Madhumeha kc010 udp

A CLINICAL STUDY ON THE EFFECT OF

ASANADI KWATHA IN MADHUMEHA

By ANIL KUMAR G. B. A. M. S.

Dissertation submitted to the

Rajiv Gandhi University of Health Sciences, Karnataka, Bangalore

In partial fulfillment Of the requirements for the degree of

DOCTOR OF MEDICINE (Ayu)

In

KAYA CHIKITSA

Under the guidance of

DR.U.N.PRASAD, M.D. (AYU) Professor

Department of Kaya Chikitsa

Co-Guide

DR. V. K. SRIDHAR HOLLA M. D. (Ayu) Assistant professor

Department of Kaya Chikitsa

S.D.M. COLLEGE OF AYURVEDA,

KUTHPADY, UDUPI 2006

I

Ayurmitra

TAyComprehended

Rajiv Gandhi University of Health Sciences

DECLARATION BY THE CANDIDATE

I hereby declare that this dissertation / thesis entitled “A clinical study on the

effect of Asnadi kwatha in Madhumeha”is a bonafide and genuine research

work carried out by me under the guidance of Dr. U.N.Prasad. M.D. (Ayu),

Professor, Department of Kaya Chikitsa and co-guidance of Dr. V.K. Sridhar

Holla M.D.(Ayu), Assistant Professor, Department of Kaya Chikitsa.

Date: Signature of the candidate

Udupi Anil kumar.G

II


CERTIFICATE BY THE GUIDE

This is to certify that the dissertation entitled “A clinical study on the effect of

Asnadi kwatha in Madhumeha” is a bonafide research work done by Anil

kumar. in partial fulfillment of the requirement for the degree of DOCTOR OF

MEDICINE (Ayu)

Signature of the co-guide Signature of the Guide

Dr.V.K.Sridhar Holla, M.D.(Ayu) Dr.U.N.Prasad, M.D(Ayu) Asst.Professor, Dept.Of Kaya Chikitsa Professor, Dept.Of Kaya Chikitsa

Place - Udupi Date:

III


ENDORSEMENT BY THE HOD, PRINCIPAL / HEAD OF THE INSTITUTION

This is to certify that the dissertation entitled “A clinical study on the effect of

Asnadi kwatha in Madhumeha” is a bonafide research work done by Anil

kumar.G under the Guidance of Dr.U.N.Prasad. M.D. (Ayu), Professor,

Department of Kaya Chikitsa and co-guidance of Dr. V.K. Sridhar Holla.

M.D. (Ayu), Assistant Professor, Department of Kaya Chikitsa.

Signature of the H.O.D Signature of the Principal Dr.U.N.Prasad Dr.Bala.Krishna.Bhat

Date: Date:

Udupi Udupi

IV

COPYRIGHT

Declaration by the candidate

I hereby declare that the Rajiv Gandhi University of Health Sciences, Karnataka

shall have the rights to preserve, use and disseminate this dissertation / thesis in print

or electronic format for academic / research purpose.

Date: Signature of the Candidate Udupi:

Anil kumar.G

© Rajiv Gandhi University of Health Sciences, Karnataka

V

DEDICATION

I Would Like to Place This Dissertation on the Lotus Feet of My Parents

Date: Signature of the Candidate Place: Anil kumar.G

VI

ACKNOWLEDGEMENTS

I am Ever Indebted To Lord Almighty,

My Venerated Parents,

Respected Teachers And

Affectionate Friends

VII

ABSTRACT Background and Objectives: Besides the miraculous achievement of modern medical

science, humanity is passing through a horror of disease and drug phobia, particularly in

developing countries like India, where poverty and illiteracy account for the man’s

ignorance towards the principles of healthcare. Symptomatology of Madhumeha is

equivalent to the features of Diabetes mellitus in modern medical science. Among the

several health problems, Diabetes mellitus is a giant disease considered as one of the arch

enemy of the mankind. Diabetes and its complications pose a major threat to future

public health resources throughout the world.

Thus it becomes a challenge for ayurvedists to search for an effective treatment.

The present study is focused on the literary review & clinical study of the Madhumeha

and to evaluate the effect of Asanadi Qwatha in patients of Madhumeha with out

alteration in their routine dietary and physical activities.

Methods: It is a single blind clinical study with pre and post test design where in 20

patients diagnosed as Madhumeha between the age group of 30 – 75 yrs and FBS

between 120 mg/dl to 180 mg/dl; PPBS level between 160 mg/dl to 300 mg/dl. And

NIDDM patients devoid of other systemic complication were selected. All were

administered with Asanadi Qwatha for a period of 30 days. The relevant investigations

were adopted for diagnosis and to assess the improvement.

Results: Good remission in the symptoms of Madhumeha and significant reduction in

FBS, PPBS was recorded. Paired t test also proved the statistically highly significant

improvement in prabuta mutrata, avila mutrata, karapada daha, karapada suptata, trushna,

FBS, PPBS. No improvement was observed in Sthoulya.

Keyword: Madhumeha, Diabetes mellitus, Asanadi qwatha.

VIII

IX

TABLE OF CONTENTS

1. Introduction Page No. 1- 4

2. Objectives Page No. 5

3. Review of Literature Page No. 6 - 108

4. Methodology Page No. 109 - 113

5. Observation and Results Page No. 114 - 133

6. Discussion Page No. 134 - 143

7. Conclusion Page No. 144 - 145

8. Summary Page No. 146 - 150

9. Bibliographic References Page No. 151 - 165

10. Annexure-Profoma

IX

LIST OF TABLES S.No. Table No. Content Page No.

1 1 Nidana 20 - 22

2 2 Classification Of DM 43

3 3 Poorva Roopa 47

4 4 Samanya Upadrava 62

5 5 Vishishta Upadravas 62

6 6 Prameha Pidakas 63

7 7 Sapeksha Nidana 66

8 8 Differential Diagnosis 67

9 9 Mutra Laxana In Different Diseases 70 -71

10 10 Pathya in Sthoola Madhumehi 93

11 11 Pathya in Krusha Madhumehi 94

12 12 Apathya Ahara, vihara, vichara 95

13 13 Ingredients of Asanadi Kwatha 97

14 14 Asanadi Kwatha - Rasa panchaka 108

15 15 Age Incidence 117

16 16 Sex incidence 117

17 17 Marital Status 118

18 18 Educational status 118

19 19 Religion Incidence 119

20 20 Socio - Economic Status 119

21 21 Occupational Incidence 120

22 22 Incidence of Addictions 120

23 23 Dietary Habits 121

24 24 Deha Prakruti 121

25 25 Sara incidence 122

26 26 Samhanana 122

27 27 Satva incidence 123

X

28 28 Rasa Satmyata 123

29 29 Status of Agni 124

30 30 Bala incidence 124

31 31 Family History 125

32 32 Effect on Prabuta mutrata 128

33 33 Effect on Avila mutrata 128

34 34 Effect on Kara pada Daha 129

35 35 Effect on Kara pada suptata 129

36 36 Effect on Bahuashee 130

37 37 Effect on Trishna 130

38 38 Effect on Ati Sweda 131

39 39 Effect on Daurbalya 131

40 40 Effect on Sthoulya 132

41 41 Effect on FBS 132

42 42 Effect on PPBS 133

43 43 Effect on Urine Sugar 133

XI

LIST OF FIGURES Sl.No. Graph No. Name of the Graph Page No.

1 1 Age Incidence 117

2 2 Sex incidence 117

3 3 Marital Status 118

4 4 Educational status 119

5 5 Religion Incidence 119

6 6 Socio - Economic Status 120

7 7 Occupational Incidence 120

8 8 Incidence of Addictions 121

9 9 Dietary Habits 121

10 10 Deha Prakruti 122

11 11 Sara incidence 122

12 12 Samhanana 123

13 13 Satva incidence 123

14 14 Rasa Satmyata 124

15 15 Status of Agni 124

16 16 Bala incidence 125

17 17 Family History 125

18 18 Effect on Prabuta mutrata 128

19 19 Effect on Avila mutrata 128

20 20 Effect on Kara pada Daha 129

21 21 Effect on Kara pada suptata 129

22 22 Effect on Bahuashee 130

23 23 Effect on Trishna 130

24 24 Effect on Ati Sweda 131

25 25 Effect on Daurbalya 131

26 26 Effect on Sthoulya 132

27 27 Effect on FBS 132

XII

28 28 Effect on PPBS 133

29 29 Effect on Urine Sugar 133

XIII

Prologue

PROLOGUE

The present era is full of chaos, stress & strain due to life style modifications,

change in dietary habits, urbanization and industrialization. This has lead in the upsurge

of many diseases and one of them is Madhumeha. Though Madhumeha is a disease

known since ancient times to the mankind, its upsurge is quiet alarming. On the basis of

its symptomatology Madhumeha can be correlated to the features of Diabetes mellitus.

. DM is one of the major killers of the modern world. It is a disorder which is sparing

neither the developing nor the developed nations. Irregular food habits, lack of exercise,

stress and strain are some causative factors that make an individual more prone to

develop diabetes at an early age. India has been projected by the W.H.O. as the country

with the fastest growing population of Diabetics. It is estimated that By 2025 the Indian

diabetic population will be 79,441,000. W.H.O. has predicted that the new millennium

population may see an epidemic of Diabetes. The reasons of its fast spread in the urban as

well as in the rural areas are ill understood. Diabetes mellitus is all the more dreaded

because of its complications in almost every part or rather every cell of the body.

The modern management of diabetes inspite of many advances still remains

unsatisfactory. Drug intolerance, hypersensitivity and resistance to insulin, the danger of

acute and chronic complications, the fear of hypoglycemic episodes with Sulfonylureas

makes it all the more important to search out safe, effective and cheaper remedies. Such

remedies could be explored from the huge wealth of Ayurveda which still remains

unexplored on the modern technological advances.

1

Prologue

Previous works on Madhumeha

1. A Study on Madhumeha by Dr.B.V.Prasanna –1981-GAMC, Mysore.

Trivanga bhasma and Jambu phala Beeja majja choorna was selected for clinical

study. 10 patients on drug and diet; 5 patients only on diet. Moderate Results were

observed in drug and diet group.

2. A clinical study on the role of Asana and Guduchi Rasayana in the management of

Madhumeha (DM). – 1999 Dr.Ranjana D. Siddhapathaki GAU, JAMNAGAR.

Group I - Asana Kashaya in two divided doses per day prepared from 40 gm of

Asana coarse powder - 2months; Group II – 6 gm Guduchi churna and then same

quantity of Asana Kashaya in two divided doses per day – 2 months; Group III –

Asana vati 4 gm of drugs in three divided doses per day – 2 months; Asana Kashaya

showed better relief.

3. Effect of Salasaradi gana basti on Stoolamadhumehi Dr.Kiran.M.Goud – 1999 –

GAMC – Mysore. Group A - 17 pts. – Pancha kola churna (10gm/tid)

Salasaradi basti therapy 16 days; Cap. Nishaamalaki 32 days with diet & exercise.

Group B – 17 pts - pancha kola churna (10gm/tid) cap. Nishaamalaki 32 days

Placebo. Cap for16 days with diet & exercise. Group A showed better results.

4. A clinical study on the effect of Nisha amalaki in Madhumeha – a controlled study

Dr. Kishore kumar.R –2002 – S.D.M.C.A, UDUPI.Group I –12 pts - Nishaamalaki

choorna (4 gm tid ) along with diet & exercise, before food for 60 days Group II –

12 pts - Placebo with diet & exercise Group I showed better results.

2

Prologue

5. A comparative study on the role of Basti Therapy and Pramehaghna drugs in the

management of Madhumeha (DM) – 2003 by Dr.Pawar Anand M. – G.A.U,

Jamnagar. Group I – Pramehaghna vati to15 patients - 2 gm tid; Group II-

Pramehaghna Basti to 8 patients. Total of 16 Basti including Niruha and Anuvasana

(Kala Basti) Group III - placebo group - 6 patients were given empty capsules with

strict diet pattern. Group I showed better results as compared to group II in the

management of DM.

More than 200 thesis works were conducted all over India on Madhumeha

in the form of shodhana and shamana line of treatment. In shamana chikitsa different

formulations have been used so for, in the form of kashaya, vati etc.

Asanadi Kwatha is anubhuta yoga which is been prescribing in S.D.M.

Ayurveda hospital, Udupi, Karnataka. Since 20 yrs. This being Tikta, Katu, Kashaya

Rasa, Katu Vipaka, Laghu, Ruksha & Tikshna Guna pradhana Aushadhi may easily

help in the dissociation of Pathogenesis of Madhumeha. They also possess mehagna,

medhohara, Rasayana, Deepana and Pachana properties and anti diabetic action.

Hence Asanadi Kwatha has been selected for the present study.

The present dissertation work entitled “A CLINICAL STUDY ON THE EFFECT OF

ASANADI KWATHA IN MADHUMEHA” consists of following parts.

Conceptual study

Clinical study

Discussion

Summary and conclusion

3

Prologue

The conceptual study includes three separate chapters. The historical aspect of the

disease Madhumeha is elaborated in the chapter on historical review. Nidana panchaka as

well as treatment of this disease is made clear in the second chapter. Full account of the

composition of Asanadi Kwatha is given in the chapter on drug review.

The details of the present research work that include material and methods, observation,

results and statistical analysis all are methodically presented in chapter entitled clinical

study.

The critical analysis of the results obtained is the subjective matter of the chapter

discussion. The conclusion drawn from this clinical study is listed in the final chapter

summary and conclusion.

4

A CLINICAL STUDY TO EVALUATE THE EFFECT OF VAMANA AND SHATYADI CURNA IN PATIENTS OF

TAMAKA SHWASA.

By

MADHUSUDHANAN.I.K., B. A. M. S.

Dissertation submitted to the Rajiv Gandhi University of Health Sciences, Bangalore,

Karnataka in partial fulfillment of the regulations for the award of the degree of

DOCTOR OF MEDICINE (AYU)

IN KAYA CHIKITSA

GUIDE:

DR.G. SRINIVASA ACHARYA., M.D. (AYU)

Asst. Professor, S. D. M. C. A., Udupi

CO-GUIDE

DR.SHRILATHA KAMATH.T., M.D. (AYU)

Lecturer , S. D. M. C. A., Udupi.

DEPARTMENT OF POST GRADUATE STUDIES IN KAYACIKITSA S. D. M. COLLEGE OF AYURVEDA, UDUPI – 574 118

2005 - 2006

I


DECLARATION BY THE CANDIDATE I hereby declare that this dissertation entitled “Clinical study to evaluate the effect of

Vamana and Shatyadi Curna in patients of Tamaka Shwasa” is an above-board

research work carried by me under the guidance of Dr.G.Shrinivasa Acharya., M.D.

(Ayu) and co-guidance of Dr.Shrilatha Kamath.T., M.D. (Ayu).

MADHUSUDHANAN.I.K.

B.A.M.S.

Date:

Place: Udupi.

II


CERTIFICATE BY THE GUIDE This is to certify that the dissertation entitled “A Clinical study to evaluate the effect of


research work done by Madhusudhanan.I.K in partial fulfillment of the requirement for

the degree of M.D. (Ayu).

