at the end of spinal cord

Beeja: Sperm and ovum

Beeja bhaga: Chromosomes

Beeja bhagavayava: Genes

Beeja dosha: Defect in chromosomes

Benign tumor: Arbud

Besan ka cheela: A baked gram flour bread

Bhang: Marijuana

Bharmari: A specific breathing exercise in yoga

Bhastrika: A specific breathing exercise in yoga

Bhed nidan: Differential diagnosis

Bhedaatmak nidan: Differential diagnosis

Bhedan: Piercer

Bhhagna tantu: Broken tissues in urine

Bhrajak Pitta: One of the five pitta humours necessary for skin colouration

Bhrukuti: Space between the two eyebrows

Bhujangasana: Serpent pose

Bhujapidasana: A yoga pose

Bhuta: Panch mahabhuta or Five great elements- earth, water, fire, ether and air

Biochemic:‘bios’ is a Greek word meaning chemistry or chemic

Biochemic therapy- Theory of 12 tissue salts

BMI: Body Mass Index

Boil: Masurika

Bradycardia: heart rate < 50/min

Brahan: To increase

Brahan ahaar-aushad: Medications for strengthening body tissues

Brahan nasya: Restorative nasal medicine

Brahan vasti: Restorative enema

Burfi: A sweet dish made of milk and sugar

Burning sensations in feet: Pada-Dah

Burning urination: Kledakshayajanya Dah

Cactus milk: Nagfani ka doodh

Castor oil: Arand tel

Cataract: Lingnash

Cervical spondolytis: Manya-stambh

Chakkar: Vertigo

Chakras:Psychic centres which provide spiritual energy to the body organs

Chakrasana:Pose like a wheel or a circle

Champi:Anointing oil over head


Changeri:Oxalis corniculata

Chapati:A baked bread


Chastity: Brahmcharya


Chedan:Lopping of substances

Cheena:Proso millet


Chi:Enegy in Chinese medicine

Chickenpox: Sheetala

Chikitsa sutras:Code of cures

Chinta-bhaya nari:Pulse of a person with worries and fear

Chintya virya:Established medicinal act



Chowmin:Chinese dish

Chronic colitis: Sangrahni

Chronic obstructive jaundice: Halimak

Chukander:Beet root

Chullika granthi:Thyroid

Chunchunahat:Tingling sensation

Cleaning: Shodhan

Cold allergy: Sheet-pitta

Cold feet: Pada-sheet

Cold season: Sheet ritu

Colitis: Grahni

Common cold: Pratishaya

Conjunctivitis: Vataja abhishyand

Crown chakra: Centre of spiritual energy over the head

Durgandh: Bad odour

Dusht meda: Abnormal lipid profile

Dushtiyukt beeja: Diseased genes

Dushyas: Abnormal bio-molecules in plasma, heterogenous tissues

Dysmenorrhoea: Nishpachadaharti

Dysuria: Mutra-krracha

Dagna:Superficial burning of spoilt parts

Dah:Burning sensation

Daliya: Porridge

Dantobhedak rog: A disease of the gums and teeth in infants

Daurmanasya: Emotional depression

Day routine: Dincharya

Decreased immunity: Pratirodhshamtakshaya

Decreased menstrual bleeding: Arajaska yoni

Deepan: Appetizer, which ignites jathragni, the fire of stomach

Deepan-pachan: Appetizer-digester

Deficiency conditions: Degeneration

Deh-sanshodhan: Body reformer or purifier

Dehydration  Delirium: Aptantrak

Dementia and forgetfulness: Buddhi hrash, Smriti naash

Dhaniya: Coriander

Dhanurasana: Pose like a dhanu– bow

Dharana: Concentration .

Dhatukshaya: Loss of vital body nutrients

Dhatukshayajanya madhumeha: Type 2 diabetes

Dhatus:Body tissues, also called ‘Lus Zun’ in tibetan medicine

Dhatwagni: Metabolizing enzymes of tissues

Dhauti: Cleaning of stomach

Dhokla: A local eating dish

Dhruva:A star

Dhumrapan:Medicated smoking ‘Inhalers’

Dhwajbhang: Impotence

Dhyana: Meditation

Dhyanasana: A pose for meditation

Diabetalogy: Study of diabetets

Diabetic vatik pad vrin: Non-healing diabetic foot ulcer

Dilatation of the heart : Vikartika Hirrdaya Rog

Din-charya: Disciplines of day life

Distension of abdomen : Affara

Doshas and dushyas: Body humours and vitiated body tissues

Dosha shanti: Subsiding of vitiated humours

Doshahar vasti: Enema which subsides humours

Doshakarak: Measures which produce abnormal humours

Down’s syndrome: Triosomy or translocation of chromosome 11, 66

Drava sweda: Liquid diaphoresis

Dravatwa: Liquidity

Dravibhootha medoama: Liquified immature fats

Drishti kshaya:Loss of eyesight

Drishtiheenta: Blindness

Drishtipatal vahini vikriti:Retinal angiopathy

DSME: Diabetes self management education

Dugdh: Milk

Dugdh vikar: Milk products

Dukh ayu: Unblessed age

Dukha: Pain

Durgandh: Bad odour

Dusht meda: Abnormal lipid profile

Dushtiyukt beeja: Diseased genes

Dushyas: Abnormal bio-molecules in plasma, heterogenous tissues

Dysmenorrhoea: Nishpachadaharti


Eka pada:One leg

Emchi: Tibetan therapy, Emchi and diabetes

Emesis therapy: Vaman treatment

Emphysematous cholecystisis: Pittakshaya shoth

Emphysematous cholecystitis- Clostridia bacterial infection of Gall Bladder

Endometrial hyperplasia: Yoni-kand

Energy: Tej

Epilepsy: Mirgi

Excrements: Malas

Extended anuvasan vasti: Retention enema

External sanshaman: Purification

Facial paralysis: Ardit

Ferrum phosphoricum: ferrum phosphate

Filariasis ‘elephant foot’: Shrilipaad

Fistula: Nari-vrin

Fistula in ano: Bhagandar

Folic Acid- pteroylglutamic acid

Foot ulcer: Vatik pada-vrin

Forehead chakra: A centre for spiritual energy situated in the middle of the forehead

Fracture bones:Asthi-bhang

Fruit kalp: Eating only fruits nothing else

Galgand: Thyroid swelling

Garbh-naash: Abortion

Garudasana: An eagle pose

Gastro-enteritis: Vishuchika

Gauri, lasika: Lymph

gchin-nyi: A pre-diabetic condition in Emchi

gChin-snayi: A diabetic condition in Emchi

Generalised abdominal discomfort: Vatodar

Ghee: Clarified butter

Gingivitis: Jivyah rog

Ginseng: ‘panax ginseng’

Gita: The holy book of the Hindus

Glucoma: Adhimanth


Gokhuru: Small Caltrops

Gomukhasana: A cow face pose

Gradhrasi: Sciatica

Grahi: Astringent

Grahni: Chronic colitis

Grishma ritu: Hot season

Gud pak: A disease of the infants

Gulab jal: Essence of rose flower

Gulab jamun: A sweet dish

Gulm: Distension of abdomen, Formation of a lump of air in abdomen

Guru: Heaviness

Habitual abortion: Sahaja garbhpat

Haematmasis: Raqt-pitta

Halasana:A pose of hala– plough

Hamsasana: A pose like a hamsa– swan

Hanmaans parikshaya: Myocardial degeneration

Hanmansopachiti: Hypertrophy of heart

Hastimeha: Lymphuria

Hatha Yoga: Difficult Yoga

Havishtha: A special food which is offered at the time of Yajna

Headache: Shir-rog

Healer: A person with high spritual power, capable of treating diseases by Pranic Therapy.

Heart fail: Hridgraha

Heen: Less

Heen kapha:Minimum increase in phlegm humour

Heeng: Astoefidia

Hemant ritu: Winter season

Hetu: Risk factors

Hicchki: Hic-cups

High blood pressure: Uchha raqtdab

Hit: Benefactors

Hit ayu: Beneficial age

Horripilation: Romharsh

Hot season: Grishma ritu

Hrid Dah: Retrosternal chest burning

Hrid shool: Vatik heart angina pectoris

Hrid stambh: Heart block and heart fail

Hridaya dah: Heart burn

Hridaya chakra: A centre of spiritual energy situated in the heart

Hridaya shula : Angina Pectoris

Hridgraha: Stopping of the heart

Hridjanya shwas: Cardiac asthma

Hridpradesha: Chest region

Hrit Griha: Ischemic heart disease

Hrithgraha: Heaviness in heart

Hrithstambh: Heart fail

Hritshool: Angina pectoris

Hydrocoel and hernia: Vriddhi rog

Hypertensive cardiomegaly: Hanmaanso-pachiti

Hypoglycemia: Atilanghan

Santarpan janya madhumeha: Obese Diabetes; T2D

Ikshumeha: Alimentary glycosuria

Imarti: A sweet dish

Immature abcess: Apripakva vrin

Incoherent behaviour: Pralapak

Incoherent talk: Pralaap

Indigestion: Ajeerna

Infected erruptions on whole body:Visphot

Infected gangrene:Vata-raqt

Infected wound:Agantuj vrin

Infection in blood: Advanced vata-raqt

Infection on penis: Shuk dosha

Infertility: Baanjhpan

Inflammation: Shofh

Inflammation in vertebral column:Dhanurvata

Inflammation of foot: Pada-shoth

Inflammatory foot: Vatik pada-shoth

Intentional bleeding: Raqt mokshan

Internal abcess: Antar vidradhi

Internal sanshaman: Internal pacification

Intestinal paralysis: Alsak

Ischemic heart disease: Vikshepika hridayrog

Jaharmohara: Serpent stone

Jal vayu: Season, Climate

Jalebi: A sweet dish

Jaleeya dhatus: Liquid nutrients

Jalini: Carbuncle with sieve like appearance

Jaliya: Watery substances

Jaliyansh: Water ratio

Jamalgota: Croton oil seed

Janmajaat vikriti: Congenital deformity

Janu Sirashasana: A Yoga posture

Jara: Premature ageing

Jara drishti: Presbiopia

Jarta: Rigidity

Jatah pramahi: Probable diabeic

Jatara Parivartanasana: Pose like a hill

Jatharagni daurbalya: Diseased digestive fire

Jathragni: The fire of stomach

Jaundice: Kamla

Javitri: Mace

Jeera: Cumin seed

Jeerna atisar: Chronic diarrhoea

Jeerna phuphsh shoth: Chronic lung infection

Jeshthikasana: A Yoga posture

Jhuchini: A Chinese herb

Jivhyastambh: Paralysis of the tongue

Jowar: A small grain


Jwar: Fever

Kaal: Time, Functional period

Kabavah: Piper cubeba

Kabj: Constipation

Kacchapika: A special type of boil in diabetics

Kachori: Stuffed fried chhapati

Kaju: Cashewnut

Kakthan: Gangrene

Kal samprapti: Duration of the illness

Kali muraiticum: Potash chloride

Kali phos: Potassium phosphate

Kali sulph: Potassium sulphate

Kalimirch: Black pepper

Kalmeha: One of the 20 types of prameha

Kama-krodha nari: Pulse of a person with anger and lust

Kamoshma: Basal metabolic requirement

Kamp: Tremors

Kanji: A home made drink, acidic juice

Kapalabhati: A breathing exercise which help in disciplining the brain

Kapha dosha: Water element, Phlegm

Kapha medodushti: Vitiation of phlegm with body fats

Kapha nari: Pulse of a patient suffering with excess of phlegm

Kapha praseka: Expectoration

Kaphajanya mutrakracch: Heaviness in urinary bladder along with pain

Kaphakarak: Foods and activities which increase kapha humour

Kapolarunya: Malar flush

Kapoor: Camphor

Karn shool: Ear-pain

Karna bhedan: Ear piercing

Karna-nad: Abnormal sounds in ears

Karya siddha: Capable of completing work

Kasa:  Cough- dry and wet

Kashay ras: Pungent taste food

Kasht sadhya: Treatable with difficulty

Kashtsadhya vyadhi: A disease difficult to cure

Kathin: Difficult


Kauni: Foxtail millet

Kaval: Mouth paste

Kayagni: Basal metabolism

Keto-acidosis: Raqtamlata

Khalli: Spasm in thigh, calf and lower arm muscles

Khand: A less purified sugar

Khar or Karkash: Harsh,Tough

Kheer: A sweet dish

Kheshkekala: Pedalium murex

Kidney failure: Vrrika sanyas

Klebyata: Impotence

Kleda: Water driven out of protoplasm and plasma and accumulating in urinary bladder as urine

Kledan: One which stirs

Klinefelter’s syndrome: karyotype 47 xxy; mosaics

Klom vyadhi: Pancreatitis

Klum: Early fatigue

Konda: A cereal

Krishta: Asthenia

Kriyas: Actions

Kruddha vata humour: Aggravated wind

Kshetra: Amniotic fluid

Kshut: Minimising food

Kubjta: Hunchback

Kukunak rog: A disease of the infants

Kulaja roga: Familial disease

Kulla: Gargling

Kumbhak: Holding of breath in pranayama

Kussmaul’s respiration: Rapid respiration followed by a long pause

Laghu: Small, Lightness

Langhan: Omission

Laryngitis: Swar-bhang

Lasika: Lymph

Lassi: Curd diluted with water

Laulyam: Polyphagia

Laulyam: Pleasurable eating

Lavan ras: Salty foods

Lavang: Cloves

Lekhan: Thinning of the body

Lekhan vasti: An enema which brings smallness in the body

Lepan: Besmearing

Leucorrhea: Shweta pradar

Lingnaash: Cataract

Lock jaw: Hanugrah

Lohit/dhamni: Artery

Lolata: Desire to eat more

Loong: It is a type of kaphaj prameha

Loss of sensation: Twakshoonya

Loss of sensation in foot: Vatik pada-shoonya

Lower respiratory tract infection: Urakshata

Lus-zun: Nutrients in the plasma in Tibetan therapy

Maadira: Barnyard millet

Maans: Muscles

Maans dhatu: Muscles

Maans sankoch: Muscular atrophy

Maansgat fats: Muscular fat

Maanskshaya: Muscular atrophy

Maansvah shrotas: Channels through which nutrients for muscles flow

Madak: Intoxicating

Madhutelak vasti: Enema with nutrient substances

Madhumeha: Diabetes mellitus

Madhumehaj drishtipatal vikriti’: Diabetic retinopathy

Madhumehaj Vrikka Vikriti: Diabetic nephropathy

Madhur ras: Sweet relish

Madhusudini: A gland which secretes pittagni

Madhya: In between

Madhyam: Medium or average

Madhyam pitta: Medium increase in pitta/bile

Mahatyaya: Life threatening

Majja: Bone marrow and white cerebral tissue

Majja-shool: Lancinating pain inside bones

Majja-shosh: Depletion of bone marrow

Majjameha: Albuminuria

Majjavah shrota: Channels through which nutrients flow for majja

Makarasana: Dolphin pose

Makshika sarpan: Flies on body

Malavrodh: Intestinal obstruction due to faeces

Mal sanchaya: Accumulation of excreta in body

Malabaddhatha: Stool binding

Maladrav: Faecal fluid

Malas: Excretions

Malignant otitis externa: Infection with Pseudomonas aeruginosa in middle ear

Mana or Chitta: Brain

Mand: Feeble/Dullness

Mandagni: Less digesting energy due to increased kapha or phlegm

Mandua: Finger millet

Mansopachit: Diabetic cardiomyopathy

Mansopachaya: Pseudohypertrophic muscular atrophy

Mantras: Holy chants

Mardan: Rubbing and body massage

Marichyasana: Pose of Marichi- a sage

Marut: Taking in air

Mastishk vikar: Diseases of the brain

Matsyasana: A pose like a fish

Mature abcess: Paripakva vrin

Maya: Craze for physical things

MCG: Magnetic cardiogram

Meda dhatu: Adipose tissue

Medagni: The metabolizing energy of the fats

Medications: Aushadh

Medo-ama: Abnormal immature lipoproteins

Medovah shrotas: Channels through which raw material for adipose tissues flows

Medovahashrotas avritatva: Obstruction of fat channels inside human body

Medovardhak: Increase adipose tissues

Meetha: It is poison

Meghavardhani drug: Increasers of intelligence

Meng meinchakra: Centre of spiritual energy

Menorrhagia: Raqt-pradar

Meridian: Imaginary electro-magnetic lines over the body

Methi: Fenugreek

Metrorrhagia: Vataj raqt-pradar

Mkhrispa or tripa type: A type of diabetes in emchi

Moh: Altered sensorium

Moh-Moorcha: Semi-consciousness

Mookta: Dumbness

Moonga bhasma: Ash of coral stone

Moorcha: Unconciousness

Mriduta: Softness

Mudras: Definite body poses in which extremities are locked with each other to prevent loss of vital electricity generated during Yoga

Mukta hasta: Untied hands

Mutra jathar: Severe pain below the navel

Mutra vahi shrota: Channels in which urine flows

Mutraansh: Body water used for making urine

Mutraghat: Obstructive uropathy

Mutragranthi: Sudden development of stone like structure at pubic region which is very painful

Mutrajathar: Distended urinary bladder

Mutrakracch: Painful uropathy

Mutrakshaya: Suppression of urine

Mutrasad: Scanty urination

Mutrasanga mutrakracch: Piercing pain in micturition

Mutrasankchya: Burning and scanty micturition

Mutrashukra: Semen flows the wrong way into urine

Mutrateet: Incontinence of urine

Mutravaha shrotas: Glomerulus

Mutroksaad: When urine is dry, yellowish and burning is also present duing micturition

Mutrotasang: Sudden stoppage during micturition gives rise to this problem

Nabhi: The navel

Nadi sodhana: Purification of nerves

Nari shoth: Neuritis

Naswaar: Tobacco or medication through nose

Nasya ‘shiro virechan’: Nasal medicine

Natrum muraiticum(Nat.mur): Sodium chloride

Natrum phosphoricum: Sodium phosphate

Natrum sulphuricum: Sodium sulphate

Nauli: Churning of stomach muscle and inducing vomiting

Nausea and vomiting: Jee-michalana, vaman

Navasana: A very useful yoga practice in diabetes

Navel chakra: Centre of spiritual energy at navel

Neela/Shira: Vein

Neelmeha: Indicanuria

Neem tree: Margosa

Neembu Ghas: Cymbopogon Citratus

Nephritis: Vata-vasti

Nephrotic syndrome: Vrikka jalodar

nes pa: In Emchi the three body humours

Neti: Cleaning of nose and throat

Netra madhyapatal shoth: Choroiditis

Netra pratighat: Opthalmoplegia

Netrabhyantar patalasth vibransh: Detachment of retina

Neurogenic pain: Snayu-shool

Nidaanarthakara vyadhi: Modifiable risk factor

Nidan: Diagnosis

Nidra: Sleep

Nidranaash: Disturbed sleep

Night routine: Ratricharya

Night blindness: Rattondhi

Nimbu pani: Lemon juice in water

Niralamba Sarvangasana: A head down Yoga pose without support

Nirbija Samadhi: Contemplation without seed

Niruh: Decoction enema

Niruhan: Dislodging of substances

Nishpichadaharti: Dysmenorrhea

Nishthapak: Assimilation of food

Nitya karma: Daily chores

Niyama: Laws

Non healing foot ulcer: Vata-Raqt-Kapha

Obstruction of wind/faeces: Aadhman, Aanah

Oja or ojus: Essence of all dhatus, body tissues

Ojakshaya: Loss of oja

Ojomeha: Loss of oja in urine, Diabetes mellitus

Ojopchhar: Treatment for oja rejuvenation

Oligozoospermia: Shukranukshaya

Optic neuritis: Netra-narishoth

Osteomylitis: Baahya vidradhi

Pachak pitta: Bile for digestion

Pachan: Fine digestion

Pachan ayushad: Digester

Pacification: Doshas shaman

Pad dah: Burning in feet

Pad harsh: Hyperasthesia

Pad sheet: Coldness in feet

Pad shofh: Swelling of the feet

Pad shoonya: Complete loss of sensations in feet

Pad vidirnata: Torn up skin of the foot

Pad-sheet: Cold feet

Pad-supti: Loss of sensations in leg

Padam: Lotus flower

Padmasana: A lotus pose

Pain during intercourse: Vipluta yoni

Pain in abdominal organs: Udavrat

Pain in eyes: Vataj netra-shool

Painful distension of abdomen: Adhman

Painful swelling of vagina: Parilupta yoni

Painful vagina: Yoni shool

Painful vagina with discharge: Uppluta yoni

Pak: Proper digestion of food

Pakkwatisara: Bacterial diarrhoea

Pakora: A fried potato dish

Pakshaghat: Hemiplegia

Pakwa mal: Formed stools

Pancha-Mahabutas: Five great elements

Panchbhutic swaroop: Constitution of human body as per these five great elements- earth, fire, water, ether and air

Pancreatitis: Klom-rog

Pandu rog: Anemia

Panduta: Paleness

Panelu: Pale Body

Pankreas (French)- Pancreas

Papad: A salted snack

Paralysis: Pakshaghat

Parigarbhik: Intra uterine

Parsva: Flank

Parsvaika pada: Leg on side

Parsvottanasana: Parsva– side/flank, a Yoga pose

Parthiv dravyas: Earthly substances

Partial blindness: Timir rog

Parvatasana: A mountain pose

Paschimottanasana: A Yoga pose, paschima– west

Pashrva shool: Chest pain

Patanjali: Founder of Indian Yoga

Peripheral neuritis: Ugrasnayuvata

Pharyngitis: Gala rog

Picchil: Sliminess

Picchil vasti: Enema which produces stickiness

Pichhilatwa: Stickiness

Pidika: Boil or carbuncle

Pidikayen: Several boil

Pin-prick sensation on body: Vata twak shool

Pinasa: Rhinitis

Pipasa: Thirst

Pishtameha: Severe phosphaturia

Pitta: Bile

Pitta dosha: Fire element, a body humour

Pitta nari: Pulse of a person with diseased pitta

Pitta Humour: A substance which helps producing energy in human body

Pitta-kapha nari: Pulse of a person with diseased kapha-pitta

Pittagni: Insulin

Pittaj klebya: Impotence due to vitiated pitta

Pittaj: A disease arising out of increased pitta

Pittajanya mutrakracch: Fire burning pain in urethra during micturition due to excess pitta

Pittakarak: Foods/activities which increase pitta

Plavani: A specific type of Pranayama

Pleeha chakra: Energy centre at spleenic area

Pleeha vriddhi: Enlargement of the spleen

Poisonous animal bite: Vish dansh

Polydipsia: Trisharog

Polyphagia: Bhashmak rog

Polyuria: Bahumutratha

Prabhav: Effect of a medical measure

Prabhuthamutratha: Excess urination

Pradeshik dah: Burning sensation on an organ

Prakriti: Nature

Pramada: Unsettled mind

Pramathi: Scavenger

Prameha: Turbid and excess urine

Prameha nashak: Destroyer of prameha

Prameha pidika: Boils and carbuncles in prameha

Pran: The vital energy which flows in the body

Pranaghna: Life threatening

Pranayama: Specific breathing exercises

Pranic energy: Spiritual energy

Pranic therapy: Healer treats diseases with his spiritual energy

Pranvah shrotas: Channels through which pranas move inside the body

Prapan: To fulfill

Prashaman: Pacification

Pratisaran: Toothpaste

Pratishyay rog: Catarrh

Pratishyaya: Common cold

Pravahika: Diabetic diarrhoea

Pravar: Superior

Prayashchit: Penance

Pre-diabetes: gChin-snayi in emchi

Premature ageing of hair: Palit rog

Prinam: To satisfy

Psharmeha: Alkalineuria

Pulsation: Dhamni pradhaman

Purak: Inhalation

Purishvah shrotas: Pores through which excreta gets out of the body

Purnamasi: A night with full moon

Purva rupa: Prodormal symptoms

Purva vrikkiya: Pre nephrotic

Pushti: Nourishment

Puti mamsa: Muscular degeneration

Qi: Energy, in Chinese medicine it is called chi

Ragi: A cereal

Rainy season: Varsha ritu

Raisin: Munnaka

Raja Yoga: Supreme stage of Yoga

Rajas: Immobile, static

Rajasic: With inertia

Ranjak pitta: One of the five type of pitta humour

Raqt: Blood

Raqt dhatu: Blood and its constituents

Raqt mokshan: Intentional bleeding

Raqt-pitta: Ketosis

Raqtatisara: Bloody dysentry

Raqtmeha: Hematuria

Raqtvah shrota: Channels in which blood flows

Ras: Nutrients in plasma

Ras shira: Hepato-portal vein

Rasayan: Substances for strengthening of body

Rasayan chikitsa: Alchemy treatment

Rasvah shrotas: Channels in which body fuel circulates

Ratri-charya: Disciplines of night living

Rechan: To exhale, Laxative

Renal colic: Vasti-shool

Retinal detachment: Netrabhyantar patalasya vibhran

Retinopathy: Antah-patal ka rog

Retrosternal burning: Hriday-dah

Rhinitis: Peenus

Ritu: Season

Ritu charya: Disciplines of living in a season

Rochak: Appetizer

Roktham: Prevention

Romharsh: Asthesias and parasthesias

Roopan: Healing of the wound

Ruksh: Dry

Rukshan: Drying of the body

Rung or loong type diabetes

Rupa: Prodormal symptoms

Saatamya ahaar: Regimen diet

Sabija Samadhi: Contemplation with some thought

Sacroillitis: Trikshool

Sadhak: One who practices Yoga

Sadhya: Curable

Safra: A body humour

Sahaj Yoga: Easy Yoga

Sahaja: General, Since birth

Sahaja klebya: Hereditary impotence

Sahaja medorog: Hereditary obesity

Salabhasana: Pose like a salabha- a locust

Salamba Sarvangasana: Salamba- with support

Salamba Sirshasana: Headstand with support

Salvan: Lepan by oil comprising ample quantity of salt

Samadhi: Contemplation

Samadhist awastha: State of contemplation

Saman: One of the five vayu humours in the body

Samanya adhimand: Simple glaucoma

Samanya madhumehaja drishtipatal vikriti: Simple retinopathy

Samanya rupa: General features

Samanya samprapti: General pathogenesis

Samitoshna: Neither hot nor cold

Samprapti: Pathogenesis

Samyak ahaar: Regimen diet

Samyoga: Eating systematically

Sandhi-bhang: Joint damage

Sandhidrava: Synovial fluid

Sandhigatah: Into the joint

Sandrameha: Phosphaturia

Sandratwa: Concentrate

Sanghaniya muscles paralysis: Ciliary paralysis

Sangrahak: Absorbents

Sangrahi: Accumulator

Sangrahni: Colitis

Sangyanash: Anaesthesia

Sangyashoonya: Numbness

Sankatasana: A Yoga pose

Sannipataj diseases: Where all humours are vitiated at once

Sannipataj mutrakracch: Severe urinary infection

Sanshaman: Pacification

Sanshamaneeya vasti: Dosha pacifying enema

Sanshodhan: Purification

Sanskar-bhed: Consecration

Santap: Feeling of intense weakness

Santrashan: Severe diarrhoea with medicines

Samyog: Eating properly

Sapta-dhatuvah shrotas: Channels through which all seven vital dhatus flow in human body

Sarpimeha: A type of vataja prameha

Sarshapika: A specific type of boil

Sarv ras ahaar: Diet containing all nutrients

Sarva guna: Full of all good qualities

Sarva virya: Both powers of coolness and warmth in a substance

Sarvangadah: All types of good smells

Sarvangasana: A Yoga pose

Sarvras: All relishes

Satalu: A food

Sattva: Pure, Pureness and goodness of everything in nature

Satyanarayan diwas: The day on which lord Satyanarayan is worshiped by Hindus

Savasana: A corpse pose; posture like dead man

Savda: The name of kapha humour in Tibetan medicine

Scanning: A method of treatment in Pranic therapy

Schizophrenia: Unmad

Sciatica: Gradhasi

Scleredema: Twacha sankoch

Scrotal infection: Vrashan krachhu

Semi-coma: Sanyas

Semi-consciousness: Ardh-moorcha

Septicemi: Visarp

Setu bandha: Bridge formation

Severe loose motions: Pravahika

Severe pharyngitis: Mukhpak

Shabdavahi shrota: Larynx

Shaithilya: Low energy

Shaman: Pacification

Shanermeha: Obstructive uropathy

Shanti karma: Prayer therapy

Sharad ritu: Winter season

Sharavika: A specific type of boil in diabetes

Shareerastha kleda: Body fluids

Sharkara mutrakracch: Sand like particles obstruct the urinary tract and produce pain

Shastrokta: As per religious books

Sheet kal: Winters

Sheet-virya: Substances wih ‘cool’ property

Sheetameha: Renal glycosuria

Sheetjanya dhatu vinash: Reynold’s disease

Sheshagni: The metabolizing enzymes of the different nutrients and tissues

Shirshool: Headache

Shira: Arteries and veins

Shira griha: Obstruction in blood vessels

Shira shool: Ischemic pain

Shira-grah: Atherosclerosis

Shira-mokshan: Intentional bleeding

Shira-sankoch: Ischemic diseases

Shiravrodh: Obstruction in arteries and veins

Shirovasti/nasya: Nasal drops or spray

Shirsasana: A Yoga pose with head down

Shishir ritu: Cold season

Shleshmak: Mucus/smoothness

Shock: Aptanak

Shofh: Oedema

Shool: Pain

Shool: pain in body parts

Shool: pin-pric pain

Shool: severe piercing pain

Shool and dah: Pin-prick and burning sensations

Shosh: Asthenia, body look of a tuberculosis patient

Shosh and Jeerna Phuphus Shosh: Pulmonary tuberculosis

Shoth: Inflammatory swelling

Shrava: Secretions

Shrotavrodh: Blocking of the body pores and the channels

Shuddhi: Purification

Shukra: Reproductive tissue, semen and atarva

Shukra dhatu: Semen, atarva and ojus

Shukra-heenta: Semen deficiency

Shukradosha: Oligospermia

Shukrakshaya: Loss of semen

Shukral: Spermatic

Shukrameha: Spermatorrhoea

Shukranu: Sperms

Shukravah shrota: Channels through which reproductive material flows

Shula: Neurogenic pain

Shushk kasa: Dry Cough (vata)

Shwas: Breathlessness

Shwasan rogi: Patient with lung infection

Siddh vasti: A special type of enema

Siddha yog: Proved medicine

Siktameha: Lithuria

Silajeet suddha: Pure essence of hard rocks

Similia similibus curentur: The principle of homeopathic medications

Sir: Mobility due to gravitational force or heaviness

Sitali: A special type of Pranayama

Sitkari: A special type of Pranayama

Skin abrasions: Pada-twak vivarnta

Snayu: Ligaments, tendons

Snayu shool: Neuralgic pains

Snayugat: Within the ligaments

Sneh nasya: Oily nasal drug

Sneh-dhu: Smoke of medicated oils

Snehan: Oleiation therapy

Snehan: Oiling of the body tissues

Snehan: Oils/ghee in food

Snigdh: Oiliness/greasiness

Solar plexus chakra: Centre of spiritual energy in the ribs of the chest

Somagun: Water content

Sookshm: Fine/minuteness

Sparsh-shool: Parasthesias

Spermatouria: Shukrameha

Sprain in ankle: Vata-kantak

Stabilizing: A technique used in Pranic therapy

Stambh: Rigidity, Sudden stopping

Stambh or Jarta: Difficulty in movement

Stambhan: Obtrusive therapy

Sthir: Firm/steady/immobile

Sthul: Bulky

Sticky vagina: Pischil yoni

Stomatitis: Mukh pak

Suchi: Refers to needle

Suchi shastra: Science dealing with the use of the neddle

Suchi tod: Piercing of the needle

Sugandha: Pleasant odour

Sukh ayu: Blessed age

Sukh sadhya: Easy to cure

Supari: Betel nut


Supt hridaya shool: Silent myocardial ischemia

Supti: Loss of touch sensation

Surameha: Acetoneuria

Surya Namaskara: Morning prayer of Sun God

Sushmma nadi: Spinal cord

Swastikasana: Swastik is a holy symbol- a body pose like swastik

Swedadhikya: Excess of sweat

Swedan: Perspiration

Swedan: Medicinal perspiration

Swedavah shrotas: Pore through which sweat flows

Swedavrodha: Obstruction of pores through which sweat flows in body

Swelling on foot: Pada-shofh

Syphilis: Firang

Tadasana: A mountain pose

Takra: One third curd and rest water-stirred well

Talukantak rog: A disease of the infants

Tamaladi vishaj drishtimaandh: Tobacco amblyopia

Tamas: Loss of vision, darkness

Tap sweda: Temperature perspiration

Taramandal shoth: Iritis

Teekshagni: Increased metabolic rate due to pitta excess

Teekshan nasya: Shiro virechan, Acrid nasal drops

Teekshna: Sharp, Acrid

Tennis elbow: Upbahuk

Thyroid gland: Chullika granthi

Tikt ras: Acrid

Time factor: Kaal

Tingling sensation in feet: Pada-harsh

Tod: It refers to enter/to pierce

Trataka: To gaze

Traumatic mutrakracch: Painful obstruction and retention of urine

Tridosha nari: Pulse of a person with all three humours vitiated

Tridoshaj: Having all three vitiated humours

Triphla: Avla (emblic myrobalan)+Harad (myrobalans)+Bahera (beleric myrobalans)

Trisha: Excessive thirst

Trishna: Desire

Trisutra: Three codes

Trit/trisha: Keeping thirsty

Tulya dosha dushyata: A principle of ayurveda to decide curability or incurability of a disease

Tundi rog: A disease of the infants

Tushti: Satisfaction and contentment of all 10 sense organs

Twacha rog: Skin diseases

Twag-shosh: Drying and mild swelling

Twak shoonya: Loss of sensation

Ubtan: Anointing herbal ointment

Udakmeha: Diabetes incipidus

Udakvahi shrota: Channels present at the palate and the pancreas

Udan: One of the five vital wind humours

Udarshool: Pain in abdomen

Udavarta: Pain in abdomen due to wind

Udharvakshepan: Throwing up

Ugravat: Excess wind

Ujjayi: A special type of Pranayama

Unani hakims: Physicians practisizing in Unani therapy

Unconsciousness: Apatanak

Unmad: Insanity, madness

Upadrav: Complications

Upkshaya: Management/treatment

Upnah sweda: Medicated perspiration

Upnishada: Most ancient holy scriptures

Uptarakamandal shoth: Iridocyclitis

Uranium nitrate: Moriate

Urdhva padmasana: A lotus like pose

Ushanavata: Urination with difficulty

Ushn: Warm/Hot

Ushn kal: Summer season

Ushn sweda: Hot fomentation

Ushn vata vrikka: Infection of urinary system

Ushn virya: Substances with warm property

Ustkhaddus: Brunella vulgaris

Utkatasana: Sitting on an imaginary chair

Utkleshan: Pulling out forcefully

Uttanasana: Hand to foot pose

Uttar vasti: Enema through vagina/rectum

Uttarayan or Adankal: The period in which the sun is nearest to the earth

Utthita Trikonasana: Extended triangle pose

Vaginitis ‘candidiasis’: Yoni sankraman

Vama Pavanamuktasana: A Yoga posture

Vaman: Vomiting

Vamankarak: Substance which induces vomiting

Varsha ritu: Rainy season

Vasa: Fat

Vasameha: Lipouria

Vasti: Combined name of kidney, urinary bladder, nephrone, ureter etc.

Vasti: Enema, Enema fluid

Vasti bhed: Pain in urinary system

Vasti dushti: Diseased urinary system

Vasti shool: Renal colic pain

Vasti tod: Peircing pain in urinary system

Vasti vikar: Urinary system disorders

Vata: Wind

Vata dosha: Air humour ‘air element’

Vata Moorcha (amlotkarsh): Ketotic coma

Vata nari: Peripheral nerves

Vata vasti: Retention of urine

Vata-kapha nari: Pulse of a person suffering from

Vata-pitta nari: Pulse of a person suffering with

Vatadusti: Vitiation of vata humour

Vataj abhishyand: Conjunctivitis

Vataj adhimand: Glaucoma fulminans

Vataj gulm: Gaseous distension of abdomen

Vataj prameha: One of the 20 types of prameha

Vataj shir rog: Diseases of the head due to vata

Vatajanya mutrakracch: Tearing pain in urinary bladder along with urethra

Vatakarak: Foods and acivities which increase vata humour

Vatakundalika: Painful dribbling of urine

Vatanari shoth: Peripheral neuritis

Vatasthila: A prostate disorder in which there is dribbling of urine

Vatavasti: Painful obstruction of urine

Vata vikar: Diseases due to vitiated vata

Vatik mutraghat: Autonomic bladder

Vatik pad shoth: Inflammation in leg tissues

Vatik pratishyay: Common cold

Vatik udar rog: Generalised enlargement of the abdominal organs

Vatik vrin: Non-healing ulcer

Vatikdhatukshaya: Loss of body tissues due to vitiated vata

Vayu shaman: Pacification of vata dosha

Vayviya: Airy substances, dispersible, diffluent

Vedas: The sacred scriptures of the Hindus

Vedotpattik: One which is originated from vedas

Vicharan: Thought provoking

Vichushika: Cholera like disease

Vidahi: Very sour, inflammatory

Vidarika: Big abcess

Videah: One which can be mixed in any herbal drug

Vidradhi: Deep seated infection

Vidradhika: A special type of boil in diabetics

Vikashi: Dryer of ojus

Vikratih: Distorted

Vikshepika hridaya rog: Angina pectoris

Vilapi: Viscous food

Vilodan: Vigorous stirring

Vinita: A specific type of boil in diabetics

Vipak: Digestion

Viprita karani mudra: Reverse body posture

Virabhadrasana: Virabhadra was a powerful man created by Lord Shiva to destroy evil people. This yoga posture is named after him

Virasana: A champion pose

Virasta: Tastelessness in the mouth

Virechan: Intestinal cleaning

Virya: Power of a substance

Virya kshayajanya klebya: Exhaustive impotence

Viryavardhak: Spermatogenic

Visarp: Septicemia

Vish: Poison

Vishad: Anti-humid and rigid

Vishadatwa: Clearness

Visham dharmi: Having opposite properties

Visham drishti: Astigmatism

Visham kriya: Heterogenous reaction

Vishesh rupa: Specific features

Vishmagni: Disordered body metabolism due to excess of vata humour in the body

Vishta: Excreta

Vishtambhi: Increases abdominal gas

Vishwachi: Carpel tunnel syndrome

Vishwachi: Frozen shoulder

Vishtambhak: One which increases and obstructs vayu in intestines

Visuchika: Cholera like symptoms

Vitiate: Dooshit

Vomiting : Vaman

Vrakkanu: Nephrones

Vrashan-shool: Pain in testicles

Vrashya: Spermatogenic

Vrikka sanyas: Renal shutdown

Vrikka shoth: Nephropathy, Nephritis, swelling in kidneys

Vrikkakathinyatajan: Nephro-sclerotic stage

Vrikkiya awastha: Nephrotic stage

Vrikshasana: A tree like pose

Vrin: Infected Ulcer

Vrin ropar: Wound healer

Vrishanaavadarana: Scrotal skin infection

Vrishti kal: Excessive raining

Vyadhi: Disease or disorder in body

Vyadhi har: Removing of disease

Vyadhi prabhav: Characteristic features of a particular disease

Vyan: One of the five vata humours

Vyapat: Deformation

Vyayama: Exercises

Wet cough: Kaphaj kaas

Wrinkles on face: Jhaain

Wrist stiffness: Vishwachi

Yaapya: Palliable diseases

Yagyopaveet: A sacred thread worn by Hindus

Yakrat shoth: Hepatitis

Yang: Strong

Yapan vasti: Digestive and diarrhoeal enema

Yavago: Semi-solid food

Yin: Weak

Yog: Combination of herbs

Yoga nidarasana: A body posture

Yoga sutras: Aphorism of yoga

Yogamudra: A body posture

Yogasanas: Body postures

Yogvahi: Medium

Yon chakra: It is situated in lower abdomen

Yuktarath vasti: A special type of enema

Za-khu: It is body’s water ‘kleda’


Note :- (h) stands for Hindi, (e) stands for English, (l) stands for Latin

Indian medicinal herbo-minerals for the treatment of diabetics.


Aak (h), Mudar (e), Calotropis gigantea (l)

Aam (h), Mango (e), Mangifera indica (l)

Aarcha (h), Pheum qustrale (l)

Abhrak bhasma (h), Ash of mica (e)

Abutilon indicum (l), Indian mallow (e), Atibala (h)

Acacia arabica (l), Acacia tree (e), Babool (h)

Acacia catechu (l), Black catechu (e), Kher (h)

Aconite leaved kidney bean (e), Phreseolus (l), Moth (h)

Aconitun heterophyllum (l), Indian atees (e), Ateesh (h)

Adrakh (h), Ginger root (e) Zingiber officinale (l)

Adusa (h), Malabar nut (e), Adhatoda vasica (l)

Aegle marmelos (l), Bengal quince (e), Bel (h)

Agar (h), Eagle wood (e), Aquilaria agallocha (l)

Agast (h), Mimusops elengi (l)

Aquilaria agallocha (l), Eagle wood (e), Agar (h)

Ajmod (h), Gelery fruit (e), Apium graveolens (l)

Ajwain (h), Ajova seeds (e), Ptychotis ajowan (l)

Akarkara (h), Pellitory root (e), Anacyclus pyreth (l)

Akhrot (h), Walnut (e), Juglans regia (l)

Allium sativum (l), Garlic (e), Lahsun (h)

Allua (h), Common Indian aloe (e), Curacao aloe (l)

Almond (e), Badam (h), Prunus amygdalus (l)

Aloe vera (e), Aloe barbadensis (l), Gheekuwar (h)

Aloo-kashthalu-kandalu-pindalu (h), Potato (e), Dioscorea (l)

Alsi ka tel (h), Linseed oil (e)

Amaltash (h), Pudding pipe tree (e), Cassia fistula (l)

Amchur (h), Dried rind of raw mango (e)

Amia haldi (h), Mango ginger (e), Curcuma amada (l)

Amil ke phal (h), Salicifolia’s fruit (e)

Amorphophallus kanjae (l), Kanjae mannam (e)

Amrood (h), Guava (h), Pasidium guava (l)

Anantamool (h), Indian sarsaparilla (e), Hemidesmus Indicus (l)

Anar (h), Pomegranate (e), Punica granatum (l)

Angoor (h), Grapes (e), Vitis vinifera (l)

Anthocephalus kadamba (l), Wild cinchona (e), Kadam (h)

Aparajita (h), Winged leaved clitoria (e), Clitoria ternatea (l)

Apple (e), Sev (h), Pyrus malus (l)

Apricot (e), Khubani (h), Prunus armeniaca (l)

Arachis hypogea (l), Groundnut (e), Moongphali (h)

Arand (h), Castor oil plant (e), Ricinus communis (l)

Arbi (h), Colocasia antiquorum (l)

Arhar (h), Pigeon pea (e), Cajanus Indicus (l)

Arjun (h), Arjuna myrobalan (e), Terminalia arjuna (l)

Arni (h), Premna integrifolia (l)

Artemicia Maritima (l), Worm wood (e), Kirmani azawain (h)

Ashok (h), Saraca Indica (l)

Ashwabala, Methi (h), Fenugreek (e), Trigonella foenum graecum (l)

Ashwagandha (h), Winter cherry (e), Withania somnifera (l)

Asparagus adscendens (l), Shweta musali (h)

Asparagus racemosus (l), Shatavari (h)

Atees (h), Indian atees (e), Aconitum heterophyllum (l)

Atibala, Kanghi (h), Indian mallow (e), Abutilon Indicum (l)

Avla (h), Embelic myrobalan (e), Embelica phyllanthus (l)

Azadirachta indica (l), Margosa (e), Neem (h)

Ajwain (h), The Bishop’s weed,Ajova seeds (e), Ptychatis ajowan (l)


Baanjak- koda (h), Paspalum scrobiculatum (l)

Babool (h), Acacia tree (e), Acacia arabica (l)

Bada Gokhuru (h), Big caltrops (e), Pedalium murex (l)

Badam (h), Almond (e), Prunus amygdalus (l)

Badi muli (h), Big sized radish (e), Raphanus sativus (l)

Badi neem (h), Neem tree (h), Melia azadirachta (l)

Badi-elaichi (h), Greater cardamom (e), Amomum subulatum (l)

Baheda (h), Beleric myrobalans (e), Terminalia belerica (l)

Baingan (h), Bringal (e), Solanum melongena (l)

Bajra (h), Millet (e), Pennisetum typheideum (l)

Bakayan (h), Persian lilac (e), Melia azedarach (l)

Balsamodendron mukul (l), Indian bdellium (e), Gugal (h)

Bala or Khareinthi (h), Country mallow (e), Sida cordifolia (l)

Balchad (h), Spikenard (l), Nardostachys jatamansi (l)

Baliospermum montanum (l), Crotten seeds (e), Danti (h)

Bambusa arundinacia (l), Vanshlochan (h)

Banana (e), Kela (h), Musa sapientum (l)

Bar (h), Banyan tree (e), Ficus bengalensis (l)

Bariyara (h), Country mallow (e), Sida cordifolia (l)

Barley (e), Yav (e), Hordeum vulgare (l)

Basa (h), Malabar nut (e), Adhatoda vasica (l)

Base (e), Kshar (h), Impure carbonate of soda (l)

Bashinda, Kamalnaal (h), Lotus stem (e), Nelumbium speciosum (l)

Basmati (h), A variety of rice

Bater (h), Pheasant (e)

Bathua (h), Lambs quarters (e), Chenopodium album (l)

Beetroot (e), Chukander (h)

Bel (h), Bengal quince (e), Aegle marmelos (l)

Bel giri (h), Fruit pulp of bengal quince

Belia pippal (h), Ficus retusa (l)

Ber (h), Plum (e), Zizyphus jujuba (l)

Berberis aristata (l), Indian berberry or Wild turmeric (e), Daruhaldi (h)

Bhaat (h), Cooked whole rice (e)

Bhang (h), Indian hemp (e), Cannabis sativa (l)

Bharangi (h), Clerodendron serratum (l)

Bhasma of sevar (h), Ash of Vellisneria spiralis (l)

Bhatkataiyya (h), Solanum xanthocarpum (l)

Bhillava (h), The marking- nut tree (e), Semecarpus anacardium (l)

Bhring Raj (h), Eclipta alba (e), Eclipta alba hassk (l)

Bicchu grass (h), Girardina heterophylla (l)

Bijasar (h), Indian kino tree (e), Pterocarpus marsupium (l)

Bijore lemon (h), Citron (e), Citrus medica (l)

Bilvadi panchmool- bel, gambhari, arni, pathal and sonapatha or arlu mool (h), Roots of Aegle marmelos, Gmelina arborea, Premna integrifolia, Stereospermum suaveolens, and Oroxylum Indicum respectively

Bimbi (h), Ivy- gourd (e), Coccinia Indica (l)

Bitter gourd (e), Karela (h), Momordica charantia (l)

Black berries (e), Jamun (h), Eugenia jambolana (l)

Black gram (e), Chana (h), Cicer arietinum (l)

Black musali (e), Curculigo orchioides (l)

Black pepper (e), Piper nigrum (l)

Black salt (e), Kala namak (h), Unaqua Sodium chloride (l)

Boerhaavia diffusa (l), Hogweed (e), Punanarva (h)

Boswellia sesrata (l), frankincense, Shallaki (h)

Brahat panchmool- bel, gambhari, arni, pathal and sonapatha or arlu mool (h), Roots of Aegle marmelos, Gmelina arborea, Premna integrifolia, Stereospermum suaveolens, and Oroxylum Indicum respectively

Brahmi (h), Bacopa (e), Bacopa monnieri (l)

Brahmkamal (h), Saussurea obvallata (l)

Brinjal (e), Baingan (h), Solanum melongena (l)

Buffalo, Bhainsa (h)

Burans (H), Rhododendron arboraum (L)

Butter (Cow milk) butyrum, Makkhan (h)

Butter milk, Chaach (h)


Cactus (e), Nagfani (h)

Camphor (e), Kapoor (h), Camphora (l)

Cardamom (e), Ilaichi (h)

Carrot (e), Gajar (h), Daucus carota (l)

Custard-apple (e), Sharifa (h), Annona squamosa (l)

Cassia auriculata (l), Avartaki (h)

Cashewnut (e), Kaju (h), Anacardium occidentale (l)

Chukander (h), Beet (e), Beta vulgaris (l)

Chest nut (e), Akhrot (h), Juzlans regia (l)

Cheena (h), Proso millet (e), Panicum miliaceum (l)

Cassia fistula (l), Pudding pipe tree (e), Amaltas (h)

Clove (e), Laung (h), Caryophyllus aromaticus (l)

Cacao seeds (e), Cocoa (l)

Castor seeds (e), Arand (h), Ricinus communis (l)

Cauliflower (e), Phool gobhi (h), Brassica oleracea (l)

Cabbage (e), Band gobhi (h), Brassica oleracea (l)

Centella asciatica (l), Indian pennywort (e), Brahmi, Mandukparni (h) 143

Chachinda (h), Snake gourd (e), Trichosanthes anguina (l)

Chakotra (h), Big sized lemon (e)

Chameli (h), Jasmine (e), Jasminum arborescens (l)

Chana (h), Gram, Bengal gram, Chick pea (e), Cicer arietinum (l)

Chandan (h), Sandal wood (e), Santalum album (l)

Changeri (h), Indian sorrel (e), Oxalis corniculata (l)

Chatraka (h), Mushroom (e), Agaricus campestris (l)

Chaulai (h), Prickly amaranth (e), Amaranthus spinosus (l)

Cheeku (h), Bully tree (e), Achras sapota (l)

Cheeta (h), Ceylon leadwort (e), Plumbago zeylanica (l)

Chhir-kakoli (h)- these are disappeared herbs and ashwagandha (Withania somnifera) root can be used at their place.

Chiekling vetch (e), Lathyrus sativus (l)

Chilgoja (h), Edible pine (h), Pinus gerardiana (l)

Chinese dolichos (e), Dolichos sinensis (l)

Chiniya kapoor (h), Cinnamomum camphora (l)

Chirayta (h), Chireta (e), Swertia chirata (l)

Chirchira (h), The prickly – chaff flower (e), Achyranthes aspera (l)

Chironji (h), Buchanania latifolia (l)

Chitrak safed (h), White leadwort (e), Plumbago zeylanica (l)

Chitrak mool (h), Ceylon leadwort (e), Plumbago zeylanica (l)

Chook (h), Bladder dock (e), Rumex vericarius (l)

Cholai (h), Prickly amaranth (e), Amaranthus spinosus (l)

Chopchini (h), China root (e), Smilax China (l)

Choti elaichi (h), Lesser cardamom (e), Elettaria cardamomum (l)

Cichorium intybus (l), Chicory (e), Kasni (h)

Cinnamomum tamala (l), Indian cinnamum (e), Tejpatra (h)

Clerodendrum phlomidis (l), Arni (h)

Coccinia indica (l), Ivy-gourd (e), Kanduri or Bimbi (h)

Coconut (e), Nariyal (h), Cocos nucifera (l)

Coleus aromaticus (l), Indian gentian (e), Pashanbhed (h)

Colocasia (e), Ari (h), Colocasia antiquorum (l)

Coriander (e), Dhaniya (h), Coriandrum sativum (l)

Corn (e), Anaj (h)

Crab, Kekara (h)

Cucumber (e), Kheera (h), Cucumis sativus (l)

Curcuma longa (l), Turmeric (e), Haldi (h)

Curd, Dahi (h)

Custard apple (e), Sharifa (h), Annona squamosa (l)

Cyamopsis tetragonoloba (l), Gwar gum (e), Gwar (h)


Dal (h), Cooked pulses

Dalchini (h), Cassia cinnamon (e), Cassia cinnamomum (l)

Danti (h), Boliospermum montanum (l)

Daruhaldi (h), Indian berberies (e), Berberis (l)

Dashmool (h)- Sarivan, pithvan, badi kateri, bhatkatyya, gokhuru, bel, gambhari, pathal, arni, and sonapatha (h) mool, Ichnocarpus fruitescens, Uraria lagopoides, Solanum Indicum, Solanum xanthocarpum, Pedalium murex, Aegle marmelos, Gmelina arborea, Stereospermum suaveolens, Premna integrifolia, and Oroxylum Indicum root respectively.

Dates (e), Khajoor (h), Phoenix sylvestris (l)

Daucus carota (e), Carrot (e), Gajar (h)

Devdali (h), Bristly luffa (e), Luffa echinata (l)

Devdaru (h), Pinus deodara (l)

Dhaniya (h), Coriander fruit (e), Coriandrum sativum (l)

Dhatki or Dhay (h), Woodfordia floribunda (l)

Dhatura (h), Datura (e), Datura stramonium (l)

Diascorea bulbifera (l), Varahikand (h)

Digitalis (e), Digitalis purpurea (l)

Dolichos lab lab (l), Flat bean (e), Sem (h)

Dooba (h), Creeping cynodon (e), Cynodon dactylon (l)

Dudhi (h), Euphorbia hirta (l)


Eekh (h), Sugarcane (e), Saccharum officinarium (l)

Elaichi (h), Cardamom (e), Elettaria cardamomum (l)

Embelia ribes (l), Babrenge fruits of embelia ribes (e)

Emblica officinalis (l), Indian gooseberry (e), Avla (h)

Enicostemma litlorale (l), Chiraita (e), Chota chiraita (e)

Eugenia jambolana (l), Jambul tree (e), Jamun (h)


Faran (h), Liliaceae(E), Allium strachyi (l)

Farhad (h), Coral tree (e), Erythrina Indica (l)

Fenugreek (e), Methi (h), Trigonella foenum graecum (l)

Ficus bengalensis (l), Banyan tree (e), Barr (h)

Ficus glomeruta (l), Fig tree (e), Gular (h)

Field pea (e), Pisum sativum (l), Matar (h)

Fitkari (h), Alum (e)

Fumaria India (e), Fumaria Indica (l), Pitt papada (h)


Gaj pippal (h), Scindapsus officinalis (l)

Gajar (h), Carrot (e), Daucus carota (l)

Gambhari (h), Gmelina arborea (l)

Gandhak bhasmas (h), Ash of sulphur

Garlic (e), Lahsun (h), Allium sativum (l)

Gathivana (h), Leonifes hepetaefolia (l)

Ghuiyan (h), Great leaved calendium (e), Colocasia antiq (l)

Giloy (h), Tinospora (e), Tinospora cordifolia (l)

Ginger (e), Adrakh (h), Zingiber officinale (l)

Ginseng (e), Arlia quinquefolia (l)

Glucamanon (e), Konjac-mannan (l)

Glycine maxmess (l), Soyabean (e)

Glycyrrhiza glabra (l), Liquorice root (e), Mulathi (h)

Gmelina Arborea (l), Gambhari (h)

Godhuma, Gehun (h), Wheat (e), Triticum sativum (l)

Gogia (h), Elephantopus scaber (l)

Gokhuru (h), Small caltrops (e), Tribulus terrestris

Golden eagle, Baaj (h)

Gomeda (h), Urine of holy cow

Gorakhmundi (h), Sphaeranthus Indicus (l)

Gorochan (h), Serpent stone (e), Bezoar (l)

Gram (e), Cicer arietinum (l)

Grapes (e), Vitis vinifera (l), Angoor (h)

Green pepper (e), Hari mirch (h), Capsicum annum (l)

Ground nut (e), Mungfali (h), Arachis hypogea (l)

Guar (h), Gualin (e), Cyamopsis tetragonoloba (l)

Guava (e), Amrood (h), Pasidium guava (l)

Guduchi (h), Tinospora (e), Tinospora cordifolia (l)

Gugal (h), Indian Bdellium (e), Balsamodendron mukul

Gular (h), Fig tree (e), Ficus glomerata (l)

Gulaskari (h), Sida spinosa (l)

Gur (h), Jaggery

Gurmar (h), Gymnema sylvestre (l), Screw tree (e)

Gwar patha or Ghrit kumari (h), Common Indian aloe (e), Aloe barbadensis (l)

Gymnema sylvestre (l), Screw tree (e), Medhashringi or Gurmar (h)


Haldi (h), Turmeric (e), Curcuma longa (l)

Hara kasis (h), Sulphate of iron (e), Fery sulphas (l)

Harad or Haritaki (h), Chebulic myrobalans (e), Terminalia chebula (l)

Harsanghari (h), Vitis quadrangularis (l)

Hartal (h), Orpiment (e), Yellow arsenicum sulphidum (l)

Heeng (h), Asafoetida (e), Ferula narthex (l)

Hingoth (h), Balanites roxburghii (l)

Hinsar (h), Rubus ellipticus (l)

Hogweed (e), Boerhaavia diffusa (l)

Honey, Shahad or Madhu (h)

Hordeum vulgare (l), Barley (e), Jaun or Yava (h)

Howber (h), Juniperus communis (l)

Hur-hur (h), Cleome vicosa (l)


Indra jav (h), Kurehi (e), Holarrhena anti dysenterica (l)

Indrayan (h), Colocynth (e), Citrullus colocynthis (l)

Issapgol (h), Plantago ovata (l)


Jaangal (h), Wild or Forest (e)

Jack fruit (e), Kathal (h), Artocarpus integrifolia (l)

Jaiphal (h), Nutmeg (e), Myristica fragrans (l)

Jaitun tel (h), Olive oil (e),Olea europoea (l)

Jal (h), Water, Aqua (e)

Jal kumbhi (h), The wester lettuce (e), Pistia stratiotes (l)

Jamalgota (h), Parging broton or Croton seed oil (e), Croton tiglium (l)

Jamun (h), Black berries (e), Eugenia jambolana (l)

Janghal manns (h), Beasts with fleshy legs

Jatamashi (h), Spikenard (e), Nardostachys jatamansi (l)

Jatrofa (e), Jatropha glandulifera (l), Junglee arand (h)

Javasa (h), Camelphorn (e), Alhagi mawrorum (l)

Javitri (h), Mace (e), Myristica fragrans (l)

Jawakhar (h), Impure carbonate of potash (e), Potasii carbonas (l)

Jeera (h), White cumin seed (e), Cuminum cyminum (l)

Jeevanti (h), Leptadenia reticulata (l)

Jhufa (h), Hyssopus officinalis (l)

Jimikand (h), Amorphophallus campanulatus (l)

Jingani (h), Odina wodeir (l)

Junglee gulab (h), Wild rose (e), Rosa invalucrata (l)

Jwar (h), Sorgum vulgare (l)


Kabila (h), Kamala (e), Mallotus philippinensis (l)

Kachnar (h), Mountain ebony (e), Bauhinia variegata (l)

Kachoor (h), Zedoary (e), Curcuma zedoaria (l)

Kadam (h), Anthocephaius cadamba (l)

Kaduu (h), Vegetable marrow, Field pumpkin (e), Cucurbita pepo (l)

Kafal (h), Bay-berry (e), Myrica nagi (l)

Kagji nimbu (h), Lime (e), Citrus medica (l)

Kainth (h), Wood apple, Feronia elephanttum (l)

Kaju (h), Cashew nut (e), Anacardium occidentale (l)

Kak machi or Macoy (h), Garden nightshade (e), Solanum nigrum (l)

Kakad, Kakada singhi (h), Pistacia integerrima (l)

Kakoda (h), Momordica dioica (l)

Kakri (h), Snake cucumber (e), Cucumis utilissimus (l)

Kaktundi (h), Asclepias curssavica (l)

Kal Megh (h), Andrographis paniculata (l)

Kala basa (h), F. Acanthaceae

Kala dhatura (h), Dhatura (e), Datura innoxia (l)

Kala hinsar (h), Black rubus (e), Rubus ellipticus (l)

Kala namak (h), Black salt (e), Unaqua sodium chloride (l)

Kala jeera (h), Black caraway seed (e), Carum carvi (l)

Kala loha (h), Black iron

Kalihari (h), The glory lily (e), Gloriosa superba (l)

Kalimirach (h), Black pepper (e), Piper nigrum (l)

Kamal-kesar (h), Tendrils of the lotus flower (e), Nelumbium speciosum (l)

Kamalgatta (h), Lotus seed (e), Nelumbium speciosum (l)

Kamalkand (h), Sacred lotus (e), Nelumbium speciosum (l)

Kampilak (h), Kamala (e), Mallotus philippinensis (l)

Kamrakh (h), Carambola (e), Averrhoa carambola (l)

Kandkari or Choti kateri (h), Solanum xanthocarpum (l)

Kaner (h), Nerium odorum (l)

Kanghi (h), Abuliton Asiaticum (l)

Kantkari (H), Solanum Indicum (l)

Kapas (h), Cotton plant (e), Gossypium herbaceum (l)

Kapoor (h), Camphor (e), Camphora (l)

Karanj (h), Indian beech (e), Pongamia glabra (l)

Karela (h), Bitter gourd or Carilla fruit (e), Momordica charantia (l)

Karonda (h), Carissa carndas (l)

Karvi tori (h), Luffa amara (l)

Kaseru (h), Water chest nut (e), Scirpus kysoor (l)

Kasni (h), Chicory (e), Cichorium intybus (l)

Kasturi (h), Musk (e), Moschus (l)

Katai or Badi kateri (h), Solanum Indicum (l)

Katechu (h), Acacia catechu (l)

Kateri choti (h), Solanum xanthocarpum (l)

Kathal (h), Jack fruit (e), Artocarpus integrifolia (l)

Kauni (h), Foxtail millet (e), Setaria italica (l)

Kathumar (h), Ficus hispida (l)

Kattha (h), Ixora parviflora (l)

Katuparni (h), Mexican poppy (e), Argemone mexicana (l)

Kaunch (h), Cowhage (e), Mucuna pruriens (l)

Kavaka or Chatrak (h), Mush-room (e), Agaricus campestris (l)

Kayaphal (h), Bay-berry (e), Myrica nagi (l)

Kela (h), Banana (e), Musa sapientum (l)

Keshar (h), Saffron (e), Crocus sativus (l)

Khair (h), Black catechu (e), Acacia catechu (l)

Khajoor (h), Date palm (e), Phoenix sylvestris (l)

Khand (h), Sugar

Kharbuja (h), Muskmelon (e), Cucumis melo (l)

Kharenti (h), Country mallow (e), Sida cordifolia (l)

Khas (h), Cuscus grass (e), Vetiveria zizaniodes (l)

Kheera (h), Cucumber (e), Cucumis sativus (l)

Khensari (h), Chickling vetch (e), Lathyrus sativus (l)

Kher or Khair (h), Black catechu (e), Acacia catechu (l)

Khurashani ajvain(h), Henbane (e), Hyoscyamus niger (l)

Kidney bean (e), Phaseolus rediatus (l)

Kingora (h), Indian berberry (e), Berberis aristata (l)

Kishmish (h), Currant (e), Vitis vinifera (l)

Kodo (h), Punctured paspalum (e), Paspalum scrobiculatum (l)

Koha or Arjuna (h), Arjuna myrobalan (e), Terminalia arjuna (l)

Kooth (h), Costus root (e), Saussurea lappa (l)

Krishna Sariva (h), Arsaparilla (e), Ichnocarpus fruitescens (l)

Kulathhi or Kulthi (h), Two horse gram (e), Dolichos bifloru (l)

Kusha (h), Eragrostis cynosuraides (l)

Kusumbha (h), Safflower (e), Carthamus tinctorius (l)

Kut (h), Costus root (e), Saussurea lappa (l)

Kutaja (h), Conessi (e), Holarrhena antidysenterica (l)

Kuth (h), Costus root (e), Saussurea lappa (i)

Kutki (h), Picrorhiza (e), Picrorrhiza kurroa (l)

Kwacha (h), Cowhage (e), Mucuna pruriens (l)


Laghu panchmool- sarivan, pithvan, badi-kateri, bhatkatyya and gokhuru (h) mool, Ichnocarpus fruitescens, Uraria lagopoides, Solanum Indicum, Solanum xanthocarpum, and Pedalium murex root respectively

Lahasun (h), Garlic (e), Allium sativum (l)

Lai (h), Lac (e), Laceifer lacca (l)

Lajvati (h), Mimosa pudica (l)

Lakhshman (h), Atropa mandragora (e), Mandragora autumnalis (l)

Lata kasturi (h), Psoralea seed (e), Psoralea corylifolia (l)

Latjeera (h), The prickly – chaff flower (e), Achyranthus aspera (l)

Lauki (h), White gourd (e), Lagenaria vulgaris (l)

Lavang (h), Clove (e), Caryophyllus aromaticus (l)

Lead (e), Seesa (h)

Lemon (e), Nimbu (h), Citrus medicavar acida (l)

Linseed (e), Til (h), Sesamum Indicum (l)

Lodh (h), Lodh (e), Symplocos racemossa (l)

Lodocia malldivica (l), Sea coconut (e), Samudri nariyal (h)

Loha bhasma (h), Iron Ash

Long pepper (e), Peepal (h), Piper longum (l)

Loquat (h), Eriobotrya japonica (l)

Lotus (e), Kamal (h), Nelumbium speciosum (l)


Macoy (h), Garden nightshade (e), Solanum nigrum (l)

Madanphal (h), Emetic nut (e), Randia dumetorum (l)

Maadira (h), Barnyard millet (e), Echinochloa frumentaceamandua (l)

Madhuhari (h), Stevia rebudiana (l)

Maha Meda (h), Poly gonatum (l)

Maha-panchmool- Bel, gambhari, padhal, arani and arlu mool, Aegle marmelos, Gmelina arborea, Stereospermum suaveolens, Premna integrifolia, and Oroxylum Indicum root respectively.

Mahua (h), Basia latifolia (l)

Mainfal (h), Emetic nut (e), Randia dumetorum (l)

Maize (h), Makka (h), Zea mayas (l)

Majheeta (h), Madder root (e), Rubia cordifolia (l)

Makhana (h), Fox nut (e), Euryale ferose (l)

Mal-kangani (h), Staff tree (e), Celastrus paniculatus (l)

Mameri (h), Thalictrum foliolosum (l)

Mandookparni, Brahmi (h), Indian pennywort (e)

Mandur (h), The waist of hot iron

Mandua (h), Finger millet (l), Eleusine coracana (e)

Mango (e), Aam (h), Mangifera Indica (l)

Manjeeth (h), Madder root (e), Rubia cordifolia (l)

Manshil (h), Realgar (e), Arsenicum sulphidum (l)

Margosa (e), Neem (h), Azadirachta Indica (l)

Marua (h), Sweet marjoram (e), Origanum majorana (l)

Mashparni or jangli urad (h), Teramnus labialis (l)

Masoor (h), Lentil (e), Ervumlens (l)

Matar (h), Field pea or Garden pea (e), Pisum sativum (l)

Mattha (h), Butter milk

Medhashrangi (h), Gymnema sylvestre (l)

Meetha (h), Aconitum balfourii (l)

Meetha vish (h), Aconite (e), Aconitum ferox (l)

Mehandi (h), Lawsonia inermis (l)

Melon white (e), Cucumis melo (l)

Methi (h), Fenugreek (e), Trigonella Foenum graecum (l)

Methi Sahajana (h), Horse radish tree (e), Moringa (l)

Milk, Doodh (h)

Mint (e), Pudina (h), Mentha spicata (l)

Mishri (h), Sugar candy

Mochras (h), Gum of silk cotton tree (e)

Molshiri (h), Mimusops olengi (l)

Molu (h), Bahvhinia vahlii (l)

Momordica charantia (l), Bitter gourd (e), Karela (h)

Moong (h), Green gram (e), Phaseolus aureus (l)

Moonga Bhasma (h), Ash of red corel (l)

Moorva tulsi (h), Ocimum tenuflerum (l)

Morphine or Opium (e), Afaim (h) 46

Morva tulsi (h), Ocimum tenuflerum (l)

Mota chaval (h), An ordinary variety of the rice

Moth (h), Aconite leaved kidney bean (e), Phreseolus (l)

Moti (h), Pearl (e),

Mandukparni (h), Indian pennywort (e), Centella Asiatica (l)

Mucuna prureins (l), Cowhage (e), Kauch (h)

Mukta or Moti bhasma (h), Pearl ‘margarita’ ash (e)

Mulaithi (h), Liquorice root (e), Glycyrrhiza glabra (l)

Mulberry (e), Sahtut (h), Morus Indica (l)

Muli (h), Radish (e), Raphanus sativus (l)

Munakka (h), Currants (e), Vitis vinifera (l)

Mung (h), Green grain (e), Phaseolus aureus (l)

Mungfali (h), Groundnut (e), Arachis hypogea (l)

Musa sapientum (l), Banana (e), Kela (h)

Musk melon (e), Karbooja (h), Cucumis melo (l)

Mustard seeds (e), Sinapis nigra (l), Sarson (h)

Myrica nagi (l), Box myrtle (e), Kaifphal (h),

Myristica fragrans (l), Nutmeg (e), Jaiphal (h)


Nag Keshar (h), Cobra’s saffron (e), Mesua ferrea (l)

Nagar Motha (h), Cyperus scariosus (l).

Nagbala (h), Sida veronicaefolia (l)

Narangi (h), Orange (e), Citrus reticulata (l)

Nariyal (h), Coconut (e), Cocos nucifera (l)

Narshal (h), Wild tobacco (e), Lobelia nicotianaefolia (l)

Nashpati (h), Pear (e), Pyrus communis (l)

Naushadar (h), Sal – ammoniac

Neela Chitrak (h), Plumbago capensis (l)

Neelkamal (h), Water lily (e), Nymphaea stelleta (l)

Neem (h), Margosa (e), Azadirachta indica (l)

Neembu ghas (h), Cymbopogon citratus (l)

Nilathotha (h), Blue vitriol

Nilupher (h), Water lily (e), Nymphaea alba (l)

Nimbu (h), Lemon (e), Citrus medica

Nirgundi (h), Indian privet (e), Vitex negundo (l)

Nisoth (h), Turpeth root (e), Operculina turpethum (l)

Nycanthus arbor-tristis (l), Night jasmine (e), Parijaat (h)


Ocimum sanctum (l), Holy basil (e), Tulsi (h)

Olea europea (l), Olive (e), Jaitun (h)

Onion (e), Pyaj (h), Allium cepa (l)

Orange (e), Santara (h), Citrus reticulata (l)

Oroxylum indicum (l), Sonapatha (h)


Padam or Kamal (h), Sacred lotus (e), Nelumbo nucifera (l)

Padamakh (h), Mild Himalaya cherry (e), Prunus puddum (l)

Paederia foetida (l), Chinese flower plant (e), Gandha prasarani (h)

Pakar (h), Ficus intectoria (l)

Palak (h), Spinach (e), Spinacia oleracea (l)

Palash (h), The forest flame (e), Butea frondosa (l)

Pan (h), Betel leaf (e), Piper betle (l)

Panchkol (h) mixture of pippal , pippalamool , chavya, cheeta, and sonth (h), Piper longum (dried catkins), Piper longum root, Piper officinarum, Plumbago zeylanica and Zingiber officinale root respectively

Panja ‘salav’ (h), Enlophia campestris (l)

Papita (h), Papaya (e), Carica papaya (l)

Parad Bhasma (h), Mercury ash (e)

Partridge (e), Jal-murgabi/Teetar (h)

Parval (h), Sespadula (e), Trichosanthes dioica (l)

Pashanbhed (h), Indian gentian (e), Gentiana kurroo (l)

Patha (h), Velvet leaf (e), Cissampelos pareira (l)

Pathal (h), Stereospermum suaveolens (l)

Pathanilodh (h), Symplocos crataegoides (l)

Patol (h), Trichosanthes dioica (l)

Pattagobhi (h), Cabbage

Peela Bhringraj (h), Eclipta (e), Wedelia calendulacea (l)

Peet Basa (h), Barleria prionitis (l)

Petha (h), Pumpkin (e), Benincasa cerifera (l)

Phalsa (h), Grewia Asiatica (l)

Phaseolus mungo (l) Black gram (e)

Phool priyangu (h), Callicarpa macrophylla (l)

Phyllanthus niruri (l), Bhuavla (h)

Pigeon pea (e), Cajanus Indicus (l)

Pila geru (h), Oker (e), Bolerubra (l)

Pindalu (h), Randia uliginosa (l)

Pineapple (e), Ananas (h), Ananas comosur (l)

Pipalli (h), Long pepper (e), Piper longum (l)

Piper nigrum (l), Black pepper (e), Kali-mirach (h),

Pippalamul (h), Piper root (e), Piper officinarum (l)

Pishta (h), Pistachio (e), Pistacia vera (l)

Pitasala or Vijaysaar (h), Indian kino tree (e), Pterocarpus marsupium (l)

Pitta papra (h), Fumaria India (e), Fumaria Indica (l),

Plumbago zeylanica (l), Ceylon leadwort (e), Chitrak (h)

Podina (h), Spearmint (e), Mentha spicata (l)

Pohkar root (h), Orris root (e), Iris germanica (l)

Polygonem Effiny (l), Polygonem (e)

Pomegranate (e), Anar (h), Punica granatum (l)

Pongamia glabra (l), Indian beech (e), Karanj (h)

Poppy, Afim (h), Opium (e), Papaver somniferum (l)

Potato (e), Alu (h), Solanum tuberosum (l)

Prasharni (h), Paederia foetida (l)

Praval ‘moonga’ bhasam (h), Red coral ‘coralium rubrum’ ash (e)

Priyangu (h), Callicarpa macrophylla (l)

Pterocarpus marsupium (l), Indian kino tree (e), Vijaysaar (h)

Pudeena (h), Spearmint (e), Mentha spicata (l)

Puerasia tuberosa (l), Vidarikand (h)

Punnarva (h), Hogweed (e), Boerhaavia diffusa (l)

Putranjeeva (h), Putranjiva roxburghii (l)

Pyaj (h), Onion (e), Allium cepa (l)


Raal (h), The sal tree (e), Shorea robusta (l)

Rabbit, Khargosh (h)

Rabia cordifolia (l), Madder root (e), Majeetha (h)

Radish (e), Muli (h), Raphanus sativus (l)

Ragi (h), Himalayan silver fer (e), Abies webbiana (l)

Rai (h), Indian mustard (e), Brassica juncea (l)

Raisin (e), Munnaka (h), Vitis vinifera (l)

Rajamash, Lobhiya (h), Chinese beans (e), Vigna catiang (l)

Rajat Bhasma (h), Silver ash (e),

Rajat makshik bhasma (h), Rajat makshik ash (e)

Raqt shali (h), A variety of the rice

Rasna (h), Pluchea ianceolata (l)

Rasoot (h), Extract of Indian berberis (l)

Rauwolfia serpentina (l), Sarpgandha (h)

Red chilli (e), Lal Mircha (h)

Renuka (h), Vitex agnus- castus (l)

Revand chini (h), Rhubarb (e), Rheumemodi (l)

Rice (e), Oryza sativa (l), Chawal (h)

Riddhi-vrridhi (h), these herbs had disappeared and varahikand ‘Dioscorea bulbifera’ (l) can be used at their place

Rishbhak (h), Vidarikand (h), Pueraria tuberosa (l)

River fish, Nadeya machli (h)


Saal (h), The sal tree (e), Shorea robusta (l)

Saambhar (h), Deer

Sabudana (h), Sago (e), Metroxylon saga (l)

Sada Bahar (h), Catharanthus roseus (l)

Safed musali (h), Asparagus adscendens (l)

Sahijana (h), Horse radish tree (e), Moringa pterygosperma (l)

Sajjikhar (h), Barilla (e)

Salad (h), Garden lettuce (e), Lactus sativa (l)

Salam mishri (h), Eulophia campestris (l)

Samundrik namak (h), Salt produced from the sea water

San (h), Ambari hemp (e), Hibiscus cannabinus (l)

Sandal wood (e), Chandan (e), Sontalum album (l)

Sanjeevani (h), Actinopteris radiata (l)

Sar Punkha (h), Tephrosia purpurea (l)

Sariva ‘krishna’ (h), Black sariva (e), Ichnocarpus fruitescens (l)

Sariva ‘shwet’ (h), White sariva (e), Hemidesmus Indicus (l)

Sarpgandha (h), Rauvolfia serpentina (l)

Sarson peeli (h), Yellow sarson, Indian colza (e), Brassica campestris (l)

Satavari (h), Asparagus racemosus (l)

Sateen (h), Rind of peas (e), Pisum sativum (l)

Saunf (h), Fennel fruit (e), Foeniculum vulgare (l)

Sea fish, Samundriya machili (h)

Seb (h), Apple (e), Pyrus malus (l)

Sem (h), Flat bean (e), Dolichos lablab (l)

Semal (h), Silk cotton tree (e), Bombax malabaricum (l)

Sendha namak (h), Chloride of sodium or sodii chloridum (e)

Sesamum seed (e), Til (h)

Sesum (h), Dalbergia sissoo (l)

Shahatuta (h), Mulberry (e), Morus Indica (l)

Shallaki (h), Indian olibanum (e), Boswellia serrata (l)

Shankahuli (h), Convolvulus pluricanlis (l)

Shankh pushpi (h), Winged leaved clitoria (l)

Shatavari (h), Asparagus racemosus (l)

Shimbi, Sem (h), Flat bean (e), Dolichos lablab (l)

Shuddh Shilajit (h), Asphalt ‘asphaltum punjabinum’ (l)

Shweta ghunguchi (h), Jequirity (e), Abrus precatorius (l)

Shweta musali (h), Chlorophytum arundinaceum (l)

Shyonac (h), Oroxylum Indicum (l)

Sida spinosa (l), Nagbala (h)

Sihora (h), Streblus asper (l)

Sinapisalb (e), Brassica cempestris (l)

Singara (h), Water caltrops (e), Trapa bispinosa (l)

Sisamum niger seeds (e), Sisamum Indicum (l)

Snake, Saanp (h)

Solanum melongena (l), Brinjal (e), Baigan (h)

Somlata (h), Sarcostemma brevistigma (l)

Sonapatha (h), Oroxylum Indicum (l)

Sonchar (h), Black salt (e), Unaqua sodium (l)

Sonph (h), Fennel fruit (e), Foeniculum vulgare (l)

Sonth (h), Dry ginger root (e), Zingiber officinale (l)

Soya, Soyabean (h), Indian dill fruit (e), Anethum sowa kurz (l)

Spinach (e), Palak (h), Spinacia oleracea (l)

Sugandhbala (h), Indian valerian rhizome (e), Valeriona wallichii (l)

Sugarcane (e), Ganna or Ekha (h), Saecharum album (l)

Supari (h), Betel nut (e), Areca catechu (l)

Swaranmakshik bhasma (h), Swaranmakshik ash (e)

Swarna Bhasma (h), Gold ash (e)

Sweet lime or Mozambique orange (e), Musambi (h), Citrus sinensis (l)

Sweet potato (e), Shakarkand(h), Ipomoea batatas (l)

Swertia chiraita (l), Chireta (e), Chiraita (h)


Tagar (h), Indian valerian rhizome (e), Valeriama wallichii (l)

Takra (h), Butter milk

Talish patrya (h), Himalayan yew (e), Taxus baccata (l)

Tamarind (e), Imli (h), Tamarindus Indica (l)

Tamba bhasam (h), Copper ash

Tarbuja (h), Watermelon (e), Citrullus vulgaris (l)

Tejapat (h), Cassia (e), Cinnamomum tamala (l)

Tel (h), Oleum (e)

Terminalia arjuna (l), Arjuna myrobalan (e), Arjun (h)

Terminalia belerica (l), Beleric myrobalans (e), Bahera (h)

Terminalia chebula (l), Chebulic myrobalans (e), Harad (h)

Thuner (h), Taxus baccta (l)

Til (h), Gingelli (e), Sesamum Indicum (l)

Tinda (h), Citrullus vulgaris (l)

Tendu (h), Gaub persimon (e), Diospyros embryopteris (l)

Tinospora cordifolia (l), Tinospora (e), Giloy or Guduchi (h)

Tobacco (e), Tambakhu (h), Nicotiana tabacum (l)

Tori (h), Acuteangled cucumber (e), Luffa acutangula (l)

Tran panch mool- Sarivan, pithvan, badi kateri, bhatkatyya, and gokhuru (h) mool, Ichnocarpus fruitescens, Uraria lagopoides, Solanum Indicum, Solanum xanthocarpum, and Pedalium murex root respectively

Tribulus terrestris (l), Small caltrops (e), Gokhuru (h)

Tricuta- Kali mirch+pippali+soth (h), Black pepper+long pepper+dry ginger (powdered)

Trigonella foenumgraceum (l), Fenugreek (e), Methi (h)

Trijatak (h)- Dalchini, Tejpetra, ellaichi (h), Cinnamomum zeylanicum, Cinnamomum tamala, and Amomum subulatum (l)

Triphla- Avla+Harad+Bahera (h), Emblica myrobalan+Belleric myrobalan+Myrobalan Chebuli (powdered)

Tulsi (h), Holy basil (e), Ocimum sanctum (l)

Tumburu (h), Zanthoxylum alatum (l)

Turmeric (h), Haldi (h), Curcuma longa (l)

Tuvraka (h), Hydoncarpus wightiana blume (l)

Twoflowered dolichos (e), Dolichos biflorus (l)


Urad, Mash ki dal (h), Black gram (e), Phaseolus mungo (l)


Vach (h), Sweet flag (e), Acorus calamus (l)

Valerica wallichii (l), Indian valerian rhizome (e), Tagar (h)

Valli-panchmool (h)- Vidarikand, sariva, haldi, giloy, and kakdasingi (h), Pueraria tuberora (l), Ichnocarpus fruitescens, Curcuma longa, Tinospora cordifolia, and Pistacia integerrima respectively

Van ajvain (e), Wild thyme (e), Thymus serphyllum (l)

Van tulsi (h), Common sweet basil (e), Ocimum basilicum (l)

Van haldi (h), Wild turmeric (e), Curcuma aromatica (l)

Van kakri (h), Indian Podophyllum (e), Podophyllum hexandrun (l)

Vang bhasam (h), Nickle, Ranga ash (e)

Vanshlochan (h), Bamboo (e), Bambusa arundinacia (l)

Varahikand (h), Dioscorea bulbifera (l)

Vat (h), Banyan tree (e), Ficus bengalensis (l)

Vatshnabh (h), Aconite (e), Aconitum ferox (l)

Vayvidang (h), Babreng fruits of embelia ribes (e), Embelia ribes (l)

Verna (h), Vitex peduncularis (l)

Vid namak (h), Vid salt (e)

Vidari kand (h), Pueraria tuberora (l)

Vijayasar (h), Indian kino tree (e), Pterocarpus marsupium (l)

Vishkar (h), Birds which firstly scatter their food and then eat

Vishnu kranta (h), Evolvulus alsinoides (e),

Vitis vinifera (l), Grape seeds (e), Angoor (h)

Vrihat panchmool- Bel, gambhari, arni, pathal and sonapatha or arlu mool (h), Roots of Aegle marmelos, Gmelina arborea, Premna integrifolia, Stereospermum suaveolens, and Oroxylum Indicum respectively


Walnut (e), Akharot (h), Juglans regia (l)

Water melon (e), Tarbooj (h), Citrullus vulgaris (l)

Wheat (e), Genhu anaj (h), Triticum sativum (l)

White babool (e), Safed babool (e)

White mustard, Indian colza (e), Safed sarson (h), Brassica canpestris (l)

White semal (h), Safed semal (h), Ceiba pentandra (l)

White surma (e), Safed surma (h)

Withania sominifera (l), Winter cherry (e), Ashwagandha (h)


Yashada Bhasma (h), Zinc ash (e)

Yav, Jaw (h), Barley (e), Hordeum vulgare (l)

Yava kshar (h), Impure carbonate of potas (e), Potasil carbonas (l)

Yellow geru (h), Oker (e), Bolerubra (l)


Zafara (h), Bixa orellana (l)

Zingiber officinale (l), Ginger root (e), Adrak (h)

(II) Important Chinese herbs useful in Diabetics

Aloe-vera: Aloe vera, var. officinalis (l)

Alfalfa: Medicago sativa (l)

Angelica: Angelica archangelica (l)

Arnica: Arnica montana (l)

Barberry: Berberis vulgaris (l)

Boneset: Eupatorium perfoliatum (l)

Burdock root: Arctium lappa (l)

Caraway: Carum carvi (l)

Cardamon, Sha-ren: Malabar cardamon (l)

Cedar berries: Juniperus virginiana (l)

Chamomile: Matricaria chamomilla (l)

Chickweed: Stellaria media (l)

Cinnamon: Cinnamomum tamala (l)

Comfrey root: Symphytum officinale (l)

Corn silk: Zea mays (l)

Cumin: Cuminum cyminum (l)

Dandelion: Taraxacum officinale (l)

Echinacea: Echinacea angustifolia (l)

Elder flowers: Sambucus nigra (l)

Elecampane: Inula heminum (l)

Eucalyptus: Eucalyptus globulus (l)

Fennel: Foeniculum vulgare (l)

Flaxseed: Linum Vistatissimum(l)

Geranium: Pelargonium graveolens (l)

Garlic: Allium sativum (l)

Ginger: Zingiberis officinalis (l)

Ginseng: Panax ginseng (l)

Golden seal: Hydrastis canadensis (l)

Gotu kola: Centella asiatica (l)

Gravel root: Eupatorium purpureum (l)

Ho shou wu: Polygonum multiflorum (l)

Juniper: Juniperis communis (l)

Liquorice root: Glycyrrhiza (l)

Mullein: Verbascum tapsus (l)

Oregon grape root: Berberis aquifolium (l)

Psyllium seed: Plantago psyllium (l)

Red clover: Trifolium pratense (l)

Sage: Salvia officinalis (l)

Senna: Cassia acutipolia (l)

Uva ursi: Arctostaphylos uva ursi (l)

Worm wood: Artemisia absinthium (l)

Yellow dock: Rumex crispus (l)

(III) Important herbs used in Unani and Tibetan medicine for treating Diabetics

Aarar: Juniperus communis (l)

Afsanteen: Artemisia absinthium(l)

Akarkara, Pythron: Anacyclus pyrethrum (l)

Anjeera adam: Ficus glomerta (l)

Ashwatya fruit: Juniperus communis (l)

Darakhte sinna: Aloe vera (l)

Fennel:Foeniculum vulgare (l)

Gogirda: Brimstone (l)

Guldaudi: Chrysanthemum coronarium(l)

Hirakasi, Jaja asphar: Ferry sulphaz (l)

Jaharmohara: Serpant stone (l)

Jaitun: Olea europea (l)

Juniper oil: Juniperis communis (l)

Kabavah: Piper cubeba (l)

Kheshkekala: Pedalium murex (l)

Oil of Carrot, eucalyptus, fennel, lemon and geranium

Phalenda: Eugenia jambolana (l)

Philphilashyah: Piper nigrum (l)

Talamkhana: Hygrophila spinosa (l)

Ustkhaddus: Brunella valgaris (l)


“hitahitam sukham dukhmayustasya hitahitam” (CharakSamhita.Sutra.L.1.S41). This implies that, ever since the origin of life, living beings have been taking care of their safety and protection. Man has been well aware of things both beneficial as well as harmful to his health and life. Life has always had and will forever have a strong relationship to knowledge. In fact, it is natural science alone which is the mother, guardian and patron of all the sciences and especially medical science. The earliest description of medical science is obtained from the mythological Hindu scriptures- the four vedas.

In ancient times, a few learned Rishis of the Aryan community were having a meeting in the Himalayas. The topic was ‘the ills that flesh is heir to’ meaning that body and illness go hand in hand. They were discussing the four main functions to be performed by human life as virtue, wordly deeds, pleasure, and liberation. Once this human body becomes a victim of diseases, it becomes lean, weak and incapable of performing those four functions. A diseased body also experiences pain, becomes an obstacle to the body’s functioning, and may even be the cause of untimely death. How can a person be happy after having these enemies (disease) and how can he then carry out the worldly functions assigned to him?


Table-1 Treatment through sun bath.

The sun rays are the most hygienic and curative agents in the whole world. Even the most dangerous bacteria can not remain alive in the presence of sun rays. Apart from this property the sun rays are also necessary for the growth of the body.

One can understand the value of sun rays by observing that a plant which is not kept under proper sunlight remains under developed, similarly if a child does not get proper sun exposure he may remain dwarf and may develop rickets. An adult needs sun rays to keep away several diseases.

Sun rays not only reach the uppermost layer of the skin but also penetrate deep into the bones, muscles and the nerves. The blood circulation and the functioning of the internal organs including heart, brain and kidneys also improve on exposure to sunlight.

The exposure to sun rays relieves from tensions and stresses. The effects of the sun bath are almost similar to that of the electric light bath.

Sun rays are not only the source of radiant (heat) energy but they also act as strong tonic through their actinic rays. If a red coloured glass is placed in between the sun and the patient then the rays with calorific effect are separated and only actinic rays with human growth property are filtered. And for filtering calorific rays a blue coloured glass is used.

Method of sun bath: One should remove all clothes and cover eyes before taking sun bath. Initially it should be taken for 1/2-1 h and the time can be increased by practice. But if one feels uneasy the time can be reduced to 5-10 minutes initially and can be increased later on. Optimum sweating is indicative of proper sun bath. After taking sun bath one should also take hip bath in a tub filled with water and it should be followed by a few steps walk under the sun.

The best time for sun bath is between 10 am to 3 pm. It is very useful for all diabetics.


This led to further discussion among the Rishis about ways to remove these obstructions. During this series, they faced Maharshi Bhardwaj present in the congegration and requested him : “Oh Rishivar, you are the most capable, learned and wise amongst us, so please go to Brahmgyani Maharaj Indra, who has systematically and deeply studied Ayurvigyan, and learn from him this deep science, Ayurveda (study of keeping human body in good health with the help of natural measures), and thus prevent and safeguard the human species from disease.”

To this Rishi Bhardwaj replied “it shall be so” and he went to the God Indra and told him that he had been sent there by a team of erudite men to learn medical treatment from him in order to relieve humans from the curse of disease. He said: “I request you to impart to me the knowledge of Ayurveda”. Thereafter Indra and the master of vedas, Lord Brahma, imparted full knowledge of Ayurveda to Rishi Bhardwaj, stating the trisutra (code of cures) of Ayurveda to be : “hetulingaushadhgyanam swasthatur parayanam; trisutram shashvatam punyam bubudheyam pitamah.” (CharakSamhita.Sutra.L.1S.24).

Rishi Bhardwaj imparted this knowledge to capable people with the warning: “Do not share this knowledge with people who will use it for earning endless money for luxury and will misuse it for their personal benefit. But distribute it among simple, sober and God-fearing people”.

The ancient natural science of Ayurveda is a part of Atharva and Rig vedas. The foremost, greatest learned man of medicine was the Professor of Medicine, Lord Punarvasu, who came from the Atri dynasty. Maharaj Atri was the son of Lord Brahma, the learned author of vedas possessing all spiritual knowledge. But it was Acharya Charaka who became the knowledgeable Maharashi to consecrate and establish Ayurvigyan in writing, thus making it available to the present generation, for which we should be grateful. All these medical documents are in writing, systematic, in series, and full of reason. These treatments can never be a false “code of cures”. Even in a short period, if a person comes in close contact with them he will come to know the reality. Acharya Charaka says a person with equal dosha-dhatu-malas (body humours-body tissues-body excretions), with balanced and working organs is enjoying good health : “samdoshah samagnishch samdhatumal kriyah; prasannatmondripamanah swastha ityabhidhiyate.” (S.Su.L.15.41).

Along with medicinal science, the work of establishing the science of surgery was accomplished by Acharya Sushruta (300 B.C.). He was the student/disciple of King Devadas of Banaras. Among several wise man in Ayurveda, one learned man was Dhanvantari (57 B.C.) who was the court physician to Maharaj Vikram, and he invented the ‘elixir of life’, capable of giving rebirth at least once to the dead.

The scripted developmental cycle of medicinal science has been incessantly continuing since its origin in rigveda (this most ancient grantha is said to have its origin about 5 to 50 thousand years before Christ), atharva veda, samveda and is still doing so.

According to natural science, there are six basic cardinal elements involved in the development and destruction of the human body. They are akash (ether), vayu (air), agni (fire), jal (water), prithvi (earth) and chetna (consciousness). Any imbalance or radical change in the ratio or quality of any one of these becomes the cause of disease.

In atharva veda there are detailed descriptions of various parts and procedures of body science, medicine and treatment, including the causes and solution of diabetes. The natural circumstances present thousands of years ago were not as they are today, similarly the living conditions prevalent 50 or 200 years ago were different. Therefore, the causes of diabetes have also changed in comparison to those in ancient days. This is obvious from the huge increase in the number of diabetics.

Nature’s products change properties according to the environment. We can see this by taking the example of neem (margosa), which has yet not developed resistance to germs even though it has been thriving for thousands of years. Just as an antibiotic becomes ineffective after being used a few times, so it is with modern medicine for diabetes (after constant use they become ineffective). In scientific language, this is known as primary and secondary drug failure.

On the contrary, if we understand the principles of natural science, which follow self renewal, and then try to find a solution to diabetes, we will certainly get it. At present and in the near future, this natural science will prove most beneficial in decreasing the severity of the disease and in total prevention of diabetes due to environmental factors, which accounts for 80-90% of diabetics.

For achieving aarogyata ‘good health’ and prevention of diseases, several methods are mentioned in natural science. Out of these, one is divine medicine, which has been used for thousands of years to alleviate the scourge of this disease. Man himself is experiencing the effects of these medicines on himself and by changing them according to need he is making them useful for curing the disease. Natural science has developed from the learning of thousands of years. Hence it has no bad effects, is permanent and besides giving aarogyata to the body, it also purifies the soul. These God-gifted natural measures are beneficial at all stages of diabetes and should certainly be used.

The most ancient grantha of natural science is known as Ayurvedic science. Ayurveda is a science that is capable of explaining the importance of natural measures in a systematic, logical and effective way hence it should be properly understood. For treatment by natural science besides medicine a few other actions are also essential:

* Simple life style involving physical labour.

* Optimistic attitude to life.

* Attitude of happiness and satisfaction.

* Purification of the mind and body by bathing, meditation, yogaand pranayama.

Besides these, a few other nature cure techniques, which are being used today for treating diabetes and its complications have been in vogue since ancient times although their names have been changed. For example, swedan, dhoop sewan, achman, jal sparsh, vasti, sanshaman, sanshodhan, aptarpan, rasayan, mud treatment and massage by siddha snehas are today given the following names respectively, diaphoresis, sunbath, water sipping, sitz bath, enema, pacification of humours, purification of body, fasting, nutriments, mud packs and medicated oil massage.

Tratak of the past produces the same effect as laser treatment of today. Today’s air cure technique is the pranayama of the past. Chandyoga upanishad advocates use of fasting and water treatment techniques for the purification of the human body. Knowledge of fasting (rules of aptarpan) is good for removing diseases. Hydropathy (water treatment) was explained in detail by Dr. James Kusi in 1717 who showed how it can keep the body disease free. Ayurveda had mentioned this as far back as 4000 years ago. Our minds feel happy as well as satisfied by the gifts of nature when we bathe in a waterfall and think of the importance of water in our lives. Mahatma Gandhi, the father of the Indian nation was an ardent follower of natural treatment but it is really sad to say that we did not quite learn from him.

Two Greek Physicians, Herodicus and Democritus, developed this natural science and presented it to mankind by giving measures of curing disease by mere changes in eating and living habits, without the need of medicine.

The father of Western medicine, Hippocrates (460-377 B.C.) said, “It is only nature which cures disease, the physician is just a part or symbol of that treating process”. This great, learned scholar who lived a long life of 109 years gave the following message to physicians: “A physician should be well aware of the usefulness of natural principles and the benefits of natural substances. He should also understand dietetic treatment, all types of massage, and astrology and astronomy, too”.

Hippocrates named impurities in blood, bile, phlegm and water as the cause of disease and the same had been established in rigveda and ayurveda earlier. Various learned scholars agree with the fact that ‘medical miracles are in reality only the result of certain unsolved effects of nature’. Hence, no extraordinary medical experience should be left unsolved considering it to be a miracle. Instead one should find the cause of that miracle. In the modern age Mr. Louis Kuhne (1888) achieved expertise in the field of naturopathy, and told the world about his experiences of treatment without medicine.

The great, brave EmperorDuleep used to go on a milk diet sometimes and also spend time in the forest. King Dashratha of Ayodhya and his queens went on fruit diet after which they were blessed with sons as Lord Rama and Laxman. Lord Buddha named clay, cow dung and cow’s urine helpful in treating poisoning ‘vishdansh’, and also named steam bath to be very effective for good health. In modern times, Dr. James Currie, Sir John Floyer, Dr. Venkat Chelapati, Dr. L.N. Chowdhary, Dr. Janaki Sharan Sharma, Dr. Baleshwar Prasad and other prominent persons have explained to us the importance of natural science, and by treading the path shown by them, we can make our lives long and healthy.

In this blog, by making diabetes treatment our base we shall be able to gather some knowledge about the important medical efforts that have been made so far for keeping the body disease free. It is essential to know about the origin of these medical treatments, which at present are most ancient in written form and there is no information prior to them.


The information regarding the anatomy and physiology of the human body was given by great Ayurvedacharyas Charaka and Shushruta as early as in 600 BC in their famous medical books namely Charaka Samhita and Sushruta Samhita. They also clearly mentioned that secretion of the pancreas that is, pittagni or Insulin also known as ‘pachak pitta ‘ (equivalent to insulin) is essential for conversion of food into nutrients, body tissues and energy.

About 2200 years back (131-200 BC) Galen collected and corrected the available medical literature and laid the foundation of analytical work.

Hippocrates,known as the father of allopathy had already estabilished the importance of glandular secretions in the normal functioning of the body about 2500 years ago (460-377 B.C.) In 1902 Bayliss and Sterling discovered ‘Hormones’. It was in 1922 that Benting discovered Insulin.for curing diabetes.

In diabetes , invariably every cell’s, function and structure are adversly affected to some degree. This is because of the need to convert glucose to energy by every cell to sustain life; when the energy production becomes disordered it deposits the harmful metabolites of glucose in the various tissues.

The constitution of almost all cells generally remains the same. But according to the functional need of the body, changes take place in their shape, size and composition. As a result the development of specific cells as epidermal, nerve, muscle and glandular cells takes place. A group of cells of almost same size and function form tissues, groups of tissues form an organ, groups of organs form an organ system, and groups of organ systems give rise to the human body.

All cell formation takes place by combining organic and inorganic elements. The atoms of chemical elements obtained from food unite with each other in the body to form organic atoms that in turn unite to form cellular fluid, mitochondria, plasma membrane, nucleus, genes and other smaller parts of the cell. The cell membrane is a special porous structure through which the essential molecules (glucose, sodium chloride, fatty acids etc.) can pass in a controlled manner (diffusion, secretion, absorption mechanisms are operational). The glucose burns in the mitochondria releasing energy, hence it is also known as ‘the power house of the cells’. Life is impossible without this bio-energy.



They are the chemical compounds produced by the plants to protect themselves from virus, bacteria and fungi. There are more than 600 phyto-chemicals recognized in nature. Their exact role in prevention of the diseases in human bodies is not clear. However they surely protect the body against some cancers, heart diseases, and infections.

A few of the phyto-chemicals are enlisted below.

1. Carotenoids: Rich sources- Carrot, potato, apricot, papaya, and green vegetables.

2. Indoles: Rich sources- Cabbage, cauliflower, broccoli, brussels sprouts etc.

3. Vitamin C: Rich sources- Citrus fruits, sweet pepper, apple, orange, and grapes.

4. Phytosterols and isoflavones: Rich sources-Soy, dried beans, green peas, sem etc.

5. Allelic sulfides:Rich sources- Garlic, onion, ginger root, and chives.

6. Lycopene: Rich sources- Watermelon, tomatoes, pink grapefruits etc.

7. Ellagiac acid:Rich sources- Grapes, apple, and mangoes.

NoteAdvertisements of pills containing phyto-chemicals keep appearing in the papers. It is not practical to eat all kind of pills. A better option would be to eat a diet rich in above substances regularly.

kanti diabetic centre



Human body contains the following main endocrinal glands:

1. Pineal

2. Pitutary

3. Thyroid

4. Parathyroid

5. Pancreas

6. Adrenals

7. Hormones secreting tissues in testis, ovaries and placenta

Hormones are those type of messenger (chemical messenger), which carry coded information from one organ of the body to another for regulating and stimulating the vital biochemical actions and reactions.

Hormones are secreted from specific glandular tissues and reach the blood directly without being assimilated or passing through any duct (hence endocrinal glands are also called ductless glands). They reach their target cells directly and are destroyed after performing their function. It is impossible to store these hormones in any tissue or body compartment, nor can they be supplied through food. They are normally made by body proteins, fats and carbonic fatty acids as per body’s requirement. they are secreted by the endocrinal glands, according to natural science, are fast in action and controlled by a feed back system (negative and positive feedback mechanism).

Normally the hormones secretec by each endocrinal gland perform a specific function only. But if any function involves the use of hormones secreted by more than on gland then these glands must also be related to each other in some way. We can see this clearly in diabetic patients. Four endocrinal glands play an important role in carbohydrate metabolism: Pancreas, Thyroid, Suprarenal ‘adrenals’ and Pitutary gland. We shall now3 discuss them individually.


The word pancreas means sweet bread (Greek). In ayurveda this gland is called madhusudini =agnyashay, a gland which secretes madhunishudini shrava (insulin hormone). This 15 cm long, mixed gland (98% of the whole gland is the exocrinal tissue which secretes digestive enzymes , plus 2% is the endocrinal tissue which secretes insulin nand glucagon hormones) is situated behind the stomach in a difficlt retropreitonial space.

Theendocrinal tissue was discovered by Paul Langerhans in 1869, hence was named ‘islets of langerhans’. There are about 1 to 2 million islets in a healthy human pancreas. Ilets of langerhans consist of Alfa, Beta and Delta cells which secrete glucagon, insulin and somatostatin hormones respectively.

The Beta cells synthesize insulin by using protein (amino acids) in the following manner: Amino Acid Monomer (Disulphide linkages) produce Poly Peptides ( alfa and beta) next Pre Pro Insulin next Pro Insulin and finally Insulin.

Insulin remains totally ineffective up to the level of pro-insulin. This is converted to effective insulin only after repeated purification (blood test of several diabetics reveal an abundance of immature insulin which is of no use).

Active insulin highly increases the permeability of glucose into all body cells (except in the brain cells and red blood corpuscles, as these cells are extremely permeable to glucose even without insulin) and thus more and more glucose enters these body cells where it is correctly metabolized.

INSULIN HORMONE: It helps in introducing glucose into the cells, and thereby in building up of body fuel stores. Besides it also has the following important functions.

* Fulfillment of basal metabolic requirement of the body cells.

* Synthesis of RNA, DNA and other proteins inside the cells.

* Glycogenesis: Synthesis of glycogen from glucose in the liver and muscles.

* Lipogenesis: Synthesis of fats in fatty tissues.

Thus the clear effect of Insulin is to stimulate anabolism and helps in development of the body. Today scientists are manufacturing human insulin commercially by using the DNA recombinant technique.

GLUCAGON HORMONE: It was discovered in 1923 by Kimble and Merlin. As soon as the blood glucose level drops down below a certain limit the alfa cells of the islets of langerhans start secreting glucagon hormone,which work as follows:

* Glucogenesis: Breaking up of fat and protein molecules by the liver to produce glucose.

*Glycogenolysis: Production of glucose from glycogen, which is stored in the liver and muscle tissues .

* Lipolysis: Breaking down of fats residing in adipose tissues.

Glucagon proves life saving in diabetics and in normal persons sometimes, as in the case of hypoglycemia, caused by excessive labour, prolonged fasting and over use of blood glucose lowering agents. Glucagon is also injected into pateints with a very low blood glucose level produced from overzealous treatment such as excess insulin or sulphonylureas drugs, crash dieting and execissve exercising. Normally insulin and glucagon hormones are secreted in accordance with the level of glucose in blood. These secretions are controlled by a limit control mechanism or negative feedback system.

SOMATOSTATIN HORMONE: It is secreted from the alfa cells of the pancreas. Its main function is to create obstacles in production of secretions from both alfa and beta cells (glucagon and insulin hormone respectively). It also slows down the digestion of food, as well as the rate of absorption of digested components of food (glucose etc.), due to which the utility of food sustains effect for longer times.

PP (F) CELLS OF THE PANCREAS:  They secrete a hormone called pancreatic polypeptide that hinders the secretion of pancreatic digestive enzymes and the somatostatin hormone.


The two hormones secreted by this gland are thyroxin (T3 & T4) and thyrocalcitonin. The former is associated with glucose metabolism whereas the latter deals with calcium metabolism.

About 0.08 mg of T4 and 0.004 mg of T3 are produced by the thyroid every day in a normal human body. T3 is more potent than T4. The secretion of thyroid hormones is regulated through a thyroid stimulating hormone (TSH) secreted from the master gland pitutary. During winter and in pregnancy, the secretion of thyroxine increases.

The main function of thyroxine is to catalyse the oxidative metabolism of the body cells and thereby increase the use of glucose and oxygen by them. It leads to an increase in the energy production rate and basal metabolic rate of the body cells and tissues. These hormones have a calorigenic effect and increase the ‘tempo of life’. They are necessary for healthy living and growth.

The thyrocalcitonin hormone stimulates bone formation, opposes disintegration of bones and increase the secretion of calcium in urine. Deficiency of thyroid hormone, which may be due either to a hereditary disorder or a decreased intake of iodine, may lead to cretinism, myxoedema (swelling of the body) and simple goitre (swelling of the thyroid gland).

Hyperthyrodism leads to thyrotoxicosis (it may be hereditary but is usually due to infectious diseases, pregnancy or overeating). Increase in body temperature, blood pressure and heart rate are its significant manifestations.


One pair of adrenal glands is situated on top of the the kidneys. The important endocrinal secretions are adrenaline (also called epinephrine), noradrenaline (norepinephrine) and corticosteroids. The regulation of these hormones is through the pitutary gland and also the autonomic nervous system.

Adrenaline increases the basal metabolic rate of each body cell, which in turn helps stimulate the body, as astivity and excitability in tissues also increase. One of the vital function of these hormones is to increase the activity of the autonomic nervous system upto ten times whenever required ( this system governs almost every activity of internal organs: digestion, respiration, heart rate and temperature regulation .

The hyper-secretion of adrenal hormones leads to tissue (muscles) wasting, generalized oedema, hyperglycemia (diabetes mellitus), and sometimes paralysis also. Their deficiency may lead to Addison’s disease, which is characterized by hypoglycemia, dehydration, hypocalcaemia and diarrhoea. Extreme hypocorticism (very low level of these hormones) may even lead to death.

Adrenal hormones are also used as medicine as they prove life- saving in various life threatening situations. But excessive and frequent use of steroids may even lead to diabetes. On prolonged use of steroids as medicine, a patient usually develops a swollen face and other swollen body organs due to sodium and water retention.


This gland is situated in the brain near the hypothalamus. It is also called the master gland (weighing 0.5-1 g) as it governs the secretions of all the other important endocrinal glands. The pituitary gland secretes several hormones, which perform important functions as growth and development of the body and also regulate and coordinate activity of almost all the other endocrinal glands.

Deficiency of one of its hormone vasopressin causes “diabetes incipidus”. The oxytocin hormone is responsible for the contraction of the uterus and the ejection of milk from a lactating mother’s breasts. The growth hormone is responsible for DNA, RNA and protein synthesis in all the body cells as well as for the growth and maintenance of all bones and muscles. It increases the synthesis of glucose from amino acids (gluconeogenesis) and glycogen from glucose (glycogenesis) in the liver. It also helps in decreasing the use of glucose for energy production and stimulates the disintegration of fats (lipolysis). Its influence increases protein production, decreases fats and conserves carbohydrates in the body.

Somatomedins or ‘Insulin-like growth factors’: Like the insulin hormone, the growth hormone, too, stimulates production and secretion of a few special type of growth substances (insulin like growth factors IGFs) in the liver, muscles, bones and other body tissues. These growth factors are called somatomedins. Normally they help in building body tissues but in starvation or fasting conditions these elements work against insulin and under their influence there is an increased use of fatty acids for energy production. But in this process excessive ketones are produced giving rise to a serious disorder called ketoacidosis.

In African pygmies there is a severe lack of somatomedins in the blood. Persons who remain extra small due to deficiency of growth hormone are fully mature mentally and also have normal reproduction capability to some extent. Nowadays growth hormones are being commercially produced by a recombinant DNA technique for therapeutic use.

Excess growth hormone results in over-growth and leads to proportionate gigantism in childhood, but in the adult it causes disproportionate gigantism and is also termed acromegaly and hirsutism. The chances of diabetes increase several times in such patients because excess growth hormone also causes hyperglycemia. Such diabetics have increased chances of ketoacidosis, too, because of excess disintegration of fats for energy production.

In females breast development takes place by combined effect of prolectin, thyroxine, insulin and growth hormone. Follicle stimulating hormone (FSH) and leutinizing hormone (LH) help secrete estrogen in females and testosterone in males (sex hormones). ACTH (adreno cortico trophic hormone) and TSH (testosterone stimulating hormone) hormones regulate secretions of adrenal and thyroid glands respectively.

Apart from the endocrinal system, other systems and organs of the body also play important roles in maintaining good health. Their brief description will aid the better understanding of diabetes and diabetes related complications.

Hence in the following text the structural and functional aspects of various organ systems present in the human body are discussed. Uncontrolled diabetes adversely affects almost every human cell and biochemical reaction. And therefore understanding of anatomy and physiology of different body organs and systems is compulsory, which is described below.


  1. Integumentary System

2. Endocrinal System

3.Muscular System

4. Skeletal System

5. Digestive System

6. Circulatory System

7. Respiratory System

8. Uro-genital System

9. Nervous System

10.Immune System ‘defence against diseases’

1. Integumentary System

It provides a covering to all the outer and inner organs besides being the first line of defence against pathogens. All the related cells of this system form a covering (in one or more layers) for the internal as well as the exposed parts of the body, in the same way as rind (peel) of fruits or vegetables. The skin and mucosa are two important components of this system. The skin is a multi-layered structure, the cells of which are nourished by very small arteries. The mucus membrane lining on the inner side of hollow organs (gastro-intestinal tract, respiratory system, and genito-urinary system) also secrete mucous besides providing protective covering to these internal organs.

The integumentary system not only protects the body from bacteria and other harmful substances but also acts as an impervious barrier also giving shape to body organs and tissues. The very minute holes present in skin and mucus membrane also help in selective exchange of substances through processes such as excretion, secretion, absorption, and gaseous exchange.

These coverings also receive general sensations such as pain, touch and temperature, and special sensations such as vibration, pressure (baro-receptors), position sense, and equilibrium. The cells of the integumentary system have the remarkable capability of regeneration, and this quality is used in healing wounds. In diabetes, due to insufficient nutrition, integumentary system suffers badly (unhealthy skin and mucosa) giving rise to several disorders.

2. Endocrinal system: Described in earlier pages.

3. Muscular system: The locomotion of the body and movements of various organs are performed by these muscles only. Muscle cells together combine to form muscle tissues and a group of such tissues gives rise to muscles. Muscle cells are long, narrow, cylindrical or spindle shaped. They are also called muscle fibres and contraction is their most important speciality. There are three types of muscles :

1.Skeletal muscles are voluntary muscles (striated muscles) and they are mostly connected at both ends to bones by their tendons (these are tough but elastic specialized tissues). They are responsible for the movements of hands and legs and locomotion of the body. The muscle fibres contain glycogen, fat globules and soluble protein myoalbumin. These muscles fulfill most of their energy requirement themselves (from fuel stored in them) by releasing energy from glucose and fatty acids. Skeletal muscles are under control of voluntary motor nerves.

2. Smooth muscles are involuntary muscles (unstriated muscles) and they are usually found in hollow internal organs, such as G.I. tract, urinary bladder, uterus, penis, eyes, skin and sphincters. They are governed by the autonomic nervous system (involuntary nerves).

3. Cardiac muscles, or myocardium, are made from those muscles which are similar to skeletal muscles in structure except that they are involuntary and independent. A few special tissues (cardiac muscles) of the myocardium are capable of self-excitation (Sino-atrial node), and a few others called Purkinge’s fibres, are capable of conducting excitation impulses (Atrio-ventricular node) further in the myocardium.

The heartbeat (normally 70-75 beats a minute) originates in these specialized muscles (SA node) by self-excitation. It is from this impulse that the heart beats rhythmically life long. The contraction in heart muscles is initiated through these impulses only which are propagated into the myocardium by the Purkinge’s fibres (these are also specialized cardiac muscles). Although neurogenic stimulation is not required for production of heart beat, yet, the autonomic nerves affect the rate of the heartbeat to a certain extent approximately 30% (sympathetic and parasympathetic stimulation increases and decreases heart rate respectively).

In diabetes, due to deficiency of essential nutritious substances and lack of exercise the shape of the cardiac muscles change (dilate) and diminish their ability to contract. With increasing weakness the muscles expand in shape and size also in dilated cardiomyopathy.

As all muscles (skeletal, smooth and cardiac muscles), require ample calcium ions (Ca++) and potassium ions (K+) to contract, poor nutrition causing deficiency in body calcium and potassium stores may lead to generalized muscle weakness. A nutritious diet full of vitamins, and regular exercise in fresh air keep the muscular system healthy and energetic.

4. Skeletal System: For giving support and maintaining the shape of the whole body and assisting the movements of the body there is an endo-skeletal framework made of skeletal tissues. The skeletal system consists of two types of tissues:

1.Cartilage is a jelly-like extremely resilient structure made up of water, proteins and minerals. Cartilage is an integral component of all joints, as it greatly helps in their normal functioning. A few cartilages contain elastic tissues, too.

2. Bones are extremely dense and strong. The ground substance of bone is made up of salts (calcium and magnesium phosphate) and carbonic substances. Bones are a storehouse of calcium and phosphorus salts and are helpful in the regulation of these ions throughout the body with the help of blood and kidneys. The bone marrow inside the bones produces red blood corpuscles. The bone cells are known as osteocytes.

In diabetics there are destructive changes in cartilages and bones. With the decrease of elasticity, flexibility and smoothness of cartilage, diseases such as frozen shoulder, tennis elbow, cervical spondilytis, and charcot’s joint, develop. An unbalanced diet leads to a lack of minerals in bones and less capability in carrying weight. Weakening of bones also results in less blood formation. For healthy bones vitamin D and calcium are essential nutrients.

5. Digestive System: It consists of the oral cavity, pharynx, oesophagus, stomach, small intestine, large intestine and accessory digestive organs such as teeth, tongue, salivary glands, tonsils, liver, gall bladder and the pancreas.

The hygiene of mouth, teeth, gums and tongue are of utmost importance because one (more particularly a diabetic) is more susceptible to developing an infection in the oral tissues. The salivary glands present in the mouth take part in food digestion and for their proper functioning healthy tissues are necessary. The pharynx and oesophagus are structures for the conditioning and propelling of food into the stomach. The stomach acts as a reservoir where food is disinfected and mixed with water to form a lump of pulpy food called ‘chyle’. The stomach opens in the duodenum through the pyloric sphincter. The re-entry of food into the oesophagus is restricted by a cardiac sphincter situated at the junction of the stomach and the oesophagus. The abdominal cavity is separated from the chest by a diaphragm. Stomach contains around 3-4 billion gastric glands, which secrete gastric juice comprising mucus, hydrochloric acid, digestive enzymes (as pepsin, gastric lipase) and a hormone named gastrin. All other secretions except gastrin are mixed in food for its proper digestion.

The small intestine is a 6 metre long and 2.5 cm broad structure made-up of smooth muscles, mucosal lining and an extensive capillary bed (a net of minute blood vessels embedded in the peritoneum).

The pancreas is situated in between the two arms of the first part of the small intestine that is, the duodenum. The pancreatic duct, carrying secretions of its exocrine gland (pancreatic juice), opens in the duodenum whereas the endocrinal secretions (insulin and glucagon) mix directly with the blood.

Importance of Pancreatic Juice

1-1.5 litres of pancreatic juice is delivered to the small intestine every day. It is a complete digestive juice because it digests carbohydrates, proteins, fats and nucleic acids present in food. Its constituents and their functions are:

1. Pancreatic amylase It converts all complex carbohydrates ‘polysaccharides’ into maltose ‘disaccharides’.

2. Pancreatic lipase It digests lipids into monoglycosides and fatty acids.

3. Pancreatic esterase It digests cholesterol.

4. Phospo-lipase It separates fatty acids and phospho-lipids.

5. Endo-peptidase It is a proteolytic enzyme which coverts complex proteins into small polypeptides.

6. Carboxy-peptidase It converts polypeptides into amino acid monomers.

7. Nucleases They digest nucleic acids (DNA and RNA) present in chyle.


Excessive alcohol use, obstruction of the pancreatic duct, cancer and a viral infection in pancreatic tissues induce inflammation of the pancreas resulting in chronic pancreatitis. Pancreatic enzymes may also be activated in pancreatic tissues during acute pancreatitis, leading to auto-digestion of the pancreas.

Liver: It is a 15 cm long and 20 cm broad structure, situated below the diaphragm, mainly on the right side of the abdomen and weighing around 1.5 kg. Liver cells are called hepatocytes. It also contains one gall bladder with its duct opening in the duodenum. The hepatic artery and the hepatic portal vein enter into the liver whereas the hepatic vein and the bile duct leave it. Metabolites of the hepatocytes either enter the blood circulation or bile (which reaches to the gall bladder).

Gall bladder: The gall bladder is an 8 cm long and 4 cm broad, egg shaped structure, which collects and concentrates bile. Later on this bile is poured into the intestines where it performs an important function that is, it helps digestion of fats (as fats can only be absorbed into enterocytes with the help of bile elements). Excess concentration of bile or an increased amount of cholesterol in the bile may lead to crystal formation (cholesterol bile stones).

Hepatocytes are metabolically very active. Apart from being an important digestive gland, the liver performs following important functions:

1. The bile salts and pigments make the chyle alkaline (necessary for activating the pancreatic enzymes), kill bacteria and help digest fats.

2. Glycogenesis (glucose® glycogen), Glycogenolysis (glycogen ® glucose) and Gluconeogenesis (amino acids and fatty acids ®glucose).

3. It converts ammonia (a by-product of protein catabolism) into urea, which is excreted by the kidneys.

4. It also helps excrete excess cholesterol in stools through bile and also detoxifies byproducts of the body metabolism (prussic acid) and toxins.

5. Regeneration of iron from disintegrated RBCs, synthesis of blood proteins (albumin, globulin) and vitamin A, activation of vitamin D and storage of vitamin A, B12, D, E, K and destruction of bacteria in blood (if present) are other functions of hepatocytes.

In diabetes the liver cells get badly damaged because of accumulation of fat globules (fatty liver) inside them. Alcohol injures hepatocytes as well, and prolonged use causes fat accumulation in and around the hepatocytes. No effort should be spared to prevent hepatitis that is, inflammation of hepatocytes (due to viral infection or chemical use) as it is lethal in a diabetic. Liver cirrhosis and hepatorenal syndrome (failure of liver and kidneys simultaneously) ultimately prove fatal.

The large intestine consists of three major structures: caecum, colon and rectum. Important diseases of the large intestine are appendicitis, colitis, amoebiasis, fissures and hemorrhoids (piles).

 6. CIRCULATORY SYSTEM: The circulatory system, comprising the vascular and lymphatic system, is responsible for supplying the digested nutrients and oxygen to all living body cells and organs. It is also responsible for maintaining the continuous inflow and outflow of chemicals (enzymes, hormones, ammonia etc.) within various body tissues. It helps in achieving homeostasis (a steady state of equilibrium between the temperature, pH of body tissue fluids and chemical constitution of the body tissues). The vascular system comprises heart, blood and blood vessels (arteries and veins). The lymphatic system comprises lymph, lymph vessels and lymph nodes.


It is a closed-fist shaped, conical, pulsating and hollow structure made up of muscles. It weighs about 300 grams and is 12 cm long, 9 cm broad and 6 cm thick. It is situated on the left side of the upper middle half of the human body. The outer covering of the heart is called the pericardium. Internally the heart is divided into four chambers, which are interconnected through the valves.

The right side of the heart (right atrium and ventricle) contains impure blood which has to go to the lungs for purification, and the left side (left atrium and ventricle) contains pure blood which has to reach to all body organs through arteries.

The beatingof the heart is the result of its rhythmic contractions. The first stage is called systole and the second diastole. During systole (as the muscles contract) the volume of the heart decreases and the blood is pushed out of the heart with force (pressure). All cardiac musculature does not contract as a whole at one time, instead it contracts rhythmically that is, first, auricle (upper chambers) then ventricle (lower chambers), hence blood flows in one direction only (unidirectional blood flow). In diabetics due to damage in the SA node, AV node or Purkinge’s fibre (which are responsible for originating and propagating excitation impulses to heart muscles of the auricles and ventricles for contraction) this rhythm may be broken.

Cardiac cycle

After contraction during diastole, when the volume of the heart comes to normal the impure blood reaches the right auricle through veins. Under normal circumstances, on contraction, impure blood from the right auricle is pushed out to the right ventricle through the tricuspid valve. From there it goes to the lungs for purification through the pulmonary valve (pulmonary arch). After purification the pure blood reaches to the left auricle and from there the blood goes to the left ventricle through mitral valve. From left ventricle the blood reaches the arch of aorta (systemic arch) through the aortic valve.Normally the heart rate is around 75/minute and therefore each such cycle (cardiac cycle) is completed in less than 0.8 seconds.

In diabetics, due to the weakness of the myocardium the heart does not contract so well. Moreover, due to expansion of muscles the effective pumping of blood from the heart becomes severely reduced (decreased ejection fraction).

Blood vessels

William Harvey (1628) discovered the fact that blood circulates in human body in a definite circuit (pathway). The heart pumps blood into some vessels called arteries (distributing vessels) which distribute it all over the body and then a few collecting vessels (veins) bring blood back to the heart. The total length of these blood vessels in human body is around hundred thousand kilometre.


There are three types of arteries in the human body: 1. Elastic arteries; 2. Muscular arteries; and 3. Arterioles. The elastic arteries (also called conducting arteries) are the biggest arteries having maximum pressure of the blood. Their inner lining (tunica intima) is thickest having more of elastic fibres and less muscular tissue. The most important property of thesearteries is their elasticity as they expand easily to accomodate more and more blood. The middle and the external layer of these arteries are called tunica media and tunica externa respectively. Presence of elastic fibres in these layers also help in making these arteries more elastic.

In diabetes it is the tunica intima which suffers very badly giving rise to a condition called atherosclerosis (damage in arterial wall giving rise to obstruction in blood flow). The muscular arteries arise from the elastic arteries and reach to different body organs. These arteries have more of muscle tissue because it helps in vasodilation and vasoconstriction. These are also called distributing arteries. Lastly the thinnest arteries which originate from muscular arteries are called arterioles. These arteries also help in regulating the blood flow into the tissues as they have a great capacity to constrict or dilate under the influence of hormones or autonomic nerves.

Blood Capillaries

They arise from arterioles and penetrate deep into the tissue fluid (arterial capillaries). Their wall consists only of a thin endothelium which is permeable to different nutrients, hormones, gasses and other selected chemicals. The nutrients diffuse into tissue fluid and body cells take the nutritious elements and excrete the waste products of their metabolism (carbon dioxide, urea) into the tissue fluid. These byproducts also diffuse (as they are more concentrated) from the tissue fluid into the venous capillaries (the far end of arterial capillary constitute venous capillary).


In tissues the net of venous capillaries constitute venules. These venules collect together to form small veins, small veins combine and form medium veins and medium veins constitute large veins. Particularly those veins which bring impure blood from lower extremities to the heart consist semilunar valves. These valves allow only unidirectional blood flow (they open only towards heart) in large veins.

Vasa vasorum

The tissues present in arterial wall get their nutrition through the blood supplied by very thin arteries called vasa vasorum. Similarly the vessels supplying blood to nerve tissues (peripheral nerves) are called vasa nervosa.


In a healthy person the blood is red in colour and 5-6 litres in volume. Blood is comprised of plasma (fluid connective tissue), which contains suspended cells and cell fragments called blood corpuscles. The pure blood comes out from the heart through a big artery, reaches the smaller arteries, and finally the minute arteries called capillaries, which are spread as a net throughout the body (from roots of the hair to the nail of the big toe). Each cell gets oxygen, water, nutrients, and hormones, through pure blood as required. The waste products (carbon dioxide, urea, and ammonia) which are obtained after metabolism in cells are absorbed back by the impure blood.

Blood corpuscles

The blood corpuscles are of three types that is, red blood corpuscles, white blood corpuscles and platelets. The function of RBCs is to carry CO2 and O2 throughout the body with the help of hemoglobin present inside them. The deficiency of hemoglobin in the blood is called ‘anemia’. The main function of WBCs or granulocytes is to protect the body from infections. With a decrease in the number and efficiency of the WBCs, the immunity system and ability of the body to fight infections weakens. In diabetics, due to incorrect nutrition and deficiency in stored glycogen, these white blood cells are produced in smaller quantity. The result is that even a small infection (respiratory tract infection, boil) takes a serious form (septicemia) and may prove extremely harmful.

The main function of blood platelets is the clotting of the blood. Another main function of blood is controlling the body temperature and internal homeostasis. In diabetics, due to the continual increase in blood glucose and lipid levels the walls of the arteries become hard (and inelastic) and the lumen narrows resulting in high blood pressure and a decreased blood supply to the vital organs.

Lymphatic System

It consists of lymph vessels and the lymph flowing in these vessels. The lymphatic net is also spread throughout the body organs. Its function is to carry any blood left in tissue fluid from arterial capillaries (which is not able to reach venous capillaries) and the debris from worn out cells back into the blood stream. Its other functions are strengthening of the body’s immune system and destruction of bacteria and other microbes (with the help of lymph blood corpuscles called lymphocytes). Apart from lymph and lymphatics the other components of the lymphatic system are: lymph nodules, lymph nodes, spleen, thymus gland, tonsils and red bone marrow. The functions of these tissues are :

1. Production of lymphocytes

2. Filtration of lymph

3. Synthesis of antibodies which help in destruction of the microbes

4. Removal of the harmful substances present in tissue fluid and lymph itself

5. Purification of the blood (through spleen). If there is chronic infection or spread of cancerous cells in body the related lymph nodes (lymph nodes which are adjacent to the diseased organ) swell and many of them are palpable even from outside (it is an important sign which helps in staging of several carcinomas).

8. RESPIRATORY SYSTEM: Cellular respiration is the most basic requirement for energy production in a living being. Oxidative degeneration of glucose (cell fuel) yields energy plus carbon dioxide (and it is called internal respiration). The carbon dioxide is carried to the lung tissues (alveoli) which exchange it with oxygen inhaled from external environment into the lungs (external respiration). The organs of this system are the nose, pharynx, windpipe, larynx (sound production), lungs, trachea, bronchi and alveoli. Diabetics are more prone to develop upper and lower respiratory tract infections such as laryngitis, bronchitis, pneumonitis and pleurisy. Pulmonary tuberculosis, a contagious disease is also quite common in uncontrolled diabetics.

9. URO-GENITAL SYSTEM: It consists of two systems, the urinary and the reproductive systems. A few organs participate in both the systems.

I. Urinary System

It consists of a pair of kidneys and ureters, one urinary bladder and one urethra. The prostate gland in males also contributes to this system.


The byproducts of body metabolism as toxic substances, waste material, excess salts and elements all in water soluble form, are excreted from the kidneys with the help of osmo-regulation through the semipermeable membrane of nephrones called basement membrane.

The normal size of a kidney is 12 cm ´ 7 cm ´ 2.5 cm. Initially there is swelling in a diabetic’s kidney, but in later stages of diabetic nephropathy both kidneys contract and become non-operational. The renal parenchyma consists of two portions : cortex and medulla. There are about 12,00,000 nephrones in the renal parenchyma (the number is determined genetically and, once destroyed, nephrones do not regenerate), which are responsible for urine formation.

The nephrone is the smallest functional unit of the kidney. Each nephrone has four parts. The first is the bowman’s capsule, which is a cup shaped structure, comprising of 50-60 fine capillaries making a bunch called glomerulus. The epithelial membrane of the bowman’s capsule and finer membrane of the capillaries, unite to form the glomerular membrane or basement membrane. The impurities travel from the blood into the hollow cavity of the bowman’s capsule through pores present on the glomerular membrane. Hence, it also acts as a sieve (filter). The urine collected in each tubule undergoes innumerable changes (exchange of various ions and water in between glomerular filtrate and the blood). Lastly the formed urine comes to the urinary bladder for final disposal.  

Other than blood purification, the important functions of the kidneys are: homeostasis, regulation of the pH and osmolality of body fluids (water and electrolytes balance) such as serum, cerebro-spinal fluid, and production of erythropoietin (an enzyme which stimulates the production of red blood corpuscles).

II. Genital System

Human beings are not only unisexual but they also have ‘sexual dimorphism’ such as women do not have a beard or chest hair, milk glands are suppressed in men, more subcutaneous fat around buttocks exists in women, and the voice difference in men and women.

(a) Reproductive system in man 

Reproductive system of men comprises testes, prostate and penis with associated structures such as reproductive ducts, epididymis, seminal vescicles, ejaculatory duct and bulbous urethral glands. Impotence, infertility and retrograde ejaculation are the three major problems common in diabetics.

Sperm are made in the testis (in semeniferous tubules) under the influence of the male hormones. They may live up to one month in reproductive ducts, which provide nutrition to these sperms. Infection, hormone imbalance, or obstruction in reproductive ducts may all lead to azospermia or oligozospermia.

Structure of the penis: This knowledge is helpful in the understanding of impotence. The penis is made up of corpora cavernosa and corpora spongiosum muscles, which are divided into many hollow spaces (thus making them spongy) by a tough membrane called tunica albagenia. At the time of sexual excitation these hollow spaces are filled with blood (sixteen times more than normal) supplied by the penile artery (any disease obstructing penile artery will lead to vasculogenic impotence) after which the penis enlarges and hardens.

Prostate gland: It secretes a few enzymes, which contribute to semen formation. After fifty years of age, swelling in the prostate gland (benign hyperplasia prostate or BHP) may cause several difficulties in the urogenital system.

Retrograde ejaculation: The ejaculatory duct opens in the urethra near the internal urethral orifice to deliver semen. At the time of ejaculation, the urinary bladder opening (internal urethral orifice) shuts so as to stop the urine flow in urethra. In few diabetics this normal physiology is disrupted, and as a result the semen flows the wrong way that is, into the urinary bladder.

(b) Reproductive system in woman

It consists of the uterus, vagina, ovaries and associated organs such as breasts. There is one pair of ovaries, which produce female hormones and ova. The ovum travels to the uterus through the fallopian tube. The uterus is a muscular structure providing developmental facilities to the fertilized egg (ovum + sperm = embryo). Sometimes as an exception pregnancy takes place in the fallopian tube (ectopic pregnancy).

Vagina: It is a 7.5-10 cm long contractile tube which the penis enters at the time of intercourse. A mucus secretion from its wall is necessary for pleasurable sex. Infections of vagina (bacterial and protozoal) are common in diabetes mellitus patients.

All somatic cells, except ‘sex cells’ (gametes) contain 23 pairs of chromosomes (sperm and ovum contain only half the number of chromosomes). Genes are situated at specific places on each chromosome. They contain numerous characteristics of a human being. One sperm and one ovum unite together to form a zygotic cell which creates (by mitotic division) a new life.

Limiting of human fertility: It is possible through various measures as follows:

Sterilization; Hormonal contraception; Intra-uterine devices; Barrier methods; Chemical methods; Induced abortion; Physiological methods and Coitus interruptus

Coitus interruptus is totally safe in terms of any of the side effects of mechanical or chemical contraception; three days prior to and three days after ovulation, one should avoid sexual intercourse (as ovulation takes place on about the fourteenth day.


It consists of the brain, spinal cord and nerves. Our eyes, nose, skin, and tongue act as external sensory organs. There are different types of sensory receptors present over these organs. They transfer environmental stimuli to these nerves, the sensory nerve carries these stimulus to the nervous system which reacts (responds) according to the stimulus and transfers the message (if required) lower down which reaches to the effector organs again with the help of nerves (motor unit). The conduction of various informaions in nerves takes place electro-chemically.

Nerve cells (neurones) are the smallest functional and structural units of the nervous system. There are about 100 million neurones in the brain alone. The quality of self-excitability is a particular feature. One more speciality of the nerve cell is the growth of one or more processes (axon) from its nucleus whose length may vary from 1 mm to several metres in a human body; this quality is not seen in any other body cell.

The cell body is the circular central part of the nerve cell. The grey matter of the central nervous system is produced only by these cell bodies. The long part bifurcating from the central cell body is called axon. The velocity of impulses travelling in the peripheral nerves is around 130-200 m/s. The structural as well functional configuration of nervous system is as follows and comprises two parts:

I. Central Nervous System

‘CNS’:It controls and regulates (directly or indirectly) each action and reaction in the human body. Its constituents are the brain and the spinal cord.

The brain is divided into three parts: forebrain, midbrain and hindbrain. The forebrain is the centre of intelligence and forms 80% of the whole brain. Its main functions are intellect, will power, knowledge, memory, speech, contemplation, laughter, weeping, urination, and excretion. Thalamus (smell) and hypothalamus (control of autonomous nervous system) are its other parts. The midbrain regulates muscle actions and eyeball movements. The hindbrain consists of pons and cerebellum and its functions are respiration control, co-ordination of the body organs during standing or locomotion, posture and balancing of the body besides coordination of all voluntary actions.

The spinal cord is a 42-45 cm long, 2 cm thick brain-like hollow structure situated in the vertebral canal. The peripheral nervous system is connected to the brain only through spinal cord.

II. Peripheral Nervous System

‘PNS’ : These are branched nerves whose net is spread throughout the whole body. They form an extensive communication system in the body by joining the CNS with the various sensory organs, muscles (effector organs) and glands (endocrinal and exocrinal).

The peripheral nerves are formed by the combination of one or both sensory and motor nerve fibres (a few nerves are purely ‘sensory’ or ‘motor’ and others ‘sensory-motor’). Sensory fibres receive and conduct the sensory input to the central nervous system whereas the motor fibres originate from the brain to carry out its orders through motor nerves.

‘Reflex action’ phenomenon works only with the help of these nerves. In the case of a burned hand by a hot plate, the sensory root (of the concerned peripheral nerve) carries burning sensation to the spinal cord and immediately the motor unit of the concerned nerve is activated in the spinal cord so as to cause the hand to be removed from the hot plate; the brain is not involved in this reflex action (it all occurs within a tenth of a second). In fact the spinal cord is involved in these types of involuntary acts. In diabetics these sensory and motor nerve cells are badly affected resulting in many serious problems, which will be discussed in detail later in the book.

The autonomic system (ANS) is that part of PNS which controls and regulates the activities of the visceral (internal) organs. Here also sensory and motor nerve fibres do exist, but they are not under voluntary control. Sympathetic and the Parasympathetic are the two divisons of the autonomic nervous system.

There are five main sensory receptor organs, which accept external stimuli that is, sensory input and these are: ear, eye, nose, skin and tongue. A brief understanding of their anatomy and physiology is as follows:


Besides receiving sound sensations the ears also help to maintain body equilibrium while walking and standing. The external ear extends from the pinna to the eardrum. The middle ear consists of the tympanic cavity, three ear ossicles (malleus, incus and stapes) and the eustachian tube. The internal ear is formed of the vestibular and cochlear apparatus. Ducts, canals and semicircular ducts are components of internal ear. Sound waves strike the eardrum, and the middle ear converts this sound energy into mechanical energy and thus transfers vibrations to the internal ear. The cochlear apparatus of the internal ear performs hearing whereas the vestibular apparatus is involved in providing balance to the body and its upset often leads to vertigo.


They act as photoreceptors. Apart from the eyeball, its other constituents are eyelids, eyebrows, tear ducts, eye muscles and optic nerves. Eyelids and eyebrows provide protection to the eye. The lacrimal gland secretes tears (lysozyme) which act as antibacterial, too. Six eye muscles provide motion to the eyeball. A defect in these muscle functions may cause strabismus. The cornea, pupil and lens (the other constituents of the eyeball) remain suspended in eyeball fluid (vitreous fluid). The retina resides in the rear portion of the eyeball where images are formed.

Light rays enter the eye through the cornea, which causes them to focus them on the lens. The aperture through which these light rays enter the eye towards the lens is called the pupil and the muscle tissues involved in it make the iris which has the capability to constrict or release. Like the diaphragm of a camera the pupil diameter controls (by constricting or dilating) the amount of light rays to be focused on the lens. Lens (triconvex) is a transparent, crystalline, colourless and elastic structure, which is mainly made of protein. Irregular and unnatural changes in the lens shape weaken the eye. Due to old age or diabetes the whitening of the lens gives rise to cataract.

Images are formed on a screen called ‘retina’ at the backmost portion of the eye. Pigmentary, neural and sensory cells constitute the retina.

Neural cells (rods and cones) help in visualizing and differentiating the colours of objects.

The optic nerve fibres converge on a point on the retina called the optic disc. Many brain diseases, such as brain tumors, raised intracranial tension, and stroke can be diagnosed correctly by examining the optic disc (papiliodema swelling of the disc, or optic atrophy). One can say that the reflection of the brain health can be known by examining fundus of the patient, with the help of an opthalmoscope (fundoscopy is a non-invasive test).

A most extensive network of capillaries is present on the retina and these minute capillaries supply blood to the retinal tissues. In diabetes the lens and the retina suffer most. Glaucoma is another disease (common in diabetics) which is related to the fluid imbalance inside the eyeball.

Nasal organs

There are two nasal cavities lined by the olfactory epithelium (neuroepithelium) and mucosa having glands of Bowman. These cavities are separated by one nasal septum. Sensory nerve cells of the epithelium extend towards the brain as olfactory nerve, which is connected to the thalamus portion of the brain. Different odours are recognized there.

Tongue (organ of taste)

Small taste buds, which are made by ‘chemo-sensory cells’, are spread over the whole tongue. These taste buds receive (chemo-reception) various taste sensations through the pores situated on their top and transmit them to the brain, which recognizes these tastes. Human beings can perceive four type of taste: sweet, salty, sour and bitter. A few diabetics complain of sweetness in the mouth when their diabetes is uncontrolled. A few herbs supposed to be anti-diabetic have the capability to paralyse the taste buds (especially of sweet taste); this is due to an excess of copper salt in them.


Free, branched and naked endings of sensory nerve fibres constitute the cutaneous sense organs, which are three in number. Pain receptors (wound, inflammation), tactile receptors (contact, pressure) and thermo receptors (cold, heat) are situated on the skin, conjunctiva, mucosa and external genitalia.

11. IMMUNE SYSTEM ‘Defence against Disease’

It is also called the body defence. A human being is protected against various diseases and disorders from birth. This inborn resistance is possible through the skin, mucous membrane, anti-microbial substances in body fluids as interferon, or transferins, natural killer cells (lymphocytes, phagocytes) and an increase in body temperature (fever).

Once a pathogen enters the tissues after breaking the skin barrier, the first line of defence that is, the macrophages (white blood corpuscles) play a significant role. The second line of defence is provided by the neutrophils and the third line of defence consists of monocytes. The specific defence system of the body (acquired resistance) that is, immunity is provided by T and B lymphocytes. Once an antigen such as bacteria, virus or toxin gets entry into the blood, production of antibodies (which are different for different pathogens) from lymphocytes start. These antibodies neutralize antigen, and as a result the disease process is immediately stopped. Lymph, lymph nodes and spleen also provide safety against several types of infections.

The malfunctioning of the immune system may also lead to allergy (hypersensitivity) or immune deficiency syndrome (nil immune response). A heavy dose of allergens in a hypersensitive person leads to generalized severe inflammation, which may cause severe shock and death, too. For a healthy immune system one needs optimum proteins, vitamins, minerals and elements in the diet.ay of menstruation).


“yatha hi varnanam panchanamutkarshapakarshkraten sanyog visheshen shabalbabhrukapilkapotmechkadirna varnanamnekeshamutpattirbhavati, evmev doshadhatumalaharvisheshenottakarshapakarshkriten sanyog visheshen pramehanam nanakaranam bhavati.” (Sushrut Samhita .Nidan.L6.S26).

In the above shloka regarding origin of pre-diabetes (prameha), God Punnarvasu says: Just as by combination of five colours in excessive or little quantities dark, bright and several other colours are obtained; similarly by combination of various types of doshas, dushyas and malas in excess, and deficiency of food, prameha is resulted. Pramehas are of 20 types and if spoiled or enraged they lead to madhumeha or diabetes.


We get ancient written information on the human body and its physiology from the Vedas of the Hindu culture (atharveda and yajurveda). Charaka and Sushruta (500-600 B.C.) scientifically interpreted human anatomy and physiology on the basis of this ancient literature by their own extensive research in the medical field. Hippocrates, Aristotle and Galen (150-350 B.C.) laid down the foundation of allopathy.

Pancha Mahabhuta (5 great elements) and their Association with the three body humours (doshas) i.e., Vata, Pitta and Kapha,    

For better understanding of vedotpattik medical science one should firstly know about a few fundamental facts and then only the further text can be meaningful. The body is composed of five elements that is, vayu (air), agni (fire), jal (water), akash (ether) and prithvi (earthly substances) in definite proportion and any abnormal change in them often leads to disease.

In the Vedas, these five elements are known as ‘pancha mahabhuta’. Sage Charaka calls them: “pancha mahabhuta shariri samvayah purush ityuchyate” which implies that to keep oneself healthy, the amount of these five constituents and their mutual ratio should remain normal in the body.

Whatever we eat, drink or breathe, consists of these pancha mahabhuta, which in turn are responsible for production of the three doshas (humours) in the body namely vata (wind), pitta (bile) and kapha (phlegm). These three doshas carry their respective functions in normal healthy persons as Bhavprakash says : “vayuh pittam kaphacchshreti trayo doshah samasatah; vikratavikrata deham ghananti samvardhyanti ch.” (Bhav Prakash.Prakaran2.S105).

Here it is also important to understand that the word dosha does not mean defect, rather it is the name of a few substances (vata– air, pitta– substance which helps producing energy, and kapha- water content or body fluid) without which the existence of body and life is not possible. But when these doshas (body humours) become disproportionate, they actually transform into ‘kupit doshas’ (vitiated body humours) which are responsible for diseases in human beings. These vitiated doshas may have adverse effects on the human body individually or in combination. One mechanism of disease production is that vitiated doshas disrupt the natural constitution of the body dhatus (produce heterogeneity in body tissues), which in turn leads to some or the other disease.

In general allthe three vitiated humours are pathogenic but due to two reasons the first one ‘vata or vayu’ humour is most serious. Firstly, it is the supplier of pran vayu (oxygen), without which life is impossible and pran also runs in nervous tissues. Secondly as vayu with its force helps in propagation of each and every, small or big particle inside the body, it also spreads the other two doshas throughout the body. In case the other dosha is vitiated, the result will be fast spreading of the vitiated dosha, too, with the help of aggravated vayu. The vayu element also imparts motion to all body organs and its secretions. It is also responsible for voice production and normal functioning of the nervous system.

The fire element’ also known as ‘pitta dosha’ provides the most important thing for life, energy. Pitta is necessary to convert food into energy and every bodily action requires energy, which is possible only due to this pittagni element. It can be also used as a synonym of insulin. Life ceases once this bio-energy finishes. Pitta is responsible for pittagni just as insulin is necessary for food metabolism. If pitta is vitiated it develops the metabolic diseases such as diabetes.

The‘water element’ or the kapha dosha’ is responsible for easy transportation of various substances inside the human body. This is because almost all the substances in the body are water-soluble. Fluidity and solubility are the most important properties of kapha dosha. If water is not present in sufficient amount, then different substances inside the body will not be able to reach the places where they are supposed to act. Apart from this, most of the biochemical reactions occurring inside the human body need water and if it is not available in sufficient amount, life will become impossible. Water is also necessary as a solvent, carrier, blood constituent, for disposal of harmful byproducts of metabolism through urine, and several other functions. In Diabetes a patient loses kleda (kapha and important bio-molecules) in urine.

The ‘earth element’ provides all carbonic and non-carbonic substances, which are obtained from the earth only and forms the basis of body composition. Therefore the physical body structure is provided by earth element.

The akash element (space/ether) provides space to every cell for getting its specific shape. Space is an integral part of the body. Even the most minute structure, an atom, occupies space. Any sort of movement is possible only when space exists.

All substances (eatables, minerals and drugs) including plants and animals consist of the above mentioned five elements in different proportions. And every element has some principal characteristics which also reflect in the substances made of them. These panch tatva (five basic elements) also constitute the three body humours.

Consciousnessis the result of a proportionate mixture of all these five great elements and it adorns the human body as a godly bliss.

Normally diseases result due to some flaw or abnormal changes in the natural ratio of these elements inside the body. Vata, pitta and kapha doshas in a normal healthy body get affected under various combinations leading to all diseases. The important causes of these doshas being adversely affected are dietary imbalances, sedentary life style, improper physical and mental hygiene and environmental pollution.

Dosha (body humours), Dhatu (body tissues) & Malas (excretions) In Normal Human body In Disease Free Human Body 

The food moves forward from the mouth to the stomach, and then to the intestines, with the help of vayu dosha only. The digestive process in the stomach and intestines divides the food into smaller molecules with the help of saman vayu. This division is necessary for absorption of the food ingredients from the intestines into the blood. Besides nutrients (nutritious elements) watery part of the meal also reaches the blood through absorption in intestines. Rest of the indigestible food along with some watery part comes out of the body as faeces with the help of apan vayu.

The great store of the absorbed nutrients in the blood, also called ras ‘body fuel’, is capable of supplying essential elements to all the body cells as required. By the use of these nutrients various types of cells are capable of performing their ascertained functions such as heart muscles perform beating, gland cells perform secretion, brain cells provide wisdom and so on.

The new molecules produced in the body with the help of nutrients in blood, constitute the smallest unit of life that is, the cell. These cells form tissues which are also known as dhatus. These dhatus (body tissues) are necessary for healthy living and prevention of diseases. The seven dhatus which are present in a healthy person are as follows: 1. Ras (micronized nutrients), 2. Raqt (blood), 3. Maans (muscles), 4. Meda (adipose tissue), 5. Asthi (bone), 6. Majja (bone marrow and cerebral tissue) and 7. Shukra (reproductive tissue)

Purification of the three doshas and the seven dhatus produces waste material called malas or excrements, which must be excreted out from the body. The essence of digested food is called ‘ahaar ka sar’ that is, rasas (nutrients and water), which reach into the blood through intestinal absorption. The remaining portion in the intestine is the viscous excretory part ‘mala drava’. From this more water ‘jaliyansh’ is absorbed into the blood which goes out of the body through urine. And the semi-solid excretory substance ‘vishta’ is excreted as faeces with the help of apan vayu.

Excrements or Byproducts (malas) of the Seven Dhatus i.e., Body Tissues

All the three doshas and seven dhatus consist their specific agnis that is, separate-separate metabolic enzymes and pathways. These metabolites get purified with the help of their own specific metabolic energy and become useful for human being (some of the dhatus generate energy whereas others make the body tissues). In this process few metabolic byproducts are produced and these with a few waste products constitute excretions (malas). For successful functioning of the body the excretions also play important role as follows.

1- Mala of ras is kapha (excreta of plasma is water).

2- Mala of raqt is pitta (excreta of blood is bile).

3- Mala of maansis filth of ear (excreta of muscle is ear discharge).

4- Mala of medais perspiration (excreta of adipose tissue is sweat).

5- Mala of asthi is nakh (excreta of bone is nails).

6- Mala of majja is netra ka keechad and twacha ka sneh (flimsiness in eyes and oiliness of skin).

7- Shukra dhatu does not have any mala because it is the most purified dhatu, which only converts into semen and ojus(Charaka samhita).

These malas when excreted out of the body bring relief from several diseases. But an abnormal increase in the quantity of a few malas is also one of the prodormal symptoms of diabetes.

DOSHA, DHATUS AND MALAS IN THE DISEASED HUMAN BODY (Body Humours, body tissues and excretions in diseased human body)

As mentioned earlier all diseases start due to an increase or decrease in the amount or ratio of the three ‘doshas’. And heterogeneity in the ‘dhatus’ (dhatuvaishamya) makes the disease even more serious. Improper excretion of waste also gives rise to complications.

The knowledge of doshas, dhatus and malas and their role in healthy and diseased state of the body is all necessary for understanding of the etiopathogenesis of diabetes and its complications.

Dosha or the Body Humours

They are three in number. 1. Vata; 2. Pitta; and 3. Kapha.

1. VATA (vayu) DOSHA Air humour: Vata is responsible for transporting the other two doshas, seven dhatus and malas (excretions) present in the body, from one place to another, besides several other functions. The other characteristics of vayu humour are its fast spreading quality and minuteness as mentioned by Acharya Sharang : “dehasya sukshmachidreshu vishedyatsukshma muchyate”. (SharangSamhita.Prakaran4).

Vayu is so minute that it can enter the minutest of body pores and shrotas. The other properties are: it is cool, lightweight and a potent pusher of substances present inside the body channels. The natural sites of vayu collection in the human body are fixed as gastro-intestinal tract, heart, brain and lungs, from where it is distributed to the other body parts and serves its purpose.

Vayu also takes along with it the other two doshas namely kapha and pitta so that these doshas reach the proper places to fulfill their duties. Every organ requires these three humours according to its need. But since vayu affects the other two humours also, hence an imbalance in the quantity of vayu also causes disorders in pitta and kapha and thus greatly harms the body.“yatha loke tatha shareere”.According to this law vayu performs the same functions within the body as it does in the outside world; it is life giving as well as a destroyer too. Vitiated vata leads to big damages. Madhumeha or diabetes mellitus is also a disease dominated by vayu dosha.

Acharya Charaka and Sushruta both name five types of vayu in the human body (pran, apan, saman, vyan and udan). But Acharya Madhav writes in his book ‘Madhavnidan’ that principally vayu is of two types pran and apan. The latter three (saman, vyan and udan) are merely the extensions of the pran and apan vayu. In the ‘Gita’ also two types of vayu- pran and apan are described as : “pranapano samo kritva nasabhyantarcharino”.

The doctrine of vata word is va gatigandhanyoh (gati = movement and gandhan = information) that is, one which carries the information of senses from one place to the other in the body is to be connected with vata. In simple language vata means the whole nervous system.

Kaviraj Gannath Sen assumes pran as cervical plexus and apan as sacral plexus. There is another view which assumes that pran and apan both are widespread in the whole body and their clear cut demarcation is not correct. Though nerve tissues associated with sensory functions are predominant in pran vayu (sensory areas of brain and nerves), and those nerve cells associated with motor functions are dominated with apan vayu (motor areas of the brain and nerves). The ‘sthul’ (bulk) portion of vayu or vata is nerve substance but the ‘sookshm ansh’ (minute portion) is the impulse travelling within it (sookshm vata). The natural abode, functions of five types of vayu and diseases caused when these are vitiated are as follows:

Pran Vata

Normal residing place: The brain and the heart.

Activity: Inspiration-expiration, intake of food, spitting, sneezing, belching and carrying of food upto intestines are its main actions. It also controls the intellect, heart, sense organs and mind. The pran vayu does prapan functions (to obtain) such as it provides informations to the brain (sensory functions); the stomach and the intestines get food with its help only (vayu forces the food inside).

Main diseases: Diseases of the sensory areas of brain (loss of sensations), somatic sensory loss, hiccups, heart, and respiratory diseases.

Apan Vata

Normal residing place: The anus and the large intestine.

Activity: All motor functions of the brain and functions like defaecation, excretion of urine and semen, child birth, secretions of endocrinal and exocrinal glands and perspiration are all the main functions of apan vayu.

Main diseases: Constipation, hormonal imbalance, diseases of motor areas of the brain and nerves, abortions, impotence, and sweating disorders.

Udan Vata

Normal residing place: The chest, throat and nose.

Activity: Both the lungs, the heart, the throat and the respiratory tract are all included in the working field of udan vata. Its main functions are sound production; articulation; accepting of substances; increasing of oja, strength, varn (skin colour) and memory; energy production and respiration. It also involves functions like udharvakshepan (throwing up).

Main diseases: The functions of udan vayu are performed correctly only when this vayuis pure. The diseases produced are voice disorders, weakness, memory loss and respiratory diseases.

Saman Vata

Normal residing place: The stomach, the small intestine and coordinating neurones.

Activity: Digestion (secretion of digestive enzymes); separation of digested food into ras ‘essence’ and kitt ‘excretory’ part; food absorption and coordination between sensory and motor nerves.

Main diseases: Gastric acidity, indigestion, malabsorption and loss of coordination between sensory and motor functions.

Vyan Vata

Normal residing place: The whole body and the heart.

Activity: It has high velocity and it conducts in the whole body. It also helps propagation of blood and ras in blood vessels, heart beating, pulse formation, and motion related acts (picking up something, throwing, opening and closing of eyes, walking, running, contraction, dilatation and movements in internal organs). Because vyan vata is spread all over the body it can also be regarded as a part of the peripheral nerves.

Main diseases: Diseases of the blood circulation, arrythmias, dysfunctioning of the internal organs, peripheral neuritis, and movement disorders.


‘fire element or pitta humour’: Pitta is a warm, yellow coloured, thin and sour substance, which increases ‘jathragni’ (the fire of the stomach)and digests the food. It also separates the hidden nutrients (ras), mala, urine and doshas from the digested food.

The pancreatic pitta firstly reacts (forms a covering) with the digested nutrients in blood and only then this complex (pitta + nutrient molecules) is made available to all the body cells for metabolism where energy is generated and new tissues are formed.

Pittagni is equivalent to insulin as when it combines with other nutrients (carbohydrate, protein and fat present in digested food) then only the human body can make use of these nutrients otherwise not as has been said by Bhavprakash :

“pachakam pachate bhuktam sheshagnibalvardhanam” (Bhavprakash.Prakaran.2.131). Modern science also emphasizes that energy production in the cells is due to the reaching of the glucose molecule from blood into the cells, with the help of insulin only. Besides this insulin is also required for food preservation as glycogen, adipose tissue and muscle tissue synthesis. The five types of  pitta  ( the bile humour), their functions and diseases caused when vitiated are as follows:

Pachak Pitta

Normal residing place: Pancreas.

Activity: Helps in food metabolism by making the nutrients available to the cells.

Main diseases: Carbohydrate intolerance, Diabetes mellitus.

Ranjak Pitta

Normal residing place: The liver and the spleen.

Activity: Blood formation.

Main diseases: Anemia.

Sadhak Pitta

Normal residing place: The heart.

Activity: Intellect and memory.

Main diseases: Loss of memory and decreased IQ.

Bhrajak Pitta

Normal residing place: The skin.

Activity: Skin colour and lustre.

Main diseases: Vitiligo.

Alochak Pitta

Normal residing place: The eyes.

Activity: Vision.

Main diseases: Blindness.


‘water element or kapha humour’ :It is a sweet watery fluid. It is an integral part of each body tissue and body secretion (enzymes, synovial fluid, and blood). It also plays important role in majority of biochemical reactions. It is the connecting medium of doshas, dhatus and malas and makes them move from one part of the body to the other. Excess of kapha causes prabhuthamutratha (excess urination), madhumeha (diabetes mellitus) and many other diseases such as asthibhangurta (arthritis), jalodara (generalized swelling) etc. Critical deficiency of this element may cause death (dehydration) also.

The water element is the main factor performing good or bad functions of kapha dosha . The five types of kapha doshas, their functions and diseases caused when they are vitiated are as follows:

Kledan Kapha

Normal residing place: The stomach.

Activity: Mixing of the food.

Main diseases: Indigestion and anorexia.

Avalamban Kapha

Normal residing place: The heart.

Activity: Functioning of the heart.

Main diseases: Heart disorders, swelling over the body.

Rasna Kapha

Normal residing place: The oral cavity.

Activity: Taste.

Main diseases: Loss of taste.

Snehan Kapha

Normal residing place: The brain.

Activity: Sensory motor functions.

Main diseases: Brain disorders.

Shleshmak Kapha

Normal residing place: The joints.

Activity: Formation of synovial fluid.

Main diseases: Osteo-arthritis.

Symptoms of Dosha Collection in the Human Body

According to Charaka the increase or decrease in symptoms of doshas should be considered as symptoms of vitiation of the doshas as : “dosha prakrati vaisheshyam niyatam vriddhi lakshanam” (CharakaSamhita.Sutra.L18.S53).

General Symptoms of ‘Doshas’ collection are :

1. Yellowness of eyes and face.

2. Decrease of agni (energy).

3. Heaviness and laziness.

4. Hatred for food and activities responsible for the particular dosha collection.

Due to several reasons (most important are wrong eating and living habits, and heredity) on increasing of doshas, the dhatus of the body also get vitiated, and as a result either they increase or decrease, besides becoming heterogeneous also in amount (dhatu vishamta). This state of the body when the tissues start deforming is most serious, but still the disorder remains in the curable stage. However on delay of correct treatment the disease becomes incurable. Nourishment and cleanliness of all dhatus (body tissues) are two important essentialities for Aarogyata ‘good health’.

DHATUS (Body Tissues) and their Functions

“prinanam jivanam lepah sneho dharanpurane; garbhoatpadachra karmani dhatunam kathitani hi.” (Bhavprakash.Prakaran2.S160). It means the functions of seven dhatus are as follows: function of ras is prinam (to satisfy), raqt gives life, maans performs the function of lepan (envelopment), meda that of snehan (oiliness), asthi performs the work of bearing, majja that of puran (completion) and shukra that of reproduction. The seven dhatus (important biomolecules and body tissues) and their normal functions are as follows:

Ras dhatu (nutrients):Glucose, fatty acids, amino acids, vitamins, minerals and elements along with water present in the blood constitute the ras dhatu. It reaches all the body cells as required to nourish them and also to activate their production. All the other successive dhatus are made by the use of the ras dhatu (yoni– mother dhatu) which contains all necessary substances. Most of the poorly treated diabetics have deficiency of this important dhatu.

Raqt dhatu (blood) The base of life is pure blood. Impure blood should be made pure and if required it should be removed. Further dhatusare also formed with the help of the blood as it contains all nutrients and circulates throughout the body.

Maans dhatu (muscles) Muscles are made by combining ushma (energy), raqt dhatu (ingredients of blood) and vayu dosha. There are about 500 small and large muscles in a human body described by Acharya Sushruta. The veins, nerves, bones and joints strengthen up by adhering to these muscles. Muscles provide motion to the body and body organs. They also store energy for emergency requirement besides giving strength to one’s body.

Meda dhatu (adipose tissue) It is a heavy, strong and nourishing substance. In normal amount it is beneficial to a human being. But its excess aggravates vayu dosha, which in turn leads to prameha and madhumehabesides several other diseases.

Asthi dhatu (bone) Asthi (bone) is formed by ripening with the help of agni and drying with the help of vayu of the meda dhatu. There are about 300 small and major bones in the body. These bones provide infrastructure to the body and contain ‘majja’ inside them. They also protect several other important internal organs such as the brain, lungs and heart by providing a covering.

Majja dhatu (bone marrow and white cerebral tissue) The essence of bone and ras dhatu (nutrients) form the bone marrow and white cerebral tissues. Majja dhatu forms several other important substances, such as red and white blood cells.

Shukra Dhatu (Reproductive tissue) Semen, Atarva and Ojus Shukra is the purest dhatu in the body and is formed from ‘ras ka sar’ (the essence of all the dhatus). Semen, ovum and ojus all the three are formed with the help of shukra only. As against common belief (shukra is synonym to semen and it remains only in genital organs), shukra dhatu is spread in each and every cell of the human body. When a person is happy and feels satisfied while performing sex with a woman, this ‘virya’ (shukra), which is living in all the body cells, becomes apparent in the shape of semen. In the absence of sex testicles produce oja only.

The raj or atarva (menstrual bleeding) is again an essence of ras dhatu and appears in females only once in a month (it starts after the age of 11-12 years and remains till 50 years of age). This atarva is because of the shukra dhatu. And atarva made over one month with the help of the ras dhatu flows as menstrual bleeding for three days. After attaining pregnancy the pathways of atarva are blocked, hence bleeding stops and this atarva and pathway combine to form the placenta. Some atarva goes to the breasts of the pregnant woman and makes them healthy. The ojus is also formed with the help of the shukra and is dealt in detail later on.

The seven main dhatus have their updhatus, too, which contribute in healthy as well as diseased states of the body. The seven dhatus are: ras, raqt, maans, meda, asthi, majja and shukra and their updhatus are: milk, menstrual bleeding, free fats, sweat, teeth, hair and ojus .



“sarv ev pramehastu kalenapratikurvatah; madhumehatvamayanti tadasadhya bhavanti hi.” (SushrutSamhita.Nidan.L6.S27). It means all types of prameha if left untreated or partially treated convert into asadhya madhumeha (incurable diabetes). Prameha is a disease characterized by prabhuthamutratha’- excessive urination and ‘avilamutratha’- turbid urine.

As history reveals, the knowledge of the syndrome of diabetes mellitus, existed with the Indians since prehistoric age. Its earliest reference in Ayurveda is found in a mythological tale, where it is said to have originated by eating Havishtha (a special food which used to be offered at the time of yajna) organized by DakshaPrajapati, the father inlaw of Lord Shiva (CharakSamhita.Nidan.L11).

What is pre-diabetes?

Pre-diabetes is a state of the body characterized by ‘a potential abnormality of glucose tolerance’ that is, glucose (carbohydrate) intolerance in an otherwise healthy individual. This decrease in ability to utilize glucose for energy production may be due to two important reasons-.

1. Slow destruction of insulin secreting b-cells (insulin or madhusudini vikriti).

2. Relative insulin deficiency (vraht vayudosha).

Because of the above two reasons there are certain changes in the body physiology leading to a few symptoms, which caution against the impending big problem, ‘diabetes mellitus’.

According to modern medicine, development of diabetes is a long process and takes around 1-15 years (either due to exhaustion of b-cells ‘secretory defect’, or decreased activity of insulin hormone ‘peripheral insulin resistance’). Ayurveda, Chinese, Tibetan and other ancient therapies also mention that diabetes develops due to a long time disorder in the form of vata/yin vitiation.

This long period prior to overt diabetes may be referred to as pre-diabetic stage and symptoms of this stage can be called prodormal symptoms of diabetes. Certain symptoms can be easily recognized but there are a few symptoms/signs, which can only be identified by investigations as blood or urine analysis. If efforts are made to check and prevent these prodormal symptoms, it will become possible to put a check on diabetes. Everybody interested in preventing diabetes in oneself, should know how to recognize these early symptoms, because probability of developing diabetes at one stage or the other of life, exists with everyone in modern days.

For confirming of diabetes, the results of the fasting blood glucose level FBG >140 mg/dL (>7.77 mmol/l) and 2 hours after meals PPBG >200 mg/dL (>11.1mmol/l), repeated at two different occasions, are most necessary. If blood glucose levels range between more than normal but less than diabetic status, then it is said, that the person has probability of developing diabetes. In such a situation, one must start taking the proper precautions.

There are several diseases, which are considered precursor (forerunner) of diabetes in the long run. Hence if a person is able to recognize the symptoms at the so called ‘prodormal stage’ of diabetes itself, he can be cured of pre-diabetes; and there is full probability of not developing diabetes at all in the future, too. Thus prevention of disease is possible. It is very satisfying to note that ayurveda and a few ancient therapies notably chinese therapy (yin/yang/chi theory of diseases) and homeopathy (which advocates theory of nervous diabetes) have done enormous work in this field and guided mankind to recognize these abnormal states (pre-diabetic conditions) at the earliest and treat them optimally to prevent diabetes. Unfortunately modern science does not talk much of complete eradication of the probability of diabetes.