Signature of the Guide:

DR.G. SRINIVASA ACHARYA., M.D. (AYU)

Assistant Professor, S. D. M. C. A., Udupi.

Signature of the Co-Guide:

Date: DR.SHRILATHA KAMATH.T.M.D. (AYU)

Place: Udupi. Lecturer, S. D. M. C. A., Udupi.

DEPARTMENT OF POST GRADUATE STUDIES IN

KAYACIKITSA

III


ENDORSEMENT BY THE HOD, PRINCIPAL / HEAD OF THE INSTITUTION

This is to certify that the dissertation entitled “A Clinical study to evaluate the effect of


research work done by Madhusudhanan.I.K, under the guidance of Dr.G.Shrinivasa

Acharya., M.D., (Ayu) and co-guidance of Dr.Shrilatha Kamath.T., M.D. (Ayu).

Signature of the H.O.D. Signature of the Principal

Dr. U. N. Prasad, M.D. (Ayu) Dr.K.Balakrishna Bhat., B.S.A.M

Professor and H.O. D., PRINCIPAL

Department of P.G Studies in Kayachikitsa. S. D. M.C.A, S.D.M.C.A, UDUPI.

S. D. M.C.A, S.D.M.C.A, UDUPI.

Date:

Place: Udupi.

IV

COPYRIGHT

Declaration by the candidate

I here by declare that the Rajiv Gandhi University of Health Sciences, Karnataka shall

have the rights to preserve, use and disseminate this dissertation / thesis in print or

electronic format for academic / research purpose.

MADHUSUDHANAN.I.K

B.A.M.S

Date:

Place: Udupi.

© Rajiv Gandhi University of Health Sciences, Karnataka

V

Review of Literature History

HISTORY

Study of sequential evolution is prime step in the research field. Study of history

is important to know about the systematic development and progress of the subject to

determine the future plans for further establishment and research designing. History of

Medicine starts from the very moment when the human being came into existence that is

why the ancient treatise is full with description of diseases and their treatment. Here the

present review related to Madhumeha is explained.

The evolution of Madhumeha can be traced from Vedas but in rudimentary form,

when we go through the Atharva Veda there is a reference related to the disease 'Asrava'

along with its management. Sayanacharya opined that Asrava means 'Mutraatisara' the

English translator Whitney (1962) interpreted it as flux and Griffith (1962) as morbid

flow, while layman has translated the meaning of Asrava as Diabetes Mellitus.

Sayanacharya highlighted the vatic nature of this ailment.

(A) Samhita Period: Explorative description of disease Madhumeha occurs at

Samhita period.

(1) Charaka Samhita: In this ancient treatise of medical science, Charaka explained

the etiology, pathogenesis, symptomatology, complications and treatment Modalities in

detail in Nidana 4th and Chikitsa 6th chapter. While in Sutrasthana 17th chapter he

described the Avaranajanya pathogenesis of Madhumeha, this is the unique contribution

of this treatise.

(2) Susruta Samhita: Susruta also explained the Madhumeha in elaborative manner

with separate chapter on its management. He used 'Kshaudrameha' synonym to

Madhumeha in Nidana 6th chapter. He typically mentioned the kashayas according to

6


each type of Prameha and mentioned the body constitution and symptoms related to

Sahaja and Apathyanimittaja Prameha.

(3) Astanga Hrudaya: Detail description about the disease is given as in Charaka

and Sushrutha samhitas with slight moderations. He added some new herbs and herbal

compounds as well as rasa aushadis for the treatment.

(4) Harita Samhita: Harita mentioned it as Papajanya and enumerated 13 types of

Prameha with nomenclature different than above treatise like, Puyameha, Ghritameha etc.

(5) Bhela Samhita: He described Prameha is of two types i.e. Svakrita and

Parakritameha.

(6) Kashyapa Samhita: He mentioned the symptoms of Pramehi child in

Vedanadhyaya and noted the disease as Chirakari.

(B) Medieval Period: In this period commentaries mainly written, but most of them

contains only the collection of thoughts from previous authors.

(1) Madhava Nidana: He collectively repeated the description of Charaka, Susruta

and Vagbhata in 33rd chapter.

(2) Gayadasa: Explained the Avilamutrata because of the presence of Doosya in it.

(3) Sharangadhara Samhita: Only mentioned the 20 types of Prameha in Prathama

Khanda 7th chapter.

(4) Bhavaprakasa: He described Prameha and Madhumeha along with some new

herbomineral preparations in Madyama khanda 38th chapter.

(5) Yogaratnakara: Explained Prameha and Madhumeha along with treatment.

7


Some of inventive landmarks about the DM:

(1) Areatus (Christian era): Firstly he mentioned the disease as diabetes.

(2) William Cullen (1709 AD): Added suffix mellitus to the diabetes.

(3) Mathew Dobson (1775 AD): He found that sweetness of urine is due to sugar.

(4) Thomas Cowley (1781 AD): He suggested that pancreas may be the cause of

diabetes.

(5) Poul Langarhans (1869 AD): Name itself suggests that he described the group of

cells in pancreas.

(6) Gusteve Edouard Laguosse (1893 AD): Named after Langerhans as islets of

langerhans

(7) Opie (1901 AD): He put forth the hypothesis that, diabetes is due to alteration in

the islets of langerhans.

(8) FG Babting and Charles best (1922 AD): Discovered insulin.

8

Review of Literature Nirukti and Paribhasha

NIRUKTI AND PARIBHASHA

I. Nirukti: Madhumeha is a compound word made up of Madhu and Meha.

Madhu: The word madhu is derived from the root ‘mana’ and the meaning as ‘manaava

bhodane’ i.e. which brings gratification to the mind1.

Meha: Meha is derived from the root ‘Miha’, which is employed in the sense of Sinchana

(to moisten), Ksharana (to flow) Prasrava (to flow excessively).

Prameha: is derived from Pra + Miha. A condition characterized by excessive outflow

and a condition where there is excess urine flow.

II. Paribhasha: Madhumeha is a Mootradosha2, characterized by Bahumootrata, which

resembles Madhu in Rasa or Varna.

III. Paryaya: Prameha: Means Prakarshena mehati – excessive urine out flow3

Meha: Is referred to as Prameha by Amara4.

Mootradosha: A urinary disorder.

Bahumootrata: A disease where there is excessive urination.

Madhumeha: A condition characterized by excess urination, resembling honey either in

colour or taste. This word has been used synonymously with Prameha.

Kshoudrameha: Kshoudra is a synonym of Madhu.

Ojomeha: Ojas is considered as Tejas or essence of all Dhatus, which is a casualty in

Madhumeha hence Ojomeha has been used by Charaka to describe this disease.

Paushpameha: Narrated in Anjana Nidana. Paushparasa is again resembles with Madhu.

From above synonyms, we can postulate that unanimously all Acharyas mentioned the

urine culture concordant with Madhu.

9

Review of Literature Nirukti and Paribhasha

Diabetes Mellitus

Definition5: The W.H.O. expert committee on Diabetes mellitus (DM) in its second

report has defined DM as a chronic disease caused by inherited and/or acquired

deficiency in production of insulin by the pancreas, or by the ineffectiveness of the

insulin produced. Such a deficiency results in increased concentrations of glucose in the

blood, which in turn damage many of the body's systems, in particular the blood vessels

and nerves. Sir. William Osler in his book The Principles & Practice of medicine

published in 1923, defined DM as a disorder primarily of carbohydrate & secondarily of

fat & protein metabolism due to the failure of the system to burn sugar and dependent on

the deficiency or absence of internal secretion of pancreas resulting from functional or

organic disease of islet cells of Langerhans. This definition is held valid to this day.

10

Review of Literature Nidana

NIDANA

Knowledge of Etiological factors and their role in the pathology is very much

necessary to find out the vitiated constituents like dosha, dushya, mala, progression of the

disease and their role in diagnosis and prognosis.

Nidana has been classified under various headings with different views. Among

them, one classification is bahya hetu and abhyantara hetu. Bahya hetu is an extrinsic

cause to the shareera to cause a vyadhi and this includes ahara, vihara, achara,vichara,

kala etc,. Abhyantara hetu is an intrinsic cause and this mainly comprises the

doshas.Bahya hetus of Madhumeha is the discussion of this chapter and abhyantara hetu

will be discussed in the samprapti chapter.

For the convenience of the study, the bahya hetus are being classified into

samanya and vishesha hetu. Specific nidanas are explained for Madhumeha only by

charaka. The samanya nidanas of Prameha and vataja Prameha nidanas are attributed to

Madhumeha, as Madhumeha is one of the types of Prameha and vataja Prameha.

Samanya Nidana

The key word in Samanya nidana of Prameha is the Hetu, which causes Kapha

vriddhi (Kapha kriccha sarvam)6. It becomes contextual here to take note of the fact that

Kapha is the main dosha involved in Prameha and hence all those Hetu that cause Kapha

vriddhi automatically become the Hetu for Prameha7. The samanya nidana can again be

classified into A). Ahara Sambandha, B).Vihara Sambandha.

A). Ahara8: Any Ahara which is Madhura and Lavana rasa pradhana, Guru, Manda,

Sheeta, Snigdha, Shlakshna, Sandra, Sthira, Picchila guna pradhana, Madhura vipaka and

Sheeta veerya, including unboiled, unroasted, unfried food articles and Anoopa mamsa, if

11


taken in excess quantity increases Kapha which attains ‘Aparipakwa Avastha’ and mainly

effects the Medas and Kleda leading to Madhumeha due to Avarana.

B).Vihara9,10:

1. Atinidra: it aggravates kapha and tamasa guna and results in accumulation of

medas.

2. Asya atisukha: Excessive Asya sukha and Swapna sukha causes Snigdhata leading

to Kapha vriddhi

3. Divaswapna: Causes inertia in the body and the accumulation of Prithvi and Ap

mahabhoota, leading to aggravation of Kapha.

4 Vyayama varjana: A man is generally supposed to balance between the nutrient

intake and energy spending to maintain equilibrium. When this balance is not

maintained, it results in accumulation of Medas and Kapha. Hence adequate amount

of Vyayama is necessary to avoid Prameha.

5. Alasya: It is nothing but the state of lethargy of mind where a man is unable to

carry out or undertake any enthusiastic task not because he is incapacitated due to ill

health but only because he is unwilling to do it. This results in inactivity causing

excessive nourishment. This mainly because of kapha and medha.

6. Chinta tyaga: An attribute of the mind that is antagonistic to Kapha and Medas.

When a person becomes free from Chinta, he starts accumulating excess Kapha and

Medas.

7. Samshodhana varjana: Samshodhana therapy is essential in any individual for

cleansing the body. Being a form of Langhana, Samshodhana causes Medas and

Kapha kshaya. If this is not resorted, it causes accumulation of Kapha and Medas.

12


8. Mruja varjana: Mruja is udvarthana and its varjana leads to Kapha and medha

dushti.

Vishesha Nidana: Though the Kapha is the Arambhaka dosha in the Samprapti of

Madhumeha, Pitta and Vata play an important role in complicating the disease. For e.g. if

an affected person starts indulging in Pittakara ahara vihara then 6 types of Pittaja meha

manifest. Similarly when Kapha and Pitta are in Ksheenavastha, the Vata causes 4 types

of Vataja Prameha.

1. Kaphaja Prameha nidana: Are the same as explained in Samanya nidana because

kapha is dosha vishesha in Prameha but it should be in bahu drava.

2. Pittaja Prameha nidana11:

Ahara Sambandhi: 1. Ushna guna ahara atisevana 2. Amla rasa ahara atisevana 3.

Lavana rasa ahara atisevana 4. Katu rasa ahara atisevana 5. Ahara sevana in spite of

Ajeerna. 6. Vishama ahara sevana.

Vihara Sambandhi: 1. Ati atapa sevana, 2. Ati santapa, 3. Shrama, 4. Krodha.

3. Vataja Prameha Nidana: The causes for aggravation of Vata can be mainly grouped

into two categories 1. Margavarana12 2. Dhatu kshaya13

The Margavarana is a result of accumulation of Kapha or Pitta dosha in the Vatavaha

srotas due to the respective Nidana sevana, this leads to Vataja Prameha. In Prameha,

Dhatu kshaya is an invariable consequence of Aparipakvata of Dhatu. This leads to

aggravation of Vata causing Vataja Prameha. Apart from this pathological classification

of Vataja nidana14, the following factors are also responsible for aggravation of Vata.

A. Ahara Sambandhi: 1. Katurasa ahara atisevana, 2. Kashaya rasa atisevana, 3. Tikta

rasa ahara atisevana, 4. Laghu and rooksha guna ahara atisevana.

13


B. Vihara Sambandhi: 1.Vyavaya atiyoga, 2.Vyayama atiyoga, 3.Vamana atiyoga,

4. Virechana atiyoga, 5. Asthapanaatiyoga, 6. Vega sandharana, 7. Anashana,

8. Abhighata, 9. Atapa sevana, 10.Udwega, 11.Shoka, 12.Shonita ati sechana,

13.Ratri jagarana, 14.Vishama shareera nyasa.

All these factors are basically designed to provoke the Rajasika guna in the body.

Vata that is predominantly Rajasika gets aggravated leading to Vataja pramehas.

Sahaja (Hereditary):

Sushruta mentioned the Sahaja word showing genetic predisposition in the

pathophysiology of the disease Madhumeha. He narrated two causative factors there i.e.

patient is eating dry and less food and is always want to wonder (unstable)15.

Charaka, while describing the prognosis of Madhumeha Clearly noted that this is

Kulaja Vikara resulting due to defect in the Beeja. Chakrapani opines that it can cause by

Father, Mother or grand parents, it means the disease inherited from generation to

generation16. Charaka narrated that Sahaja type of diseases can occur due to defect in

beeja, beejabhaga or beejabhaga avayava. We can correlate beeja to ovum and sperm,

beejabhaga to chromosomes and beejabhagavayava to genetic coding17.Chakrapani

commented that this defect is because of the indulgence of faulty foods at the time of

pregnancy. Caraka narrated that indulgence of Madhura rasa by mother at the time of

pregnancy causes Madhumeha and Sthaulya18

.

Thus genetical predisposition and the over indulgence of etiological factors at the

time of pregnancy by mother helps to precipitate the disease Madhumeha, but the

important thing is genetic predisposition.

14


AETIOLOGY19,20,21

Genetics: The mechanism of inheritance of DM either insulin dependent or non-insulin

dependent is unclear. The genetic predisposition is probably permissive and not casual.

Genetic susceptibility in IDDM: This probably involves more than one gene. Candidate

loci have been proposed on chromosomes 2, 6, 11, & 15 though primary genetic site in

humans is believed to be located in the major histocompatibility locus on the short arm of

the 6th chromosome. While definite associations exist between class I alleles & type 1

DM, the D locus is considered of primary importance (A, B, C & D are the four loci of

HLA human leucocyte antigen) encoded by the MHC (Major Histocompatibility

Complex) found to be closely associated with IDDM]

Genetic Susceptibility in NIDDM: Modes of inheritance of NIDDM in variant called

maturity onset DM of the young (MODY) have been more or less conclusive than the

other forms. It is highly likely that ordinary NIDDM is polygenic. Genetic influence is

powerful. Since the concordance rate for DM in monozygotic twins with type 2 disease

may be as high as 80%, risk to offspring and siblings of patients with NIDDM are higher

than in type I DM. Nearly 4/10ths of siblings and 1/3

rd of offsprings eventually develop

abnormal glucose tolerance or frank DM.

Autoimmunity: The basic pathology of DM spins around one factor i.e. insulin and its

source of production viz. islet β cells. Complete or partial destruction of islet β cells or

peripheral resistance of insulin is causal of DM, but an autoimmune process destroying

the islet β cells is nevertheless Insulin dependent. The autoimmune destruction of the β

cells may be best explained by the existence of a β cell specific protein that for unknown

reasons acquires auto-antigenic properties and eventually becomes target for autoimmune

15


reaction. Gradual β cell loss becomes clinically manifest only when β cell mass is

reduced to a critical part after which metabolic compensation is not possible.

Heredity: The mechanism of inheritance of IDDM is unclear. At various times,

transmission has been postulated to be autosomal dominant, autosomal recessive and

mixed. While IDDM occurs with increased frequency in some families, familial

aggregation is uncommon. So, deduction of mechanism of inheritance is difficult.

Analysis of pedigrees shows a low prevalence of direct vertical transmission. The chance

of a child developing type 1 DM when another first-degree relative has the disease is only

5-10%. HLA identity in a sibling increases the risk. The presence of NIDDM in a parent

increases the risk for IDDM in the offspring. It is not known whether the intermixing of

IDDM and NIDDM in the same family represents operation of a single genetic trait or

whether two common genetic predispositions coexist in a family by chance. While the

low rate of transmission of IDDM makes it difficult to discern the mechanisms of

inheritance through study of families, they are reassuring to diabetics who wish to have

children. The risk of type 1 DM is up to five times higher when the father has the disease

than when the mother is a diabetic.

Environmental factors:

Viral Infections: As noted earlier, the fact that a significant proportion of monozygotic

twins remain discordant for IDDM suggests that non-genetic factors are required for the

development of DM. An environmental factor in many cases is believed to be a viral

infection of a β cell. A viral etiology was originally suggested by seasonal variations in

the onset of the disease and by what appeared to be more than a chance relationship

between the appearance of DM, preceding episodes of mumps, hepatitis, infections,

16


mononucleosis and coxakie virus infections. The isolation of coxakievirus B4 from

pancreas of a previously healthy boy who died after an episode of ketoacidosis and

induction of DM in animals inoculated with isolated virus also suggested a viral etiology.

Further support for viral theory comes from the observation, that about 1/5th of

individuals with congenital rubella develop DM. Despite its attractiveness, the viral

theory should be treated with considerable caution. Serological studies seeking evidence

of recent viral infection in patients with new onset IDDM are inconclusive at best.

Bovine albumin: It has been suggested that exposure to cow’s milk or milk products early

in life predisposes to autoimmune DM. In an initial study, diabetic subjects were found to

have attributes to bovine albumin. Exposure to cow’s milk is presumed to induce an

immune response to 17-amino acid fragment in some infants and cross reactivity of the

antibody. This hypothesis has not received wide support.

Obesity: Type 2 DM is almost non-existent in individuals with a body mass index below

22 Kg/m2 and increased risk of DM with obesity has a strong familial tendency. When

one or both parents are diabetic, 100% offspring’s will develop DM, if they become

sufficiently obese. If neither parent has DM, less than 20% of obese offspring develop

DM.

Life Style: Epidemiological studies of type 2 DM provide evidence that over eating,

especially when combined with obesity and under activity is associated with development

of type 2 DM.

Malnutrition: It is proposed that malnutrition in utero and in infancy may damage β cell

development at a critical period predisposed to type 2 DM at a later stage. Impaired β cell

17


function and peripheral insulin resistance have been major factors involved in NIDDM.

Pregnancy also induces NIDDM in genetically susceptible individuals.

Causes of secondary DM

a) Secondary to Pancreatic disease: Congenital Pancreatic Aplasia, Acute and Chronic

Pancreatitis, Pancreatic Carcinoma, Cystic fibrosis & Haemochromotosis.

b) Secondary to Endocrine Disorders: Hormones with an insulin antagonistic affect such

as, Growth hormone, glucocorticoids, catecholamines, thyromine and glucagon cause

impaired glucose tolerance or even overt DM when produced in excess as a result of

tumor or hyperplasia of the respective gland of origin. Endocrine syndromes frequently

associated with carbohydrate abnormalities of variable intensity are Acromegaly,

Cushing’s syndrome, Phaeochromocytoma, Glucogonoma, Hyperthyroidism, Cons

syndrome and Carcinoid syndrome.

Chemically induced DM: Two groups of drugs causing permanent or transient

hyperglycaemia can be distinguished. 1) Substances with cytotoxic effect on β cells and

2) Substances inhibiting insulin secretion without β cell destruction. The first group

includes Alloxan, Glyoxal Streptozotocin, Oxine dithiazone and recently Asparaginase,

Pentamidine Esthionate, N-3-Phyridyl methyl N- p- mitro ethyl urea (PNU). The second

group includes Diazoxide, Diphenyldydation Cyproheptadine and Manaoheptolose.

Majority of these drugs have been used only experimentally in laboratory animals.

Rare causes of DM: Numerous rare genetic syndromes (Lipoatrophic DM,

Leperchaunism, Acanthosis Nigricans types A & B, Ataxia Telangiectasia, Stiff man

syndrome, Bardet Biedl syndrome) may be associated with either glucose tolerance or

overt DM. Special islet lesions have not been described in any of these syndromes, there

18


is an absolute or relative insulin deficiency in such diseases. The high coincidence of

cirrhosis and DM is long established (Naunyn’s DM). This may be due to reduced insulin

degradation by cirrhotic liver with subsequent hyperinsulinism and insulin resistance.

a) Pituitary DM: The growth hormone of the pituitary appears to have diabetogenic

power (Houssay). Administration of hormone leads to atrophic changes in the β cells

associated with an early reversible phase of DM, followed by an irreversible phase with

complete destruction of β cells. DM may be associated with Acromegaly.

Hypophysectomy will arrest the course of DM in the experimental animal.

b) Adrenal DM: There is convincing evidence that Adrenal cortical hormones may affect

both the experimental and human disease. Adrenalectomy will arrest or modify the

progress of experimental DM. Adrenal hyperplasia or tumors may be associated with

DM. The administration of hydrocortisone causes DM by inhibiting insulin action.

c) Gestational DM: During normal pregnancy, insulin sensitivity is reduced through the

action of placental hormones and this affects glucose tolerance. The term gestational DM

refers to hyperglycaemia occurring for the first time during pregnancy. Repeated

pregnancy increases the risk of developing permanent DM especially in obese women.

19


Table No. 1: Nidana and Guna Karma Nidana Predominant of Rasa, Guna, Veerya, Vitatiates Vipaka 01) Guruguna ahara Prithvi,Ap Madhura rasa Kapha, Medas 02) Snigdhaguna ahara Prithvi, Ap Kleda 03) Dravaguna ahara Ap Kapha & Kleda 04) Picchilaguna ahara Prithvi, ap Kapha & Kleda 05) Sheetaguna ahara ap Udaka & vata

with dravaguna 06) Madhura rasa ahara Snigdha, Guru, Kapha, Rasa, Rakta, Sheeta veerya, Mamsa, Medas, Madhura vipaka Majja, Shukra and Ojas 07) Lavana rasa ahara Kleda, Kapha vilayana

Milk & its products 08) Goksheera Kapha & Medas 09) Mahisha ksheera Atisneha, Atinidra, Kapha & Medas Mandagni 10) Avika ksheera Abhishyandi Pitta and Kapha 11) Dadhi Kapha & Medas 12) Godadhi Kapha & Medas 13) Mahisha dadhi Kapha & Medas 14) Avika dadhi More abhishyandi Kapha & Medas 15) Mandaka Mootrala Tridosha Ghrita 16) Goghrita Kapha & Medas 17) Mahisha ghrita Kapha & Medas 18) Piyusha, Morata, Kapha

Kilata Sugarcane and its products Kapha

19) Ikshu Madhura rasa Kapha Sheeta veerya Snigdha and sara Guna and vidhahi 20) Phanita Guruguna Guru in guna Tridosha abhishyandi 21) Guda Kshara, Madhura Kapha & Medas in rasa, Snigdha, Sheeta in guna and veerya 22) Matsyandika, Snigdha, Guru Kapha & Medas

Khanda sharkara guna, Madhura rasa vimalajatha

23) Madhusharkara Rooksha guna, Liquifies Kapha dosha (Crystals of honey) Kashaya, Madhura rasa, Chedini in action, - Madhura vipaka

Vegetables (shaka) 01) Trapusha (Cuccumis sativas) Guru guna Kapha, Medas

20


02) Irvaruka (Cuccumis memordika) Madhura rasa Kapha, Medas Sheeta veerya 03) Keluta Vishada in guna Kapha, Medas & 04) Kadamba (Adina cardifolia) Sheeta veerya mootra 05) Nadi Masha Abhishyandi 06) Induka 07) Tarata 08) Shrungataka (Trapabis spinosa) Guru guna, Kapha & Medas 09) Shaluka (Nymphase lotus) Sheeta veerya 10) Krounchadana (A water tuber) and Vishtambhi 11) Kasheruka (Scripus crossus) in nature 12) Ankoladya (Root of sweet lotus) 13) Kamuda (Nymphae lotus) Sheeta veerya Kapha & Vayu

14) Utpala, nala, phala and pushpa Madhura kashaya in (A blue lotus) rasa 15) Pushkara beeja shaka (Nymphase stellata) 16) Vidarikanda (Convolvulus paniculatus) Madhura rasa Mootra & Kapha sheeta veerya, balya and mootrala in action 17) Upodika (Basella cordifollia) Madhura rasa & Kapha Vipaka, Snigdha in guna, Sheeta veerya 18) Chatraka Sheeta veerya, Kapha Madhura rasa, Guru guna 19) Phalanki (Spinacia alleracea) Guru, sara, pichilla, Kapha guna, sheeta veerya 20) Ardraka Tikta, Madhura in Mootrala rasa, Mootrala in action 21) Palandu (Alium cepa) Snigdha guna, Kapha Madhura rasa & vipaka, guru pichilla in action 22) Tanduliyaka (prickly Amaranth) Sheeta veerya, Kapha Madhura rasa and vipaka 23) Munjataka Snigdha, Sheeta, Kapha & Medas Guru guna, Madhura rasa, Brimhana in action 24) Kooshmanda (pumpkin) Madhura rasa and Kapha 25) Tumba vipaka, 26) Kalinja Vishtambana and 27) Karkaru (Cucumis utilismen) Abhishyandi in 28) Tindisha (A kind of cucumber) action 29) Chanaka (Pancium miliaceum) 30) Chirbhata (Cucumis memordica) 31) Hayanaka (A red variety of rice) Madhura rasa, Guru, Kapha & Mootra 32) Yavaka (Hordeum vulgare) Snigdha guna 33) Uddalaka (Phaseolus aconitifolium) Snigdha, Guru guna, Kapha & Medas Madhura rasa, Balya

21


34) Vreehi Madhura rasa, Guru Mootrala guna 35) Tila (Sesamum indicum) Snigdha guna, Kapha Madhura rasa

Krutanna Varga 1) Vilepi (variety of Prepared with Mamsa and Shaka is Amla Kapha & Medas cooked food) in Vipaka 2) Krushara Kapha and Pitta 3) Payasa (Food like Guruguna, Vishtambhi, Balya in action Kapha & Medas rice, wheat boiled with milk and sugar) 4) Palala (Tila churna Kapha

preparation) 5) Pishtanna Abhishyandi Kapha abhishyandi Madhya Dravaguna and Agni bhoota Dravaguna Gramya, Anoopa and Audaka mamsa

Anoopa 1) Koolachara (living eg. Gaja, Gavaya, Madhura rasa and Mootrala & at river side) Mahisha etc. vipaka, Sheeta, Kapha vardhana veerya, Snigdha guna 2) Plava (Birds eg. Hamsa, sarasa Sheeta veerya, Mootrala which swim) Krouncha etc. guna, Madhura rasa and vipaka 3) Koshastha (Live eg. Shanka, Shukti Madhura rasa and Shleshma vardhana

In burrows) Shambooka etc. vipaka, Sheeta veerya Snigdha guna 4) Padina (which eg. Koorma, Balya Mootrala have limbs) Khumbeera, Shishumora etc. 5) Matsya a) Nadeya (Fishes Madhura rasa, Guru Shleshma of river) and Snigdha guna b) Samudra (Fishes eg. Timingala Guru, Snigdha, Ushna Shleshma of sea) Kulisha etc. guna, Madhura rasa and vipaka Vihara 1) Nidra atisukha Increases Tamoguna Shleshma vardhana 2) Asya atisukha Increases Tamoguna Shleshma vardhana 3) Diwa swapna Increases Tamoguna Shleshma vardhana 4) Tyakta chinta Kapha and Medas 5) Mruja varjana Inactiveness, laziness Kapha and Medas 6) Tyakta vyayama Increases Agnimandya, Shareera gourava Kapha and Medas 7) Alasya prasakta Kapha 8) Failure to perform Tridosha

Samshodhana therapy

22

Review of Literature Samprapti

SAMPRAPTI

Samprapti is defined as the description of the evolution of the disease in

sequential order, commencing with dosha vaishamya till the disease manifest fully22. It

includes the vaishamya of dosha, dushya, agni, srotas. Knowledge of this is very helpful

to the physician both for correct diagnosis of the disease and also for deciding the

appropriate treatment.

According to Sushruta, too much indulgence in the etiological factors related to

Prameha results into Aparipakva Vata, Pitta, Kapha and Meda, which further proceed

through the Mutravaha Srotas to get localized in the Basti Mukha and thus leading to

disease Prameha23. Sushruta has stated that, all the Prameha if left untreated or treated

improperly get terminated into Madhumeha24

Vagbhata described two types of pathogenesis of Madhumeha i.e.

Dahtukshayatmaka and Dosha Avaranatmaka. Further, Vagbhata25 interpreted that in all

types of Prameha, the Dosha and Dushya remain same but still the difference in Mutra

Pravritti is due to specific type of Samyoga between specific Dosha and Anukula

Dushya26. Charaka has explained the pathogenesis in a detailed manner i.e. Samanya

Samprapti of Madhumeha and vishesha Samprapti of Madhumeha.

Samanya Samprapti of Madhumeha27:

Charaka has explained Samanya Samprapti of Madhumeha elaborately. It may be

explained on the basis of Shat kriyakala. The Samanya Samprapti process commences

from the Nidana Sevana.

23


1. Sanchaya: The excessive indulgence in Nidana Sevana of Guru, Snigdhadi Ahara and

Avyayamadi Vihara leads to Kapha Dosha Sanchaya. It is important to mention that the

Kapha Dosha, which gets Sanchita here is having the quality of Bahudravatva, vividly

supported by Charaka28. Due to Nidana Sevana the kapha dosha gets Bahudravatva.

2. Prakopa: The three factors i.e. Nidana, Dosha and Dushya get combined together in

such a precise way that they lead to Prakopa of Bahudrava Kapha rapidly and

Madhumeha in future.

In the first two stages the Anukulatva between Nidana and Dosha ensues. Kaphakara

Ahara Vihara vitiates Kapha Dosha without any resistance due to similar properties.