Symptoms of pre-diabetes (as  per ayurveda):

Ayurveda says when prameha (pre-diabetes) changes to madhumeha (diabetes) then development of the following symptoms takes place : “danta deenam maladhayatwam pragrupam panipadyoh; dahashrichakkanata dehe trit swadvasyam cha jayate” (Vagbhatt.Nidan.10) and also “talugalgivhadanteshu malotpattih” (SushrutSamhita.Nidan.L6.S5).If an otherwise normal individual develops any of the following symptoms, he or she must become cautious.

1. Paleness in the skin, eyes and urine.

2. Profound weakness and fatigue without any apparent disease.

3. Repeated infections of the urinary tract, respiratory tract, and the skin.

4. Rapidly increasing obesity or sudden loss of body weight.

5. Loss of concentration and deterioration in memory.

6. Desire to lie down and feeling of avoiding all physical activities.

7. Extreme oiliness or dryness of skin.

8. Habitual abortion.

9. Feeling of sweetness in mouth and hatred for sweet items.

10. Loss of lustre in the face and shine of the body.

11. Inflammation in the palm and the sole of foot.

 Above symptoms are the pointers of diabetes in ‘evolution phase’.


It implies to :

A few diseases or conditions, which can give rise to diabetes and some other complications if not treated completely.

A few diseases or conditions, which precede diabetes that is, ‘impending diabetes’ or first stage of diabetes.

There are a few diseases or conditions, which appear before diabetes and they also predict the probability of developing of diabetes. These are:

1. Pre-clinical diabetes or chemical diabetes.

2. Prameha or pre-diabetes ‘the precursor of madhumeha or diabetes mellitus’.

3. Impaired glucose tolerance test (IGTT).

4. Gestational diabetes mellitus (GDM).

5. Obesity related diabetes in teens.

6. Malnutrition related diabetes mellitus (MRDM).

7. Stress diabetes.

8. Diseases of the endocrinal glands other than the pancreas.

9. Viral diseases: Coxsackievirus, mumps, measles, hepatitis, infectious mononucleosis, and rubella.

10. Diabetogenic drugs.

11. X-syndrome.

12. Other genetic syndromes.

1. Pre-Clinical Diabetes or Chemical Diabetes

The diagnosis of symptomatic diabetes is not difficult. When a patient presents with the signs and symptoms attributable to an osmotic diuresis (polyuria) and is found to have hyperglycemia, essentially all physicians agree that diabetes is present. The problem arises with an asymptomatic patient who for one reason or the other is considered to be a potential diabetic but has a normal fasting blood glucose concentration i.e., <140 mg/dL. If such patients with or without reason (illness or other cause) get their blood glucose level tested after eating (carbohydrate overloading), usually it comes out more than normal (blood glucose level >140 mg/dL) but less than the diabetic status (blood glucose level <200 mg/dL). But on taking normal food and when body becomes healthy (no other illness or precipitating factor as stress) then their increased blood glucose level touches normal. This subset of patients are said to be having ‘chemical diabetes’.

It is not possible to assess exactly which of these patients may become diabetic in due course of time. This is because several persons (>80%) suffering from chemical diabetes do not develop diabetes at all in life that is, 80% patients diagnosed as chemical diabetics do not develop overt diabetes at all.

Normally sub-clinical diabetes is diagnosed when a person gets blood test done due to some other illness or just in routine and his blood glucose level comes out to be more than normal (>160 mg/dL). At this stage if symptoms of preceding diseases (as hormonal imbalance, infections, decreased immunity) are present then symptoms of sub-clinical diabetes also appear.

Those persons who are more susceptible to develop diabetes due to heredity (positive family history of diabetes) should get regular investigations done because if diabetes is diagnosed at the earliest stages itself (pre-diabetes), it is possible to remove any further damage to the pancreas at this stage itself.

Note: As per latest guidelines of WHO the Abnormal Fasting Plasma Glucose Level is considered to be >126 mg/dL instead of >140 mg/dL.

2. Prameha or Pre-Diabetes ‘The Precursor of Madhumeha i.e., diabetes’

‘Madhumeha’ signifies diabetes mellitus which is one step further to prameha (advanced state of prameha is overt diabetes). As we know several diseases of the body are manifestations of the misbalance of the three humours that is, vayu, pitta and kapha. The condition worsens when the dhatus are also adversely affected by the doshas and vitiated dhatus convert into dushyas.

Prameha is a disease in which all the three humours (doshas) are adversely affected (tridoshaj disease) and when disease remains unattended, the nutrients such as glucose, protein, adipose tissue, minerals and elements are excreted in urine (dhatukshaya) and gradually prameha becomes incurable. It is rightly said in ayurveda that all pramehas change into madhumeha if not timely treated “sarv ev pramehastu kalenapratikurvatah” (SushrutSamhita.Nidan.L6.V27).

Wordly Meaning of Prameha

Pra : excess in both frequency and quantity and Miha: watering. The word Prameha is derived from the root Miha Sechane meaning ‘watering’. In reference to the diseases of human beings, it may have a meaning of passing urine, qualified by prefix ‘pra’ meaning excess in both frequency and quantity. Vaghbhat says : “samanyam lakshanam tesham prabhutavilmutrata” (Vagabhatt.Nidan.S10) i.e., passing out of deformed urine (avilmutra) in excess quantity (prabhuta pariman) is one of the most common symptom of this disease.

Definition: The name prameha is self-explanatory. It is defined as a stage when a person urinates excessively and frequently (prabhuthamutratha) and the urine is turbid (avilamutratha) as said by Sushrata :“tatravil—-“ (SushrutSamhita.Nidan.L6.V6). Moreover there is dominance of kapha in all the pramehas as Charaka says : “bahurdravah shleshma dosha visheshah” (CharakSamhita.Nidan.L4.S6) i.e., extremely fluid kapha dosha is present in prameha. Prabhuthamutratha (polyuria) is said when a person passes more than 2000 ml of urine/d (normal urine output = day time 39 ounces + after sunset 13 ounces, a total 55 ounces or 1500 ml).

Many times people confuse frequent urination (common during urinary tract infection) with polyuria. Polyuria means more than normal amount of urine but mostly it is also associated with increased frequency of urination. Most of the times polyuria is non-serious and may be due to extremely cold climate, drinking of more fluid or diuretic property drinks. But it can be pathological also such as in prameha and madhumeha.

The causes of avilamutratha (turbid urine) are several as : presence of phoshphates, chyle, albumin, pus, fibrin, bases, bile pigments, hemoglobin, indican, blood, oxalate, urate, casts, fats, semen and glucose also.

Hetu (causes): Ayurveda had established the general causes of prameha and madhumeha very clearly 4000 years ago and these causes are proving even more relevant today.

Rishi Sushruta says : “dwo prameho bhawatah- sahajopathyanimittashcha; tatra sahajo matrapitrabeejadoshkritah ahitahaarjoapathyanimittah” (SushrutSamhita.Chikitsa.L11.S3). It implies prameha developing due to wrong eating habits and unhealthy mental thinking and heredity is its yet another important cause. Acharya Madhavkar also says : “kruddhe dhatukshayadvayo doshavritpathethva” (Madhava.Nidanam.L.33.S24) i.e., prameha developing due to severe dhatukshaya (loss of body tissues in urine) or avrita vayu (obstructed vayu) is fatal.

Rishi Vaghbhat also clearly pointed some environmental triggering factors for the development of pramehasuch as sedentary life style, midday nap, lack of exercise and obesity.

Rishi Charaka said prameha may be hereditary or one may develop it later in life by distorted eating and working habits (ahaar-vihar nimitta). The latter cause is proving to be true in the present times as the number of diabetics is growing at a very rapid pace. Stating the causes of prameha Rishi Charaka says :“asyasukham swapnasukham dadheeni gramyodakanuparsah payansi; navannpanam gudvaikritam ch prameha hetuh kaphakricchsarvam” (CharakSamhita.Cikitsa.L6.S4). The meaning of the above shloka is described in the coming text.

Asyamsukham ‘eksthanasanratih’& a person who comfortably carries out his works sitting at one place only. swapnamsukham ‘shayanam vidhivarjitam’& excess sleep is harmful. dadhini&products made from curd as cream, butter, and ghee. gramyodakanuparsah& beasts with excess fat as goat, cow, and pig. navannpanam& grain from new harvest. In ayurveda meaning of apathya is heavy food (one which digests with difficulty). gudvaikritam& products of jaggery, molasses or sugar. kaphakriccha ‘kaphavardhak’ products& items made from milk or excess water. All the above are the definite causes of prameha. Sushruta has considered kapha increasing products as the main cause of prameha and also mentioned the predominance of water element (kapha) in all types of prameha.

In the following shloka Rishi Sushruta writes in detail about the causes of prameha and madhumeha as “divaswapnavyayamalasyaprasaktam sheet snigdhamadhurmedyadravannpan- sevinam purusham janiyat pramehi bhavishyateeti”(SushrutSamhita.Nidan.L6.S3). It means persons who sleep in the afternoon, do not excercise, are always lazy and take in oily, sweet, fat increasing diet have tendency of developing prameha. Today modern science also accepts that besides heredity there are certain environmental risk factors which are extremely helpful in developing diabetes and these are lack of labour in daily routine, sedentary life style and unbalanced diet containing excess fats and calories.

Whether females develop prameha and madhumeha or not?

A few Acharyas have said prameha is not found in females as there is a shloka in Tantrantar: “rajah prasekannarinam masi masi vishudhyati; sarvshariram doshashrach na pramehantyatah striyah”. It implies, menstrual cycle of females, too, plays a role in the development of prameha. Madhumeha and other types of prameha are seen in females but those in whom the menstrual cycle is regular do not develop prameha. It develops in those ladies only in whom menstruation is irregular and unsteady or scanty. But Dalhancharya does not consider the above theory to be absolutely true as he says : “ettatu na yuktam, sarvtantraprasiddhe pratyakshvirodhacch”. This is however sure that females suffer from diabetes to a lesser degree than males.


Acharya Charaka says : “sadhyah kaphotha dash, pittajah shad yapya, na sadhyah pawanacchtuskah; samkriyatvadwishamkriyatvanmahatyatvacch yathakramam te.” (CharakSamhita.Cikitsa.L6.S7). There are 10 kapha, 6 pitta and 4 vata pramehas.

Though prameha is a tridoshaj vyadhi (a disease arising due to vitiation of all three body humours simultaneously), the relative predominance of one dosha and specific dushyas, enables its classification into vataj, pittaj and kaphaj prameha.

These have further been classified into 20 subtypes: kaphaj-10, pittaj-6 and vataj-4. The sixteen types (kaphaj-10 and pittaj-6) differ in the physical characteristics of urine as colour, density, odour and volume depending upon the different properties of kapha and pitta humour. Vataj prameha has been sub-classified into 4 subtypes depending upon the dushyas (vitiated dhatus) being excreted through the urine. The urinary characteristics of these patients also differ from others. There are several classifications in use as:

1. Humoural (doshic) classification : The main causes of kaphaj, pittaj and vataj prameha are deformities in vata, pitta and kapha body humours. But once the specific dushyas (when the body tissues such as the muscles, and the adipose tissue get vitiated by humours they are called dushyas) reach the vasti (urinary system) and are eliminated out in urine with respective humours then 20 types of prameha result.

Important dhatus, which are adversely affected in prameha are called dushyas and they are raqt (blood), meda (adipose tissue), maans (muscles), ambu (water), asthi (bones), majja (bone marrow), shukra (reproductive tissue), oja, lasika (lymph) and vasa (lipids). Normally these dushyas are not abandoned out through urine. But in prameha specific dushyas reach the bladder and are eliminated out through urine.

2. Classification based on the body constitution : Charaka divided pramehis in two broad groups : 1. Lean and thin ‘asthenic’ (krisha) pramehi; and 2. Obese (sthula) pramehi. Rishi Charaka says: A patient of apathyanimittaja (related to disordered eating) prameha is called a sthula/strong/obese pramehi and a person of sahaja (congenital or hereditary disorder) prameha is called krisha/durbal/lean and weak pramehi. Further he says that a strong and obese pramehi is one in whom there is dominance of specially the kapha humour. Hence a ‘sthula mehi’ is one in whom prameha develops after birth due to intake of apathya food. On the contrary one in whom vata dominance occurs and is of asthenic body, then one is a ‘sahaja mehi’. These pramehis only, later on turn to obese (type 2) and asthenic (type 1) diabetics respectively. Rishi Sushruta says a weak pramehi should always be specially protected.

3. Classification depending upon inheritance: Rishi Sushruta, founder of ayurveda shalya chikitsa (surgery) classified prameha as: 1. Congenital (sahaja) prameha It develops due to beeja dosha (inherited from parents or forefathers). It is incurable and one has to live with it.  2. Acquired (apathyanimittaja) prameha It develops due to faulty eating habits and life style and is fully curable, if timely treated.

Sushruta says : “dwo prameho bhawatah- sahajoapathyanimittashch; tatra sahajo matrapitra beejadoshakritahahitahaarjoapathyanimittah.” (SushrutSamhita.Cikitsa.L11.S3). It means sahaja prameha is hereditary ‘kulaja rog’ and apathyanimittaja prameha is because of ‘ahit ahaar’ (harmful diet).

Sahaja prameha, whose cause is hereditary, seems to be equivalent to asthenic built krisha pramehi, and probably juvenile onset diabetes according to modern science.

Apathyanimittaja prameha, which is equivalent to obese prameha, is the leading cause of an explosive increase in the number of obese diabetics, because these are the pramehis who have full potential to convert into diabetics in the future. In allopathy the apathyanimittaja madhumeha is also called adult onset diabetes; if correctly treated these diabetics never require insulin injection.

4. Classification based on management guidelines: Acharya Sushruta says : “tatra krishmannpan- pratisanskritabhih kriyabhishrichikitset, sthulampatarpanyuktabhih” (SushrutSamhita.Cikitsa.L11.S4). This means a krisha (weak) patient should be treated by a diet including sneh (oil) that is, santarpan, and an obese patient by aptarpan processes as exercise, and restricted diet.

As regarding management also there are two groups of pramehis and madhumehis. Treatment of lean patient is firstly done by brahan chikitsa ‘promotary treatment’; and that of an obese patient by vaman ‘emesis’ (if kapha is increased) or virechan ‘purgation’ (if pitta is increased); and finally both are given purification and pacification treatments respectively.

5. Prognostic classification: Acharya Sushruta says that in equilibrium ten kaphajanya prameha are sadhya (curable), six pittajanya prameha are yapya (palliable) and, four vatajanya prameha are mahatyaya (which may kill a patient) and therefore asadhya (incurable). And all these if not treated in time become incurable.

Rishi Charaka says: “sapurvaroopah kaphapittamehah kramen ye vatkritashrach mehah; sadhya na te pittakritastu yapyah sadhyastu medo yadi nam pradushtam.” (CharakSamhita.Cikitsa.L6.S56). It means : apathyanimittaja prameha are curable whereas hereditary (since birth) pramehaare incurable.

As far as the prognosis in prameha is concerned, treatment at a very early stage makes it sukh sadhya (curable), in the middle stage kasht sadhya (curable with difficulty) and in the later stage asadhya (incurable) but still treatable.


If a person wants to prevent himself from diabetes then he should make proper efforts by identifying the symptoms at the early stage of prameha (pre-diabetes) only. As has been mentioned earlier, prameha if not treated in time surely leads to diabetes hence all efforts must be made to cure it at the earliest stage possible. For this a person should be able to identify properties of abnormal urine at prameha stage (pre-diabetic stage) itself as colour, quantity, odour etc. By saying 20 types of prameha one does not mean 20 types of diabetes. Infact these prameha are a reflection of the various disorders in the functioning of the body tissues/dhatus, which one can recognise through the symptoms as change in physical properties of the urine. At the most prameha can be considered as pre-diabetes.

The diabetes spreading in developing countries today is the spoilt form of prameha. As far as curability and incurability of the disease is concerned it can be said it is curable in the initial stages and not in the later stages.

Purva Rupa (prodormal symptoms)

The prodormal symptoms of prameha are as follows : “swedoangagandah shithilangata ch shayyasanswapnsukhe ratishrach; hrajnetrajivhashravanopadeho ghananghata keshanakhati vriddhih” (CharakSamhita.Cikitsa.L6.S13) i.e., bad smelling sweat, weakness in extremities, letharginess, deposition of malas in chest, ear, nose, and tongue, and extra growth of nails and hair.

Further Charaka says : “sheetpriyatvam galtalushosho madhuryamasye karpaddah; bhavishyato mehagdasya rupam mutreabhidhavanti pipeelikashrach.” (CharakSamhita.Cikitsa.L6.S14) It implies: more infinity to cold substances, drying of the throat and palate, sweetening of the mouth, burning sensations in the hands and the legs, and coming of ants where one urinates, are a few early symptoms of prameha. But prior to developing symptoms of specific prameha one may experience the general symptoms of abnormal humour accumulation (dosha sanchaya) as follows:

(a) Common symptoms of vata vikar (disorders due to vitiated vata humour)

1. Weakness, loss of strength and desire for heat.

2. Stiffness in organs and palpitation.

3. Concentrated urine.

4. Loss of sleep.

(b) Common symptoms of pitta vikar (disorders due to vitiated pitta humour)

1. Weakening of the sense organs and desire for cold.

2. Paleness of the stools, urine, eyes and the body.

3. Increase in the body temperature and spells of unconsciousness.

4. Decrease in urination.

(c) Common symptoms of kapha vikar (disorders due to vitiated kapha humour)

1. Heaviness, rigidity and coldness in joints.

2. Body temperature falls and increase in sleep.

3. Whiteness in stools.

4. Increased salivation.

Vishesha rupa (specific symptoms)

Rishi Charaka says : “varn rasam sparshamthapi gandham yathaswadosham bhajate pramehah; shyavavaruno vatkritah sashulo majjadisadgunyamupaityasadhyah.” (CharakSamhita.Cikitsa.L6.S12). All pramehas get colour, ras (taste), sensation (consistency) and odour in urine according to the type of the humour which is vitiated.

There are different symptoms in urine for recognizing different prameha. The urinary characteristics helpful in identifying the twenty types of prameha (kaphaj 10 + pittaj 6 + vataj 4 = 20) are as follows:


1. Udakmeha syn. diabetes incipidus : The urine is clear, water like, in more quantity, odourless and cool. Important diseases associated with udakmeha are kidney diseases, high blood pressure, disorders of adrenal and pitutary glands. Less important conditions are excess intake of water, drinks containing diuretic property such as tea, cocoa or diuretic drugs and mental tension.

2. Ikshumeha syn. alimentary glycosuria : Patients passing urine as sweet as sugarcane juice are called ikshumehi. Because of improper metabolism and assimilation of glucose in body the excess (unproductive) glucose spills in urine. Vaghbhat says diabetes and ikshumeha are two separate diseases as : “sarveapi madhumehakhya madhuryacch tanoratah”. The treatment of ikshumeha is simply reducing high carbohydrate diet and exercises (pathya aahar-vihar). By doing so the disease subsides itself.

3. Sandrameha syn. phosphaturia: Modern doctors call it phosphaturia. In this disease if the urine is kept for some time in a container it becomes thick. This state is either because of pus or fibrin in the urine.

4. Surameha syn. acetoneuria: The urine remains clear at the surface but concentrates at the bottom of the container. The colour of the urine is just like wine and it smells as fruits.

5. Pishtameha syn. severe phosphaturia: Charaka calls it shklimeha. Urine becomes as white as rice water and patient experiences chills while urination.

6. Shukrameha syn. spermatorrhoea: The urine is like semen or mixed with semen. The urine may contain sperms as it is a complication seen in diabetics (retrograde ejaculation). The semen like urine can also be present in situations such as kidney, liver, nerve and heart diseases.

7. Siktameha syn. lithuria: There are small pieces of stone (like sand) in the urine. Patient may also complain of urinary stone.

8. Sheetmeha syn. renal glycosuria: The urine is sweet and cold. It contains glucose along with nitrogen and ammonia. The renal glucose threshold lowers only because of excess nitrogen and ammonia in the urine (ammonia lowers temperature and thus reduces renal glucose threshold) and this leads to excretion of glucose at a lower blood glucose level (<180 mg/dL).

The blood glucose level of these patients never rises to diabetic range i.e., >200 mg/dL and glycosuria is only present under the influence of ammonia in the blood and the renal tissues. This disorder also does not require anti-diabetic treatment.

9. Shanermeha syn. obstructive uropathy: This disorder develops because of some obstructive pathology in the urinary tract (pelvis, ureter or urethra). The patient urinates slowly and repeatedly, and urination is often associated with pain.

10. Alalameha syn. albuminuria: The urine is fibrousand sticky (snigdh and pichhil) as it contains albumin. Rishi Sushruta had called it phenmeha because it makes too much phen (lather/foam) while urinating. There are several simple and serious causes of this condition such as deterioration of diabetes, prolonged standing, high protein diet (meat and milk) etc.

Note: Ikshumeha and sheetmeha (kaphaj prameha) and ojomeha (vataj prameha) are conditions synonymous to glycosuria, where the patient passes sweet (glucose) urine. Among these ojomeha refers to diabetic glycosuria while ikshumeha and sheetmeha are non-diabetic glycosuria.


1. Psharmeha syn. alkalineuria : Generally the urine is slightly acidic. But if the urine is retained in the urinary bladder for a long time it becomes slightly alkaline. The causes of this disease are: 1. prolonged holding of the urine; 2. swelling in the prostate (BHP); 3. urethral deformity; and 4. chronic cystitis. The colour, smell, taste and touch of the urine is similar to that of a base.

2. Neelmeha syn. indicanuria: The colour of the urine is blue and it contains a substance called indican. When putrefaction of albumin (protein) takes place anywhere in the human body, usually in the large intestine, indican is produced which reaches the kidneys with the blood and filters into the urine giving rise to classical symptoms. This state of the body can be because of chronic constipation, intestinal obstruction, diarrhoea, cholera, inflammation of intestines, pulmonary inflammation and advanced pulmonary tuberculosis. Colour of the urine is initially normal but changes to blue after some time.

3. Kalmeha syn. ?Carbolic aciduria: Because of excess of pitta the colour of the urine becomes black like ink. It occurs because of several reasons such as presence of red blood cells, indican, indole, pus, melanin and carbolic acid in urine. Kalmeha also develops because of putrefaction of proteins and collection of pus in the muscles. In melanotic sarcoma one can get this type of urine.

4. Haridrameha syn. bilirubinuria : The colour of the urine becomes turmeric yellow and it is because of excess bilirubin in urine. It is also called bileuria. Sometimes the normal constituent of the urine that is, urobiline is in excess in the urine giving rise to this condition. Besides jaundice this condition also arises during anemia, complicated fevers, renal tumor and black water fever when only hemoglobin comes into the urine (not the whole RBCs).

5. Majisthameha syn. haemoglobinuria : The normal colouring agent of the urine is urobiline. When there is an excess of this agent because of abnormal breaking of haemoglobin, the colour of the urine becomes smoky, it smells like uncooked food (amagandh) and also looks like a decoction of majistha. It all occurs because of hemorrhage in the ureter or the kidneys.

6. Raqtmeha syn. hematuria : The red blood cells come in the urine. The urine is smelly, warm, salty and blood like in colour. It occurs in hemorrhages in the urinary bladder, kidney tumors, hemophilia, purpura and scurvy.


1. Vasameha syn. lipouria : Fats and pus are present in such type of urine. According to modern medicine it may be called lipouria (when lipids are present) or pyuria (when pus is present in urine). It occurs in kidney or urinary tract infection, gonorrhea or decaying of the urinary tract tissues.

2. Majjameha syn. albuminuria: The urine of these patients contains albumin. It means that there is loss of the body proteins. It is equivalent to dhatukshayajanya prameha. It occurs in kidney diseases, overeating of proteins, severe infection in the body tissues, tuberculosis of the kidney, diabetic nephropathy and a few other diseases.

3. Ojomeha syn. diabetes mellitus : Sweetness of the urine is only because of oja in it. When a person starts losing ‘apar oja’ (there are two types of oja- par oja and apar oja) in his urine he gets diabetes mellitus very soon. The taste of the urine can be sweet or pungent. Modern science calls this state as diabetes mellitus or madhumeha.

4. Hastimeha syn. lymphuria: A patient urinates like an elephant that is, forceless urination and dribbling of urine all the time. It may contain lymph and this disease may be caused by autonomic bladder (in brain stroke and hemiplegia), renal stones and prostate enlargement.

Conclusion: The above 20 types of prameha have individual characteristics in the urine and if one gets proper treatment at the right time, he can terminate the chances of diabetes in him. If masses can be educated about them a large section of the society can be prevented from diabetes as well as many other serious diseases simultaneously.

In Conclusion the Twenty sub types of prameha and there synonyms in allopathy and identification by urine characteristics are as follows:

Name of Prameha                 Syn. in Allopathy                   Urine Charteristics

Kaphaj prameha

1. Udakmeha                         Diabetes incipidus                  Urine is cool,    clear, water like sp. gravity, odourless, and frequent.

2. Ikshumeha                        Alimentary glycosuria            Urine is cool, sweet, turbid, sticky, like sugarcane juice, and in excess.

3. Sandrameha                       Phosphaturia                        Sedimentation and thickening of collected urine in a short time.

4. Surameha                             Acetonuria                              Colour and smell of urine is like alcohol or acetone.

5. Pishtameha                          Chyleuria                             Urine is white in colour like rice water.

6. Shukrameha                           Spermaturia                        Semen like or sperm mixed urine.

7. Siktameha                          Lithuria                            Minute sand like particles are present in urine.

8. Sheetmeha                                Renal glycosuria             Urine is sweet and very cool suggesting low body temperature.

9. Shanermeha                              ——-                       Patient frequently passes small amount of urine slowly and without force.

10. Alalameha                              Albuminuria                          Urine is thread like and having picchil (sticky) consistency.

Pittaj Prameha

1. Psharmeha                               Alkalinuria                         Smell, colour, flavour, and touch of urine is like that of an alkali mixed in water.

2. Kalmeha                                       ?Indicanuria                         Urine is like black ink in colour and warm.

3. Neelmeha                                       Indicanuria                            Urine is blue in colour and acidic.

4 Haridrameha                                   Bilirubinuria                             Urine is yellow coloured and bitter. Burning in micturition.

5. Majisthameha                              Hemoglobinuria                       Urine is smoky, blood coloured, and also smells like mango.

6. Raqtmeha                                  Haematuria                          Urine is red, warm, mango smelling, and also contain salts.

Vataj Pameha

1. Vasameha                                   Lipuria                                 Urinecontains fats along with its colour, consistency, and smell.

2. Majjameha                                  Albuminuria                             Urine contains albumin and bone marrow like substance. Sarpimeha ‘Sushruta’

3.Hastimeha                                                                              Constant dripping of urine in large quantity. Urine comprises lymph also.

4 . Ojomeha                              Diabetes mellitus                    Urine is sweet, pungent, yellowish, rough having high specific gravity.

Note: The patients of ‘Ikshumeha’ and ‘Sheetmeha’ is temporary and on decreasing sugar items in one’s food, the glucose in urine disappears and the disorder is completely cured (Charak). Charak stressess that ‘Ikshumeha and Sheetmeha’ are due to deformities in kapha dosha (humour) predominantely and not the vata dosha.                         


Samprapti: The evolution of prameha can be understood in the following two steps:

I’st step

The first step is to understand the normal physiology of the human body. Food enters into the stomach and gets digested and absorbed into the blood through the intestines. In the blood it provides nutrients and water (ras and ambu dhatu respectively) for the nourishment of the dhatus. A substantial part of nutrients get converted into energy with the help of pittagni (insulin) and the waste of the food and metabolites is excreted predominantly through the faeces and urine.

II’nd step

The body physiology in prameha is now being described. Everything remains normal till the nutrients and water reach the blood. But due to deficiency of pittagni the nutrients do not convert to energy properly and these excess nutrients reach vasti (vasti word is used for all the components of the urinary system) for filtration. Because of accumulation of abnormal humours in the body and the vasti both, these nutrients and water are excreted in the urine which is not a normal phenomenon. And instead of being utilized in the body, the excretion of these nutrients prove very dearly to the human body. This is the beginning of prameha and madhumeha.

Charaka says the deformity or disorder in the vasti is essential for the development of prameha and madhumeha. This point seems to be very important because it is the kidneys only which get adversely affected in diabetes primarily and all the other major complications are linked to it such as hypertension, heart disease, stroke, retinopathy, micro and macro vascular complications and so on and so forth.

Sushruta also fully agrees with Charaka as he says : “tasya chevam pravrattsyaparipakka ev vatapittashleshmano yada medsa sahekatvamupetya mutravahishrotamsyanusrityadho gatva bastermukhamashritya nirbhidhyante tada pramehanjjanyanti” (SushrutSamhita.Nidan.L6.S4) i.e., ama doshas start excreting out of the body with meda and vasa only through the dysfunctioning vasti and later on more dhatus are also excreted out forcefully giving rise to diseases like pre-diabetes and diabetes. In fact ama doshas and ama dhatus (immature humours and body tissues respectively) both have high affinity to renal tissues and therefore only it all happens (excretion of glucose and protein in urine).

Atidravatwa’ in dhatus (liquidity of body tissues)

The vitiated humours mainly kapha in association with vata and pitta pollute the body tissues all over. Firstly kapha enters in disproportionate amount into the body tissues especially the meda (adipose tissues) increasing its liquidity. Similarly kapha also vitiates the muscles and the other vital body tissues. This abnormal association of kaphawith the other body tissues makes the latter more fluid and unstable, too. This abnormal change in the vital body tissues becomes responsible for disordered functioning. Thus different body organs and organ systems (made of these tissues) cannot function properly giving rise to several symptoms and disorders.

Due to mixing of kapha with the dhatus, the stability of the vitiated dhatus also suffers badly (vital tissues no longer remain solid and stable). The excess vayu drives these liquified dhatus (initially meda, kleda and maans dhatu) towards the kidney. And weakened kidneys (vasti) of a diabetic do not find themselves capable of resisting the loss of vital tissues in the urine. It is noteworthy here that Sushruta has clearly stated that vasti dushti (diseased urinary system) is essentially present in all diabetics that is, diabetes develops only when there is structural or functional deformity in one’s kidneys and urinary system (also read chapter 2, normal functions of the kidneys).

It should be noted that one segment of the kidneys, the glomerulus, simply acts as a seive which filters the blood (and the filtrate is almost identical to blood except blood cells and proteins) but remaining portion of the kidneys, the tubules help reabsorption of the nutrients and water back into the blood stream. As the humoral abnormalities increase, the other important nutrient bio-molecules like vasa, majja, lasika, and oja also start excreting in the urine because malfunctioning kidneys do not retain these immature humours and body tissues, too.

Specific Etio-Pathogenesis of the Three Types of Prameha

There are various patho-physiological changes, which take place before and during the evolution of prameha and madhumeha. When food items and activities capable of increasing the particular humour or humours are observed for a long duration, one’s body tissues ultimately get vitiated and severe loss of the nutrients takes place (dhatukshaya) and thus the proportion of the nutrients in the body also does not remain normal. It all leads to heterogeneity in tissues which is the root cause of dysfunctioning of several organs.

Different humours are responsible for the different nutrient bio-molecules being excreted in the urine. This is because every humour has affinity with a particular set of nutrients for example kapha finds properties of meda, kleda and maans closer to its own properties and therefore it primarily reacts with them and makes them unstable, too. The vitiated humour attracts the nutrients with similar properties towards the vasti (kidney) and once they reach there, the humour is excreted in the urine along with the vitiated body tissues (doshas and dushyas both are excreted in urine).

Prameha updrava i.e., Complications of Pre-Diabetes

The important complications of prameha are: trishna (desire for food and drinks), atisara (diarrhoea), dah (burning sensation all over the body but especially extremities), and daurbalya (debility). Sushruta has mentioned malabaddhata that is, severe constipation as a very common complication of prameha. As the body of the diseased person is loaded with meda (fatty tissue) one develops severe constipation which does not respond to common laxatives/purgatives in usual doses also. The complications of prameha also guide us about the early stages of pre-diabetes and diabetes.


(a) Acute Complications of Prameha

Name in Hindi/Sanskrit   English Translation   Meaning

Trisha                              Excessive thirst          More drinking of water

Alasya                             Laziness                    Loss of interest in work

Pratishyaya                      Influenza                    Common cold

Shaithilya                        Tiredness                   Loosening of body organs

Atisara                             Loose motions            Watery diarrhoea

Jwar                                 Fever                         Increased body temperature

Dah                                 Burning sensation        Feeling of body burning

Arochak                          Loss of appetite           Disinterest in food

Apach                             Indigestion                 Decreased & disordered digestion

Kapha praseka                Sputum/Phlegm          Expectoration

Chardi                            Nausea/Vomiting         Feeling of vomit

Vasti-bhed                      Pain in micturition       Renal pain

Amlika                           Acidity                       More acid formation

Laulyam                         Epicure                      Desire of spicy food

(b) Chronic Complications of Prameha

Name in Hindi/Sanskrit   English Translation    Meaning

Makshika sarpana           Flies on body               Body secretions attract flies

Mamsopachaya              Increased muscles        Unnatural muscle growth

Shushk kasa                   Dry cough (vata)           Cough but no expectoration

Ardra kasa                      Wet cough (kapha)        Productive cough

Shwasa                           Breathlessness             Dyspnoea

Vrishanaavadarna           Ripping of scrotum         Infection of the scrotal skin

Panelu                            Pale body                     Anaemic body

Nidranash                       Loss of sleep                 Difficulty in falling asleep

Kamp                             Tremors                         Trembling of body

Baddhapurishatva          Constipation                  Improper evacuation of bowels

Hridaya shool                 Angina pectoris         Typical cardiac ischemic chest pain

Shool                             Neurogenic pain     Pin-pricking type of pain in extremities

Lolata                             Desire to eat more      Polyphagia

Anidra                            Less sleep                 Disturbed sleep

Prameha pidika              Boils and carbuncles   Skin infections

Putimamsa                     Muscle degeneration    Decaying of body tissues

Vidhradi                         Abscess                     Collection of pus

Note :Symptoms as unconsciousness, vomiting, high fever, dyspnoea, septicemia and heaviness signify advancement of the disease.

Genetic Factors in Prameha

Including ayurveda all authentic medical therapies mention a strong relationship between thedevelopment of prameha and heredity. Acharya Charaka and Sushruta had described this relationship in great detail. In Charaka samhita and Sushruta samhita one finds description of prameha and madhumeha as familial diseases or ‘kulaja rog’ and the causes of their origin as genetic or chromosomal disorders ‘beeja dosha’.

Sushruta says “tatra sahajo matrapitrabeejadoshakritah” (SushrutSamhita.Cikitsa.L.11.3) i.e., sahaja prameha (equivalent to type 1 diabetes) is due to a defect in the beeja (ovum and sperm). But one can also develop this disease even if it was present in forefathers and not necessarily in the parents.

Charaka has not only explained about beeja dosha but the minutest details of beeja anatomy and pathology also in great detail. He confirms the role of beeja (sperm and ovum), beejabhaga (chromosomes) and beeja bhagavayava (genes) in the pathogenesis of pre-diabetes and diabetes. One really gets emotional on reading how our ancestors even without any advanced means made such important discoveries just by their hard education, immense labour and experience and scripted them down to keep a man healthy.

Today modern researches have proved that the above facts are true. Acharyas have also said that on accumulation of thehumours on thesperms and theovum, due to apathya ahaar-vihar (wrong eating and living habits), the chromosomes also get vitiated and carry diseases called ‘hereditary diseases’ and transfer them to thenext generation. Today scientists call it genetic mutations (abrupt changes in genes) and no reason has been given for this in modern medicine.


The approach to the treatments of all types of pramehas is common. Patients who are asthenic must be advised promotary treatments first. It is necessary as they can be put on purification treatment only when they are in a position to bear its effects. Emesis, purgation, and enema measures are employed to purify the body from various abnormal humours. Obese patients can be put directly on purification measures. After purifying one’s body from abnormal humours, santarpan (nutritious diet) should be given to all the patients. Medicines which pacify abnormal humours (anti-prameha medication) at the same places where they are situated should be tried next in all the patients, if required.

The treatment of glycosuria presents difficulties. According to Rishi Charaka, the glucose in the urine of the patients of ‘ikshumeha’ and ‘sheetmeha’ is temporary and on decreasing sugar containing items (carbohydrates) in one’s food, glycosuria is fully cured. He stresses that the above two disorders are due to the deformities in kapha dosha and not vata dosha.

Vataj Prameha is of two types curable and incurable. Curable vataj prameha is that type of prameha in which the vata increases with simultaneous increase in pitta and kapha humours. Incurable vataj prameha is that type of prameha in which the vata increases due to extreme weakening of pitta and kapha and severe dhatukshaya.

All Acharyas agree that by timely treatment, all types of pramehas are curable. The detailed treatment (medicinal and extra-medicinal) of prameha is dealt later.


It is observed many times that the blood glucose level does not remain normal after consuming a diet rich in simple carbohydrates in a few persons. In fact in these persons glucose metabolism does not take place properly; as a result the glucose load is not cleared by the body and blood glucose level increases. But to label these persons as pre-diabetic or diabetic is incorrect.

Today the facility of testing the blood glucose level is available very easily in every household which has its own benefits but the disadvantages are also there nonetheless. Due to improper knowledge regarding diagnosis of diabetes many times wrong conclusions are drawn after checking the blood glucose profile of a previously unknown diabetic person. Blood glucose level after consuming carbohydrate rich diet or 75 g of glucose (2 h later), if comes out in the range of 160-199 mg/dL (8.8-10.9 mmol/l) then the diagnosis of pre-diabetes is incorrect as it has been proved in researches that more than 80% patients of this category do not suffer from diabetes for the next five years at least.

In fact these persons could be kept under the category of IGTT (impaired glucose tolerance test). A person having impaired carbohydrate or glucose tolerance should balance his diet and improve life style (regular exercising and timely sleep) and try to remain tension free. But in no case should he always keep thinking that he is susceptible to diabetes in the future. In reality these persons are also as much prone to developing diabetes as other normal persons without carbohydrate intolerance.

4. Obesity Related Diabetes in Teens

A few years back this disease was considered as a ‘non-entity’. But today we are observing an unanticipated rise in the number of type 2 adolescent age diabetics. Genetic factors, changes in life style and other environmental risk factors are the important causes of development of diabetes in children, adolescents and adults alike. It is normally seen that children who are obese (due to eating of excess fat and sugar containing food) have increased danger of developing insulin resistance that is, insulin is being produced in normal quantity but remains inactive (less active) thus resulting in increased blood glucose levels.

Studies on heredity reveal that if both mother and father are suffering from obesity then chances of obesity in children are very high (~75%). With no family history of obesity the chances of obesity in children are only about 15%, especially in developing countries. Besides obesity the hormonal changes in teenage, stress and lack of physical activity are also the contributory risk factors for developing of diabetes. Habit of eating while watching television, excessive use of fast foods and cold drinks and family tensions are all other triggering factors (Couch Potato Syndrome). For prevention of this disease in children, preventive education of masses is essential. Even if it develops then removing the known risk factor in the child may cure the problem.

5. Malnutrition Related Diabetes Mellitus (MRDM)

Children belonging to the lower income group of society suffer from malnutrition due to lack of food (low buying capacity) and those belonging to the upper class due to lack of correct knowledge (and practice) about healthy food. Under these circumstances if any triggering factor (infection, strong medicine) is present which results in an increase in insulin requirement then the healthy pancreas may not generate sufficient insulin so as to normalize elevated blood glucose levels only because of the deficiency of raw material for insulin in the blood. Thus the result is malnutrition related diabetes mellitus.

The b-cells of pancreas make insulin with the help of first class proteins, vitamins (mainly vitamin E) and chromium (Cr) element. If our food lacks in any one of these substances, sufficient active insulin production is not possible. In developing countries ~75% (three-fourths) of diabetics also suffer from malnutrition related diabetes and when their diet is balanced then production and activity of natural insulin increase by at least 25% in 3 months only.

For prevention of malnutrition related diabetes in children and adults, too, the masses should be educated regarding balanced diet and inclined towards eating home made products. Toffee, chocolate, fast food, coke, chips and other fat or sugar containing items should be avoided and stress should be laid on healthy nutritious foods such as roti (chapati, bread), daliya (porridge), dal (lentils and pulses), rice, milk, fruits, fresh vegetables, and white meat.

6. Stress Diabetes

Much evidence suggests that the standard oral glucose tolerance test (OGTT) over diagnoses diabetes to a remarkable degree, probably because a variety of stresses produce abnormal test. The operative mechanism is thought to be epinephrine (adrenaline) discharge especially when a person is under severe mental or physical stress. Epinephrine blocks insulin secretion, stimulates glucagon release (a hormone having opposite properties of insulin), activates glycogen break down (glycogenolysis) and impairs insulin action at target tissues (insulin helps deposition of glucose and fatty acids in target tissues). It affects in such a manner that hepatic glucose production is increased (neoglucogenesis) and the capacity to dispose of an exogenous glucose load is impaired (slows glycogenesis).

A good example of stress diabetes is as follows. A very interesting finding noted in practice is that even anxiety over venipuncture (a procedure for collecting blood) may generate sufficient epinephrine so as to produce an abnormal blood test that is, the blood glucose levels may increase upto 200 mg/dL, simply due to various types of anxieties.

Concomitant illness, inadequate diet and lack of physical exercise during stress period also contribute to false positive examinations (high blood glucose levels). Stress hyperglycemia sometimes is due to an endogenous release of glucagon and catecholamines. The examples are severe burns, acute myocardial infarction and other life threatening illnesses.

In the changing environment of today we find that 1 out of every 10-12 people that is,10-12% people are suffering from diabetes in the developing countries. Whereas in developed countries this figure is much less. Unfortunately most of the diabetics in developing countries are adolescents and of young age who are in the most productive period of their life and have to suffer greatly due to diabetes. If we are able to normalize (cure) more than half the patients of this group with the help of natural measures, it will definitely be a great service to mankind.

Firstly, all sections of the society (of all age group) should know that stress diabetes is a curable disease, but it needs certain positive changes in life style and corrective measures in eating habits. Secondly, one should know how to prevent this disease totally or even if it develops then how to put a check on it in the earliest stages itself. For achieving the above aims education regarding causes, symptoms and prevention of prodormal diabetes and overt diabetes is essential.

7. Diseases of Endocrinal glands other than the Pancreas

Besides the pancreas, the other three endocrinal glands, which play important role in carbohydrate metabolism are the pituitary, the thyroid and the adrenals.

Hyperpituitarism : Due to over secretion of the growth hormone from the pituitary gland the blood glucose level rises and patient may develop diabetes mellitus. One can diagnose pituitary diabetes by observing a few bodily features. During growing years (child and adolescent) due to excess secretion of growth hormone the body grows too fast and the development of all body organs is far more than normal and height may also reach ~8 feets (proportionate gigantism).

But after growth period (>20 years of age), excess secretion of growth hormone leads to gigantism but height does not increase. The bones of hands, legs, lower jaw become extra large and enlarging of tongue, eyelashes, nose, chin and dense hair on body giving appearance of ‘gorilla’ are all its important recognizing features. Mammary glands increase and hunchback appears. This stage is called ‘acromegaly’. If left untreated, it gives rise to pituitary diabetes. But by recognizing the excess secretory stage of pituitary gland in the earliest stages itself, this type of diabetes can be totally prevented.

Hyperthyroidism : Excess secretion of thyroid hormone ‘thyroxine’ (T3 and T4 ) is caused by infectious diseases, pregnancy, and over eating. Its classical manifestations are increase in the body temperature, heart rate and blood pressure. Such patients complain of irritation, tiredness, weakness, insomnia, irritation, perplexity, trembliness and diarrhoea. The patient of hyperthyroidism is recognized by his bloating eyes and swollen throat. Due to the effect of thyroid hormone the utilization of glucose in cells increases (simultaneously neoglucogenesis also increases) which results in an increase in energy production, basal metabolic rate and blood glucose level.

The calorigenic effect of thyroid hormones increases the‘tempo of life’. Whereas deficiency of this hormone (hypothyroidism) also slows down the above processes. Several complications result in diabetes when the thyroid gland does not function properly.

Adrenals : Cushing’s syndrome occurs due to an excess secretion of adrenaline hormone from the adrenals (how adrenaline and noradrenaline contribute in the development of diabetes has been explained under the topic stress diabetes). Moon face, buffalo hump, fatty stomach, coarse voice and thick hair, moustache and beards in girls are its features. By surgical treatment of adrenals, prevention from diabetes is possible.

‘Pheocromocytoma’, a tumour of adrenal gland (sometimes it may occur in ganglions of the autonomic nerves as these nerve cells also secrete catecholamines) secretes excess catecholamines, which are capable of developing norepinephrine and epinephrine stress hormones. The main symptoms of this disease are high blood pressure (hypertensive crisis), seizures and anxiety attacks, which do not respond to ordinary treatment. Over half of the patients have impaired glucose tolerance due to suppression of insulin and stimulation of hepatic glucose output under the influence of stress hormones. The impaired glucose tolerance almost never requires specific treatment and disappears after removal of the tumour cells.

8. Viral Diseases (coxsackievirus, mumps, measles, hepatitis, infectious mononucleosis, rubella etc.)

An environmental factor believed to be a virus plays detrimental role in onset of diabetes especially in children (juvenile onset insulin dependent diabetes). The sequence of events in the development of type 1 diabetes due to virus is as follows: Virus attacks the normal b-cells of a healthy person who is probably genetically predisposed and then the following chain reaction takes place.

Normal b-cells + virus® insulitis (virus protein merging with b-cell wall protein)® inflammation of b-cells® conversion of b-cell from ‘self’ to ‘nonself’® activation of the immune system ® destruction of b-cell by b-cell auto-antibodies® insulin dependent diabetes mellitus (IDDM).

Points Favouring ‘Virus’ as a Causative Agent of Diabetes

1. Seasonal variation in the onset of disease.

2. More than a chance relationship between appearance of diabetes and preceding episodes of mumps, measles, hepatitis, infectious mononucleosis, rubella, coxsackievirus infections.

3. Induction of diabetes in experimental animals by infecting them with coxsackievirus.

4. Rise in titer of neutralizing antibody to coxsackievirus in few patients of insulin dependent diabetes.

Thus there is strong possibility that a virus (yet not identified) can cause diabetes especially in children and possibly in persons with a defective immune system. No convincing evidence of recent viral infection such as raised antibody titers is against the theory of viral etiology. All efforts must be made to avoid viral infections especially in children as it helps in prevention of type 1 diabetes to a certain extent. Preventive measures as: immunizations against polio, measles, mumps, rubella, and hepatitis should be conducted thoroughly at the right age. Defective immunity can also be rectified through proper medication along with use of genetic engineering in treating the defective gene.

9. Diabetogenic Drugs

Several drugs used for treating other diseases can also lead to hyperglycemia, but most simply they produce only impaired glucose tolerance, which is transient and abolishes on stopping of the concerned drug. Therapeutic or iaetrogenic use of steroids may also lead to diabetes or deteriorate previously existing diabetes. Chronic alcohol consumption leads to pancreatitis and later on ‘secondary diabetes’. Phenytoin sodium, a commonly used drug for epilepsy competes for sulfonylureas (a potent drug to decrease blood glucose level) and as a result hyperglycemia sets in. Diuretics (drugs which cause increased urination and thus help in reducing high blood pressure), psychoactive agents (such as lithium containing salts), catecholaminergic agents (used in nervous system disorders) and analgesics (usual pain killers as aspirin, acetaminophen), all these drugs may lead to temporary hyperglycemia.

10. X-Syndrome

It is a disorder of young age related with the fast life style of the metropolitan cities. It is characterized by four important features:

1. Mild diabetes (elevated blood glucose levels).

2. Mild hypertension (elevated blood pressure).

3. Obesity (increased BMI).

4. Ischemic heart disease at young age (premature IHD).

Various studies have confirmed the origin of x-syndrome totally because of changed wrongful life style. X-syndrome arises due to the downfall in human values and the mental agony thereafter, in the modern highly mechanized life. It can be treated by removing the above mentioned disorders of life style.

11. Other Genetic Syndromes

The incidence of type 2 diabetes increases in a number of inherited syndromes as down’s syndrome (triosomy or translocation of chromosome 21), turner’s syndrome (karyotype 45 xo; mosaics) and klinefelter’s syndrome (karyotype 47 xxy; mosaics) and their physical characteristics are easily recognizable. By observing proper precautions diabetes is preventable in these patients.


Who Should Get Diabetes Checked Up?

If any of the following combination is present.

Age 45 + Over weight

Age 45 + Hypertension (high BP)

Age 45 + Strong family history of DM

Age 45 + History of IGTT

Age 45 + Family h/o premature IHD

 If obesity (>40%) is present with any of the conditions mentioned below.

Age >55 years

Either parent/blood relative is diabetic

Chest pain or breathlessness

Sedentary life style

Heavy alcohol intake

If any two of the following are present.

Age >60 years

Obesity >40% of B.M.I.

I’st Degree relative is diabetic

Hypertension/Premature IHD

Intellectuals/businessmen who have to do sitting work most of the time.

The diagnosis of symptomatic diabetes is not difficult but the true prevalence of diabetes is difficult to determine because of differing standards of diagnosis. When a patient presents with sign and symptoms attributable to an osmotic diuresis and is found to have hyperglycemia, it is almost certain that diabetes is present in him/her. Similarly there is a little disagreement about an asymptomatic patient but having persistently elevated fasting plasma glucose concentration (³126 mg/dL or ³7.7 mmol/l). To label a person diabetic the following parameters must be fulfilled:

1. Fasting (overnight) blood glucose level: Venous plasma glucose concentration

             ³126 mg/dL (³7 mmol/l) at least on two separate occasions.

2. Post prandial (2 h after meals) blood glucose level: Venous plasma glucose concentration ³200 mg/dL (³11.1 mmol/l) at least on two separate occasions.

If random blood glucose concentration is found to be elevated (³200 mg/dL) fasting venous plasma glucose concentration should be checked. And if it is also found to be elevated on two separate occasions (³126 mg/dL) the diagnosis of diabetes is almost certain.

Difficulty in the Diagnosis of Diabetes

The problem arises with the asymptomatic patients who for one reason or the other are considered to be ‘potential diabetics’ but have a normal fasting blood glucose concentration. Such patients are often given an oral glucose tolerance test and if abnormal values are found, they are diagnosed as having pre-diabetes or ‘chemical diabetes’. There seems to be no question that normal glucose tolerance test is a strong evidence against the presence of diabetes, but the predictive value of a positive test (impaired glucose tolerance test) is less certain (rather totally uncertain). However most of the physicians perform glucose tolerance test for confirming diabetes mellitus.


After overnight fasting, a morning sample of venous blood is taken empty stomach (for fasting blood glucose level). Following this the patient is asked to drink 75 g of glucose dissolved in two glasses of water. One should note the timings of drinking glucose. Further blood samples are collected at ½ h, 1 h, 1½ h and 2 h duration after the ingestion of 75 g of glucose.

Interpretation of Results

Much evidence suggests that the standard glucose tolerance test over diagnoses diabetes to a remarkable degree, probably because a variety of stresses can produce an abnormal response, which contribute to false positive examinations. National Diabetes Data Group of the National Institute of Health revised criteria for the diagnosis of diabetes following a challenge with oral glucose. The two criteria are:

1. Overnight fasting venous plasma glucose concentration

      ³126 mg/dL (³7 mmol/l) on at least two separate occasions.

2. Following ingestion of 75 g of glucose venous plasma glucose concentration

      ³200 mg/dL (³11.1 mmol/l) at 2 h and on at least one other occasion during the 2h test that is, two values ³200 mg/dL must be obtained for confirming the diagnosis of diabetes.

Impaired Glucose Tolerance Test (IGTT)

If the 2 h value of whole venous plasma glucose level is between 126 and 200 mg/dL (7–11.1 mmol/l) and one other value during the 2 h test period is equal to or greater than 200 mg/dL, a diagnosis of impaired glucose tolerance test (IGTT) is suggested.

Factors, which influence the results of GTT : A variety of stresses can produce an abnormal response. The operative mechanism is probably adrenaline discharge, as it blocks insulin secretion, stimulates glucagon release, activates glycogen breakdown and impairs insulin action in target tissues such as the liver. The hepatic glucose production is increased and the capacity to dispose of an exogenous glucose load is impaired. Many stresses such as severe burn, life threatening accident, acute myocardial infarction, mental strains and stresses, depression and even anxiety over venipuncture may generate enough adrenaline to produce an impaired GTT. Few other factors such as concomitant illness (if any), drug use (other than hypoglycemic agents) and lack of physical exercise may contribute to false positive results.

Glucose tolerance test if used to predict diabetes has its own limitations. In clinical practice its usefulness for screening of diabetes also remains doubtful. It is because the interpretation of impaired glucose tolerance (IGTT) would be that the patients of this category are at increased risk for the development of fasting hyperglycemia or symptomatic diabetes but that such progression is not predictable in an individual patient. Most patients (~75 %) with impaired glucose tolerance test never develop diabetes, and subjects diagnosed as having diabetes by the second criterion (2 h³200 mg/dL plus at least at one other occasion during the 2 h test ³200 mg/dL venous plasma glucose level) may never manifest fasting hyperglycemia or symptomatic deterioration. Hence in clinical practice considering all aspects of GTT, it does not deserve much credence as far as labeling a person diabetic, though it is useful as a research tool.

Glycosylated Hemoglobin


Blood glucose concentrations may fluctuate widely in relation to food, physical activity and medications. Traditional parameters of blood glucose concentrations at different times reflect the glycemic status only at the time of blood sampling and are a poor reflection of what has happened over the past periods (days, weeks or months before). An indicator of long term glycemic status was essential to sort out the above problem. This requirement was fulfilled by the discovery of glycated hemoglobin (GHb) test. This test has added much to our understanding of different aspects of glycemic control.


GHbs are a series of stable minor hemoglobin formed slowly by a chemical reaction between hemoglobin molecules and circulating blood glucose. GHb represents the glycemic history of erythrocytes (which contain Hb) during preceding 120 days in a person with normal erythrocyte life span. 50% of GHb value is contributed by glycemia in the preceding 4 weeks, 40% by glycemia between 4-12 weeks prior and only 10% by more distant glycemia. Thus GHb values are more weighted by immediately preceding past rather than more distant past.

Classification of GHb

Total GHb = HbA1a + HbA1b + HbA1c + lysine glycated.

HbA1 (Fast hemoglobin) = HbA1a + HbA1b + HbA1c.

HbA1c = Numerically the most prevalent species of GHb.

There are different methods of GHb measurement and each has its limitations that is, advantages and disadvantages. Overall GHb measurements have following merits/demerits.


It indicates average glycemic control in preceding four months. A patient can rely on this test that is, if the tests reveal normal values, one can be sure of preventing oneself from late diabetic complications, which occur due to prolonged hyperglycemia.


There are no categorical disadvantages of this test however one should choose a well equipped lab with modern scientific instruments. Hypoglycemia can only be diagnosed through blood glucose estimation. A good physician is needed to explain its results.


It is important to remember that figures obtained in one laboratory cannot be and should not be compared with those obtained in another lab. It is better to perform serial tests in the same patient in same laboratory by the same method so as to make useful comparisons.

 Values: HbA1c < 4-6% Normal.

7% or Mean Plasma Glucose- 170 mg/dL     Good control

6% or Mean Plasma Glucose 135 mg/dL      More Stringent Target

8% or Mean Plasma Glucose 205 mg/dL     Uncontrolled Diabetes

9% or Mean Plasma Glucose 240 mg/dL     Poor Control

10% or Mean Plasma Glucose 275 mg/dL   Very Poor Control.

> 10% Severely Uncontrolled Diabetes

Note: Rise of 1% HbA1c is equvilent to 35 mg/dL plasma glucose level

Which one is better for diagnosing diabetes ‘GHb’ or ‘GTT’?

GHb reflects sustained glycemia rather than the short-lived glycemic excursions. GHb may be near normal in a person with normal fasting blood glucose and widely swinging post glucose excursions (ups and downs in post prandial blood glucose levels). Individuals diagnosed diabetic because of higher blood glucose values at 2 h following ingestion of 75 g glucose (glucose tolerance test) but normal fasting blood glucose concentrations may have a completely normal GHb level and ~75% patients diagnosed diabetic with above mentioned criteria that is, by GTT alone do not show symptomatic deterioration or fasting hyperglycemia later in life. Hence these patients should not be diagnosed as having diabetes. Thus to prevent over diagnosis of diabetes GHb i.e., HbA1c should be preferred over OGTT (oral glucose tolerance test).

GHb as a tool for self-monitoring of diabetes: It has been over 40 years that GHb is in clinical use and has added much to our understanding of different aspects of glycemic control. It should be used in conjunction with clinical examination and periodic monitoring of blood glucose level, urine glucose level, urine albumin and urine ketones. GHb is not an alternative for home measurements of capillary blood glucose levels that is, ‘SMBG’ (self monitoring blood glucose).

Though highly significant correlation exists between the above two measurements (GHb and SMBG) but there is an obvious scatter of results around the regression line. Besides intrinsic differences in rates of glycation, vitamin C, vitamin E and aspirin use may also influence GHb values. The usefulness of GHb in preventing chronic diabetic complications is beyond any doubt.


Diabetes appearing because of autoimmune destruction of insulin secretingb-cells of the pancreas is called type 1 diabetes. This destruction may be acute or sub-acute in origin and usually more than 95% b-cells become dead in a span of few weeks or months requiring exogenous insulin for treatment.

The greatest problem before a physician comes when a person between 16-30 years of age is diagnosed as a diabetic. Under these circumstances it becomes very difficult to adjudge whether insulin injection is necessary or oral medicines (diet restrictions and exercising) themselves are capable of controlling diabetes. At this stage a few tests are capable of diagnosing whether the patient is suffering from type 1 insulin dependent diabetes or not. These investigations also reveal the rate of deadening of b-cells and its causes.

Serum Auto Antibodies Estimation (The Body’s Immune System Forms Antibodies Against Following Tissues)

In type 1 diabetics islet cells, insulin and insulin receptors are the three antigens against whom the body produces auto-antibodies and these auto-antibodies are known as islet cell auto-antibodies (ICA), insulin auto-antibodies (IAA) and insulin receptor auto-antibodies (IRAA) respectively. Besides helpful in diagnosing type 1 diabetes these auto-antibodies titers also provide useful information about the probability of type 1 diabetes in first degree blood relative ‘FDR’ (relatives with titers of >40 JDF units carry high risk of IDDM) and therefore have predictive value also. The predictive value of IAA is less then ICA though increase in IAA alone can be correlated with younger age of onset of, and faster progression to, type 1 diabetes. The two additional auto-antibodies recognized in recent years which also help in predicting IDDM in FDR are GAD (glutamic acid decarboxylase) and ICA 512 auto-antibodies.

In type 1 diabetes the body’s immune system becomes unable to recognize its own insulin secreting b-cells and behaves (produces antibodies) with them in the same manner (reaction between antigen and antibody) as it would have reacted against any foreign protein that is, antigen (bacteria, virus).

In fact in such patients the immune system forms antibodies against its own pancreaticb-cells (which it starts recognizing as foreign protein or antigen) which are called b-cell auto-antibodies. These antibodies destroy b-cells beyond repair (antigen antibody complex). If the concentration of b-cell (islet cell) auto antibodies in blood is detected in abnormal limits the diagnosis of type 1 diabetes is certain because in type 2 diabetes b-cell auto antibody titer never comes high.

A high level of ‘islet cell auto-antibodies’ in blood verifies type 1 diabetes whereas rise in the levels of ‘insulin auto-antibodies’ signifies considerable insulin damage and the rise in ‘insulin receptor auto-antibodies’ titer indicate presence of severe peripheral insulin resistance mostly in type 2 diabetics.

Serum C-peptides and Serum Insulin Estimation

For knowing the state of b-cells and the quantity of insulin being produced in the patient’s body, an investigation called C-peptides estimation in serum proved very helpful. As this test is simple and clear, more informative and economical than testing of blood insulin levels, it is practiced widely.

In the pancreas during conversion of pro insulin to insulin, C-peptides are produced in equimolar quantity (exactly in same amount as insulin). Hence as the number of livingb-cells decrease the C-peptides level also decreases. And on checking serum insulin level it also comes out low (only if patient is not using insulin injection). In case patient is using insulin injection the serum insulin levels may come normal or high but C-peptides level will remain critically low. Therefore C-peptides test has superiority over serum insulin estimation (because it truely indicates b-cells functional status).

Mostly children (1-12 years of age) are victims of type 1 diabetes (6-8 years of age is most crucial), in teenagers and adults (upto 70 years of age) also a small percentage suffer from type 1 diabetes. But the results of investigations of these old age patients are a little different from that of young patients and have been summarised in the table given below.



Patients who don’t receive self-management training are four times more likely to develop acute and chronic (short and long term) complications of diabetes. If DSME is to become more effective, then interventions such as computer generated calls to patients (to achieve dietary goals), follow up support through telephones and other automated systems need to be done to increase patient’s involvement in their own case. By self-monitoring one learns from mistakes and thus improves on the previous performance. Not only cardio-vascular mortality reduces by 50%, but 90% cases of impaired glucose tolerance test (IGTT) do not develop diabetes just by positive changes in diet and daily exercise (Kanti Diabetic Care Centre, Rishikesh).

These patients (with DSME) report fewer symptoms of depression, fewer days in bed, greater self-efficacy for self-care activities and quality of their health outcomes. Tobacco dependence counselling increases sustained quit rate of smoking. DSME motivates patients to take responsibility for their health behaviours. This process naturally advances forward as newer outcomes and treatments become available. A patient learns to adjust treatment on the basis of the frequency and magnitude of glycemic excursions.


The objectives of treatment in diabetes are to prevent diabetes (over diagnosed patients return to euglycemic status without any drug treatment); relieve symptoms; improve quality of life; attain and maintain near normal body weight in adults and ensure normal growth patterns in children; attain and maintain good metabolic control in order to prevent, arrest or revert the complication of diabetes. These objectives are achieved by effective meal planning, exercise and anti hyperglycemic therapy, and periodic monitoring.

The ideal monitoring system should be simple, cheap, full proof, reliable, possibly non-invasive and painless and give immediate information. There are two methods to monitor diabetes control:

1. Subjective methods; and 2. Objective methods.

1. Subjective Methods

It is sometimes observed that a diabetic starts crash dieting and over exercising in an effort to bring a strict control on blood glucose level. In these circumstances the blood glucose level immediately becomes normal or sub normal but the strength of the patient decreases and symptoms of weakness that is, loss of body weight, trembling, fatigue, and vertigo start occurring and after sometime due to vitamin deficiency the immune system of the patient also weakens. In few patients due to malnutrition even the insulin production level decreases (malnutrition related diabetes mellitus or MRDM).

For prevention of such a stage a simple measure is to recognize and observe the symptoms of hyperglycemia and hypoglycemia and how a person is feeling (the sense of well being, good health and full energy indicate good diabetes control).

The main symptoms of hyperglycemia that is, increased blood glucose level are frequent urination (which also results in dryness of mouth), polydipsia and polyphagia. If the patient observes that on a certain night he has urinated 3-4 times (which was not happening before), he should understand that it is due to increased blood glucose level only (or deterioration of overall diabetic control) and should immediately take optimum measures against it. But if there is trembling of hands and feeling of anxiety in performing the daily chores then one must understand that symptoms of low blood glucose level are appearing.

On the other hand despite the blood glucose level being slightly above the normal limit, if the patient feels no weakness, vertigo or anxiety and his body feels energetic then it can be said that his diabetes is under control and moreover there are least chances of developing diabetic complications in the near or distant future.

Limitations of Subjective Methods

Monitoring by subjective methods however has its limitations. Subjective methods are based on the expression of feelings and experiences with regard to diabetic control but this at times may be unreliable and it is in this context that objective methods are employed for measuring diabetes control. Subjective feelings (in relation to glycemic control) are also not useful in case of asymptomatic hypoglycemia or hyperglycemia because the alarming system of the body that is, autonomic nervous system gets involved adversely in chronic diabetics thus the alarming symptoms do not appear. Infants and children also are unable to express subjective symptoms correctly. It should also be borne in mind that patients vary in sensitivity, too, thus sometimes subjective feelings are not reliable for monitoring control of diabetes.

Advantages of Subjective Methods

There is an added advantage of subjective methods of monitoring diabetes as it makes a person more self-conscious and one gives sufficient attention to his body weight, shape of the muscles, colour and texture of skin and gracefulness. According to ayurveda a poorly treated diabetic is deficient in ojus (as shine on face and skin disappears).

To top it all the patient gets the feeling that by adopting simple measures (which he can plan and do himself) also, he not only can monitor and keep his diabetes under control but can remain healthy and work like other persons of his age group. This feeling generates a new ray of hope in his life. Practically also it has been seen that medicine doses of such patients decrease upto 75%. For better monitoring of diabetes these natural measures are very helpful. Use of objective methods is also important for recognizing and understanding subjective methods correctly.

2. Objective methods 

These are as follows :

A. Estimation of body weight.

B. Urine analysis for glucose, albumin, and ketones.

C. Quantitative urine glucose measurement.

D. Home monitoring blood glucose ‘HMBG’.

A. Estimation of body weight : A major objective of treatment is to attain and maintain normal body weight. Unexplained weight gain may be attributable to dietary indiscretion, excessive diet and drugs or hypothyroidism. Unexplained weight loss could be due to anorexia, crash dieting, overzealous exercise, imbalanced diet, uncontrolled hyperglycemia, calcific pancreatitis, hyperthyroidism, chronic constipation, diarrhoea or other intestinal diseases.

One should have normal body weight according to his age, sex and height and it is called ideal body weight. BMI that is, body mass index is another method of examining healthy body weight.

B. Urine analysis for glucose, albumin and ketones : It is performed by physical examination and chemical analysis of the urine.

I. Physical examination : A patient can easily recognize a few symptoms by physical examination of the urine at home itself and may judge the level of his diabetes. These symptoms differ from a normal person’s urine in the amount, colour, smell, temperature, touch, texture and specific gravity of the urine and can be differentiated with careful physical examination.

Ayurveda provides a lot of useful information in this subject. 20 subtypes of prameha, which are potentially diabetogenic do have separate urinary characteristics (and can be recognized by physical examination of the urine only).

Glucose does not come out alone in the urine but takes along with it several important proteins, minerals, elements and also water out of the body. This is why a diabetic’s urine is unlike a normal person’s urine. One can get a glimpse of diabetic complications also by seeing a few symptoms in urine. And therefore the importance of physical examination of the urine in treatment of diabetes is as important today as it was in ancient times. A few important observations are as follows:

* Excessive and frequent urination and turbid, odourless and sweet tasting urine are all strong proof (evidence) of diabetes mellitus.

* If the urine is pungent, honey coloured, sticky, heavy or with roughness, and occurs repeatedly then these all are indications of advanced diabetic stage.

* If sediments deposit (in short interval) in a container in which a diabetic’s urine is collected, then it indicates phosphates in urine.

* If the urine smells like fruits and has the colour and smell of alcohol (acetone) it indicates presence of ketones in urine.

* Warm, odourless, whitened and froth containing urine indicates presence of albumin in urine.

* When glucose is present in urine then at the place of urination (if it is an open place as garden) presence of ants and flies is a normal phenomenon.

II. Chemical analysis : It is simple to do chemical analysis of urine at home itself. Micro albuminuria tested in a pathology laboratory can give vital information about the status of kidneys.

(a) Urine glucose estimation : It is cheap, non-invasive, easy to perform and an useful investigation. Urine testing of glucose is an indirect reflection of blood glucose levels. Because as soon as glucose level in blood starts rising above 180 mg/dL (>9.99 mmol/l) the extra glucose in blood starts coming out with urine. Estimation of glucose in urine is influenced by renal glycemic threshold, which has a wide range (54-270 mg/dL, mean value 180 mg/dL) and blood glucose levels.

Urine testing does not warn of hypoglycemia. Drugs such as vitamin C, analgesics, and x-ray contrast media influence its results. In cases of diabetic nephropathy (renal threshold increases and glucose does not filter in urine even when the blood glucose level is >250 mg/dL) this test is not recommended. During pregnancy and in children the renal threshold may decrease upto 110 mg/dL but still this test is useful in these patients, too. Apart from other patients, young children (<10 years of age) who may find ‘SMBG’ unacceptable, this test is very helpful.

Method of home urine glucose testing: The two methods of urine glucose testing are :

1. Test tube method: Take 2 ml benedict’s reagent in a test tube. Add 4 drops of urine to it and warm on a spirit lamp. When it starts boiling, start counting till 100 (1 minute) and compare the colour obtained in test tube with the colour chart printed on the bottle of the benedict’s reagent.

2. Uro-diastix method: Dip the uro-diastix in urine and take out immediately. Compare the colour developed on the test strip with the colour chart printed on the bottle of the uro-diastix exactly after 30 seconds.

Interpretation of the results

No change in colour  Urine glucose ‘nil’    blood glucose level (b.g.level) <180 mg/dL.

Green colour develops     Urine glucose ‘+’         b.g. level 180-200 mg/dL.

Yellow colour develops     Urine glucose ‘++’      b.g. level 200-250 mg/dL.

Red colour develops         Urine glucose ‘+++’    b.g. level 250-300 mg/dL.

Brown colour develops      Urine glucose ‘++++’  b.g. level >300 mg/dL.

Note: If renal threshold for glucose is high due to diabetic nephropathy the glucose may not excrete in urine despite of high blood glucose level. And if the renal threshold is low as in children or during pregnancy urine glucose can be detected at much lower blood glucose levels.

(b) Urine ketones analysis: Presence of urinary ketones is an indirect reflection of raised blood glucose level. Insulin deficiency leads to hyperglycemia and in this situation body cells start utilizing fats (neoglucogenesis in liver) to fulfill their energy requirement and in this process ketone bodies are generated in excess amount.

If blood ketones remain elevated for longer periods then all body excretions such as urine, sweat and breath also start excreting ketones which give fruity smell (acidotic breath). This state of the body is called ketosis which is a serious complication mostly seen in insulin dependent diabetics. Ketones can be easily detected by keto-diastix available in the market. If one finds urinary ketones positive, he should immediately report to a diabetalogist.

(c) Urine albumin analysis: Though the earliest sign of diabetic nephropathy is micro albuminuria (>20 micro g/min), which can be detected in laboratory only, still home urinary albumin excretion monitoring is useful because it detects macro albuminuria, which is also an important earlier manifestation of diabetic kidney damage. Moreover it can be tested easily at home by patient himself, and also provides enough information regarding balancing of dietary proteins in normal as well as patients of diabetic nephropathy.

Method of Home Urine Albumin Testing: The two methods of urine glucose testing are-

1. Test tube method: Take 2 ml of urine in two test tubes and warm one on a spirit lamp. Let the urine boil till you count 100 (approximately 1 minute). Now compare the colour of the boiled urine with that of the unboiled urine (second

test tube with unwarmed urine). If there is no colour change, it implies that the kidneys of the patient are unharmed (undamaged by diabetes). But if milky colour appears on boiling then add 2 drops of 2% acetic acid and stir it, wait for 30 seconds. If milky colour disappears it indicates phosphates only in urine (the white colour is because of phosphates) and if it doesn’t disappear and remains white it confirms albumin in urine.

In the first situation that is, phosphaturia just cut down salad, milk, meat and a few vegetables in diet and phosphaturia will disappear but patients with albuminuria should consult a physician (as there are several serious/non-serious causes of albuminuria besides diabetic nephropathy).

2. Albumin dipsticks method: Albuminuria can be tested at home easily by these test strips. Dip one strip in the urine and then take it out immediately. Compare the colour developed on the strip with the colour chart printed on the bottle exactly after 30 seconds.


Quantitative glycosuria is the measure of total urine glucose excreted over a period of 24 h; alternatively it can be fractionated over a period of 6 or 12 h also. Glucose excretion <3% of the daily carbohydrate intake or less than 10 g (total glucose excreted in urine) over a period of 24 h is accepted as within normal range in a diabetic.

The advantages of this investigation include wide acceptability, accuracy in estimation of total urinary glucose losses, facilitation of checking the accuracy of pre-meal tests and serving as an adjunct to ‘SMBG’. The limitations of quantitative measurement of glucose include inaccuracy in event of altered renal threshold and incorrect estimation of glycosuria in instances where the urine is diluted such as over zealous use of water.


Just as urine glucose test strips are available to a patient these blood glucose estimation strips also provide an approximate reading of blood glucose levels. If one uses an instrument called Glucometer then with these strips far more accurate results are obtained. The procedure of testing is given on the bottle of the strips itself or booklet provided with the instrument. Advantages and limitations of ‘HMBG’ are as follows:


1. One can immediately find out his blood glucose level and thus the effect of different medicines can be analyzed at home itself very easily.

2. It is helpful in adjusting the dose of medicine(s).

3. It is difficult to recognize low blood glucose by symptoms alone in children, aged and unconscious persons. In that case HMBG is very helpful in identifying hypoglycemia that is, low blood glucose level.

4. It is useful during pregnancy, surgery and at emergency situations.


1. There may be a difference of 10-20% (+ or -) in the reading of blood glucose levels as compared to lab test.

2. It is slightly expensive. Occasionally results of glucometer should be compared with readings obtained by testing blood in a laboratory (whole venous blood).

3. At times the results are unexpected so one should educate himself enough to explain them correctly.


 When we talk about the general investigations of blood then in our minds we are thinking of those investigations by which any type of problem developing within the body even though without symptoms may be identified. These examinations are: Hb, TLC, DLC, ESR and GBP.

Haemoglobin and Red Blood Corpuscles i.e., Hb and RBCs

By saying how much blood a body contains we refer to the reading of haemoglobin in blood and the number of red blood cells. This is because the active part of blood taking part in bio-chemical reactions is haemoglobin only, which is protected within covering of red blood cell. Several times it happens that the general red blood cells count is normal but haemoglobin is not present within red blood cells in normal amount due to which the assigned functions (here carrying of oxygen and carbon di-oxide) are not performed properly.

Only 80-90 % haemoglobin is present in blood of majority persons living in cities whereas in healthy and persons doing hard physical labour (like village folk) it is upto 100 percent.

The average quantity of haemoglobin in a healthy person ranges from 14 to 18 g/dL (8.7 to 11.2 mmol per liter) in males and 12 to 16 g/dL (7.4 to 9.9 mmol per liter) in females. Normally haemoglobin is tested by taking out blood from vein or puncturing in finger. Haemoglobin is tested by two ways: 1. Concentration of haemoglobin in blood; and 2. Assessment of red blood cells in blood and then concentration of haemoglobin in them.

Effects of increase or decrease in haemoglobin on human health : Decrease in quantity of haemoglobin in blood is known as anemia. In all anemic patients there is certainly low haemoglobin content but there are differences in the number and form of red blood cells in various patients and by this only the cause of anemia is identified (ascertained). Mostly in anemia the haemoglobin concentration within red blood cells is low but in pernicious anemia haemoglobin deficiency occurs due to decrease in number of red blood cells and not the haemoglobin concentration within the red blood cell.

Anemia in which number of red blood cells does not decrease (chlorotic anemia) are cured easily in comparatively less time whereas patients of pernicious anemia are very difficult to cure.

Effect of decrease or increase in red blood cells on human health: The concentration of red blood cells in human blood is 4.5-5.5 millions/mm3. In newborn infants, empty stomach, excessive perspiration and in persons living in height this number increases to 6-70 millions/mm3. After menstruation, childbirth or drinking excess water this number normally decreases.

Increase in red blood cell number : In few stages of some diseases the RBCs count increases like in chronic bronchitis or those lung diseases in which proper oxygenation of blood does not occur or those in which air does not properly reach the lungs. A few other diseases are also there in which RBCs count increases as vomiting, diarrhoea, repeated urination or fever in which blood concentrates.

In few heart diseases due to hole in inter ventricular septum (ventricular septal defect (VSD) due to which blood flow in lungs decreases, low heart rate, in case of more than 20% burn, excessive use of iron and sudden bleeding also the number of red blood cells increases in the body.

Decrease in red blood cell number:A decrease in RBCs occurs in case of bleeding, leukemia and secondary anemia patients as in pernicious anemia the RBCs count decreases.

White Blood Cells i.e.,  WBCs

In a healthy state the number of white blood cells in blood ranges from 4,000 to 10,000/mm3. Their number is known to increase (leucocytosis) in case of pregnancy, after taking of meals, taking bath in cold water and exercise. The most common type of leucocytosis is ‘polynuclear neutrophils’ leucocytosis either in healthy or diseased state.

In few fevers there is an excess increase in counts of neutrophils (leucocytosis) whereas in others their number may decrease also (leucopenia). This information is mainly useful in identifying tropical fevers (leucopenia). One more important point to note is that in case of pus formation in body leucocytosis definitely occurs.

Leucocytosis is definite in the following few cases : Abscess, suppuration, septicemia (spreading of infection in body), bone inflammation, pneumonia, tubercular meningitis, cancer and majority of bacterial infections.

Several diseases lead to leucocytosis but to identify disease it is necessary to know the type of white blood cells, which have increased. For this slide of blood is stained and seen.

Leucocytosis pattern

1. Total count of white blood cells i.e., TLC is greater than normal.

2. Only one type of WBCs have increased.

3. Or there is a change also in cells shape and size of WBCs with leucocytosis.

All the above three stages are called leucocytosis.


Total Leucocyte Count “TLC”: 4,000 to 10,000/cmm

Differential Leucocyte Count:  “DLC”

     Polynuclear ‘neutrophils’ “P”: 60-70 %

     Small Mononuclear Leucocytes ‘lymphocytes’ “L”: 20-30 %

     Large Mononuclear Leucocytes ‘monocytes’ “M”: 2-5 %

     Transitional Stage: 2-5 %

     Eosinophils “E”: 1-3 %

     Basophils or Mast cell: 0-1 %

Polynuclear neutrophils constitute the largest number among the white blood cells. In case of fever, pneumonia, septicemia, meningitis and other brain infections, abscess and inflammation cases, appendicitis and osteomellitis etc., there is an increase in number of neutrophils.

Typhoid is such a fever in which the number of neutrophils greatly decreases (this information differentiates it from other fevers). It has also been seen that on glycogylation (reaction with glucose) of white blood cells the process of their breaking up accelerates.

A small part of white blood cells is made of eosinophils. Their count increases abnormally in a few types of blood cancer, allergies and various types of skin diseases. In asthma (breathlessness disease) eosinophilic count increases upto 25%. Breathlessness is not due to heart problem can be proved when eosinophilic count comes to normal in dyspoenic patients. In allergy and other defects in asthma these cells can be seen stuck to respiratory tubes in excess (bronchus, bronchioles and alveoli).


Lymphocytes named white blood cells are seen to increase mostly in those diseases, which are present in the body since a long time. In a few specific infections as tuberculosis (infections of lungs, kidneys etc.) and viral infections the number of lymphocytes increases unexpectedly. Besides these diseases in which immune system is activated lymphocytosis is seen. In chronic diseases as arthritis, collagen disorders and chronic colitis also lymphocytosis develops.

Erythrocyte Sedimentation Rate “ESR”

The measure of sedimentation of red blood cells is know as ESR. This is mostly measured by taking the upper surface of the serum and upper surface of the sedimented RBCs (in mm) in a specially designed glass tube.

Venous blood (in which a chemical is mixed to prevent it from solidifying) is filled in a special glass tube upto the mark of 100 and kept in a stand. Exactly after 1h the fall is noted and this is ESR “O” (observed) reading. In reality ESR develops due to difference in specific gravity of the plasma and the red blood cells. But a few other factors also affect it.

Significance of ESR

ESR is an investigation, which confirms hidden physical disease within the body. It is found to be increased in chronic and acute infections, cancer, disease of collagen tissues, kidney disease and all those other diseases in which there is an abnormal increase in blood protein levels. ESR is found to be increased in anemia also. The factors capable of causing irregularity in this examination when corrected the result is known as corrected ESR. Pregnancy and old age are two stages when slight increases in values of the ESR are normally seen.

General Blood Picture “GBP”

Staining a slide of blood and seeing it under a microscope various shaped blood cells are clearly seen. There are several diseases which have effect on the shape and internal structure of the blood cells. By this clear information of disease is obtained. For example in pernicious anemia the red blood corpuscles are of the shape of flask. In secondary anemia developing due to cancer, nephritis etc. these cells become kidney shaped. The infections as malaria, kalazar and filaria are identified by this test only (blood parasites can be seen in the blood film under the microscope).

Routine Urine Examination

When a person does normal testing of urine then following facts come out. Firstly urine is tested by seeing its physical properties as observing colour, smell, reaction, specific gravity, any type of sedimentation and quantity of urine. Then by chemical analysis presence of albumin, glucose, phosphates, ketones, bile elements and salts etc. are observed. And finally the physician looks for any types of deposits (as red blood cells, calcium oxalate crystals, pus cells, casts etc.) under a microscope. Routine examination of urine should be done not only keeping kidneys in mind but also other diseases.

Different colours of urine in different diseases: Normally the colour of urine is decided on the basis of the concentration of pigments present in urine. Normal bile pigments are ‘urobiline’ and ‘urachrome’ which are respectively the metabolic remains of blood and bile ‘pitta’. But under abnormal conditions (in case of disease) there are several such elements which when present in urine change its natural colour.

1. The colour of urine in acute nephritis, fever or excess perspiration is yellowish and is more concentrated/thick. The specific gravity is also increased (normally it is between 1015 to 1025).

2. In diabetes mellitus and in cases of bahumutrata “polyuria” the urine is slightly yellowish in colour. Whereas in patients of diabetes incipidus the urine is of watery colour.

3. In presence of bile salts in urine (jaundice) it is slightly orangish and increases to brown and in presence of bright sun light it appears slightly greenish (urobilinuria).

4. When blood is present in urine its colour changes to red, dark red and finally smoky. Thick and smoky coloured urine is obtained when excess blood cells break (heamoglobinuria).

5. In presence of melanin (normally present on skin) and some other elements like indican the colour of urine changes from brown to black.

6. In chloromas urine is green coloured, in chyluria it is white, on taking salicylates dark green or black colour may appear.

7. Different medicines and foods (and colour in them) may change the colour of urine accordingly.

For seeing the reaction (pH) of urine it should be tested by litmus paper. Normally urine is slightly acidic hence on testing with blue litmus paper it changes to red. Urine testing for glucose has already been dealt with in detail earlier.