The Bahudrava Kapha is prone to develop Madhumeha and as it is already present in

excess quantity from the beginning, hence it gets aggravated rapidly when the Anukula

Nidana are continued. This type of Anukulatva may be seen in person having Kaphaja

Prakriti and who are having genetic predisposition for Prameha.

3. Prasara: In this stage, the provoked Kapha gets spread all over the body owing to

Sharira Shaithilya. Sharira Shaithilya being one of the Anukula factors for Nidana

towards the Dosha.

4. Sthana Sanshraya: Vikrita Kapha has affinity towards Bahu-Abaddha Meda due to

their similar properties and gets lodged there. Vikrita Kapha after combining with Bahu-

Abaddha Meda causes its vitiation; the other important Dushya are Sharira Kleda and

Mamsa, which are already increased in large quantity, prior to vitiation of Kapha. The

provoked Kapha with vitiated Meda gets combined with Sharira Kleda or Mamsa or both.

24


This is an important stage because the prodromal symptoms of the disease are manifested

in this stage. It is essential to diagnose the disease at this stage to prevent further progress

of the disease for better prognosis.

5. Vyakta: In this stage, two types of manifestation will occur:

1. Puti Mamsa Pidika due to Mamsa Dhatu vitiation – The vitiated Kapha and Meda

combines with Mamsa Dhatu leading to Puti Mamsa pidika.

2. Mutravaha Srotodushti due to Sharira Kleda Dushti – If vitiated Kapha and Meda

come in contact with Sharira Kleda, then it changes in Mutra, the vitiated Kapha impedes

the openings of Mutravaha Srotas, which are already filled with vitiated Meda and Kleda,

thus producing the disease Madhumeha.

The above two manifestations of Kleda and Mamsa Dushti will occur simultaneously or

in two stages.

6. Bheda: In this stage various complications of the disease manifest and the disease

progresses towards Asadhyata i.e. the disease becomes incurable. The Madhumeha

attains Sthairya (stability) and Asadhya (incurability) status because of its Prakriti and

Vikriti.

Here Chakrapani has explained the term Prakriti and Vikriti that if all the natural

properties of Kapha become abnormal, the Prameha gets chronic and if Kapha gets

provoked further condition of incurability ensues. Involvements of Raktadi Dhatu which

are not similar in qualities to Kapha are considered as Vikriti.

25


VISHESHA SAMPRAPTI:

1) Kaphaja Prameha: The etiological factors first cause the provocation of Kapha

because of its close similarity to the related Hetu. This aggravated Kapha then spreads all

over the body rapidly due to Sharira shaithilya. Meda Dhatu being excess in quantity,

Abaddha and having similar properties with Kapha, the provocated Kapha while

spreading gets amalgamated with Medha Dhatu causing its vitiation. This annexation of

vitiated Meda and Kapha comes in contact with Sharira-Kleda and Mamsa, which are

already in excess quantity resulting Putimamsapidaka On the other hand the vitiated

Kleda gets converted into Mutra. The Kapha along with Meda and Kleda impede the

openings of Mutravaha Srotas resulting into Prameha29

Sushruta narrated Dushya in each Doshik type of Prameha. He narrated vitiation

of Kapha along with Vata, Pita and Meda in Kaphaja Prameha30

2) Pittaja Prameha: Due to its etiological factors provoked Pitta manifests as Pittaja

Prameha. Here similar pathogenesis occurs as described in Kaphaja Prameha31

Depending on different properties of Pitta Dosha the Paittika Prameha develops into six

types. Pittaja Prameha is not entirely Paittika but it does have Pitta predominance as it is

mentioned Charaka. There is dominance of Pitta Dosha in comparison to Kapha Dosha

and Vata Dosha, in Paittika Prameha.(Chakrapani). Sushruta related Shonita along with

Vata, Kapha and Meda in the pathogenesis of Pittaja Prameha32

(3) Vataja Prameha: Here Vata gets provoked due to its own etiological factors and

draws out Vasa-Adi Dhatus from the body towards Basti resulting into four types of

Vataja Prameha. When Oja is drawn towards Basti due to vitiation of Vata, the natural

26


Madhura Swabhava of Oja due to the Ruksha Guna of Vata gets transformed into

Kashaya Rasa leading to the manifestation of Madhumeha33

One more pathogenesis of Vataja Prameha is described in Chikitsa Sthana. Here

provoked Vata due to depletion of other two Dosha carries vital Dhatus towards Basti,

resulting into Vataja Prameha34 As per Sushruta Kapha, Pitta, Meda, Vasa and Majja take

part in pathogenesis of Vataja Prameha35.

Madhumeha due to Margavarana:

Due to the Nidana sevana, the kapha, Pitta & Medas attain an Ati

pravruddhavastha. This causes Margavarana of Vata, resulting in Vata dushti. The Dushta

vata does the Adana of the Ojas into the Basti producing Madhumeha. The Vata, Pitta

and Kapha doshas start manifesting their symptoms intermittently depending on their

extent of Dushti. Subsequently, they attain Kshayavastha due to Kshaya of Dhatus again

leading to Vata vriddhi. Here kshaya avasta means pitta and kapha are less severely

vitiated when compared to vata.

This process of Margavarana of Vayu due to Kapha & Pitta occurs in two kinds of

people, firstly in those who are Sthoola and secondly in those who are not Sthoola but

have indulged in Kaphamedokara ahara and vihara. If the Nidana for Pitta are significant

then it also gets Dushta. Anyway, it should be remembered that the role of Pitta is only

secondary in nature. In Sthoola people, the Sthoulya is the result of two reasons. First is

due to excess indulgence in Kaphakara ahara vihara and second is due to Beeja dushti. In

the former case, the vriddi of Medas occurs due to the Nidana sevana. Whereas in the

latter case, the Medo vriddi occurs even in the absence of Kaphamedokara ahara vihara

as the Beeja dushti would have occurred in the Medas in such a way. In both the cases,

27


the Kapha, Medas and Pitta if involved cause Margavarana of Vayu leading to

Madhumeha. Hence, this variety of Madhumeha has been conspicuously identified by

Sushruta as Apathya nimittaja Madhumeha36.

Madhumeha due to Dhatukshaya:

This variety of Madhumeha is triggered by Dushta vata due to Dhatu kshaya. The

Dhatukshaya avastha is essentially seen in Sahaja Madhumehi and as a terminal

consequence of other Prameha. The patients with Sahaja Madhumeha are Krusha,

Alpashee, Pipasubhrisham and Paribhramanasheela unlike Sthoola Madhumehi who are

Sthoola, Bahvashee and with Shayyasana swapna sukherati. Madhumeha occurs in

Sahaja Madhumehi as a direct consequence of Vata because of the inherent nature of

such Rogi.

But Madhumeha as a result of Dhatukshaya in patients, who were Sthoola in the

beginning but became Krusha due to long standing disease, aggravates further due to

Dhatukshaya janya vata vriddhi. This stage can also be seen a terminal consequence of

Prameha due to other causes.

Samprapti of Sahaja Madhumeha:

Madhumeha has been described as a Sahaja vyadhi because it is caused due to

Upatapa of Beeja, Beeja bhaga or Beejabhaga avayava, resulting in Madhumeha

arambhaka dosha dushti in parents suffering from Madhumeha. Hence, this disease is

transmitted from generation to generation making Madhumeha a Kulaja vikara, justifying

Sushruta’s inclusion of Madhumeha under Adibala pravrutta vyadhi.

28


The Beejabhaga avayava responsible for the genesis of Vapavahana, undergoes

Upatapa during the formation of Garbha depending on the existence of the disease in

Mata, Pita or both of them. The extent of Upatapa depends on the predominance of the

Doshas during the formation of Garbha. This results in “Jatah khavaigunya”. The

development of the disease in such people also depends on the predisposition to the

disease in the factors like Prakruti, Desha, Kala, Bala, Nidana and the resultant Dosha

dushya sammurchana. Accordingly, the disease manifests early in the Balya avastha or in

later stages of life depending on when one or more of these factors exert their influence.

Hence, it can be conveniently inferred that a patient born to parents, both of

whom are Madhumehis has a higher chance of developing the disease than a patient one

of whose parent is Madhumehi. Moreover, the patient whose Mata is a Madhumehi is

more likely to develop the disease than in the patient whose Pita is Madhumehi, because

the Dushyas in Madhumeha are mainly Matruja avayavas and Dhatus like Vapavahana,

Medas, Mamsa and so on.

The Sahaja Madhumehi hence is usually Krusha, Alpashee, Pipasabhrisha and

Paribhramanasheela leading to Dhatukshayajanya vata dushti. Therefore a preexisting

Khavaigunya in Vapavahana is initiated by Dushta vata leading to Madhumeha38.

SAMPRAPTI GHATAKA OF MADHUMEHA:

Dosha: Shleshma Pradhana Tridosha. Shleshma is the Pradhana dosha responsible for

Madhumeha inspite of the fact that Madhumeha is a Tridoshaja vyadhi. Hence it is also

called Madhumeharambhaka dosha. It is known that Shleshma is a Rasa mala. The

Shareerastha shleshma is continuously nourished by this Rasa mala shleshma during

Parinama of the Ahara rasa into Rasa dhatu by the action of Rasadhatvagni. When a

29


person indulges in Shleshmakara ahara vihara as in Madhumeha, the Agnimandya of

Jatharagni leads to Asamyak ahara parinama of ahara especially with relation to

Shleshma resulting in Aparipakvata of shleshma or in other words, Amaroopi sleshma

utpatti.

This Amaroopi shleshma attains Aghanata as there is loss of Samhanana in the

Kaphaswaroopa. This leads to Bahudravata of Shleshma set to cause further Dhatu

dushti. Therefore evidently, Shleshma is the primary dosha of the diseas, the other

Doshas like Vata & Pitta only trigger off this Samprapti and associate as Anubandha.

Dushya: Rasa, Rakta, Mamsa, Meda, Majja, Shukra, Vasa, Oja, Lasika, Kleda and

Acording to Vaghbhata Sweda.

Srotodushti: The Srotodushti lakshana occur as Sanga of Kapha leading to

Vimargagamana and Atipravrutti of Kleda through the mootra.

Agni: Vaishamya of all Agni (or Dhatvagnimandya)

Ama: Medogata Ama produced due to Jatharagnimandya and Dhatvagnimandya.

Adhisthana: Basti

Udbhavasthana: Amashaya

Bhedavastha: Occurrence of Upadrava such as Puti Mamsa, Pidika etc.

Nature: Chirakari, Anushangi39

(A) Dosha: All the three Doshas are responsible for manifestation of Madhumeha.

i) Kapha: It plays the dominant role in the Samanya Samprapti of Madhumeha. It is the

first Dosha to get vitiated. Acharya Charaka while describing the causative factors used

30


the term ‘Kaphakrut Cha Sarvam’ in it. It indicates the significance of this Doshadushti in

Madhumeha. Sharirashaithilya is the consequence of Bahudrava Kapha. Other ensuing

manifestations are Alasya, Atinidra, Tandra, etc.

(ii)Pitta: Here, in Avaranajanya Madhumeha mainly the symptoms manifest because of

Vriddhi of Pitta Dosha (Trishna, Daha, Kshudha and Trunshavriddhi) 40 Pitta is in

Kshaya Avastha as compared to Vata in the Vataja Prameha pathogenesis. So, Kshaya

Lakshana of Kapha Dosha and Pitta Dosha may manifest in Kshayajanya Madhumeha. 41,

Pitta Kshayajanya Lakshanas are Mandagni, Prabhahani, Shitata etc while Kapha

Kshayajanya Lakshanas are Bhrama, Hriddrava, Slathasandhita etc.

(iii)Vata: This is the prime Dosha in the pathogenesis of Madhumeha. Here Vata get

aggravated either because of its own etiological factors or because of Avarana caused by

Kapha Pitta and Meda. This provoked Vata carries the vital constituents of the body like

Vasa, Majja, and Oja towards Basti and excretes them outside through urine resulting in

depletion of the Dhatu. Thus due to severe depletion of Dhatus, the symptom manifests

are Karshya, Daurbalya, Angasuptata and Parisaranshila nature.

In Sushruta samhitha it is described that Vyana and Apana are the main culprits in

Prameha. Here mainly the function of Vyanavayu gets hampered because of the

accumulation of vitiated Dushya at macro and microcellular level. Thus in all the

Samprapti of Prameha Vyana acts as gatherer of Kleda and Apana as excretor.The

function of Apana Vayu gets aggravated resulting excretion of vital Dhatus through the

urine outside the body42.

31


(B) Dushya: Nidana, Dosha and Dushyas are the three factors responsible for the

manifestation of every disease. But when they are having Anukulatva disease establishes

in its way. So Anukulatva of these factors is important in Madhumeha. The following are

Dushya involved in Madhumeha:

i) Rasa: Rasa is the seat of Kapha Dosha and at the same time it is the Mala of Rasadhatu.

So provoked Kapha has affinity towards the Rasadhatu. The symptoms like Alasya,

Gaurava, Karshya, Hrillasa, Angamarda, Sada, Pandutva, Klaibya etc. are produced as a

result of Rasa Dushti.

ii) Rakta: It mainly gets vitiated in Pittaja Prameha. The Rakta Dusti Lakshana are Daha,

skin diseases like Kustha, Visarpa, Pidika, Dadru, Charmadala, Pama, Kotha,

Asramandala or the systemic diseases like Kamala as Raktapradoshaja Vyadhi43 are

produced as a result of Rakta Dusti.

iii) Mamsa: Mamsa and Kapha are having the same qualities i.e. both give strength to the

body. When Kapha gets vitiated, Mamsa losses its normal consistency and develops

Shaithilya and provides space in between for the accretion of morbid matter. This

consequently results into the Puti Mamsa Pidika. "Mamsaleshu Avakasheshu"44

iv) Meda: It is the dominant Dushya in all types of Prameha. It gets vitiated both

quantitatively and qualitatively. Kapha and Meda have close resemblance as they have

the same qualities. Both get vitiated more or less by same etiological factors.

In Madhumeha vitiation of Meda results in two ways:-

32


Qualitative [Abadhdha, (Asamhata)]: Normal function of Meda is to produce

unctuousness in the body along with Dridhatva i.e. compactness. So this Abaddhatva

causes derangement in the structure of Meda producing Shaithilya in the body.

Quantitative (Bahu): Here in the pathogenesis, Meda is in excess quantity. This Medo

Dhatu is Aparipakva (Ama). 45

Meda Dhatu is the most Anukula Dushya for provoked Kapha Dosha. Guru Snigdhadi

Ahara and Avyayamadi Vihara leads to. Bahutva of Meda Dhatu, due to

Dhatvagnimandya. Whatever food obese persons take, it gets converted into Meda and

other Dhatus remains under-nourished leading to Dhatukshaya. Along with Bahutva,

Dhatvagnimandya also results into Abaddhatva of Meda. Such an Abadhdha Meda gives

‘Sharira Shaithilya’ and instead of doing Asthi Poshana; Meda Dhatu gets itself over

burdened which is harmful to the body.

Meda Dushti may manifest in many ways .The deranged Meda produces following signs

and symptoms which are the eight Doshas of Atisthula person. 46

Ayushorhrasa, Javoparodha, Kricchravyavayata, Daurbalya, Daurgandhya, Swedabadha

Kshudha-Ati Matra, Pipasa-Atiyoga.

By observing above description certainly it can be asserted that in Samprapti of

Madhumeha, Meda plays the foremost role.

v) Majja: Due to Vata Prakopa Kshaya of Majja Dhatu occurs. Thus vitiated Majja

produces clinical symptoms like, Netragaurava. Angagaurava in Madhumehi47

vi) Shukra: Shukra Dhatu gets affected in the pathogenesis of Prameha, which due to its

vitiation produces symptoms like Daurbalya and Kricchravyavayata. In Sahaja Prameha

33


Shukra has an important role to play. Prameha is a Kulaja Vikara and occurs as result of

Beeja Dosha. Sushruta has described that Shukra Dosha and Prameha get precipitated

because of the vitiation of Vyana and Apana Vayu. Vata causes depletion of Shukra

Dhatu and also Shukrameha. So one can appreciate the importance of Shukra Dushti in

Prameha.

vii) Vasa: It is an Upadhatu of Mamsa and is ‘Sleshmika’ in character. The provoked

Vata draws Vasa towards Basti and excretes it through the urine in the form of Sneha. In

case of Madhumeha, the Dushti is illustrated in the form of Bahutva as well as

Abaddhatva (Chakrapani) but still the manifestations are not described concerning Vasa

Dushti.

viii) Lasika: The aggravated Vata propels Lasika towards the Basti and then excretes it

through the urine leading to increased micturation. Lasika is described as a Dushya in

Hastimeha.

ix) Oja: Oja is supreme extract of all the Dhatus and gives strength and immune power to

the body. Oja is the purest quality of Sleshma in its constitution, Guna and Karma. Oja is

an important Dushya in the Samprapti of Madhumeha. Here provoked Vata transforms

the Madhuratwa of Oja into Kashayatwa and carries Oja towards Basti and excretes

through urine leading to Ojakshaya. So the symptoms of Ojakshaya like Murccha,

Mamsakshaya, Moha, Daurbalya (excessive weakness), Vyathita Indriya, Rukshata,

Gurugatrata, Nidra, Tandra etc. may manifest.

x) Kleda: It is also an important Dushya after Meda. The literal meanings of Kleda are –

wetness, moisture, dampness etc.). It has been mentioned by Charaka that Kleda gives

34


Shaithilya to Sharira. Charka has given Ambu as a synonym to Kleda. Normal function of

Mutra and Sweda has been described by Vagbhata as follows.48

Under normal physiological conditions Mutra and Sweda maintain balance of

Kleda in the body. If this Kleda gets vitiated it directly affects the Mutra and Sweda and

disrupts the physiology of bodily elements causing Shaithilya. Arundatta has mentioned

that absence of Kleda may lead to the dryness of the body. In the Samprapti, Kleda

Dushti is in the form of ‘Vriddhi’ and not the Kshaya. Hence, Bahu Kleda will manifest

as Prabhuta Mutrata and Avila Mutrata because extensively increased Kleda is excreated

out of the body as Mutra. The other manifestations of Kleda Dushti may be Shithilangata,

Ati Sweda Pravritti, Visra Sharira Gandha (due to excessive sweating), Sharira Mruduta,

Snigdhata etc 49

xi) Sweda: This Dushya has been mentioned only by Vagbhata. Sweda is mainly related

with Meda and Kleda. Due to the vitiation of Meda and Kleda, Swedavaha Srotodushti

occurs leading to the manifestation of Ati Swedapravritti, Daurgandhya, Picchilagatrata,

Snigdhagatrata Visra-sharirgandha etc. Sushruta mentioned that in Madhumeha Sweda

becomes Sweet in nature 50 The whole pathological phenomenon described in Kleda and

Sweda Dusti can be correlated with water and electrolyte imbalance.

C) Srotodushti: In the Samprapti of Madhumeha two types of Srotodushti are found:

1. Atipravritti 2.Vimargagamana

D) Agni:

Madhumeha is a complex metabolic disorder which results from the Dhatwagnimandya.

All the metabolic activities are governed by Agni and its derangement leads to so many

35


metabolic disorders and Madhumeha is one of them. Agni functions at the level of

Jatharagni, Bhutagni and Dhatwagni. When they function properly, each & every Dhatu

is nourished & formed properly. But when there is derangement in these Agni, then

Dhatu are not nourished & formed properly. In case of Avaranajanya Madhumeha due to

Kaphakara Nidana, Dhatvagnimandya & particularly Medodhatvagnimandya develops

and due to this, excessive but Sama Medodhatu is formed leading to more vitiation of

specific Dhatu which obstructs the Gati of Vata leading to its provocation. Due to this

provocation of Vata, Jatharagni gets stimulated leading to increased appetite. This cycle

goes on. Therefore, in Madhumeha the Dushya Dushti mostly occurs in the form of

Vriddhi reflecting Dhatvagnimandya. Due to Medodhatvagnimandya there is less

nourishment to further Dhatus which results into Kshaya Lakshana of Majja and Shukra

Dhatu.

E) Ama: Sushruta has illustrated the role of Ama in the pathogenesis of various

disorders. He mentions that the Samprapti of Prameha takes its origin from the Ama only.

He states51 that is from the very beginning, Agnimandya has been developed due to Guru,

Snigdhadi Ahara and Avyayamadi Vihara which leads to production of Ama. Dalhana

adds that not only Dosha but Meda Dhatu is in the Ama form. Hence Ama is a part and

parcel of Samprapti. Ama means Aparinamitta. Anything which remains in undigested

form, being harmful to the body is Ama. It is Apakva (undigested), Asyaukta (Shithila),

Durgandhi, Picchila in nature and it produces Gatrasada. In the Samprapti of

Madhumeha, we also get the dominance of Ama regarding Kapha Dosha, Meda Dhatu,

Mamsa Dhatu, and Kleda. The undigested Kapha and Meda acts as Ama vitiating the

36


Mutravaha Srotas leading to Madhumeha. This vitiation is in the form of Srotas

obstruction.

CLASSIFICATION AND PATHOGENESIS OF DIABETES MELLITUS52

Primary DM: The basic categories of classification of DM are based on the

recommendations by the National diabetes data group. The disease DM is divided

broadly into Primary DM & Secondary DM. Primary implies that no associated disease is

present while in the secondary category some identifiable condition causes or allows a

diabetic syndrome to develop. Insulin dependence in this classification is not equivalent

to insulin therapy rather the term means that the patient is at risk for diabetic ketoacidosis

(DKA) in the absence of insulin. Many patients classified as non-insulin dependent

require insulin for control of hyperglycemia although they do not become ketoacidotic if

insulin is withdrawn.

The term type 1DM is often used as a synonym for insulin dependent diabetes

mellitus (IDDM) and type 2 DM is considered equivalent to non insulin dependent

diabetes mellitus (NIDDM). This linkage is not ideal because subsets of patients with

apparent non-insulin dependent DM become fully insulin dependent & prone to

ketoacidosis. Hence a modified classification has been suggested so that the terms,

insulin dependent & non-insulin dependent describe physiologic states (Ketoacidosis

prone & ketoacidosis resistant respectively) while the terms type 1 and type 2 refer to

pathogenetic mechanisms (immune mediated & non immune mediated respectively).

Using such a classification three major forms of primary DM would be recognized, Type

1 IDDM, Type 1 NIDDM and Type 2 NIDDM.

37


Category (2) is an intermediate range of autoimmune destruction in which the capacity to

produce insulin is sufficient to prevent ketoacidosis but not to maintain normal blood

glucose. This variant likely occurs when the autoimmune process begins at an older age

and progresses more slowly than usual. A subset of obese people with apparent non-

insulin dependent can become transiently insulin dependent and develop diabetic

ketoacidosis. Such individuals do not have markers of autoimmunity suggestive of type 1

DM and may not require insulin permanently after recovery from DKA. Presumably

diminution of insulin renders such subjects vulnerable to stress induced metabolic

decompensation & causes transient insulin dependence.

Secondary DM: There are several secondary forms of DM. Pancreatic disease

particularly chronic pancreatitis in alcoholics is a common cause. Hormonal causes

include pheochromocytoma, Acromegaly, Cushing’s syndrome & administration of

steroid hormones.

“Stress hyperglycemia” associated with severe burns, acute myocardial infarction

and other life threatening illness is due to endogenous release of glucagons &

catecholamines. Hormonal hyperglycaemia results from various combinations of

impairment of insulin release and induction of insulin resistance. A large number of drugs

can lead to impaired glucose tolerance or hyperglycaemia and even ketoacidosis can be

due to quantitative or qualitative defects in the insulin receptor or to antibodies directed

against it. The mechanism is essentially pure insulin resistance.

Genetic syndrome associated with impaired glucose tolerance or hyperglycaemia

includes the lipodystrophies, myotonic dystrophy and ataxia telangiectasia. The final

category i.e. others is poorly defined and is meant to include any condition that does not

38


fit elsewhere in the aetiologic scheme. The appearance of abnormal carbohydrate

metabolism in association with any of these secondary causes does not necessarily

indicate the presence of underlying DM although in some cases mild asymptomatic

primary DM is made overt by secondary illness.

Pathogenesis of IDDM: Pathogenesis begins with a genetic susceptibility to the disease,

with the destruction of islet β cells of pancreas almost complete due to an autoimmune

process. Viral infection is a triggering factor but non-infectious agents may also be

involved. Autoimmune attack then follows. The islet β cells become infiltrated by

monocytes/macrophages & activated cytotoxic T cells. This infiltration is usually called

Insulitis or sometimes called Isletitis. Multiple antibodies against β cells antigens are

present in the blood. The patients’ state while the immune attack is underway but

unrecognized is termed pre-diabetes. This stage may by brief or prolonged and may be

progressive and uninterrupted or intermittent. What is clear is that the insulin reserve

steadily diminishes until it is insufficient to maintain blood glucose within normal limits.

At this point the diagnosis is DM. Rarely type 1 DM develops exclusively from an

environmental result, as from the ingestion of Vacour-a rat poison. It is also possible that

an autoimmune DM can develop in the absence of an environmental trigger i.e. can be

purely genetic. Usually however the pathogenetic sequence is,

Genetic predisposition

Environmental insult

Autoimmune destruction of β cells

Diabetes mellitus (IDDM)

39


Destruction of β cells and development of IDDM: The loss of insulin reserve occurs over

a few to many years. The earliest sign of abnormality is the development of islet cell

antibodies when the blood sugar & glucose tolerance are normal and when insulin

responses to glucose load are intact. The second phase ensues after this where there is

only decreased glucose tolerance. Fasting blood sugar remains normal. This is the last

pre-diabetic stage. In the third phase, fasting hyperglycemia develops but ketosis does not

occur even when the DM is poorly controlled and the clinical appearance is that of

NIDDM. Continued destruction of β cells then leads to insulin dependent stage and a

propensity for ketoacidosis especially during stress. Once this stage is acquired the

patient ordinarily requires lifelong insulin therapy. The immune directed destruction of β

cells probably involves both humoral & cell mediated mechanisms. Cells involved in the

attack on β cells include natural killer cells, activated cytotoxic T lymphocytes and

macrophages cell destruction may be at least partially due to release of cytokines such as

interlukin I (IL-I)) and tumour necrosis factor α (TNF α) from activated macrophages.

Cytokines may work through induction of nitric oxide or of super oxide. β Cells have a

low capacity for free radical destruction and are especially vulnerable to oxygen toxicity.

Pathogenesis of NIDDM: NIDDM is more common than IDDM. Its pathogenesis is less

well understood. The relation between the β cells abnormality and insulin resistance is

not resolved. The major environmental factor is obesity. Both β cell defects and insulin

resistances are present in the overt disease, which more commonly exhibits familial

aggregation. Patients with type 2 NIDDM have two physiologic defects viz. abnormal

insulin secretion and resistance to insulin action in target tissues, which of the

abnormalities is primary is not known. Descriptively, three phases can be recognized in

40


the usual clinical sequence. In the first phase, plasma glucose remains normal despite

demonstrable insulin resistance because insulin levels are elevated. In the second phase,

insulin resistance tends to worsen so that postprandial hyperglycaemia develops despite

elevated insulin concentrations. In the third phase, insulin resistance does not change but

declining insulin secretion causes fasting hyperglycaemia and overt DM. Most authorities

believe that insulin resistance is primary and that hyper insulinaemia is secondary i.e.

insulin secretion increases to compensate for the resistance state. However, hyper

secretion of insulin may cause insulin resistance i.e. a primary islet cell defect causes

insulin hyper secretion and insulin hyper secretion in turn leads to insulin resistance.

Explanatory hypotheses increased fat synthesis in the liver and enhanced fat transport

(Via very low-density lipoprotein VLDL) leading to secondary fat storage in the muscle.

Increased fat oxidation could impair glucose uptake and glycogen synthesis most patients

with NIDDM are obese and obesity per se causes insulin resistance, but obesity is not the

sole cause for insulin resistance. It is also true that a modest reduction in weight often

results in major improvement in the blood sugar control in obese patients of NIDDM.

The late decline in insulin release could be due to the underlying genetic defect or to

metabolic toxicity in β cell. High levels of glucose or increased tissue levels of long chain

fatty acids (lipotoxicity) could be the damaging molecules.

In summary, it is likely that an insulin secretory defect and insulin resistance are

both required for DM to be expressed since massively obese persons with marked insulin

resistance may have normal glucose tolerance. Presumably the β cell lesion is not present

in such persons. This fact suggests that the primary defect resides in the insulin producing

cells. β cell mass is intact in type II NIDDM in contrast with the situation in type 1

41


IDDM. The α cell population is increased resulting in an elevated ratio of α to β cells and

in excess of glucagon relative to insulin that characterizes all hyperglycemic states

including NIDDM.

Role of Amylin: Although insulin resistance in type II NIDDM is associated with

decreased numbers of insulin receptors most of the resistance is post receptor nature. It

has long been known that deposits of amyloid are found in the pancreas of patients with

type 2 DM. This material is a 37 amino acid peptide termed Amylin. Amylin is co-

packaged with insulin in secretory granules and is released simultaneously with insulin in

response to insulin secretogogues. In animals, amylin has been reported to induce insulin

resistance but in diabetic subjects an amylin derivative has hypoglycemic effects

apparently because it causes delayed adsorption of nutrients from gastrointestinal tract.

Amylin deposition in islets may be the consequence of overproduction secondary to the

insulin resistance to which it contributes. Alternatively accumulation of amylin in the

islets might contribute to the late failure of insulin production with long standing

NIDDM. A definitive role for amylin is not established.

42


Table No. 2: Classification of DM:

I. Primary

1) Autoimmune (type 1) DM

a) Non insulin dependent Diabetes mellitus (type 1 NIDDM) - Transient

b) Insulin dependent Diabetes mellitus (type 1 IDDM)

2) Non Auto immune DM

a) Insulin dependent Diabetes mellitus (type 2 IDDM) - Transient

b) Non insulin dependent Diabetes mellitus (type 2 NIDDM)

c) Maturity onset Diabetes mellitus of the young (MODY)

II. Secondary

a) DM caused by pancreatic disease

b) DM caused by hormonal abnormalities

c) Drug or chemical induced DM

d) DM caused by insulin receptor abnormalities

e) DM associated with genetic syndromes

f) DM of other causes.