Serum Chromium : Normal limit: 94.2 to 183 nmol per liter

Creatinine Clearance : Normal limit: 90 to 120 mL/min.

It denotes the functioning of both kidneys. The decrease in creatinine clearance is indicative of decrease in glomerular filtration rate. Urine creatinine 8.8 to 15 mmol per day.

                     Urine creatinine (mmol/l) x vol/min

Calculation —————————————————

                    Plasma creatinine (mmol/l)

GFR (glomerular filtration rate)

                         Normal Limit

     Young age : 90-150 mL/min

         Old age : 70-140 mL/min.

Lipid Profile (at the age of ~50 years)

      Total Plasma Cholesterol : 150-270 mg/dL (Men); 145-260 mg/dL (Women)

                                                                   (Ideal in diabetics: 200 mg/dL)

      Plasma Triglyceride : 60-320 mg/dL (Men); 50-220 mg/dL (Women)

                                                                   (Ideal in diabetics: 150 mg/dL)

      Plasma LDL Cholesterol : 95-200 mg/dL (Men); 75-165 mg/dL (Women)

                                                                   (Ideal in diabetics: 100 mg/dL)

      Plasma HDL Cholesterol : 30-65 mg/dL (Men); 35-85 mg/dL (Women)

                                                                  (Ideal in diabetics: 45mg/dL)

  Total cholesterol/HDL Ratio >5.0 (High risk for coronary artery diseases)

Plasma Insulin (fasting) : Normal Limit: 6 to 26 mU per mL

Plasma C-Peptide : Normal Limit: 0.5-2.5 mg per liter

Plasma Calcium ‘Ca++

         Total : 9 to 10.5 mg/dL [2.2 to 2.6 mmol per liter]

         Ionized: 4.5 to 5.6 mg/dL [1.1 to 1.4 mmol per liter]

Serum Creatinine : N <1.5 mg/dL (133 mmol per liter).

This investigation has special significance for all age group diabetics. Creatinine is a substance produced in human body as a byproduct of muscle metabolism. Kidneys filter all the creatinine they get through the blood for filtration. Normally serum concentration of a healthy person does not rise above a definite limit. Temporary elevations are seen infrequently (as in muscle degeneration) and therefore if one finds even slight elevation in s.creatinine values he should consult his physician as it could be due to diabetic nephropathy which is a serious problem. It is observed that once s.creatinine starts rising above normal the life expectancy gradually reduces and it is said that increased level of s. creatinine is inversely proportional to life expectancy.

Serum Urea : N: 10 to 50 mg/dL (3.6 to 18 mmol per liter)

The urea is produced in human body as a by product of protein catabolism. Kidneys filter almost 100% urea entering into it through blood. But renal tubules reabsorb some of the urea back into the renal tissues. It is because urea plays important role in making urine optimally concentrated. Serum urea can increase in several renal and extra renal diseases and the rise can be temporary or a permanent phenomenon (depending upon the cause). Whatever may be the cause if blood urea increases to abnormal limits the signs and symptoms of uremia start appearing. Urea increasing as a result of diabetic nephropathy is usually irreversible and denotes significant renal damage.

SGOT, AST (serum glutamic oxaloacetic transaminase): 10-40 karmen units per mL

It denotes damage in cardiac muscles specifically. Though an increase in SGOT is also observed when there is substantial damage in hepatocytes. Thus the normal values of SGOT can increase in cardiac as well as hepatic disorders.

SGPT, AST (serum glutamic pyruvic transaminase): 10-40 karmen units per mL

It denotes damage to liver cells i.e., hepatocytes. In cases of hepatitis and fatty liver (mostly because of diabetes and alcohol use) SGPT values exceeds its normal limit.

Serum Proteins

Serum proteins are essential for several functions in human body. The most important are: 1. As raw material for production of different hormones and enzymes; 2. Formation of colloidal osmotic pressure in blood (protein holds water in blood due to its cohessive force).

S. Proteins

      Total : 6.5 to 8.0 gm/dL [65 to 80 g per liter]

      S.albumin : 3.5 to 5.5 gm/dL (50 to 60 percent) [35 to 55 g per liter]

       S.globulin : 2.0 to 3.5 gm/dL (40 to 50 percent) [20 to 35 g per liter]

Serum Amylase: 55-180 somogyi units per dL

Serum Uric Acid

            M : 2.5 to 8.0 mg/dL

            F : 1.5 to 6.0 mg/dL

Serum Alkaline Phosphatase : 21 to 91 per liter at 37 0C (I.U.)

Serum Electrolytes

         S. sodium ‘Na+’ : 136 to 145 mmol per liter [136 to 145 meq per liter]

         S. pottasium ‘K +’ : 3.5 to 5.0 mmol per liter [3.5 to 5.0 meq per liter]

         Serum phosphorus (inorganic): 3 to 4.5 mg/dL [1.0 to 1.4 mmol per liter]

TSH (thyroid stimulating hormone) : < 5mU/mL

        Thyroxine (T4) : 65-150 nmol per liter

        Triiodothyronine (T3) : 1.0-3.0 nmol per liter


        Protein : up to 150 mg [<0.05g per day]

        Protein in pregnancy : up to 300 mg [<0.1g per day]

        Albumin : up to 25 mg per day

        Creatinine : 1.0 to 1.5 g per day [7.5 to 15 mmol in 24h]

        Fat : 3-5g per day


       Total amount of stool ~200g

       Fat ~5g

       Protein : Minimal

Note : To convert values from mmol/l to mg/dL divide by 0.02586.


About 2500 years before, Charaka said : “kashaya madhuram pandu rooksham mehati yo narah; vatakopadsadhyam tam pratiyanmadhumehinam.” (CharakSmhita.Nidan.L4.S44). It means a person whose urine is sweet or pungent in taste, pale and harsh definitely has diabetes developing due to vata humour. According to Sushruta diabetes refers to the flowing of urine as sweet as madhu ‘honey’ (“kahaudrarasvarnam“- Sushut Samhita.Nidan.L6.S12).

By the above example it is clear that until the urine does not contain glucose consistently (for a long period) and symptoms like polyuria, and paleness, do not appear it is not wise to call a person diabetic. According to modern medicine, too, blood glucose level at this stage should be around 200 mg/dL.

History of Diabetes Mellitus or Madhumeha

It is fascinating and one bows his head out of respect towards the Hindu scriptures, ‘Vedas’ written more than 5000 years ago, which give us information about the different features of diabetes mellitus including its etiopathogenesis, complications and treatment.

Maharshi Charaka collected, corrected and published the medical accounts of his time and laid the foundation of ‘Ayurveda’. We get detailed information of the disease from ‘Charaka samhita’ written in 600 B.C. by Maharshi Charaka and ‘Sushruta samhita’ written in 500 B.C. by Maharshi Sushruta. Later on Acharya Vaghbhat (100 B.C.) and in the recent past Bhavprakash, Madhavkar, and others worked extensively on this subject. In due course of time Hippocrates (300 B.C.), father of ‘Allopathy’ and Aristotle (250 B.C.), father of ‘Unani Medicine’, described this disease in detail. Voluminous publications and interest of physicians from ancient times towards diabetes show the seriousness of the disease.

On studying ancient medical writings it is clear that intensive research work spread over unaccounted period of time (probably 100-200 generations) must have been conducted because then only such useful information regarding diabetes is present in the ayurvedic medical writings.

The causes of pre-diabetes and diabetes described by Rishi Charaka thousands of years ago are applicable today also as he states : “kashayakatutiktrookshalaghu—–vatah prakopmapadyate” (CharakSamhita.Nidan.L4.S36) meaning that by use of pungent, bitter, tikt (acrid), dry, light and cold food items; excess intercourse; excess exercise; vomiting; purgation; deep sorrow and anxiety; starvation; excess bleeding and untimely sleep or keeping awake for long hours; and in an obese person following a sedentary life style, the vata humour gets vitiated and the result is diabetes. All the causes mentioned by Charaka in the above shloka need special attention.

Thereafter, medical writings of Chinese (2300 years ago), Egyptian (1500 years ago), Greek and Tibetan (1000 years ago) civilizations also consider diabetes as a serious disease and give vital information regarding its prevention and treatment. Homeopathy, Biochemic, Naturotherapy, Acupuncture, Chromo therapy, Hydro therapy, Magnet therapy and other therapies also give detailed information regarding its management. In the last decade of 18’th century Dr Van Merring and Minkovisky proved the role of pancreas in developing of diabetes.

Origin of Madhumeha ‘Diabetes Mellitus’

The two schools of thoughts are: 1. According to first account diabetes is hereditary and transmitted from one generation to the other and to some extent wrong eating habits, sedentary life style and a few other risk factors are responsible for its development. 2. According to the second school of thought diabetes develops more due to dysfunctioning of the nervous system but disorders of the digestive and urinary systems can also cause it or assist in its pathogenesis.

Charaka, Sushruta and Vaghbhat first of all gave the information that diabetes is not an infectious disease (agantuj disease) but strong familial tendency (diabetes in parents or close blood relatives) and a few other environmental risk factors play detrimental role in its development. Sushruta writes that in some people diabetes may be due to hereditary disorders (genetic defect) only and he named them ‘sahaja madhumehi’. Charaka also writes that one main cause of diabetes is ‘beeja dosha’ (defect in genes) but continuous intake of improper diet (as it fills the body with vitiated humours) and sedentary life style, too, are responsible for its development.

According to Chinese medicine (400 BC), the second most widely practiced and ancient medical science, founded two and a half thousand years before (which seems to be influenced or probably originated from the ancient medical science that is, ayurveda) an imbalance in Yin and Yang (light and heavy substances, which create a human body) plus gross deficiency in Chi (energy that flows in the body) are the two sole reasons responsible for diabetes. According to Unani therapy whose pioneer was Aristotle, a mutual imbalance of the three humours, present in the body, is the main cause of diabetes. Homeopathy (founder Dr Samuel Hahnemann 1820) considers defects in nervous system to be the main cause of development of diabetes and today we can clearly see that a sudden rise in number of diabetics is more due to excess mental tension and strains rather than excess food.

According to Biochemic system of medicine (Schusller 1873, became the founder of the biochemic system of treatment which advocates that diseases can be cured by supplementation of one or more cell salts out of the total twelve cell salts) diabetes and its complications occur due to deficiency of certain cell salts which if replenished greatly help in curing diabetes.

There is an interesting tale in the Vedas, about the origin of diabetes, where it is said to have originated by eating Havisha (a special food which is offered during a religious ceremony) at the time of yajna organized by Daksha Prajapati, the king of Himalayas in India, thousands of years ago (CharakSamhita.Nidan.L11).

Galen (131-200 B.C.) put the foundation of anatomical work. Ernest H. Sterling 1866-1927 introduced the term hormones. Louis Kuhne 1888 introduced and practised naturopathy and established that the serious result of interfering with nature is diabetes but if man takes support of nature then he can prevent himself from other diseases also besides diabetes. Sir Frederic Gowland (1899) established the identity and need for treating the disease through naturopathy. Bayliss and Sterling (1902) discovered hormones and Benting and Best (1921), discovered the use of ‘insulin’ for cure of diabetes.

Definition of Diabetes

Diabetes is characterized by metabolic abnormalities and long-term complications such as involvement of the eyes, kidneys, nerves and blood vessels, and by a lesion of the basement membrane of the nephrone (nephrone is the functional unit of kidney). The initial signs and symptoms of diabetes are attributable to an osmotic diuresis ‘polyuria’ which leads to polydipsia and polyphagia. The symptoms in old diabetics pertain to specific organ damage in them.

Diabetes is that stage of the body in which the body finds it difficult to properly utilize its main fuel glucose and metabolism of the other nutrients like fats and proteins also get disordered. Due to a gross disorder in food metabolism, a defect occurs in the composition of the body tissues and important biochemical reactions necessary to keep the body alive. This occurs due to deficiency or malfunctioning of the insulin hormone. As a result the body is unable to produce optimum energy and the nourishment of the body tissues also hampers badly. Both these reasons produce extreme weakness, letharginess and early fatigue in a diabetic patient.

Insulin deficiency leading to non-utilization of glucose, fats, proteins and other essential nutrients causes increase in blood glucose and lipid levels. Lack of nourishment such as protein deficiency also leads to weakening of the muscles, the bones and the nervous tissues. There are two more types of diabetes mellitus that is, latent and brittle diabetes besides overt diabetes.

1. Latent diabetes

This is also known as hidden or unclear diabetes. In this disease no clear symptom is present in the patient except high blood glucose level (usually after meals). It is considered to be of only one type.

2. Brittle diabetes

Without any symptom, assimilation of glucose starts in the blood and diabetes results abruptly. In these patients the blood glucose level sometimes goes very high and at other times very low (unstable glycemia).

‘Conjugal Diabetes’ is said to occur when husband and wife both are suffering from diabetes. All offsprings of these types of couples have greater probability of developing diabetes.

According to ayurveda diabetes is described as follows: Since a diabetic passes out sweet urine like honey and the body, too, contains sweetness hence all types of advanced pramehas in which the urine also consists sugar besides other classical symptoms (in patient) are called diabetes.

Prevalence of Diabetes

The prevalence of diabetes is difficult to determine because numerous standards, many now no longer acceptable, have been used in its diagnosis. The overall prevalence in western societies is about 5% (type 1 and type 2 both). Whereas in the Indian subcontinent the prevalence is touching 10% figure and is expected to go further more. The prevalence of IDDM has been estimated to be ~2% by age of 20. Among diabetics one-fourth cases have insulin dependent disease while three-fourth are non-insulin dependent. The frequency and chances of insulin dependent diabetes decreases after the age of 20 years.

The alarming rate at which this disease is spreading can be anticipated from the fact that about 25-30 years back in a city (in India) with 10,000 population the number of diabetics could be counted on fingertips. But today this number has reached to 1,100 per 10,000 people (in Indian subcontinent). What is the reason of this upserge in diabetic population is a matter of great concern? But the good aspect is that more and more people are becoming health conscious and have started adopting a few natural preventive measures such as balanced diet, yoga and daily exercises.

Diagnosis of Diabetes

Utmost care should be observed before labeling a person diabetic. National diabetes data group of the national institute of health has provided a criteria for the diagnosis of diabetes and a detailed description has been given in the previous chapter. A few case histories (Kanti Diabetic Care Centre, Rishikesh) along with the results of their investigations have been discussed below. One can take help of the following examples to correctly make diagnosis of diabetes himself.

Case no. 1

Patient’s name: Mr. Vinod

Age/Sex: 44 y/m,

Profession: Chartered Accountant.

Presenting Features: Polyuria, polydipsia and +ve family history.

Investigations: Overnight fasting plasma glucose level (FPGL).



Overnight FPGL: 170 mg/dL N : <126 mg/dL


Overnight FPGL: 161 mg/dL N : <126 mg/dL

Interpretation: Two reports of FPGL >126 mg/dL (whole venous blood) are conclusive of diabetes.

Case no. 2

Patient’s name: Master Vibhu

Age/Sex: 11 y/m,

Profession: Student Class VI

Presenting features: Semi consciousness and acidotic breath.

Investigations: Random plasma glucose level (RPGL).



RPGL : 499 mg/dL N: <200 mg/dL (<11.0 mmol/l)

Urinary Ketones: ++++

Interpretation: RPGL >200 mg/dL and positive Urinary Ketones is conclusive for diabetes.

Case no. 3

Patient’s name: Mr. Ashok Kumar

Age/Sex: 51 y/m,

Profession: Teacher

Presenting features: Asymptomatic but +ve family history for diabetes and ischemic heart disease.

Investigations: ‘Glucose Tolerance Test’ 75 g of glucose, dissolved in two glasses of water are made to drink by the patient. A series of blood samples are taken at 30 minutes, 60 minutes, 90 minutes and 120 minutes following ingestion of 75 g glucose.



30 minutes PGL : 141 mg/dL N: <200 mg/dL (<11.1 mmol/l)

60 minutes PGL : 144 mg/dL N: <200 mg/dL (<11.1 mmol/l)

90 minutes PGL : 209 mg/dL N: <200 mg/dL (<11.1 mmol/l)

120 minutes PGL : 212 mg/dL N: <200 mg/dL (<11.1 mmol/l)

Interpretation: Two reports of whole venous PGL >200 mg/dL at 90 and 120 minutes, are confirmatory of diabetes.

Case no. 4

Patient’s name: Mr.Rishi Gupta

Age/Sex: 42 y/m,

Profession: Bussinessman

Presenting Features: Asymptomatic, +ve family history of diabetes, stressful life and poor eating habits.

Investigations: ‘Glucose Tolerance Test’ procedure as described in Case no. 3



30 minutes PGL : 134 mg/dL N : <200 mg/dL (<11.0 mmol/l)

60 minutes PGL : 146 mg/dL N : <200 mg/dL (<11.0 mmol/l)

90 minutes PGL : 189 mg/dL N : <200 mg/dL (<11.0 mmol/l)

120 minutes PGL : 202 mg/dL N : <200 mg/dL (<11.0 mmol/l)

Interpretation: The diagnosis is impaired glucose tolerence test (IGTT). It is because one reading (at 120 minutes) is >200 mg/dL and all other readings are <200 mg/dL.

Difficulty in the Diagnosis of Diabetes

The problem arises with the asymptomatic patient who for one reason or the another is considered to be a potential diabetic but has a normal fasting plasma glucose concentration. Such patients are often given an oral glucose tolerance test (OGTT) to find out whether they are diabetic/non-diabetic/potential diabetic. Case number 3 and 4 are examples which may help in this regard.

Several patients diagnosed diabetic by GTT may never show symptomatic deterioration or elevated fasting plasma glucose levels later in life that is, ~75% patients of impared glucose tolerance test ‘IGTT’ do not develop diabetes in later 5 years.

Golden Parameters for Diagnosing Diabetes

The following methods and parameters were used for diagnosing diabetes in good olden days and they still have not lost their significance. These are as follows:

* A diabetic prefers standing to walking, sitting to standing, lying down to sitting and sleeping to lying down (SushrutSamhita.Nidan.L6.S25) position.

* Presence of boils/carbuncles in patients with symptoms like polyuria, polydipsia and polyphagia are almost confirmed diabetics.

* The patient himself diagnoses the disease by tasting urine (honey taste).

* Presence of flies and ants at the place where the patient urinates indicate glucose in urine and possibility of diabetes “CharakSamhita.Cikitsa.L6.S14” (for more details read prameha).

Differential Diagnosis of Diabetes

Does excessive and repeated urination always occur in diabetes only? Can sugar spill in the urine in other diseases also besides diabetes? The answers to these questions are as follows: The main symptom of diabetes that is, repeated and excessive urination ‘prabhuthamutratha’ (more than normal quantity of urine per day due to osmotic diuresis) can develop in several other diseases also and sweetness, too, can occur in other pathological states. Besides, ‘prabhuthamutratha’ the other symptom ‘avilamutratha’ (turbid urine), another finding in diabetics can also be present in other diseases, too, such as ikshumeha (alimentary glycosuria) or sheetmeha (renal glycosuria).

‘Prabhuthamutratha’ (Polyuria or bahumutra)

Normal urine output is 50 ounces a day out of which, roughly 37 ounces is during the day and 13 ounces during the night. More than this amount of urine per day indicates bahumutratha, which can occur in the following circumstances:

1. Diabetes mellitus.

2. Diabetes incipidus.

3. Acute glomerulonephritis.

4. Acute renal failure (diuretic phase).

5. Severe increase in ‘vata’ humour.

6. Excessive cold.

7. Nervousness, anxiety and fear.

8. Stroke and post epilepsy.

9. Plenty of semi solid foods.

10. Liquid drinks as squash etc.

11. Natural diuretics as tea, coffee, and wine.

12. Diseases of adrenal glands.

‘Avilamutratha’ (turbid urine)

In natural states, the urine is light and straw coloured. But when unnatural substances start coming in the urine, then its colour and specific gravity both change. Main causes of turbid urine are:

1. Glucose in urine.

2. Acute renal failure (oliguric phase).

3. Nephrotic Syndrome and a few cases of Chronic Renal Failure.

4. Sweating, vomiting, diarrhoea.

5. Prolonged high fever.

6. Presence of phosphates, chyle, albumin, pus, fibrin, base, bile pigments, hemoglobin, indican, blood, oxalate, urate, hyaline cast, fat, and semen in the urine.

Under natural (normal) circumstances glucose does not spill in the urine. In children and pregnant women glucose may appear in the urine at blood glucose levels around 110 mg/dL (lowered renal threshold for glucose) but in adults it has to be >170-180 mg/dL. The level of glucose in the urine increases in the same proportion as that of blood glucose level after 200 mg/dL that is, in a diabetic with normal renal threshold for glucose if blood glucose level reach 200, 250, 300 and 350 mg/dL the urine glucose will show .5%, 1%, 1.5% and 2% respectively. But in some cases due to kidney failure despite high blood glucose levels glucose does not spill out in the urine.

Presence of Glucose in Urine

Glucose may be present in the urine of the patients of following four disorders:

1. Ikshumeha (alimentary glycosuria).

2. Ojomeha (diabetes mellitus).

3. Sheetmeha (renal glycosuria).

4. Non-specific glycosuria.

If glucose in urine is present due to violation of renal threshold by excessive intake of carbohydrate rich food then it is not a serious situation (alimentary glycosuria). But in a few patients the renal threshold decreases and despite normal levels of blood glucose, glucose spills in urine (as in sheetmeha due to ammonia). Diabetic glycosuria is said when a patient persistently has glycosuria without any other apparent disease and normal renal threshold. In ojomeha also one loses glucose in the urine but it is of permanent nature and very serious disorder which soon converts in overt diabetes.

According to ayurveda in ‘sheetmeha’ and ‘ikshumeha’ also the urine is sweet in taste, though the patient is non-diabetic. There are certain drugs and chemicals which also give false positive test for urinary glucose. The problem disappears are stopping of these drugs.

Presenting Features of Diabetes

The development of subjective symptoms definitely occurs on developing of diabetes but the capability of recognizing the severity of these symptoms is different from patient to patient. On interpreting the symptoms it becomes easy for the physician to optimally diagnose and treat the disease. By presence/absence and severity of symptoms one can also judge the level of diabetic control in himself. Broadly diabetes is of two types :

1. Primary Diabetes

A. Type-1 or Insulin dependent diabetes mellitus ‘IDDM’ Synonym (ayurveda)- Sahaja madhumeha or Avrita vatajanya madhumeha.

B. Type-2 or Non-insulin dependent diabetes mellitus ‘NIDDM’ Synonym (ayurveda)- Aahar-viharjanya madhumeha or Dhatukshayajanya madhumeha.

2. Secondary Diabetes

Described later in tthe blog.

Both these types (IDDM & NIDDM) of diabetics reach the physician with different early presenting features, but the late symptoms are almost identical (symptoms of the late complications of diabetes). Presenting features in diabetes can be grouped under three categories :

1. Early or primary symptoms of type 1 diabetes (IDDM) or Avrita vatajanya madhumeha.

2. Early or primary symptoms of type 2 diabetes (NIDDM) or Dhatukshayajanya madhumeha.

3. Delayed or secondary symptoms of type 1 and type 2 diabetes.

1. Early or Primary Symptoms of Type 1 Diabetes (IDDM) or Avrita vatajanya Madhumeha

The symptoms of this disease are sudden, severe and serious in nature. Sushruta called these patients as ‘krish madhumehi’ and modern medicine recognizes them as ‘insulin dependent diabetes mellitus’. The patient normally is of minor age (average age is 8 years) and very normal until the time of getting ill (usually a few days back). Sudden onset of fever (in several cases even mild fever is not present) and excessive urine are the initial presenting symptoms and soon the patient reaches semi-conscious state.

This semi-consciousness occurs due to keto-acidosis, which if left untreated, soon converts into ketotic-coma. This is so because the intrinsic insulin production drastically reduces due to irreversible damage in ‘beta cells’. This leads to excess utilization of fats instead of glucose utilization for fulfilling body’s energy requirement and during this process excessive production of ketone bodies takes place. Since ketones are like poison for nerve cells, if the patient is not timely treated he lands firstly at the stage of semi-consciousness, soon deep coma and ultimately dies.

 Identifiable Symptoms of Ketosis

The most common and easily identifiable initial symptom of ketosis is a fruity (acetone like) smell present in breath, sweat and urine of the patient. This is because excess blood ketones are excreted in these secretions and they smell like fruits. The symptoms of more advanced stages like forgetfulness, over anxiety, irritation and confusion, also appear in children. Advancement of the disease leads to serious symptoms like unconsciousness, semi-coma and coma.

Relation of Age with Severity of the Disease

As the age at which IDDM has appeared advances, the severity of initial presenting symptoms reduce. A boy developing insulin dependent diabetes at the age of 5 years will have more intense symptoms and disease profile as compared to a 10 years aged patient. The common presenting features are:

1. Sudden loss of body weight.

2. Repeated urination.

3. Excessive thirst.

4. Excessive hunger.

5. Acidotic breath.

6. Mental and physical weakness

2. Early or Primary Symptoms of Type 2 Diabetes (NIDDM) or Dhatukshayajanya Madhumeha

Rishi Sushruta says: “sa chapi gamnat sthanam sthanadasanmichati aasanad vrinute shayyamshayanat swapnamichati” (SushrutSamhita.Nidan.L6.S25) i.e., a diabetic prefers standing to walking, sitting to standing and lying down to sitting and sleeping to lying down. ~75% diabetics suffer from this type of diabetes. It has various names but most common is obese diabetic (synonym: ‘sthula madhumeha’ ).

These patients are normally of more than 30 years of age, they have more than normal body weight (obese) and are usually lethargic. Weakness and early fatigue are common complaints.

The Early Presenting Features of NIDDM

1. Polyuria (increased urination).

2. Polydipsia (dryness of mouth).

3. Dah (burning sensation).

4. Frequent change in specs.

5. Paleness of skin.

6. Sexual weakness (impotence).

7. Repeated bacterial infections.

8. Irregularity in menstruation.

9. Increase in appetite (polyphagia).

10. Sudden loss/gain in body weight

Breathlessness while climbing stairs and retrosternal chest discomfort are a few other non-specific symptoms. But occasionally they may be because of high blood pressure or premature ischemic heart disease.

3. Delayed or Secondary Symptoms of Type 1 and Type 2 Diabetes

These delayed symptoms develop due to: dhatukshaya that is, decline, waste or vitiation of muscles, blood, bones and other dhatus; accumulation of harmful and toxic substances amyloid (ama) and sorbitol in the body tissues as cardiac muscles, nephrones, and retina; and damage in shira (arteries and veins), vatanari (nervous tissue) and snayu (ligaments, tendons). Anemia, muscular atrophy, leanness, osteoporosis, bone marrow depression, oligospermia, decreased immunity, dehydration and loss of vitality are a few more disorders which give rise to characteristic delayed symptoms (clinical features) of diabetes.

The arteries provide pure oxygenated blood to all the living cells of the body, hence if they are occluded then all the body organs, systems and biochemical reactions also suffer badly and the consequences are:

1. Brain clots or intra-cranial hemorrhage, leading to paralytic attack.

2. Blockage in coronary arteries, lead to angina and heart attack.

3. Narrowing, clotting and subsequent obstruction in peripheral arteries such as femoral artery occlusion causes intermittent claudication initially (calf cramps) and on complete stoppage of blood supply gangrene of the foot.

4. Damage in retinal arteries gives rise to visual loss (retinopathy).

5. Premature cataract and glaucoma (loss of eyesight and severe pain respectively).

6. If a diabetic wears glasses he may frequently need change in his specs and it is because the shape of the lens also keeps changing.

7. The basement membrane of the nephrones get choked, giving rise to symptoms like swelling, nausea, vomiting, and altered consciousness.

8. Erectile impotence in diabetic males.

Ayurveda differentiates between type 1 and type 2 diabetes by the suddenness and severity of symptoms, the age at which diabetes has developed and whether the patient is strong or weak. In former (sahaja madhumeha– insulin dependent diabetes) the symptoms are very fast to appear and in latter case (apathyajanya madhumeha– obese diabetes) they appear slowly. The former type of diabetes appears at much younger age as compared to the latter. Apathyajanya diabetics are usually obese but sahaja (janamjaat- since birth) diabetics are thin and emaciated.


Efforts have been made in all the therapies (ancient and new) to classify diabetes mainly on the basis of etiopathogenesis and treatment plan.


Modern medicine classifies diabetes into two groups: 1. Primary; and 2. Secondary diabetes.

Primary diabetes implies that no associated disease (disease responsible for diabetes) is present whereas in the secondary type some other identifiable conditions (such as defect in thyroid or adrenal glands) cause or allow the development of diabetic syndrome. Primary and secondary diabetes is further divided into subgroups as follows :

 1. Primary Diabetes

It is of two types : Type 1 and Type 2.

1. Type-1 or ‘ketosis prone diabetes’ (IDDM)

It includes those patients who need insulin injection life long because they do not produce insulin any more (all b-cells of langerhans are dead) and therefore are unprotected against ketosis, a specific body state, rarely seen in type 2 diabetes.

Ayurveda also recognized this disease entity as it says in a few vataj prameha the body tissues so severely and quickly dissappear from the human body that most of the time the patient can not even reach a doctor and dies. The symptoms of the disease are hyperacute and the condition of the patient deteriorates very fast and because of lack of effective herbs the disease becomes incurable and deadly. The Acharyas have rightly called it a deadly disease because insulin in injection form was not available to the physicians of those times.

In most of these cases the insulin secreting b-cells get destroyed very fast (auto-immune damage) and the patient is known to be having IDDM. But in a few patients the damage process may prolong for 1-5 years (why it is so, is yet unconfirmed) and these are known as non-immune mediated IDDM patients (probably a large chunk of such patients has originated from sahaja pramehis). The final outcome in both the groups is similar that is, insulin production reduces to nil and these patients have asthenic (lean/thin) bodies.

Normally type 1 diabetes is diagnosed when a young patient reaches a doctor with symptoms of keto-acidosis or diabetic coma. Usually there is no major preceding illness but a few precipitating events such as severe infection, major accident or surgery, may be present. In fact during stress period insulin requirement of the body increases and a person destined to develop diabetes may not be able to fulfill this requirement and the result is diabetes, but a little earlier than anticipated.

At this stage these patients require insulin injection. But as soon as the stressful situation passes they can stay normal without insulin injection for a considerable period spreading over some months to a few years. This period is known as the ‘Honeymoon period’ of a diabetic. After passing this period, again symptoms of severe insulin deficiency appear.

Symptoms of immune mediated IDDM appear very fast. Normally the patient reaches the physician with complaints of mild fever (for 1-2 days), repeated urination, severe weakness, acidotic breath and semi-conscious state.

These patients are normally of 8-10 years of age (80%) but this disease can also occur at 20-45 years of age (15%). It rarely occurs after the age of 50 years. In IDDM patients the level of antibodies against insulin and ‘beta cells’ are found greatly increased (serum level of IAA and ICA). Within one month of appearing of symptoms, the insulin production becomes almost negligible. Decreased concentration of C-peptides (insulin and C-peptides are produced in equimolar amount in healthy (Beta cells) in blood is one of the main identification feature of this disease.

In ayurveda these patients are described as having ‘avrita vatajanya madhumeha’. According to ‘Sushruta Samhita’ such patients are recognized by sudden appearance of symptoms (suddenly vata humour increases many times and produces disease), semi consciousness and finally coma.

Immune and non-immune mediated IDDM, both are referred to as type 1 diabetes. Several type 2 diabetics may also require insulin injection at some point of time during their life. But the belief that by just using of insulin injection a patient converts to IDDM is not true. Hence insulin dependence should not be kept in the same class or equivalent to insulin therapy. Several type 2 diabetics, who are using insulin injection do not develop ketoacidosis even after stopping of insulin injection (some residual insulin secretion prevents keto-acidosis in type 2 diabetics).

2. Type-2 or ‘ketosis resistant diabetes’ (NIDDM)

These patients are those who do not require insulin injection for treating their disease. These patients are mostly adults and ketosis resistant. The serum insulin auto antibody titer and islet cells auto antibody titer usually do not show abnormal values (whereas in type 1 patients the auto antibody titers are always high). Thus as contrary to IDDM the ’beta cells’ of these patients are not destroyed by immune mediated injury. This fact indicates that ’beta cells’ are alive and they are secreting insulin (may be less) and it can further be confirmed by estimation of serum insulin and C-peptide levels, which most of the times show near normal values.

In reality the cause of hyperglycemia in early stages of this disease does not come out to be gross insulin deficiency but something else, and it may be insulin receptor resistance or insulin post receptor resistance. In obese type 2 patients hyperglycemia (born out of peripheral insulin resistance) puts an extra load continuously over insulin secreting ’beta cells’ (as they over function to normalize increased level of blood glucose) and due to this reason the ’beta cells’ exhaust and partially lose the ability of synthesizing normal amount of insulin that is, development of secretory defect. Type 2 diabetes can be of two types : a. Non-obese and; b. Obese diabetes and resembles apathyanimittaja madhumeha described in ayurveda.

(a) Non-obese NIDDM

These are those diabetics who are capable of controlling their diabetes by oral medications alone and insulin injection is not required. But it has also been observed that patients of this category may convert to insulin dependent diabetics after a few years of the disease and then they are equally susceptible to ketoacidosis as type 1 patients. The subsets of patients in this category are non-obese subjects who carry HLA-DR3/DR4 phenotype and may exhibit islet cell antibodies in the blood.

(b) Obese NIDDM

These are the patients whose pancreas functions properly at least in the earlier stages of the disease, but due to eating high caloric diet (almost all obese indulge in this eating pattern) insulin requirement increases very much, which becomes difficult to fulfill by the pancreas and the result is secretory defect (after few years). Peripheral insulin resistance (decreased activity of insulin) also plays detrimental role in development of diabetes in these obese people.

First of all peripheral insulin resistance does not allow insulin to function properly and as a result blood glucose level rises which, further puts burden on the ’beta cells’. This vicious cycle goes on and ultimately even maximum functioning of the ’beta cells’, too, becomes incapable of meeting out increased insulin requirement and the result is exhaustion and subsequent malfunctioning of the ’beta cells’. It all leads to decreased insulin production over a period of few years (secretory failure).

The probability of diabetes increases to 300% if one gets obesity and obese persons are 3 times more susceptible to develop diabetes as compared to the normal persons. And since in these patients obesity is the sole cause of disease hence through correct treatment of obesity diabetes can be prevented as well as cured also. As there is no involvement of autoimmune destruction of ’Beta cells’, the patient can remain healthy life long.

Today it is being seen that comparatively young people (12-35 years of age) are also developing obese NIDDM (a few years back it was a non-entity). But through proper treatment these patients can also control their disease lifelong without requiring insulin injections (as against the common belief that all juvenile age diabetics are IDDM). There is another subset of patients called maturity onset diabetes of young that is, ‘MODY’. These are the young patients in whom ’beta cells’ destruction has not taken place completely and therefore they behave as NIDDM for a few initial years and then convert into insulin requiring diabetics.

2. Secondary Diabetes

In this type of diabetes some other identifiable conditions which cause or allow the development of diabetic syndrome are discussed as follows:

1. Pancreatic disease.

2. Endocrinal disease other then pancreas.

3. Drug or chemical induced diabetes.

4. Insulin receptor abnormalities.

5. Genetic syndromes.

6. Others: it includes all conditions which do not fit elsewhere in the etiological scheme.

Inflammation of the pancreatic gland, pancreatitis, whose main cause is chronic alcoholism, greatly destroys the ’beta cells’ resulting in secondary diabetes. A few endocrinal abnormalities such as pheochromocytoma, acromegaly, cushing’s syndrome and excessive use of steroid hormones, sex hormones (male and female) as medications may also lead to diabetes. ‘Stress hyperglycemia’ is because of excess secretion of catecholamines and glucagon hormones in situations like severe burn, life threatening illness, myocardial infarction (heart attack), major accident, complicated surgery etc. Hormones (other than insulin) affect blood glucose level in two manners:

1. Firstly they may obstruct production and secretion of insulin.

2. Secondly they may neutralize insulin action in body (anti-insulin).

Medicines used in treating other diseases such as hypertension or epilepsy may become the cause of temporary diabetes (high blood glucose level persists till these medicines are in use) and even ketoacidosis. But most of the time the abnormality is limited only upto ‘impaired glucose tolerance test’, which is purely the result of ‘peripheral insulin resistance’. This dysfunction may be due to quantitative or qualitative defects in the insulin receptors itself or due to abnormalities directed towards it.

Several types of genetic syndromes are also related to impaired glucose tolerance and hyperglycemia. The three main syndromes are: Lipo dystrophy, Myotonic dystrophy, and Ataxia telangiectasia.

Others include all conditions, which do not fit in the above etiological scheme. The appearance of abnormal carbohydrate metabolism in association with any of the secondary causes does not necessarily indicate the presence of underlying diabetes although in some cases a mild, asymptomatic, primary diabetes may be made overt by secondary illness.


In ayurveda, the most ancient and authentic classification of diabetes i.e., Madhumeha was published by Maharshi Charaka as he recognized the importance of heredity in the prevention, development and treatment of diabetes 3000 years ago and accordingly divided diabetics into two major groups:

1. Congenital or Sahaja madhumeha

2. Acquired or Ahaar-viharjanya madhumeha.

Both the above conditions are preventable, the first one by cleaning beeja dosha (beeja suddhi– purification of genes through herbal preparations) in parents, and the second one by improving food and life style habits.

There is another classification depicting the ultimate result of diabetes treatment that is, sadhya and asadhya diabetes. Sahaja diabetics are either asadhya (incurable) or yaapya (as long as medicines are in use the disease is under control) and all other diabetics including sthula diabetics (type 2) are either curable or treatable with difficulty (kashta sadhya).

In Charaka and Sushruta samhita (the two most important ayurvedic text books) diabetes is included in kulaja roga (familial disease) that is, a disease, which runs in families. As Charaka says : “shukrashonitjeevsanyoge tu khalu kukshigate garbhasangya bhavati” (CharakSamhita.Shareersthanam.L4.S5) i.e., the origin of foetus is a combination of male beeja (sperm), female beeja (ovum) and the soul. Further he says : The properties (guna and dosha) of the first two (genetic cells) play a definite role in the health and disease status of a child. It means that physicians at that time knew about a few diseases as having hereditary predisposition and diabetes was one of them.

It has also been said : “jatah pramehi madhumehino va na sadhya uktah sa hi beejadoshat” (CharakSamhita.Cikitsa.L6.S57) i.e., it is quite probable that the offsprings of a diabetic are likely to be diabetic, too, and it occurs due to deformity in the beeja (genetic cells) itself.

Th e synonyms of avrita vatajanya madhumeha are : sahaja madhumeha, krisha (constitution) madhumehi, insulin dependent diabetes, juvenile diabetes and type 1 diabetes. Whereas dhatukshayajanya madhumeha is equivalent to apathynimittaja or sthula madhumeha, non-insulin dependent diabetes, obese diabetes, adult onset diabetes or type 2 diabetes.

For better treatment plan diabetes is divided into two types : 1. Krisha constitution (asthenic) diabetic; and 2. Sthula constitution (obese) diabetic and again these can be compared with type 1 and type 2 diabetics respectively. Recently a third type of diabetes has been recognised and named as lean type 2 diabetes or apathyajanya madhumeha with weak body constitution (lean iatrogenic type 2 diabetes).


According to Chinese therapy (yin/yang method of diagnosis) diabetics are classified into two groups : 1. Patients of Yin (weak) constitution; and 2. Patients of Yang (strong) constitution and both have deficiency of Chi (energy). Every substance in nature belong to either yin or yang category. Even plants have yin and yang elements. The leaves and flowers are yin and the seeds and root are yang. Yang rich medicines are essential for the former whereas the latter group of diabetics need yin rich medications.


Tibetan system of medicine that is, Emchi (~500 A.D.) says nes pa (body humours) and lus zun (nutrients in plasma) along with some mental and spiritual factors are responsible for the development of pre-diabetes (‘gChin-snayi’ ) and fully developed diabetic syndrome is called as ‘gichin-nyi’. There is deposition of dusht meda (abnormal fats) and badkan humour (normal quantity of badkan is 3 fist full which increases several fold in diabetes) in the body of a diabetic. And increased badkan combines with za-khu and collects in the urinary system (‘za’ means to use and ‘khu’ refers to liquidity). Actually za-khu is body’s water element (shareerastha kleda) and dissolved nutrient molecules (glucose, fats, proteins, salts). The weakened kidneys transfer za-khu out of the body through urine.

There are three main types of ‘gChin-snayi’ : 1. Rung or lung type; 2. Mkhrispa or tripa type; and 3. Badkan type and also 20 subtypes 10 lung, 6 tripa and 4 badkan. And the causes of ‘gichin-nyi’ or diabetes syndrome include serious eating and living habit disorders beside nervous disorder.


According to pranic therapy there are 11 chakras in the human body which provide energy and nourishment to the body organs besides controlling nervous system. The solar plexus chakra is congested and the pancreas is also found slightly swollen up in diabetics. The cause of diabetes is damaging of the pancreas due to slightly brownish red pranic energy. In diabetes it is seen that ajna, navel and basic chakras are badly affected giving rise to two types of diabetes : 1. Extra pancreatic diabetes: Insulin activity is mainly affected (decreased); and 2. Pancreatic diabetes: Patients with less amount of insulin. In allopathy the first pathology is called ‘peripheral insulin resistance’.


Acupuncture considers diabetes as a ‘wasting and thirsting’ disease. Yin deficiency and empty energy are the main causes of this wasting and thirsting disease or diabetes. Yin can become cause or complication of diabetes. There are three types of diabetics : 1. Upper wasting LU Heat; 2. Middle wasting ST Dryness; and 3. Lower wasting KD Yin.


Unani or Greek medicine described diabetes as a curable disease if treated at early stages itself. Exercising, regimen diet and use of a few volatile oils as medication cures several diabetics.

The great philosopher, Aristotle (384-320 B.C.), court physician of King Amyntas of Macedonia, was the founder of this system. Pythagoras who is known as father of greek medicine named the three body humours safra, savda and balgum ‘phlegm’ responsible for diabetes. Plato also had same views on the origin of diabetes.


Homeopathy divides diabetes into two groups: 1. Neurogenic; and 2. Hormonogenic. According to homeopathy mostly diabetes is of nervous origin and digestive disorders (hormonogenic diabetes) are secondary and today we are finding it very correct.

Thus we see that normally all important and popular therapies divide diabetics into two groups out of which treatment of a few is easy whereas others are difficult to treat. Association of diabetes with nervous system is also confirmed.


According to the biochemic system of medicine, the development of diabetes is mainly due to complication and defects in the nerves ‘neurogenic diabetes’, and there is a deficiency in those cell salts which nourish the nerves. Due to this only the nerves are unable to properly carry out their main function of stimulating the pancreas (pancreatic diabetes). This disease is seen mostly in the people of Jewish community and those with hereditary pre-disposition.

The main cause of diabetes is considered as disordered eating in persons with nervous temperament. Obesity (which is the cause of ‘auto-toxication’, that is, the work of causing bad effects on one’s own body cells, tissues and systems) and excess cholesterol in the body causes all the body cells to become less sensitive to insulin secretion (peripheral insulin resistance).

Moreover cholesterol and other bad lipids causes neurological damage also to the nerve cells. According to biochemic medicine, the above two reasons are sufficient for the development of diabetes. Under these circumstances, certain harmful chemicals as diacetic acid and oxybutyric acid cause damage to the

b-cells of the pancreas, hepatocytes of the liver, nephrones of the kidneys, besides other body cells, and cause chronic complication of diabetes.


Diabetes as per Ayurveda 


Acharya Charaka says: “asyasukham swapnasukham dadheeni gramyodakanuparsah payansi; navannpanam gudvaikritam ch prameha hetuh kaphakricchsarvam” (CharakSamhita.Cikitsa.L6.S4). It implies that the causes of sthula diabetes or apathyanimittaj madhumehaare wrong eating and drinking habits and incorrect life style.

The word madhumeha was first used by Rishi Charaka 3000 years ago, who gave it a place in twenty subtypes of prameha or pre-diabetes. Sushruta used ksaudrameha in place of the word madhumeha. The literal meaning of both ‘madhu’ and ‘ksaudra’ is honey. However Sushruta, too, has defined ksaudrameha as the damaged and spoiled stage of prameha. Rishi Vaghbhat’s observations are also similar as he observes : “sarva eva pramehastu kalenapratikarinah” i.e., all illtreated pramehas convert into madhumeha.

According to great ayurvedacharyas like Charaka, Sushruta and Vaghbhat diabetes is primarily of two types that is, ‘Avrita vatajanya madhumeha’ or type 1 diabetes and ‘Dhatukshayajanya madhumeha’ or type 2 diabetes.


Charaka and Sushruta both have named ‘beeja dosha’ or defect in the genes as one of the main factor responsible for this disease. Charaka has described anatomy of beeja (semen or shukra and ovum or dimb); which may be correlated as beeja = semen, beejabhaga = chromosomes and beeja bhagavayava = genes (CharakSamhita.Shareer.L4.S30).

According to them beeja dosha can occur at any level either at beeja level, beejabhaga level or beeja bhagavayava level. They also say that as blindness since birth can occur in children without parents being blind (congenital blindness), similarly if beeja dosha is present in the parents without active diabetes in them the children still have probability of suffering from hereditary ‘sahaja’ diabetes. It proves that since ancient times only, physicians knew about the role of inheritance in the development of diabetes.

We can analyze this fact easily by seeing this disease being placed in the category of ‘kulaja diseases’. It has been mentioned in Sushruta samhita that genetic involvement in diabetes can be understood only by keeping in mind four factors mainly kshetra, ambu, beeja and ritu. Here kshetra refers to female genetalia, beeja to sperm and ovum, ambu to the watery contents (amniotic fluid) that give nutrition to the foetus, and ritu to the environment (homeostasis) around the fertilized ovum or foetus.

According to Sushruta the future of the baby to be born depends upon the food taken by the probable mother and her mental and physical health (as these factors may cause vitiation of ovum). Therefore, due to beeja dosha that is, defective genes, the probability of developing diabetes at any stage is more in these persons as compared to a normal person born without beeja dosha.

If a few risk factors in the same proportion are present in two persons, one born with beeja dosha and the other without beeja dosha, then the former is more prone to develop diabetes at a very young age itself and the latter may or may not develop it at all. Maharshi Charaka also informs that vitiated body humours in the parents influence their beeja as abnormal humours get settled in genes and in due course of time this beeja dosha leads to diabetes in the offsprings.

Primary diabetes mentioned in ayurveda is the most serious form of vataj prameha. Secondary diabetes is the spoilt form of all pramehas that is, pre-diabetic conditions whose proof is the complications developing in one’s body prior to overt diabetes. Both primary and secondary diabetes develop as a result of sudden and prolonged excess of vata respectively in human body.

The sudden increase in vata humour is due to two reasons. Due to hollowing of the body tissues because of their abnormal and excess excretion through the urine, vata finds unnatural pathways and residing places, where it can collect in abnormal amounts, giving rise to increase in vata, which is responsible for primary diabetes. Secondly because other humours that is, pitta and kapha obstruct the natural passage of vata in the body, vata collects in abnormal amounts giving rise to avrita vatajanya madhumeha or type 1 diabetes.

On the other hand if the amount of vata has increased only because of a decrease in other two humours (change in ratio) and there is chronic dhatukshaya also, one is more prone to develop a milder form of diabetes called type 2 or apathya ahaar-viharjanya madhumeha.

Disease developing as a consequence of the former phenomenon (avrita or obstruction) is fulminant from the very beginning and can also be identified as insulin dependent diabetes developing at a very young age. And diabetes as a result of the latter phenomenon (proportional increase in vata) develops slowly and steadily, and all the three humours are found vitiated in it. Kapha vitiation is expressed by excess urination, pitta vitiation through obesity and vata vitiation leads to loss of oja, lasika, majja and vasa, nutrients in the urine.

Tulya Dosha Dushyata’ and Progression of Pre-Diabetes into Diabetes

According to the principle of ‘Tulya Dosha Dushyata’ (homologous etiological factors of vitiation of doshas and dushyas) vataj prameha is the precursor of diabetes and its treatment is very difficult because drugs which cure vitiated humours increase dushyas and drugs which decrease dushyas increase humours, and therefore the treatment of this disease becomes visham kriya that is, heterogeneous treatment as said in : “na ch tulyaguno dushyo na doshah prakritirbhavat”. Generally all the three major types of pramehas (vataj, pittaj and kaphaj) are curable in their initial stages, some easily and some with difficulty. What is the reason behind their difficulty in treatment can be understood by understanding the law of ‘tulya dosha dushyata’.

Tulya Dosha Dushyata

The law of tulya dosha dushyata is all about the fact that homologous etiological factors for a disease vitiate doshas and dushyas with same properties. There are a few risk factors which have the capacity to vitiate a particular dosha (because of similar properties) besides also vitiating those dushyas which have similar property as that of the dosha. If such a drug is available for a disease which have similar effects on both doshas and dushyas, the treatment is easy; but if a disease is such in which only those drugs/food are available which have opposite actions on vitated dosha(s) and dushya(s) the treatment will become difficult. And according to the above principle the prodormal stage of diabetes that is, vataj prameha is considered a difficult disease to treat (kashtsadhya vyadhi) whereas the kaphaj mehas are amenable to treatment.

Progression of Pre-Diabetes into Diabetes

The main cause of all pre-diabetic conditions is consumption of kapha dominant dravyas (substances) and activities which help in increasing kapha in the body. Dhatus which are adversely affected in pramehas are also of kapha grade(tissues as meda, kleda and maans have properties similar to kapha and also have affinity to kapha). Substances having properties like katu-tiqt-kashay ras decrease both the vitiated humour (kapha) and dushya (meda, kleda and maans) in kaphaj prameha and therefore the disease is easily curable at this stage only. However if proper anti-disease measures are not taken at this stage itself kaphaj prameha converts into vataj prameha very soon only to become kashtsadhya or asadhya vyadhi.

Obesity or hypercholestremia (medo-rog) has been proved as an important cause of diabetes in modern days and in ayurveda it is described as a ‘nidaanarthakara vyadhi’ (having modifiable risk factor). Charaka says : “bina pramehampyeta jayante dustmedasah” (CharakSamhita.Sutra.L17.S104) i.e., dushtameda (e.g., hypertriglyceridimia) can produce prameha pidika (a serious diabetic complication) even before the development of diabetes. Most of the obesities are acquired (hence treatable) but a few which are of hereditary origin (sahaja medo-rog) are difficult to treat.

In case of pittaj prameha the dosha is of pitta category but the dushyas (same as in kaphaj prameha that is, meda, kleda and maans) are of kapha category. Sheet/cold and madhur/sweet property substances subside pitta but increase kapha and therefore the treatment becomes difficult. But a careful mixture of drugs (which decrease pitta but do not increase kapha) still cures the disease. If not treated in time it also coverts into vataj prameha.

Vataj Prameha (including ojomeha equivalent to madhumeha) which is very close to diabetes is the most difficult disease to treat. And this is because dhatukshaya (loss of nutrients in the urine and heterogeneity in body tissues) becomes so severe and rapid that proper herbs/diets are not made available to replenish the vital dhatus, without which no treatment will be successful.

The treatment of vataj prameha is also difficult because anti-vata measures are often medovardhak (increase adipose tissues, blood fats and kapha which again increase diabetes) and anti-meda (anti obesity) measures are vatavardhak, and diabetes is because of vitiation of vata. The equation is that medovardhak treatments decrease vata but increase kapha and medorodhak treatments (anti-obesity measures) decrease kapha but increase vata, so therefore in both the situations removal of the disease becomes difficult (as per the law of Tulya dosha dushyata).

Vataj prameha which develops because of either excessive langhan (deliberately reducing quantity of food and over exercising which may give rise to malnutritional diabetes) or excessive santarpan (eating of excessive fats plus a lethargic life style may lead to obese diabetes) are both totally preventable and curable according to ayurveda (CharakSamhit.Cikitsa.L6.S16,17,18). But in patients of vataj prameha where vataitself gets vitiated and attracts other body tissues towards the kidneys, thus leading to their excessive loss in the urine and resulting into disease, the treatment becomes more complicated and difficult.

The most recent studies have confirmed that it is the resistance towards insulin action which plays detrimental role in the pathogenesis of resistant diabetes but modern science has not yet come up with any satisfactory explanation for this phenomenon as to why a person is diabetic while he is having sufficient insulin (75% patients of the total population of diabetics have this state of the body in the initial years of diabetes) and if it is only because of insulin resistance then what are the exact reasons and pathogenesis?

Role of Extended (Increased) Vata in Progression of Diabetes

Vedic science has the answer to this phenomenon and they call it extensive vrihat vata dosha which is spread all over the body cells. Dusht vata destroys all good actions of pittagni (insulin) and does not allow the cells to produce their energy from glucose and fat metabolism as Charaka clearly says: The energy production in the human body with the help of pittagni suffers badly when pitta is vitiated “agnirev sharire pittantargatah kupitakupitah shubhashubhani karoti” (CharakSamhita.Sutra.L.12.S11). Similarly Acharya Bhavprakash also says : “pittashayeadhikah shleshma vahimandhyam prabhakshayah” (Bhavprakash.Prakran.6.S87) i.e., the loss of pittagni action leads to deficiency of energy in the human body.

As it was explained earlier vata humour is most dangerous because it has the necessary quality and force to disperse other doshas and harmful substances very quickly all through the body cells.

Role of Dusht Meda (abnormal lipids in blood) in Progression of Diabetes

So far the studies suggest that after vata the second important cause of diabetes is dushtmeda/abnormal lipids. In association with vata it reaches all over the body shrotas/pores present over the cell membrane, which get choked developing peripheral insulin resistance. As a result the fats, glucose, proteins and other nutrients do not get entry inside cells and thus largely remain unutilised. This causes deficiency of energy, accumulation of fats in the body, weakening of body tissues besides increase in blood glucose levels.

After some time these unutilized nutrients start appearing in the urine in deformed shape and a patient suffers with various nutritional disorders as deficiencies of essential amino acids, good lipids, vitamins, minerals and elements. In allopathy, too, the reason of insulin resistance is supposed to be the blocking of glucose channels and dysfunctioning of insulin receptors because of harmful lipids.

Acharya Madhavkar has inumerated various reasons for collection of abnormal lipids and the most important are : “avyayamadi—“, “madhuroannarasah—“, “medasaavratmargtwadvayuh—“ i.e., lack of exercise, plenty of sweets and carbohydrates in diet and obstruction of medovahashrotas by vatadi doshas respectively (Madahavnidan.L.4.S1). Acharya Charaka says : “medovahashrotas avritatva” i.e., encircling meda is the root cause of the disease.

Sushruta also gives vital information, as he says : “srotashyannavahe pittam paktou va yasya tishthati” (SushrutSamhita.Sutra.L46.S497) meaning this disease is the result of pitta dushti and annavahashrota dusti that is, defective pittagni causing abnormal food metabolism. Medodushti increases vata and kapha, and the result is prameha. Therefore medodushti because of encircled vata causes diabetes. Vaghbhat says it is a disease of those people who do not indulge in physical work.

The tissues/dhatus which create a human body, on getting vitiated with humours are called dushyas and they are: Ras (plasma), Raqt (blood), Maans (muscles), Meda (adipose tissues), Vasa (free fats and lipoproteins), Lasika (lymph), Asthi (bone), Majja (bone marrow and white cerebral tissue), Shukra (semen and atarva), Ambu (fluids) and Ojus (essence of all dhatus).

Shareerastha kleda can be described as that necessary portion of water inside the body tissues without which life is impossible. And when it is forcefully separated from the tissues, the result is slowing down of life, which gradually leads to death. The seat of accumulation of doshas, dushyas and shareer kleda is vasti (kidney and urinary bladder) through which they are excreted out of the body. For the accumulation of dushta meda in the body medovahashrotas avritatva (encircling or covering of fat), vata vitiation, jatharagni vriddhi (increase in appetite) and kapha medovardhaka nidan (causes which increase body fats) are necessary. It is a fact that obese persons are more prone to develop diabetes and kapha medodushtialso appears in the body.


Sushruta defines development of diabetes as : “divaswapnavyayamalasyaprasaktam sheetsnigd- hmadhurmedyadravannpansevinam purusham janiyat pramehi bhavishyateeti” (SushrutSamhita.Nidan.L6.S3). It means persons who sleep in the afternoon; keep away from physical labour; are lazy; and make excess use of oily, sweet, fat rich food items are prone to develop diabetes. Vaghbhat says : “ekstanasanratih—–” (Vagbhat.Nidan.L10) i.e., persons sitting at one place only all the time are more susceptible to diabetes and “shayanam vidhivarjitam—–“ (Vagbhat.Nidan.L10) i.e., unnecessary sleep taken by breaking all rules as overlooking time, place and age is surely harmful and one important cause of diabetes.

In the following shloka Charaka has named a few causes of diabetes as: “asyasukham swapnasukham dadheeni gramyodakanuparsah payansi; navannpanam gudvaikritam ch prameha hetuh kaphakricchsarvam” (CharakSamhita.Cikitsa.L6.S4). It means : ‘Asyasukham swapnasukham’ This refers to persons who escape from labour and lead an easy, sedentary life style. ‘Dadheeni ’ Dairy products, which have lactose and lesser number of carbohydrate chains ‘simple carbohydrates’ and are easily metabolized. ‘Navannpanam’ Intake of newly harvested paddy which is rich in carbohydrates. ‘Gudvaikritam’ Food items made of sugar and jaggery. ‘Payansi’ Liquid diets as they increase kapha humour. ‘Gramyodak’ animals that is, flesh of animals which reside near human habitations and ‘anupa’ animals that is, animals living in water as fish (as these are ‘abhishyandi’ or ponderous foods and how they help in development of diabetes will be described later in the book) are all the causes of diabetes. As per modern science it can be concluded that the above said animals have more fats as compared to animals residing in forests.

The food, which is ingested gets assimilated and utilized by jatharagni in a normal body whereas in a diabetic due to vitiation of jatharagni, impairment in above mechanisms begin. Thus free glucose increases in the blood and one glucose molecule collects seven water molecules and gets filtered through ‘mutravaha shrotas’ (glomerulus), and reaches the vasti (renal tubules), where reabsorption mechanism fails and thus sweet urine is witnessed. In ayurveda all components of the urinary system are named as vasti.

According to ayurveda fats, glucose and proteins all three present in food, may increase meda in diseased as well as healthy body. And as meda accumulates within and outside the body cells and also obstructs various channels and in turn causes obstruction in the passage of air and pittagni. As these two are necessarry for burning the body fuel their vitiation leads to disordered substrate metabolism (low energy production, fat and glucose deposition).

Modern science also accepts that insulin is essential for making glucose molecules reach inside the cells for metabolism. But the satisfactory answer to the question how diabetes develops despite normal serum insulin levels, in obese diabetes, can only be found in theVedas, which mention that it is the pittagni/insulin which makes the nutrients reach within the cells by the force of vayu. And within the cell, energy is being produced by burning of glucose. Hence if flow or force of vayu is not proper but obstructed then energy production will also not be proper and the result is diabetes. All the causes which help vitiate vata and pitta are developers of diabetes.


‘Jathragni Daurbalya’ i.e., weakening of stomach fire

First of all jathragni daurbalyata meaning the weakening of the fire of the stomach is observed in those patients who eat an unbalanced diet and lead an adverse life style. Then due to increased kapha humour, agni (metabolizing energy) is reduced due to the cooling property of kapha. Indigestion or ajeerna is the result of this agni dushti (disordered metabolism). This ajeerna can be of several types as vatakarak (foods which increase vata such as dry and hot foods), pittakarak (foods which increase pitta such as oils and oily foods) or kaphakarak (foods which increase kapha such as flesh of water animals, dairy products, sweets) foods. And as a result the illdigested humours in the food constitute ama that is, apripakwa ras or immature humours. In diabetics ama of vatakarak foods constitutes amavata, which is a very harmful substance for body cells (just as sorbitol). The researches made till now agree that glucose with the help of a few enzymes reduces to sorbitol through ‘polyol pathway’ and sorbitol acts as poison for the body tissues and the cells.

Agni Dushti’ i.e., disorders of metabolizing enzymes

Agni (pitta) disturbances combine with immature doshas and reach the other dhatus of the body and vitiate them leading to their heterogeneity. The vitiation of the dhatus start from the first dhatu that is, ras dhatu or plasma. The essence of food that is, ‘saar’ mixed with ‘ama’ or ‘amasaar’ (ill digested nutrients) reaches the blood and vitiates the whole plasma that is, the ras dhatu. Once in the blood this ama along with agni dushti spread all over the body to each and every cell resulting in gross disturbance in cell metabolism causing peripheral insulin resistance. The above pathology explains why people are diabetic even when their serum insulin levels (pittagni) are near normal (even increased).

Sequence in which Metabolic Disorders spread in the Dhatus

The metabolic disturbance spreads in a specific manner and the first set of polluted dhatus is ras (plasma), raqt (blood) and maans (muscles) and the second set is asthi (bones), majja (bone narrow) and shukra (ojus). The uttan dhatus that is, the first as well as the second set of immature dhatus is accessible to treatment (auto-corrective mechanism), whereas adipose tissue (dushta meda) residing in between these two groups is inaccessible for correction.

In fact auto-corrective mechanism’ of the body acts as a protective mechanism and makes the rectification in these dhatus (SushrutSamhita.Sutra.L15.1S8). This rectification process converts immature dhatus into mature dhatus and also does balancing act as one dhatu can convert into another and vice-versa. The dhatus thus produced or matured become immature dosha free. This protective auto-corrective mechanism is controlled and executed through the nerves and secretory glands. But meda can not be corrected completely by auto-rectification mechanism therefore its timely prevention and treatment is essential otherwise it may lead to pre-diabetes, diabetes, prameha pidika (boils/carbuncles), obesity, dyslipidemia, hypertension and many more diseases.

Abnormalities in Ojus Dhatu in Diabetes

The ojus is produced as a result of several times rectification of ras and all other dhatus. Ojus can not be produced in normal amount in the body cells if the other dhatus of a person are unhealthy (heterogenous). The essence of all dhatus is named as ojus (SushrutSamita.Sutra.L15.S19,20).

According to Sushruta oja is the best energy substance made by the essence of all dhatus from ‘ras to shukra’. Just as fats are invisibly present in milk, similarly ojus is present in each and every healthy body tissue. Oja provides strength (bal) and energy (tej) to the body cells. On increasing of oja only rise in tushti (satisfaction, contentment of all 10 indriya), pushti (nourishment) and bal (strength) occurs. A human being remains alive as long as one is having sufficient amount of oja (CharakSamhita.Sutra.L17).

Charaka and Sushruta, the two great ayurvedacharyas have emphasized the importance of ojus in diabetes, so far so that they named a disease ‘ojomeha’, which is another name of diabetes. As oja is synonymous to strength and lustre in the body therefore it assumes much importance in healthy living of a person. Apart from strength, oja controls all the physical, psychological, neuronal and hormonal functions in the human body.

Charaka described ojus as a biochemical element of the body, which is reddish white, and slightly yellowish in colour and resides in the heart, brain, and other vital organs in substantial amount, and in all the other body cells in minute quantity. Sushruta links oja with the life span of a person and further elaborates that this honey tasting material when thrown out of the body in the urine always gives rise to severe diabetes.

In diabetics the amount and quality of ojus suffers badly in two ways: 1. Through obstruction in vessels (srotavrodha); and 2. Due to degeneration in the body tissues that is, dhatukshaya. Every attempt should be made to prevent ojokshaya and restore it with the help of proper food and medications.


“Pravrittasyaparipakwa” which means, inclination of doshas to excrete in the urine in immature stage itself and similarly coming out of ama dushyas (mainly non-metabolized glucose amaras and immature fats medascha apripakwam) in the urine through the kidneys (mutravahi shrota) are the two important factors responsible for developing diabetes.

According to Gayadas “medascha aparinamammiti asamyak parinatam” i.e., an abnormal increase in the body fats results in its misbalance. Modern science considers this fat imbalance as lipid abnormalities (cholesterol, triglyceride, VLDL and LDL levels in plasma are elevated), which are definitely considered very important reasons of developing diabetes nowadays.

Formation of meda (fats) from other nutrients inside the liver does not stop in diabetes (glucose converts into lipids). As fats are manufactured from the different types of carbohydrates present in one’s food, the new fats also have some properties of its raw material (type of carbohydrates). The newly formed fats are usually of bad properties and in excess may harm a diabetic.

According to modern medicine different food items contribute different types of fats, a few are health friendly while others are not. Besides this the liver also forms fats like cholesterol, triglycerides, HDL from the glucose obtained through several types of carbohydrates in the food and sends them into the blood circulation. It is astonishing to see that our learned Maharshis were knowing this fact which we in modern times were able to find out only a few years back.

‘Ama Ras Vadati Snigdham i.e., immature doshas make ras and the other dhatus greasy and oily. Oiliness is a natural quality of fat but in diabetes it is more sticky (pichhilatwa) and viscous (atidravta). It is this meda, which comes out of the body through the urine carrying along with it its fluidity. The dhatus vitiated with medaalso become fluid and come out easily through the urine. Glucose, fats, proteins and minerals present in the urine make it sticky and thick (dense).

Patho-Physiology of Dushta Meda

Due to impaired jatharagni and dhatwagni all the dhatus and doshas of the body remain immature and more viscous thus becoming unstable (in a normal person the dhatus remain in a stable form). These dravibhutha medadi dhatus with more fluid, are driven to the vasti (the kidneys and the urinary bladder) only to be excreted in the urine. Immature doshas and dushyas carry out body kleda, water driven out of the protoplasm and plasma and the other immature dhatus in the urine. Teekshanagni, increase in jatharagni and pachakagni and decrease in fat utilization medagni are the causes of obesity.

Medo-rog and madhumeha have close proximity. This can be proved by observing a few similarities in their causative agents that is, in both the diseases the intake of madhur ras (sweets) and snigdh guna dravyas (food items with oil or property of oiliness) are helpful in kapha vriddhi (increase in kapha humour) which is a main feature of both the diseases.

‘Santarpanotha vikar’ meaning obesity and diabetes are the diseases developed due to heavy food (santarpan measures) that is, eating diet rich in calories and avoiding all physical labour. These two diseases usually develop one after another. An astounding similarity is also found in their symptoms like early fatigue, unexplained weakness, letharginess, boils, polyphagia, and excess sweat (Madhavnidan.L34.S1,2).

By limiting the use of kaphakarak and medovardhak food items one can prevent medo-rog and diabetes both. Increase in medagni and kayagni (metabolic energies of different nutrients) and normalizing increased jatharagni and pachakagni with the help of pathya ahaar-vihar (balanced diet and life style) and medications cure both the diseases. A minor difference between medo-rog and diabetes is that in the former case ras, raqt and mamsagni (protein metabolising enzymes) are spared, whereas medagni is vitiated; but in diabetes all are involved. The result is defective metabolism of all the nutrients.

Sequence of Vitiation of the Body Tissues

Kapha dosha alone without vitiation of pitta and vata is unable to develop diabetes. A serious defect in all the three doshas of the body is essential for development of pre-diabetes and diabetes. Vitiation of dhatus takes place in following chronological order :

Meda (adipose tissue) ® Raqt (blood)® Shukra (semen)® Ambu ‘shareer kleda’ (water) ® Vasa (lipids)® Lasika (lymph)® Majja (bone marrow)® Ras (plasma)®Ojus(strength).


Vata dosha is the most important disorder in diabetes but the reasons, which are responsible for increase in vata, also help decide the curability or incurability of this disease. The purva rupa or prodormal symptoms, samanya rupa or general features, vishesh rupa or specific features, hetu or risk factors and sampraptior pathogenesis also provide important clues regarding further behaviour of this disease in the near and distant future.

Almost in all diabetics, there is an increase in kapha dosha in the initial stages. This abundance of kapha itself causes prameha (excess and turbid urine) and because it destabilizes the other dhatus and helps in bringing them in the urine along with excess meda, the ultimate result may be diabetes. In the following lines the above pathophysiology is explained in detail.

The excess kapha combines with meda only to make it more thin, simultaneously the other two doshas react easily with liquefied meda and thereafter this dusht meda also vitiates the other important dhatus. In the meantime vitiated vata and pitta also reach these dhatus only to make them worse. The presence of excessive doshas, vitiated dhatus and ama (substances which block glucose channels), all combined, lead to diabetes.

Note: Excessive vitiation of ojus does not permit a person to live long and therefore protection of ojus through diet, herbs and healthy activities is necessary to live a normal life.



The two types of diabetes insulin dependent and non-insulin dependent have different pathogenesis. The process of development of diabetes in both is entirely different though the result is almost the same. Understanding of pathogenesis helps in prevention of pre-diabetes, diabetes and diabetic complications, besides also proving helpful in correct treatment. The ratio of type 1 and type 2 diabetes in the total population of diabetics is around 1:5 that is, one out of every six diabetics is an insulin dependent diabetic.

(A) Pathogenesis of Type 1 Diabetes (IDDM)

By the time a patient is diagnosed as having type 1 diabetes, his b-cells are almost destroyed. This is caused by the body’s own immune system which is actually meant for defending body cells from outside pathogens. But instead by auto-immune destruction it destroys its own very important organ, the pancreas. A short description of the pathogenetic sequence is described in the following lines. Firstly, genetic susceptibility to the disease must be present in a probable patient. And secondly, an environmental event, which initiates the pathology in susceptible individuals, is also essential. Viral infection is believed to be a common triggering mechanism. Along with genetic susceptibility presence of an environmental event, probably a viral infection of the pancreas is most essential for the evolution of this disease. This can be confirmed from the fact that if one, out of a pair of monozygotic twins has type 1 diabetes then only in 50% cases, it is seen that the other, too, develops it. Hence, if this disease would have been purely because of a genetic disorder, then it should have been present in almost 100% cases of monozygotic twins, but it is not so. By this fact we come to know that on being genetically susceptible, the probability, only, of environmental event (viral infection) increases.

Viral Pancreatitis

Viral infection becomes very common specially when the weather changes. Just as other infections in the body tissues cause inflammation, similarly when infected with virus, the b-cells (beta cells) react, and it leads to inflammation called ‘insulitis’. The inflamed pancreatic islets are flooded with ‘T-lymphocytes’. These lymphocytes get access into the b-cells of the islets of langerhans. This lymphocytic infiltration changes the genetic identity of the b-cells and makes them stranger (self to non-self) to their own body’s defence system. As a result, the immune system of the body starts producing antibodies against its own b-cells. The reaction between the b-cells and the antibodies destroy both. This irreversible damage leads to type 1 diabetes. The pathogenetic sequence can be summarised as follows :

Virus infects the b-cells of a person with genetic predisposition ® environmental insulitis ® conversion of the islets of b-cells from self to non-self ® activation of the immune system ® production of anti b-cell auto antibodies ® antigen (non-self b-cells) antibody complex ® destruction of the b-cells ®result is type 1 diabetes mellitus.

Genetics in IDDM

Although quite often this disease is observed within families, still its transmission to other generations cannot be known and therefore it is not based on any standard ‘mandelian law’ (which tells that if both parents are having diabetes then the chances of becoming diabetic in the off springs are almost 100% and if only one parent is diabetic, then the risk is halved and without parents being diabetic, if only a distant blood relation is diabetic, the chances of developing diabetes are only 25%). And the chances of developing type 1 diabetes in a child when another first-degree blood relative has the same disease, is only 5-10%.

However, as compared to IDDM the presence of NIDDM in one or both the parents, somehow increases the risk for IDDM in the off springs. Low rates of transmission of IDDM make it difficult to discern mechanisms of inheritance through the study of families but are reassuring to diabetic parents who may wish to have children.

One of the susceptible genes in IDDM likely resides on the sixth chromosome. In view of the strong associations between diabetes and certain human leukocyte antigens ‘HLA’ (HLA- DR3, DR4, DW3, DW4, B8, B15) were coded by the major histo-compatibility region on this chromosome. When compared with the general population, the risk for IDDM imposed by the presence of susceptible gene is four to ten times. However many persons carrying ‘high risk’ genes never develop diabetes. There are certain people and tribes in the world where type 1 diabetics are almost negligible in number. In other way we can say that certain people and tribes are protected from IDDM and this protection occurs in these people due to the presence of a special gene structure (probably antigens B7, DR2) in their chromosomes.

IDDM is an immune mediated disorder; hence, if there is a genetic abnormality in the immune system itself (T-cells) then also this disease may develop without the person being infected with a virus. Under these circumstances the white blood cells do not recognize the

b-cells of its own body itself and start fighting against them (auto antibody production) considering them as foreign bodies. The result is destruction of the b-cells.

To fight against virus and other infections there are certain special substances in the body (cell mediated immunity), which recognize the body proteins, but not the outside proteins (in this case virus). When this external protein sticks on the outer membrane (which is also a protein structure) of the

b-cells of langerhans then body’s immune system considers this whole complex (virus + b-cell) as external and fights against it, resulting in destruction of both. Virus infection plays a definite role in the development of IDDM. It can be verified by looking at the following facts.

1. Seasonal variation in the onset of IDDM.

2. More than a chance relationship between appearance of diabetes and preceding episodes

of viral diseases such as mumps, hepatitis, measles, rubella, and coxsackievirus infection.

3. Finding of coxsackie’s virus B4 from the pancreas. On infecting experimental animals ith this virus many developed IDDM.

4. Moreover in few patients the antibody titers against this virus are found to be elevated.

5. 20% patients of congenital rubella may also develop IDDM.

Note: Unfortunately, no such virus has been discovered to date, which is solely responsible for the development of IDDM.

Viral infection causes damage to pancreas : It is possible through two mechanisms : 1. Direct injury to islets (insulitis); and 2. Through previously described auto-immune process. And by the time, diabetes appears most insulin producing cells disappear forever.

The average weight of the pancreas in a normal person is almost 80 g, whereas, the pancreas of IDDM patient may reduce upto just 40 g. The weight of endocrinal cell mass(a, b and d cells) reduces from 1400 mg to 400 mg only and the insulin secreting b-cells, which weigh approximately 850 mg in normal person, get reduced to almost nil in IDDM patients. Auto-immune mechanism is the reason for IDDM and is well supported by the fact that a majority of IDDM patients also suffer from more auto-immune diseases as compared to NIDDM patients.

Prediction of IDDM

The question now arises, can persons prone to develop IDDM in the near future, be recognized from the past itself or can this disease be identified in the initial stages itself (when no significantb-cell damage has occurred). The answers to these questions are few genetic markers can indicate which person is at high risk and by no means is it possible to recognize this disease in the early stages, as yet. However some prediction regarding the course of the disease is made possible by few investigations as anti-insulin antibody titer, anti b-cell antibody titer, and C-peptides value.

Role of Immuno-Suppressent Drugs in Prevention of IDDM

The other very important question is whether use of immune suppressive drugs provides prevention or at least some relief in IDDM? The answer is no. On identification of the virus, the development of anti-viral vaccine can also be looked into in the future.


The question as to how type 2 diabetes develops has been unanswered since a very long time and still there are no specific signals of advancement in this field. This disease runs in families but the mode of inheritance and pattern of transmission are not yet exactly known.


Till now, no gene has been found, which is capable of carrying this disease from one generation to the next. However, in a few patients (mostly maturity onset diabetes of young that is, MODY) a definite pattern of inheritance has been found out, which is as follows :

1. If both parents are type 2 diabetic, then the offsprings have 100% chances of developing this disease.

2. If one parent is diabetic, half the numbers of offsprings are prone to develop type 2 diabetes.

3. Besides parents, if any first degree blood relative is suffering from type 2 diabetes then the probability of this disease in children reduces to 25%.


As compared to type 1 diabetes, in type 2 diabetes it has not yet been known whether their chromosomes contain those genetic markers, which are helpful in the development or inheritance of this disease. Type 2 diabetes is not an auto-immune disease as type 1 diabetes. No proof has been found, of any virus, which attacks persons of a typical genetic composition. By observing that type 2 diabetes runs in families, this is certain, that there is definitely some powerful genetic influence, which carries this disease from one generation to the other generation.

It is an irony only, that diabetes, which occurs in majority of people and spreads from one generation to the other and has assumed such a big problem, still remains undiscovered as no definite gene or chromosome has yet been identified which transfers this disease from one generation to the other.

Physiological Defect in NIDDM Patients

Almost in all type 2 diabetics two physiological defects have been identified but in different proportions. First is abnormality in the insulin secretion (secretory defect) and the second is resistance to insulin action in the target tissues (peripheral insulin resistance). Which defect occurs first and which one is more powerful? These are the two questions whose answer is decided by proper history taking, careful examination and a few investigations in type 2 diabetic patients.

Hyperinsulinemia in Obesity

It is seen that most of the type 2 diabetics are obese (especially in the beginning) and this obesity is responsible for obstructing insulin activity called ‘peripheral insulin resistance’. Due to improper insulin action blood glucose level increases. As hyperglycemia is the single strongest stimulant of insulin secretion, the insulin secretion increases (sometimes hyper-insulinemia) in obese persons who are also having peripheral insulin resistance. But this increased blood insulin level does not serve its purpose completely and if the causes of insulin inaction are not taken into care, this vicious cycle continues till all the

b-cells are exhausted that is, decrease in insulin secretion called ‘secretory defect’. This fact proves that primary defect is decrease in insulin functioning capability and secondary defect is decrease in insulin secretion (pancreatic dysfunctioning occurs in later years).

Why do not all obese people get diabetes?

The question now arises that if obesity is the cause of insulin resistance and it is a compulsory requirement for the development of type 2 diabetes, then, why don’t all obese people develop this disease? And whether lack of obesity ensures keeping away from type 2 diabetes?

All obese people do not develop diabetes, because insulin resistance (due to obesity) is not the only factor responsible for diabetes. Instead a decrease in the

b-cell responsiveness (blood glucose level is the driving force behind insulin secretion), either due to genetic or environment risk factors may be essential pre-requisite for the development of type 2 diabetes. Therefore over a period of time, either due to defective genes (present in a person destined to develop diabetes as per his genetic constitution) or due to overuse of b-cells (exhaustive failure), once capacity of insulin secretion diminishes.

Insulin resistance, provoked by obesity (and may be some more reasons) plays secondary role in pathogenesis of type 2 diabetes. And it definitely plays a detrimental role in the appearance of diabetic symptoms, especially in early stages of the disease. The following conclusions can be drawn by reading above text:

1. Not all, but a few, ~40% obese people develop type 2 diabetes.

2. Type 2 diabetes can develop even if a person is not obese. In these patients, besides secretory defect, deficiency of insulin is capable of developing insulin resistance.

The knowledge of secretion and physiology of insulin, role of insulin receptor and post receptor resistance are all useful as described later.


Teachings of both vedic and modern medicine agree with the fact that deficiency in insulin secretion (synonym ‘pittagni’) by the pancreas is one most important cause of diabetes. Production and secretion of immature insulin (amapitta) and deformities in insulin action make the situation worse.

The exocrine cells of the pancreas produce pancreatic enzymes and the endocrine cells ‘islets of langerhans’ produce glucagon and insulin hormones (secreted from a and b cells respectively). Pancreatic enzymes digest the complex carbohydrates, proteins and fats present in food and change them to very minute molecules of glucose, amino acids and fatty acids respectively.

The number of b-cells in a human body ranges between 2-3 lakhs and their total approximate weight is 750 mg. Their number does not increase and always remains the same, as at the time of birth. If they are destroyed they can not be regenerated. The insulin secreted by the cells reaches the blood directly without passing through a pancreatic duct. The function of glucagon is to increase blood glucose level and decrease insulin secretion. Before going into the details of insulin functions, one should know about a few terms as described below:

* Chemical Digestion of the Food

It includes digestion of carbohydrates, proteins, lipids and nucleic acids, as different digestive enzymes and bile elements convert them into very minute substances called glucose, amino acids, fatty acids and nucleotide units, which also break in nitrogenous substances, glucose and phosphates.

* Absorption of Food

All the digested nutrients (glucose, fatty and amino acids) are in water soluble form; then only they become diffusible through the mucous cell membrane of the intestines into the blood capillaries (90% absorption of nutrients occurs in the small intestines).

* Assimilation of Food

Glucose, lipoproteins, free fatty acids, glycerol, phospholipids, cholesterol, glycosides, amino acids, urea, water, minerals, nitrogenous substances and vitamins are always present in the serum (blood). Out of these urea is metabolized by the kidneys only. The body cells utilize the other substances as raw food as per their required metabolism. As soon as they reach within the cells these substances start taking part in reactions relating to the synthesis of complex substances and become part of the protoplasm and also get dissolved for energy production.

* Metabolites

The assimilated substances are called metabolites.

* Metabolic Reaction

It includes all those biochemical events, which are taking place in the cells either to produce energy or to conserve energy. The former reactions are called catabolic and the latter anabolic reactions. Muscles, adipose tissue, and glycogen are all stored food ‘body fuels’.

Correlation between the Functions of Insulin and Pitta Humour

As insulin is necessary to help assimilation of nutrients for further action (metabolism) similarly, pittagni is also associated with different processes of food metabolism which are necessary to make use of foods and sustain life. The description of functions of pitta and after effects of pitta dushti (vitiation of pittagni) provide enough knowledge of the pathogenesis and treatment of diabetes.

According to ayurveda, pitta is liquid in consistency (thin, dilute), warm in temperature and yellowish in colour. It is of five types that is, pachak, ranjak, sadhak, alochak and bhrajak.

“rasadidhatugatah—–tadvraddhikshayavraddhikshayatmakah” (Bhavprakash Prakaran2.S134). In the above ‘shloka’ the importance and functions of pitta have been expressed. The pachak pitta digests the food and separates the ras (nutrients), mutraansh (water for urine), mala (excretory products) and doshas (humours) available in the food. Then the pitta situated in the pancreas intermixes with the nutrients by its own power and then only the nutrients can be used by the body (this process is equivalent to glucose insulin complex in blood). If pachak and ranjak pitta are insufficient, then food digestion and subsequently substrate metabolism also slows down. Sadhak, alochak and bhrajak pittas are also related to several metabolic processes. Vitiation of pitta leads to insufficient fuel storage and energy production.