43

Shareera kleda

increase Ojo

aparipakvaDhatu. Agnimandya

Beeja Upatapa (Sahaja)

Shleshma Dushti &

Vata Vriddhi

Margavarana of vayu

Vapavahana dusti

Bahu abadha medas mamsa

etc.

Basti

Mootra

Dhatukshaya Madhumeha

Kaphakara ahara and vihara

(Apathya Nimittaja)

Illustration 4.1: Samprapti of Madhumeha

Review of Literature Poorva roopa

POORVAROOPA

Poorvaroopa are indications of impending diseases. They occur prior to complete

manifestation of disease and may suggest the forthcoming illness. During the course of

the Samprapti of an illness, the morbid Doshas circulating ubiquitously in the body tend

to localize in an area and produces some of the unique symptoms and is referred by the

name Poorvaroopa. Diagnosis at this stage of the illness gains paramount importance, as

the effective treatment at this stage definitely reduces the possible organic damage as

well as degree of morbidity.

As Madhumeha is classified under the Vatika type of Prameha, Purvarupa of

Prameha can be taken as Purvarupa of Madhumeha. If all the Pramehas are neglected

then it results in to Madhumeha. This may be the reason for not mentioning the specific

poorva roopa by our Acharyas for Madhumeha and most of the poorva roopa mentioned

in our classics are the clinical features and complications of Diabetes Mellitus. So, the

poorva roopas of Prameha in general is discussed in this context. Our Acharyas have

given more importance to poorva roopas. According to Sushrutacharya, if all the poorva

roopas are clearly exhibited and if the patient notice a slight increase in mootra, then one

can infer that patient may suffer from Prameha in the near future. If half of the

poorvaroopa are exhibited clearly and patient notice adhikamootra pravritti, then it is the

clear indication of the presence of Prameha.

In olden days vaidyas used to detect the presence of sugar in urine by

pipeelikaabisarana. A patient use to approach a vaidya only when he suffered from

prabhoothamootrapravritti . But he neglected the symptoms like snigdhata of the body,

atinidra etc. which occur much more earlier than the above mentioned cardinal feature.

44


That is why our Acharyas have considered these early stages as poorva roopa.

From the above description it is clear that the Acharyas were able to diagnose

Madhumeha only at a later stage. In the present era due to the advanced technologies the

same can be diagnosed well in advance by examining the sugar level in blood and urine.

Thus we can say that, most of the poorvaroopa mentioned in our classics are actually the

clinical features and complications developed due to Diabetes Mellitus.

Pre-Diabetic States53

Sometimes a patient with abnormal hyperglycemia may not have full clinical

symptoms of Diabetes mellitus and often pre-diabetic states are asymptomatic. Mild

symptoms if manifested go unrecognized but the identification of such stages can go a

long way in prevention of an overt disease. The British Diabetic Association has

suggested a classification that is accepted by W.H.O. expert committee on Diabetes. They

are as follows:

Potential Diabetes: These are persons who have high probability of developing Diabetes.

They do not show any evidence of impaired glucose tolerance. They include, a) Identical

twin of a diabetic, b) Persons with both the parents diabetic, c) Persons with one parent

diabetic, the other non-diabetic parent having a diabetic parent or a diabetic sibling or

their offspring having Diabetes.

Latent Diabetes: a) Persons with a normal G.T.T. at present, but had an abnormal G.T.T.

sometime in the past viz. during pregnancy, infection when under stress or when obese,

b) Persons with a normal G.T.T. under standard conditions but an abnormal one with

provocative tests.

45


Asymptomatic Diabetes: This stage is variously known as chemical, subclinical or

subliminal Diabetes. They always show an abnormal G.T.T. but the fasting blood levels

may be normal in the early stage. Later on, even these levels may be raised.

46


Table No. 3 - Poorva roopa54, 55,56

Sl. No.

Poorvaroopa Charaka Samhita

Sushruta Samhita

Ashtanga Hridaya

1 2 3 4 5 6 7 8 9

10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40

41 42

Sweda Angagandha Angashaithilya Angasada Shayya sukherati Swapna sukherati Asana sukherati Hridayopadeha Netropadeha Jihwopadeha Shravanopadeha Taluni malotpatti Danteshu malotpatti Ghanangata Kesha ativruddhi Kesha jatilibhava Nakha ativruddhi Sheeta priyatwam Galashosha Talushosha Asya madhurya Kara daha Pada daha Mootrapipeelika abhisarana Madhura mootrata Shukla mootrata Snigdha gatrata Picchila gatrata Guru gatrata Pipasa Shwasa dourgandhya Tandra Kara suptata Pada suptata Anga suptata Alasya Mukha shosha Kayachidreshu upadeha Sarvakale nidra Shatpada pipeelika abhisarana on shareera Shatpadamootra abhisarana Pipeelika shareera abhisarana

+ + + - + + + + + + + - - + + + + + + + + + + + - - - - - + - + + + + + + + + +

+ +

- + - + - - - - - + - + + - - + + - - - - + + - + + + + + + + + - - - - - - - - - -

+ + + - + + + + + + + - - + + - + + + + + + + + - - - - - - - - - - - - - - - - - -

47

Review of Literature Roopa

ROOPA

Under the heading Roopa the signs and symptoms produced in an individual as a

result of sequential changes in the disease process can be studied. Roopa of a disease will

be produced in the fifth stage of samprapthi i.e. vyaktavasta. In this stage doshadooshya

sammurchana will be capable to produce its laxana.

In classics, laxana of Madhumeha are only ascribed to mootra and mootra

pravrutti which remains incomplete without the study of sarvadaihika laxana explained in

the contexts of aapatyanimitaja and sahaja madhumeha by Sushruta. Hence the laxana of

Madhumeha are mainly grouped under two categories, that is 1.mootra sambandi laxana

2.sarvadaihika laxana.

MOOTRA SAMBHANDI LAXANA:

The laxana in relation with mootra are to be studied under two heads A. samanya laxana

B. vishesha laxana.

A. SAMANYA LAXANA:

1. Prabhootha mootrata: This is the cardinal sign described by all Acharyas.

Vagbhata mentioned Prameha as the disease of Mutraatipravrtija Patient Voids urine

more in quantity and frequency57. Gayadasa opines that this excess urine quantity is

because of liquification of the Dushyas and their amalgamation58.

2. Avilamutrata: Patient voids urine having hazy consistency or having turbidity.

Gayadasa and Dalhana both opine that, this characteristic feature of urine is because of

the nexus between mutra, Dushya and Dosha59 Vagbhata also emphasized that this

turbidity of the urine is because of its annexation with the dhatus60.

48


Kashyapa61 mentioned following symptoms of Prameha to be observed in pediatric

patients

Akasmat Mutra Nirgama: Child excretes urine suddenly with no intention.

Makshika Akranta: Flies get attracted towards the urine.

Shweta and Ghana Mutra: Child excretes urine having Shweta colour and solid

consistency i.e. turbidity

B. VISHISTA LAXANA62:

1. Madhurata: Here Madhurata refers to madhura rasa that is entirely due to Apakva ojas.

The Rasa of Ojas is Madhura and hence also of the Mootra as is evidenced by the

attraction of Shatpadapipeelika towards the Mootra.

2. Rooksha: Refers to the Guna and Rooksha guna is due to vriddhavata.

3. Pandu: Refers to the Varna of urine. The urine would have lost its normal varna as a

result of abnormally increased Shareera kleda.

4. Kashaya: The term Kashaya denotes both Rasa as well as Kashaya kalpana which are

usually dark brown to black in colour. Bhavaprakasha in his description of the condition

mentions that the word Kashaya should indicate the Varna of Kashaya i.e. dark brown to

blackish. But when we analyze this description, it becomes evident that the Rasa of urine

cannot be Madhura and Kashaya at the same time. Moreover, if the Kashaya rasa had

been an accompaniment of Madhura rasa, it must have been less predominant because,

the Pipeelikas or ants are drawn towards only Madhura rasa. If we consider Kashaya as

Varna in Madhumeha it is almost a non-occurrence in cases of Madhumeha, as we

understand it in the form of Diabetes. The Kashaya varna can be an occurrence in

conditions of Nephropathy as a sequel of DM. Hence, this speculation can be clarified

49


with an argument that does not nullify the opinion of Bhavamishra and therefore the

Kashaya varnata could be understood as a terminal manifestation of DM.

5. Madhusama mootra63: Varna, gandha, rasa of mootra will be similar to that of madhu.

It is due to the ojonissarana in mootra. This situation is similar to the previous one that

can be analyzed on the basis of Vagbhata’s statement, that the Samanya roopas of

Prameha are Prabhoota and Avila mootrata and the other Vishesha roopas are seen

depending on the Dosha and Dushya samyoga where, the urine assumes the respective

character in terms of Varna, Rasa, Sparsha and Gandha. When this is applied to

Madhusamam, it can mean that urine resembles honey in taste, colour, touch and smell

but clinically and literally the disease favors more towards resemblance of urine with

honey in its taste rather than other qualities, Nevertheless the Varna of honey is also

darkish brown and can be understood as discussed earlier under the previous heading of

Kashaya.

SARVADAIHIKA LAXANA64:

Apathyanimittaja madhumeha:

1) Sthoulya, 2) Bahvashee, 3) Snigdha, 4) Shayya asana swapna sheela.

Sahaja Madhumeha:

1) Krisha, 2) Alpasheela, 3) Rooksha, 4) Paribhramanasheela

Other than these, some other laxana are found in different context in Ayurveda. They are

1. Tanumaduryata65: Due to the circulation of madhura, snigdha, bahudravashleshma

along with aparipakwa rasa dhatu through out the body because of shareera shithilata one

can notice tanumaduryata.

2. Vranaha kruchrena sidyanthi: Delayed healing of wound is seen in Madhumeha. For

50


this Chakrapani gives reasoning as Dustadushyataya.

3. Sushruta explains the nature and the extent of klama of a Madhumehi by the following

version. He says that Madhumehi prefers to stand instead of walking , he likes to sit

instead of standing, he desires to lie down instead of sitting and he prefers more to sleep

than all the above

Apart from these Pratyatma roopa, the mootrasambadhi roopa Kaphaja,

Pittaja and Vataja Prameha are described as follows66, 67, 68

Kapha Pradhana Vatanubandha Madhumeha (Kaphaja Prameha):

Prameha Mootra lakshana

1) Udakameha : Accha, Bahusita, Sheeta, Nirgandha, Udakopama

2) Ikshuvalika rasa meha : Atyartha madhura, Sheeta ,Ishatpicchilam,

Avilam, Kandekshu rasa sankasham.

3) Sandrameha : Paryushita, Sandribhavati bhajane

4) Sandraprasadameha : Samhanyante mootram

5) Shuklameha : Shukla, Pishtanibham, Abhikshnam

6) Shukrameha : Shukrabham, Shukramishram, Muhurmehati.

7) Sheetameha : Atyartha madhuram, Sheetam

8) Sikatameha : Katina mootrata

9) Shanairmeha : Mandam, Mandavegam, Kruchram

10) Alalameha : Tantubaddha iva, Alalam, Picchilam

11) Surameha : Suratulyam

51


12) Lavanameha : Vishada, Lavana tulyam

13) Pishtameha : Pishtarasa tulyam

14) Phena meha : Stokam stokam, Saphena

Pitta pradhana Vatanubandha Madhumeha (Pittaja Prameha):

1) Ksharameha : Kshara tulya varna-rasa-sparsha

2) Kalameha : Masi varna, Ajasram, Ushnamootra

3) Neelameha : Chashapakshi nibham, Amlam

4) Raktameha : Visra, Lavanam, Ushnam, Raktam

5) Manjistameha : Manjistodaka sankasha, Visra

6) Haridrameha : Haridrodaka sankasha, Katuka

7) Amlameha : Amla rasa, Amla gandha

Vata Anubandhya Madhumeha (Vataja Prameha):

1) Vasameha : Vasamishram, Vasabham

2) Majjameha : Majjanam

3) Hastimeha : Hastimatta iva ajasram, Lasika.

4) Madhumeha/Kshaudrameha : Kashaya,Madhura, Pandu varnata, Ruksha

5) Sarpimeha : Sarpiprakasham

52


CLINICAL FEATURES69

The manifestations of symptomatic diabetes mellitus vary from patient to patient.

Most often, symptoms are due to hyperglycemia (polyuria, polydipsia, polyphagia), but

the first event may be an acute metabolic decompensation resulting in diabetic coma.

Occasionally, the initial expression is a degenerative complication, such as neuropathy, in

the absence of symptomatic hyperglycemia. The metabolic derangements of diabetes are

due to a relative or absolute deficiency of insulin and a relative or absolute excess of

glucagon. Normally, a rise in the molar ratio of glucagon to insulin leads to metabolic

decompensation. Changes in this ratio can be caused by a fall in insulin or a rise in

glucagon concentration, separately or together. Alteration in the biologic response to

either hormone would have the same effect. Thus, insulin resistance could cause the

metabolic effects expected of an elevated glucagon/insulin ratio, even if the ratio found

by immunoassay of the two hormones in plasma were normal or even decreased (the

glucagon being biologically active, the insulin relatively inactive). Typically, the clinical

features of IDDM and NIDDM are distinctive.

Insulin-Dependent Diabetes IDDM usually begins before age 40; some patients develop

type 1 diabetes late in life, with a first episode of ketoacidosis occurring at age 50 or even

later in rare instances. These patients, who on the basis of age should have type 2

NIDDM, are usually not obese. Onset of symptoms may be abrupt, with thirst, excessive

urination, increased appetite, and weight loss developing over several days. In some

cases, the disease is heralded by the appearance of ketoacidosis during an intercurrent

illness or following surgery. As outlined in type 1 patient may have normal weight or

may be wasted, depending on the length of time between onset of symptoms and start of

53


treatment. Characteristically, the plasma insulin level is low or immeasurable. Glucagon

levels are elevated but are suppressed by insulin administration. Once symptoms develop,

insulin therapy is required. Occasionally, an initial episode of ketoacidosis is followed by

a symptom-free interval (the "honeymoon" period), during which no treatment is

required.

Non-Insulin-Dependent Diabetes: NIDDM usually begins in middle life or later. The

typical patient is overweight. Symptoms begin gradually, and the diagnosis is frequently

made when an asymptomatic person is found to have an elevated plasma glucose level on

routine laboratory examination. In contrast to IDDM, plasma insulin levels are normal to

high in absolute terms, although they are lower than predicted for the level of the plasma

glucose; i.e., relative insulin deficiency is present. Stated in another way, if plasma

glucose concentrations in nondiabetic subjects were raised to levels equivalent to those

found in NIDDM patients, insulin values would be higher in the normal group. This

relative deficiency reflects the previously mentioned insulin secretory defect in NIDDM.

Glucagon metabolism in NIDDM is complex. While the elevated fasting plasma

concentrations can be lowered by large amounts of insulin, the exaggerated glucagon

response to ingested nutrients cannot be suppressed; i.e., alpha cell function remains

abnormal. For unknown reasons, patients with NIDDM do not develop ketoacidosis but

are susceptible to development of hyperosmolar, nonketotic coma.

54

Review of Literature Upadravas

UPADRAVA

Upadrava are manifestations of severe forms of the Roga, and are Rogashraya.

They occur alongside the disease or as a sequele. In either form, they mark the beginning

of fatality. Unless so severe as to warrant a special attention, they subside with disease.

The disease Madhumeha, when severe, involves almost all Dhatu and the

respective Srotas. Accordingly, Upadravas appear as and when a particular Srotas is

affected. The Upadravas of Madhumeha can be studied under the following headings. 1.

Samanya upadravas 2. Vishishta upadravas. The classification of Upadravas as

Samanya and Vishishta has not been done in any of the Granthas. Charaka and Bhela

have listed and described common Upadravas at random. Sushruta, Vagbhata and

Bhavaprakasha have described them separately as Kaphaja, Pittaja and Vataja

1. Trushna: Person will not satisfy even after drinking water continuously is known as

trushna70, Pipasa is its synonym. Trushna will manifest as a upadrava due to excessive

loss of kleda through mootra. Pitta with its Ushna guna is the main Dosha here71. Trushna

may manifest as a poorvaroopa where the degree of vitiation is comparatively less.

2. Atisara: The long standing vitiation of vata affects its sthana that is pakwashaya which

in turn causes atisara. Westerners have also observed atisara as an upadrava in

Madhumeha and they have termed it as diabetic diarrhea. Intermittent or persistent

painless diarrhea has been observed in long standing severe diabetics. The stools are

watery and large. Typically diarrhea is nocturnal it may last for a few hours to few days.

3. Paridhupana/Daha: Daha may manifest in kara and pada or savanga. It is a Pittaja

nanatmaja vikara and is described as Sarvanga dahanamiva santapa72 and develops in

55


conditions of Pitta pradhanyata in Madhumeha. It can be appreciated as diabetic

peripheral neuropathy.

4. Jwara: is mainly due to Pitta pradhanya and the manifestation seen is that of Jeerna

jwara. Pitta pradhanyata is usually seen in the second stage of the disease where there is

relatively more involvement of Medas and Rakta. Here, as a result of Dhatu kshaya and

reduced Vyadhikshamatva, Jwara develops.

5. Dourbalya: It is because of dhatvagni mandya, which later results in ojokshaya, hence

ojokshaya leads to dourbalya.

6. Arochaka: Is a condition where there is Virasa mukhata and the patient experiences

disinclination in swallowing the food which is already in the mouth as described by the

sentence Mukhapravishtasyapi nabhyavahara. The main dosha involved is Kapha but

Pitta also causes Arochaka.

7. Avipaka: Is the Ajeerna occurring as a result of Agnimandya by Kapha.

8. Pootimamsa pidaka73, 74: These pidakas manifest due to the vitiation of mamsa, meda,

shonita with increased kleda results in development of Pidakas, which develop Shotha

resulting in Pooya vriddhi. The Shopha may or may not burst. If not treated, the Pooya

attains Abhyantara prapti and Utsanga, resulting in Asadhyata. The development of

Pidakas has been described as limited only to the lower limbs as the Rasayanis there are

Durbala. Clinically also, the incidence of diabetic ulcers occurring in the lower limb is

maximum. The Pidakas are the most important Upadravas of Madhumeha as negligence

in treating them renders the disease Asadhya.

9. Brama: Is the condition where the patient feels Chakravat bramana of gatra (as if the

body is being rotated like a wheel). And whenever he gets brama usually falls down

56


(bhoomau patati) 75. It is mainly due to Pitta or Vata or both and due to Raja dosha of

Manah76. This Upadrava is produced when Gambhira dhatus like Majja are involved.

10. Tama: Tamah can be caused by Pitta77 causing Rakta prakopa78 and Vata causing

Rasa samvahana abhava. This can occur during the course of the illness as a transient

phenomenon or during the terminal stage leading to death.

11. Shoola: It is due to Vata along with Gambira dhatus like Majja involvevment79. Apart

from this, Shoola can be understood as udara shoola which is due to badda purishata and

udavarta, which is also an Upadrava of Madhumeha.

12. Kandu: This is mainly a due to Kapha80 which has attained Bahudrava avastha and

due to excess Sweda as a result of Dushta medas. The patient is hence susceptible to skin

diseases. Clinically, the incidence of Yoni kandu and Medra kandu are more in

Madhumeha Besides, Kapha pradhana kushta have Kandu as a predominant symptom,

which is not uncommon in Madhumeha.

13. Alasya: Means anutsaha81 this is due to Kapha and meda.

14. Pratishyaya: This is due to Kapha, Vata and Oja kshaya and Pranavaha srotodushti.

15. Shaithilya: The Dhatu kshaya leads to Anibida samyogata (loss of compactness)

leading to Dourbalya82.

16. Mamsopachaya: Is characterized by Mamsa sanghata83 due to Mamsa pradosha and

hence a Madhumehi can develop Adhimamsankura vikaras.

17. Makshikopasarpana: This condition is the result of Tanu madhuryata and subsequent

Madhura bhava of Sweda84. This attracts more Makshikas as this Laxana has been also

mentioned in Poorvaroopavastha. This condition should be considered as a symptom

57


indicating Asadhya avastha, which is likely to be preceded or succeeded by Murccha adi

upadrava.

18. Kapha praseka: Means excess Lalasrava due to Kapha bahudrava.

19.Chardi: This can also be a symptom of Marma85 which is an occurrence in

Madhumeha.

20. Nidra: It is due to Kapha dushti and Tamoguna.

21. Kasa & Shwasa: Are result of Prana vaha srotodushti by Vriddha kapha and vata.

22. Vrushana avadarana: It may be a result of Kandu or Kushta affecting Vrushana.

23. Bastibheda / Medratoda: This is due to Vata dushti.

24. Hritshoola: is due to Vayu dushti as a result of Avarana by Kapha and Pitta and is

also a symptom of Hridroga due to Madhumeha.

25. Amlika: Means Amlodgara as a result of Shuktapaka due to Agnimandya caused by

pitta.

26. Moorcha: It is also called as moha and defined as Chetanachyuti86 where there is

Kashtavat patana of the patient and he is unable to experience Sukha and Dukha. This is

mainly due to Pitta, Rakta and Tamo guna dushti.

27. Nidranasha: It is due to Vata and Pitta vriddhi.

28. Panduroga: This is a Pittapradhana vyadhi where due to Dhatvagnimandya, there is

Rakta dhatu poshaka sara bhaga kshapana leading to Panduroga87.

29. Hridgraha: A condition where patient experiences as if his heart is being pulled out it

is mainly due to Vata dushti or due to Kaphapitta avarana.

58


30. Loulya: Is abnormal desire to have all rasa, described as Sarvarasa abhi kanksha like

vataja grahani where it is mentioned that guddihi savarasanam88. And it is due to vyadhi

prabhava and dathu kshaya.

31. Sthambha89: Means Nischalikarana it is due to Vata vriddhi.Gatra stamba is due to

ojo kshaya.It can be correlated with diabetic neuropathy.

32. Kampa: It is due to Vata vriddhi where there is Gatrakampana especially of

Hastapada tala.

33. Baddha pureeshata/udavartha: Though there is difference between in baddapurishatva

and udavartha the mechanism of manifestation in Madhumeha one and same. Apanavayu

in normal course controls the mechanisms of vata, mootra and purisha pravritti. Thus

vitiated vata produces badda puishatwa and it further leads to udavartha. The mechanism

of constipation is attributed to diabetic autonomic neuropathy.

34. Shosha: Occurs due to Dhatu kshaya and vata prakopa.

35. Atiprasruta: Is described as Atisrushtam mootram (excessive urination).90

36. Angamarda: Udweshtanamiva vedana(Squeezing or twisting type of pain) due to

Vyana vata dushti.91

Complications of Diabetes mellitus92

The complications of Diabetes mellitus can be acute or chronic. Acute complications are

the medical emergency and need immediate medical management, otherwise the patient

may go into coma and ultimately death may occur. Among the acute complications,

hypoglycemia is the most serious one encountered in the medical field.

They can be classified as follows:

59


I. Acute metabolic complications:

1. Diabetic ketoacidosis 2. Hyperosmolar coma 3. Hypoglycemia

II. Chronic complications:

A) Angiopathic complications

1. Microangiopathic: Retinopathy, Cataract, Glaucoma, Nephropathy, Neuropathy.

2. Macroangiopathic: Coronary artery disease, Cerebrovascular disease, Peripheral

vascular disease.

B) Infections: Skin infections, Pulmonary Koch’s, Urinary tract infections, Vaginal

Candidiasis, Balanitis, Gangrene of the feet etc.

C) Others: Gastro paresis, Diarrhea, Sexual dysfunction.

I. Acute metabolic complications:

1. Diabetic ketoacidosis: it is seen primarily seen in individuals with Type 1 DM due to

the insulin deficiency. The patient complains of nausea, vomiting, abdominal pain,

associated with tachycardia, hypotension, glycosuria, ketonuria, kussmauls respiration,

acetone breath, lethargy, central nervous depression followed by coma and death.

2. Hyperosmolar coma: It is most commonly seen in elderly individuals with Type 2 DM.

Its clinical features include polyuria, orthostatic hypotension, altered mental status,

lethargy, seizure and coma. Insulin deficiency and inadequate fluid intake are the

underlying causes of hyperosmolar coma.

3. Hypoglycemia: Among the acute complications, hypoglycemia is the most serious one

encountered in the medical field.

60


II Chronic complications:

Blindness is the primarily the result of progressive diabetic retinopathy and

clinically significant macular edema. Duration of the DM and the degree of glycemic

control are the best predictors of the development of retinopathy. Diabetic nephropathy is

the leading cause of DM related morbidity and mortality.

Diabetic neuropathy occurs in approximately 50% of individuals with long

standing Type 1 and Type 2 DM. Diabetic peripheral neuropathy presents with distal

sensory loss, hyperesthesia, paresthesia and pain also occurs. Paresthesia is

characteristically perceived as a sensation of numbness, tingling, burning that begins in

the feet and spreads proximally.

Autonomic neuropathy affecting the cardiovascular system causes a resting

tachycardia and orthostatic hypotension. Reports of sudden death have also been

attributed to autonomic neuropathy.

The most prominent GI symptoms due to autonomic neuropathy are delayed

gastric emptying (gastroparesis) and altered bowel motility (constipation or diarrhea).

Gastroparesis may present with symptoms of anorexia, nausea, vomiting, early satiety

and abdominal bloating.

Diabetic autonomic neuropathy may lead to genitourinary dysfunction including

cystopathy, erectile dysfunction, and female sexual dysfunction (reduced sexual desire,

dyspareunia, reduced vaginal lubrication).

Infections diabetics have increased susceptibility to various infections, such as

tuberculosis, pneumonia, pyelonephritis, carbuncles and diabetic ulcers. This may due to

poor blood supply, reduced cellular immunity or hyperglycemia.

61

Review of Literature Upadrava

Table No.4 : Samanya Upadrava93,94

Upadravas Charaka Bhela 1) Trushna1

2) Atisara1

3) Jwara1

4) Daha1 5) Dourbalya1

6) Arochaka1

7) Avipaka1

8) Pootimamsa pidaka2 9) Angamarda2

10) Kasa2

11) Bhrama2

12) Tama2

13) Shoola2

+ + + + + + + + - - - - -

+ - - - - - - + + + + + +

Table No. 5: Vishishta Upadravas95,96,97

Upadrava Sushruta Ashtanga hridaya Bhavaprakasha A. Kaphaja Prameha upadrava 1) Makshikopasarpana 2) Alasya 3) Mamsopachaya 4) Pratishyaya/peenasa 5) Shaithilya 6) Arochaka 7) Avipaka 8) Kapha praseka 9) Chardi 10) Nidra 11) Kasa 12) Shwasa

+ + + + + + + + + + + +

- - -

+ - + + - + + + -

- - - + - + + - + + + -

B. Pittaja prameha upadravas 1) Vrushana / mushka avadarana 2) Bastibheda 3) Medratoda 4) Hritshoola 5) Amlika 6) Jwara 7) Atisara 8) Arochaka 9) Vamana 10) Paridhupana 11) Daha 12) Moorcha 13) Pipasa / Trushna 14) Nidranasha 15) Panduroga

+ + + + + + + + + + + + + + +

+ + + - + + + - - - + + + - -

+ + + - + + + - - - + + + - -

62

Review of Literature Upadrava

16) Peeta vit 17) Peeta mootra 18) Peeta netra

+ + +

- - -

- - -

C. Vataja prameha upadravas 1) Hridgraha 2) Loulya 3) Anidra 4) Sthambha 5) Kampa 6) Shoola 7) Baddha purushata 8) Udavarta 9) Shosha 10) Kasa 11) Shwasa

+ + + + + + + - - - -

+ + + - + + - + + + +

+ + + - + + - + + + +

Table No. 6 : Prameha Pidakas

Pidaka Charaka Sushruta Vagbhata (i) Sharavika (ii) Kacchapika (iii) Jalini (iv) Vinata (v) Alaji (vi) Vidradhi (vii) Sarshapika (viii) Masoorika (ix) Putrini

(x) Vidarika

+ + + + + + + - - -

+ + + + + + + + + +

+ + + + + + + + + +

63

Review of Literature Arista laxana

ARISTA LAXANA

Arista laxana are those signs and symptoms which herald the oncoming death, just as the

flowers indicate the next coming fruit, the smoke indicates the fire and clouds the rain.

There is no death without arista laksanas and there will be no life after their appearance.

Hence the physician should acquire the knowledge of the asrista lakshanas.

In Madhumeha the following forms of Lakshanas signal imminent death.

1. If a person dreams of drinking various types of sneha in association with chandalas

(out cat men) he dies of Prameha.98

2. If a Madhumehi dreams of consuming water then he dies of Prameha.99

3. The meeting of the messenger and the physician near the pond or along with water

then the progress will be bad.

4. In spite of regular bath and the application of perfumes if the flies attach concurrently

on a Madhumeha rogi, then he will die soon.100

5. If Madhumeha present with the upadravas it is to be considered as arishta.101

6. If he is lethargic, obese, atisnigdha and is a voracious eater, then death impends in the

form of Prameha.102

7. A person who likes Abhyavaharana and hates Snana and Chankramana will fall victim

to the disease Prameha just like the eggs of a Pakshi in its Vasavruksha (Needadruma)

that falls prey to its predators, as it is unable to move and rescue itself due to the inherent

inertia of the egg.103

64

Review of Literature Sapeksha Nidana

SAPEKSHA NIDANA

Sapeksha nidana plays a vital role in establishing the exact identities of the

disease wherever identical signs and symptoms prevail in two or more diseases making it

very difficult in arriving at a true diagnosis.

Regarding diagnosis of Prameha Charaka acharya says that Madhura Mutrapravritti like

honey is manifested in both i.e. Vataja Prameha and Kaphaja Prameha. To differentiate

both these Prameha, knowledge of Nidana Sevana is proper way to reach the diagnosis. If

Nidana sevana is Kaphakara, the Mutramadhurya is definitely the manifestation of Kapha

Prameha. On the other hand, if etiological factors favor Vata dosha then Vataja Prameha

(Madhumeha) may be diagnosed.