Pittagni helps in storing the nutrients inside the liver, spleen, muscles, blood and heart cells besides increasing the release of energy ‘sheshagni’ which is also helpful in metabolizing the other nutrients. Every dhatu (body tissues and bio-molecules) has its own metabolic enzyme and pathway which may be termed as ‘dhatwagni’ according to ayurveda.

According to modern science metabolism of carbohydrates, fats and proteins, inside the body, occurs separately but all these three nutrients can get inter-converted also with the help of several metabolizing enzymes (dhatwagni). By controlling agni (metabolizing enzymes or ATPase) of the seven dhatus and the three doshas the body can be kept energetic and lively besides curing of diabetes.

How important is the contribution of pancreas in energy synthesis?

Rishi Vaghbhat has explained it in the following example as : “yatha grahasthapitani ratnani khadyotvad durbhasvarani tanyapi deepjyotisha durprakashkani bhawanti; tatha agnyashayasthpachkagnite jasa sarveagnyo balwanto bhavanti” (Bhavprakash.Prakaran2.S134).

Just as the shine of a jewel increases and reachesfar, when even minute light of diya (lamp) falls on it; similarly the pachak pitta present in the pancreas makes available the important metabolites to all the body cells and thus accelerated metabolism takes place (Bhavprakash Prakaran2.S135). The quantity of pittagni is described equivalent to a sesamum seed (in vedic science) and incidently the weight of b-cells is also only 750 mg.

Jathragni (the fire of stomach), with its power, is capable to disintegrate food into tiny particles and also retains its original properties. These particles after absorption into the blood, get distributed among all the body cells. Further what happens with them and where do they go? It can be understood by this example. Just as the sun resides so far in the sky but still dries up the lakes/ponds merely by its rays, similarly pittagnipresent in the pancreas (insulin) accelerates all the food molecules present throughout the body into releasing energy thus becoming useful for the body.

The synonym of agni is pittagni. Pitta is the source of fire/energy; the heat and power generated through it wanders throughout the whole body in blood. It provides kayagni (basal metabolism) to all the cells and thus kamoshma (basal metabolic requirement) is fulfilled. Pitta with its many functions is responsible for keeping the body alive and active, too.


Initially, the healthy b-cells, capable of insulin bio-synthesis synthesize pre-pro insulin molecule (one molecule of which is 11500 daltons), but its half-life is merely a few seconds. Very soon it breaks into pro insulin molecule, weighing 9000 daltons. Thereafter pro insulin matures more and again breaks up into two parts that is, insulin and C-peptide. They are immediately secreted after their synthesis but a small proportion of insulin may be retained (stored) in the b-cells with the help of zinc element.

The human, porcine and beef insulins are remarkably similar in their molecular structure. An ordinary change in the molecular structure of beef and porcine insulin causes no hindrance in being used for treating diabetics.


Immature insulin is inactive and any amount of it is ineffective in the body (pre-pro insulin® pro insulin ® insulin). It is surprising to read that 3000 years ago our learned Rishis knew of the fact that pittagni, a secretion of the pancreas after repeated maturation only, gets enough power to carry nutrients all over the body. Aparipakva pitta converts to paripakva pitta. It has been said in Charak samhita that immature pitta gives rise to disease only and ‘not the energy’.

Regulation of Insulin Secretion

According to ayurveda the pittagni, responsible for food metabolism and controlling of the other sheshagnis, is itself controlled as follows. As the food pushes down by the force of vayu from the mouth towards the stomach, the secretion of pittagni from the pancreas starts and increases proportionately. It implies that the amount of food decides the secretion of pittagni. In the allopathic system amount denotes calories in the food whereas in ayurveda amount denotes ‘guru’ or ‘laghu’ food. Advanced investigations reveal that the pancreas secrete insulin in three phases.

The first phase is known as ‘cephalic phase’, which starts as soon as the food reaches the mouth and is under neuronal control.

The 11thcranial nerve ‘Vagus’, carries a few parasympathetic nerve fibres originating in the hypothalamus region of the brain and reaching the b-cells, where they help in regulating the quantity and speed of insulin secretion. As pranvata (an important wind in human body) constitues the nerve cells of the brain and its functions are also under control of pran vayu, vata vitiation definitely plays important role in disordered functioning of parasympathetic neurones giving rise to diabetes.

The second phase of insulin secretion starts when the food reaches the stomach. A few gut hormones and presence of simple carbohydrates in the food influence insulin secretion. In ayurveda also the food is considered as the most potent stimulator of pittagni.

The third phase of insulin secretion is regulated by the quantity of glucose and fatty acids reaching the blood from the intestines. If they are in high concentration (in the blood), the insulin secretion will increase and if low the secretion will decrease. Secretion of pachak pitta is also dependent upon dhatwagnis.

At last we can say that the brain cells, along with the blood glucose and fatty acid levels, control the level of insulin production, secretion and regulation. Just as the brain plays an important role in insulin secretion similar is its role in insulin suppression. It is made possible by the sympathetic nerves which also travel to the pancreas through the vagus nerve. A small amount of insulin secretion takes place all the time and is called basal insulin secretion, which is crucial in the restraining of catabolism (prevents much breakdown of reserved food).


A few decades back, diabetes was considered purely as a glandular disease (pancreatic origin). But today it is not so. As we know that the brain and insulin secretion are deeply inter-related and activation of sympathetic nervous system leads to suppression of insulin secretion. As a person gets nervous, depressed, worried or anxious there is sympathetic over stimulation which may cause decrease in insulin secretion.

And how can irregular and sedentary life style full of tensions be held responsible for development of diabetes can be understood well by knowing about the recently discovered ‘syndrome-X’ as it has four features that is, young age, hypertension, mild diabetes and coronary artery disease. All have been proved to be due to fast changing life style and not the genetic background.

In ancient books on medicine and more particularly in ayurveda, it has been mentioned that vayu dosha, which mainly resides in the brain, controls secretion of pittagni (Charaka Samhita). Therefore severe defect in vayu dosha (wind humour) will definitely cause impaired insulin secretion.

Insulin Receptors

These are the structures made of proteins, which are present on the semi-permeable cell membrane of each and every cell of the body. Numerically it is not possible to count them as their number keeps changing; they increase or decrease according to the body’s requirement (several factors are involved, too).

The presence of insulin receptors on the cells is necessary for letting the glucose molecules (and also fatty acids and amino acids) enter the cells and tissues. It is only through them that the glucose molecule can reach within the body cells.

Functioning of Insulin Receptors

The physiology of insulin receptors has therapeutic importance and is helpful in treating diabetes as it may help to minimise the use of anti-diabetic medicine.

A mature normal insulin molecule fixes four glucose molecules on its one end. The other end is connected to the outer end of insulin receptor (present on the cell membrane). The inner end of the insulin receptor is connected to microsome bound glucose transport units, which are always present within the cells though a diabetic may have deficiency of these units. Insulin + glucose + insulin receptor + transport unit all combine and make a complex, which easily crosses the cell membrane and reaches the mitochondria, ‘the power house of the cell’. There the glucose burns down to release energy, necessary for life and a certain part of glucose gets converted into glycogen and is stored inside the cell itself as reserved fuel. Any defect in this link-up will give rise to dysfunctioning of insulin and therefore of glucose utilization.

Recycling &/or Resynthesis of Insulin Receptors and Glucose Transport Units inside Cells

The insulin receptor and glucose transport unit which reach inside the cell with glucose and insulin, either reach back to their original site, the cell membrane or are broken down by lysosome into amino acid within the cell itself. God’s creation is so great that each cell of the body has enough means and power, so as to rebuild/resynthesize these insulin receptors and glucose transport units within the cell itself.

The level of insulin in the blood decides the number of insulin receptors present on cell membrane. As the number of insulin receptors is inversely proportional to the level of insulin in blood, hence those diabetics who are mostly insulin deficient, definitely have more than normal insulin receptors on their cell membrane.

Insulin, Insulin Receptor and Glucose Metabolism

The pancreas release insulin directly into the hepatic circulation, which also consists nutrients absorbed from the intestines. The hepatocytes (functional units of the liver) utilize 75% of the total insulin produced in the pancreas, for important metabolic functions. It is thus clear that maximum utilization of insulin occurs in the liver. Rest of the insulin reaches the kidneys through the peripheral blood circulation. The two kidneys utilize 15-18% insulin out of the remaining 25% to fulfill their metabolic need. A small quantity of insulin filters out of the body through the kidneys in the urine. Remaining 8-12% of the total insulin proves sufficient for fulfilling metabolic requirement of the rest of the body’s cells. How the kidneys and the liver utilize so much of insulin can be understood in detail by knowing a few effects of the insulin hormone on these target tissues.

Active insulin molecule makes the entry of glucose possible inside the cell, only through insulin receptors present on the cell wall. Therefore, it is understandable that not only sufficient quantity of insulin in the blood circulation, but presence of sufficient insulin receptors on the cell wall along with normal amount of glucose transport units inside the cells are all mandatory for controlling of the blood glucose levels.


Insulin receptors also appear to be regulated by the amount of insulin that they are exposed to. Thus in ‘chronic hyperinsulinemia’, the number of receptors decreases and it is called ‘down regulation’.


Number of insulin receptor a  —————————————

                                             serum insulin concentration

Conversely in ‘hypo insulinemic states’ such as untreated insulin deficient diabetes, the number of insulin receptors increases.

The classical example of down regulation is obesity. If an obese patient observes food restriction, there is an immediate increase in insulin affinity, and then a slower increase in the receptor number. This regulation of receptor number may be a protective mechanism. Thus in obesity with hyperglycemia, the cells become less responsive to insulin to limit, for example, triglyceride synthesis and deposition (to prevent fat deposition and thus obesity). A vicious circle can, however, result with more and more insulin secreted to overcome the fall in receptor number and activity, a sequence of events, which can lead to diabetes in a susceptible individual when insulin secretion has reached a maximum along with insulin inaction.

On increasing of the number of occupied insulin receptors (on which insulin + glucose complex sticks) the affinity of unoccupied receptors towards insulin decreases. The use of this knowledge is being made in discovering such elements (medicine), which can activate the unoccupied insulin receptors. Similarly a few elements will definitely be there which decrease activity of the insulin receptors and if we can remove them the blood glucose profile may improve.

In fact the above subject needs more research to be conducted. During one of the experiment on fat cells, it was seen that, only 10% of the total number of insulin receptors present at any time on the cell membrane, were proved enough for fully utilizing insulin present at that particular time in the blood. This discovery disclosed that the other receptors (90%) at that time were either embedded in the cell membrane itself or were covered up by the other neighbouring cells.

Just like in hyper insulinemic states the principle of ‘down regulation’ is used similarly on continuous lowering of blood insulin level, there is an increase in the number of insulin receptors called ‘up regulation’. This is normally seen in those patients who are fighting against chronic insulin deficiency. Let us now make efforts to understand how and why insulin resistance develops and what is the role of insulin receptors in this process?

Insulin Resistance and Type 2 Diabetes i.e., NIDDM

Non-insulin dependent diabetics are mostly obese and their serum insulin levels during initial stages of the disease come out to be perfectly normal. However if carbohydrate load is put on these patients (carbohydrates rich diet or 75 g of glucose is consumed to perform glucose tolerance test), they fail to metabolize the extra glucose and therefore the blood glucose level increases.

Why doesn’t the extra glucose get converted into glycogen and fats, despite normal insulin level? This is because to prevent the body from more obesity, the body’s homeostatic system (auto-corrective mechanism as described by Sushruta 2500 years before) decreases the effectiveness (functioning capability) of the insulin receptors present on the cell membrane (insulin resistance). As a result the glucose does not enter the hepatocytes in unlimited quantity and is not converted to fats ‘triglyceride’ so it can not be stored in the body and hence obesity is comparatively checked.

But this protective mechanism has its adverse effects, too. Due to insulin receptor resistance, besides the liver, glucose is unable to reach the ‘mitochondria’ of the rest of the body cells, hence there is a decrease in the release of energy in the patient’s body, and moreover the blood glucose level also increases. After a certain stage this increased glucose in blood starts spilling out through the urine and comes out of the body resulting in decrease in body weight of the patient. Symptoms and complications as a result of hyperglycemia also start developing in a patient.


As is well known the blood glucose level directly influences the secretion of insulin. So in obese patients the blood glucose level is increased due to taking high calorie food and as a reaction the blood insulin level also increases and this stage is called ‘hyperinsulinemia’ (more than normal levels of insulin in blood). On increasing of blood insulin levels the number and activity of insulin receptors on cells also decrease which again hampers glucose utilization.

          hyperinsulinemia a insulin resistance

Hyperinsulinemia increases insulin resistance, which again causes hyperinsulinemia. The result is a vicious cycle when the insulin secretion reaches maximum in the patients and insulin resistance also increases unexceptionally, then the symptoms of diabetes (repeated urination, thirst and others) start appearing. When these patients improve upon their diet and do exercise then activity of the insulin receptors increases and insulin resistance decreases suddenly. Since more insulin is being secreted in the blood, the blood glucose level starts decreasing fast and symptoms of low blood glucose start appearing in the patient.

In a few patients (especially non-immune IDDM where the disease developing period is 1-12 months) in whom

b-cells are slowly destroyed the number of insulin receptors increases greatly (up-regulation). Therefore in such patients, initially, a little dose of insulin can prove so effective that the blood glucose level decreases to dangerous levels (severe hypoglycemia).

Post Receptor Resistance

In several diabetics the number of insulin receptors and their functioning both are completely normal and the blood insulin level is also normal, still they suffer from diabetes. Why it is so? The answer is that it happens due to the presence of post receptor resistance. Earlier researches made on experimental animals showed that ‘microsome bound glucose transport units’ perform the function of carrying glucose from the cell membrane to the cell.

Earlier it was thought that the insulin receptors only, are required to carry glucose from the semi-permeable membrane to the mitochondria through diffusion within the cell itself. But now it is clear that the function of carrying glucose from the cell membrane to the cell’s powerhouse is performed by the above said intercellular glucose transport units and not the insulin receptors alone. If due to any reason there is a decrease in the number of glucose transport units present inside the cell, then the glucose reaching the cell membrane with the help of insulin is not utilized fully (as it does not get entry into the cell) and the result is diabetes. It is called post receptor resistance.


In several diabetics fasting blood glucose level comes out abnormally high; whereas post prandial glucose levels do not increase in the same proportion. Among these patients there are several patients in whom wide fluctuations in blood glucose are observed during the whole day (sometimes low and sometimes very high blood glucose level). In addition to uncontrolled hyperglycemia these patients also show tendency of weight gain.

There is another category of patients who have fasting hyperglycemia, in addition to it there are some patients in whom fasting blood glucose is high but postprandial blood glucose does not increase in the same proportion and wide fluctuations in blood glucose level are not seen during the day. Most of the patients of this category show static body weight or the body weight decreases. In situations of morning hyperglycemia dose increase in anti-diabetic medication is the only correct treatment and the evening dose of all such patients should be increased. But it is not correct because increase in evening dose does not cure the problem of all patients. Instead this complication can take more severe stage. How it is possible and what should be done to treat moderate hyperglycemia in all these patients can only be understood after knowing about following two important physiological reactions.

1. Somogyi Effect

2. Dawn Phenomena

Morning hyperglycemia, increase in body weight, polyphagia (other systems of hyperglycemia as polyuria and polydipsia may or may not be present), wide fluctuations in day time blood glucose (sometimes very high and sometimes very low) make one suspicious about this complication. The principle of somogyi effect is rebound hyperglycemia following an episode of hypoglycemia. As it is well known in situations like hypoglycemia the body’s protective mechanism produces some hormone such as epinephrine, glucagon etc., which prevent from hypoglycemic coma. These hormones are also called counter-regulatory hormones. They have anti-insulin effect and under the influence of these catabolic hormones the liver converts more and more fat and glycogen into glucose and thus makes it available to the blood and thus the decreasing blood glucose level not only becomes normal but also increases more than normal (generally the protective mechanism overeacts). The cause of above phenomena is over dosing of medicine (usually the evening dose of insulin is more which gives rise to midnight hypoglycemia causing rebound morning hyperglycemia). The treatment consists of the reduction in doses of insulin/OHAs especially in the evening dose.

Dawn phenomena and several diabetics with early morning hyperglycemia do not have this because of somogyi effect (i.e., they do not suffer with midnight hyperglycemia). The nocturnal surge of growth hormone release is thought to be a major factor. Increased clearance of insulin also occurs in the early morning hours, but the changes are probably not of major importance. Infact, growth hormone has some anti-insulin effect, which plays a major role in these patients.

It is necessary to differentiate between dawn-phenomena and post hypoglycemic hyperglycemia i.e., Somogyi effect because the latter can be avoided by decreasing the evening dose of anti-diabetic drug, whereas patients with dawn’s phenomena require increased amount of anti-diabetic medication to maintain euglycemia in morning.

How to Differentiate between the Patients of Somogyi Effect and Dawn Phenomena?

It can be decided by doing blood glucose test in the night at around 2’o clock. In patients of Somogyi effect, the blood glucose is detected very low at this time but in morning hours because of the effect of counter regulatory hormones, the blood glucose level increases unexpectedly and the result is morning hyperglycemia. Because the reason of Somogyi effect is severe hypoglycemia at night, therefore it can be avoided by increasing a few calories in dinner and decreasing the medicine dose.

But if at 2 a.m, the blood glucose level is detected normal or slightly more than normal then there is full probability that in coming hours because of production of natural growth hormone (maximum secretion of growth hormone takes place around 3 a.m.) the blood glucose level increases more and more and by early morning high blood glucose level are observed. In such a situation, to normalize hyperglycemia the calories in evening meals should be a little decreased and the dose of anti-diabetic medication should be a little increased.


Biochemical Background of Food Utilization

It is essential for the patient and the doctor to have some knowledge of the fundamental biochemical processes which underly normal nutrition, such as the supply and utilization of energy containing nutrients upon which life depends; the control of the metabolism of proteins, fats and carbohydrates; and results of imbalance between the fuel supply and demand. It is necessary to know how the metabolic fuels are provided to the tissues, and which biochemical changes occur in a patient deprived of food and so on.

Need and supply of metabolic fuels 

The body requires energy for various functions. These include the synthesis of new tissues, the maintenance of ionic exchange, the process of secretion and detoxification, the generation of heat, and the performance of exercise and locomotion. To provide this energy, the body tissues oxidize glucose from carbohydrates, fatty acids and ketone bodies from fat, and amino acids from proteins. These energy containing substrates or metabolic fuels are provided as a mixture to the tissues through the blood stream, and their proportional utilization depends on several factors.

Oxidation of the fuels

The oxidation of these fuels is linked to the generation of the high energy phosphate of adenosine triphosphate (ATP) through various cycles (TCA or Citric acid). A high proportion of ATP is generated in the mitochondria through oxidation but additionally it can also be formed anaerobically such as during glycolysis (breakdown of glycogen) but this amount is insignificant. Glucose, fatty and amino acids produce ‘acetyl-Co-A’, whose cyclic oxidation (use of Oxygen and release of carbon-di-oxide) forms ATP. Oxidation of a single molecule of glucose can result in the formation of 36 molecules of ATP.

Energy requirements

A male of 65 kg under the age of 50 years will require roughly 2300-3100 KCal/day (light work) and 3600-4400 KCal/day (hard work) and a female of same stature 1800-2200 KCal/day (light work) and 2400-2700 KCal/day (hard work). After the age of 50 years it reduces by 10%. In a healthy person, the energy consumption increases considerably with exercise, fever, surgery, burns, and cancerous growth. 90% of the total caloric expenditure is utilized by the skeletal muscles (30%), abdominal organs (25%), brain (20%), and heart (11%). Rest 9% energy is utilized by all the other body cells. During exercise, the energy requirements of the muscles may increase upto 10-15 fold. Whether burning body fuels through exercise beyond a certain limit can help in maintaining normal health in a diabetic? The answer is obviously no as a diabetic is already suffering from the problem of food storage deficiency in reserved food. One will not be benefitted by doing excess exercises and this subject is discussed separately later in the book. It is also noteworthy that energy expenditure decreases after middle age.

Body composition and metabolic fuels

In normal circumstances the body comprises of 60% water, 18% fats, 16% proteins, 5% minerals, and 1% carbohydrate. The available metabolic fuels in a normal adult of 70 kg body weight during fasting state are: 15 kg fat (135,000 calories), 6 kg protein (24,000 calories), 0.2 kg glycogen in the muscles (800 calories) and 0.2 kg glycogen in the liver (800 calories).

The post meal ‘circulating’ metabolites in the blood are : glucose 20 g (80 calories), glycerol 3 g (12 calories) and free fatty acids 3 g (27 calories). In comparison, the energy to be derived from circulating metabolites is insignificant (1000 times less than the stored energy).

 The above description tells that 99.99% energy expenditure of the body every day is contributed by stored food, and it can only be stored in normal amount when sufficient insulin is present in the body.

Can body proteins be used as the main fuel in place of glucose and fats?

There are two main important sites of protein storage in the body, ‘intracellular’ and ‘extracellular’ compartments. The intracellular protein present in the muscles can be utilized for fulfilling fuel requirement; whereas the extra cellular protein present in the bone matrix, and skin is not readily available as a source of fuel. The significance of the differences between the muscle and adipose tissue as source of potential energy becomes obvious when it is recalled that 4 g of muscle protein gives only 4 calories (17 kj/g) to the body, whereas 1 g fat gives 9 calories (38 kj/g) and 1 g glucose yields 4 calories.

 The dietary protein (protein in the food) contains 4 calories/g, but in the muscles one protein molecule contains 3 times more water as compared to its own weight; thus the effective weight of amino acids remains only 1 g out of every 4 g of muscle proteins, thus yielding only 4 calories/4 g of muscle protein, whereas the adipose tissue yields 9 calories/g.

 In non-fasting persons there are a number of minor short-term body stores of fuel such as glycogen, free glucose, free amino acids and free fatty acids. The main metabolic fuels circulating in the plasma as their constituent are proteins as amino acids, fats as fatty acids and glycerol and carbohydrates as glucose and lactate during exercise. Ketone bodies formed in the liver are also a source of energy.

Note : The ideal fuel of the human body (diabetic and non-diabetic both) is glucose that is, carbohydrates in diet, but a small contribution is also made by fats deposited in the body. But a condition in which the body proteins (reserved in muscles) are needed to generate energy for day to day living should not arise. This is because of two main reasons:

1. The byproducts of protein catabolism like urea, ammonia, and uric acid are harmful for the body tissues especially the kidneys, joints and brain.

2. The energy produced from reserved muscle proteins is very less and the loss incurred to the muscles (severe and sudden muscle wasting) is very high.


The liver occupies a central position as the transformer between the fuel supply and the tissues, which utilize it. After the rapid utilization of short term fuel stores such as glycogen, the main suppliers of further fuel are fat and protein and the main utilizers are the muscles, nervous system, abdominal organs and the blood cells. The ratio of the carbohydrates, fats and proteins to be utilized is decided by the concentration of a few hormones and other metabolites in the blood.

Basic metabolic requirement (roughly 1800 KCal/day) of a normal fasting man are fulfilled by 75 g of proteins, 160 g of triglycerides and 180 g of glucose released from the liver. Brain utilizes 75% of the total glucose present in the blood as its own fuel and the rest 25% glucose is converted into lactate and pyruvate (through the kidneys and bone marrow), which again goes to the liver and reconverts into glucose so as to prevent gluconeogenesis from proteins (because excess protein utilization has its own drawbacks).

In addition to complete oxidation of glucose in the brain and glycolysis in the red blood cells, the remaining tissues as the heart, kidney and skeletal muscles in fasting state, use free fatty acids or ketone bodies as their energy providers. The hepatocytes, which convert ‘glucogenic amino acids’ into glucose, themselves require energy, which is again provided by free fatty acids (non-esterified fatty acid).

In normal persons the intake and utilization of the food appear to be closely linked, so that, in healthy person body weight and composition remain virtually constant for years together. Intake of food is influenced by appetite and hunger and probably by some other unidentified endocrinal or intestinal signals. The role of the hypothalamus in this regard can not be overlooked.


Following basic principles regulate substrate metabolism.

(a) Availability of Substrate

The concentration of a particular substrate in the circulation represents the balance between its utilization and production either from endogenous or dietary sources. Probably it is the most important regulatory factor besides neuro-hormonal regulation.

The total amount of substrate (oxidizable fuels) in the blood is remarkably constant in various physiological states but the proportion of glucose, free fatty acids, ketone bodies and amino acids may vary considerably. For example, decreased insulin concentration in the blood leads to increased lipolysis and production of ketone bodies, and increased utilization of proteins. Normal blood flow also helps in controlling metabolism.

(b) Permeability to Substrate

How substrates circulating in the blood reach inside the cells? There are two important ways:

1. By ‘simple diffusion’ through the semi-permeable membrane of the cell.

2. By a specific transport system, whose activity is alterable by hormones. Glucose reaching inside the cells with the help of insulin and insulin receptors is an example of the specific transport system.

(c) Entry into metabolic pathway

Although the majority of substrates eventually yield ‘acetyl-Co-A’, which further oxidizes to produce energy, each substrate has its own metabolizing initiating enzyme, which helps in converting or limiting the process by which a particular substrate changes into actyl-Co-A. It is again astonishing to find that ayurveda had explained metabolites physiology in great detail, as it says every dhatu has its own agni that is, ‘dhatwagni’. All nutrients have their ‘separate metabolic energy’, though they are very much interconnected.

(d) Intracellular Regulation of Substrate Metabolism

It is now well established that many regulatory hormones as hexokinase, glucokinase, lipoprotein lipase, acetyl-Co-A synthetase, and glutaminase in particular those concerned with storage or mobilization of stored fuels fat or glycogen, exist in active and inactive forms which can be readily inter-converted within seconds. In fact these enzymes act as catalyst and speed up the reaction in which they are involved that is, forward or backward reactions in metabolic pathways. The above knowledge may help in treating diabetics if disorders of glucose and lipid metabolism regulating enzymes are corrected with the knowledge of ayurveda itself.

(e) Substrate Interaction

Changes in substrate concentration in the blood can in certain situations regulate the utilization or production of another substrate (for example, excess glucose converts into fat in the liver). In starvation or semi-starvation very common in most of the diabetics due to under eating, or in anticipation that it will help in bringing down the elevated blood glucose levels to normal, the body muscles stop utilization of glucose so that glucose can be spared for the brain cells and instead they use ketones, non-esterified fatty acids (free fatty acid or NEFA) and amino acids for their activity/energy requirement.

Another important example of substrate interaction is the production of glycerol, which is released on mobilization of adipose tissue triglycerides, which convert into glucose in the liver. Ketone bodies themselves stimulate the pancreas to produce insulin so as to reduce fat utilization. It all confirms that all substrates are inter-related to each other somehow or the other.

Food Metabolism in Diabetes

Glucose ‘main fuel’

Although many types of fuels are present in the blood circulation, glucose occupies a central role. It is so, because it serves as an optimal fuel for so many tissues and an obligatory fuel for the brain, red blood cells, and renal medulla. Glycogen is the storage form of glucose in many tissues especially the white blood cells and hepatocytes.

Glucose can be liberated from the liver by the action of an enzyme, glucose 6 phosphatase, which is absent in the muscles. After an overnight fast, about 25% of the 180 g of glucose required daily by a 70 kg man, is produced from glycogen; the rest is formed from fats (glycerol) and amino acids (gluconeogenic protein). In the fed state the concentration of glucose in the blood remains very constant. And it is made possible by very rapid disposal of glucose. The main organ for its disposal is the liver, where glucose is rapidly converted to glycogen and fatty acids.

Anabolic and Catabolic Reactions

Inside the body, all chemical reactions related to food storage are called ‘anabolic’ and those related to conversion of stored food to energy are called ‘catabolic’ reactions. When both these opposite reactions are in equilibrium then only the body weight remains steady and ideal. Our body tries to bring a co-ordination (regarding the supply of nutrients ‘to be read as fuel’ to the body cells) between periods of fasting and post meal duration.

Disposal Of Glucose Load By Hepatocytes

After taking food, surplus of glucose, fats and proteins reach the hepatocytes (liver cells). Hepatocytes (in healthy state) are designed in such a manner that they can easily assimilate any amount of the above mentioned nutrients. In the presence of insulin the hepatocytes metabolize these food ingredients in a proper manner and do not let the blood glucose level increase beyond normal. How the hepatocytes balance the extra carbohydrate load can be understood from the following example.

When we take 100 g of glucose in diet, then the glucose level in fluid content of our body should increase to 30-35 mmol/l (600 mg/dl), whereas in reality it increases by only 2-3 mmol/l (50 mg/dl). How it is possible and what happens to the extra glucose? In fact this extra glucose gets converted by liver cells into glycogen and fat (fatty acids, triglyceride etc.). Both are then absorbed in hepatocytes and adipocytes respectively.

Body proteins

Body proteins are the complex molecules of amino acids. They are being continuously broken down and resynthesized. The rate at which protein turnover takes place is in between 3-3.5 g/kg of body weight in a young man that is, around 200 g of protein is daily broken in healthy state. But if it is not restored by equivalent protein synthesis, the rapid loss of muscle bulk can happen as occurs in patients of malnutrition related diabetes.

Body cells synthesize these complex structures as per their need but the raw material is provided through the amino acid molecules reaching the blood from intestines. Various digestive enzymes in the digestive tract break down these complex protein molecules to simple amino acid molecules wherein they are absorbed in the intestines and reach the liver through portal circulation.

The liver cells normally oxidize a few amino acid molecules but majority of them are stored in muscle tissues. Amino acid molecules are not stored as such. Infact they have to get converted to protein first and then only can they be stored. This protein synthesis from amino acid is possible and accelerated only in the presence of sufficient insulin.

During amino acid utilization in liver (gluconeogenesis), urea is produced which has to be excreted in the urine. Alanine, an amino acid from muscles reaches the liver for deamination (as a result glucose and urea are produced) and liver supplies glucose to these muscles in exchange of those amino acids. Not all the types of amino acids can be metabolized in the liver cells, many reach the muscles, too, surpassing liver metabolism such as leucine and isoleucine.

Body fats

Fats are an integral part of food and body composition. According to their caloric value these are of two types: Firstis white adipose tissue, which contains 9 cal/g and second is brown fat, which has upto 180 cal/g. Brown fat is only found stored in infants and not in adults.

Dietary fat is insoluble in water and consists of triglycerides largely (including fatty acids in their structure) but small amount of cholesterol and fat-soluble vitamins are also present in them. After ingestion the fats form a coarse emulsion in the stomach. Thereafter pancreatic lipase enzyme does hydrolysis of triglycerides where after two fatty acid molecules are obtained along with a beta monoglyceride.

Bile salts reaching the intestines from gall bladder react with these fatty acid and monoglyceride molecules to form a water-soluble complex called mixed micelle. Except bile salts, which remain in the gut the latter is readily absorbed through enterocytes that is, the cells of the digestive system which absorb digested food. Once within the enterocytes triglycerides are resynthesized.

These intracellular aggregates of triglycerides, coated with phospholipids and proteins are called chylomicrones, which also carry some cholesterol and fat-soluble vitamins with them. Within the enterocytes the chylomicrones are easily secreted into intestinal lymphatic system, which opens up in hepatic blood circulation. Thus these substances reach inside the blood after being consumed in the food.

Triglycerides with medium chain fatty acids are readily digested and absorbed into the blood circulation and if they are present in one’s food, they may reach inside the blood very fast as their digestion does not take much time. Within the body fat is absorbed into adipose tissues as these tissues are made by combination of fat cells (adipocytes), minute blood vessels and connective tissues. In these fat cells, fatty acids remain stored in the form of fat globules. Under normal circumstance free fatty acids convert into triglycerides and vice versa. During this process some quantity of fatty acids is made available to circulating metabolites pool.

But when alternate fuel is required in condition of long period of starvation then it is fulfilled by glycerol obtained from triglyceride, oxidation of fatty acids (muscles fulfill their own 90% energy need by fatty acids only) and from metabolism of ketone bodies made from fats.

Lipolysis: Inside adipose tissues there is continuous breakdown of triglycerides into glycerol and free fatty acids. The former is converted into glucose through hepatocytes, whereas the latter may again change into triglycerides or be used by the body to produce more energy. During insulin deficiency more and more free fatty acids are released into the blood, where they may be used directly as fuel or get converted into ketone bodies in the liver itself.

Except red blood cells and nerve tissues all other body cells can utilize free fatty acids to fulfill their energy requirement and sometimes the muscles even favour free fatty acids as compared to glucose.

Ketogenesis: There are a number of conditions in which the body uses these ketone bodies as fuel. The production of ketone bodies can increase either when increased amount of free fatty acids and glycerol are present in the blood (due to insulin deficiency) or when long chain fatty acids increase in amount and reach the liver cells for oxidation (glucagon sensitive) and in this process large amount of ketone bodies are formed.

During starvation or severe insulin deficiency the blood ketones level crosses 2-5 mmol/l. Utilization of these ketone bodies depends upon individual organ whether that organ has his own alternate fuel or not; brain and nerve tissues utilize them selectively.

Glucose Lipid Interactions

The relationship between the utilization of glucose, hepatic carbohydrate status and lipid metabolism are of considerable importance in the management of diabetes. As we know ‘actyl-Co-A’ is the ultimate carrier of energy and its ‘actyl’ group is derived from glucose, fatty acids and a few amino acids; this molecule is oxidized in the cells to produce energy. Therefore if enough glycogen is not present in the liver cells, so as to produce enough glucose, then fatty acids get converted to glycerol in the adipose tissues. Glycerol on reaching the liver delivers glucose and simultaneously free fatty acids are also converted into ketone bodies in the liver.

In fact the increased blood concentration of ketones inhibit gluconeogenesis in the liver and on the other hand normal glycogen stores in liver prevent oneself from ‘ketogenesis’. The above description is sufficient to understand the relation in between these two metabolites. This knowledge is of great help in ketosis prone diabetics.

Biochemical Effect of Starvation

While a person is fasting, his energy requirements are fulfilled by the stored fuel. Except a brief period of fed state, rest of the day ‘during fasting which is about 20 hours a day’, the brain, nervous tissues and kidneys have an obligatory requirement for glucose amounting to 180 g/day. 80% of this is needed in overnight fasting and this is primarily supplemented (90%) by stored glycogen in the liver.

As the time of fasting increases the brain cells start utilizing ketone bodies and thus an attempt is made to prevent glycogen and stored first class proteins (vital amino acids) from being exhausted. Gluconeogenesis is also a source of energy in fasting stage. This glucose is formed from lactate, pyruvate, amino acids, glycerol and other alternate fuels. During period of deficiency of fuel/energy the kidneys and other tissues reduce their energy requirement to even less than half.

The results of short and long-term fasting specially in diabetes prone persons are as follows:

Effects of short-term fasts (in between the meals and overnight fast)

Their effects on metabolism are described above that is, glycogen, fat and protein utilization serve the purpose of providing fuel.

Effects of long-term fast

When glycogen and fats are already utilized it has very deleterious effect on muscles as their protein becomes body fuel and produces some glucose (some glucose in blood is necessary to keep oneself conscious). In fact the production of glucose from muscle, proves very-very costly, because proteins in muscles contain three times more water in comparison to their weight that is, 4 g of muscle protein will provide only 1 g glucose ‘4 calories’; whereas 1 g of dietary protein provides 4 calories, which is equivalent to 1 g of glucose. So if a person has starved to such an extent that his glycogen and fat stores are almost empty then the deterioration of the body becomes very-very fast. A diabetic patient should always keep the above fact in his mind; malnutrition must not be present at any cost.

In extreme cases the brain starts using ketones as substitute of glucose, the liver reduces gluconeogenesis and the kidneys become the main sites of glucose production with the help of ‘deaminated amino acids’. As starvation continues the basic energy requirement of the body also falls. This happens because of decreased physical activity and some hormonal changes that is, fall in T3 (low levels of thyroxin hormone reduces metabolic rate) and also very significant fall in serum insulin levels. Therefore starvation, partial or complete should never be practiced by obese diabetics in anticipation that sudden and significant decrease in obesity will help them regaining normal status.

Target Tissues of Insulin

Although insulin hormone has its effect on the whole body but the liver, kidneys and muscles are its target organs. The cells of these tissues also perform important functions such as energy production and fuel storage. More description about these organs is as follows:


The liver provides unrestrained and uninterrupted supply of glucose to all the body cells. Gluconeogenesis (glucose from protein and fat) and glycogenolysis (glycogen into glucose) reactions take place in the liver with the help of insulin hormone. The liver does not let the stored food to be exhausted quickly. Carbohydrate load, developing after the intake of food is managed by the liver with the help of insulin hormone.


Apart from proteins, the muscles also contain glycogen and fat. Insulin converts some glucose into the glycogen for storage in muscles. But this stored muscle glycogen is of no use to the other body cells, instead in dire emergency it converts into lactate and pyruvate which on reaching the liver reconvert into glucose and is made available to other body cells.

Insulin has a major effect on muscle protein metabolism, as it enhances amino acid transport into the muscles, helps protein synthesis, helps repair damaged cells and decreases amino acids utilization for energy purposes and prevents protein degradation, too. Insulin also causes increased potassium ions store in muscle cells. Health status of a diabetic is indicated by estimation of his blood proteins level and shape of muscles.

Adipose tissues

They are the reservoirs of main fuel fats. These energy stores are situated primarily beneath the skin. Mainly the fats come through diet but are also synthesized by surplus glucose in liver. Adipocytes contain fatty acids and triglycerides as fat globules. ‘Lipolysis’, as a result of insulin deficiency also takes place in the adipose tissues. Fatty acids themselves come and go through the adipose tissues and thus always provide an alternate fuel to the body. On deficiency of insulin the level of ketone bodies reaches to dangerous levels.

Effect of Hormones on Metabolism

Hormones influence metabolism in two ways:

1. They influence the level of metabolism regulatory hormones inside the body.

2. The rate of transport of substrates into the cells is also under hormonal control.

Changes in concentration of circulating substrates (as glucose) represent direct response of hormones. For example, following a carbohydrate meal, high blood glucose levels and a few gut hormones stimulate the pancreas to produce more insulin which results in decrease in catabolic activity (decreased neoglucogenesis, lypolysis and glycogenolysis) and increase in anabolic activities (storage of fuel as glycogen and fatty acids).

There are various fast and long-term effects of hormones, but insulin, glucagon and stress hormone (catecholamines and growth hormone) are of the first variety and greatly influence glucose metabolism. The effects of various hormones are described elsewhere in the book but insulin, glucagon, cortisole and catecholamines need break explanation because they are closely related to substrate metabolism with regard to diabetes.

Functions of Anabolic Hormones


Protein, glycogen and fat synthesis is stimulated but lipolysis and gluconeogenesis is inhibited under the influence of insulin. Detailed description is given later in this chapter.

Functions of Catabolic Hormones

Blood levels of catabolic hormones determine the level of blood glucose in diabetics as well as normal persons, too. As they balance and oppose insulin actions, these hormones are more active empty stomach whereas immediately after food intake, insulin actions predominate. The following hormones come in the category of catabolic hormones.


This is secreted from the ‘alpha cells’ of the pancreas. Its main work area is limited to the liver only. This hormone mainly plays role in gluconeogenesis (production of glucose from alternate fuel) and partly in glycogenolysis (breaking down of glycogen to glucose) and thus increases blood glucose level. The main function of glucagon is accelerating the work of gluconeogenesis by making gluconeogenic amino acids available to the liver cells. In the presence of glucagon, fatty acids easily reach the powerhouse of liver cells, where they produce energy by self-oxidation and then change into ‘acetyl-Co-A’, ketone bodies and other such fuels and thus become available to other body cells for energy production.

Adrenalin and Noradrenalin ‘Stress Hormones’

The target tissues of these hormones are the liver and adipose tissues. In the presence of stress hormones the process of lipolysis in adipose tissues and gluconeogenesis and glycogenolysis in liver are accelerated. Due to all these effects the level of glucose, ‘acetyl-Co-A’ and ketone bodies in blood increase.


These hormones do not let the glucose go out of the blood due to which glucose can neither be utilized for storage nor can it enter the cells for production of energy. This hormone is also helpful in mobilizing the stored fatty acids in adipose tissues and making them available to the body as fuel. Later on these fatty acids convert into glucose.

The most dangerous effect of cortisole hormone is accelerating protein degradation in the muscles. In its presence like other body fuels protein, too, is utilized for energy production (normally it is not so) and hence the muscles become thin and weak (wasting of muscles).

Growth Hormone

It increases glucose uptake by muscle cells and also promotes lipolysis which is a catabolic action (breakdown of fats). But its main function is to excite the body cells for amino acid uptake and protein synthesis that is, anabolic action.

After having knowledge of insulin production, insulin regulation, insulin functioning and anti-insulin hormones, the effects of partial or total deficiency of insulin on the body and how this information can be helpful in better treatment of diabetes, become easy to understand.

(a) Partial Deficiency of Insulin

Though insulin deficiency definitely occurs in type 2 diabetes, too, the residual insulin secretion remains sufficient to restrain catabolic effects such as lipolysis, ketogenesis and proteolysis. Gluconeogenesis and glycogenolysis slightly increase during hypo insulinemia.Partial deficiency of insulin also leads to inadequate disposal of carbohydrates reaching the blood through intestines. Fat and protein deposition in the body tissues also hamper in hypoinsulinemic phase.

The net result of all these biochemical events can be summarized as ‘decreased stores of body fuels’ that is, decreased glycogen stores, decreased protein synthesis and depleted fat deposits. Inadequate activation of adipose tissues, lipoprotein, and lipase due to hypoinsulinemia ensures high cholesterol, triglyceride, LDL and VLDL serum levels. Glucagon secretion increases during insulin deficiency states and thereby enhances gluconeogenesis and as a result, blood glucose level increases and stored fuel quantity decreases.

(b) Total Deficiency of Insulin

The consequences of absolute insulin deficiency are drastic and life-threatening. To summarize they are :

1. The body’s storing capacity of the fuels slowly decreases and ultimately finishes completely.

2. The blood glucose and cholesterol levels reach alarmingly high levels and ultimately short and long-term diabetic complications start developing.

3. The glucose supply to the cells slowly finishes off. And in this situation the body cells start utilizing the remaining fats. Once they are also finished body starts utilizing muscle proteins but soon this fuel also exhausts and a person dies because of non-availability of body fuels.

4. Ketone bodies (normal level <7 mg/dL, severe ketosis >150 mg/dL) are like poison for the nervous system and in absence of quick treatment ketotic coma ensures resulting in sure death.

5. Hypo insulinemia leads to an increase in the serum levels of catabolic hormones that is, glucagon, cortisole, adrenaline and growth hormone.

(c) Relative Insulin Deficiency

It is that state of the body in which insulin secretion remains almost same as before (slightly deficient) but due to several factors insulin requirement goes high thus producing relative insulin deficiency. One of the important factors leading to relative insulin deficiency is increased concentration of ‘anti-insulin hormones’ due to several reasons. And to counter catabolic effects of these hormones more secretion of insulin by the pancreas is required which is not possible in most of the diabetic patients.

Generally hormones that oppose insulin functions that is, stress hormones, are secreted in more than required quantity in periods of stresses like myocardial infarction, major accident, severe acute infection, septicemia, or burn etc. And this leads to immediate severe increase in blood glucose levels. To meet out this extra requirement insulin by injection is necessary. But as soon as the stress is overcome the need of extra insulin is no longer required.

Insulin Resistance Syndrome

Insulin resistance- When normo-glycemia is not possible despite normal levels of insulin in the blood then this state is called ‘insulin resistance’. In simple words it is that stage in which insulin is unable to carry out its prescribed functions to full capacity. Insulin resistance of type 1 insulin dependent and type 2 non-insulin dependent diabetes differ.

Normally, the blood insulin levels in obese type 2 diabetics remain only slightly deficient (or normal) as compared to a similar obese non-diabetic person. For developing of the initial symptoms of diabetes in these obese patients, a decrease in the functioning power (capacity of the insulin molecule to push glucose inside the cells) of insulin is most crucial.

Why only a few obese people develop diabetes whereas others do not? The answer is, that the main reason of developing diabetes is that the insulin responsiveness of body cells decreases in these susceptible obese persons as compared to non-susceptible obese persons.

Susceptibility depends upon several factors such as genetic, environmental risk factors, drug intake, and other glandular diseases. It implies that in these persons insulin makes glucose reach less easily and in low quantity (usually 1 molecule of insulin carries 4 glucose molecules) across the cell membrane into the cell, resulting in diabetes mellitus (hyperglycemia). On the contrary in non-susceptible obese persons insulin responsiveness remains intact and therefore blood glucose level remains normal.

It is seen that in most of the obese diabetics due to hyperinsulinemia the number of insulin receptors decrease (down regulation). In such cases if insulin is given by injection then blood glucose may increase even more instead of decreasing. This is because in these obese diabetics (who are also supplementing insulin from outside) hyperinsulinemia may itself cause decrease in the number of insulin receptors (because the number of insulin receptors is inversely proportional to the amount of insulin present in blood). This state of the body is called insulin resistance.

Exhaustive research and minute analysis reveal that in majority of type 2 diabetics insulin resistance does occur but the number and activity of insulin receptors does not decrease in that proportion so as to explain massive insulin resistance seen in them. In fact insulin responsiveness (activity) decreases only when more than 80% insulin receptors become inactive and this state can only lead to diabetes. When there is no serious defect present at the level of insulin receptors then how is insulin still incapable of functioning can be understood from the following information.

Post Receptor Resistance

The production of insulin + glucose + insulin receptor complex occurs at the level of the semi-permeable cell membrane itself. There are glucose transport units present (described before) to carry these complexes within the cell that is, from cell membrane to the mitochondria. If there is a great decrease in the number of these glucose transport units then no matter how high the blood insulin level is the blood glucose level increases and can not remain normal. This state is called ‘post receptor defect’. Microsome bound glucose transport units are made from high quality proteins and the cells themselves produce them (intracellular production).

Anti-Insulin & Anti-Insulin Receptor Antibodies

Normally antibodies do not develop against the insulin molecule (which is also a protein) produced by the body itself. The body’s immune system is activated so as to produce antibodies against the insulin only under certain special circumstances that is, when insulin molecule attaches itself to another protein molecule and the result is changed protein configuration of the natural insulin molecules itself. As this new structure is ‘non-self’ for one’s immune system and therefore it acts like a foreign protein ‘antigen’. The pathophysiology of the insulin receptor antibodies is similar to that of anti-insulin antibodies. These insulin and insulin receptor antibodies inactivate insulin molecules as well as insulin receptors.

The chances of development of anti-insulin antibodies are more in patients who are taking insulin injections so as to control their diabetes (on using human insulin injections the problem of anti-insulin antibodies production becomes less as compared to using bovine ‘animal’ insulin). By use of unrefined insulin the antibodies, which are being produced in large numbers, become capable of making the body’s insulin also ineffective and the result is insulin resistance.

The excessive secretion (more than normal) of catabolic hormones, too, results in insulin resistance. Anti-insulin hormone glucagon is secreted in large quantity in type 1 diabetics (juvenile insulin dependent diabetes) and thus contribute insulin resistance to a large extent. Temporary insulin resistance is also seen in ketoacidosis (due to increased production of catabolic hormones, acidemia and hypothermia). If daily insulin dose exceeds 200 units, the patient is said to be suffering from serious insulin resistance requiring hospitalization. One should take all precautions and necessary steps as to prevent it from happening in oneself.

Treatment Code of Vitiated Pittagni (Defective Insulin)

“tatra swayonivardhananavya pratikarha” (SushrutSamhita.Sutra.L.15.S8) that is, inloss of doshas as pitta dosha, are should try to use these diets and drugs which help in increasing body metabolism due to loss of insulin. As Charaka said- “dhatavah punah sharirah samangunnaih samangunbhuyishtheh va vayvaharvihareh abhyasya maneh vriddhim prapnuvanti” (CharakSamhita) i.e., increase the substances causing increase in blood. The yoni (mother dhatu) of pitta is blood (pitta is the by product of blood metabolism) so do those measures which increase plasma- blood.

Achrya Sushruta says if pittadi doshas are increased then treat them with purification and suppression medical measure (Sushrut Samhita.Sutra.L.15.S17).

Consequences Of Abnormal Food Metabolism

The aim of diabetic treatment is to achieve near normal glycemic control so that one can prevent himself from acute as well as chronic complications of hyperglycemia (uncontrolled diabetes). Severe hypoglycemia especially iatrogenic (because of over zealous treatment) should not be allowed to occur as severely low blood glucose level may cause paralysis, coma and even death.

Maximum damage in body tissues occur because of blockade in small and large blood vessels. A peculiar substance amyloid (in ayurveda it can be compared with ama) developing in long term uncontrolled diabetics, if gets deposited in various tissues of the body, does great damage in vital organs such as kidneys (k.w. syndrome) and nervous tissues.

Tight control of blood glucose concentration definitely reduces the chances of complications. But uncontrolled diabetes always leads to complications is not correct. In fact etiology of different diabetes complications is different except one common factor that is genetic influences. Few genetic markers of specific complications have been discovered recently. Their presence in oneself predicts the vulnerability for that particular disease.

So far the scientists have discovered a few diseases as having confirmed genetic background and they are cataract, ischemic heart disease, kidney disease, hypertension in diabetics etc. Large vessel damage in diabetes is primarily linked to hyperinsulinemia and hyperlipidemia (lipid disorders). Similarly small vessel disease is said to be due to hyperglycemia. Diabetic neuropathy, a most common complication of diabetes is the result of hyperglycemia, sorbitol accumulation in nerve tissues and disordered fuel supply (vasa nervosa are occluded). Normal metabolism of carbohydrates, fats and proteins along with normal intake of minerals, elements and vitamins in diet are all essential to prevent complications and keep the body fit.



As Per Ayurveda

By the use of rough and imbalanced food, over zealous fasting and exercising, and improper living habits, the drying of ras and dhatu (plasma and body tissues respectively) occur. As a result the dried nutrients are unable to spread evenly all over the body tissues resulting in malnourishment of muscles, bones and other vital tissues, ultimately leading to a lean and thin body. Such patients are incapable of tolerating the power of anti-diabetic medications and can not perform tasks requiring power and energy of the body as fighting with infections or overcoming stresses. And one or the other serious complicatory diseases resulting in death then besiege these lean diabetics.

There is a very well defined disorder in ayurveda which describes the pathogenesis of aptarpan janya madhumeha (diabetes due to excessive purification processes). It states that drastic treatment measures like crash dieting, purgation, and emesis therapy lead to the hollowing of body tissues and as a result vata humour enters in tissues in excessive amount giving rise to diabetes (CharakSamhita.Cikitsa.L.6.S16,17). And to prevent this diabetes Acharyas instructed santarpan chikitsa (promotary treatments).

As Per Allopathy

Several type 2 diabetic patients of developing countries look asthenic and malnutrited (~75%). Although as per diabetic patho-physiology these type 2 diabetics should have been having bulky physique instead they look thin and emaciated.

In medical language the word ‘iatrogenic’ means those disorders which are not produced as a result of the primary disease itself (these are not the complications of the disease) instead they are the results (byproducts) of wrongful treatments. These problems are inflicted over the patient by none other than the treating doctor.

In respect to diabetes a complication like leanness and asthenia usually develops not because of the diabetic process itself but wrong treatment and most importantly wrong advice regarding diet and exercise. The excessive use of metformin, severely cutting down of diet and over exercising on physicians advice are a few reasons of this big problem. A large section of the above category of diabetics are residing in countries like India and Bangladesh.

Generally this disorder is the result of a hypocaloric diet (prescribed by a physician) which was being consumed by these patients for a long time either because of the mistake on part of the patient himself or under guidelines given by an unexperienced physician. Unnecessary restriction of several food items such as fruits, rice, potato, milk, egg, bread, and meat in diet in an attempt to reduce elevated blood glucose levels lead to such a problem.

In fact this condition is totally preventable, and correct education regarding balanced diet and the use of these informations in making one’s diet healthy and nutritious helps a lot. But unfortunately it does not happen; even educated patients are unaware of this fact that hypocaloric diets (a diet containing less number of calories which his body needs every day) result not only in decreased body strength, but insulin production of the patient also falls upto 40% less than one’s insulin secretory capacity at that time.

It means that if that person would have been eating the required number of calories in diet his insulin secretion would have been better. This condition is totally avoidable as a normocaloric diet would have prevented it and instead of leanness and asthenia a diabetic would have been having ideal body weight and full energy, besides having good control on diabetes. How a hypocaloric diet results in such a great loss and how much benefit a patient can gain by improving his dietary habits is the matter to be discussed in this chapter.

Promoting Weight Gain As A Therapeutic Option

It is interesting to observe that an increase in calories not only improves one’s insulin secretory capacity but also makes his body more solid (stout/robust). As insulin secretion increases more food starts storing as reserved fuel (this is the sole function of insulin hormone that whatever nutritious elements that is, carbohydrates, protein and fats one consumes in diet, insulin with the help of hepatocytes convert them in such a form that they can be stored in one’s body as reserved fuels (glycogen in liver, proteins in muscles and fats in adipocytes respectively). This leads to the following two important events: (a) Because food is utilized the blood concentration of glucose and fats comes under normal limits. (b) Body gains some weight and increases in strength.

On the contrary if one is not eating optimum calories according to his total caloric requirement the events which occur in one’s body are:

1. The food which one eats is utilized for two purposes : firstly nourishment and repair of the body tissues and production of new cells, hormones, enzymes etc., and secondly production of bio-energy necessary to keep oneself alive. As carbohydrates, fats and proteins are utilized for energy production as well as remain available in the blood for the production of hormones and new tissues, therefore on eating hypocaloric diet there are full chances of developing weakness and reduction in insulin secretion.

2. If a person is alive and active, it means his body is utilizing certain definite number of calories because without getting energy above acts are impossible. Now if most of these calories are not coming from diet as diet is hypocaloric, then the question is from where are they coming? In fact these calories are coming from the stored food and body reserves. The body is utilizing its own muscles and adipose tissues besides a small amount of stored glycogen. Only upto a maximum of 50 g of glycogen that is, ‘stored glucose’ exists in one’s body and that, too, when a person is eating normal diet, which is only one-fourteenth of the calories which one spends in a day. Therefore if a diabetic is undergoing long periods of partial starvation maximum calories come only from muscle proteins and fatty acids present in the adipose tissues. This leads to marked decrease in strength and body weight of a diabetic patient besides reduction in insulin secretion.

A hypocaloric diet harms from one more angle. Mostly such diets are imbalanced, too, and therefore give rise to problems like deficiency diseases due to lack of multiple vitamin-mineral-trace elements, anemia and hypoproteinemia that is, less protein and hemoglobin in blood. It all complicates the disorder. A balanced diet is one which not only includes calories as per total caloric requirement/day of a patient but caloric distribution should be such that 50-60% calories come from carbohydrates, 20% from proteins and 15% from fats; besides such a diet should also contain all essential trace elements, minerals and vitamins in right proportion.

A number of studies and long trials have proved that in the Indian subcontinent a huge diabetic population is observing hypocaloric diet and as a result people are suffering from ‘iatrogenic lean type 2 diabetes’. Optimization of calories in their diet for 3-6 months resulted in marked improvement in health as they gained some weight and their insulin secretory capacity also increased by 25-50% in more than 80% patients. Several studies have been done in this regard at Kanti Diabetic Care Centre Rishikesh. A conclusion of these studies and a few observations made will help in understanding this issue better.

Material methods

Out of 800 patients who attended KDCC in a period of 6 months (1 January to 30 june 2010), 75% were found as having less than normal body weight. The average BMI was 15 kg/m2 whereas the normal limit is around 24 kg/m2. Most of the patients were also having hypoproteinemia.

After an exhaustive session of history taking and examination it was observed that more than 80% patients were consuming only 68% of their total caloric requirement (total caloric requirement/day = ideal body weight in kg x 36 in males and 34 in females + necessary corrections according to age, sex and nature of job (see diabetic’s diet).

In this centre, these patients were given individual computerised diet charts depicting all about their caloric requirement, protein intake per day, food quantity, food stuffs, expected weight gain, alternative foods, and a book guiding all about the caloric and food value of common eatables. A dietician explained individually about the diet schedule and answered their individual queries. After this all patients were given the opportunity of talking to the physician for any further problems by telephone, e-mail, letters or personal visits. Patients were asked to come back after 2, 3 or 4 months and thereafter 6 months. Their body weight and serum proteins were measured at these intervals. In few patients some dietary and medicinal corrections were also made in between the study. The results can be summarised as below:

1. At the end of 6 months upto 70% patients had gained weight (with an average of .5 kg/month that is, a total of 3 kg in 6 months).

2. Almost all patients (~95%) who continued the treatment said they were feeling better and some of these patients despite an unsatisfactory glucose control described the feeling of well being in them.

3. The serum protein levels also showed remarkable improvements as a mean increase in s. albumin was 1.1 g/dL (4.1 against 3.0 g/dL at the beginning of the treatment).

4. The most crucial investigation, the results of blood glucose profile (indirectly indicating insulin secretory capacity) can be summarised as below:

* 80% patients out of those who completed the study did not need any increase in their anti-diabetic drug (type 2 patients) which was prescribed first time on day 1. And their blood glucose levels and average urine sugar estimations were all within normal limits despite an increase in their diet.

* Around 30% patients needed reduction in their anti-diabetic drug as they experienced repeated mild to moderate attacks of hypoglycemia.

* 16% patients required minimal increase in their anti-diabetic drug as their blood glucose level was not touching normal values.

* Approximately 80% of type 2 diabetics who were taking insulin and OHAs both needed either stopping of insulin in them or marked reduction in daily dose of insulin.

* There were about 25 patients of type 1 juvenile onset diabetes in this study. It was observed that by liberalising and regulating their dietary habits almost 90% showed marked improvement in different features. As the number of hypoglycemic attacks had practically reduced to nil, the results showing high sign on glucometer were much less and strangely they gained weight as well as their blood glucose levels were stabilized on almost same amount of insulin which they were taking before or prescribed at the centre on day 1, about six months back. The serum albumin concentration also showed an increase of around 1.2 g/dL.


All studies conclude that optimization of dietary caloric intake is essential for better control on diabetes. As this study has also shown increase in insulin secretion though indirectly (s. insulin levels or C-peptides tests were not conducted and increase in body weight and lowering of blood glucose level were the criteria used to recognize increased insulin secretory capacity). It is certain that optimum caloric food increases body weight, insulin production and both these factors help in normalization of blood glucose levels and no medical measure can normalize blood glucose level if the diet of a patient is hypocaloric (and imbalanced).

One important point which a physician should keep in his mind is that an initial increase or change in medications may be required and this can be learned by experience only. Second point is that any change in dietary habits should be volunteered, slowly, according to the wishes and habits of the patient.

No dramatic change in diet is required to correct hypocaloric diets. One has to do only this much that he should motivate the patient towards improving dietary habits at the first meeting, telling him all about food and difficult points must be explained patiently because the only aim of the physician at this moment is to somehow motivate the patient to such a limit that he increases his diet by 400-500 calories/day.

The importance of balancing of diet besides the need of whole grain flour, fresh fruits, fresh vegetables, fat free milk, roasted meat and avoidance of non-nutritious calories should all be explained at the first meeting with a flexible and liberal approach. Monitoring of diabetes through non-expensive measures like urine glucose estimation by benedict’s reagent should be practically shown to the patient and if possible a small kit containing 1 test tube, 100 mL bottle of benedict’s solution, test tube holder, spirit lamp (it costs only Rs. 50 and a patient can make almost 50 tests) should be given. Patient should be encouraged to keep a record of urine test, blood test (SMBG) and body weight every month preferably by the same weighing machine.


“hridgraho laulyamnidra stambah kampah shoolam baddhapurishatvam cheti vatajanam” SushrutySamhita.Nidan.L.6.S13). Regarding the most severe complication of diabetes Sushruta (400 B.C.) recognizes it as ‘hridgraha’ due to which the natural movements of the heart are restricted and as a result the pulse, too, beats irregularly. ‘Stambh’ rigidity of movable parts, ‘kampah’ trembliness, ‘shoolam’ piercing pain, ‘baddhapurishatvam’ obstruction in stools are a few other complications of diabetes. Some of these patients die untimely due to ‘hritstambh’ or heart failure.

A diabetic develops complication only when the vitiated body humours increase with the help of bad humours obtained through one’s diet and poisonous environment. In this situation the amount of vitiated doshas inside the body increases manifold, which is followed by vitiation of the other body components. Not only this these vitiated doshas have the capability of changing the normal flow of healthy body humours and dhatus (nutrients & body tissues) inside the human body (as obstruction in blood circulation). They can obstruct the pathway of one dosha causing shrotavrodh or can change the property of another dosha (one humour vitiates another). They can also destabilize the healthy body humours and tissues as Charaka says : “shareerkledastu shleshmmedomishrah” i.e., immature kapha and meda combine together to increase kleda or wetness. The vitiated doshas also disturb and distort various physiological and biological reactions necessary for healthy living.

Entry of humours in the human body

“vayuh pittam kapahashrechati trayo doshah samasatah; vikratavikrata deham ghananti samvardhayanti ch.” (Bhavprakash.Prakaran.2.105). This means vata, pitta and kapha humours if vitiated destroy the human body and in pure form keep a person alive. There are two wordly meaning of doshas:

1. Dosha meaning body humours as vata, pitta and kapha doshas.

2. Dosha meaning malfunctioning, deformity and inequality in humours.

These doshas are the components of various eatables in panchbhautic swaroop or five basic elements which in diseased state vitiate the body tissues and excretions as Bhavprakash says : “malashrach te rasadinam malinikarnanmatah” (Bhavprakash.P.2.S110).

To keep oneself alive and also to carry out all worldly functions, every living being takes solid as well as liquid food from the mouth and also consumes air. The sun rays are also responsible for the development of certain substances in our body. If these external elements as solid and liquid food, air and sun rays entering the body are pure and in right proportion then prevention of various diseases including diabetes is very much possible. Rishi Charaka says : “ahaar shuddho satva shuddhih dhruvasthitih” i.e., if diet is pure, the plasma will be pure and when plasma is pure the health of a person will be as stable as Dhruva, the polar star. Acharya Sushruta also stressed upon equilibrium in dosha-dhatu-malas in the body as he says : “samdoshah samagnishcha samdhatumalkriyah, prasannatamendriyamanah swastha ityabhidheeyate” (Sushrut Samhita.Sutra.L.15.S41).

Role of heredity in diabetic complications

Single, most influential risk factor for the development of diabetic complications is the probality of a disease since birth and because diabetes itself has connections with hereditary diseases therefore a few complications of genetic background are more likely to arise in a few diabetics. Acharya Sushruta also stated that it is not necessary that the presentation or clinical features of a familial disease must be present since birth or childhood, but they can also appear much later in life.

Acharya Charaka says diseases arising out of beeja dosha are difficult to treat as : “jatah pramehi madhumehino va na sadhya uktah sa hi beejadoshat” (CharakSamhita.Cikitsa.L.6.S57). These disorders are more common in close blood relative but can also be due to ancestors (poorvaja). As 3000 years back Charaka said “pramehoanushanginam” i.e., prameha is a genetic disorder. Sushruta elaborates the reason of diabetic complications as pollution of parental beeja (genetic material) by vitiated humours. Again deformity in beejabhaga (chromosomes) or beejabhagavayava (genes) occurs when a person observes doshakarak measures (improper eating, faulty life style and mentality) for a prolonged period as the doshas enter into the beeja and the offsprings born out of these vitiated beejas definitely have more chances of a genetically monitored disease.

Manifestations of hereditary disorders

Sushruta has given a classical example of recessive and dominant genes as he says congenital blindness in offsprings of normal parents can occur because of this disease being present in forefathers. This example shows that the genes responsible for blindness were present in parents but without being expressed. Similarly a person can also develop diabetes though his parents were not having overt diabetes only because of genetic reasons.

Acharya Charaka says : “shukrashonitjeevsanyoge tu khalu kukshigate garbhasangya bhavati” (CharakSamhita.Sha.L.4.5) i.e., with physical and mental characteristics the genes responsible for various diseases (if present) can also transfer from parents to the offsprings through chromosomes. But sometimes only genetic predisposition is not enough for expression of a pathological gene and a few environmental risk factors are also linked to it. For example, out of four children born of diabetic parents one develops diabetes at the age of 30, the other at 50 and the third one at 60 years but one may not develop diabetes all throughout his life.

In fact, it is the influence of environmental risk factors (such as obesity, prolonged illness, imbalanced food) that matters more. Sushruta also advocates this theory as he uses the word “ahitahaarjoapathyanimittah” (SushrutSamhita.Cikitsa.L.11.S3) i.e., these diseases are dependent on wrongful eating and living habits, and so much so that one can even develop them at very young age itself. Diseases that may have familial origin are: defects of kidney, eyes, heart, brain and defects since birth that is, vrikka vikar, netra vikar, hrid vikar, mastishk vikar, janmajaat vikriti respectively.

Relation between prameha (pre-diabetes) and diabetes

Prameha is regarded as a preceding disease of diabetes. All 20 types of prameha if not cured in time may convert into diabetes as Sushruta says : “pidkapiditam gaadhmupsrishtamupdraveh madhumehinmachashte sa chaasadhyah prakirtitah” (Sushrut Samhita.Nidan.L.6.S24) i.e., diabetes is a complication of prameha. Since diabetes develops as a result of prameha upadrava (complication of pre-diabetes) similarly when diabetes remains illtreated several complications start arising in the human body. And as these are consequences of vitiation of dhatus (body tissues) with vatadi doshas hence named as vata vikar, vata-pitta vikar, vata-kapha vikar, sannipataja vikar and dhatukshaya vikar. In fact treatment of diabetes in real terms means:

1. Fully controlled diabetes is as good as non-diabetes.

2. Prevention, postponement or cure of diabetic complications is sufficient to live a long life and it can be regarded as equivalent to diabetic cure.

Upadrava (complications) of diabetes

Uncontrollable dhatukshaya and high vitiation of tridosha (vata-pitta-kapha) along with disorders in malas (excretions) give rise to diabetic complications. As diabetes can develop in two manners that is, avritavatajanya or type 1 diabetes and dhatukshayajanya or type 2 diabetes in short and long periods respectively; the diabetic complications also arise in same manner that is, acute (in short period) and chronic (in years) complications respectively.

1. Acute complications (a feature of type 1 or avritavatajanya diabetes) develop suddenly within ‘1-12 weeks’ of diabetes detection.

2. Chronic complications develop over many years (a feature of type 2 or dhatukshayajanya diabetes) with permanent damages in the body organs.

In avritavatajanya or sahaja diabetes the complications are more severe and acute or hyperacute. As this disease is fulminant since starting so are its complications. These patients look asthenic and usually have much reduced body mass. Acharya Madhavkar says symptom like extremely thin body at young age is the hallmark of hereditary diabetes. The complications in these patients are severe only because kaphadi doshas suddenly obstruct the natural passage of vayu (air) thus causing abrupt increase in the amount of vata humour. Thus all vata actions also suffer severely (predominantly vatanari sansthan, the nervous system).

Vatkopajanya moorcha probably ‘ketotic coma’ and opsargic trisha ‘inquenchable thirst’ both are life threatening. As Charaka says : “jwarmehakshyashoshshravasadyupsrishtadehanam” (CharakSamhita.Cikitsa.L.22.S17). Trisha of this nature is incurable and equivalent to severe dehydration in ketosis as it dries the body tissues. Persistent vomiting (a classical feature of diabetic ketosis) and severely reduced body mass are symptoms of the terminal stages as Charaka further says : “ghoropadravayuktasatrishna maranay vigyeyah” (C.Ci.L.22.S18).

But diabetes developing as a result of prameha upadrava (complication of pre-diabetes) and dhatukshaya does not cause incurable or life threatening trisha as mentioned by Charaka: “dehorasjoambubhavo rasshrach tasya kshaya ch trishyeddhi” (C.Ci.L.22.16). Sushruta has described it more elaborately as he says ranjak pitta that is, pittagni or insulin gets vitiated more and produces heat in body tissues, and because of deficiency of ras, liquid dhatus of the body dry and do not get proper nourishment. As a result the patient desires more and more water as he says : “doshadhatumalkshino balkshinoapi vanarah; swayonivardhanam yattdannpanam prakandakshati” (SushrutSamhita.Sutra.L.15.S29). The symptoms of this type of diabetes are slow and less severe in nature and are called chronic complications of diabetes.

As Acharya Sushruta says in ahaar-viharjanya/dhatukshayajanya diabetes the complications like weight loss and vision loss are gradual and slow. Acharya Madhavkar says complications arising in ‘dhatukshayajanya’ diabetes are slow to appear but they are irreversible to a great extent as vrikkasanyas (renal failure), lingnash (cataract), dristipatalvibhransh (retinal detachment) etc. Acharya Sushruta says chronic complications are more common in patients of secondary diabetes and mostly they are untreatable. Madhavkar says complications of vatikdhatukshaya diabetes are slow to develop but are of permanent nature.

Sahaja (insulin dependent) and mithya ahaar-viharjanya (non-insulin dependent) diabetes both may have different etiology, symptoms and pathogenesis, but they all develop almost similar chronic complications. In sahaja diabetes the complications develop very fast and cause a few acute complications like vatik moorcha (keto-acidotic coma), hridgrah (cardiac arrest), visarp (septicemia), pakshaghat (stroke) and may take away life within a short period. According to Charaka avrita vatajanya diabetes is incurable only because of the nature of its complications. Charaka further says that treatment of only those disorders are possible which arise because of vata vitiation and not because of the complications of vataj prameha and mentions : “yavatamehan prati purvamukta vatolbananam vihita kriya sa” (CharakSamhita.Cikitsa.L.6.S52).

Treatment of the acute complications is also difficult because timely administration of strong shaman (pacification) drugs is not made possible mostly because of poor availability of the effective drug especially in old days. Secondly in primary diabetes the events occur so rapidly that patient reaches a physician very late and very less time is left for treatment.

One should also be familiar with the meaning of a few terms mentioned below that is, vata, avritavata, vatavikar, vataraqt, ama, amavata, medoama, medovridhhi, medokshaya as all these are associated with diabetic complications.

What is vata, vatadushti and vatavikar?

Dietary irregularities, waking up whole night, untimely panchkarma janya diabetes (iatrogenic santarpan janya ‘overeating’ diabetes), excessive exercises (atilanghan induced diabetes), dhatus deficiency (malnutrition related diabetes mellitus) or dhatukshaya because of other illnesses, worries, sadness, weakness and on top of all asatamya ahaar vihar (wrong eating and living habits) are a few causes of vatadushti.

The vitiated vata (dry vata without having properties like oiliness, softness, smoothness) or ruksha vata obstructs several types of shrotas (e.g., glucose channels, calcium channels) and thus produces local as well as generalised diseases “rukshashuddhanilartanamatah snehaan prachshmahe; vividhan vividhvyadhiprashmayamratopman” (CharakSamhita.Cikitsa.L.28.S118).

The question arises what does vata vyadhi mean to a patient? If vata (air humour inside body) is vayu and vayu itself is a disease or disease arising because of vayu is vata vyadhi? In fact both are incorrect definitions. The correct definition is as Charaka says : “vikritvatajanitoasadharano vyadhirvatavyadhih” meaning thereby a disorder arising out of deformed vayu (obstructed and more than required amount of air in the body) is vata vyadhi.

Vata and its association with nervous system

Vata means “va gatigandhanyoh”, that is, Va- ‘with’, gati– ‘movement’ and gandhan denotes ‘to inform’. Therefore some substance in the body which conducts and spreads several informations (sensory or motor) is called vata.

In the human body the informations are in two forms: 1. Sensory; and 2. Motor and all body actions (physical as well as mental functions) are conducted and coordinated by these two acts. The physical existence of vata can be anticipated within these sensory and motor nerve cells also. The natural abode of vata spread over the whole body is this vatanari sansthan (nervous system). Every living cell of the body is in contact with nervous tissues. And therefore every activity of even a single cell is perceived by the brain with the help of vatanari (sensory areas of the brain) and response to the information is also carried from the brain to the effector organ with the help of motor areas of the brain.

In fact vayu in human body is only of two types: pran and apan (the other three udan, saman and vyan are its subtypes). Charaka says : “prakarshen unyati jeevyati iti prana, prakarshen aanyati va pranah” i.e., function of pran vata is ‘prapan’ that is, all the informations are carried to the sensory areas of the brain with the help of pran and therefore it should be called ‘pran vata sensory nervous system’. Similarly “apaanyati doorikaroti iti apanah” one which takes informations away from brain is called apan and these areas of the brain are comparable with ‘apan vata motor areas’.

Pran’s functions are those which carry or bring something to the centre of the body that is, towards the heart and brain and apan vata helps in all actions which take away something out of the centre or the body. The udan vata, a part of apan vata helps propulsion, saman vata interlinks pran and apan and also coordinates their functions. Vyan vata is spread all over the body and can be compared with peripheral nerves in which pran and apan vata exist sometimes alone and sometimes in combination (sensory, motor and sensory motor peripheral nerves).

Primarily vayu is one but because of its different sites of action and nature of functions it is of five types viz., pran, apan, vyan, udan and saman. Vayu is invisible as Vaghbhat says: “rooprahitah shabdasparshvan vayuh”. Charaka describes the properties of vata as: “vayuayurbalam vayurvayurdhata sharirenam” and “vayurvishravamidam sarvam prabhurvayushrach kirtetah”. Vayu is the regulator and generator of body’s each voluntary and involuntary actions and responsible for keeping strength and life steady. The above acts are solemnized with the help of the nervous system (vatanari sansthan) and therefore one can presume that vata is synonymous to vatanari sansthan.

Vata is not only present in physical form in the vatanaris, rather as electricity flows in live electric wires, similarly vata has full control over the functions of the nervous system (moreover it is the reason of activity). Nerves are meant only to provide means to vata for its activities. Nervous system functioning is dependent on vata and vata requires nervous system to act.

Normal functions of vata

Acharya Charaka says : “vayustantrayantradharah—–bhawatyakupitah” (CharakSamhita.Sutra.L.12.S8) i.e., vata (wind- air in natural motion) provides power to tissues as the blood vessels, heart, lungs, liver, brain and other organs which are spread all over the body. With the force and properties of vayu these organs perform their activities. Vata produces movements in muscles through vatanari sansthan (nerve). Controlling of brain and mental functions are also dependent on vata. All sense organs (gyanendries) and organs related with actions (karmendries) get power of vata through the nerve fibres as these organs are heavily supplied with pran and apan vata that is, sensory and motor nerve fibers.

Touch, taste, vision and smell etc., sensations are perceived by pran vata and conducted through them only to brain and spinal cord. Vata stabilizes all the dhatus (body tissues) of the body at their respective places. Speech is dependent on udan vata. Agni (metabolic energy) can indulge in its own actions only through the help of udan vata. Apan vata helps excretion of urine and stool and moving out of the foetus. All these functions are directly in control of vatanaris (each and every part of the body is linked to the central nervous system through an extensive network of sensory motor nerve cells).

Acharya Chakrapani and Gangadhar have said : “tantram shareerdhatunam niyamah” i.e., vayu only bears the living body. Acharya Sushruta says : “pakwaamshyayoh madhyam siraprabhava nabhih naam marm” (SushrutSamhita.Shastra.L.6) that is, primary abode of vayu is nabhi ‘the navel’. The internal nabhi is that place where all small territories of hepato-portal system join and take away nutrients absorbed from intestines into the blood to liver through hepatic portal vein.

Vitiation of vayu produces several physical and mental illnesses. The distortion of pran vata (which resides in brain and heart) gives rise to the diseases of the heart and the lungs. Vitiated udan vata causes voice related disorders (such as laryngitis) and respiratory diseases. Vitiated vyan vata is the most important cause of dysfunction of smooth muscles (involuntary muscles), disorders of the heart rate, blood pressure and pulsation (dhamni pradhaman), weakness, asthenia, shosh (body look of a tuberculosis patient), maanskshaya (muscular atrophy) and deficiency of living energy. The symptoms related to autonomous nervous system dysfunctioning also appear.

One must know that stimulation of peripheral nerves provides nutritional effect to the muscle fibres (activation causes nutritive effect and non-stimulation has atrophic effect). A diabetic patient with active vatadushti develops cardiomyopathy (cardiac muscles degeneration) only because of this very reason. When saman vata is vitiated the disorders of digestive system start appearing such as ajeerna, indigestion, constipation, aanah, shooting body pains, grahni, and diarrhoea. Apan vatadushti causes diseases such as retention of urine, piles, urinary stones, burning sensation in micturition and diseases of the foetus “kupitastu —– pranamshrachoparunadhhi” (CharakSamhita.Sutra.L.12.S9).

Charaka says : “yatha loke tatah shareere” vayu produces those very symptoms within the body which it does in the outside world (CharakSamhita.Sutra.L.12.S10). Vata vyadhis have two important characteristics: 1. The symptoms are short term but of recurrent nature (vata is inconstant, ‘chanchal’); and 2. Laghuta (constriction or smallness) in the organ systems as Acharya Madhav says : “gata vega bhavate swasthyam sarveshvakshepkadishu”.

The symptoms of vata-vikar are inconstant as there is waxing and waning of symptoms. Smallness in affected organ or tissues is because of dryness and absorption of jaleeya dhatus (liquid nutrients) from the cells due to the effect of increased vata (in kapha diseases, the size of the affected organ or tissue increases; in pittaj vikars there is smallness associated with burning sensation). Charaka says that the specific reason(s) of vata vitiation and its abnormal presence in a particular body component are two important factors which determine symptoms (of vatadushti) which are of diverse nature. The name of the vyadhi (disease) is dependent on the site of disease (where vitiated vata is residing) and the specific symptoms.

Tridosha or vitiation of all three body humours

It is an important feature of diabetes which may be present since birth (beeja dosha janya) or developed later in life (apathya ahaarvihar janya) and harms the body very much as it definitely leads to serious complications if not treated in time. Vayu dosha being a predominant feature in diabetics gives rise to its upadrava (complications) early. Patients who have beeja dosha (hereditary background of diabetic complications) are more severely affected by vatadushti.

In diabetes the quantity and speed at which doshas are spreading and reaching other places are all important features, which determine the site and severity of diabetic complications. The position and condition of kapha and pitta humours in the body and their ratio against vayu dosha also play definite role in the appearance of diabetic complications.

The three increased doshas and ama (undigested humours which attain toxic stature) mix together in different proportions and help vitiate other dhatus also in various proportions to give rise to complications of different severities as said by Sushruta also : “shukradoshapramehastu vyanapanprakopjah” (SushrutSamhita.Nidan.L.1.S20).

When vyan and apan vata mix and vitiate, together they give rise to diseases such as pre-diabetes and shukra dosha (impotence). If all the five vatas of a person vitiate together then death is imminent : “pranamshrochparunnaddhi” (CharakSamhita.Sutra.L.12.S9). Acharya Madhav says: “vatavyadhirasadhyoyam devyogat prashamyati” (Madhavnidan.L.22) i.e., if vata vyadhis are not optimally treated in time they certainly leave some permanent deformity.

Purva rupa (general symptoms) of vata vikar

The joints of hand and foot (small as well as medium joints) shrink due to the effect of vata, decaying of joints and bones along with osteoporosis (asthi-shosh). The patient cries with pain. The tissues of the hands, feet and back shrink and patient can not sleep properly only because of severe pain. There is loss of foetus, semen and menses. There is flickering and loss of sensation in the tissues. The ear, nose and mouth may angulate ‘ardit, facial palsy’.

Samprapti (pathogenesis) of vata vikar in diabetes

The pathogenesis of vata vikar in diabetes is two fold:

1. Due to sudden massive loss of dhatus, the air gets a chance to spread here and there at undesignated places inside the organs; the body tissues become hollow due to sudden and severe dhatukshaya.

2. Obstruction in the natural passages of air by vitiated dosha-dhatu-malas lead to an increase in vata along with its vitiation (vayu can remain pure only when it is free flowing, so obstruction in its pathway ‘avritavata’ gives rise to its pollution). In patients of avrita vatajanya diabetes the symptoms of excess kapha and pitta may also be present (SushrutSamhita.Nidan.L.1.S34, 39) because these two simultaneously increase and then only obstruct air passages.


Ama and other highly poisonous substances in human body develop as follows: When proper digestion of food doesn’t take place in the intestines (due to pachakagni daurbalya) then the immature ras (plasma) goes to the main residing places of kapha that is, the vasti (kidneys and urinary bladder), stomach and joints through blood, where it combines with certain humours. In the stomach jatharagni daurbalya does not allow proper digestion of ama and when back in blood it again chemically reacts with immature vata only to produce a highly toxic substance called amavata (as per allopathy it can be called amyloid, a poison for body cells).

Amavata is gravely injurious to healthy cells as it destroys and inactivates body cells and tissues on coming in contact. It is said that in whichever part of body amavata collects that organ starts malfunctioning shortly. Amavata is of grave consequence in diabetics, as it collects in the body tissues such as naris (nerves), snayus (ligaments), kidneys, brain, spinal cord, connective tissues, joints, blood cells, skin etc., and harms them greatly i.e., “yatrasthamamam virujettmev desham visheshen vikarjateh” (Madhavnidan.L.6.22).

Sushruta says : “taso amah dhamnibhi prapadyate, dhamnimarge sa chalati bhayodushitah atishayen dushitah.” i.e., the ama collects in ras shira (hepato-portal vein which carries absorbed nutrients from intestines to the liver tissues) through blood circulation and obstructs various entry points ‘pores’ present on the cell membrane of hepatocytes, adipocytes and muscle cells through which glucose, fatty acids and amino acids enter for storage or energy production purposes. Simultaneously amaras (undigested food) does not convert into nutrients necessary to nourish the body tissues. Weakness arising because of this pathology gives rise to several serious diseases such as decreased immunity, multiple nutritional deficiency syndromes, muscular atrophy and even diminished mental strength.

Shrotavrodh (blockage of innumerable channels and pores present in body tissues and cells) because of amavata is similar to peripheral insulin resistance described in allopathy. According to ayurveda despite having full amount of pittagni (insulin) in one’s blood, nutrients do not produce energy only because of this amavata. Simultaneously increased and vitiated pittagni produces other upadrava. As per allopathy excess insulin in the blood causes several diabetic complications such as ischemic heart disease and stroke.

Acharya Charaka describes a simple method to check whether a person is suffering from ama or not and the procedure is as follows : “majjatyama gurutvadwit pakka tutplavate jale; binaatidravsanghatshaityashleshmpradushanat” (CharakSamhita.Cikitsa.L.15.S94). It implies: immature stool drowns in water whereas if stools are properly digested they float on water. It is because immature stool is heavy and mature stool is always light. If a person is found to be having immature stools the chances of developing amadosha increase.

Upadrava (complications) of amavata 

Amavata causes complications in all people but in diabetics they are more injurious as Bhavprakash says : “angmardoaruchistrishna chalasyam gauravam jwarah” (Bhavprakash.M.K.Ama.Vata.8) i.e., amavata with repeated vitiation leads to the following disorders in diabetics: Shool (pain in body parts), Aarochakta (dislike for food), Trisha (excessive thirst), Alasya (laziness), Heaviness (ponderousness), Jwar (fever), Ajeerna (indigestion), Sangyashoonya (numbness), Bahumutratha (excess urination), Vaman (vomiting), Shofh (swelling), Shaithilya (low energy), Hrithgraha (heaviness in heart) and Hrithstambh (heart fail). Amavata on being vitiated by pitta and kapha humours causes other diseases such as Jatharagni daurbalya (significant digestive disorder), Shofh (swelling), Shoth (inflammatory swelling), Shool (pin-prick sensation) and Dah (burning sensations).

Amavata and sandhinash

The defect in joints (arthritis) can be because of two reasons: 1. Tissues supporting a joint that is, snayu ‘ligaments’ get damaged by amavata (sandhinash). 2. The lubricant present within the joint gets vitiated with amavata resulting in its drying (sandhivata).

In the first category patients only the functions of the joints are defective, whereas in latter type the cartilage which prevents friction between the two bones gets permanently damaged and the fluid inside that is, synovial fluid also thickens and becomes useless. It all leads to deformity. The former condition in modern language is called arthritis and the latter is sino-arthritis. In diabetics it is called charcot’s joint (severe osteoarthritis + loss of pain and proprioception or both; knee, hips and ankles are the usual sites) which is caused by vatanaris (defective nerves) and destruction of the joint is its main feature.

Medoama, Medovridhhi and Medokshaya in diabetes (immature fats, increase in fats and loss of fats)

Acharya Charaka says : “sthulah pramehi balwanihaikah krashastthaikah paridurbalshrach” (CharakSamhita.Cikitsa.L.6.S15) i.e., a patient with intact medas (adipose tissues) and ojus is a healthy patient and one who does not become weak and asthenic. Body fats include mostly adipose tissues and lipids (cholesterol etc.) present in blood and muscles. But excess fat is also associated with several problems as 75% mortality and morbidity in diabetics is related to lipid abnormalities. Obesity is also one of the most important reason of impotence. Hypertensive kidney disease and retinopathy (resulting into blindness) are other conditions indirectly related to body fats (due to high blood pressure). Silent myocardial infarction (painless M.I.) is also common in diabetics.

It is also proved that bad cholesterol in blood helps in progression of these disorders whereas good cholesterol protects the heart. It is surprising to see that our ancient physicians had recognised this pathology 5000 years back and said it is the medoama (abnormal lipoproteins) which is responsible for all this and normal meda (adipose tissues) in a person is not a sign of disease rather it shows strength in body as Charaka says : A diabetic patient who doesn’t have dusht meda (abnormal lipid profile) should be considered sadhya i.e., curable “sadhyastu medo yadi nam pradushtum” (C.Ci.L.6.S56).

Pathogenesis of Abnormal Lipid Metabolism

Jathragni daurbalya leads to improper digestion of fats. Once in the blood the ill-digested fat does not reach within the cells for metabolism and thus becomes useless for the human body, instead it collects in more and more quantity and starts blocking the various shrotas or body channels. Acharya Gayadasa says that an increase in the quantity of meda mainly leads to its vitiation. He further elaborates that in these patients conversion of madhuradi ras (carbohydrates) into meda (fats) does not stop, rather meda produced develops the qualities of ama (immaturity). Sushruta calls it ‘medascha aparipakwam’ which is the main cause of diabetic complications.

Amatwa (dyslipidemia) in meda leads to medascha aparipakwam which in turn produces pichhilatwa (stickiness) with atidravata (liquidity) in itself and also in the other body dhatus (making the body tissues less stable). Later on the dravibhootha medoama (liquified immature fats) drags other dhatus and amadoshas in vasti (renal system) only to be excreted through urine called mootrasya kledavahanam.

Ama auto-corrective mechanism

Medovridhhi is more prominent among patients who in their initial years of diabetes are taking more calories and to normalise blood glucose levels they are also taking more medicines. In this situation ‘ama-auto-corrective mechanism’ also becomes helpless.

The sar (digested food minus faecal matter = sar or extract) contains all necessary ingredients for the nutrition of body tissues. And body tissues utilize these nutrients as per their caloric and nutritional requirement in a balanced manner. The body has an inherent mechanism by which it controls the production of body tissues (so that they remain in normal limits in a healthy body) and despite preponderance of nutrient(s) in blood their production does not go beyond permissible limits (such as amount of plasma, blood cells, bones, density of bone, bone marrow, body muscles always remain within prescribed limits). All dhatus obey this rule but not the meda dhatu- ‘medaschya aparinitam’ that is, any amount of fat can be deposited in the body tissues.

Jathragni daurbalyta is the first defect detected in these patients. And agni dushti due to increased kapha is one step further as it leads to various types of ajeerna (indigestion towards specific substances) according to the predominant dosha associated. The agni disturbances follow with ama in pachakagni and spread to ras, the yoni (mother) of all other dhatus. The deformed agni (defect in metabolising enzymes) further gets rooted in the successive dhatus where first three make one set and latter three make another (in all there are seven dhatus in human body which are described earlier in the book). In between these two the meda dhatu is not easily accessible for treatment. The ama auto-corrective mechanism acts and makes the rectification of ama in uttan dhatus (ras, raqt and mamsa). This protective mechanism seems to be under the neural or hormonal control (or both), but medas can not be get corrected by auto-rectification.

Pathophysiology of Ama-Auto-Corrective Mechanism

In fact the pathophysiology of the above protective mechanism can be understood by observing the following two principles:

1. If a dhatu in plasma is in more than required concentration it converts into other dhatu for example, excess glucose converts into fat by liver cells (it was discovered by our learned Acharyas thousands of years before and allopathy could rediscover it just recently).

2. Body can also change its sheshagni (basal metabolic rate) and therefore in conditions of excess the BMR will increase and during deficiency states it may decrease. These variations in the rate of metabolism directly control blood levels of different nutrients and regulate the quantity of body fuels in the human body.

Excess blood fats neither change into other dhatu (liver converts only that much amount of fat into glucose which is required to feed hungry cells and that too whenever needed) nor the BMR can be increased beyond certain limits. In this situation aparipakwameda or abnormal lipids are produced in abnormally high amount.

Causes And Effects of Increased Fats in the Human Body

Acharya Madhavkar says : “avyayama divaswapnashleshmalaharsevinam madhuroannarasah prayah snehanmedah pravardhayet” (Madhavnidan.L.34.1) i.e., lack of exercise, day time sleeping, kaphakarak and atisnigdh ahaar-vihar are all the developers of obesity. Then he says : “medasaavratmargtwat pushyantyanye na dhatawah” (Madhavnidan.L.34.2) i.e., shrotavrodh prevents nutrition of other tissues and a person constantly suffers with weakness and fatigue syndrome (as nutrients remain unutilized).

Complications of Medo-Roga

Madhavkar says : “medasyateev samvraddhe sahsevaniladayah; vikaran darunan kritva nashyantyashu jivitam” (Mahavnidan.L.34.8) i.e., excess medas suddenly increase vata humour in abnormal proportions and produce severe complications and markedly reduce the life span of a diabetic (as also proved in allopathy). Medavriddhi leads to fatty degeneration of the heart (dilated heart) and the liver (fatty liver followed by cirrhosis), klebyata (impotence), jara (ageing), prameha pidika (carbuncles), shiravrodh (obstruction in arteries and veins), trisha (thirst), deterioration in immune system and capability of doing physical work.

Medokshaya’ or Loss of Body Fats

In majority of diabetics meda is constantly lost through urine and medokshaya is common in diabetics. But it does not become apparent soon because it is stored in ample quantity in the body and a non-regimen diet (apathya ahaar) also provides excess amount of meda along with more meda formation inside the liver from ‘madhur dravyas’; and all these conditions are helpful in increasing medas. As meda is full of energy, as long as, one is having it in ample quantity, one will not complain of excessive weakness though excessive perspiration and early fatigue are a few common complaints of almost all obese diabetics. But when body weight starts decreasing and one loses substantial weight body weakness is inevitable.

In sahaja or type 1 diabetes the body is lean from the beginning only and there is severe deficiency of meda. Therefore both type of diabetics at some stage start showing symptoms of medaksheenta (deficiency of body fats) such as destruction of joints, cracking and harshness of skin besides profound weakness, splenomegaly and decreased immunity etc.

Pathogenesis (samprapti) of Diabetic Complications

Lord Krishna says to Arjuna”As long as living, dietary and thinking habits remain healthy one will entertain good health” (Gita). Complications arise in diabetes due to increase in vata-pitta-kapha (wind-bile-phlegm) body humours, presence of immature meda in body and urine, deficiency of several dhatus and collection of malas in the human body and most of it happens due to faulty ahaar-vihar (wrong eating and living habits).

The vitiated vatadi doshas are helpful in dhatukshaya as they make the stable dhatus liquefied and then take them away through urine. The dhatukshaya motivates more vata vitiation (because in hollowed tissues vata enters easily) and thus this vicious cycle doesn’t end easily. So therefore a diabetic loses dhatus for various reasons and simultaneously the dhatus adopt immature status (leading to their defective assimilation and metabolism too) which then are easily lost in urine. They also carry important body elements out of the body through urine resulting in deficiency of nutrients, vitamins and minerals in the body which themselves causes several problems.

Sushruta says : “purvah purvoativriddhtvadwardhyeddhi param param; tasmadatipravriddhanam dhatunam hrasanam hitam.” (SushrutSamhita.Sutra.L.15.S18). It means self increased dosha-dhatu-malas are dangerous, but they are more dangerous when the increase in one dhatu is due to the increase in the other dhatu (it happens either when one dosha obstructs the pathway of the other dosha or when one dhatu increases, the production of next dhatu increases automatically). For example :

1. If kapha humour increases (as in kaphaj prameha) and at one stage starts obstructing the natural passage of vata then a new disease will take birth due to avrita vata dosha (obstructed vata) and it leads to great damage in the body.

2. If blood increases abnormally because of its own reason e.g., the special living conditions as high altitude or nutritious diet then it is less serious as compared to its increase because of the increase in the other dhatu in this case maans (proteins).

This is because on increasing of the first dhatu the next dhatu also increases (as increase in ras ‘plasma’ causes increase in raqt ‘blood’). Similarly on increasing of second dhatu the first dhatu also increases (increased raqt increases ras).

In fact when a dhatu (in this case blood) increases only because plasma (ras dhatu is yoni of raqt) contains its ingredients in some more amount it does not create a serious condition. But when one dosha or dhatu increases because of abnormality of another dosha-dhatu it constitutes a serious disorder especially in diabetes as most diabetic complications are because of the above mechanism. For example:

1. Shrotavrodh of one type gives rise to the shrotavrodh of another type (explained further).

2. Increase in peripheral insulin resistance (due to accumulation of abnormal lipids on cell wall obstructing glucose channels)if corrected by a decrease in fat intake alone may prove less effective as compared to cutting of carbohydrates along with low fat diet.

3. Avrita vatajanya diabetes which is equivalent to insulin dependent diabetes is more dangerous than diabetes produced as a result of conversion of prameha into madhumeha. The difference in these two is that in former case vata is aggravated because of obstruction in its natural pathway avritavata dosha, whereas in latter case vata increases only because its two natural accomplices kapha and pitta have reduced because of various reasons and therefore the ratio of vata increases in body tissues.

Abnormal body humours also bring abnormalities in the body tissues such as their amount, consistency, molecular structure and the quality of stability that is, remaining firm at their respective places in the human body.

Obstruction in excretion of waste products is a complication as well as an important cause of diabetes. The vital role of excretions in making the internal environment of the body suitable for cells can not be overlooked. Any major increase or decrease in the amount of excretions definitely has deleterious effect on one’s health. Mostly the excretions are more in initial years of diabetes such as increased production of malas in shwasa (foul smelling breath), talu (palate), throat, tongue, teeth, nails and urine and later on they decrease as less sweating (swedavrodha) and decreased urination (mutravahi shrotas are obstructed) become apparent. Constipation usually accompanies obese diabetes but as diabetes becomes chronic the chances of diabetic diarrhoea (diabetic autonomic neuropathy affecting intestinal functions) too increase (CharakSamhita.Cikitsa.L.6.S13,14).

The collective adverse effect of all the vitiated dosha-dhatu-malas determine the structure and seriousness of the complication. As all three doshas, seven dhatus and three malas are involved in disease formation practically all the tissues (organs, organ systems) and biochemical functions in human body are potentially much more prone to develop disorders in diabetes which we name as diabetic complications. And as we know one defect produces other; the other defect produces another; and this vicious cycle assumes dangerous proportions in diabetes. There is not even a single tissue or biochemical reaction in the human body which is totally protected against diabetes and there is no disease which does not assume serious form if the patient is a diabetic and his diabetes is also uncontrolled, and therefore almost all diseases and disorders have some relationship with diabetes.

 Importance of knowing about diabetic complications

It is not only the control of hyperglycemia which matters in diabetes management (for longevity and good quality life) but the ability of successfully keeping body away from various complications is much more important apart from being urjavaan (energetic). A diabetic can have complete normoglycemia yet have serious diabetic complications. Too many restrictions on diet will lead to several degenerative conditions such as general muscular weakness, cardiomyopathy, various nutritional disorders comprising vitamin deficiency diseases like beri-beri (heart failure), night blindness, scurvy, osteoporosis and blood clotting disorders, different neuropathies because of faulty nutrition and vitamin deficiency, low energy states because of less availability of body fuel and decrease in mental functions (brain including total nervous system utilizes glucose only for smooth functioning and 24 h unhindered glucose supply to the brain is only possible if body stores of glycogen and fats are sufficient and liver is functioning normally because it is the hepatocytes only which convert fatty acids into glucose).

More and more exercising for keeping the blood glucose level under control may prove very harmful as it depletes reserved food stores in one’s body. One wastes his precious body fuels by over exercising and harms himself greatly as body fuels can only be replenished with the help of insulin. Besides it also leads to severe klum (fatigue) and damages in joints as knee etc.

Thus it can be said that it is very much possible to keep blood glucose concentration under normal limits by eating less calories and doing excessive exercise but it does not mean that one’s diabetes is perfectly under control and will not cause any loss of health.

Ayurveda tells the parameters of optimum diabetic control. It is only when all symptoms related to excess vata, dhatukshaya or collection of abnormal dosha-dhatu-malas are not present in body, the body is stout, well energetic, the skin shining and oja is intact one can say that his diabetes is fully under control. And this stage of a diabetic can be regarded as a proof to good health and give an assurance of immunity against diabetic complications in future, too.

Practically one can also observe that diabetics who over exercise and eat very less (dieting) get some serious disease such as severe infections (pulmonary tuberculosis, foot ulcer etc.), heart failure, stress fracture, osteoarthritis and decreased resistance against several diseases as compared to those diabetics who have maintained a stout body (maintaining of optimum body weight is a positive sign). This is also true that a body with optimum snehan (sufficient body fats) and strong dhatus faces other diseases in a better manner than a dry, lean and thin (asthenic) body.

The role of dhatukshaya in the pathogenesis of diabetic complications

The loss of body tissues, dhatukshaya (a condition in which one loses those important elements in urine which are the raw material for building and nourishing all the body tissues) is one of the most prominent feature of diabetes and its complications as one may lose them in massive proportions too (a severe weight loss upto 10-40 kg in 2-3 months only can be observed).

There are seven important dhatus in the human body. Matters as to which dhatu gets affected first or whether there is any sequence of losing them and how their dushti (abnormalities) assumes central position in development of diabetic complications are all which need further elaboration.

Dhatukshaya in type 1 diabetes

In sahaja or type 1 diabetes no fixed pattern of dhatukshaya exists, instead there is sudden massive loss of all dhatus in a person who was otherwise healthy a week ago. This indicates that the cause of type 1 diabetes, too, must be massive and serious and it is exactly so. A massive vata increase due to uncertain reasons is the main driving force behind the massive loss of dhatus in urine. In such a condition no specific sequence is seen in losing one’s dhatus. Instead whichever dhatu comes in way of kruddha vata (agitated vata), is immediately melted and excreted into the urine.

Dhatukshaya in type 2 diabetes

But in patients who have gradually developed diabetes that is, type 2 diabetes there is a well set pattern of dhatus being shed into urine. These patients are those who were suffering from illness (kaphaj, pittaj and vataj prameha) from a long time and a gradual deterioration in their condition was found. It is because of increase in dosha sanchaya (collection of the abnormal humours) and continuously passing out of dhatusthrough urine.

There is set of doshas and dhatus which are being excreted in urine at different stages of the disease. As in kaphaj prameha kapha, meda, maans and kleda are lost in urine; in pittaj prameha pitta, kapha, meda, maans and kleda are lost in urine; and in vataj prameha, theprodormal stage of diabetes, vata, kapha, vasa, majja, ojus and lasika are excreted in urine. Acharya Vaghbhat has described the order in which these dhatus called dushyas are being lost in urine as : “kaphah sa pittah pawanshrach dosha, medoasrashukrambuvasalashikah; majjarasaujah pishitam ch dooshyah, pramehinam vinshatirev mehah” (Va.Ni.10) i.e., Meda (adipose tissue) ® Maans (protein) ® Vasa (good cholesterol) ® Majja (bone marrow) ® Lasika (lymph) ® Asthi (bones) ® Shukra (reproductive tissue) and ® Oja (ojus).

The set mechanism is that firstly vitiated meda followed by kapha and kleda start excreting in urine. And as a result of vitiation with meda and kapha, maans and raqt also start being excreted. In the absence of proper treatment, vitiated vayu and pitta humours along with medoama take out vasa, asthi, majja, shukra and ojus dhatus with them into the urine.

Shareerastha-kleda and jaliyansh (body fluid and water) of the body are also lost in huge quantity. All patho-physiological reactions involving doshas and dushyas vitiation and their excretion take place in vasti (nephrones and urinary bladder)and therefore it seems necessary that vastiis essentially diseased in diabetes.

Vitiation of body tissues and humours (dhatus and doshas) in diabetes

Vitiation of ras : The essence of properly digested food once absorbed into the blood is called ras (plasma). It is the most nutritious dhatu among all as it consists all nutrients essential for energy production and also for maintenance of all the body tissues. And if ras is having weakness or is immature then all other dhatus, updhatus and malas are affected adversely as their normal nutrition, development and repair is not possible.

Vitiation of raqt and maans : The second dhatu, raqt is a substance in which life resides. Its deficiency causes all type of weaknesses, asthma, neurogenic problems, infections and unconsciousness. Under normal circumstances after the pak (coction) of raqt, the thickened portion (condensed blood) transforms into maans (flesh). The vayu then divides maans into various muscle fibres which together take the shape of a muscle (there are 500 muscles in the human body as per ayurveda).

Muscles along with their fibres encircle almost all the body components such as veins, ligaments, bones and joints and thus strengthen them. The destruction of maans dhatu is common in illtreated diabetics (due to improper nutrition) and it also leads to loss of strength and power. Diseased muscles also give rise to impotence, heart enlargement and generalized weakness. Abnormalities in fat metabolism are described earlier in this chapter.

Vitiation of asthi, majja and shukra : Bones are formed with the nutrients available in plasma and its mother dhatu, adipose tissue. On weakening of asthi (bones) following disorders result: asthi-shool (bone pain), bhangur-asthi (osteoporosis), asthi-bhang (stress fracture), breaking of nails and teeth etc. When majja dhatu weakens, the result is as follows: sandhi-bhang (joint damage), asthi-shoonya (numbness of bones) and nidra-shool causing nidra-naash (loss of sleep due to lacerating nocturnal pain in bones). The essence of bone is bone marrow which provides blood corpuscles in the blood. Its weakness causes anemia.

On weakening of shukra, klebyata (impotence), shofh (non-inflammatory swelling), vrashan-shool (pain in testicles) and shukra-heenta (semen deficiency) take place. On destruction of oja defects in nerve and brain functioning along with slackness in all gyanendries (as sense organs) and pain in all karmendries (as extremities) also occur.

Vitiation of updhatus : Ayurveda has described a few more important tissues in human body apart from the regular tissues (dhatus) and named them ‘updhatus’. Acharya Charaka says milk, menstrual secretions, muscle fats, sweat, teeth, hair and oja are the updhatus of ras, raqt, maans, meda, asthi, majja and shukra dhatus respectively. In uncontrolled diabetes the updhatus are also vitiated. In fact when the yoni (mother) dhatu becomes thin the updhatu also gets reduced.

Updhatu of ras is the milk in a mother’s breast. If the mother who has just delivered a baby is a diabetic and malnourished then there can be scarcity in mother’s milk and the breasts may also reduce in size. Updhatu of blood is raj (menses) in ladies, which may have several irregularities. Due to vitiation of raj by doshas, chances of arbud (endometrial tumour) increase by 400% as compared to a non-diabetic female.

Updhatu of maans is vasa (lipids), excess of which obstructs the shira (blood vessels) and the nari (nerves) thus leading to symptoms of raqtavrodh (obstruction in blood flow). The main diseases are: hridaya-shool (angina pectoris) and vatanari (peripheral neuritis) such as pad-sheet (cold feet), pad-shool (pain in calf muscles) and pad-supti (loss of sensations).

Vasa also provides taralta (fluidity) to the blood so that it does not become abnormally viscous and their should be smooth flowing of blood. Modern scientific researches call this type of vasa as high density lipoprotein (HDL) which does not allow the blood to deposit in the arteries. The findings of ayurveda, reveal that mixture of vasa and maans(fats and proteins = lipo-proteins) is useful in many ways to the human body. But its excess (or vitiation) also causes serious diseases as heart attack, stroke and clotting in large peripheral arteries.

The updhatu of meda is sweda (sweat). In people with increased meda even slight labour leads to profuse sweating and klum (unusual fatigue). Due to excess excretion of sweda the body salts and water stores deplete. Deficiency of sweda, too, causes diseases such as dah (body burning sensation), prameha pidika (carbuncles) and low grade jwar (fever) not responding to medication.

The updhatu of asthi are teeth, which are damaged untimely if asthi dhatu is weak. If majja weakens it becomes the cause of untimely falling of the hair, premature ageing and pandurog (anemia). And on weakening of ojus which is an updhatu of shukra, the whole body is damaged.

Vitiation of apdhatu ‘jal’ (water)

After digestion of the food, the nutrients and water are absorbed into the blood, and the remaining part of the food which is left in intestines is called maladrav (faecal fluid). Maladrav goes to the large intestine, where water and a few more nutrients left are absorbed into the blood leaving only solid waste called vishtha (faeces) which comes out through the rectum with the help of apan vayu.

In the process of filtration of the blood urine is formed in vasti. The water which is lost in form of urine is called ‘jaliyansh’ (the quantity of water which is absorbed by kidneys in the process of blood filtration, and excreted out in shape of urine is called jaliyansh). In diabetes this jaliyansh does not come in right proportion and more than normal amount of water is absorbed by the kidneys from the blood. This is because for clearing extra blood glucose load, more production of urine is required and for this water comes in abnormal amounts from the blood (and the body cells) leaving the body and body cells dehydrated as rightly said by Acharya Sushruta “tatravilprabhootmutralakshanah sarv ev prameha bhawanti” (S.Ni.L.6.6). Moreover the vitiated doshas and dushyas (vitiated dhatus as glucose) present in urine cause irreversible damage to the vasti. Slowly and slowly as the damages increase the quantity of urine starts decreasing and ultimately urine formation stops altogether resulting in vrikka sanyas (renal failure).

As more water is required to clear extra load of glucose in blood more and more jaliyansh is absorbed from maladrav (in large intestine) leaving the stools more hard. As a result the stools formed become less wet. On top of it the ugra apan vayu (increased wind) dries up the faeces further more and converts it in bullet (guthlidar mal) like hard structures. Thus defecation becomes difficult and insufficient. Sushruta has defined this stage as baddha purishatva “baddhapureeshatvam cheti vatjanam—–“ (SushrutSamhita.Nidan.L.6.S13) and is more common in obese diabetics. Normal purgatives can not correct it and often strong purgation (kathin virechan) as nishoth or jamalgota and niruh vasti (decoction enema) are required.

When excreta gets accumulated in the rectum and obstructs the natural path of apan vayu many more complications arise. Deformed apan vata vitiates the other two vayus that is., saman and vyan and moves upwards in gastro-intestinal tract instead of going down. As a result wind passing becomes difficult and causes pain in heart area (hridshool), restlessness, acidity, hiccups, retrosternal burning and some other pachak rog (digestive diseases) like gulm, ajeerna, udavrat and anaah.

In a diabetic it is very difficult to differentiate between a heart disease (as classical referred chest pain is absent during heart attack in most of the diabetics) and simple gastric vayu (gas) as the symptoms of both are common as: restlessness, suffocation, heaviness and chest discomfort (bharipan and bechaini) and retrosternal burning. Hence a diabetic must take all necessary precautions so as to prevent oneself from such a confusing situation.

‘Vata Vyadhi’ (complications of vitiated vata)

Diabetes is predominantly a vata vikar. A description of such 80 vata vyadhis is mentioned in ayurveda and a diabetic can develop any of them more so if diabetes is also uncontrolled.

The commonly affected organs and systems due to aggravated vata are: blood, bones and muscles, eyes, mouth, nose, and tongue and systems as urinary, genital, cardio-vascular, respiratory, immune, brain and nervous system. The diseases arising from vatadi doshas (equivalent to diabetic complications in diabetics) are as follows: shira-grah (atherosclerosis), bahu-shosh (frozen shoulder), gridhrasi (sciatica), pad-harsh (hyperasthesia), pad dah (burning sensation in foot), pakshaghat (paralysis), ardit (facial palsy), kamp (tremors), tod (piercing feeling), shira-sankoch (ischemia), garbha-nash (abortion), moh (altered sensorium), and moorcha (unconsciousness).

Apan vata gets vitiated at its natural abode- the colon and rectum, and then fills the three cavities that is, chest, abdominal and pelvic cavity in uncontrolled diabetics. It then produces diseases such as kabj (constipation), mutraghat (dysuria or anuria), anaah (obstruction of faeces and urine along with distension of abdomen), addhaman (distension of abdomen), gulm (formation of a lump of air in abdomen), atisar (dysentery), trisha (thirst), vaman (vomiting), hicchki (hiccups), ajeerna (indigestion), aatop (desire of defecation along with gargling sounds in abdomen) and baddha purishatva (stool like hard bullets).

The vitiated vata in chest causes diseases as pashrva shool (chest pain), shwasa (breathlessness) and kasa (cough-dry and wet), hritgraha (abnormality in heart rate or arrythmia), hrid shool (vatik heart or angina pectoris) and hrid stambh(heart block and heart fail).

The vitiated vata in skin(twag gat vata)causes supti (loss of touch sensation), chunchunahat (tingling feeling), shool (severe piercing pain), rom-harsh (hyperasthesia), sparsh-shool (parasthesias), twagvidhirnta (cracks in skin) and twag-shosh (drying and mild swelling) like skin disorders.

Avrita (obstructed) vata in meda (adipose tissues) and maans (muscles) causes shofh (non-inflammatory swelling usually allergic), shoth (inflammatory swelling), vrin (wound), prameha pidika (boils and carbuncles), mansopachit (diabetic cardiomyopathy), mansopashaya(pseudohypertrophic muscular atrophy) and the body becomes heavy, fatigued and immobile and pain like beating with a cane occurs.

The vitiated vayu in bones gives rise to asthi-shoth (ostitis and periostitis), asthi-shosh (bone-tuberculosis), asthi-ksheenta (depletion of minerals in bones), asthi-bhangurta (osteoporosis), asthi-shool (bony pains), nidranaash (loss of sleep due to severe bony pains), majja-shool (lacinating pain inside bones), majja-shosh (depletion of bone marrow) and vidhradhi (oesteomyelitis). Vatik asthi patient feels as his bones are empty and he suffers with a strange pain of hollowness which does not respond to massage, pain killing ointments and non-narcotic non-steroidal analgesics as Madhavkar says : “hanti sandhigatah sandhiy shoolatopo karoti ch” (Madhavnidan.Nidan.L.22.21) i.e., vitaiated vata destroys bones and joints and causes great pain.

Vitiated vata destroys asthi-sandhi (degenerative changes in bony joints) and leads to pain and inflammation, too. Vata in snayu causes stambh or jarta (difficulty in movement), kamp (tremors), bahyayama (bending of vertebral column outside like a bow), antarayama (kyphosis, forward bending), khalli (spasm in thigh, calf and lower arm muscles), kubjta (hunchback) and localized tender swelling (tendonitis). Vata vitiation in the tissues of the shoulder causes vishwachi (frozen shoulder). Acharya Vagbhat says gridhrasi (sciatica) is because of snayugat vata as : “snayusthitah kuryad gradhashyayam kubjatah” (Astang.H.Nidan.L.15) but can also occur when vata is vitiated at lumbosacral joint.

The shukragat vata causes premature ejaculation and sometimes semen is totally blocked. Similarly pregnancy and child birth have several difficulties in females suffering from vata. Acharya Sushruta says : “apravrittah pravittiva vikratih shukragenile” i.e., a child born with a vata dushtiyukt beeja (diseased genes) may have congenital defects too. Dhwajbhang (impotence), shukradosha (oligospermia), anatarva (amenorrhoea), garbh-naash (abortion) and baanjhpan (infertility) are a few other complications of shukragat vata.

Vitiated vata destroys the power of auditory nerve (hearing), optic nerve (vision), olfactory nerve (smell), taste nerve endings (tastes), and sensory nerves which are engaged in perceiving cold, hot and other sensations.

Vyan vata is spread all over the vessels and its one of the main function is to protect and nourish vessel walls (tissues). Besides this in arteries the blood flows with the power of vyan vata and if it is uncontrolled different disorders of blood circulation such as thrombo-embolic phenomenon in coronary, cerebral, renal and leg vessels may occur. Vyan vata also helps in activities like: distension (such as diastole in heart), contraction (systole, pupillary changes), velocity (blood circulation and all other glandular secretions), throwing and a few other movements within and outside the body. Vyan vata also controls sweating which is a very important measure to control the body temperature. Several painic disorders (ischemic pains) in the human body are as a result of vata in vessels as Vaghbhat says : “shiragath shoolam—–shiraswadhamanriktata” i.e., the cause of pain in these patients is shiragat vata (vata within the arteries).

Raqtgat vata (vitiated vata in blood) has all the properties of high blood pressure such as discolouration of skin, santap (feeling of intense weakness), aruchi (unliking), body heaviness and bodyache, warmness, and irregular heart beat (CharakSamhita.Cikitsa.L.28.S36). Pravadha raqtdab as described by Charaka and Madhav occurs when vitiated vata enters into blood and becomes avrita (obstructed) and giving rise to increased raqtdabaor hypertension.

In Akangaghat (it is a form of upper motor neuron paralysis) ugra vata (of unknown etiology) dries the vata naris (pran vata, cerbral cortex) and usually flaccid paralysis of a single limb occurs. In hemiplegia the ugra vata dries the vata nari (below cortex) and usually produces spastic hemiplegia (one half of the body). The face is spared.

Diplegia is a congenital disorder in which vatanari suffers with stambhyukt akangaghat (spastic paralysis). In paraplegia the vatanari sansathan suffers with ugra vata and usually results in complete paralysis with loss of control on bowels and bladder. All those pathologies in which loss of touch and other sensations, along with loss of activity in one half of the body occur, can be included in pakshaghat and it is a very serious matter, too, as many such patients die. The incurable type of hemiplegia is one in which vatadushti is associated with kapha, pitta dushti and dhatukshaya. When paralysis occurs in association of dhatukshaya the prognosis is bad. This is because sensory as well as motor neurons get destroyed and regeneration of neuron is not possible as Madhavkar says : “vatavyadhirsadhyoayam daivyogen sidhyati; pratyakhyanen kurvanti chikitsam na pratigyya” (Madhavnidan.Ni.L.22). Acharya Sushruta says krish(asthenic) patients suffer more with these disorders.

When vata deforms tissues present in head, nose, eye muscles, ears, lips and forehead a disease called ardit (comparable with bell’s palsy or facial nerve paralysis) results, which is usually unilateral and temporary. In allopathy a similar condition where recurrent episodes of facial paralysis occur is T.I.A. (transient ischemic attack). Usually these attacks are indicators of a big disease ahead such as stroke. Lower motor neuron facial palsy is also common in uncontrolled diabetics (mostly reversible and the cause lies in facial nerve). Acharya Sushruta described its causes as shouting, eating very hard and dry substances, excessive cold air, heavy weight lifting and others.

When vata bends the bodylike dhanush (bow) it is called dhanurvata (synonymous- tetanus). A disease called hanugrah is because of the dislocation of the jaw. It can be because of eating very dry and hard substances. Jivhyastambh (paralysis of the tongue) can also result when vitiated vata destroy nerve fibres supplying to the tongue muscles.

Vata also destroys the vocal apparatus and produces badhirya (muteness). In the ears it causes severe pain and swelling karnashool. It fills in the vessels around the anus and in association with pitta-raqt produces arsh(piles).

Most of the time vata gets vitiated primarily by its own reasons and causes complications. But many times other doshas may obstruct vata and thus help in its vitiation and abnormal increase. In this regard Acharya Sushruta says ‘avrita vata’, obstruction of vata in its natural pathway by other doshas/dushyas leads to dangerous complications.

A person badly affected by ugra vayu (excessive vata) usually develops initial symptoms like jarta (rigidity), aakshep (fits), aswap (nidra naash or insomnia), shofh (oedema), shool (severe pain) and udavarta (pain in abdomen). When pittadushti (in a vatik body) also becomes significant one develops burning sensation, restlessness and unconciousness. Similarly when kapha dushti also vitiates a vatik body one develops excessive cold (extremities remain cool despite observing warming measures), weakness, lassititude, swelling, ankylosis and ponderousness (heaviness).

Vataraqt and raqtvata are two different conditions. When vata and raqt vitiate separately (due to different reasons) and then combine together the condition is called ‘vataraqt’. But when dushit vata vitiates blood the condition is known as ‘raqtvata’. The latter disorder leads to hypertension whereas the former is the main reason of gout as rightly said by Madhavkar “raqtachha vatracha iti raqtvata” (Madhavnidan.L.22).

When highly vitiated vataraqt circulates in the body several symptoms arise such as: pinpricking sensations, asthesias, hyperasthesias and loss of touch (classical symptoms of diabetic polyneuropathy). When vata and pitta both aggravate and vitiate blood the result is vatapittaraqt. Similarly vata, kapha and raqt vitiation leads to vatakapharaqt.

Vataraqt, vatapittaraqt and vatakapharaqt in diabetes synonymous- diabetic foot

These pathologies may arise in diabetics more easily as compared to normal persons. And because legs are predominantly involved therefore they are of much importance in diabetes. In allopathy three types of diabetic feet are described: 1. Neurogenic; 2. Vasculogenic; and 3. Infected foot. But in ayurveda diabetic foot is even better described as all the above mentioned major disorders have prodormal symptoms which a person should be able to recognize (thus ayurveda helps in early diagnosis) as follows:

Vataraqt causes touch parasthesias in lower extremities along with piercing pain, skin abrasions, dry skin and swapa(loss of touch, temperature and pain sensations). It also causes swelling, inflammation and severe pain in knee joints of a diabetic.

The prodormal symptoms of vataraqt are: hardness, wetness (perspiration), warmness, skin abrasions and heaviness in lower extremities. The symptoms of life threatening vataraqt are: tearing and blackening of tissues, pus discharge and rottening of muscles.

In vataraqtpitta there is severe burning in body along with dryness of mouth and mild swelling in legs and sometimes all over the body. Dah (burning) in soles and below knee portion is the main complaint of a diabetic which does not permit him to take sound sleep.

Predominance of kapha in vataraqt leads to eczema in upper thighs and armpits, dermatitis, tingling sensations and the colour of the skin becomes pale white and the temperature lowers down (the touch is cold), the legs swell and swiftness also vanishes.

When highly vitiated vataraqt causes necrosis of the leg tissues then quvathan (gangrene) the poisonous substances produced as a result of necrosis spread all over the body and may cause visarp (septicemia).

Three doshas vata, pitta and kapha and four dushyas raqt, lasika, skin and muscles all contribute in the pathogenesis of visarp. Visarp word means a substance moving inside the body like a snake (sarp). Abnormal humours when spread with tremendous velocity, reach important organs like outer coverings of heart, brain, and lungs in a very short period and cause visarp. The equivalent to visarp in allopathy may be called erysipelas (an infection because of ‘streptococus erysipelatis’ bacteria). And this may take the form of septicemia as vatadik visarp may be life threatening.

The last but not the least complication of vata dosha is that it spreads other humours inside the body that is, the doshas can spread with the help of vata only as Charaka says : “vata pitta kapha dehe sarvashrotonusarinah, vayurev hi sukshmatwadvayostatrapyudiranah” (CharakSamhita.Cikitsa.L.28.S59).

Loss of strength in diabetes

Acharya Sushruta says : “tatra rasadinam shukrantanam dhatunam yat par tejastatkhalvojastdev balmityuchyate” (SushrutSamhita.Sutra.L.15.S19) i.e., the essence of ras to shukra dhatus is the strength of a person. Symptoms of great labour even on doing little physical work, early fatigue, idleness, deterioration of mental as well as physical strength, weakness (thinning) and frigidness in muscles, symptoms of tiredness in all gyanendriya (sense organs) and karmendriya(work organs), lean body built, absence of lustre in face all indicate uncontrolled diabetes.

It is believed that this lack of strength occurs in a diabetic due to splitting and damaging of shukra dhatu and ojus. Acharya Charaka says : The total essence of all dhatus is shukra (and ojus) and it is responsible for stability in muscles, growth, smooth functioning of physical and mental compartments, voice, bright colour of the skin and functions of all outer and internal sense organs (intelligence and nervous system). Deterioration in shukra occurs due to dhatukshaya as well as misuse of shukra dhatu, greed, excess sex, anger, grief, anxiety and hunger.

Ojus and its vitiation with doshasin diabetes

Vaghbhat describes strength and ojus as “prathak ch prastam proktmojomasatisharetsam” (Astang.H.Shastra.L.3) i.e., a person who is lacking oja is like a dead man. It is the ojus, the essence of all dhatus that is responsible for steadiness of body, increase in flesh, unobstructed speed of physical as well as mental functions, purity of sound and colour and proper functioning of all the external as well as internal sense organs.

Sushruta says : “tasya vishranso vyapat kshaya iti trayo doshah lingani bhawanti—–” (SushrutSamhita.Sutra.L.15.S24) i.e., there are three pathologies involved with oja loss and they are: 1. Displacement from its natural abode; 2. Vyapat or deformation; and 3. Loss and reduction in amount of oja. When oja leaves its place (displacement) it gives rise to symptoms like dislocation of joints, severe pain in body, difficulty in physical and mental activities. Symptoms of impure oja are stiffness in joints, heaviness in body, swelling, lassitude and fatigue. When ojus is lost one develops unconsciousness, loss of muscles, dizziness and death.

Acharya Charaka says: The displacement of ojus from its place is the reason of diabetes and similar are the views of Acharya Chakrapani. Vedas give a sacred writing ‘mantra’ to rebuild ojus as : “tejoasi tejo mayi dehi; ojoasi ojo mayi dehi”. This prayer to God should be recited to regain ojus. The ojais produced inside the human body as described below.

There are two types of secretions from the testis: 1. Exocrine that is, semen including sperms; and 2. Endocrine that is, secretion of ojus. Oja is the endocrinal secretion of testicular glandular cells. After being produced in testis oja gets distributed among all the body cells. Normally the testis produce ojus constantly but during intercourse due to the effect of vayu (breathing increases during sex and vata stimulation leads to increased blood flow towards penis and reproductive tissues) the secretion of ojus is stopped altogether and semen starts getting produced in the testis.

How does it happen? It happens because there is a change in the rate of flow of blood during intercourse, and in testis the dhatus which produce ojus normally start producing semen, the exocrinal secretion. At this time the internal secretion (endocrinal) becomes nil. The endocrinal secretion, oja has two parts ‘par’ and ‘apar’. Normally damage occurs in apar oja, which is the root cause of deterioration in strength and apar oja is distributed in all the body cells and tissues and different type of diseases appear once it is displaced but loss of ‘par’ oja leads to death.

 Degeneration of vital body organs

Normal and similar functioning cells come together and form tissue. There are several systems in the human body such as nervous, digestive, muscular, skeletal, connective, cardio-vascular and integumentary system and all have different tissues. And tissues which perform almost similar functions or assist each other for completion of a job combine to form organs and similarly group of organs collectively form organ system. When all these systems function correctly and are integrated one keeps alive and leads a normal active life.

In the human body several dhatus (nutrients) combine to form different tissues and these tissues are nurtured by the ras dhatu (nutrients in plasma) itself. If any one or more of the dhatus are missing (as they are lost continuously in urine in uncontrolled diabetics) and they are not replenished externally through food or medications, it becomes impossible, as to run all the organ systems smoothly and the result is an unhealthy body.

How can one say that the tissues are degenerating only because of diabetes because normally also ‘wear and tear phenomenon’ goes on within the body. The production of new tissues and repair of old is carried out by nutritious diet but the destruction process also goes on naturally without any reason and is called ‘the law of natural destruction’.

In these circumstances if a few new reasons develop which cause heterogeneity in body tissues then the repair process will definitely suffer adversely along with more destruction and lesser development of new tissues for growth or repair. And therefore the quantity of tear will increase whereas that of reconstruction will decrease. And the body will progress towards unwanted and premature destruction.

In uncontrolled diabetes the destructive process dominates only because the dhatus of such a diabetic are defective and they do not provide healthy nutrition to body tissues and thus repair and growth are retarded and one loses healthy body tissues not because of ‘the law of natural destruction’ but only because of heterogeneity in his dhatus. Therefore it is necessary that a diabetic should not permit heterogeneity in dhatus because then only he may be able to lead a normal active life. A diabetic must observe several measures to keep his body stout and fit.

The deformity arising in oja also contributes in destruction of tissues. Every cell of the human body gets strength and energy from oja and as Charaka says: Diabetes is equivalent to ojomeha (one loses oja, which is of sweet taste in urine) and deficiency of oja leads to decreased functioning of body tissues. According to allopathy, glycogen which is a form of stored glucose inside the body cells provides substrate for energy production and without glycogen (a stored fuel) human body can not survive; same is the case with oja as a person dies if ojus stores are very much depleted. Decreased amount of ojus causes rapid destruction of body tissues and several diseases such as cardiomyopathy, neuropathy and vision disorders.

Blood, proteins, adipose tissues, bones, bone marrow, shukra and ojus all these dhatus need continuous supply of nutrients through ras/plasma to keep them healthy and energetic besides being used for repair purposes. Failing to do so (imbalanced eating) will lead to inactivity of the respective dhatu depending upon which nutrient is deficient. Finally a tissue/organ/organ system may become lifeless. It occurs mostly in those diabetics who are not consuming all the necessary natural food items.

One must observe utmost care in eating as most of the human tissues once dead or degenerated can not be regenerated except a very few body cells such as skin or mucosa cells. It is also important to understand that one type of tissues can not replace the other that is, one type of tissues perform only those functions for which they are designed, and therefore can not be used at other places of the body successfully. Therefore it is mandatory to keep all the tissues healthy.

The vayu (wind) in an open area is always pure ‘vegvan vayu is pran vayu’, whereas, vayu encircled in a closed and humid area becomes impure (just as a typical odour and discomfort is felt if one enters in a room which has remained closed for a long time). Similarly within the body if the path of vayu is clear/open, it will give life, but if it is obstructed somewhere in an organ system it becomes motionless thus vitiated and instead of giving life only gives diseases and death.

As the organs do not get shuddh vayu (pure air) they start failing and become dysfunctional. Deficiency of clean vayu or vitiated vayu in the tissues, both give rise to premature ageing of the cells and therefore the decaying of tissues takes place soon. This untimely ripening of tissues produces those diseases which normally arise in old age such as: loss of eyesight, cataract, impotence, heart weakening, breathlessness, and osteoporosis.

A few other degenerative diseases are cerebral atrophy, alzheimer’s disease, dementia, parkinsonism, ligament fibrosis and fatty degeneration of the liver and the heart. As tissue destruction occurs, slowly and slowly symptoms of life decrease and ultimately a patient dies. Since in a diabetic more than one dhatu can weaken at a time similarly several complications can take place simultaneously. Sudden or slow both types of dhatukshaya leads to diseases.


Vitiated doshas and adverse activities which are involved in the pathogenesis of a particular disease may further create another disease, which may be trivial or major, but is usually responsive to the management of original disease, and is called an ‘upadrava’ or complication. It is a matter of great relief that those medical measures which cure the original disease also cure its complications (special quality of ayurvedic treatments).

If the above statement is seen as regards to a diabetic then we can say that all those medicinal or extra medicinal measures, which are helpful in treating diabetes, treat diabetic complications, too. By following this principle and normalizing the proportions of dosha, dhatu and malas inside the human body one can prevent himself from diabetic complications completely. Just maintaining of normal blood glucose levels by constant cutting down on intake of food is not only insufficient but harmful, too. Dosha purification or pacification is necessary in dealing with diabetic complications successfully.

Classification of Madhumeha Upadrava (Diabetic Complications)

Ayurveda classifies diabetic complications keeping in mind their practical utility for example, it recognizes complications by the nature and severity of deformities (dosha-dhatu-malas involvement status) and to which extent these deformities have spread inside the human body (external or internal disease). It has also laid down a parameter of sadhyata/asadhyata for classifying complications such as sukhsadhya, kashtsadhya and asadhya vyadhi (cures with ease, difficulty or incurable respectively).

The most useful aspect of ayurvedic classification of diabetic complications is that when the disease is in early stages itself called ‘samanya vyadhi’, it gives rise to common symptoms which get recognized and eliminated quickly. But as it assumes a more serious form, ‘deep disease or sansathangat vyadhi’ (involvement of internal organs and organ systems), symptoms of organ or organ system dysfunction start appearing and diseases become a little more difficult to treat.

Symptoms of both samanya or sansathangat vyadhis can be recognized by the patient himself and enable him to assess the actual condition whether his diabetes is totally under control or not. For recognizing the symptoms of prodormal stages of acute and chronic diabetic complications the following text will prove helpful. There are three main groups of diabetic complications namely:

1. Ordinary complications (superficial or external diseases)

2. Specific complications (deep or internal diseases)

3. Complications of organ systems (complicated internal diseases)

Note : There are two words ‘Shira’ and ‘Snayu’ which are commonly used in ayurveda and need clarification. One should not confuse with the meaning of shira as veins (which collect impure blood and carry it upto the heart). Instead as Acharya Sushruta says vessels which carry raqt, pitta, kapha and vata separately throughout the body should be called shira and they are four in number as: 1. Lohit (dhamni or artery); 2. Neela (shira or vein); 3. Gauri (lasika or lymph); and 4. Arun (vatanari or nerve).

Several people believe ligaments and nerves both are included in the word snayu. Whereas it is incorrect as snayu literally means one which stabilizes the tissues or bones in human body. They are the important components of one’s joints. Sometimes it becomes difficult to differentiate between the two such as in case of Gridhrasi nidan (differential diagnosis of sciatica) as it can be due to diseases of ligaments and nerves both (Madhavnidan).

1. Ordinary Complications (Superficial or External diseases) Of Diabetes

These are ordinary diseases which have reversible adverse effects on human body, meaning that these diseases can be cured completely and easily. In fact these arise because of an increase in vata and resolve by taking proper treatment. And as vayu is chanchal (unsteady, always keeps moving) so are its initial disorders. These can be present during the time of diagnosis of diabetes and later on also.

The appearance of a complication indicates that diabetes is becoming uncontrolled besides the intensity and complexity of the main disease. Superficial diseases can be regarded as primary symptoms of complicated diabetes.

Ayurveda has different views which are much more advanced than modern medicine regarding the prodormal symptoms of a disease (they are of the time when disease is yet not formed but deformities in form of ‘collection of doshas’ necessary to produce the disease have started) and it helps in actual prevention of the more complicated disease or the serious diabetic complications.

The importance of general complications have great value in knowing the immediate effect of a treatment schedule and the effect of any new medical measures as exercising, sunbath, dieting etc. Besides presence and absence of general disorders predict chances of serious complications.

If a patient is responding positively to the treatment of the original disease either these general diseases will not be present and if they were present previously one would expect their removal. Therefore efficacy of a treatment can be judged simply by observing presence or absence of general disorders. This special relationship between the original disease, its general complications and treatment efficacy is rarely found in respect to other diseases and also the other two classes of diabetic complications. This is because organ system disorders that is, serious complications take much more time to develop; their symptoms are not so pronounced and of less intensity; the symptoms are slow to come and also slow to disappear because the chronic complications are often of non-reversible nature; and one needs much more dosha-dhatu deformities to develop and collect before appearance of more serious complications.

Therefore even if symptoms of chronic complications (organ or system damage) are recognized they are not as helpful in controlling of diabetes as symptoms of general complications. Ordinary complications do not require much accumulation of doshas and time also and therefore appear very early.

A person develops these complications at the time of diagnosis of diabetes and later on also if diabetes is worsening. The increases in blood glucose level and strength loss are two chief reasons behind these complications. The ordinary complications are as follows:

‘Trisha’ (thirst) Polydipsia

The vitiated pitta and vayu rise upwards and affect the tissues situated at hard palate and pancreas (udakvahi shrotas)and vitiate them to produce trisha/increased thirst. The two important causes of polydypsia are: 1. Deficiency of water in the body; and 2. Increase in vata and pitta humours.

Trisha caused due to the vitiation of udakvahi shrotas may even lead to death of a patient as Acharya Sushruta says : “udakvahe dwe tayormulam talu klom tatra vidwasya pipasa sandhyomaranam ch”.

Vitiation of mutravahi and swedavahi shrotas secondary to udakvahi shrotas vitiation may lead to gradual but permanent decrease in urine and sweat formation which may often prove fatal causing renal failure.


A patient can be lazy because of the two reasons: 1. Weakness in reality; and 2. Lavish life style. The Acharyas have also described alasya as : “sa chapi gamanat sthanam sthanadasanmichati; asanad yrinute shayyam shayanat swapnamichati” i.e., a diabetic patient prefers standing in comparison to walking, sitting in comparison to standing, lying down in comparison to sitting and sleeping in comparison to lying down and these are the characteristics of a diabetic (Sushruta samhita).

‘Laulyam’ Polyphagia

In the stomach and intestines pachak pitta becomes strongly active and digests the food very fast (teekshagni). The aggravated vata abnormally takes out the food (glucose and other dhatus) from blood into the urine. Because of these two reasons a diabetic feels hungry again and again (Charaka samhita).

‘Stambh’ Rigidity

The tridoshas get vitiated and cause rigidity. As a result the patient feels pain in walking, sitting, standing and other body movements and the rigidity and pain increase in the winters.

‘Anidra’ Sleeplessness

Ugra vayu (aggravated wind) makes the patient suffer in several ways and does not let him take a sound sleep. Severe nocturnal vata shool (piercing pain) also does not allow a person to sleep.


Vata on excess vitiation affects the pranvayu in brain and thus produces tremors in the body. Sushruta says : “snayupraptah stambhkampo shoolmakshepanam tatha” (SushrutSamhita.Nidan.L.1.S27) i.e., kamp is a symptom of snayugata vata.

‘Shool’ Pain

An uncontrolled diabetic remains restless due to pain in the whole body especially severe nocturnal pain in calf muscles and thighs. It is a symptom of excess vata in the body tissues. Whichever organ is affected with vitiated vata develops piercing pain.

‘Malavrodh’ Intestinal obstruction due to faeces

Sometimes hard bullet like faeces not only obstruct the lumen but also causes intestinal swelling and inflammation of the tissues because of the friction. One reaches to this stage only because vitiated apan vata dries the stool, and absorption of more water from faeces makes stool further hard (for clearance of excess glucose load, body has to arrange more water for urine formation in diabetes). Hence one should take every precaution to prevent hardening of stools and if it occurs it should be specially treated.

Klum’ Early fatigue

Without doing much labour a patient feels fatigue and the normal functioning of lungs, karmendris and gyanendris is adversely affected. Klum is a most common symptom of diabetes (especially uncontrolled diabetes).

‘Vata moorcha’ (amlotkarsh) Ketotic coma

This mostly happens in sahaja ‘krisha’ diabetics (IDDM). In this condition the patient sees the sky as blue, black or red and becomes unconscious. There are tremors and severe burning pain in body, acidotic breathing and blackening of the skin. These patients are usually lean and thin but it can also occur in very obese diabetics (coma without acidosis).

‘Dah’ Burning sensation

The patient complains of severe burning sensation all over the body. Any reason which decreases somagun (water content) and kapha and increases pitta will lead to dah. The association of vitiated vata with pitta is necessary for the development of dah.

2. Specific Complications (Deep or Internal Diseases)

When the body tissues deform because of excessive dosha accumulation one is likely to develop specific complications. In such situations symptoms pertaining to specific organ damage such as vishwachi (frozen shoulder), gridhrasi (sciatica), and cataract (lens whitening) occur. A few important biochemical reactions and body actions also show abnormalities such as weakness, impotence, improper digestion, listening difficulty, decreased lustre on the skin etc.

A diabetic develops specific complications once his all three body humours get aggravated along with dhatukshaya. In these patients vata dosha alone increases several folds in a short period and damages other body organs. Dhatu vitiation or heterogeneity is an integral part of the pathogenesis of diabetic complications.

In both type 1 and type 2 diabetics the main culprit is vata which reacts with the other two doshas (pitta and kapha) present in different organs in different proportions thus producing different dysfunctions (pertaining to different organs). Acharya Charaka says : The vitiated vayu produces strange symptoms in accordance to the reasons due to which it is produced or is unsystematised (by vitiation of dhatus). Depending on the vitiated elements and developed symptoms various diseases result.

Once a diabetic develops any specific disease the treatment complicates but still remains kashtya sadhya or cures with difficulty only if timely detected. Uncontrolled diabetes for long periods gives rise to the following complications:

Drishti kshaya’ Loss of eyesight

When vitiated doshas cover the whole drishti mandal/visual area and alochak pitta, which is responsible for supplying energy to eye components is also vitiated then drishti kshaya or loss of vision occurs rapidly. Initially it starts from night ‘ratondhi’ (night blindness) and gradually produces complete blindness. The vitiated humours also reach to drishti mandal from other diseased parts of the body (like nephropathy leads to retinopathy) besides involving eyes directly.

Maans sankoch’ Muscular atrophy

There is a decrease in muscle proteins in uncontrolled diabetes. The muscles also become strengthless and weak in these patients. This leads to contraction and reduction in size or atrophy of the muscles. Acharya Sushruta says muscular atrophy also leads to loosening of joints and blood vessels. A diabetic must protect his muscles and body proteins carefully.

Puti mamsa’ Muscular degeneration

The problem of tissue necrosis arises when doshas reach the blood first and then vitiate body tissues especially of the muscles of upper and lower extremities (vataraqt). The necrosed tissue (gangrene) is also more prone to develop infection (sadan or rottening) as the dead tissues, spoiled blood and pus are a good source of nutrition to pathological bacteria. The symptoms of life threatening vataraqt are: tearing, blackening and rottening of tissues and pus discharge.

‘Jara’ Premature ageing

If body tissues ripen before age, one develops the following symptoms: loss of strength and memory, glani (feeling of weakness), whitening of hair, loosening of teeth and irritating behaviour. Dhatu vishamta (heterogeneous tissues) and dhatukshaya are its important causes.

‘Gridhrasi’ Sciatica

Rigidity, loss of power and severe piercing pain in and around hip joint, lower back, buttock, thigh and leg are the characteristics of the disease called gridhrasi. When vitiated vata enters into snayu/ligaments this disease results and usually it is unilateral. Exposure to cold air, too much of forward bending, carrying heavy weight on back, and sprain are all the causes of this disease. Sometimes the intervertebral disc may rupture to give rise gridhrasi. The most distressing features of the disease are severe nocturnal pain and inability to walk.

‘Ashmari’ Stones in urinary system, gall blader etc.

Kidney, gall bladder, salivary gland and spermatic cord are a few common places where stone of the size of sand particle to a big potato can develop. In diabetics urinary stones are formed because of the drying of kapha, pitta or shukra by ugra vata (which provide nidus for further deposition of salts).

‘Vishwachi’ Carpel tunnel syndrome

The ligaments present over the wrist, elbow and shoulder joints get vitiated with vata and destroy, too (radial-ulnar neuritis or radio-ulnar paralysis). The pathogenesis of vishwachi and gridhrasi are almost identical.

‘Vasti bhed’ Pain in urinary system

Ugra vata produces severe pain in the urinary bladder. The swelling produced by vata in urinary tract is the reason of several complications along with severe piercing pain. Diabetics often suffer with this problem.

‘Pandu rog’ Anemia

Paleness on the skin, eyes, urine, stools, face and nails only occur when jeerna tridosha (chronic vitiation of all the three humours) develops in a diabetic’s body. The deformity and deficiency of dhatus make a person look like a dead person. Krish (asthenic) and sthula (obese) both category diabetics can suffer from this disease.

‘Chakkar’ Vertigo

When vata reaches upto the neck and brain a person starts feeling dizziness and as disease progresses these symptoms become more severe and make a person physically handicapped as he can not walk or stand because of the vertigo. In later stages vertigo is present even when a patient is lying down.

Galgand’ Thyroid swelling

The tissues present inside chullika granthi (thyroid) develops inflammation sometimes because of nutritional deficiencies and at other times due to congenital disorder (hereditary). But in both the situations there is disordered secretion of hormones which cause imbalance in blood glucose levels.

‘Arsh’ Piles

Vayu inflates the bunch of minute blood vessels situated at the anal sphincture and produces bleeding. The same pathology gives rise to moles which are present on the skin.

‘Shira shool’ Ischemic pain

Vayu in shira always produce pain. Vayu also causes calf cramps and night pains in legs.

‘Shira griha’ Obstruction in blood vessels

It causes sign/symptoms of large artery blockade especially in legs such as: cramps, coldness, colour change (blue-black) and cracks in the skin. Later on gangrene of the foot may also occur. The obstruction of large arteries of the head and of coronary arteries lead to life threatening situations as stroke and myocardial infarction.

Bahushosh rog’ Frozen shoulder

Vata in shoulder joint dries the synovial fluid and joint ligaments and as a result there is painful restriction of shoulder movements.

‘Twacha rog’ Skin diseases

Vata dries the ras (plasma) and makes skin dry, blackish, stretched and full of pricking pain and abrasions. The sensing power of the skin also destroys in these circumstances but pin pricking sensations and hyperasthesias can exist.

‘Kulaja rog’ Genetic disorder

A child born of a diseased beeja, beejabhaga or beejabhagavyava (sperm, chromosome or gene respectively) usually has congenital anomalies. But a few other familial diseases which may appear later on at any age are diabetes, hypertension, polycystic kidney and genetic syndromes. A diabetic should try to rectify and pacify his doshas and only after that he should plan a child as this may help in prevention of familial diseases in his offsprings.

Mookta’ Dumbness

When vayu covers up/obstructs the shabdavahi shrotas (larynx) and becomes still then the person becomes dumb.

‘Karn shool’ Ear-pain

When vayu forces its way through head and neck and reaches the ears then severe pain in ear develops.

‘Arbud’ Benign tumour

When ugra vata vitiates the maans and raqt dhatu in any part of the body then serious shofh (non-inflammatory swelling) develops. This is a vata rog and specially causes benign (non-cancerous) tumour in the uterus of females.

‘Gulm’ Distension of abdomen

The round (gaanthi) knot made of air which exists between the heart and the kidney (vasti) is called gulm. This vayu keeps moving or remains constant and increases or decreases in that region. When vayu becomes calm then only gulm pacifies.

‘Moh-moorcha’ Semi-consciousness

Due to the presence of aggravated vata in the sensory area of the brain (pran vata) sudden darkness appears and person falls down like a piece of wood and loses all his senses. This stage is called moh-moorcha.

‘Hrit griha’ Ischemic heart disease

All three doshas get vitiated and stay in the heart. Together with this on vitiation of vyan vayu and oja various types of chest pains and feeling of tightness occur in and around the heart. In allopathy it is called angina pectoris.

‘Udavarta’ Pain in abdominal organs

Pitta and kaphadi doshas vitiate the normal vayu residing in the stomach. At this stage the kledan kapha and pachak pitta present in the intestines also do not remain untouched and cause various types of stomach diseases (along with pain and agony).

‘Shosh and jeerna phuphus shosh’ Severe asthenia and pulmonary tuberculosis

A few diabetics get infected with serious infections as rajlakshma (tuberculosis) and slowly their body starts shrinking and ultimately they die.

‘Aarochak’ Loss of interest in food or anorexia

One feels hungry in aarochak disease but does not develop desire to eat. The reasons can be physical (gastritis) or mental (anorexia nervosa) both. Due to vitiation of ras vahi shrotas one loses all desire for food. It may occur in diabetics frequently. In vataj aarochak there is severe retrosternal pain.

‘Kasa’ Cough

Due to excess kapha deposition in the respiratory ducts (trachea, bronchus, bronchioles and alveoli) the motion of pran vayu does not remain normal. So the vayu behaves unnaturally and goes through different-different paths and reaches the lung tissues and thus patient develops kasa and breathlessness.

In fact kasa is a symptom of several diseases. The causes can be cold air, pollen grains, dust, smoke etc. Apart from this when amaras (illdigested food) comes towards the mouth one develops kasa rog. Due to excess of vata, dry cough and excess kapha leads to wet cough. In pittaj kasa burning in chest, fever and stomatitis are some other main features.

‘Shwas’ Breathlessness

Long-term kasa changes into shwas. Apart from this it also occurs when the natural unobstructed flow of pran vayu in the lungs and blood vessels is obstructed. This is because of obstruction in pran vahi shrota which destroys natural cycle of air in the body. The attack of shwas mostly starts from the stomach (on expanding of diaphragm). Sometimes vata in the heart does cause similar symptoms (cardiac dyspnoea). This can prove fatal also.

 Hicca-shwas can be because of nervous system and digestive system disorders. The pathogenesis of shwas is described by Acharya Charaka who says shwas is not only because of the diseases of pran vata in the lung but brain is also connected with this pathology (CharakSamhita.Cikitsa.L.18) and it is clear by observing the fact that asthma worsens during mental stress and worries.

’Hrid stambh’ Heart fail

There is obstruction in natural heart rate (suddenly the flow of vata is obstructed in excitatory muscles of the heart ‘S.A. node’ which may lead to complete cessation of heart beat). The pulse beats unnaturally at intervals. On benumbness of mobile ingredients (electric flow in cardiac muscles) even death may occur. Charaka says in vatik heart disorders like kampan (palpitation) and stambh (arrythmias or heart blocks) are two important symptoms.

‘Prameha pidikayen’ Boils and carbuncles

“upekshayaasth jayente pidikah sapt darunah” (CharakSamhita.Sutra.L.17.S82) i.e., due to negligence in diabetic treatment sometimes the doshas spread in the skin, the muscles and the adipose tissues and produce pidika (boil and carbuncles) at joints, muscular parts and delicate portions of the human body. Charaka says : “bina pramehamapyeta jayente dushtmedasah” (C.Su.L.17.S104). Though generally obese diabetics develop these pidikas more frequently but in some other weak conditions (chronic fever) one can also develop these pidikas. According to modern science ‘staphlococcus bacteria’ is responsible for them.

Pidikas (boil and carbuncles) can be of seven types :

1. Sharavika: They look like sharav, the corners are up and there is a pit in the middle. The colour of skin is black and it is a very painful situation.

2. Kacchapika: Externally it looks like the back of a tortoise and there is burning pain at the site of the pidika.

3. Jalini: It is extremely painful and is covered by maans (muscles). The outer appearance is characteristic (carbuncle with sieve-like appearance) that is, there are tiny holes present all over the pidika and a web of shirajal (minute blood vessels) is also visible over them.

4. Sarshapika: A big pidika is in the centre and it is surrounded by several small mustard seed like (in size and colour) pidikas. It matures early and is painful, too.

5. Alaji: It takes the form of red and black blisters, which are painful. They are red and black in colour, with burning pain and often lead to unconciousness because of high fever.

6. Vinita: It is very painful, often appears on the back, and there is a depression in the middle of it. It excretes sticky secretions.

7. Vidradhika: These are big abcesses which are of two types: a. Baahya (external) vidradhika is present on the skin, ligaments, muscles, and adipose tissues; and b. Abhyantar (internal) vidradhika is present in the organs like intestines, gall bladder and other internal organs. These are all very painful and often lead to the death of the patient.

‘Vidarika’ Big abcess

It is round and hard like vidarikand. These pidikayen are incurable in patients who are suffering from trishakasa etc., and persons who have low energy and are lean and thin.

Jwar’ Fever

Mithya aahar-vihar (wrong eating habits and unhealthy life style) gives rise to diabetes and it is also the most important factor in pathogenesis of fever (amadoshas are associated with all kind of fever- CharakSamhita.Cikitsa.L.3). Pittadushti is necesarry for diabetes same is also true with fever (SushrutSamhita.Uttartantram.L.39). Acharya Madhavkar says ‘krodhat pittam’ that is, aggravation of the pitta dosha and mithya aaharviharabhyam (antipathic food and living habits) both are associated with fever.

Low-grade fever produces bodyache and extreme fatigue. Fever can be a prodormal stage of several diseases or it can be the symptom of several diseases. Fever itself may be a disease (independent disease as pyrexia of unknown origin or PUO) or it can be a natural treatment of some diseases (in high body temperature during fever several pathogens do not survive and hence are killed). Low grade fever with evening rise can be a presenting feature of pulmonary tuberculosis. In diabetes one can have fever only due to weakness also besides other causes. Sannipataj jwar (in which all the three dosha are simultaneously increased) is a serious condition.

Daurbalya’ Weakness

This is a common and genuine problem of a diabetic and greater part of the treatment of this condition is in the hands of the patient himself. Apart from a good nutritious diet keeping the body dhatus neat and clean is a very effective manner of preventing daurbalya. Many patients do not observe sarvras in their diet and therefore greatly harm themselves.

Avipak’ Indigestion

The deformity in pitta and kapha dosha is responsible for this pathology. Nausea and chest burnning are its cardinal symptoms.

‘Sandhi shoth’ Swelling of the joints or arthritis

Vitiation of kapha occurs in majority of the diabetics as Acharya Charaka says : “prameha hetuh kaphakrichha sarvam” (CharakSamhita.Cikitsa.L.7) i.e., consumption of kaphakarak substances is the most powerful cause of arthritis as vayu and kapha both on vitiation reach the joints of the bones throughout the whole body and vitiate dhatus (ligaments, cartilages) there and produce shoth. There is severe pain and swelling in joints.

3. Complications of the Organ Systems (Complicated Internal Diseases) in Diabetes

These are much serious form of diabetic complications, as body tissues as well as organ systems develop permanent deformities and as time passes and one remains untreated the signs and symptoms of organ system (as cardiovascular, nervous, uro-genital) disorders start appearing. Besides this the process of excretion of waste products is also adversely affected as seen in decreased urination and malbaddhata in complicated diabetics.

As a result of shrotavrodh (blocking of various pores and channels throughout the body) one develops significant adverse affects in metabolism of several dhatus such as glucose and fat. Simultaneously the elimination of harmful substances also becomes abnormal as is evident by lesser urine output, less sweating, severe constipation and acidosis (decreased carbon dioxide excretion through lungs also contributes in acidosis).

Nature has gifted a lot of reserve to all the body organs and systems and therefore they face adversities for a long period without much harm to the body tissues and bodily functions. But in absence of timely treatment irreversible tissue damage takes place. Systemic disorders take long period to develop but they do not produce early or prodormal symptoms and their delayed symptoms are of lesser intensity and therefore not detected early (though the defect is very large) but of permanent nature.

A diabetic should observe optimum prevention against these complications because they are usually painless (as silent myocardial infarction, chronic renal disease) and do not give rise to prodormal symptoms.

Rishi Sushruta says : “serv ev pramehastu kalenapratikarinah madhumehatvamayanti tadaasadhya bhavanti hi” (SushrutSamhita.Nidan.L.7.S27) i.e., if proper and timely treatment is not done all types of prameha (pre-diabetes) convert into madhumeha (diabetes) and become difficult to treat.

When diabetes remains uncontrolled for long periods, all types of body tissues and biochemical reactions suffer badly and all the vital organs can also develop complications.

Why does a diabetic suffer only when his diabetes is uncontrolled? Are these complications preventible? These are the matters to be discussed in length.

Regarding development of complications in kulaja diseases as madhumeha, Rishi Charaka had said 3000 years ago that : “yasya-yasya hyavayvasya beeje beejabhage va doshah prakopmapadyante, tam tamvayavam vikratiravishati” (C.Sha.L.4.30). This implies that if the genes responsible for developing a particular organ are defective then the organ developed will also be defective depending upon the nature of defect in the genes. And this defect can manifest at any age after birth.

In the human body there are different systems working at a time for the benefit of the body and their functions are also entirely different; but they are all inter-related and complementary to each other. If a major problem arises in any one of the systems it will certainly have adverse affects on the functioning of other body systems, too. Besides this, these deformities have very dangerous effects on the important biochemical reactions necessary for life, as energy poduction, hormone secretion, vision, and conduction of impulses in neurones. In diabetes, unfortunately these reactions may even suffer permanent damage.

Systemic diabetic complications and shrotavrodh : The involvement of systems takes place because of the dysfunctioning of different shrotas (shrotas are the pores or channels through which substances are transported within the cells and the body). As long as these shrotas remain in natural unoccluded state no serious diabetic complications develop as said by Acharya Charaka : “tadetat shrotasam prakratibhutatvann vikarerupsrajyate shareeram” (C.Vi.L.5.6). There are a few important shrotas (in modern medicine these shrotas can be compared with glucose or calcium channels present over the cell wall) which are predominantly involved in the pathogenesis of diabetic complications.

The root of pranvah shrotas is heart, and its vitiation with doshas leads to diseases of the heart, sound production and lungs. The root of udakvah shrotas is in the hard palate and pancreas, and its vitiation leads to diseases like diabetes, polydipsia and oedema. The root of annavah shrotas is the stomach and both sides of the body, and its vitiation leads to several diseases relating to abnormal digestion, assimilation and metabolism (including diabetes). All the important nutrients required for nourishing the dhatus have separate shrotas for their movement inside the body and are called sapta-dhatuvah shrotas (rasvah, raqtvah, maansvah, medovah, asthivah, majjavah and shukravah). All these shrotas have their roots and pathways different from each other and their vitiation leads to the similar complications as that of the dhatu-dushti which is to be transported through them.

In diabetes primarily three type of shrotas are affected adversely, rasvah shrotas (help in providing fuel to the body cells), medovah shrotas (help in collecting the body fuel) and mutravah including shukravah shrotas (help in production of urine and carrying out of reproductive functions). The deformity in mutravah shrotas assumes special place in development of diabetes as well as its complications. The root of mutravah shrotas is vasti (vasti is a combined name for kidneys and urinary bladder) and the symptoms of its vitiation are characteristic features of almost all the diabetics at least in beginning. The symptoms are frequency of micturition, polyuria, dysuria, deformities in urine as albuminuria and glucoseuria, pain in vasti, increased concentration of urine, falling of the urine production after some years and slowly moving the patient to irreversible kidney damage, and finally death.

The vitiation of purishvah shrotas leads to several disorders of defaecation such as constipation, diarrhoea and formation of bullet like hard stool. Swedavah shrotas dushti leads to excess or decreased sweating and disorders of the skin as burning sensation, stickiness, romharsh (asthesias and parasthesias).

It is also important to understand that if a particular shrota such as shira, nari, dhamni, pores of skin, mouth or anus is blocked it not only deforms that substance which is being transported through it but it also leads to deformity of the other shrotas and dhatus. And if causes of shrotavrodh are not removed timely this chain reaction will ultimately deform all the body shrotas and dosha-dhatu-malas.

 Adverse Effects of Diabetes on Body systems

The adverse effects of diabetes on various body organs and organ systems are being dealt in detail in the following text. The diagnosis, causes, aetio-pathogenesis, prodormal symptoms, probability of cure and prevention of these complications are all described.

Diabetes and the digestive system

The natural abode of vayu is in this system only. Hence intake of substances capable of polluting the digestive system also impurifies the vayu and produces severe diseases.

The vayu in motion that is, wind (vegvan vayu) remains pure in its primary natural abode the stomach, duodenum and rectum. If a diabetic eats improper (apathya) food and the digestive system gets obstructed then the vayu residing there (saman and apan) also gets vitiated giving rise to several problems as discussed below.

Similarly in diabetics accumulation of meda and malas in intestines and constant intake of impure food leads to mandagni (decreased digesting energy) which increases the amount of immature doshas (coction of food becomes improper). And as this vicious cycle of dosha vitiating jathragni (fire of the stomach),and vitiated jathragni (mandagni) increasing ama (immature doshas) continues, the diseases of stomach and intestine develop.

The third important factor responsible for digestive disorders is improper evacuation of malas (constipation) and deformed stools. Constipation and diarrhoea both are the features of uncontrolled diabetes and they harm the digestive system in following ways.

Firstly, due to constipation one can develop friction in the lower intestines which leads to inflammation and further problems such as sangrahni (colitis) and aggravation of piles, fissure etc. If a person is having loose motions it is most likely that most of the nutrients remain undigested and are hence not absorbed into the blood and pass out through the faeces. All the above mentioned factors deteriorate digestive functions as well as diabetes control.

Those diabetics in whom due to saatamya ahaar-vihar (regimen diet) the digestive system remains pure (proper appetite, proper digestion, absence of gas, and normal defaecation) it is seen that not only diabetes but other diseases (if present) are also cured very fast and the body remains healthy. The important gastro-intestinal disorders are as follows:

‘Vatik udar rog’ Generalised enlargement of the abdomen

When apan, saman or vyan vayu get vitiated then gurgling sounds develop in the abdomen. In this case flatulence occurs and the stomach swells up. Symptoms like pain in the whole body and joints, obstruction in wind, difficulty in walking and other movements, weakness, decrease in jathragni, mild swelling all over the body, looseness in extremities, constipation, dah (body burning) and letharginess also develop. Aml-pitta (acidity), hriday dah (heart burn), apach (indigestion), gulm (gas balloon), atisar (loose motions), yakrat shoth (swelling of liver), diseases of the rectum as arsh and bhagandhar (piles and fissures) and a few other diseases develop easily in a diabetic with vatik udar rog.

Vataj gulm’ Distension of abdomen

Unsuitable ahaar-vihar, excess exercise, obstruction of faeces and apan vayu, removal of pitta and kapha from their native places, and blocking of passages by faecal matter, leads to severe pain in the stomach. It is treated by snehan and swedan procedures.

‘Aphara’ Distension of stomach

When saman vata vitiates in stomach the result is distension of stomach. In this situation immature doshas develop tendency for evacuation from oral route. Patient remains restless and in great discomfort. Sour belching can also manifest.

‘Aadhaman-aanah’ Pain due to obstruction of wind and faeces

When saman vayu is obstructed in small intestine the patient develops symptoms of intestinal blockage such as pain and distension of abdomen. Usually this occurs when immature doshas obstruct the natural path of vayu. Such a patient also complains of constipation.

‘Atisar’ Loose motions

As constipation comes in the way of a healthy body, similarly loose motions, too, do not allow a person to lead a healthy normal life. Ayurveda describes the following common causes of atisar: intake of extra heavy, dry, hot, fluid, hard and cool foods, heterogenous food, addhyasan (eating before the previous food has yet been digested), eating uncooked food, panch karmas, drinking of toxic substances, fear, sorrow, contaminated water, alcohol, a few adverse physical exercises and worm infestation.

One should take prevention against diarrhoea because then only he can take full advantages of a nutritious diet. Ayurveda has also described neuro-muscular mechanism of developing diarrhoea as there are three mechanisms :

* Post prandial diarrhoea (due to gastro-colic reflex).

* Nervous diarrhoea as in diabetics with autonomic neuropathy (DAN) and following mental excitement such as fright (fright a component of strees reaction) and flight.

* Due to intestinal inflammation : tuberculosis, enteritis, colitis etc.

‘Amatisar’ Diarrhoea with mucus

Immature food lying in intestine acts as foreign body and therefore intestinal mucosal tissues react and the result is amatisar. Apart from this, the presence of ama leads to auto intoxication. All three doshas can be vitiated in amatisar. A stool with froth is suggestive of vatik amatisar, whitish and kapha mixed (mucus) stool is indicative of kapha amatisar and yellowish-green or reddish stool is indicative of pitta amatisar.

Pakkwatisara’ Bacterial diarrhoea

Once the food is digested in the small intestine, the stool it forms is called pakwa mal (formed stools). Because of kapha dushti one can develop severe diarrhoea and it is mostly associated with intestinal infection with gram negative bacteria.

‘Raqtatisara’ Bloody dysentry

When raqt (blood) is also present in loose motions it is raqtatisara. All pathologies remain the same as that of amatisar; bursting of the small intestinal capillaries under the influence of ugra vata is an additional pathology which also works during this disease.

‘Pravahika’ Diabetic diarrhoea

Acharya Sushruta has described about this disease as : “vayuh pravriddho nichitam balasam nudatyadhastadahitashnasya; pravahmanasya muhurmalaktam pravahikam taam pravdanti tajgyah” (SushrutSamhita.Uttartantra.L.40.S138). It means that due to smallest force, even if involuntary, a patient passes kapha mixed stool. Kapha dushti is essentially present in these patients. The patient also suffers with loose motions due to abnormalities in vata nari sansthan of the intestines as diabetic autonomic neuropathy.

‘Grahni’ Chronic colitis

Following jeerna atisar (chronic diarrhoea), or due to non-regimen diet, the jatharagni gets vitiated more and adversely affects the intestine, too. The basic defect in grahni is mandagni. The prodormal symptoms of grahni are thirst, letharginess, loss of force, acidity, delayed digestion and ponderous body. Kayasya gaurvam that is, guruta (ponderousness) in the body is one of the most prominent feature of grahni disease. The prodormal symptoms of grahni are: dryness in mouth and throat, feeling hungry and thirsty several times in a day, weakening of eyesight, bodyache, mucus in stools, chest pain, virasta (tastelessness in the mouth) and lean and thin body.

‘Visuchika’ Cholera like symptoms

When vatadi dosha cause obstruction of the intestine along with shofh (inflammation) the result is very harmful; one vomits and also loses water through watery diarrhoea. The name visuchika suggests pain like pin pricking in intestines.

‘Hrid Dah’ Retrosternal chest burning

Pitta distorts ‘vidhagdh pitta’ in a person with poor jathragni and symptoms like retrosternal chest burning, and sour belching appear. The symptoms of acidity are very distressing and prevent onself from taking normal diet. Hrid dah also results when amadosha (immature vata-pitta) does not find a normal passage in the intestines and because of vata vitiation in the stomach and the intestines, they develop a tendency to come out through the mouth. In this process ama regurgitates into oesophagus giving rise to the symptoms like ‘hrid dah’. Sometimes diagnosis of ischemic heart disease becomes difficult to rule out because of this disease as both present with retrosternal chest discomfort.

‘Klom vyadhi’ Pancreatitis

When vayu blocks the ras veins of the pancreas, then pancreatitis occurs. If it is not treated in time ugra vata and some times pittaitself destroys the pancreas (necrosis of pancreatic tissues) completely. In this condition mortality rate is quite high.

But in patients with chronic pitta disorder the clinical features and course of the disease is different. As per allopathy it can be compared with chronic pancreatitis. The prodormal symptoms of chronic pancreatitis are: agnimand (indigestion), krishta (asthenia), panduta (paleness), avsad (depression), udarshool (chronic abdominal pain), pipasa (thirst), vaman (vomit) etc.

Repeated vitiation of vayu leads to above symptoms and it indicates deterioration in diabetes. Hence if above prodormal symptoms are seen in any patient, then he should become alert.

‘Yakrat shoth’ Hepatitis

The liver cells ‘hepatocytes’ perform important and crucial body functions. The vitiation with vata and infiltration with fats make these cells weak and their functioning capability reduces markedly. In the beginning the size of the liver increases as there is inflammatory swelling in the hepatocytes. Later on the liver shrinks in size (cirrhosis) and does not function properly and ultimately the patient dies.

‘Pleeha vriddhi’ Enlargement of the spleen

When blood gets highly vitiated, or there is untimely destruction of the RBCs (a red blood corpuscle normally lives for 120 days) as in malaria andkalajar, and when there is inflammation in the liver giving rise to portal hypertension, the spleen enlarges with dangerous consequences. It may rupture also if there is more enlargement or external injury.

Diabetes and the Urinary System

According to ayurveda vasti dushti (vasti refers to kidneys, ureters and urinary bladder and dushti means derangement of functions) leads to diabetes. When vasti takes out glucose along with several other dhatus such as protein, fat, lymph, oja, calcium phosphates, minerals, and water in large amounts out of the body, then diabetes occurs. When dosha-dhatu and malas of the whole body get vitiated and collect in the vasti and take out immature liquefied dhatus and immature doshas along with urine, then diabetes occurs.

As Acharya Charaka says : “vastivikriti samyatpramehnidan achhute” i.e., there is a close relationship between diabetes and vasti. Deformation in functioning of the vasti is necessary to produce diabetes. This information is provided by modern science also that if the kidneys of a diabetic are unaffected, then one can lead a perfectly normal and healthy life.

The importance of knowing vasti vikars (urinary system disorders) according to ayurveda lies in the fact that diabetic damage in kidneys is very often symptomless (as per allopathy) but ayurvedic science tells us several methods of detection and prediction whether a diabetic person is slowly progressing towards irreversible kidney damage or not. How it is so will be described a little later in the book. First of all let us know something about the kidney and its functions.

The smallest structural and functional unit of kidney is a nephrone. There are about 10,000,00 of these small independent urine forming units in one healthy kidney which are connected in series. This number always remains the same as it was at the time of birth. In a normal person, too, after the age of forty years about 10% nephrones per year become non-functional upto the age of eighty years. But this decrease in number does not cause any problem (because of several reasons) and remaining nephrones cover up this deficiency. A nephrone can never regenerate if it has been destroyed by any disease and neither new nephrones can be regrown. Diabetes is such a disease which affects the human body mostly through its damaging effects on nephrones. As the most important function of homeostatis (making the body’s internal environment suitable for functioning and living of body cells) suffers if one’s kidneys are damaged, so uncontrolled diabetes may prove very dearly.

The process of diabetic renal damage does not complete in a year or two rather it takes decades to develop permanent damage in one’s kidneys. Because the time period taken by this pathology is very prolonged the symptoms it produces are also trivial and not acute. Generally a person overlooks certain very important but mild symptoms which appear in between these years, especially when a diabetic suffers with some other illness which is not directly linked to kidney disorder. Since almost all moderate to severe diseases have some stress effect on the body (organs) so the adverse effects on kidneys at these times produce some symptoms such as oliguria, polyuria, anuria, difficulty and burning in urination, retention of urine, pain and heaviness in the pelvic region, hotness or coldness in urine, renal colic, pus in urine, recurrent U.T.I. (urinary tract infection), discolouration of urine, sedimentation, and off and on swelling below eyelids, face and feet, loss of appetite, nausea and vomiting.

Sometimes even very prominent symptoms such as blood and albumin in urine, and increased pulse pressure, are overlooked by the patient and the physician, too. It is therefore suggested to all diabetics that if they observe any of the above mentioned symptom or any other related symptoms they must not overlook them but immediately advanced investigations should be planned. Not only this if a person finds these symptoms he must correct his eating and living habits and concentrate more on all possible medical measures which should be undertaken, because once the nephrones are destroyed they remain so for rest of the life, and there is a lack of very prominent prodormal symptoms also of diabetic renal damage.

Ayurveda has described several diseases of urinary system disorder which can give us a clue about the status of one’s kidneys and a few symptoms of these disorders are excellent guide for showing the path of prevention by recognizing or knowing of these symptoms. These diseases can be put under two categories Mutraghat (obstructive uropathy, less urine; 12 subtypes) and Mutrakracch (painful uropathy; 8 subtypes) and are as follows:

‘Mutraghat’ Obstructive uropathy, less urine

Vatasthila (prostatedisorder- dribbling of urine), vatakundalika (painful dribbling of urine), asthila (obstruction of stools, urine and wind along with severe pain in pelvic region), vatavasti (painful obstruction of urine), mutrateet (forceful retention leads to dribbling, slowing, recurrence and decrease in urination), mutra jathar (severe obstructive pain below the navel, the urine and the stools are also obstructed), mutrotasang (sudden stoppage during micturition, urine mixed with blood, pain and dribbling), mutrasanchay (burning pain in vasti and scanty urine), mutragranthi (sudden development of stone like structure in urine path which produces symptoms of stone), mutrashukra (intercourse at the time of having strong urge for urination leads to production of smoky urine), ushnavata (urination with difficulty, colour of urine is deep yellowish or reddish brown), mutroksaad(when urine is dry, yellowish and there is burning in micturition). Above diseases and their symptoms strongly indicate that a patient can develop serious kidney problem in near future and therefore he must start adopting preventive measures.

‘Mutrakracch’ Painful uropathy

Vatajanya mutrakracch tearing pain in urinary bladder with scanty urination), pittajanya mutrakracch (fire burning pain in urethra, scrotum and head of the penis; urine becomes deep yellow like turmeric and warm), kaphajanya mutrakracch (heaviness in urinary bladder, horripilation, the urine is sticky and whitish), sannipataj mutrakracch (different colours in urine with lot of pain during micturition), traumatic mutrakracch (painful obstruction and reddish brown colour of urine), mutrasanga mutrakracch (piercing pain), ashmari mutrakracch (renal colicy pain in mobile renal pelvic or uretric stones, dullache pain in big urinary stones and discolouration of urine), sharkara mutrakracch(sand like particles obstruct urine flow in ureters and neck of the bladder and cause pain and obstruction in urine). If any of the above symptom is present in a diabetic he must consult a surgeon.

Prodormal symptoms of urinary system disorders

These are nidranaash (loss of sleep), agni mandata (decreased metabolism), shofh (swelling on body), benumbed pulse and rough skin.

On increasing of vayu vikar and blood viscosity, vrikka rog (kidney diseases) occur and produce early symptoms such as yellowness of face, absence of perspiration, dry and rough skin, pain in waist, stomach and kidney region, increased pulse and drop by drop urination. On recurrence of the symptoms the disease becomes serious. The prodormal symptoms of prameha can also be included in these symptoms (read ‘prameha’ chapter).

When vayu dosha in kidney becomes severe and systemic blood also gets vitiated then kidney disorders such as vrikka shoth (nephropathy), vrikka sanyas (kidney failure), vatik mutraghat (autonomic bladder), vasti shool (renal colic pain), and secondary spleen-liver disease, karna-naad (abnormal sounds in ears), eye disease (retinopathy), dhwajbhang (impotence), moorcha (unconsciousness) and moh (altered sensorium) develop in the body. Following disorders are common in diabetics:

‘Vrikka shoth’ Swelling in kidneys : On increase of vata and other doshas, slowly swelling over the whole body starts which later changes to generalized anasarca. Ayurveda describes four stages of vrikka shoth as follows:

‘Akshikoot shoth’ Early morning swelling, which subsides as the day moves on.

‘Uchha raqt-bhar’ Less urination leads to increase in blood pressure (­BP).

Bhhagna tantu’ Broken tissues in urine are indicative of vrikka shoth.

‘Vrikka sanyas’ Urine output gradually reduces to aneuric stage.

Madhumehaj vrikka vikriti Diabetic nephropathy : In prameha and madhumeha there is initial swelling in renal tissues (vrikka shoth) because of ruksha vata situated in the minute shira (capillaries) and vrakkanu (nephrone). As the disease progresses there are nodular changes inside renal tissues (‘lasika granthi janya vrikkanu koshika kathinyata’ nodular intercapillary glomerulo-sclerosis) and in later stages the kidneys contract and look badly scarred (contracted diabetic kidney: as they remain only one-fourth of the normal size).

Ayurveda had recognized and explained this problem thousands of years before as : “jayante kupiterdoshermutraghatastrayodash; prayo mutravidhatadyairvatkundalikadayah.” (Madhavnidan.L.31.1) i.e., the vitiated doshas and especially dry vata due to forcefully stopping the urge of urination, defaecation, and eating anti-pathy diet give rise to this disease. And there are three stages as:

1. Purva vrikkiya (pre-nephrotic);

2. Vrikkiya awastha (nephrotic stage); and

3. Vrikkakathinyatajan (nephro-sclerotic stage).

In stage 1 no specific pathology can be detected in urine except that on collecting urine in a pot for 24 hours the only symptom is excessive urine. In stage 2 there are deposits as albumin, phosphates, and casts in stored urine. And in stage 3 urine output starts decreasing (<1000 mL per day) only to stop completely in near future.

‘Vata vasti’ Retention of urine : When vitiated vata produces obstruction at the outlet of urinary bladder one suffers with pain and lack of urination. It occurs because of forceful retention of urine.

‘Mutrateet’ Incontinence of urine : If one holds urine for prolonged periods urination becomes difficult and even if it occurs it does so very slowly.

Mutrajathar’ Distended bladder : Mutravega nirodhaja udavrat causes distension of abdomen by vitiating vasti through apanvata. A patient feels severe pain near navel portion (severe adhman).

‘Vrikka Shoth’ Nephritis : Highly vitiated doshas (amavata or amyloid) vitiate the dhatus of a diabetic’s kidney and also cause low grade inflammation. If not treated in time the disease progresses towards chronic renal failure.

‘Mutrakshaya’ Suppression of urine : Due to vitiation of pitta and vata the people with excessively dry or weak body develop burning pain in urination and oliguria.

‘Mutrasad’ Scanty urination : When pitta and kapha dosha (separately or combined) situated at the vasti get concentrated due to dry vata, the patient urinates slowly and with difficulty. The urine becomes dark yellow, reddish and concentrated. After a few hours of collection it becomes more thick and sediments can also be detected.

‘Mutrakrrach’ Painful urination : Excessive exercise, alcohol use, eating excess of spicy foods and non-vegetarian foods are all causes of this disorder. The patient complains of pressure in urine pathway and severe pain during micturition. Despite having full vasti (with urine) and desire for micturition, a patient does not prefer to urinate only because of the fear of developing more pain.

‘Ushn vata vrikka’ Infection of urinary system : Excess of pitta causes burning, inflammation and pain (like pouring salt over a wound) while urinating, inflammation in glans of the penis and fever with chills.

Vrikka vidradhi’ Pylonephritis : Highly vitiated doshas vitiate the raqt-maans-meda (kidney tissues) and cause inflammatory swelling in the kidneys. If it is not treated in time pus development starts.

Vrikka sanyas’ Renal shutdown : By the time this stage reaches there is intense collection of tridosha and malas in body along with dhatukshaya. And one can observe following symptoms: swelling, less urination, comparative decrease in specific gravity of urine, urine contains albumin and casts and is smoky coloured, there is raqt dosha and high blood pressure.

All above diseases or abnormalities are indicative of disordered vasti and should alarm a diabetic patient to take proper precautions and treatment.


Ayurveda had recognized the importance of beeja (sperm and ovum), beeja bhaga (chromosomes) and beeja bhagavayava (genes) thousands of years ago. It developed the principle that healthy sex is responsible for healthy generations. If either mother or father suffers from sexual diseases then certain doshas make their abode in the beeja (deformity in sperm/ovum, chromosomes or genes). This becomes the cause of birth of an unhealthy child. It is seen that sexual problems occur to a greater extent in diabetics than normal persons, hence extra efforts are required to prevent them. A male or a female both may suffer from sexual diseases due to several reasons.


The most common complaint of diabetic males is weakening of the sex. Most of these men complain of unsatisfactory erection (less hardening) coupled with unsustaining of erection for appropriate time during intercourse. Premature ejaculation is also one of the major complaint of diabetic males. All these sexual problems are considered as erectile dysfunction or impotence.

Klebyata or Napunsakta (impotence) is said to be present when a person is incapable of successful intercourse and the patient is called a kleeb (impotent). This is one main problem which is common in diabetics. Ayurveda describes its reason as excess vatain the nerves and the blood vessels of the penis. The speed of sensations in the nerves and blood flow in the blood vessels both are obstructed and lead to impotence.

In a normal male the proper erection of the penis is only made possible when vatanari sansthan (nervous system) and blood circulatory system function normally. The desire for sex arises in the brain followed by motor impulses which originate there and travel upto the muscles and blood vessels of the penis. Under the influence of nervous stimulation of the penile artery massive blood flows into the penile muscles and gets accumulated there (16-20 times more blood as compared to resting state).

During intercourse and ejaculation the sensations of pleasure (orgasm) can only be perceived by the brain (when the sensory nerves of the penis are intact as they are responsible for carrying the pleasure sensations upto the brain) and in diabetics sensory nerves may not be intact (dead or less active nerves). Acharya Bhavprakash says : “yad dravyam purusham kuryadvajeev suratakshamam tadvajikarmakhyatam munibhirbhishajam vareh” (Bhavprakash.U.3.1). It means the substances, which help a male to involve in intercourse like a horse are called bajikaran.

Kleebta (impotence) is of seven types, out of which fifth and seventh are incurable and the remaining five can be prevented or removed by bajikaran chikitsa. The seven types of impotence are:

1. ‘Mansik klebya’ Psychological impotence

If the mind of the person involving in sexual intercourse is full of sorrow, anger, fear and other pessimistic feelings or he is not at all interested in the lady with whom the act is to be performed then the penis loses erection.

2. ‘Pittaj klebya’ Premature ejaculation

By the intake of strong, sour, hot and salty foods in excess, the matured pitta vitiates giving rise to virya kshaya.

3. ‘Virya kshayajanya klebya’ Exhaustive impotence

If a person is excessively involved in intercourse and does not take in bajikaran, he becomes incapable of erection in his penis in due course of time.

4. ‘Vyadhi or aushadjanya klebya’ Other disease or drug induced impotence

This develops due to some serious disease in the penis such as syphlis, gonorrhea, or cancer. In a few systemic diseases such as nephropathy, severe ischemic heart disease, cancer and severe hypertension one can also develop this disease. A few medicines used for treating other diseases like anti-hypertensives and anti-psychotics may give rise to this condition. The treatment is to cure the secondary disease and remove the causative drug if present.

5. ‘Shirachedajanya klebya’ Vascular impotence

Due to holes in the virya vahini and the blood vessels (spermatic cord and penile artery), a patient develops this disease. It is similar to a condition described in allopathy as valvular incompetence. Here the blood does not remain in the penile muscles for optimum time due to deformity in functioning of the valves responsible for holding up blood there during intercourse. This leads to improper erection and premature ejaculation, too.

6. ‘Shukra stambh janya klebya’ Obstructive impotence

Despite a healthy body, if a person follows principle of brahmacharya (abstains from sex) then due to no outlet of virya (semen) this problem may develop.

7. ‘Sahaja klebya’ Hereditary impotence

This is the situation when a person is a kleeb since birth or due to pre-birth reasons. On excessive diseasing of vatanaris this incurable problem occurs (neurogenic impotence).

Shukrameha (retrograde ejaculation) and Baanjhpan (infertility) are the other two most common diabetic complications. The former disease takes place on shukrakshaya (loss of semen). On being vitiated by vayu the semen does not come out of the penis, but from the seminal vescicles it reaches into the urinary bladder, and comes out with urine at the time of micturition. In allopathy, this disease is called retrograde ejaculation (a common complication in diabetics due to defect in nerves controlling functions of the valve between urinary bladder and urethra). In this disease semen flows the wrong way.

The latter problem baanjhpan or infertility is again either due to excessive shukrakshaya or absence of shukranu (sperm) in the semen and in both the person loses the capability of fertility.


Just as diabetic males are more prone to develop sexual problems similarly females are equally susceptible to develop certain sexual diseases. The most common sexual problem in diabetic females is lack of lubrication in vagina during intercourse. Vaginal monaliasis is another common problem in diabetic females. The common sexual problems in diabetic females are:

1. ‘Sushk vata yoni’ Dry vagina

Due to atikshaya (excess) of vayu the essential smooth fluid which keeps the vagina lubricant dries up and the vagina becomes rough, dry, hard, harsh and full of pain and swelling.

2. ‘Bhagshishn suptijanya napunsakta’ Clitoral impotence

The blood vessels and the nerves of clitoral tissues are vitiated by vayu. In these circumstances one does not develop arousal (same as failure of erection in men) because of decreased blood flow in female genital organs. Apart from this the sexual impulses and the feeling of orgasm also does not reach the brain due to defective sensory nerves and it all leads to impotence in diabetic females.

3. ‘Vatik pradar’

A disease in which there is excess blood flow through the vagina either during menstrual period or otherwise also is called pradar. Diabetes is one main reason of this disease. Due to blood loss weakness, confusion, semi consciousness, thirst, inflammation, yellowness of face, eyes and skin, drowsiness and other vatik diseases (censures, trembliness) develop. Because of deficiency of blood nari shoth (neuritis) occurs and the patient feels burning sensations all over the body. Due to obstruction of passage and dhatukshaya, vayu dosha increases and symptoms as leanness, kamp, nidranaash, restlessness, irritation and breathlessness occur.

4. ‘Nishpichadaharti’ Dysmenorrhea

Normally during menstruation pain in lower abdomen, headache, burden, tiredness, restlessness, irritation and other such symptoms are observed and the diseases is called nishpichadaharti. If these symptoms become very severe then they are known as kricchartav.

5. ‘Raqt pradar’ Metrorrhagia

It means bleeding from the uterus in the intervals between the menstrual cycles. The doshas responsible for excess menstrual flow later on become capable of increasing time period and irregularities in menstruation.

6. ‘Shweta pradar’ Infected leucorrhoea

The bloodless white secretion coming out of the female genitalia is known as shweta pradar. This normally occurs due to swelling in uterus and vagina in association with anemia and infection and is a very common disorder in diabetics. The disease is also a sign of ill health in women. Its symptoms are : foul smelling secretion through vagina, weakness, vertigo, and cutting, sharp pain below knees and waist.

7. ‘Vipluta’

When there is constant daily pain in the vagina even without intercourse the disorder is termed as vipluta.

8. ‘Paripluta’

When there is too much of pain in the vagina during intercourse only, the condition is called paripluta.

9. ‘Udavarta yoni’

Vitiated vayu obstructs its own speed and that of raj (normal menstrual discharge) and causes udavarta (pain) in yoni (vagina).

10. ‘Bandhyatva’ Sterility

For conception both the male and the female are equally responsible. In females congenital malformations, or due to acquired reasons, defect/or destruction of the beeja (ovum) or absence of reproductive genes in the chromosomes of the beeja may lead to sterility. The above diseases develop in majority of female diabetics only due to intake of heavy and acidic food, excessive mourning, worry and deep sorrow.

Diabetes and Eyes

“chakshu rakshayamservacal—–vidyamanepi” (AstangHirdaya.Uttartantra.L.13) i.e., a man should constantly make efforts throughout his life for preventing eye diseases because despite having all worldly pleasures if a person becomes blind then day and night are the same for him and everything seems useless.

Origin of eyes and eye-sight

Eyes are formed from panch mahabhuta and their light (vision) comes from the essence of panch mahabhuta “sarvabhutgunodbhavam—–“ (SushrutSamhita.Utartantra.L.1.S10). Including the eyeballs, the eyes comprise of four parts (four layers). Defects due to diabetes start developing from the innermost layer and reach the outermost covering. Due to this reason only symptoms relating to eyesight develop late (as abnormal doshas collection starts from inside) and by that time the disease becomes incurable.

Layers of visual tissues

There are four layers (patal) in the human eye as Sushruta says : “tejojalashritam bahyam teshavanyat pishitashritam” (SushrutSamhita.Utartantra.L.1.18) i.e., the four patals are jalashrit, mannsashrit, medashrit and asthiashrit. Vaghbhat says : “chakshuh tejomayam” (AstangHridaya.L.2) i.e., eyes are made of teja. Different doshas collect in the four layers of the eyes and develop serious disease timir (temporary/permanent darkness).

Causes of timir ‘andhkar’ (darkness- vision loss)

The doshas become very severe and aggressive (and damage the eyes and vision) under the following circumstances: Intake of cold and hot products, sleeping during the day and waking up during the night, taking liquid food during night, excess weeping, anger, sorrow, grief, worry, mental conflict, physical weakness, head injury, smoking, drinking, excess intercourse, continuous watching of nearby or far off objects.

‘Samanya samprapti’ (pathogenesis) of eye disorders

Diabetic eye diseases develop either directly due to defects in the eyes or indirectly when doshas develop in any other body part and reach the eye through blood circulation. Several diseases of the body have adverse effects on the eyes and one is diabetes. Degenerative diseases such as retinopathy, cataract and diseases related to age as presbiopia, glucoma are also seen more frequently in diabetics. Sushruta has described smoking as the most injurious causative agent of eye diseases. The common and prevalent eye diseases in diabetics are as follows:

‘Vataj abhishyand’ Conjunctivitis

This disease develops due to vitiation of the doshas and the blood and the following are its main symptoms: excess secretions from eyes, pain like pin prick, tightness, grittiness, stickiness, redness, swelling and inflammation in eyes and recurrent headache.

‘Adhimand or sambal vayu’ Glaucoma

A condition in which pain occurs in the eyes and half side of the head, pricking sensation persists in inner side of eyelids, and there are excessive secretions from eye(s) is called ‘glaucoma or sambal vayu’. When these symptoms become very severe then the condition is called vataj adhimand (glaucoma fulminans). In this case the patient becomes blind within 6-7 days only and this is because vayu enters the eye vessels and dries up the tissues present very fast.

There is another condition called ‘hatadhimand’ which also causes incurable loss of eyesight (acute glaucoma). In samanya adhimand (simple glaucoma) due to defect in trigeminal nerve the vayu repeatedly produces pain in eyebrow, eye and also secretions from eye (trigeminal neuralgia).

‘Drishtiheenta’ Blindness

When the first three patals (layers) of the eye are adversely affected one develops ‘timir rog’. When defects enter into the fourth patal one develops ‘lingnash’ (cataract) as Sushruta says : “sa ev lingnaashastu neelikakatchsangyitah” (SushurtSamhita.Uttartantra.L.7). As there are three components of vision, blindness also develops in three ways:

1. General blindness:Vata dosha produces defect in the first and second layer that is, the conjunctiva and the sclera of the eye and as a result, corneal opacity develops and one suffers with partial or complete and temporary or permanent blindness.

2. Specific blindness: It occurs due to defect in the lens (fourth patal is lens) as development of cataract (lingnash). The lens develops this disease gradually (progressive cataract) as in early stages of immature cataract the symptoms of timir dominate, but later on development of mature cataract there is complete darkness.

3. Main blindness (drishtiheenta): Vision, which accepts form and shape is situated in the innermost part of the eye and is also known as sookshmdrishti (allochak pitta or macula leutea- “SharngdharSamhita.L.7”). Serious drishtiheenta occurs due to drying up of the blood vessels supplying blood to the eye tissues over there.

Out of these three the first two, if treated timely are fully curable, and in the third one probably retinal detachment occurs. If treatment is delayed then the first two also come under incurable category of blindness.

‘Timir rog’ (Dhund)Darkness

It is a group of symptoms which are indicative of the disease process in one’s eyes. As described by Acharya Sushruta a patient visualizes red or rainbow colours, dancing objects, white patches, abnormal shaped small or big distorted objects, and similar several other symptoms (SushrutSamhita.Uttartantra.L7S11,14). A diabetic should start taking optimum precautions if he develops any of the above symptoms.

Change in eyesight

According to nature and position of dosha in the eye, changes in eyesight also occur. If doshas accumulate in the lower part of the eye then nearby things can not be seen easily. Likewise, if they are in the front portion then far off things can not be clearly perceived and if they are in the middle portion then big objects are not clearly perceived. If doshas exist in two portions then two types of defects can be seen.

‘Madhumehaj drishtipatal vikriti’ Diabetic retinopathy

When vatadi dosha and alochak pitta are highly vitiated in the tissues of antaha patal (retina) or these doshas come from other diseased organs and get attached to retinal tissues drishtipatal vikriti results. The minute blood vessels become fragile because of dry vata and they break even on mild pressure (such as during coughing or running). This disease progresses as follows:

1. Drishtipatal vahini vikriti retinal angiopathy The capillaries develop aneurysm and there is bleeding, too, from these damaged vessels.

2. Samanya madhumehaja dristipatal vikriti simple retinopathy When timiradi doshas develop because of ruksha vata and vitiation of alochak pitta, a patient is said to be heading towards permanent blindness.

3. Vriddhijanya madhumehaj dristipatal vikriti proliferative diabetic retinopathy Abnormal dhatus start depositing in the internal layer ‘retina’ of the eye and patient develops symptoms as distorted vision, black spots, and diplopia. If such symptoms persist then probably the disease has reached innermost layer of the eye tissues and the next thing to happen is total blindness. This disease acquires dangerous proportions if the patient is having uncontrolled hypertension, too, and then the disorder is termed as raqtdabvriddhi-janya madhumehaj dristipatal vikriti. Another similar disorder is madhumehaj vrikka drishtipatalgat vikriti.

Miscellaneous Eye Diseases in Diabetes

Taramandal shoth (iritis) and uptarakamandal shoth (iridocyclitis) are quite common in uncontrolled diabetics. Netra madhyapatal shoth (choroiditis), ‘sanghaniya’ muscles paralysis (ciliary paralysis) and visham drishti (astigmatism) are a few more eye problems sometimes present in diabetics.

‘Netrabhyantar patalasth vibransh’ Detachment of the retina

Vataraqt vitiates the dhatus of the innermost portion (degenerative process) of the eye ‘retina’ and makes them almost dead. Hence retina of the eye detaches (drishti vitan) and a diabetic becomes blind forever.

‘Lingnaash’ Cataract

In the eye lens, vikar janya timir (progressive cataract) and later on complete lingnaash (cataract) both may occur.

Lingnaash occurs either due to hereditary disorder (kulaja vikar) or as a developmental disease. In diabetics both the reasons genetic and degenerative (nutritional) lead to premature cataract. When timiradi doshas reach to the fourth layer there is destruction of the visual power known as lingnaash. A patient develops complete darkness in front of the affected eye. Timely treatment by surgery makes the disease curable.

‘Tamaladi vishaj drishtimaandh’ Tobacco amblyopia

This disease develops due to high intake of tobacco and other intoxicating substances. The clinical features are slow deterioration of the vision. A bilateral centrocecal scotoma is the characteristic defect of tobacco amblyopia. The tobacco amblyopia induced by pipe smoking may be due to the lack of the detoxifying effect of vitamin B12 on cyanide derived from tobacco smoke.

Sub-cojunctival echymosis

This occurs when an artery ruptures due to excess of vata in the white portion of the eye ball and produces red marks (patches which later on become black).

‘Jara drishti’ Presbiopia

This disease develops as age progresses. But sometimes increased doshas affect eye tissues at a young age itself and produce decrease in vision much earlier. Usually patient complains of blurring of the vision while seeing nearby objects and only distant objects are seen clearly.

Normally this disease occurs at old age only and the cause is loss of elasticity in ciliary muscles which prevent normal functioning of the lens (with the help of ciliary muscles the focal length of the lens changes according to the need). The light rays coming from nearby objects do not focus on the retina rather they converge after retina thus preventing formation of normal image (instead a hazy image is produced). The treatment of this disorder is to use an external convex lens. Diabetics may suffer with this disease early in their life.

‘Vattarmsharkara-netra pidika’ Infected mole

There are numerous small pidika which surround a hard and painful swelling (pidika is an infected eye mole) called vattarmsharkara. This pidika takes birth when vatadi doshas spread in the venous capillaries of the eyelashes. Diabetics may catch this disease easily.


Vrikka dosha, ama, meda dushti, and improper food and life style produce serious diseases in the heart, veins and arteries. And it is vatadi doshas which cause severe destruction. Meda, vasa, raqt, ras and other dhatus also get vitiated with doshas and cause disturbances in blood and vayu (air) movements in the body thus increasing the severity of vata dosha (avrita ‘obstructed’ vata is dangerous).

Anger and alcohol consumption are the two great enemies of the heart. Acharya Charaka describes the anatomy and physiology of the heart very minutely as he says : “tudyamanam sa hridyam suchhibhiriv manyate” (CharakSamhita.Sutra.L.17.S39), if there is infection in the heart one can have pain like pricking of pins in hridpradesha (chest).

There are two distinctive anatomical divisions of the circulatory system and the heart itself that is, 1. Internal membrane ‘endocardium’ of the heart which makes the valves of the heart, too; and 2. Heart musculature and vessel walls (artery and vein). The valves regulate the unidirectional blood flow in the heart and the heart muscles provide strength for contraction and propulsion of the blood. Myocardium is highly vascularized as there is a web of coronary arteries and the venous system incorporated in the cardiac muscles.

The blood is pumped into the main artery, aorta and then circulated into all the body tissues through a network of arteries. Tissues obtain their nutrition from pure blood and also excrete metabolic byproducts into the blood (impure blood) which is collected in the minute vessels called venous capillaries, which unite together and make big veins. These ultimately pour the impure blood into the heart (inferior and superior vena cava).

The most crucial act of collecting impure blood in the lower extremities and then transporting it to the heart against the gravitational force is carried out by the veins with the help of valves present inside their lumen (as these valves facilitate only unidirectional flow of blood that is, from leg to the heart).

The normal functioning of the venous valves is necessary to transport blood in the leg veins. These valves are controlled by the autonomic nervous system which is in control of the hypothalmus region of the brain (pranvata nari). If vatanaris are diseased the venous valves develop dysfunctioning and become incapable of transporting the blood from the leg tissues to the heart and the result is varicose veins (blood pooling in veins) and swelling of the legs.

In fact the muscles in legs act as pump when they are in action, as during movement they help propelling the impure blood into the veins and due to contraction-relaxation process the impure blood gradually reaches the veins from the tissues and flows towards the heart (if muscles do not come in motion one will develop swelling in the limb as seen in cases of plastered leg or arm). The function of the venous valves is to allow the blood to flow only towards the heart and not to let it to flow downwards or backwards.

When vata and pitta both get vitiated in the human body one develops weakness in the cardiac muscles and therefore the pumping power of the heart suffers badly (ejection fraction markedly reduces). Because of lack of energy the heart muscles dilate and their pumping power decreases.

If kapha humour is vitiated there is accumulation of apdhatu jal (water) and lavan (salt) inside the body which also gives rise to high BP (hypertension).

General symptoms of heart diseases

Acharya Charaka has described several purva and vishesh rupa (prodormal and specific symptoms respectively) of the heart disorders and insisted that one should be aware of all these symptoms as they help in early recognition of the heart diseases and also help differentiate between real heart problems and simple gastric diseases (the most common is oesophagitis) which mimic heart diseases.

Acharya Charaka describes several symptoms of the heart diseases as : “vaivarnyamoorchajwarkasahiccashvasasyavairasyatrishapramohah; chardih kaphotklesharujoaruchishrach hridrogajah syuvirvividhastathanye” (CharakSamhita.Cikitsa.L.26.S78) i.e., the symptoms are: vaivarnya (discolouration of the colour of the face) and rest of the skin changes as- panduta (pallor) in anemia, shyavata (cyanosis) in ventricular septal defect and kapolarunya (malar flush) a symptom of mitral stenosis. Moorcha (unconciousness), hridjanya shwas (cardiac asthma), and jwar (fever) are important symptom of endocarditis. Kasa (cough), hicca (hiccough), and shwas (breathlessness) are a few more symptoms of heart diseases.

Kasa, hicca and shwas are obstructive symptoms which are also known as pressure symptoms and are prevalent in high blood pressure and mitral regurgitation. Raqt (in cough), chardi (vomiting), aruchi (anorexia) and shwaskrichhata (deficiency of breath or dyspnoea) are the symptoms of hritshool (angina pectoris) as described in this shloka. Acharya Sushruta has also said about symptoms of cardiac diseases as: blackening of vision, aruchi(lack of appetite), dirtiness in the eyes and swelling over the body.

Following complications are common among diabetics

Ayurveda has described several symptoms related to cardiac disorders and these are of great use for diabetics as they help in recognizing the disease in very early stages. But with advancment of time the environmental, social and psychological conditions also do not remain same and change and as these factors have close relationship with heart disorders the symptoms and nature of cardiac diseases shall also change automatically. A few disorders which were rare in previous days as ‘ischemic heart disease’ and subsequently ‘myocardial infarction’ are now very common and similarly common disorders of past times are less common now a days such as heart diseases due to ‘worm infestation’, ‘rheumatic heart disease’ or ‘infective endocarditis’.

Ayurveda has described five major types of heart diseases as vataj, pittaj, kaphaj, sannipataj and krimi janya. The symptoms, etio-pathogenesis and complications of a few heart disorders of the present times are quite similar to diseases described by Acharya Charaka and Sushruta.

‘Vataj hridrog’ described by Acharya Sushruta has several similarities with the coronary artery disease of modern times (ischemic heart disease or M.I.) as he says : “ayamyate marutje hridayam tudyate tatha—–” (SushurtSamhita.Uttartantra.L.43.S6) i.e., one feels stretching of heart, pin pricking, cutting and tearing pain in the chest and it is all due to vata entering into the heart and causing dryness and stretching of the cardiac muscles.

‘Pittaj hridrog’ as described by Acharya Sushruta is comparable to the disease called pseudohypertropy of cardiac muscles. Sushruta also says about its symptoms as : “trashnoshadahchoshah—–” (SushrutSamhita.Uttartantra.L.43S7) i.e., thirst, pradeshik dah (chest burning), weakness in the heart, smoky feeling in the chest and the throat, dryness of the mouth and unconciousness are a few symptoms of hanmaans parikshaya (myocardial degeneration).

‘Kaphajanya hridrog’ has some similarities of dilatation of the heart ‘diabetic cardiomyopathy and pseudohypertrophic dilatation of the heart’. Sushruta says about the symptoms of this disease as “gauravam kaphasanshravoaruchih—–” (SushrutSamhita.Uttartantra.L.43.S8) i.e., heaviness on the chest and the body, swelling and sweet taste in the mouth. In the following lines description of heart diseases is given according to the old system of ayurveda as it may be of great benefit to diabetic patients.

‘Hanmansopachiti’ Hypertrophy of the heart

If the heart has to do extra work as propulsion of the blood from the heart at a much higher force (due to constriction of aortic valve or systemic hypertension), the cardiac muscle mass gets hypertrophied. This stage is called compensatory hypertrophy and it occurs mostly due to obstruction in the blood movement due to vata in the heart and the arteries. The following are the symptoms of this stage: chest pain, kamp (trembling), weakness, shwas (breathlessness) and prameha (pre-diabetes).

‘Ayamic hrid rog’ Dilatation of heart

If the causes of doshas collection responsible for hypertrophy are not removed then cardiac smooth muscles become long and thin (stretching of muscle fibres) and this stage is called ‘dilatation of the heart’. Its symptoms are: confusion, breathlessness, trembling of heart, numbness in body parts, loss of strength, nidranaash (loss of sleep), generalized anasarca (swelling) and other heart diseases.

‘Hanmans parikshaya’ Myocardial degeneration

The main cause of this disease is excessive dhatukshaya developed during diabetes and accumulation of fat in the heart muscles (vasa sanchaya). A few symptoms are: kamp (shivering), low pulse, depression, confusion, and unconsciousness.

‘Vikshepika hridaya rog’ Angina pectoris

Very severe vayu all of a sudden blocks the blood vessels of the heart (sudden coronary artery spasm) or the blockage may occur due to accumulation of abnormal doshas or dhatus in the arteries and the heart. The symptoms are piercing pain in the chest, tightness, tod (pricking pain), dah (burning sensation), restraint in breathing, altered sensorium, cold perspiration and cold extremities. This disease later takes serious form of hridaynaash (myocardial infarction).

‘Hridayavarta or kshagya hridaya rog’  False heart disease

When apan vayu in the rectum is vitiated then it rises upwards and causes chest pain, restlessness, and shivering symptoms; but vayu does not do any harm by entering into the vessels and the heart as it does in heart attack. As symptoms of the two disorders are quite similar it is very often that one is mistaken for the other but the pathogenesis of both diseases are different and so are the treatments, as heart attack needs much aggressive treatment and is a much serious disorder whereas removing of constipation can cure the other problem very easily.

‘Hrid Dah’ Burning sensation in the chest or heart burn

Due to excess of pitta in the stomach one suffers with aml vata (oesophagitis) as vata brings increased pitta towards the mouth through the oesophagus. It causes severe inflammation in oesophagial tissues and subsequent burning (retrosternal) behind the chest. Cold milk (without sugar) with some cream brings this situation to normal.

‘Supt hridaya shool’ Silent ischemia

In most of the diabetics referred pain (severe pain in medial aspect of the left arm, jaw, left side of the neck and pain radiating to right side of the chest and arm too) of angina does not occur. It happens only because of drying up of pranvata in sensory naris (sensory nerves carrying pain sensations from the heart ‘ischemic injury to the myocardium’ to the brain become dead). Hence in these patients heart attack is diagnosed not by its classical symptom of excruciating anginal pain, but by other symptoms such as breathlessness, cold sweating, nausea, sinking pulse and blood pressure, retrosternal chest discomfort and difficulty in breathing, dizziness and unconciousness. Patient may land up in cardiogenic shock at the beginning itself (massive heart attack) or anytime during the illness and mortality rate soars to almost 90%.

‘Uchha raqtdab’ High blood pressure

When dushit vata vitiates the blood the condition is known as raqtvata which leads to hypertension as said by Acharya Madhavkar : “raqtachha vatshrach iti raqtvatah” (Madhavnidan.L.22.).

Severe vayu besides making the blood vessels dry, hard, brittle and inelastic also reduces their diameter. Due to this the blood has to move through thinner vessels with high pressure. Moreover the heart has to transport blood with greater force/power through the narrowed arteries hence heart muscles have to contract more forcefully and thus extra pressure is exerted by the cardiac muscles giving rise to hypertensive hypertrophy. Due to all these processes speed of the blood increases very much which leads to a great damage in the body organs like kidneys, eyes, brain and heart itself and as a result following complications develop: nephropathy, retinopathy, brain stroke and hypertensive heart failure in the above vital organs respectively.


The important organs of the nervous system are the brain, the spinal cord and the peripheral nerves. The functional and structural unit of the nervous system is the neuron. These neurons have several characteristics the most important ones are :

1. Self excitability;

2. Conduction of ‘electrical’ impulse;

3. Self control; and

4. Control over almost all the body cells and tissues (even a single cell is connected to the neurons).

Brain has several functions including memory, intellect, behaviour, coordination of motor functions and perception of sensory informations.

In diabetes there are several types of vatavikar (vataraqt shira) in the brain and the peripheral nerves. The vata can produce madness, hyper excitability, behavioural changes, memory loss and many more psychological disorders. Apart from this when blood supply to the brain is hampered stroke develops which is often life threatening and kashta sadhya (cures with difficulty). Obstruction of the minute blood capillaries (vasa nervosa supplying blood to the nerves) is hampered giving rise to ischemic injury in these nervous tissues.

Mental Diseases

“samam buddhirhi pashyati” meaningtake everything as it is. Outward pretence, show of prosperity, vanity, jealousy, anger and fear; all these are the causes of mental diseases and develop due to self made mistakes.

‘Shir shool’ Headache

It is a very important symptom of brain diseases. There are two main reasons of headache: 1. Due to pressurization or trauma to the muscles and the blood vessels of the head and face; and 2. It may be because of cerebral tumour (arbud), meningitis (shoth), increase in amount or pressure of the cerebrospinal fluid (raised intra cranial tension, hydrocephalus) and inflammation of teeth, eyes, ear, face or nose.

Acharya Chakrapani says : “anamaye yatha mule vrakshah samyak pravardhate; anamaye shirsvevam dehah samyak pravardhate” (Chakrapani.Su.L.2) i.e., just as the root is important for the tree similarly the head is important for the whole body. AcharyaVaghbhat says: If the root is protected the tree will remain alive and healthy similarly on protecting the head the other parts of the body remain protected, too.

In diabetics vataj shir rog is very common and the reasons are alcohol use, grief, sorrow, fear, anxiety, excessive weeping, increased sex and smoking. The etio-pathogenesis is : “shirogatah sira vridho vayuravishya kupyati—–” (CharakSamhita.Sutra.L.17.S18) i.e., vitiation of the tissues of the blood vessels transporting the blood to the head and the brain by ugra vata. In allopathy also it is said that due to atherosclerosis (hardening and narrowing of the arteries) blood circulation to the brain tissues suffer greatly and in such a situation a major vessel may break giving rise to internal hemorrhage and subsequently paralysis, coma and death.

Apart from the central nervous system the peripheral nerve tissues also get their nutrition through very minute blood vessels called‘vasa nervosa’ which on occlusion definitely give rise to the symptoms of nerve inflammation, injury or death (peripheral neuritis).

Symptoms of vatanari shoth (peripheral neuritis) are tingling sensation, tremors, loss of sensory sensations, asthesia, hyperasthesia, severe pain, loss of power in concerned organ (usually extremities). Akanghat (monoplegia), hangaghat (hemiplegia), and netra pratighat (opthalmoplegia) are a few more types of neuritis. Nari shoth is because of kupit kapha humour spreading into the nerves which are already vitiated with vata. In such circumstances the neurons are unable to produce energy (necessary for living) as they do not get proper supply of nutrients and neurogenic diseases arise.

Mental disease and diabetes

Vitiated vayu causes great damage in the brain giving rise to mental diseases. Vitiated pitta combines with vata and causes irritation, provocation, agitation and other such problems. The imbalance in the electrical activity of the brain gives rise to problems like epilepsy and psychosis. Important mental disorders are as follows:

1. ‘Pralap’ Unmeaningful talk

Vitiated vayu leads the diabetic to useless gossip and discourse. This is called pralap. One also does not remember any of his own acts.

 2. ‘Apsamar’ Epilepsy

Due to extreme vata/pitta/kapha doshas in the sensory tissues the person becomes ignorant (senseless) and starts throwing his hands and legs, grinds his teeth, falls down on the ground and after sometime again comes back to his senses. Loss of remembrance of the unconsciously performed act is a characteristic feature. This disease also occurs if there is blockade in vatanari.

 3. ‘Unmad’ Insanity

A person shows gestures by ‘karmendriyan’, wisdom by ‘gynandries’, thought by ‘manas’, discretion/reasoning by wisdom and his presence ‘aham’ by arrogance and other such sentiments. The routes through which these sentiments are expressed are called unmarg and if vatadi doshas develop in them then all the above feelings suffer set back and become unsettled and this situation is known as unmad (madness).

4. ‘Aptanak’ Postpartem eclampsia

Due to abortion, excessive bleeding during pregnancy or delivery of the child and severe trauma to the utreus; all this may give rise to convulsions and other symptoms of cerebral ischemia. Vayu dries up the veins and the nerves of the head and the brain and may cause death.

Brain and Nerve Diseases

Stroke is the third most important cause of mortality and morbidity in diabetes. Diabetics often do not survive after a major stroke and minor strokes keep them crippling as the neuro-muscular recovery is also poor in diabetics. Therefore prevention of stroke is necessary to live a healthy and useful life. Peripheral neuritis does not kill a patient but it certainly gives rise to a few conditions which do not allow to lead a normal active life. What are these conditions and how one can recognize them easily is all described further in the lesson.

1. ‘Pakshaghat’ Hemiplegia

It is of two types doshaj and agantuj. In the former ugravat (excess vata), madhyam pitta (medium increase in pitta) and heen kapha (minimum increase in kapha humour), all the three doshas combine and cause pakshaghat which is full of vatik symptoms. Despite orders of the mind defective sensory areas of the brain are unable to give orders to the motor areas of the brain. As a result the body can not function properly and the muscles become feeble resulting in pakshaghat (hemiplegia).

In this there is no defect in the motor area. Agantuj pakshaghat occurs due to brain shoth (inflammation) and a few other reasons. If there is shoth, arbud (tumor), bleeding (hemorrhages) in the most superior portion of spinal cord (medulla oblongata) or nearby its parts then also motor nerves become dead and agantuj pakshaghat occurs.

2. ‘Ardit’ Facial paralysis

Vayu affects the mouth and causes facial paralysis. In this disease half of the face and the nose become crooked, tremors also occur and person becomes incapable of speech. The neck also becomes crooked and there is pain in the teeth. Continuous saliva from the mouth, and pain are symptoms of extremely severe vata.

3. ‘Twak shoonya’ Loss of sensation

It is the stage when sensitivity to touch and other sensations of the skin (as coldness, hotness, softness, hardness, tremors, persue sense) are lost. It is due to vata in the nerve endings of the skin.

4. ‘Snayu shool’ Neuralgic pains

The constant pain (of excruciating nature) in the branches and sub-branches of nerves is called snayu shool. This mostly occurs in profound weakness, kidney diseases, ajeerna, and extremely cold and humid air. Snayugat vata causes piercing pain, stambh or jarta (immobility) and akshepa (fits). Patient weeps overnight and can not sleep due to pain.


Due to atikshaya dhatukshaya there is a severe drooping down in the body’s immune system due to which various agantuj rog (foreign diseases such as infections) develop. Diseases of the defective immunity are also common in these patients. Indriyans (gyanendriyas and karmenandriyas) are reduced or retract and so is their power as Acharya Charaka says : “indrayani vinashyanti khili bhavati chetna” and one also loses oja and teja (shining of skin)“ojastejashrach nashyati” .

Normal immune system

Nature has provided an excellent protective mechanism against several pathogenetic organisms which can produce diseases in the human beings. The pathogens are bacteria, viruses, protozoa (amoeba and giardia), fungi and worms infestation. As these are not required in the human body and therefore are of no use when they get entry and are usually eliminated by the body’s defence system. Almost every time a healthy body does not allow these pathogens to make the body tissues their abode and therefore resists their presence. This resistance against the presence of pathogens (they act as antigens that is, foreign proteins) is put forward by the cells of a specialized system called immune system of the body.

The immune system broadly comprises of blood and lymph. There are white blood corpuscles, special ‘killer cells’ (T-lymphocytes), macrophages and antibodies which in a systematic manner provide immunity against pathogens. For a healthy and disease free body a healthy immune system is essential otherwise one becomes an easy victim to infections. All components of the immune system require optimum energy to fight with the pathogen and it is provided by the glycogen stores only (which may be deficient in a diabetic).

Apart from necessity of proper energy, the production of the white blood corpuscles and other components of the immune system should also be normal and it is only possible if a diabetic is eating a balanced diet (optimum calories and vitamins, minerals and elements in diet) and not a hypocaloric under nutritious diet. In controlled diabetics there is a severe defect in the immunity status which is evident by the fact that these patients suffer more with infections (diabetic sepsis). Common diseases of lowered immunity are:

‘Vidradhi’ Deep seated infection

When vitiated doshas take support of the bone and spread into the skin, maans, meda and the blood then they produce painful inflammation. Moreover pus also accumulates and this stage is called vidradhi. A few main type of vidradhi are : asthi vidradhi, majja vidradhi, vrikka vidradhi and klom vidradhi. Pain and pus discharge are the two most significant features of this disease. The root of the disease lies deep down in the bones or the internal organs making cure almost impossible.

‘Vatik vrin’ Non-healing ulcer

Specially in lean and very obese diabetics a vatik vrin (ulcer) may develop which usually has low secretion, pin pricking pain and is black coloured.

‘Jeerna phuphsh shoth’ Chronic lung infection

When a diabetic with weak dhatus comes in contact with a shwasan rogi (patient with lung infection) then bacteria enter the lungs and advance in the innermost minute cells (alveoli) and cause pain, inflammation, prulent secretions and defective functioning of the lung tissues (disordered oxygenation).

Several times chronic lung infection converts in pleurisy (dry and wet both) and tuberculosis mostly in diabetics. A diabetic must not visit a hospital where chances of environmental pollution with pathogenic bacteria are high (Tuberculosis patients’ clinic) and one should also take precaution in meeting with a chronic lung patient. While travelling in crowded places (bus, train, cinema hall) optimum precautions must also be observed.

‘Vatik pratishyay’ Common cold

Vitiated vayu pollutes the dense mucus in the head, the nose and the sinuses thus producing common cold. Inflammation, excessive secretions, pain, running nose and fever are its important symptoms. The vata enters deep into the mucosa of the sinuses and produce pain in one half of the head (sinusitis and migrane). In modern science this is known as viral fever, too.



Leg problems mostly trouble a diabetic and also give rise to uncontrolled diabetes. Several studies confirm increase in blood glucose levels in patients with leg problems and the cause of this increase is multifactorial.

How do legs affect health of a diabetic?

The incidence of amputation (leg below knee) was as high as 12% of the total number of diabetics a few decades back. But today with better anti- diabetic therapy and antibiotics this figure has lowered down to just 1%. But because of increase in survival years in diabetes the chances of leg and foot problems have also increased. There are several reasons which contribute to adverse health of a diabetic’s leg. First of all the skin over the leg tissues does not remain healthy as it becomes rough and cut marks appear over it (as the first line of defence is broken).

The muscles namely calf and thigh muscles may become weak in uncontrolled diabetics (faulty nutrition is an important cause) and thus movement of the body may restrict (physical activity is seriously hampered) giving rise to high blood glucose levels. Thirdly the bones also do not remain as strong as they were before, and shooting pains may disrupt sound sleep.

Deadening of sensory nerves leads to increased probability of external injury. One also experiences distressing symptoms of peripheral neuritis. Decreased blood circulation in leg tissues gives rise to calf cramps during walk, non-healing ischemic ulcers and finally cutting of complete blood supply leads to gangrene. All the above pathologies have definite adverse effects on a diabetic’s health. A few important leg problems are as follows:

 ‘Pad shofh’ Swelling of the feet

 Vitiated vayu takes along with it vitiated raqtpitta and kapha through veins where it gets blocked and produces a large protrusion of dushyas (deformed dhatu) in between skin and maans (muscles). This is called pad shofh. It does not have tendency of pus in it. Mostly this shofh occurs as a result of kidney, heart or stomach diseases.

One property of vata is chanchalta (unsteadiness) and therefore pad shofh also appears and disappears depending upon the severity of dosha vitiation. Sometimes patient also develops sangyanash (anasthesia) and romharsh (hyperasthesia) off and on. Application of oil (tel abhyang and massage) over the affected skin is its main treatment. Mild swelling on the foot can also appear as a result of poor nutrition and prolonged standing.

‘Pad harsh’ Hyperasthesia

When vitiated vayu-kapha produce horripilation and tingling like sensations in the legs, it is called padharsh. In rainy season diabetics can easily develop this disease.

‘Pad dah’ Burning in feet

Vitiated vata-pitta-raqt produces burning feeling in the legs especially during walking. The patient complains of severe burning pain in sole of the feet while walking and sometimes even while sitting or lying down. Regarding pathogenesis of pad dah Acharya Bhavprakash says : “padyoh kurute daham pittasrikksahitoanilah” (Bhavprakash.M.K.V.Vy.162) i.e., vayu combines with pitta and raqt (blood) and thus produces burning in soles of the feet.

‘Pad shoonya’ Complete loss of sensations

Very severe doshas deaden the sensory nerves and the patient while walking feels as if he is walking on a mattress.

‘Pad sheet’ Coldness in feet

Blood flow is hampered in vata blood vessels hence skin below the knees specially remains cold.

‘Pad vidirnata’ Torn up skin

Due to vitiated vata the skin becomes torn up, which proves dearly in the long run. A diabetic should take all proper preventive measures, which help keep the skin of his legs healthy.

 ‘Vatik pad shoth’ Inflammation in the leg tissues

Vatadi doshas are highly vitiated due to faulty eating and living habits and on reaching the leg tissues give rise to symptoms like hyperasthesia or distorted sensations, tingling, pin pricking pain, and loss of sensations. The internal tissues are also affected adversely because of involvement of the autonomic nerves (part of vyan vata). The venous valves present in leg veins do not function normally leading to stagnation of impure blood in the leg tissues.

Vitiated vata affects motor nerve fibres, too, and as a result the strength of the leg muscles reduces. The reflex activity also suffers adversely because of involvement of the sensory nerve fibers of the autonomic nervous system (ANS), and as a result the patient can not retract his leg immediately even if he gets hurt by a thorn or pointed object. The loss of sensations also makes a person more prone to foot injuries and the chances of infection increase. Later on inflammation and pus formation take place and a foot ulcer which is difficult to heal may develop.

Diabetic vatik pad vrin’ Non-healing diabetic foot ulcer

Accumulated doshas beneath the skin vitiate the dhatus present over there and develop tendency of pus formation in them. Slowly and slowly it takes a form of wound. A small prick or cut in the skin is sufficient to precipitate this pathology very fast.

In vatik vrin initially pus accumulation does not occur (this is the difference from vidradhi in which pus is present from the very start). Instead a period of prolonged inflammation starts in which patient usually complains of local pain, swelling with tenderness and mild fever. In fact there is a big defect in diabetics that pus formation doesn’t take place normally as compared to non-diabetics. In fact pus is indicative of a battle fought between pathogens (foreign proteins as bacteria) and white blood cells of the body’s defence system (an uncontrolled diabetic usually lacks in good immunity).

In diabetes there is delayed and weak immunological response of an infection and moreover the lymphocytes which kill the bacteria suffer with low energy problem (deficiency of glycogen in lymphocytes). The combined effect of these two leads to delayed formation of pus (pus is a collection of dead bacteria, white blood cells and necrosed tissue debris).

After severe inflammatory stage the next stage is pad vrin (foot ulcer) in which the skin (line of defence) is uncovered (torn apart) and black coloured vrin containing scanty secretions develops (excess vayu dries the wound). On blocking of the blood flow imitable foot ulcers occur in which the dhatus in the legs dissolve/waste away producing poisonous secretions. The first major defect (full impact) of this vrin comes in the big toe, which soon spreads over other fingers, sole, ankle and even upto the knees.

When situation worsens then kakthan (gangrene) develops. The treatment is to separate affected part from rest of the healthy tissues. But if its poison mixes with the blood and then spreads all over the body, one develops visarp or septicemia which may prove fatal.

 ‘Agni visarp’ Septicemia

When visarp (bacteria and poisonous substances) enters in sensitive areas (heart, lung and brain covering membranes) thin vayu gets severely vitiated and causes painful inflammation in all affected organs. This generalized inflammatory reaction very often produces septicemic shock. The patient suffers from hiccups and breathlessness and the sleep is also destroyed. One becomes restless and lastly severe hypotension sets in which ultimately results in the death of patient. The palliative treatment at this stage is raqtmokshan and sanshaman chikitsa only.

‘Sheetjanya dhatu vinash’ Reynold’s disease

Acharya Charaka says : When blood vessels come in contact of very cold vayu then they contract and suddenly blood flow reduces markedly and this leads to romharsh (horripilation), coldness, and loss of sensations, swelling and even necrosis (dhatu vinash) may also occur. The defect lies in minute vatanaris.

 Calf cramps

 Acharya Bhavprakash says : “kaphavrito yada vayurdhamanishvev tishthati” (Bhavprakash.M.K.V.Vy.S168) i.e., when vata and kapha dosha vitiate big arteries of the leg (such as femoral artery) leaving the arterial wall hard like wood (inelastic) and when such patient walks for some time the increased need of pure blood in the leg tissues remains unfulfilled and therefore ischemic cramps appear in the calf muscles. As the problem increases the patient complains of even pain at rest which becomes unbearable while walking a few steps. The presence of above symptoms in diabetics indicate severe generalized disease in large peripheral artries such as coronary artery disease, vascular impotence and cerbro vascular disease, besides leg problems.

Note : Till now in this chapter efforts have been made to explain diabetic complications as per ayurvedic science. But the following text describes diabetic complications as per modern science.



Diabetes itself is not a disease, but it is that stage of the body in which due to various reasons proper metabolism of food does not take place that is, whatever one eats does not benefit him completely as it should have done. As a result the glucose and cholesterol levels in blood do not remain normal. Moreover there is profound deficiency of physical, mental and sexual energy. And due to several adverse reasons the organs and their functions do not remain normal and are badly affected giving rise to diabetic complications.

Acute Complications

There are a few complications which develop within a short period of time only and accordingly are named acute complications. Insulin dependent and non-insulin dependent both type of diabetics can develop these disorders though a few are more common in former whereas others in the latter group. One pecularity of these complications is that though they may be very severe (with high mortality) but are completely reversible if treated in time. The three important acute diabetic complications are: 1. Diabetic ketoacidosis; 2. Hyper osmolar (hyperglycemic) non-ketotic coma; and 3. Hypoglycemia.

Etio-pathogenesis of acute complications

Pathogenesis of acute complications is very simple. One can develop complications either due to hyperglycemia or hypoglycemia. Type 1 insulin-dependent and Type 2 non-insulin dependent both type of diabetics react in different ways while developing hyperglycemia. Type 1 patients develop ketoacidosis that is, high blood concentration of ketones. The stage at which the ketone bodies act as an alternative fuel of body cells is a very dangerous stage, as they are very toxic to neurons and especially may prove fatal to central nervous system (brain). This condition is termed as ketoacidotic coma.

Type 2 diabetics are spared from this most fatal complication. It is probably because at no point of time their insulin production comes to almost nil whereas complete insulin deficiency is a pre-requisite for developing ketoacidosis or ketotic coma. In previous decade above knowledge was used to differentiate type 1 from type 2 patients.

The procedure used is that insulin injection, which a patient is using from sometime is stopped altogether and a very close watch is kept on the patient’s blood glucose and urine ketone levels. As concentration of blood ketones becomes more than normal (indicating complete absence of insulin in the body) along with hyperglycemia the excess ketones start appearing in the body in the form of excretions like sweat, urine and breath and these can be tested in a laboratory. Not only this as ketones have fruity smell the urine and other excretions also smell like fruits. This is why one can easily recognize high blood ketones level by smelling the body or mouth odour (typical acidotic breath). Moreover the urine and sweat also smell like this.

If a patient is suffering from type 1 diabetes one usually develops ketosis within 2-3 days of stopping insulin injection. The blood glucose concentration also rises more than 350 mg/dL (>19 mmol/l). But type 2 diabetics rarely (1 in 10,000) develop ketosis even when their blood glucose concentration rises more than 600 mg/dL (>33 mmol/l.)

1. Diabetic ketoacidosis clinical features and summary of preventive measures and management

It is matter of great concern that in developing countries like India most of the cases come to know about type 1 diabetes only after suffering from ketoacidotic coma. Due to lack of facilities timely diagnosis of type 1 diabetes is not possible and most patients reach the doctor only when the disease has become complicated that is, ketoacidotic coma or septicemic (severe infection) shock.

Ketosis can develop at any age in type 1 diabetes. A few decades back, this disease was incurable but now with effective medicines 90% of the patients who reach before permanent brain damage (deep coma) are saved.

The essentialities of diabetic ketoacidosis are complete insulin deficiency coupled with absolute increase in the glucagon hormone blood level (in the hepatocytes excessive ketones are produced under the influence of ‘glucagon’ hormone).

Usually ketosis develops after cessation of insulin intake but may also result from physical such as infections, surgery, myocardial infarction or emotional stress (increased adrenalin secretion) as insulin requirement drastically increases and the amount of insulin which a patient was taking earlier becomes insufficient in new conditions. In both the above mentioned situations the blood glucagonlevel rises. Stress hormone adrenalin acts in two ways: first it stops any residual insulin secretion (left in a few type 1 patients only) and second it inhibits insulin induced glucose transport in the body tissues. Insulin deficiency, excess of glucagon and stress hormones lead to two critical effects:

1. Gluconeogenesis, leading to severe hyperglycemia which causes excessive osmotic diuresis (plasma volume depletion and dehydration are two characteristics of ketoacidosis).

2. Ketogenesis, initiation of ketogenic process and metabolic acidosis. In keto-acidotic state adipose tissues and liver both observe few changes. The first is increased formation of fatty acids from adipose tissues and subsequent increase in free fatty acid concentration in the blood and secondly over production of ketones. In situations like starvation or severely uncontrolled diabetes these fatty acids are used by the liver cells to produce ketones (after activation of hepatic oxidative machinery) that provide vital energy to all the other body cells (as glucose can not enter inside them without the help of insulin). And above reaction takes place under the influence of glucagon hormone only (the glucagon/insulin ratio also changes). Over production of ketones by the liver cells is the primary event in ketotic state.

Clinical features of ketosis

Ketosis includes early symptoms like anorexia, nausea, vomiting, and increased urination. Abdominal pain may or may not be present. If not treated in time altered consciousness or frank coma ensures. The signs of this pathology include Kussmaul’s respiration’(rapid respiration followed by a gap), signs of volume depletion, dehydration and shock, body temperature normal or below normal (fever indicates severe infection), rarely vascular collapse or renal shut down.

Metabolic abnormalities : It includes an electrolyte imbalance, initial rise in potassium and phosphorus followed by their deficiency. Serum magnesium and sodium also decrease. Hypertriglyceridemia (triglycerides in blood >400 mg/dL) and lipemia (increased fatty acids) are inevitably present. Prerenal azotemia (signs and symptoms of acute renal shut down) is a frequent finding. Plasma level of aceto-acetate, lactate and other acids contribute acidosis.

Differential diagnosis : It is simple in previously diagnosed type 1 diabetic. The problem arises when patient with no history of diabetes presents in acidosis. The differential diagnosis includes:

1.Lactic acidosis

2. Uremia

3. Alcoholic ketoacidosis

4. A few poisonings

Finding of urinary ketones indicate acidosis because of ketosis only. It is important to know that starvation for prolonged periods may itself lead to ketosis. After diabetes the most common cause of ketoacidosis is alcohol. And alcohol plus diabetes associated with ketoacidosis is a very big problem. However for the diagnosis of diabetic ketoacidosis two diseases have to be excluded:

1. Severe starvation

2. Alcoholic ketoacidosis.

The problem of diagnosis becomes manifolds in lean and thin younger diabetics who also drink alcohol.

Alcoholic ketoacidosis

It is commonly seen in chronic alcoholics. Normally it occurs within the period alcohol is taken (during drinking or a little later) but it can also occur even 24 h after taking alcohol. Ketosis (s.ketones N: 0.5-1.5 mg/dL) occurs more easily in starved alcoholics. Nausea and stomachache are its main but initial features. In more than 75% patients acute, subacute or chronic pancreatitis is also detected in ultrasound and serum amylase concentration is also high (N: 13-53 mmol/l) if pancreatic tissues are inflammed.

In most of the patients (of alcoholic ketoacidosis) blood glucose level remains <150 mg/dL (below diabetic range), in ~15% it is <50 mg/dL and in very few rarely >300 mg/dL. Plasma free fatty acid concentrations (N: <0.7 mmol/l) are almost equal to diabetic ketoacidosis (~2.9 mmol/l). The pathogenesis of ketoacidosis in these patients is two fold: 1.

Starvation activates liver and enhances ketogenesis and 2.It is not known yet why some alcoholics only mobilize free fatty acids excessively (while others do not) and later on these free fatty acids are utilized by the hepatocytes to produce ketones. In contrast to diabetic ketoacidosis, alcoholics recover very fast by giving I.V. glucose (thiamine should be added in intravenous fluids to prevent acute beri-beri ‘congestive heart failure’). Insulin is rarely required in these patients (as there is no persistent hyperglycemia).

Treatment of ketoacidosis

Intravenous fluids alone can not reverse diabetic ketoacidosis as it requires expertise treatment with insulin and some other drugs. Insulin is given as per two below described schedules:

In low-dose insulin schedules (8-10 units plain insulin intravenous every hour till blood glucose level comes to 150 mg/dL) 50-60 units are required to revert ketoacidosis. In patients with insulin resistance or patients not responding to low dose insulin regimen more drastic treatment is required such as 25-30 units/hour till blood glucose level touches normal.

Volume deficit (3-6 litres) is compensated by giving ‘isotonic saline’ or ‘ringer lactate’ through the intravenous route. As the condition improves 5% dextrose under cover of plain insulin (5-7 units each 500 mL) is infused keeping in mind the urine output and the fluid status of the body. Late cerebral oedema (swelling in brain tissues) especially in children may ensure if dehydration is not corrected fast. The suspicion of cerebral oedema gains importance when patient remains comatose or lapses into coma following reversal of acidosis.

Potassium supplement is necessary but not in initial 3-4 hours as serum K+ levels are already high. Reversal of acidosis and hyperglycemia are indications for K+ supplementations. This is because insulin causes shift of K+ into intracellular compartment leaving the interstitial fluid K+ deficient. The other important supportive treatment is use of sodium bicarbonate to antagonize acidosis (plasma ph should be maintained ~7.2). Two points should always be remembered while treating serious ketoacidosis as:

1. Despite normoglycemia insulin glucose infusion should be continued till all ketones are cleared from plasma.

2. Plasma ketones value by keto diastix are not sufficient to monitor ketosis as sticks measure only aceto-acetates and acetones whereas beta hydroxybutyrate estimation needs lab testing (total serum ketones N: 0.5-1.5 mg/dL).

A good treatment cures 90% patients of keto-acidosis. Rest 10% die because of several reasons. The most common are myocardial infarction and infections (pneumonia). Most of the children die from cerebral oedema. Poor prognostic signs are hypertension, azotemia, deep coma, respiratory distress, vascular thrombosis, and a rare fungal infection called ‘mucormycosis’.

As mentioned above ketoacidosis is not a feature of type 2 diabetes because complete stoppage of insulin secretion does not occur in these patients. Due to negligence in treatment or otherwise if blood glucose level increases too high, a condition called ‘hyper osmolar coma’ may ensure in non-insulin dependent diabetics.

2. Hyper osmolar coma non-ketotic hyperglycemic coma

As the name reflects it is a condition associated with uncontrolled forced diuresis (glucosuria). Due to sustained hyperglycemia and inability to drink sufficient water to keep up with urinary fluid losses there is always a chance to develop this disease. This usually happens in elderly type 2 patients who have contracted infection or developed ‘cerebral stroke’ along with sustained severe hyperglycemia. Hyper osmolar coma is also common in following patients:

1. Patients on dialysis.

2. High protein diet by tube feeding.

3. Use of osmotic agents such as mannitol for some reason (as raised intra cranial tension).

4. Patients on medicines like phenytoin sodium, steroids and diuretics.

Clinical presentation : As against ketotic coma no significant symptoms of this disorder occur which may compel a patient to consult physician and by the time full-blown picture develops it is too late to reverse brain damage.

The reason why only type 1 patients develop ketoacidosis and not type 2 is difficult to explain. Even the ketogenic mechanism of the liver is not stopped altogether in type 2 diabetics.

Type 2 diabetics seem to be resistant to ketoacidosis because they have some residual secretion of insulin. But an insulin dependent diabetic may develop hyperosmolar coma, too, if one is receiving insulin sufficient to prevent ketosis but not enough to control hyperglycemia (as it leads to increased osmotic diuresis, severe dehydration and hyper osmolar coma).

Central nervous system involvement and gram negative bacterial infection coupled with hyperglycemia, volume depletion and hyperosmolality leads to ‘hyperosmolar non-ketotic coma’. The plasma glucose concentrations are often very high >1000 mg/dL (twice that of common in type 1 patients of ketosis). Plasma urea and creatinine levels are also elevated. Mild acidosis because of lactic acid production rarely requires bicarbonate therapy. The mortality rate in hyper osmolar coma is very high >50%.

Treatment of non-ketotic hyper osmolar coma

It is treated with large amount of I.V. fluids (the deficiency is up to 10 litres which has to be compensated in short interval). Initially normal saline (2-3 liter) is infused with small plain insulin doses and as blood glucose level touches normal, 5% drip under insulin cover is advised. K+ supplements are needed early as compared to ketotic coma. Bicarbonates and antibiotics are given if required.

3. Hypoglycemia clinical features and summary of preventive measures and management

The word Glycemia refers to the level of glucose in blood. When we say Hypo, it means low level and Hyper, refers to a high level of glucose in the blood. Majority of diabetics recognize the symptom of hyperglycemia but are incapable of recognizing hypoglycemia. Usually hypoglycemic symptoms appear when blood glucose falls beyond 75 mg/dL but they may also appear at ~100 mg/dL if there is sudden fall of blood glucose. Recurrent hypoglycemia may result in chronic headache, impaired vision and memory loss.

(a) Symptoms of mild to moderate hypoglycemia “blood glucose level 50-75 mg/dL”

1. Headache, uneasiness and anxiety.

2. Cold sweat and pain in sole of the foot.

3. Palpitation (hearing heart beats through one’s ears) and tremors.

4. Physical unsteadiness and dizziness.

5. Hunger pains and empty feeling in the stomach.

6. Confusion and mental instability.

7. Experience of pricking like pins and needles sensation around lips.

Treatment : The treatment at this stage is eating some simple carbohydrate food as glucose, toffee or fruit juices.

(b) Symptoms of severe hypoglycemia “blood glucose level <50 mg/dL”

1. Clumsiness and letharginess.

2. Disturbed mood and inappropriate response.

3. Aggressive behaviour and irritability.

4. Convulsions-tonic and clonic generalized seizures.

5. Paralysis-complete or partial, temporary or permanent.

6. Semi coma or altered consciousness.

7. Coma or permanent brain damage (brain death).

Treatment : The treatment at this stage is urgent hospitalization, injection glucagon and intravenous glucose administration.

Important causes of hypoglycemia

1. Insufficient food and excess medications.

2. Inappropriate and unusual physical activity.

3. Attempt to achieve supernormal blood glucose level by crash diet.

4. Alcohol and missing meals thereafter.

5. Medicines for some other diseases with daily anti-diabetic dose.

Investigations in hypoglycemia : One should not delay treatment for the sake of investigations. Firstly take appropriate treatment even on suspicion of hypoglycemia and simultaneously go for any investigation.

Prevention of hypoglycemia

1. Don’t exercise empty stomach and excessively.

2. Never attempt whole day fasting.

In illnesses where food intake is reduced or one is having vomiting or diarrhoea, the usual dose of oral hypoglycemic agents is reduced except during infection (illness). Patients who are susceptible to develop hypoglycemia (as insulin users) must keep Glucagon Hypokit with them.

Caution : Children and old diabetics may not complain of hypoglycemic symptoms. In case of former it is because they are too little to complain and in latter because of the involvement of autonomic nervous system which normally functions as an early alarming system.


Complications which develop slowly in later years are called chronic complications. They are more serious and of much concern to a diabetic. This is because they slowly affect the body and patient doesn’t even come to know as initial symptoms of these disorders are usually absent or very mild.

Just as termites slowly eat up land and make the wood hollow and from looking at the surface everything looks pretty good similar situation occurs in a diabetic, too. He may even look obese but still be very deficient in power. By the time one knows of the disease it is too late and irreversible damage already takes place. These chronic complications usually occur after 10-15 years of developing of diabetes.

Pathogenesis of chronic complication of diabetes

Various types of chronic complication can occur in diabetes. Though chronic complications usually present 15-20 years later after developing of diabetes however in a few patients they can be premature, too. The mortality and morbidity in diabetes increases substantially because of them only. At a time a patient can suffer from one or more of the chronic complications.

Arteriosclerosis of the type seen in non-diabetics occurs more severely and earlier in diabetic subjects and the most probable cause seems to be glycosylation of lipoproteins. The deposition of glucose, lipids plus certain blood elements in inner layer of the arterial wall is the root cause of several serious complications. Peripheral deposits in the large arteries may also cause intermittent claudication, gangrene and in men vasculgenic impotence, too.

Surgical treatment of arteriosclerosis is often unsatisfactory because of the simultaneous presence of extensive disease of the small vessels. Silent myocardial infarction and cerebro-vascular accidents are a few serious but common problems. Heart failure without the disease of coronary arteries (ischemic heart disease) is a feature of ‘diabetic cardiomyopathy’ only.

Damage to the retina leading to blindness (no prodormal symptoms) is quite common in diabetics of the Indian subcontinent. Premature cataract, glaucoma and frequent change in eyesight are a few other problems of most of the diabetics.

Diabetic nephropathy ‘DN’ is a leading cause of morbidity and mortality in 50% of the type 1 patients. However type 2 patients are also victim of this dreaded complication in equal proportion. Diabetic neuropathy may affect any part of the nervous system with the possible exception of the brain. Though neuropathy is not a direct cause of death but a major cause of disability and distress. Severe pains (especially in night) shooting and piercing in nature, asthesias and hyperasthesias on one side of the body or complete numbness, loss of touch, pain and temperature sensations are the two extremes of diabetic neuropathy. Unawareness of hypoglycemic symptoms is the result of diabetic autonomic neuropathy (DAN).

Diabetic foot ulcer is a special problem of diabetics. Non-healing ulcers of the feet and the lower extremities may ultimately need amputation. Pregnancy in diabetics needs specialized care and treatment. Successful outcome of pregnancy depends upon several factors and one of them is good coordination between the doctor, the nurse and the patient besides strict normo-glycemia.

Infections occur more in diabetics than in non-diabetics. The three most specific infections which are characteristic of diabetes ‘diabetic sepsis’ are: Malignant otitis externa (Pseudomonas aeruginosa), Rhinocerebral mucormycosis (Mucor, Rhizopus and Absidia fungus) and Emphysematous cholecystitis (Clostridia species bacteria). These infections need specialized treatment and usually prove fatal. Infections of the skin, lungs, urinary tract, blood stream and bones are also common in diabetics.

‘Hyper-triglyceridemia’ is common in diabetes and is usually due to deficiency of active insulin. Improper disposal of low-density lipoproteins by the hepatocytes also contribute to ‘hyper-lipidemia’. Obesity is usually present in type 2 diabetics and is a major cause of diabetic complications.

Lipoatrophic diabetes, X-syndrome, Ataxia telangiectasia and a few other conditions can also be seen in diabetes. Insulin allergy is an uncommon complication, which may be present in a few diabetics who use bovine insulin. Severely allergic patients need insulin desensitization.

A variety of characteristic skin lesions such as ‘necrobiosis lipoidica diabeticorum’ a plaque like lesion usually on legs, scleredema, diabetic dermopathy, bullosis diabeticorum, fungal skin infections, vaginal fungal infection (monoliasis), lipoatrophy and lipodystrophies are a few more diabetic complications. Delayed wound healing and disorders of blood viscosity are also common in diabetics. Joint contractures and tight waxy skin over the dorsum of the hands are a few other complication of diabetes.

When more than 200 units of insulin per day are required to control hyperglycemia and prevent ketosis one is said to be suffering from insulin resistance. Hyperkalemia (high serum K+) associated with hyperglycemia is a frequent problem in diabetics and cardiac arrhythmias because of iatrogenic severe hyperkalemia (such as due to use of K+ sparing diuretics) do also occur.

What causes diabetes complications?

The reasons of chronic complications in diabetes have not been found out convincingly as yet but the reasons can be multi factorial also. The researches made till now agree that glucose with the help of a few enzymes reduces to sorbitol through ‘polyol pathway’ and sorbitol acts as poison for the body tissues and the cells. It has been experimented that sorbitol in nerve tissues helps reduce ‘myoinositol’ and activity of ATPase enzyme and these two abnormalities lead to nerve dysfunctioning. It has also been proved that if aldose reductase enzyme (which helps conversion of excess glucose into sorbitol) is taken care of with the help of medications complications like diabetic neuropathy can be prevented or treated effectively. Sorbitol toxin can be held responsible for developing of a few more complications in diabetes as: retinopathy, nephropathy, cataract, atherosclerosis and cardiomyopathy the use of the above drugs may help greatly in the management of chronic diabetic complications.

Glycated hemoglobin estimation in blood is a well known test performed to calculate average blood glucose level in last 4 months and glycosylation of hemoglobin is the mechanism behind it (in blood glucose reacts with hemoglobin on minute to minute basis and it shows a continuous reaction going on in between these two substances in all conditions, but as the plasma values of glucose remain high persistently more glucose reacts to Hb molecule and this makes the basis of GHb A1c estimation).

Similarly various body proteins on reacting with glucose can affect their structure as well as functioning. A few such common proteins are plasma albumin, lens protein, fibrin, collagen and lipoproteins which are present in the tissues spread all over the body such as connective tissue, joints, blood, skin, bones, and liver. Now it is proved beyond doubt that ‘glycosylation of proteins’is the second important mechanism, which helps in the development of chronic diabetic complications.

A few most important lipoproteins present in the blood as hdl ‘high density lipoprotein’, ldl ‘low density lipoprotein’ and vldl ‘very low density lipoprotein’ react with excess glucose and the result is increased glycosylation of lipoproteins which proves very harmful as described below:

1. Half-life of glycosylated LDL (bad cholesterol) increases.

2. Half-life of glycosylated HDL (good cholesterol) decreases.

3. Glycated collagen absorbs more of bad cholesterol from serum thus accelerating the damage in arteries (collagen is the main constituent of arterial walls) and dysfunctioing of glycated HDL seems to be the operating mechanism (described later).

4. Glycosylation of good cholesterol (HDL) plays important role in the pathogenesis of several chronic diabetic complications.

In fact collagen should remain in fluid ‘semi-viscous’ form for maintaining elasticity and texture of the arterial walls, ligaments and joint tissues or where ever collagen tissue is present. HDL cholesterol helps in keeping collagen in viscous form whereas LDL does its opposite. Once HDL and LDL cholesterol become glycated above properties change. Glycated HDL becomes less effective and the adverse properties of glycated LDL increase (it all results in loss of elasticity and smoothening properties of collagen tissues). The glycated collagen itself helps in increasing of adverse properties like less solubility and texture wise toughening. The most significant adverse effect of this process reflects upon the health status of arteries and joints. There is generalized hardening (loss of elasticity) and narrowing (causing obstruction in blood flow) of small and big all arteries supplying blood to vital organs as: heart, brain, nervous system, legs and eyes.

Apart from this some degenerative complications can be explained by the theory of glycosylation of proteins and hyperactive polyol pathway as: premature cataract, ageing, joint diseases, cardiomyopathies, skin lesions etc.

The kidney damage that is, diabetic nephropathy is clinically characterized by a steady and continuous decline in glomerular filtration rate (GFR), increasing albuminuria, hypertensionand lastly chronic renal failure ensures.

Many times diabetic nephropathy remains silent for very long periods (10-15 years) and this is the reason that microscopic lesions do not match with clinical condition of a patient (classical lesions may be present but no signs/symptoms of nephropathy). In fact during the initial years of diabetes the kidneys are hyperfunctioning making as much as 50% more urine as compared to normal state (osmotic diuresis in diabetes).

The next stage of nepropathy is microalbuminuria (urinary loss of albumin >30 mg/day but less than 300 mg/day, a normal person excretes nil to 30 mg albumin/day in urine) which can be detected in laboratory examinations (strips can detect albuminuria only when it is >550 mg/day) only.

There is a great dispute on the diagnosis of nephropathy based upon the finding of albumin in urine. In fact persistent leakage of albumin through the kidneys can be confirmed when at least 3-4 samples of urine in a span of 6 months detect albuminuria >20 µgm/h (>30 mg/day) and in this case the diagnosis of DN is almost confirmed. Practically albuminuria in range of >500 mg/day (2 or 3 readings) is sufficient for the diagnosis of DN.

Macroalbuminuria is said to occur when urinary losses touch the figure of >300 mg/day. Once the macroproteinuric phase begins there is steady deterioration in glomerular filtration rate, on an average about 1mL/min per month (that comes to around 10-12 mL/min in one year). As per this formula in 10 years the GFR will reduce from 130 mL/min to almost 00-10 mL/min only). The signs and symptoms of azotemia as: hiccough, nausea, vomiting, irritability, drowsiness, scanty urine and altered sensorium start appearing in the later stages of DN. Serum creatinine test allows assessment of the rate of deterioration in the kidney functions.

Does strict control on blood glucose levels help prevent chronic diabetic complications?

The question arises whether a strict control on the blood glucose and the lipid levels help preventing oneself from diabetic complications and whether uncontrolled levels of glucose, and cholesterol can be solely held responsible for developing and increasing of chronic diabetic complications? And why does it happen that in patients of almost similar diabetic status and environmental conditions only a few suffer from complications whereas others do not?

The answers to the above questions are not difficult to understand and are as follows:

Firstly one should know that there is a strong role of genetic factors in the pathogenesis of chronic diabetic complications and it is not only the metabolic abnormalities which are detrimental. If a diabetic has a family history of kidney disease or hypertension then he can develop nephropathy easily also. But it has also been seen that if kidney transplant has been done in a patient and his blood glucose level is uncontrolled then after a few years (3-5 years) characteristic lesions of DN also develop (it indicates metabolic origin of DN). But this problem does not arise in the patients in whom pancreas transplant is done along with kidney transplant.

A very interesting finding which confirms the role of metabolic derangement in pathogenesis of chronic complications is as follows: On transplanting of the kidney of a patient of diabetic nephropathy in a normal person, the characteristic lesions (basement membrane and arteriolar changes) of DN disappear in most of the cases. And this shows a very strong relationship between hyperglycemia and DN as a diseased kidney becomes totally normal after being transplanted in a non-diabetic.

Detailed study of the facts confirm that higher levels of blood glucose and a few other metabolites affect the kidneys. Besides this a few other risk factors are genetic susceptibility (very crucial), obesity, smoking and hypertension. Genetics also plays role in the prevention of DN as follows: It is the genetic protection only, which prevents diabetics from several chronic complications including DN despite having severe hyperglycemia for years together (there are genes obtained through parents which resist development of different diseases). Whereas in a few diabetics, diabetes is only diagnosed after developing of some chronic complications (as the privilege of genetic protection is not available to these diabetics).

Meticulous treatment of hyperglycemia by insulin showed reversal of some pathological lesions present in the basement membrane, decrease of albuminuria (improvement in renal functions), and alter motor nerve conduction velocity (improvement in nerve functions). However there is no firm evidence which shows that chronic complications can be totally prevented by near normalization of the blood glucose levels for long term.

But there is no confusion regarding the fact that good glycemic control overall helps a diabetic to live a normal healthy life, full of energy. Whether intensive therapy and that too by insulin injection upto the level of absolute glycemic control (often complicated with hypoglycemia) should be practiced or not is yet unclear because there are no proved added advantages of it.

Long-standing diabetics often lose the capability to recognize hypoglycemic symptoms just because of the involvement of autonomic nervous system. And therefore early recognition of symptoms such as nervousness, tremors, hunger and sweating is not possible and the patient may land up in a situation where the central nervous system functions are altered such as abnormal behaviour, loss of consciousness and even convulsions and finally coma. Therefore every attempt should be made to keep blood glucose levels well under control but not to the limit of hypoglycemia. This is because it is not wise to induce a condition that can cause immediate and irreversible damage to a patient in the unproven hope that late complications might be prevented by very strict control of diabetes.


The first name which gains most significance is diabetic nephropathy as it is irreversible and often proves fatal unless treated either in very early stages itself or by successful renal transplant. Diabetic neuropathy is another problem, which has no confirmed treatment even after so much advancement in allopathy. As far as arterial diseases are concerned some are easily and substantially treatable whereas others are not. The common chronic complications of diabetes are as follows:



When an adult man is unable to achieve a penile erection adequate for intercourse or loses the erection in between the intercourse itself, the patient is said to be suffering from erectile impotence. It can be purely psychological as well as organic (50-50% chances) and as compared to normal persons it is 3-4 times more common in diabetics.

Today the number of young patients is fast increasing not only because of excessive use of alcohol, drugs and smoking, but also due to a difficult arduous life style and mental tensions. In surveys 30% of patients reaching hospital with complaint of impotence are also found to be diabetic. It is more than coincidence that most of the heart attack patients also suffer from impotence, though satisfying sex is beneficial in optimally treated hypertensives and ischemic heart disease patients. Below mentioned simple observation helps a lot in determining cause of impotence. The erectile dysfunction can be of two types: 1. psychological and 2. organic.

Psychological impotence

No desire for sex at all is called lack of libido, hence there is no erection of penis. It may occur in deep sorrow, grief, and stress.

Organic impotence

The erection is improper and unsustained despite libido and there may be premature ejaculation, too. It occurs due to damage of nerves or blood vessels and imbalances in the male hormone blood level. A use of few drugs in treating other diseases in diabetics can also give rise to organic impotence. Four types of organic impotence-neurogenic, vasculogenic, hormonogenic and drug induced, are more common among most of the diabetics.

A few tests for differentiation in between the psychological and organic impotence are as follows:

1. Subjective tests by patient himself

If pain is not provoked by gentle pressure on testicles the chances of neurogenic impotence are more. Similarly if one is able to stop urinating in the middle and restart at will (indicative of healthy nerves), the chances of psychological impotence are more.

2. Nocturnal penile tumescence test

Normally, since birth till the eighth decade of life, erection occurs at least 3-4 times while sleeping. But in patients of organic impotence, at no stage does the erection of penis occur.

3. Stamp test

Patient sticks a round chain made of normal stamps at the base of his penis. If the chain is found broken in the morning it indicates a change in size of the penis, which rules out organic impotence.

4. Regiscan test

This portable machine records the degree and frequency of hardening of the penis. In patients of organic impotence the penis size does not change, even when patient is shown obscene pictures.

Pathogenesis of organic impotence

When a man gets desire (under hormonal influence), the message travels from the brain down to the spinal cord and autonomic nerves, to dilate the penile artery supplying blood to the penis so as to increase the blood circulation (15-20 times more blood than resting state accumulates in penile muscles). This results in the hardening and erection of the penis. Besides psychological causes the failure in erection can be because of damaged arteries and nerves, abnormal level of sex hormones and use of a few drugs.

Detailed past, present and family history all are important to pin point the cause of impotence. Chances of neurogenic impotence increase if some corroboratory evidence of nervous system disorder for example inabilities to perceive sensations, postural hypotension or fixed heart rate are found.

Intra-cavernous injection of Trimix, a three drug combination of papaverene, phentolamine and prostaglandinwith the help of a small needle leads to the erection of penis lasting for half an hour to 1 hour in all cases, except patients with damaged penile artery. This blockade in blood flow can be confirmed by Doppler ultrasound study.

Vasculogenic impotence is also a prelude to increased chances of future heart attack. Abnormal blood levels of sex and a few other hormones like Testosterone, FSH, LH, Prolectin, T3, and T4 may also lead to impotence. This hormonogenic impotence responds to hormone replacement therapy. A few drugs used for treating diseases such as hypertension may also cause impotence.


Counselling, good glycemic control and physique, positive thinking, nutritious diet, avoidance of tobacco, drugs and alcohol are all important. A few herbs and vitamin E (400 mg/day) act as sex tonic. Hormone replacement therapy (HRT) with testosterone/anabolic steroids is also helpful to some extent. Patient himself conducts ICI treatment under full hygienic conditions. The surgical treatment is penile artery transplant and prosthesis implant.


Incidence of DN

Approximately, one fourth of diabetics suffer from nephropathy after 20 years of diabetes. Modern equipments and investigations have made it possible to diagnose DN in the prodormal stages itself and with the help of genetic science advanced prediction of DN in an individual is also made possible (detection of patients with genetic susceptibility of DN through molecular biology).

Normal functioning of the kidneys

The functional unit of the kidney is a nephrone which has two important components: 1. The bowman’s capsule which consists basement membrane and afferent arteriole; and 2. The tubule which consists of a proximal and distal convoluted tubule, and a loop of henle.

The function of the bowman’s capsule is to filter blood which it does with the help of the basement membrane. It is a sieve like structure having two membranes overlying each other with pores in them. One cell lining is of the capillary wall and the other is of the epithelium of the glomerulus. Blood comes through the minute arteries and spreads over the membrane for filtration. The volume of filtrate is about 20% of the total blood flowing over the basement membrane, and the filtrate contains almost all the components of the plasma excluding proteins (blood – blood corpuscles = plasma; plasma – proteins = glomerular filtrate; glomerular filtrate – tubular reabsorption + tubular secretion = urine formed and excreted).

The most important function involved in urine formation is that of tubules where reabsorption and secretion of substances in and out of the tubular fluid, interstitial fluid and blood takes place. And after a complex process the urine is ultimately formed which carries all the impurities of the blood leaving optimum water and electrolytes in the body so as to prevent oneself from dehydration and electrolyte imbalance respectively. A total of around 180 litre of filtrate comes into the tubules in 24 hours and 99% of it is reabsorbed (reabsorption of water, electrolytes, glucose and amino acids) into the blood circulation only through these tubules.

As glomerular filtration rate (G.F.R.) is ~130 mL/min and 99% of this is reabsorbed in the tubules and the net urine production is only 1500 mL to 2 liter per day. But if tubular functions are hampered by 10% only the urine output may increase upto 20 liters per day.

Functions of Kidneys

1. Purification of the blood.

2. Homeostasis that is, maintain suitable environment for cell living and functioning.

3. Maintenance of base reserves in the human body.

4. Water and electrolyte (Na+, K+, Cl-) balance.

5. Activation of Vitamin D that is, 1-25 di-hydroxy-cholecalceferol.

6. Maintenance of optimum pH of the blood and the other body fluids.

Definition of DN

Clinically DN is characterized by a steady and continuous decline in glomerular filtration rate (GFR), increasing albuminuria and high blood pressure. Ultimately chronic renal failure ensures with typified lesions in the kidneys “Kimmelstiel and Wilson Syndrome”. The typical structural and functional changes in a diabetics kidney can be summarized as follows:

Morphological changes in kidneys

Slowly as kidneys fail, symptoms of uremia appear. Ultra sound studies reveal 25% increase in the kidney size initially. But as disease progresses the kidneys shrink and lastly become completely scarred (contracted kidneys).

Microscopic changes in kidneys

The kidney is made of matrix and glomeruli. In DN initially there is glomerular enlargement followed by diffuse mesangial expansion with or without nodule formation. Complete hyalinization of the glomeruli is suggestive of the end stage renal disease.

Functional changes in kidneys

In initial years the glomerular filtration rate increases. But as the disease progresses there is a steady decline in GFR. In advanced stages of the disease urine formation completely ceases.

Diabetic kidney under the electron microscope

When we examine the basement membrane under the electron microscope the diffuse changes are in the form of generalized widening and mesangial thickening (in the basement membrane). It denotes decrease in permeability of the filtering membrane as it becomes less porous and there is difficulty in diffusion of water and other substances into the filtrate. Gradually this difficulty increases and finally the basement membrane becomes totally non-permeable and there is no filtration at all.

The second defect in the basement membrane is formation of nodule like structures. Under microscope massive drop like structures (PAS positive) are found near the periphery of the glomerulus. This specific lesion is characteristic of a diabetic’s kidney (Kimmelstiel-Wilson lesion).

Not only this (apart from filteration membrane) the minute arteries supplying blood to the nephrones (afferent and efferent arterioles) also show obstruction in the blood flow as they are also found hyalinized. All these changes lead to occlusion of the glomeurli. The albumin and other proteins are also accumulated in glomerulus and tubules and thus increase the problem. The classical findings are hyalinization of glomerular arterioles and typical nodular glomerulosclerosis also called k.w.nodules.

Prediction of diabetic nephropathy

Diabetics with increased chances of DN (later in life) are as follows:

1. Diabetics with HLA A-2 genes.

2. Young hypertensives.

3. Positive family history of high BP or ischemic heart disease.

4. Diabetics in whom daily insulin requirement exceeds 150 units.

5. Old age and obese diabetics.

6. Persistent hyperglycemia and hyperlipidemia.

7. Diabetics with congenital disorders such as spina-bifida.

8. Smokers.

Clinical features of DN

Early stages are usually asymptomatic and only advanced investigations can diagnose this disease. However a few early symptoms such as fluctuating swelling on face and legs, weakness, fatigue, irritant behaviour, abnormal mental status, chronic headache and vertigo may be present. As disease advances urine formation decreases and following symptoms of uremia (chronic renal failure ‘CRF’) gradually appear.

1. Breathlessness.

2. Nausea, vomiting and hiccups.

3. Swelling of the whole body.

4. Semi-coma.

5. Coma.

Natural course of DN

It is characterized by progressive increase in urinary albumin excretion rate (UAER) and decrease in glomerular filtration rate (GFR). UAER <20 mg/min is insignificant. Micro albuminuria is said when UAER is between 20-200 mg/min and it denotes incipient DN (grade 1). UAER increases by 10% per year without treatment. Macro albuminuria that is, UAER >200 mg/min is a feature of grade 4 DN.

Albuminuria in nephrotic range (which is responsible for generalized anasarca) is a poor prognostic sign. If urine samples on three separate occasions in a span of 6 months show considerable excretion of albumin then DN is almost certain. Non-serious and transient causes of albuminuria are:

1. Sudden increase in blood glucose level.

2. Extra rich protein diet.

3. Prolonged starvation.

4. Excess labour.

5. Urinary tract infection.

GFR >140 mL/min is a feature of both uncontrolled hyperglycemia and grade 1 DN. The former condition immediately responds to blood glucose lowering drugs, as the GFR returns to normal and if kidneys are hypertrophied they too regain normal size. But in cases of grade 1 DN, increased GFR does not respond as rapidly to the above treatment. However GFR gradually reduces (10-12 mL/min/year) after initiation of grade 2 DN.

In absence of proper and timely treatment half of the patients die within 10 years. By proper treatment the rate of decline in GFR can be reduced to ~5 ml/min/year and the life expectancy increases by 2 times.

Overt nephropathy chronic renal failure

Annual incidence of overt DN is 1-4% and overall incidence of CRF is 20-25%. There is a peculiar phenomenon in timing of appearance of DN and that is, two peaks are observed, one after 16 years and the other after 32 years of diabetes. The sequence of events in DN is as follows:

* Hyperactive kidneys

* Micro albuminuria

* Incipient DN

* Macro albuminuria

* Overt DN

* End stage renal disease (ESRD)

Note: Hypertension is a constant feature of DN and both increase one another that is, high blood pressure (hypertension) increases DN and DN increases blood pressure.

Factors that influence/modulate the natural course of DN : The natural course of nephropathy is influenced by two group of risk factors as some of them are removable (or modifiable) whereas others are not.

The treatable factors are: hyperglycemia, hypertension, albuminuria, obesity and hyperlipidemia, smoking, and high protein intake. Whereas the untreatable factors are: age, sex, genetics and duration of diabetes. A short description of these factors is as follows:

Hyperglycemia: Two important observations can be made in regard to hyperglycemia and diabetic nephropathy and these are: a. Normoglycemics develop albuminuria much later in life as compared to hyperglycemics; b. Conversion from micro to macro albuminuric phase is faster in uncontrolled diabetics; and c. Optimum insulin therapy and complete normoglycemia may completely heal microscopic lesions of DN.

2. Hypertension: High BP is inevitable in DN as it occurs in all the patients. Normalization of blood pressure is an indicator of a good kidney status besides being a neccessity for healing DN. Normotensive diabetics never develop DN. At ESRD (end stage renal disease) almost all patients develop malignant hypertension and the prospects of survival dims.

3. Albuminuria: Disappearance of albuminuria strongly advocates that the treatment is correct besides being a sign of improved renal functions. But if it is left untreated the result is generalized anasarca (swelling) and CRF.

4. Obesity and hyperlipidemia: Many patients of DN also have the history of obesity but all obese diabetics do not develop DN. The two risk factors of DN that is, high BP and hyperglycemia are common among obese diabetics and therefore the chances of DN secondary to hypertension increase. Raised serum lipid values have unfavourable effect on the kidney functions, as they deteriorate very fast in obese patients.

5. Smoking: Only 7% non-smoker diabetics develop albuminuria as compared to 15% who smoke. Not only probability of DN increases but disease progression is also fast (60% more) in smokers despite treatment.

6. Protein intake: High protein diet (especially from animal sources) is injurious to the kidneys as it puts them under undue stress. The advantages of protein-restricted diet are beyond doubt in patients of DN. But is protein restriction enough to prevent DN and when should one start observing protein restriction so as to prevent this complication?

High-risk patients or patients with DN are recommended 20-25% (.6-.8 gm/kg of body weight) calories out of their total caloric requirement per day through proteins, and this much protein restriction brings desirable results in patients of DN.

7. Age, sex, genetics and duration of diabetes: These all are non modifiable risk factors. As age advances the chances of nephropathy increase and the outcome of treatment measures is also unfavourable. Some people are genetically more prone to develop kidney disorders. As the duration of diabetes increases the chances of nephropathy also increase and therefore a diabetic should take more precautions as he grows older.

Treatment of DN and renal replacement therapy (RRT)

Treatment of DN starts with screening of high-risk patients. It is far easy to treat a patient of micro albuminuric phase as compared to later stages (macro albuminuric or oliguric phase). The treatment varies as per the grade of DN. Salt and protein restricted diet, absolute normality in BP and reasonably good glycemic control bring desirable results. Physician plans a complete strategy of the treatment and alteration in an individual’s diet. Terminally ill patients require CRF supportive treatment, dialysis (5 years survival rate on hemo-dialysis is ~30%) and kidney transplant if possible.

I shall give you detailed information further in my blog relating to Diabetic Nephropathy i.e., Dn, measures of prevention of DN, management of Chronic Renal Failure i.e., CRF and Renal Replacement Therapy i.e., RRT.

Urinary Tract Infection ‘UTI’

Besides other causes, kidney failure also facilitates urinary tract infection and severe UTI does contribute to kidney failure. Hyperglycemia, dehydration, structural malformations and stones in the urinary tract are a few precipitating factors. Recurrent or multiple antibiotic resistant UTI is commonly seen in uncontrolled diabetics, especially females. The guidelines for preventing UTI are as follows:

1. Optimization of blood glucose levels.

2. Plenty of water intake to prevent dehydration in vomiting.

3. Low salt diet.

4. Timely surgical intervention of calculus, structural deformity or polycystic kidney.

5. Routine urine examination including pH and microscopic examination should be made.

6. In cases of UTI full antibiotic course (after culture/sensitivity) is necessary.


Just as electricity, voice, and picture are transmitted through wires; similarly different messages come and go through the brain to the various body organs with the help of peripheral nerves only. Neurological functions are auto controlled and are of two types: Voluntary and Involuntary. Sensory and motor nerves conduct voluntary functions whereas autonomic nerves control involuntary functions.

The anatomical and physiological changes taking place in uncontrolled diabetics leading to functional disturbances are termed as diabetic neuropathies. The defects in nerves are probably because of restricted blood flow in vasa nervosa (capillaries supplying blood to nerve) and subsequent ischemic injury to the nerve fibres. Approximately 15% diabetics after 5 years of diabetes and 50% after completing 50 years of age suffer with diabetic neuropathy. Hyperglycemia and food irregularities are the two modifiable risk factors. Diabetic neuropathy may affect any part of the nervous system except perhaps the brain tissues. A few clinically important neuropathies, their names, causes, symptoms and preventive measures are described below.

Peripheral poly-neuropathy “distal sensory-motor neuropathy”

This is the commonest neuropathy in diabetics and therefore its prevalence rate is also high ~70%. Symptoms, which are characteristically bilateral, include numbness, paraesthesia and severe hyperaesthesia and are limited to big toe, fingers and sole of the feet, but occasionally may extend to the hands and thighs.

Deep seated and severe lancinating pain, often worse at night, is a distinguishing feature. Fortunately extreme pain syndromes are self-limiting and they subside by themselves. But heart attack, foot injury, burn etc., may go unnoticed and prove dearly. Involvement of proprioceptive nerve fibers may lead to abnormalities of gait and charcot’s joint “a painful deformity of knee joint”.


Involvement of a single large nerve with unique feature of spontaneous reversibility, though less common but still a significant condition in poorly controlled diabetics. Sudden wrist drop, foot drop or paralysis of third, fourth

and sixth cranial nerve may occur. Wasting of the leg muscles along with pain and numbness, due to damage of sciatic or femoral nerve is characteristic of mono-neuropathy.

Mono-neuropathy multiplex

In this disease two or more nerves simultaneously get affected and the symptoms start with severe pain in back and hips. If the condition worsens, pain radiates towards knees and feet but hands are spared or rarely affected. There is no diminution in touch, pain or temperature sensations. Thinning and weakening of leg muscles are common. Cure of mono-neuropathy multiplex by itself is a natural phenomenon. Frequent recurrences pose some difficulties in future.

Proximal neuropathy

Identical peripheral nerves on both sides of the body are affected simultaneously. Unfortunately there are no alarming symptoms of this disease and over a period of years touch and pain sensations are lost permanently. And the muscles supplied by the motor unit of these affected nerves develop wasting (disuse atrophy). Thighs, hips, back and shoulders are the most affected parts of the human body.

Diabetic autonomic neuropathy ‘DAN’

As all internal organs are governed by autonomic nerves and any dysfunction in these nerves present with a variety of symptoms pertaining to the concerned organ or system. The foremost victim of DAN is gastro-intestinal tract. The symptoms are difficulty in swallowing, delayed gastric emptying, constipation unresponsive to laxatives and diabetic diarrhoea, which often worsens at night.

Malfunctioning of pupillary muscles leads to problems such as glare in sunshine and inability to see at night. Postural hypotension often presenting with frank syncope and collapse on standing is the hallmark of DAN. Cardio-respiratory arrest, cardiac arrhythmias and sudden death are a few conditions related with DAN. Urinary system dysfunctions include autonomous bladder with its characteristic feature of overflow incontinence, erectile impotence and retrograde ejaculation. Dysfunctions of the secretory glands are common in DAN as lachrymal gland dysfunction results in nil or excess tears.

Investigations in diabetic neuropathy : To ascertain the nature and extent of diabetic neuropathy a patient himself, can perform these investigations.

1. Damage in the sensory units of nerves is confirmed by testing touch, temperature and pain sensations with the help of a sterilized pin.

2. Damage of the motor units is confirmed by careful examination of muscles thickness for any muscle wasting.

3. An increase in the heart rate of <5/min from lying to standing posture suggests DAN.

4. A five minutes deep breathing exercise is unable to increase the heart rate by >10/min in patients of DAN.

5. Constant running for 10 minutes does not increase HR by >30/min in patients of DAN.

6. Val-salva manoeuvre (a simple method to do this manoeuvre is blowing a football bladder) for 15 seconds increases the heart rate by 15% in normal subjects whereas in patients of DAN it is not so.

Prevention of diabetic neuropathy : It is rightly said, “Prevention is better than Cure”. It is more so in DN because dead nerves can not regenerate. Neuropathies are closely related to long-term glycemic control as chronically uncontrolled diabetics easily develop them. A balanced diet, yoga, pranayama and morning walk help in prevention. Smoking, alcohol and drugs increase the risk of neuropathy by 300%.

Treatment of diabetic neuropathy : It is non-predictive and often unsatisfactory, too. Pain unresponsive to usual analgesics and non-steroidal anti-inflammatory drugs often responds to codeine, phenytoin sodium or a combination of amitriptyline and fluphenazine. Multi vitamin B1, B6, B12 injection, methcobal and vitamin E 400 mg/day may salvage some damage in the nerve tissues. Oral myoinositol stops formation of sorbitole in the nerve tissues and may cure the disease. Sarpgandha, ashwagandha and shatavar are the herbs effective in neuropathies. Diabetic diarrhoea responds to difenoxalate and atropine or loperamide. Hypotension is best treated by elevating the head-end during sleep. Sudden standing from lying posture should be avoided and one should use full-length elastic stockings to avoid syncope. 9-a-fluorohydrocortisone is useful in some of the patients of postural hypotension.

Cerebro-Vascular Accident (CVA) ‘Stroke Syndrome’

A stroke is defined as a neurological injury occurring as a result of hemorrhage, thrombus, atheroma or embolism in arteries carrying blood to the brain, giving rise to several types of paralytic syndromes. There are no prodormal symptoms of stroke as it occurs spontaneously without any alarming sign or symptom. However recurrent TIA, transient ischemic attacks may occur before a massive stroke.

When a small thrombo-embolus blocks the blood flow in a small cerebral artery giving rise to mild symptoms of paralysis it may constitute TIA. The symptoms like aphonia, aphagia or paresis in hand, finger or arm, remain only for less than 24 hours as the blood clots are removed by the protective mechanism of the body and the patient becomes absolutely normal within a day. When this process is repeated several times one becomes more susceptible for a big stroke. Hence it can be said that TIA is indicative of a big problem that is, incipient stroke ahead.

In most cases, the abrupt, dramatic onset of focal neurologic symptoms corresponding to a lesion in specific vascular territory such as hemiperisis and aphasia, suggest blockade in the middle cerebral artery territory of the dominant hemisphere. A sudden disturbance in a visual field suggests the territory of the posterior cerebral artery and a pure motor hemiperisis suggests a small ‘lacunar’ infarct in the internal capsule supplied by small penetrating branches of middle cerebral artery.

Cerebro-vascular accident is the third leading cause of death in diabetics after heart diseases and cancer. Diabetics have 200% more chances of stroke as compared to a normal person. This risk increases manifolds if diabetes is complicated with hyperlipidemia, hypertension and smoking. Insulin circulating in increasing amount in obese and insulin resistant diabetics provokes arteriosclerosis (atheroma and thrombus formation). Some times the pathology starts at a remote site, as it occurs when an embolus from the heart or extra cranial circulation lodges in an intracranial vessel, obstructing blood flow. The chances of post-stroke survival and recovery depend upon several factors as specialized treatment and care is necessary.

Apart from neuropathies and stroke syndrome, dementia, forgetfulness and inability to concentrate are some other problems. Intellect does not seem to be adversely affected by diabetes as well-controlled IDDM patients, usually children, behave and act more intelligently and maturely.



The eyes of the heart can view the inner beauty of a human, but to see and appreciate God’s wonderful creations, hale and hearty eyes are required. Diabetes may lead to partial or complete blindness, which can be reversible or irreversible, too. Diabetes contributes heavily to blindness.

Common eye complications in diabetes

1. Retinopathy, 2. Cataract, 3. Change in eyesight frequently and 4. Glaucoma


The retina, the backmost portion of the eye, behaves like a screen on which images are formed. It consists of rods and cones besides optic nerve, capillaries and connective tissue. Rods are for differentiating black and white, and cones for visualizing the different colours. The level of glycemic control, duration of diabetes, age and associated diseases like nephropathy and high BP influence the appearance of retinopathy. Retinopathic lesions are divided into two categories, simple (background) and proliferative.

In simple retinopathy, firstly the permeability of capillaries increases and thereafter substantial occlusion of capillaries takes place. On progression of disease, aneurysm formation takes place (because of narrowed lumen the pressure inside these capillaries increase and moreover the arterial walls are also weak and a combination of these two leads to aneurysm formation). And these aneurysms bleed on slightest application of force such as hypertensive crisis, forceful coughing, heavy weight lifting, 100 metres race etc.

Inner hemorrhages in the retina are dot or flame shaped and more serious pre-retinal hemorrhages are characteristically boat shaped. The body’s defence mechanism successfully removes these small hemorrhages but repeated attacks prove very harmful. Leaking of proteins and lipids from the damaged capillaries into retinal tissues form the basis of hard exudates as exudates are the avascular portions of the retina. Other vascular lesions are atrio-venous shunts accompanied with endothelial cell lining proliferation.

Proliferative retinopathy is diagnosed by cotton wool exudates, new vessel formation (hypoxia induced) and scarring on the retina. The exudates are imperfused areas surrounded by dilated capillaries on retina. A sudden increase in their number represents an ominous sign as it leads to retinal detachment (nerve cell layer separates from rest of the retinal tissues).

The hemorrhages extending into the vitreous fluid (vitreous hemorrhages) also pose a threat of sudden vision loss. The seriousness of retinopathy depends upon the acuteness of symptoms and extent of retinal involvement and if more than three-fourth part of the retina is having pathological changes, then it is indicative of the ‘Eye at risk’. Complete protection of retinopathy is impossible because there are no early warning symptoms and only regular (yearly) eye check-up can detect this disease in early stages.

The investigations in retinopathy includes: Fundus examination every year after 5 years of diabetes may reveal swelling, hemorrhages or exudates on retina. Retinal angiography and fundus photography are advanced investigations.

Prevention and treatment of retinopathy includes: Timely detection and laser photocoagulation may save eyesight as it also prevents and treats retinal detachment. But by delaying treatment 75% mild retinopathy patients reach the stage of “eye at risk” within 5 years of commencement of retinopathy and soon become blind.

Premature cataract

Cataract is described as an opacity in eye lens, whereas its original colour is black. In fact greying of lens is a normal ageing process but in diabetics it hastens. And as the colour of the lens becomes white, the light rays can not travel through it (loss of refractory power), and making of image on the retina becomes difficult, and a person becomes blind though temporarily (blindness is removed after lens extraction and implantation of artificial intra ocular lens). But non-removal of the diseased lens in time (over mature lens) may lead to permanent blindness. In diabetes cataract may appear even at 5 years of age. Medical records of Kanti Diabetic Care Centre, Rishikesh reveal 50% diabetics suffer from this complication within 20 years of diabetes.

Frequent changes in power of the lens

When there is sudden increase or decrease in the blood glucose level, the shape of the lens doesn’t remain static as it imbibes more water and swells giving rise to blurred vision.

The eye lens is a crystalline structure made up of a protein called crystallin. It is a biconvex structure which is colourless and transparent. Lens is covered with a layer of connective tissues (lens capsule) and is supported by suspensory ligaments. As we adjust focal length to get a clear picture from a camera similarly there is provision in the eye lens to adjust its focal length and it is called accomodation power (achieved by change in convexity) of the lens. But if this change in shape of the lens becomes abnormal only due to change in the osmolarity of the fluid (glucose concentration) in which the lens remains suspended one will complain of blurred vision and if there are frequent changes in the blood glucose, it will necessitate repeated change in the specs.


An increase in amount of the fluid inside the eye, giving rise to increased intra-ocular pressure is indicative of glaucoma. Its most prominent symptoms are severe headache, reddening of the eye, increased lacrimation and decreased vision. The raised ocular pressure if not corrected in time gives rise to pressure atrophy of optic nerve and permanent blindness. Glaucoma is more common, produces more damage and is more difficult to treat in diabetics as compared to normal persons. Simultaneously the chances of bacterial infection in surgery are more in diabetics.

The prevention and treatment of glaucoma is possible by good glycemic control, Vitamin A, and no smoking. The treatment is irectomy (a small nick is made in the iris to release raised intra-ocular pressure). Sudden block of the retinal artery by a blood clot can also cause blindness.



The two important pathologies, which affect the foot health adversely in diabetes, are damages in the nerves and blood vessels of the legs. In previous times, up to 20% such patients, required partial or complete amputation below the knees (otherwise gangrene or septicemia sets in). Today with better treatment and facilities, this percentage has come down considerably. But as longevity has increased with better drugs, the incidence of neuropathic foot (old age favours neuropathy) has also increased. The three important type of leg problems in diabetics are as follows:

Neuropathic foot

It is only with the help of nerves that we feel sensation like tightness of the shoes, hotness, pain due to pricking of sharp objects or an injury. The sensory informations (pain, temperature) travel from the leg tissues to the brain for proper analysis and then appropriate impulses are produced and transmitted to the concerned organ to behave in a manner suitable to overcome the problem, if any, and prevent further damage.

In this manner the nerves act as an emergency warning system. In long standing diabetes these sensations are either diminished or completely lost. But in a few diabetics distressing symptoms of neuritis as sensation of pricking of pins and needles, burning pain and numbness, hyperasthesia, itching and severe nocturnal pain in the thighs and calf muscles also appear.

Vasculopathic foot

As a part of generalized atherosclerosis, the big and small both type of arteries develop blockade. As a result, the blood supply to the tissues reducec and fixes, too. In this situation the patient complains of calf cramps while walking or running short distances. Inappropriate nourishment due to reduced blood supply leads to drying and cracking of the skin, thinning of bone density and muscles, too. More severe obstruction in the blood flow leads to ischemic gangrene. Commonly big toe is the first victim. As condition worsens slowly other fingers, foot and lastly leg below the knee joint develop gangrene and need amputation.

The symptoms of poor blood supply can be indicated by 4 C’s: cramps, coldness, colour change and cuts: 1. Cramps in the calf muscles occur initially during exercise but later on even on rest; 2. Cold legs, because of poor blood circulation skin over the legs no longer remains warm but becomes cold; 3. Colour of the skin over feet also changes. Initially it is red (when there is acute obstruction), then reddish blue and finally blackish blue, suggesting severing of blood supply; and 4. Cuts on skin, as it becomes thin, dry and fragile. Thus, a patient can himself examine his legs for any vascular lesion by analyzing above signs and symptoms.

Non-healing diabetic foot ulcer

Even a trivial foot injury may convert into a non-healing wound. The reasons are two fold that is, absence of the sensations in feet leads to repeated insult of the wound and poor blood supply hampers early healing. As infections are common in uncontrolled diabetics, the situation of the wound worsens and in such conditions infected foot ulcer necessitates surgery or amputation.

Infected gangrene, if not treated in time, may lead to even death (septicemia). The problem of uncontrolled diabetes also increases if patient becomes less mobile because of foot problems.

Prevention of foot ulcer

No effort should be spared to keep the feet healthy. The helpful measures:

1. Daily cleaning of the legs and feet with soap and luke warm water.

2. Dry the feet and spaces in between the fingers and toes.

3. The nails should be properly cut.

4. Use mustard oil to keep the skin soft.

5. Never walk bare feet.

6. Wash your socks daily.

7. The footwear should be comfortable and examined for any cracks or pebbles.

8. Do regular leg exercises.

9. Balanced diet.

10. No smoking.

Leg exercises :One should walk half an hour early in the morning as it is an exercise which suits almost every person young or aged, with or without diabetic complications. Healthy persons may also practice brisk walking. Patients with foot ulcer or severe leg problems can sit on a chair and do upper extremity exercise in morning hours as it has almost similar effect as morning walk. Early morning exercise in an open place helps in oxygenation of muscles, as myoglobin content of the muscles react directly with oxygen and thus re-energize leg muscles.



Normally pathogens are unable to gain entry into the healthy body tissues and even if they do so the body’s defence mechanism finishes them. But in diabetes due to weakening of defence mechanism, infections occur easily and recurrent infections may even be the presenting feature of diabetes. Ketosis, common in children, usually develops secondary to infections. It is also seen that almost all patients of diabetic coma also suffer from infections. A few decades back 25% of diabetics met untimely death only because of serious infections. But today effective antibiotics have brought this figure down to 1%. The body defence mechanism protects the body as follows:

The first line of defence: It is the skin and mucous lining of internal and external organs as former protects all external organs and the latter the internal organs. No pathogen can enter the body without breaking this defence.

The second line of defence: It is provided by the white blood corpuscles as they put resistance whenever pathogens get entry into the tissues through the broken skin or mucus lining. The energy required by WBCs to fight with bacteria or fungi comes from the glycogen stored in them.

The third line of defence: It is the immune system. Pathogens (antigen) entered in the blood circulation provoke formation of antibodies. It is the T-lymphocytes in the blood, which synthesize antibodies. These antibodies fight fiercely with the pathogens and eradicate infection. The other beauty of this system is its uniqueness in recognizing the same pathogens in the future and evoke severe response against them, without any delay.

It is necessary to understand food metabolism during infections as the patient’s diet usually decreases but this does not permit decrease in anti-diabetic dose of the medicine. It is because despite taking food containing lesser calorie, the blood glucose level does not fall, instead it increases dramatically due to increased production of anti-insulin hormones that is, Adrenocorticotrophin, Cortisone, Glucagon, Epinephrine and Nor-epinephrine hormones. And as these hormones promote neo-glucogenesis, the blood glucose level increases and more insulin is required by the patient. To meet out this increased demand more anti-diabetic medicine (or insulin) is required. Patient himself with the help of self-monitoring of blood glucose level best regulates the dose of anti-diabetic medications.

Simultaneously, one is encouraged to take food items such as khichri, pudding, porridge, fruit juice, milk, honey and other things, because it meets increased energy requirement of white blood corpuscles ‘WBCs’ and thus prevents depletion of glycogen in them. Starvation or insulin deficiency during infection may give rise to ketotic and non-ketotic coma in type 1 and type 2 diabetics respectively.

Two golden rules to remember during infection are : 1. Despite decreased food intake anti-diabetic dose is increased; and 2. A patient must learn the utilization of self monitoring blood glucose ‘SMBG’ for anti-diabetic dose regulation.


These are those infections, which either can appear in diabetics only or have a characteristic clinical presentation, significantly different from non-diabetics. Important infections, their causative pathogens, symptoms and easy preventive measures are described below.

Urinary tract infection ‘UTI’

The two kidneys, two ureters, one urinary bladder and one urethra constitute the urinary system. In females the vagina is an additional organ. Bacteria and fungus are two common pathogens for UTI. If a patient is not passing glucose in the urine, the chances of infection are lesser as glucose is used by pathogens for nutrition and development. UTI is more common in diabetic women and paralytic patients. The symptoms include severe burning pain in urination, passing of red or brown coloured urine, fever with chills and excessive thirst. Urine examination reveals glucose, albumin, red blood corpuscles, epithelial casts and pus cells. Normoglycemia and appropriate antibiotic course is the treatment of choice.

Respiratory tract infection ‘RTI’

It is of two types : 1. Upper respiratory tract infection; and 2. Lower respiratory tract infection. The former includes pharyngitis (inflammation of the posterior wall of the oral cavity), tonsilitis, laryngitis and the latter includes bronchitis, pneumonitis, pleurisy and tuberculosis of the lungs. Close contact with an already infected person leads to severe infections such as pulmonary tuberculosis and pleurisy. Preventing oneself from the atmosphere where chances of infection are more such as hospitals, and visiting a person suffering with RTI, and quitting of smoking are the essential preventing measures.

Skin and mucous membrane infections

Most common bacteria are streptococcus, staphylococcus and pseudomonas giving rise to boils, carbuncles, non-healing foot ulcers, infected gangrene and injection abscesses. Oral thrush (candidisis) and vaginal monaliasis are a few fungal infection.

Malignant otitis externa and media

It is a bacterial infection of the external ear by pseudomonas bacteria. Its symptoms are: fever, severe earache, swelling in surrounding tissues, pus discharge and inflammation. The word malignant does not indicate malignancy but the clinical course and outcome of the treatment is such that this disease behaves exactly as malignancy (ultimately takes the life of the patient). The involvement of cranial nerves (paralysis) is a bad prognostic sign. To eradicate pseudomonal infection extensive antibiotic treatment is required. One requires 6-8 weeks courses of effective antibiotics (culture/senstivity proved) such as tricarcillin and amikacin combination and if need arises surgical incision of the infected tissue.


This fatal fungal infection of the nose presents with facial swelling, severe pain, nasal bleeding and pus discharge. Without early treatment with amphoteracin-B, gangrene sets in and patient dies.

Emphysematous cholysistysis

This gall bladder infection with clostridium bacteria is present in men only (why it is so is unclear). Initially there is swelling of the gall bladder and lack of treatment causes its rupture and death.

Viral infection

Virus stay in passive state in the atmosphere. Their reproduction and activity is possible within living body cells only. Common viral infections are Herpes joster, Herpes opthamicus and Influenza.

Various researches point out to the fact that if a diabetic has an optimum, effective and long term control on his blood glucose level then the probability of infections are the same as that of in a normal person.



Out of every three, two female diabetics face complications during pregnancy. This puts the life of the baby and mother both in danger. The true incidence of diabetes in pregnant population is estimated around 0.5-1.0%. A pregnant lady can suffer with two types of diabetes: 1. Diabetes developing during pregnancy; and 2. Those having diabetes before pregnancy. The maternal and foetal risk are same in both and are as follows:

Risk to the mother

* Septicemia

* ‘Hyper’ and ‘Hypo’ glycemia

* Ketoacidosis

* Pre-eclampsia and Eclampsia

* Habitual abortion

* Shock

Risk to the foetus

* Still birth

* Macrosomy

* Microsomy

* Infections

* Congenital malformations

During the first trimester insulin requirement decreases as the foetus utilizes glucose obtained through the mother’s blood (35-40 g/day). Diabetic mother who fasts for a few hours may develop ‘accelerated hypoglycemia’ that is, a serious lowering of blood glucose level (~50 mg/dl) after fasting of 2-3 h. And it is only because of this phenomenon that after a brief overnight fast, a pregnant woman may demonstrate raised plasma ketones which are otherwise characteristic of prolonged starvation in non-pregnant individuals. It is thought that these responses are needed to spare circulating maternal glucose for the demands of the foetus.

In the second trimester of pregnancy, insulin requirement doubles, as peripheral insulin resistance increases due to increased production of ‘human placental lactogen hormone or HPL’.

In the third trimester, as more nutrition is required, the insulin requirement of the mother further increases.

Though the pancreas of the foetus of 11 weeks produces insulin, but this foetal insulin does not help in utilization of glucose or other nutrients. In fact it acts as a catalyst (growth factor) for the development of the foetal organs.

Neither the maternal nor the foetal insulin traverses the placenta so each individual has separate insulin compartments. The nutrients essential for development of the foetus are transported from maternal circulation to foetal circulation by several mechanisms as : 1. Glucose crosses the placenta and reaches the foetus by facilitated diffusion; 2. Amino acids (protein) are transferred by an active process; and 3. Lipids levels are almost similar on both sides and the rate is determined by the maternal plasma lipid levels.

A brief account of the maternal and foetal complications is as follows:

Macrosomy : Hyperglycemia in the mother causes hyperglycemia in foetus also, resulting in increased secretion of foetal insulin which stimulates the development of baby organs like the heart, liver, lungs, kidneys, and spleen, excepting the brain and nerve cells. These babies are born fat, round faced with red skin, long and matured hair and small neck.

Polyhydromnios : It is a rare but serious complication in the last trimester of pregnancy. Death of the foetus is inevitable and only strict diabetic control by a pregnant woman can prevent it but no cure is possible.

Pre-eclampsia and eclampsia : High BP and constant presence of albumin in the urine suggest eclampsia and chances of arterial blockage increase. Partial obstruction of placental artery leads to microsomy that is, under developed foetal organs. But near total stoppage of blood circulation only leads to foetal death. Maternal mortality is also high in eclampsia. Early recognition and normalization of BP are two essentialities. Albuminuria indicates above pathology in early stages.

Congenital malformations : Babies born to diabetic mothers have 3-4 times more chances of developing congenital defects of the cardio-vascular, skeletal, and nervous system and it is only the hyperglycemia in the first trimester of pregnancy, which has a detrimental effect. Offsprings of diabetic fathers do not show this tendency confirming that these congenital malformations are not primarily of genetic origin (but because of physiological abnormalities).

Acute respiratory distress syndrome : The lungs of a foetus remain in inactive form and soon after birth, a secretion called surfactant is released in the baby’s lung and only after that the lungs can expand. In premature babies due to deficiency of surfactant, lung expansion becomes defective and due to this free flow of air into the lungs does not take place and the result is severe respiratory symptoms that is, acute respiratory distress syndrome ‘ARDS’ and death.

Hypoglycemia in newborns : This usually develops in over-developed babies as they have more quantity of foetal insulin, which is activated after birth, and causes rapid metabolism of stored glucose and glycogen.

Infection : Mainly infections of the urinary tract and vagina are common in pregnancy and a new born baby, too, can catch these infections at the time of the birth.


It is identified by the oral glucose tolerance test ‘OGTT’ during pregnancy only (2h blood glucose> 200 mg/dL). It is a mild form of diabetes which has few symptoms and mostly can be controlled by balanced diet and exercise. Only about 3-4% patients of GDM require insulin, which is also stopped after pregnancy, as blood glucose level automatically touches normal reading.

‘GDM’ can be because of firstly, increased insulin resistance during pregnancy and secondly, extra insulin is required for the development of the foetus which is not available. As the increased demand of insulin is not meted out in these pregnant women due to several reasons, the result is reflected into an abnormality in utilizing extra load of carbohydrates in diet and subsequently gestational diabetes. The maternal and foetal complications in these women are the same as that in females who were diabetic since beginning.

Measures for successful pregnancy : It includes detailed history taking as: number of conceptions, abortions and kids, under-developed child or still birth, and complicated pregnancy. Thorough physical and per vaginal examination, timely investigations as: hemoglobin, vdrl, blood group, blood urea and lipid profile, besides long standing normoglycemia (normal GHb A1c) and healthy diabetic complication free body are all necessary.

Four step care is recommended for normal child birth

1.Insulin injection: Oral hypoglycemic agents are stopped altogether and under physician’s supervision, the patient herself starts taking insulin injection, two or three months prior to conception in previously known diabetics. Insulin dose may need curtailment in the first trimester of pregnancy, but during second and third trimester insulin doses increase. A few gestational diabetics may also require insulin treatment though most of them are cured by diet and exercise.

2. Balanced diet: During pregnancy itself the daily caloric requirement (normal total caloric requirement per day of a female is: body weight in kilogram X 34) of a female increases two folds, approximately fifty times of the body weight in Kg. Out of the total caloric intake 40-45% should be from carbohydrates, 20-25% from proteins and remaining 15-20% from fats, in food. An increase in the body weight of the mother by 3-4, 5-6 and 4-5 Kg during first, second and third trimester respectively, is a healthy sign.

3.Self monitoring blood glucose (smbg): Self monitoring of blood glucose levels and insulin dose titration with its help is necessary as sharp control of fasting (70-100 mg/dL) and PP 2 h blood glucose levels (110-140 mg/dL) are mandatory. Such type of strict control can not be achieved by urine glucose analysis alone.

4. Timely check-ups: These include weekly urinary albumin, fortnightly blood pressure and ultrasound checkup at the beginning of each trimester. Planning the time and mode of delivery (as in macrosomy delivery at full term and in microsomy and placental ishcemia pre-mature delivery through caesarian section is indicated) is also essential for safe pregnancy. Normal delivery is possible in uncomplicated cases.



The heart starts functioning in the womb of the mother and keeps on working day and night for years together. The heart is a hollow structure made up of specialized muscles, conduction and connective tissues, nerve fibres and blood vessels, and its outer covering, the pericardium.

The unidirectional blood flow is maintained with the help of valves inside four chambers of the heart, as firstly the blood enters into right atrium through inferior and superior vena cava, then to the right ventricle through tricuspid valve, then to the lungs through pulmonary valve, then from the lungs to left atrium through semilunar valves, then to the left ventricle through mitral valve and finally into the aorta through aortic valve. This heart cycle repeats at least 60 times/min in a healthy person, circulating approximately 5 litres of blood during 1 minute.

Important cardiac complications

* Premature ishemic heart disease

* Myocardial infarction or heart attack

* Heart failure

* Heart block

* Congenital heart disease

* Postural hypotension

Premature ishemic heart disease angina pectori

It is one of the most important complication of diabetes. The word premature signifies that one may develop angina pectoris at a comparatively young age that is, <40 years because usually this disease is more prevalent in elderly people (non-diabetics). Its pathogenesis and clinical features are as follows:

As a part of generalized arteriosclerosis, the coronary vessels, too, suffer narrowing and clogging in uncontrolled diabetes. It results in a decreased blood supply to the heart musculature giving rise to the symptoms. Unfortunately, referred pain of angina pectoris in middle of the chest radiating to both hands (medial aspect), jaw and back, is not a presenting feature of ischemic heart disease in chronic diabetics, because nerves carrying pain sensation from the heart tissues to the brain are almost inactive. Therefore, instead of typical angina symptom like referred chest pain, one only complains of discomfort in breathing and heaviness on chest, palpitation and cold sweat while walking or doing some physical labour.

As the disease progresses the symptoms appear at rest also. If a diabetic experiences such symptoms or even if suspicion arises he must pay utmost importance and consult a cardiologist.

Myocardial infarction ‘M.I.’

Ischemic heart disease is one of the most common and lethal 0complications of diabetes having the highest morbidity and mortality. It may also lead to a very dangerous situation called ‘silent myocardial infarction’ (a patient does not come to know that he has suffered a heart attack and by the time diagnosis is made it is already too late), which has only 20-30% survival rate of 5 years. As is evident in the research study by Dr. Deepak Joshi entitled “Clinical features, risk factors and platelet functions (PF-3 release) in myocardial infarction in young” it has become clear that diabetes is the most critical risk factor after smoking in young M.I. patients.

As typical anginal pain is absent in most of the chronic diabetics hence symptoms like discomfort in breathing, heaviness on chest, palpitation, cold sweat, breathlessness, and syncope, should not be overlooked as they may be indicative of heart attack (M.I.) in absence of excruciating chest pain. It is advisable to consult a physician even on suspicion of the above symptoms.

Sometimes in the absence of timely treatment (mostly because of delayed diagnosis) or due to massive heart attack many patients develop cardiogenic shock and die soon. Hyperglycemia, hyperlipidemia, obesity, hypertension and smoking are a few more modifiable risk factors of M.I. Whereas positive family history for ischemic heart disease (IHD) is an unmodifiable risk factor.

Sudden coronary artery spasm in an otherwise healthy diabetic causing M.I. is related with smoking habits most of the times. Thus smokers are more prone to develop sudden heart attack only because of coronary artery spasm without any prodormal symptoms of IHD.

Heart failure

The heart is a pumping station, which propels the impure blood into lungs and the pure blood into systemic circulation. The force necessary for pumping is provided by the healthy heart musculature but as it weakens in a few diabetics, the symptoms of stagnated blood circulation such as extreme tiredness and early fatigue, palpitation, dyspnoea on exertion, rest or nocturnal dyspnoea (dysponea while sleeping or lying down), swelling first on feet and face and then total body swelling and cardio-respiratory failure appear.

The reasons of weakening of the cardiac muscles in diabetics are two fold. Firstly, diastolic hypertension necessitates more forceful propulsion of the blood from heart because then only proper blood supply to the body organs can be maintained. This increased load causes compensatory hypertrophy (hypertensive cardiomegaly) of cardiac muscles and as these muscles increase in size extra quantity of pure blood is required for nourishment, which is not possible through already diseased (clogged) coronary arteries and the net result is weakness in cardiac muscles giving rise to left ventricular dysfunction and later on heart failure. Secondly, slow decaying and losening strength of the cardiac muscles due to deposition of poison like substances (amyloid, sorbitol) results in a clinical condition called “dilated cardiomyopathy”. As a result heart dilates and ejection fraction drops markedly giving rise to “congestive heart failure” (CHF) which is preventable and treatable in earlier stages only.

Heart block

Defective production and conduction of the heart beat both lead to ineffective contraction of the heart and irregularities in the heart rate. As a group of specialized cardiac muscles S.A.Node “sino atrial node having self excitatory quality” is the pacemaker of the heart which can be adversely affected in diabetes several diseased states may take place such as bradycardia (heart rate < 50/min), tachycardia (heart rate >150/min), arrythmias (irregular heart rate) and other rate and rhythm disorders (heart blocks).

After production in SA node, the impulses travel into the cadiac muscles only through specialized conduction tissues called Purkinje’s fibres or the ‘bundle of his’ (after passing through atrio ventricular or AV node). Again these are specialized cardiac muscles and if the conduction is defective and there is blockade or delay in conduction of the impulse (which is necessary for contraction of cardiac muscles to produce heart beat) it will give rise to low ventricular rate which may cause dysponea and heart failure depending upon the severity of the disease that is, right, left or complete heart block (the treatment is permanent pacemaker).

A clinical condition called “sick sinus syndrome” presents with alternating tachycardia and bradycardia along with vertigo and syncope. All the above complications are 200% more common in diabetics as compared to normal person. Smoking increases the number of these patients.

Congenital heart malformations

Ventricular Septal Defect i.e., VSD and Atrial Septal Defect i.e., ASD are congenital diseases more prevalent in offsprings of diabetic mothers. Partial prevention is possible by observing normoglycemia during pregnancy.

Postural hypotension

Severe vertigo and syncope while standing from lying down posture are due to sudden and severe fall in blood pressure. The life becomes unproductive and physical activity practically comes to nil. The diabetic autonomic neuropathy is the the main cause of this disease.


These include monthly monitoring of blood pressure and serum glucose levels, half yearly electrocardiogram and serum lipid profile, besides TMT, Holter’s monitoring, coronary angiography, thallium scan, echo-cardiography and coloured doppler as required.

Prevention and treatment

The prevention of several cardiac complications is not a difficult job provided the patient follows the given guidelines:

* No active or passive smoking

* Low fat, high fibre and nutritious diet

*Physical and yogic exercises

* Tension free living


Streptokinase and urokinase enzymes do the chemical lysis of the clot and thereby open any recent obstruction in coronary vessels due to thrombo-embolism which is mostly present in cases of acute myocardial infarction. The only drawback with this mode of treatment is that the patient must reach the physician within 4 h of developing MI because then only myocardial salvage is possible (cutting of blood supply for more than 4 h bring irreversible damage to cardiac muscles and reopening of the vessel after that interval will be of no use). Blockade in coronary arteries developing over a period of years needs physical intervention for re-vascularization in the form of balloon angioplasty or bypass surgery. Patients undergoing this expensive and difficult treatment must take measures to prevent restinosis. Avoidance of smoking in every form is a necessary requisite for success of any re-vascularization plan.

Natural coronary artery bypass

This is a very exciting phenomenon of developing collateral blood supply to the myocardium through neo-vascularization. Aerobics, yoga and pranayama along with medicinal control of ischemia provide sufficient time to generate alternate blood supply channels called collaterals’ and thus natural coronary artery bypass takes place which is far better, safe and inexpensive.

Obesity, hyper cholestremia and heart diseases

A few patients who have an inherited tendency of producing increased amount of cholesterol in the body (it is produced by hepatocytes) should curtail cholesterol rich food items in their diet and egg, meat, milk, and other eatable substances should be consumed only after consulting their physician. But it is also necessary to consume free fats in diet. The important reasons are as below:

1. These are essential ingredients of the cell membrane and also provide stability to it.

2. Fats are necessary to produce energy in the human body.

3. A few biochemicals as enzymes, lipoproteins, and lubricating fluids are made of fats only.

4. The reserve fuel of the body is stored as fats.

5. Fat insulates the human body and internal organs too.

When polyunsaturated fat is ‘hydrogenated’ a component called “trans” gets attachment to fat molecule and then fat becomes saturated (as dalda ghee) and if used in increased amount may harm human body. It is not only the saturated fats which may harm a person, but the unsaturated fats if consumed in more than required amount produce several disorders in the human body (adverse effects on defence system of the human body and decreased immunity).

It is only the defence mechanism of the body which protects a person from contagious diseases, cancers or tumors. All type of fats lead to obesity and obesity contributes in the pathogenesis of hypertension, arterial diseases and a couple of other problems besides diabetes. In nut shell we can say that optimum amount of all fats are necessary for remaining healthy.


Vedotpattik Chikitsa




All Popular Treatment Pathies

It is needless to say that the doctor fraternity of the world agrees that treatment and possible cure of diabetes is a difficult job and it is correct, too, to some extent. But the views of our learned Professors of the most ancient “vedotpatiik medical science- Ayurveda” on diabetes treatments should also be known to the world. These sacred writings are originally in Sanskrit language. The English translation of a few worth mentioning quotes has been given here as they are encouraging and may infuse a new ray of hope in the disheartened patients.

* The God of medicine, Dhanvantari says: “madhumehitvamapannam bhishagmih parivarjitam; yogenanen matiman pramehin mupacharet” (SushrutSamhita.Cikitsa.L.13.S3) that is, a diabetic who has been given up by a physician as incurable should take treatment from the mixtures prescribed byHim.

* Acharya Sushruta says : “upyujya tulamevam girijadmritopamat; vapurvanbalopeto madhumehvivarjitah” (S.Ci.L.13.12) that is, taking a concoction of pure salsaradigan herbs and grinded pure shilajitu strengthens the body and diabetes, too, keeps going.

* Acharya Charaka says : “vyayamyogervivideh pragarehrudwartaneh snanjalavsekeh” (CharakSamhita.Cikitsa.L.6.S50) that is, a pramehi (pre-diabetic) should do extra exercise because it keeps one away from prameha (however a lean patient is advised to keep away from exercise).

* Acharya Sushruta says : “ete panch yogah sarvmehanampahantaro vyakhyatah” (SushrutSamhita.Cikitsa.L.11.S.8) that is, the mentioned five yogs (herbo-minerals) cure all types of pre-diabetes. Rishi Charaka adds : “kshaudren yuktamathva haridram pibedrasenamalkiphalanam” (C.Ci.L.6.26) that is, all of these yogs should also contain embelica myrobalan juice, turmeric and honey.

* God Punnarvasu says :“ch prameha purvarupam kriti yatra drishyate kinchichapyadhikam mutram tam pramehhinamadidyot” that is, in prodormal stages all pramehas are sukh sadhya (easy to cure). He further adds : “sarv ev pramehastu kalenapratikurvatah madhumehatvamayanti tadaasadhya bhavanti hi” that is, all types of prameha if not attended to in the first stage convert to asadhya madhumeha (Charaka samhita).

* Regarding the use of honey in diabetes Acharya Charaka says : “nanadravyatamaktwacch yogavahi param madhu” that is, the sweet ras of honey is vidhey in pramehas because it is yogvahi (a substance which develops properties of the medicine in which it is mixed) and Acharya Sushruta also advocates the use of honey in all anti-diabetic formulations (SushrutSamhita.Cikitsa.L.11.S9).


The highlighted features of a great science like ayurveda and naturotherapy are: the medical principles based upon the Dosha-Dhatu-Malas theory of treating diseases through purification and pacification of vitiated body humours; methods of curing heterogeneity of the body tissues; a great emphasis on preventive measures at every step of the disease; lessons preaching diet as the best medicine of diabetes; measures which treat not only the physical but the eternal body, too; description of a healthy life style (din-charya and ratri-charya); a vast knowledge of curing properties of herbs and other substances; and moreover a vast approach towards diagnosis making and treatment measures. Ayurvedic science preaches that one should do his own practical research, too, towards finding the answers pertaining to treatment of complicated issues in diseases like diabetes. And vedotpattik chikitsa intends to provide the basic rules of the diseases, its prevention and treatments.

Note : The glucose in the blood is the most powerful stimulant for insulin secretion from the pancreas. As the blood glucose concentration rises, the signal from the brain travels to the pancreatic cells to increase insulin secretion. It happens in all healthy as well as most of the diabetic persons (~75%). In other words we can say that the best medicine for increasing blood levels of natural insulin is glucose itself. And because of this reason only most of the type 2 diabetics usually have increased serum insulin level (yet they are diabetic). Now if most of the diabetics have hyperinsulinemia then why does one get diabetes? Briefly it is due to the reason given in the following lines.

For an initial 10-15 years the insulin production of a type 2 diabetics remains almost normal and in many cases even more than normal but due to lack of proper activation and utilization, a significant amount of insulin does not serve its purpose, hence is wasted. It leads to less reduction of the blood glucose levels and as hyperglycemia persists, the pancreas is stimulated more strongly and the result is excess production of insulin. But slowly, the sensitizing capability of glucose (stimulation of b-cells) decreases. In other words we can say the b-cells become less responsive to glucose and therefore even on maximal stimulation they do not secrete insulin and this leads to decrease in insulin production.

As beta-cells have to function more to produce excess amount of insulin partially due to decrease in tissue response towards insulin action (peripheral insulin resistance significantly present in type 2 diabetes) and partly because of increased requirement in situations like overweight, stress, infections or myocardial infarction; the secretory failure sets in after a long period (beta-cells exhaust and thus insulin production decreases markedly). But if tissue responsiveness towards insulin can be normalized and a person takes care and prevents himself from those situations which overburden the pancreas, then automatically he can be cured.


A detailed description regarding nidan (diagnosis) and bhedaatmak nidan (differential diagnosis) is already present in the book. But briefly it can be concluded that symptomatic deterioration and presence of sweet urine over a long period (persistent glucosuria) are strongly suggestive of madhumeha (diabetes mellitus) demanding proper treatment.

In modern times, a slight modification can be made in the diagnosis procedure and that is, if after careful investigations blood glucose level 2h PP comes more than 200 mg/dL on at least two different occasions with clinical features (signs and symptoms) of diabetes in the patient then a diagnosis of diabetes can be made and necessary treatments should be instituted.

Introduction of ayur-diabetalogy

The foremost solid and written information regarding diabetes is in Ayurveda as the existence of this disease from the very start of present human civilization has been proved in ancient medical literature. Later on Unani (300 B.C.), Chinese (250 B.C.), Tibetan, Homeopathy, Biochemic and other medical books also described this disease prominently. Modern medicine (western and allopathic), whose father is Hippocrates, has also given serious weightage to this disease and its treatments.

Historical aspect of relevance in ‘diabetic treatments’

Treatment of diabetes mellitus has amply been described by all the medical therapies of ancient as well as present times. An extensive description of the disease process is present in the vedas especially in the atharveda (the other three vedas are: samveda, yajurveda and rigveda).

Thereafter, as civilisations developed several beneficial as well as knowledgeable facts were added to diabetic treatments. Treatment by ayurveda is even more important because it is this science only which deals with hit ayu, ahit ayu, sukh ayu and dukh ayu and tells about the methods of increasing ayushya ayu and decreasing anayushya ayu as also said by Acharya Charaka : “hitahitam sukham dukh mayustasya hitahitam” (C.Su.L.1.41). The treatment of a diabetic with the above aim in mind is only possible by the vedic treatment as nidan (diagnosis), hetu (cause), samprapti (pathogenesis), rupa (prodormal symptoms), upadrava (complications), and chikitsa sutras (code of cures) of pre-diabetes and diabetes are all well described in it.

Modern system of treatment has given one important contribution in diabetes treatment in the form of insulin by injection (human insulin which is produced outside the human body with the help of genetic technology). Plants also contain insulin called p-insulin. In the previous days high retention enema ‘asthapan vasti’ with extract of anti-diabetic plants was used to treat these patients but with uncertain results. About one century ago there was no predictable and reliable treatment for insulin dependent type 1 diabetics.

Pre-requisite for successful diabetes treatment

While treating of diabetes ‘patience’ is one most important factor both on the part of the patient as well as the physician. A patient should give sufficient time to both medicinal as well as extra-medicinal measures for getting the desired results as normal blood glucose level and optimum body weight. If one does not observe patience then unnecessary and frequent changes made in food, exercise and medicines can on the contrary prove harmful, too.

Methodology of successful ayurvedic diabetic treatment

In reality treatment starts from prevention only for which necessary instructions have been mentioned throughout this book. If our society is educated regarding this disease even partially and interested in gaining knowledge regarding aarogyata (total health) then definitely 50% cases of diabetes can be avoided. Sedentary, hectic and haphazard din-charya and ratri-charya (life style), laziness, irregularities in diet, and several more avoidable reasons are all proving disastrous as they are the biggest risk factors of diabetes today. This shows that in majority of patients this disease is not destined to happen but is due to those causes which can be cured (modifiable risk factors). Sushruta has also named this disease as : “ahitahaarjoapathyanimmittah” (SushrutSamhita.Cikitsa.L.11.S3) meaning diabetes developing due to wrong eating and improper living style.

Once the blood glucose level rises then efforts to decrease it by the use of strong medicines or lowering down of food intake is totally undesirable. On the contrary if there is no serious complication or any other necessity (as ketoacidosis, infection, surgery, pregnancy) then efforts to decrease blood glucose level very fast prove not only useless but harmful also in the near future. Thus what is required is a correct knowledge of diabetes and patience.

There are several reasons due to which even in a healthy person the blood and urine glucose levels increase temporarily (as alimentary glycosuria, renal glycosuria, drug induced hyperglycemia, glucose intolerance, and stress diabetes). There is no established investigation to date that can diagnose that the increase in blood and urine glucose levels is due to diabetes only. It is the symptoms only which greatly help in this matter. Hence if a patient keeps patience and repeats his testing in short intervals of time then only he is benefitted all the more.

In case of mild to moderate hyperglycemia, if medicines are given for lowering of the blood glucose level (despite more insulin in the blood of most of the diabetics) then firstly the pancreas become habituated to them and secondly strong medicines have some side effects also.

Homeopathy and western medicine specially consider this disease as neurogenic that is, the brain plays a main role in development of this disease. The pancreas produces insulin according to instructions from the brain and on the basis of glucose, fatty and amino acids from food which reach the blood. Hence due to various reasons if instructions from the brain are disturbed then insulin production from the pancreas is reduced and the result is high blood glucose level. Opposed/contrary mental state is capable of increasing blood glucose levels in several ways for example, it increases production of stress hormone epinephrine and does not allow a person to eat properly or exercise properly. This implies that both suitable mental states and efficient medicines capable of removing adverse mental effects are essential for eliminating this disease.

Sushruta says : “madhumehitvamapannam bhishagmih parivarjitam; yogenanen matiman pramehin mupacharet” (S.Ci.L13.3) i.e., pre-diabetes can be cured by a few yogs of herbo-mineral drugs. In fact these are the patients whose tissues/dhatus have been destroyed (majority of patients of developing nations belong to this category only). Removal in heterogeneity of the body tissues and nutrient molecules results in curing of this problem.

In Biochemic medicine also for treatment of diabetes those salts are used which nourish the brain cells primarily. In Tibetan and Unani systems of medicine, too, like ayurveda purification of all humours (vitiated elements) in the body is considered essential. Chinese medicine lays stress on normalization of yin and yang elements in the body (yin implies light whereas yang refers to heavy) and as a result generation of normal energy ‘chi’ required by the body.

Like many diseases become incurable after reaching a certain stage but are curable if they are timely treated similar is the case with diabetes, which is curable upto a certain stage only. This stage in which timely treatment cures the disease was recognized by ayurveda and given the name prameha. Sushruta has also mentioned that ‘incurable diabetes’ can be made ‘curable’ by use of certain medicines. Rishi Charaka names shilajit as sure treatment for diabetes and its complications as he says : “na soasti rogo bhuvi sadhyaroopah shilahvayam yam na jayet prasahya” (CharakSamhita.Cikitsa.L.3.65).

Western medicine, too, has mentioned that timely treatment of repeated infections, malnutrition and hormonal diseases prevents and treats diabetes successfully. By removing of hyperlipedemia and obesity in 15-20% diabetics this disease can be cured altogether. Patients suffering from X-syndrome (diabetes + ischemic heart disease) are cured by regulating life style and eating habits.

Prior to successful treatment of diabetes it should be well understood that only a very few percentage of patients are there who are totally deficient in insulin secreting cells (ketoacidosis prone diabetes). In majority of non-ketosis prone diabetics (about 80%), the pancreas secretes insulin and at no stage, even after several years, does it decrease to that extent that a patient could reach ketoacidotic stage. And because of this reason only type 2 diabetics are ketosis resistant ‘a complication which develops only when natural insulin production becomes almost nil’.

The fact is that most diabetics have live b-cells but unfortunately insulin is not being produced in the human body. In this situation it is advisable to use only those medicines which strengthen the pancreas and remove dysfunctioning and inactivity in the b-cells and thereby increase the secretion of insulin from b-cells. Regarding the food of a diabetic, Charaka points out : “tachh nityam prayunjeet swasthyam yenanuvertate; ajjatanama vikaranamunutapattikaram ch yat” (CharakSamhita.Sutra.L.5.S13) i.e., a nutritive food has full preventive capabilities ‘prophylactic’ besides treatment through phyto-chemicals, and alkaloids.

The subject of choosing the method of treatment is a little difficult and needs one’s command over diabetes because sometimes one can be treated well only through light measures but at times more harsh measures including combination therapy may be required. Ayurveda says that the treatment measures which most satisfy the patient (as he also feels happy and symptom free) and suit him should be the correct pathy which one should continue. Rishi Charaka further says : “yabhih kriyabhirjayante shareere dhatavah samah; sa chikitsa vikaranam karma tadbhishjam smritam.” (CharakSamhita.Sutra.L.16.34) i.e., the activities (medicinal and extra-medicinal) which may be able to keep the dhatus (body tissues) in normal amount, and prevent and treat complications should constitute a correct pathy.

A patient who knows his limits, follows a regular life style, and takes proper diet and medicines, always remains healthy. Several patients treated like this are completely cured and many others are greatly benefitted. Regarding treatment Acharya Sushruta warns : “doshaghnamaglanikaranvikari viparyaye” (SushrutSamhita.Sutra.L.34.23). This means the treatment which pacifies one disease, but side by side invites other complications is not correct.

Out of all known treatments there is none, which can cure diabetes hundred percent, but a certain percentage of patients are definitely cured. The experience of the author is that medicine of this disease exists in nature as in different foods, herbs, air, sun, water, salts, positive thinking, physical and mental exercises, hence it is essential that the patient makes maximum use of all natural means around him and becomes capable of understanding the importance of each measure himself. By following this line of treatment he will certainly benefit himself.

For treatment of diabetes medicines are being used since thousands of years. These medicines are taken orally and they cure or control the disease. Besides oral medication treatment of diabetes is also done by giving medicine by injection (in modern times), nasal spray (nasya) and enema (vasti) containing anti-diabetic herbs through the rectum (especially in old days).

It is now almost 50 years since insulin was discovered but no other method of injecting the appropriate amount of insulin has yet been discovered. Insulin is a protein and if given orally it breaks down by digestive enzymes in the stomach and like other proteins gets converted to amino acid molecules and is of no use in reducing of blood glucose levels. Nasal spray and enema can make insulin enter the body but their quantity can not be precisely decided (as sometimes more and at other times less medicine is absorbed through the mucus membrane).

Scientists today are trying to discover an instrument through which insulin can be sent inside the body through the holes present on the skin (jet injector) so that use of injection is no longer required. Oral allopathic medicines play a main role in normalizing of blood glucose level and to some extent they cure it also (peripheral insulin resistance) but mostly they are used for fast lowering of the blood glucose levels.

On the contrary use of herbs and other natural products help in removing the irregularities present in the body tissues and discrepancies in bio-chemical reactions as their use removes the root causes of the disease. Herbal drugs are harmless in all conditions whether one is having sub-clinical diabetes or overt diabetes, he is not harmed by these medications. Hence if abnormalities are present in the body humours or tissues they will be cured and even if they are not present the medicine shall have no negative effect on the body.

Aarogyata: Health is precious for everyone hence constant determination and efforts to preserve and conserve it give aarogyata (long healthy life). Ayurveda has defined aarogyata as : A person whose doshas, agni, malas and dhatus are in equilibrium and the body works normally as it should; moreover the body, sense organs and mind remain happy, then such a person is called healthy. Learned Rishi Sushruta says: A person with a very obese body or lean body is not ideal; a medium sized person is ideal (SushrutSamhita.Cikitsa.L.11.S3).

For successful treatment nature has laid down a few simple but very effective rules. Recognition of these boons and faithfully following them is the prime requirement for aarogyata. Natural methods have benefits beyond imagination. They fill the patient’s mind with the positive thinking that diabetes is not difficult to treat and even with the help of very light medicines one can stay healthy. Also unlike normal persons these patients prove very useful for the family, society and country because of several other qualities besides discipline.

Symptoms of a good physician : A diabetic patient himself should know the symptoms of an efficient physician before starting his treatment. Our ancestors also advice : “yogmasam tu yo vidyadeshkaloppaditam; purusham purusham vikshaya sa gyeyo bhishguttamah” (CharakSamhita.Sutra.L.1.S124) i.e., an excellent physician is one who knows and prescribes medicines to a patient after examining and testing him thoroughly.

Properties of a good medicine : Bhavprakash says regarding the qualities of a drug : “pratyakshlakshanphalah prasiddhashrach svabhavatah; naushadhirhetubhirvidwanparikshet kadachan.” (Bhavprakash.P.K.M.P.5.259).This means the medicine which has been proved effective (karya siddha) without side effects should be used by a physician even if all its properties as ras, guna etc., are not completely known.

Our Maharshis state“yasya deshasya yo jantustajam tasyoshadham hitam”. It implies that the medicines and herbs of only that place are beneficial to a human being of which he is a native. Like for an Indian, the ahaar-vihar and aushad of his own country only are more beneficial. The allopathic medicines made for Europe and other such cold countries although very beneficial there can not be said to be as effective in eastern countries.

The moment a patient starts experiencing the benefits, which he has earned himself, he boldly starts climbing step by step towards success.

“Maha Mrityunjaya Mantra”

It is believed that by worshipping Lord Shiva by reciting of this mantra, diseases are cured miraculously. If recited with pure and honest spirits it is an extremely capable weapon against diseases. It is even believed to win over death, too.

“Om Tryambakam Yajamahe Sugandhim Pushti Vardhanam

Urvaarukamiva Banadhanaan Mrityormuksheeya Maamritaat”

This shloka means: We worship the three eyed one (Lord Shiva) who is fragrant and who nourishes well all beings; may he liberate us from death, for the sake of immortality, even as the cucumber is severed from his bondage (of the creeper).


The First Pillar




Before starting treatment, first of all a complete information of the patient regarding his medical, personal and family history is taken. In the meantime the physician also examines the patient mentally. The patient’s social, literary and financial level; medium of earning livelihood; family structure; place of living; the herbs, food items and life style available; and other such informations are necessary to decide the line of treatment. A knowledge of the family history, whether the patient’s uncle, cousins or some other first blood relative is suffering from diabetes, blood pressure, heart disease, or kidney disease is also important.

The determination of the cause(s) of the disease, correct assessment of diabetic status and its complications are all helpful in instituting the correct line of treatment. For this very purpose ayurveda has instructed the following investigations:

1. Examination by history taking

2. Visual examination

3. Examination by touch

4. Pulse examination

5. Examination by hearing

6. Examination by smelling

1. Examination by history taking

A knowledge about the country, tribe, time period, diet, development of vata diseases, loss of strength, position of urine and mala, jatharagni and other such initial states and their later stages is helpful. Knowledge about the state of stomach, thirst, bahumutra and hunger, too, is helpful.

Family history: A detailed family history of diabetes, rheumatism, blood pressure, premature ischemic heart disease, unnatural death, hemorrhagic and kidney disease is taken.

Personal history: Information regarding intake of tobacco, alcohol and other intoxications and sufferance from any mental disease, fear, worry, anxiety, family tension, or professional loss in the past.

Other diseases: The physician should know whether the patient is suffering from some other disease as tuberculosis, sexual disease, heart disease, pain in chest, kidney disease, anemia, malaria, arthritis, vata-vyadhi, recurrent viral fever, major accidents, or burn and surgery.

Painic disorders: Since diabetes is a vata disease, hence different types of painic disorders (asthesias and hyperasthesias) and discomforts in different body parts are natural. History relating to body pain (especially nocturnal pains) shows the extent and seriousness of the diseases.

Disorders of excretion: Knowledge of constipation, diarrhoea, dysentery, excess urination, decrease in urine, dysuria, anuria, decreased and increased sweating (swedavrodha and swedadhikya respectively) is also helpful.

2. Visual examination

Physical examination of the eyes, tongue, and urine is done along with assessment of the severity of the illness. By physical examination, we come to know about the body’s obesity or leanness, signs of ageing, strength, colour, defects in the body organs, swelling of the body veins and the thyroid gland.

Eye examination:Eyes diseased due to vitiated vayu are rough, smoky coloured with several red lines, yellowish and sunk in. If kapha dosha also exists along with vayu dosha then eyes are full of water, without any glow, fixed and whitish in colour. Jaundice, pandu-rog and anemia are also recognized by eye examination.

Tongue examination: Due to effect of vayu the tongue becomes dry and cracked like the leaf of a teak tree. When there is excess kaphaalso, then it becomes wet and liquid. Due to imbalanced diet and stomach diseases, blisters in the tongue also occur.

Urine examination: In diabetes the urine is in excess and turbid. Greater details have been given in the chapter on prameha. In ashmari (renal stone) one may have red urine and the colour of the urine in pandu rog (anemia-paleness) is usually yellowish.

Severity of the illness:By seeing the physical condition of the body and observing the way of walking, talking and sitting the extent of disease can be assessed quickly.

3. Examination by touch (palpation)

By examining the coldness, hotness, softness or hardness of the skin disorders as pitting edema, cracking sound from a fractured bone, organomegaly (such as splenomegaly, hepatomegaly), and fluid retention in pleural, pericardial or peritonial sac are diagnosed easily. On getting fever the whole body becomes hot but if a particular organ only becomes hot then it signifies some nervous disorder ‘neuritis’ or inflammatory swelling ‘infective/arthritic pathology’.

4. Pulse examination ‘nari parikshan’’

The right hand pulse of males and left hand pulse of females is usually examined. Sometimes pulse of the both the hands need simultaneous checking.

Method of examining pulse and observations made: Three fingers should touch the pulse. The physician should examine right hand pulse of a man and left hand pulse of a woman after giving some time for relaxation. The name and properties of different types of pulses are as follows:

* Vata nari

It flows below the forefinger and moves haphazardly.

* Kapha nari

Slowly moves below the tarjani (fore finger).

* Pitta nari

It moves below the middle finger in jumping motion.

* Vata-pitta nari

It moves below the middle and fore finger in crooked pathway and jumping motion. In case of worry/fear it becomes weak/slow.

Vata-kapha nari

Moves slowly and crookedly between the anamika (the finger between middle and little finger) and tarjani.

Pitta-kapha nari

It moves below the madhyama (middle finger) and anamika in slow and jumping motion.

* Tridosha nari

It moves below all the three and becomes severe/fast. If the pulse beats in intervals, skips, is weak and very cold then it leads to death. During fever the heart beats fast thus pulse also moves fast and becomes hot, too. When agni (metabolism) becomes slow or dhatus (tissues) become weak then pulse moves very slowly. The pulse of a hungry person is swift.

Kama-krodha nari

During anger and lust the pulse moves very fast.

Chinta-bhaya nari

During worries and fear the pulse becomes small in intensity and feeble.

5. Examination by hearing

In modern times this investigation is performed with the help of a stethoscope. The rule behind this investigation is that minute sounds produced by the functioning organs are enhanced and made hearable with the help of an instrument or making an apparatus by folding a piece of paper in appropriate manner. If there is any disorder in the functioning of an organ, different type of sounds can be heard.

6. Examination by smelling

Various diseases can be diagnosed with the help of the smell coming out of patient’s excretions or breath. For example, urine of a few patients of diabetic ketoacidosis smells like fruits, in others like alcohol or ammonia. Putrefaction or gangrene formations also have a peculiar smell. Patients of intestinal disorders usually pass bad smelling wind. General hygeine status of a patient is also recognized by smell.

If a physician does the above investigations time to time in a patient then treatment also becomes very-very effective. Following terms also need clarification :


It includes all the medicines, foods and activities which provide relief to a patient. While examining the patient a knowledge of the causes, general pathogenesis, differential diagnosis, the severity of disease (bal samprapti), the time taken by dosha-dhatu to get vitiated and develop diseases (kal samprapti), prodormal signs and symptoms are all essential. By doing this only upkshaya (management/treatment) is possible. This refers to the condition in which a man finds happiness that is, making a decision regarding medicine, food and life style. Before starting treatment the state of the disease in the body should definitely be assessed because if excess medication (diet or exercise) for lesser degree of disease and low medication for greater degree of disease is given, then both are harmful.


Deciding of causes by identifying the vitiated humours is called hetu.The main causes of vata vitiation are rainy season, excess use of rough/harsh substances, excess labour, malnutrition, excess intercourse, and worries.

Samanya samprapti

It is called general pathogenesis in allopathy. The rate and extent of vitiation of humours in the body is also essential to know for correct upkshaya.

Bhed nidan

Its synonym in english is differential diagnosis meaning assessment of the degree of doshas as to which is more and which is to a lesser degree.

Bal samprapti

The causes, symptoms, and development of disease gradually or all at once are helpful in identifying the severity of the disease.

Kal samprapti

The duration of the causes and the doshas present in the diseased body helpful in development of diabetes should be known. If diabetes develops within a short period it indicates its seriousness.

Samanya and vishesh roop

Common or specific prodormal symptoms and symptoms which indicate development of disease in the near future are general purva roop. If they exist along with specific doshas they are called specific or vishesh purva roop.


Disciplines of living in day, night and changing weathers


Life style plays a very crucial role in prevention/control/cure of diabetes. If a proper life style is adopted the result is ‘aarogyata’ or total health.

Day routine ‘dincharya’

Daily routine implies to the conduct/behaviour/practice to be followed everyday. This is the behaviour to be followed daily, which is correct and capable of keeping good health. Three prahar of night (7½ h) ‘triyama’ are for sleeping only. After sleeping one should wake up in brahma-muhurt (2-3 h before sunrise) or before morning namaj (prayers offered by muslims) and drink 1-2 glasses of water kept overnight in a copper vessel. If a patient is taking some natural medicine he should take it in brahma-muhurt itself empty stomach because its effects doubles up that time (absorption of the herbal drug is far better as compared to taking it after meals).

If a patient takes in a little water through nose (jal neti) he can prevent himself from diseases of the brain, eyes and pratishyay rog (catarrh). The invisible rays of the sun a little before sunrise are extremely beneficial for the body. Moreover the air in early morning is full of good qualities hence should definitely be taken in.

Morning exercises ‘pratahkal ka vyayam’

In early morning the brain is fresh and full of liveliness/energy. If critical problems are thought over at this time then they are immediately solved and the person finds relief from tensions the whole day. All this is extremely helpful in diabetic control as the most efficient way of decreasing stress is to find proper solution to problems. Other exercises equivalent to walking are brisk walking, slow running, swimming, horse riding, badminton and other such sports. The daily household chores performed by men and women are also exercise only.

Symptoms of ‘vyayam’ exercise

Any effort (work) made by the body which is correct, for its betterment, brings happiness to mind and stability to the body and is strength increasing is called exercise. It has been said also : “shareercheshta ya cheshta sthairyaartha balwardhini” (CharakSamhita.Sutra.L.7.S31). Charaka also says: “ya cheshta shareer cheshta” i.e., exercise should bring peace to mind. He warns weak persons as well as strong persons to keep away from excess exercise as in the following shloka : “gajamsinham ivakarshan sahsa sa vinashyati” (C.Su.L.7.S35) meaning excess exercise harms the body in the same way as a lion by its bravery kills an elephant but while trying to pull the dead elephant it itself dies.

Extent of exercise and its identification by symptoms

Out of the total energy obtained by intake of ideal food only that much should be used in exercise so that more than half of the total energy is conserved for the essential body processes in rest of the day. The symptoms when half the body energy is being utilized in exercise are: breathlessness starts occurring and breath comes back slowly; perspiration occurs in the armpits and joints of hand and legs; and mouth starts drying up; then one should understand that exercising time is over.

Effect of exercise

Charaka says by exercise the body feels lively/light, enthusiasm for work is filled, jatharagni increases, loss of meda occurs and the body becomes graceful. Exercise gives the power to face mental distress, thirst, cold, and hot situations. Moreover by exercise old age is kept away just as a rabbit/jackal does not dare come near a lion (SushrutSamhita.Cikitsa.L.24.S42). Daily exercise is capable of digesting all types of food.

Persons who should avoid exercise

Exercise is prohibited for the following persons: seriously diseased very young or old persons; patients of raqt-pitta (ketosis) and indigestion; lean persons or those suffering with shosh (asthenia), breathlessness and cough; and patients with defects in vision and delusion. Also patients with heart disease, high blood pressure, kidney disease, insensitivity to sensations in legs, and foot ulcer should do exercise only after consulting a physician.

Losses by excessive exercise

Polydipsia, breathlessness, raqt-pitta, physical and mental distress, cough, fever, leanness and low blood glucose level may occur.

Exercising empty stomach is prohibited for a diabetic

“aharan pachati shikhi doshanaharavargitah; doshakshaya pachaddhatun pranan dhatukshaya tatha”

. It means that the agni of the body digests the food and if food is not available it starts digesting the body humours. On depleting of humours it starts digesting the body tissues and lastly in absence of tissues it takes life. On the contrary if the patient eats something before exercise then his health is protected by exercise only.

‘Adhwa’ Long distance journey on foot

Walking long distances makes the body old, weak and becomes the cause of ageing.

‘Chakraman’: walking and strolling

Walking and strolling till the limit it doesn’t adversely affect the body instead increases age, strength and energy and makes the sense organs vigilant and active.

Types of exercises

There are three types of exercises aerobic, anaerobic and relaxation exercises. A diabetic must not do anaerobic exercises as they may prove very harmful. Aerobic and relaxation exercises prove beneficial to a diabetic.

1. Aerobic exercise (isometric exercise)

There is a constant contraction and expansion of muscles in aerobic exercises as walking, running, jogging, badminton, and swimming. As a result the body gets toned up to face any situation. Moreover the different joints of the body also become active and perfect. In these exercises about 200-400 calories are consumed every hour hence blood glucose level also lowers down. Aerobic exercises done early morning fill the body with freshness and energy. The mind feels elevated and the cool breeze removes vayu vikar as shool, and indigestion. Exercising for ½ hour to 45 minute is beneficial for all.

2. Anaerobic exercises (isotonic exercise)

These are picking up heavy weight, 100 m sprint race, and body building. While doing these exercises the muscles of the body are involved for very little time and great strength is used for a few seconds only. In this case all the organs, joints, and muscles are not involved for more time hence this type of exercise does not give the desired result. A diabetic should never perform anaerobic exercises.

3. Relaxation exercises

Acharya Charaka has stressed that physical as well as relaxation both the exercises are necessary to maintain good health. Sushruta says there are two types of exercises physical and mental and both are helpful in the treatment of diabetes. Besides Yoga and pranayamathe below mentioned exercises remove mental tensions and can be performed in between daily chores also.

* Clinch your fist for a minute as strongly as you can and then suddenly release it.

* Stretch your body starting from big toe of the right leg and concomitantly extend this stretching to the right thigh, trunk, right arm, face, left arm, left thigh, left leg and lastly left big toe. Keep