Until and unless Haridra and Rudhira coloured Mutrapravritti is not associated with the

premonitory symptoms of Prameha, the disease can not be diagnosed as Prameha, but it

goes more in favor of Raktapitta. Here more importance is given to Poorvaroopa of

Prameha and not only to Mutra Pravritti. Regarding Madhumeha, it is to be specially

emphasized that instead of only Mutra Madhurya, ‘Sharira Madhurya’ is also found

which is not present in other types of Prameha. Apart from Mutramadhurya other

characters of urine are also helpful in differential diagnosis among various Doshika

varieties of Prameha.

Here one should essentially consider Madhumeha as a consequence of Vata vriddhi as a

result of Dhatukshaya where Vata is the Anubandhya dosha or Madhumeha as a result of

Margavarana janya vata vriddhi where Vata is an Anubandha dosha and is directly

dependent upon Kapha, which has undergone Vriddhi because of Santarpana. The factors

for differentiation are as follows. (Table no.7)

65


Table No. 7: SAPEKSHA NIDANA

Vyadhi bodhaka

Nidana

Madhumeha

(Anilatmaka)

Madhumeha

(Kaphasambhava)

Rogi

Nidana

Rogi avastha

Roopa

Samprapti

Vyadhiswaroopa

Sadhyasadhyata

Upadrava

Chikitsa

Krusha, Durbala

a) Vatakara ahara vihara

along with Vata vriddhi as a

result of Deerghakaleena

madhumeha

b) Beeja uapatapa

Bala to madhyama vaya

Vatapradhana

Madhumeharambhaka dosha

dushti leading to Vapavahana

dushti especially in Sahaja

madhumehi

Ashukari

Asadhya

Vata pradhana upadravas

Santarpana

Sthoola, Balavan

Kaphakara ahara vihara

Madhyama to vriddha

Kapha pradhana

Kaphamedodushti leading to

Madhumeha arambhaka

dosha dushti in Vapavahana

Chirakari

Sadhya in the beginning

Kapha pradhana upadravas

Apatarpana

Madhumeha is primarily a Medovaha srotodushtijanya vikara but its Pratyatma lakshanas

become Vyakta in the Mootravaha srotas with abnormal change in the Rasa, Varna,

66


Gandha, Sparsha of the Mootra and it is characterized by Prabhoota and Avila

mootrata.104

Prabhoota mootrata means Atipravrutti of mootra. It goes without saying that there

is also increased frequency of micturition along with increased quality of urine and Avila

mootrata means Atyartha Kalusha Samalam105 or Malinam akulam which means that

there is a considerable change in the quality of urine as per the above mentioned factors.

Considering these factors, it becomes contextual to enumerate the conditions where there

is increased frequency of urine and abnormality in its quality (Table No.9). Most of the

times these symptoms are associated with Mootravaha srotodusti and other diseases at

differentiating Madhumeha is not a problem for evident reasons.

Differential Diagnosis:106

Differential diagnosis between the following types are listed below,

Table No. 8: Differential Diagnosis

Characteristics Juvenile or growth

onset type I (IDDM)

Adult or maturity

onset type II

(NIDDM)

J type

Age of onset

Sex incidence

Mode of onset

Symptoms

Body weight

Ketosis

Childhood or young

age

Equal

Acute or rapid

Present

Often lost

Occurs easily

Middle age or later

More in males

Incidence

Often absent

Often gained

Absent

Young

age

-

Incidence

Present

Very lean

Absent

67


Insulin sensitivity

Plasma insulin

Response to sulphonylurea

High

Low

Poor

Low

Normal or increased

Good

Low

Poor

It becomes relevant to consider the following conditions where hyperglycemia is

a common manifestation under the heading of differential diagnosis.

I. DM & Endocrine disorders:

a) Pituitary gland: 1) Pituitary diabetes due to growth hormone, 2) Acromegaly,

3) Diabetes insipidus.

b) Adrenal Cortex: 1) Cushing’s syndrome, 2) Steroid diabetes due to administration of

steroids, 3) Primary Hyperaldosteronism.

c)AdrenalMedulla: 1)Phaeochromocytoma, 2)Addison’sdisease, 3) Adrenalectomy.

d) Thyroid: 1) Hyperthyroidism, 2) Myxoedema.

II. Pancreatic Diabetes: 1) Acute pancreatitis, 2) Mumps (rarely), 3) Chronic

pancreatitis, 4) Haemochromatosis, 5) Total pancreatectomy, 6) Carcinoma of pancreas.

III. Diabetes and Liver: 1) Cirrhosis of liver, 2) Gall Stones.

IV. Drugs & Diabetes: 1) Thiazide, Chlorthalidone, frusemide, oestrogen containing

oral contraceptives, β blockers & catacholaminergic drugs.

V. Miscellaneous: 1) Type I glycogen storage disease, 2) Down’s syndrome,

3) Turner’s syndrome, 4) Huntington’s chorea, 6) Burns.

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Conditions where there is polyuria:

The Polyuria of DM should not be confused with prostatic hypertrophy or cystitis

where it is only increased frequency of micturition & not increased quantity.

I Polyurea due to water diuresis:

a) Cranial or neurogenic Diabetes insipidus: This is due to an identifiable lesion in the

hypothalamus, pituitary or both, leading to failure of A.D.H.

2) Nephrogenic Diabetes insipidus: Familial form seen in males only, also as an

accompaniment of Fanconi syndrome.

3) Psychogenic polydipsia or compulsive water drinking: This is a hysterical condition.

There is clinically marked fluctuation here.

II Polyurea due to increased solute load: Diuretic therapy and Chronic renal failure.

69

Review of Literature Sapeksha nidana

Table NO. 9: SAPEKSHA NIDANA

Mootra Lakshana (Varna Nimitta) Vikara 1) Avila mootra/mootra dosha/prakupita mootra 2) Bhasmodaka pratikasham 3) Bastagandhitvam 4) Gomeda prakasham

5) Guru

6) Haridram

7) Krishna

8) Picchilam

9) Pita

10) Rakta (Sarakta, Sasruk, Sarudhira, Raktabham)

11) Sarkara saha

Ashmari poorva roopa108 Ashmari109 Mutra shukra110 Ashmari poorvaroopa111 Ashmari

a) Kaphaja arsha112 b) Vata kundalika113

a) Paittika gulma114 b) Pattika arsha115 c) Vishamasannipata jwara116 d) Kamala117 e) Paittika mutrakrichra118 f) Rakta pitta poorva roopa119 g) Paittika udara120 h) Ushna vata121 i) Nanatmaka pitta vikara122

a) Vatika arsha123 b) Vatika gulma124 c) Asadhya kamala125 d) Paittika mutrakrichra126

a) Kaphaja arsha127 b) Kaphaja mootra krichra128 c) Kaphaja mootraiikasada129

a) Paittika arsha130 b) Halimaka131 c) Paittika Jwara132 d) Kamala133 e) Kshiralasaka134 f) Mutrasada135 g) Paittika mutrakrichra136 h) Pandu purvaroopa137 i) Paittika pandu138 j) Paittika trushna139 k) Paittika udara140 l) Ushna vata141 m) Basti vidradhi142

a) Rakta vruddhi143 b) Ashmari144 c) Sannipata jwara145 d) Asadhya kamala146 e) Ksata kshina147 f) Mutrasada g) Mutrotsanga148 h) Paittika mutra krichra i) Raktaja mutra krichra149 j) Raktapitta poorva roopa150 k) Ushna vata151

Sarkarashmari

70

Review of Literature Sapeksha nidana

12) Sita (Sitalam)

13) Sasikatam (Sikatanuviddam matam)

14) Snigdha

15) Shukla (Shweta, sita)

16) Shyava

Sannipatika mutra krichra

Ashmari

a) Kaphaja arsha152 b) Kaphaja mutra krichra153 c) Kaphaja basti kundala154

a) Kaphaja arsha155 b) Kaphaja gulma156 c) Kaphaja jwara157 d) Mutra sada158 e) Kaphaja mutrakricchra159 f) Kaphaja pandu160 g) Kaphaja udara161 h) Kaphaja unmada162 i) Kaphaja bastikundala163

a) Vatika arsha164 b) Vatika udara165

Mootralakshana (Pravartana Nimitta) Lakshana 1) Abhikshnam (Muhuh muhuh, Punah punah subahushah, vikiranam

2) Atipravrutti

a) Ashmari166 b) Mutratita167 c) Vatika mootrakricchra168 d) Ushna vata169

a) Amavata170 b) Arsha poorvaroopa171 c) Sahaja arsha172 d) Kaphaja arsha e) Mutra praseka173 f) Upasthita prasava174 g) Chidrodara175 h) Asadhya masurika176 i) Ama jwara177

71

Review of Literature Sadya asadyata

SADHYASADHYATHA

A forecast of the probable course and termination of a disease is prognosis or

sadhya asadhyatha. Madhumeha has been described as Anushangi, which means

Punarbhavi. Therefore, one should make all efforts to prevent and control it.

Sadhyata of Kaphaja Prameha178: The ten Kaphaja pramehas are described as Sadhya

because of the following reasons.179 a) Samakriyatvat b) Atishayena medo dushitam na

bhavat.

A. Samakriyatvat: Tulya dushyata180 is a determinant of Sadhyata in Madhumeha, which

means the Guna of the Dosha and Dushya involved are the same. This makes the

treatment easier because the Katu, Tikta, Kashaya rasa and Tikshna, Ushna guna, which

are antagonistic to Kapha, are the same for Medas, Mamsa, Kleda, Lasika, and Rasa etc.

Dhatu. Hence due to Samakriyata, Kaphaja meha are Sadhya. This is the early stage of

Madhumeha.

B. Atishayena medo dushitam na bhavat: Kaphaja mehas are characterized by less

involvement of Dhatus. Here, predominant symptoms of only Kapha are only seen;

therefore, Madhumeha is Sadhya in this stage. Moreover other Dhatus are not much

involved in this stage and Upadrava are not manifested.

Yapyata of Pittaja Prameha: The six Pittaja mehas are described as Yapya because of

a) Vishamakriyatva, b) Atrapi atishayena medo na dushtava and c) Samsrushta dosha

meda sthanatvat181.

a) Vishamakriyatvat: The Dosha Pitta and the Dhatu Medas, Rasa, and Mamsa have

Viruddhaguna, which makes the Chikitsa Vishama i.e. if Pitta is treated with Sheeta and

Madhuradi dravya, they are antagonistic to Pitta but are Medo- rasadi dhatukara and if

72


Medo-rasadi dhatu are treated with Tikshna Ushnadi dravyas, they cause Pitta vriddhi

hence defeating the purpose of Shuddha chikitsa. Hence Pittaja Prameha are Yapya.

b) Atrapi atishayena medo na dushtatvat: Pittaja prameha also are characterized by

relatively less involvement of Dhatu as suggested by the term “Atrapi” which means that

the involvement of Medas and other Dhatu is too severe for it to be Sadhya, yet not

severe enough to be Asadhya. Therefore this stage of the disease is Yapya.

c) Samsrushta dosha meda sthanatva: Means “Sannikrushtam doshasya Pittasya

medashcha sthanam yasmat” i.e. proximity in the Sthana of Medas and Pitta hence Pittaja

pramehas have been called Durjaya. The Sthana of Pitta is Amashayam and that of

Medas is Vapavahana. There is proximity or Pratyasannata of these Sthanas in the Koshta

as described by the term Ekadesha. Hence there is a mutually contradictory environment

in Ekadesha; the result is Vishama kriya of the Chikitsa and therefore Pittaja pramehas

are Yapya.

Asadhyata of Vataja Prameha: The four Vataja Prameha are considered Asadhya due

to a) Mahatyayatvat, b) Viruddhopakramatvat.

a) Mahatyayatvat: means Majja prabhrutisarabhoota dhatukshaya or ashukari

Due to this guna all the Dhatu including the Gambhira dhatus undergo Nasha, Kshaya &

Apakarshana.This process involves multiple Srotas producing Upadrava and is hence

Mahavyapattikara, which means that the disease is much too savere to sustain life.

b) Viruddhopakramatvat182: The Chikitsa of Vataja Prameha involves Viruddhopakrama

which means there is a mutual contradiction in the treatment modalities as use of Snigdha

etc. are Pathya for Vata but Apathya for Medas. Hence the disease is Asadhya.

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Other situations determining Asadhyata of Madhumeha:

1) Madhumeha with all Poorvaroopa183 : It has been said by Charaka that if a disease in

Roopavastha has all the Poorvaroopa manifested then the disease becomes Asadhya184 .

Based on this principle, the inherent nature of Sadhya Asadhyata of Kaphaja, Pittaja and

Vataja meha undergoes modifications as follows.

a) Sadhyata of Kaphaja meha attains Asadhyata when associated with all Poorvaroopas.

b) Yapyata of Pittaja meha attains Pratyakhyeyata when associated with all

poorvaroopa.

c) The severity of Asadhyata increases when associated with Poorvaroopa.

Vataja Prameha has already been described as Asadhya but this term has to be

analytically interpreted in the two clinical types of Vataja mehas viz. Dhatukshaya janya

and Margavarana janya.

2) Jatah Madhumeha is Asadhya due to Beeja dosha as there is an irreversible

Madhumeharambhaka dosha dusti since the birth itself185.

3) Madhumeha with Pidaka is Asadhya

4) Madhumehi who has Bala mamsa kshaya can be left untreated186.

5) All Pramehas if left untreated terminate into Madhumeha which is Asadhya187.

6) Prameha with Gadha upadravas and Atiprasruta mootra is Asadhya.

7) Pramehas with Arishta laxana is Asadhya.

8) A patient who hates hygienic habits like Snana, Chankramana and one who has

Mandotsaha, who is Atisthoola, Snigdha and Mahashana dies of Prameha188.

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Prognosis189

The prognosis in diabetes has improved steadily since the introduction of insulin,

but even with its use the average exception life of diabetic is still less than that of non

diabetics. It may be difficult to estimate the prognosis of an individual patient because so

many variable factors have to be considered. The working capacity and longevity of a

diabetic patient to a great extend depends on the timely recognition of the disease, its

severity, complications, the age of patient and proper treatment. If diabetes develops at

early age shorten is the patients life span. The prognosis of diabetes mellitus is mainly

determined by the degree of affection of the cardio-vascular system. The commonest

cause of the death in diabetes mellitus are pathological conditions of vessels. (Myocardial

infarction, thrombosis of cerebral vessels etc.) in the neuropathy at young age.

The patients having mild diabetes are capable in their works. In moderate and severe

forms of the diabetes the working capacity is assessed individually depending on the

course of diabetes mellitus and concomitant diseases.

75

Review of Literature Chikitsa

CHIKITSA

In general Chikitsa is the method adopted for eradication of the disease from the

body. The aim of treatment is to restore swasthya. That means to restore normal functions

of agni, dosha, dhatu, mala and maintain mental health. The primary importance of

Chikitsa lies in samprapti vighatana.

SAMANYA CHIKITSA:

Nidanaparivarjana in Margavarana janya Madhumehi: An pathyanimittaja

madhumehi usually Sthoola, who likes Abhyavaharana & hates Chankramana is in a

situation just like of the helpless eggs on a tree, they cannot move to avoid their predators

& hence fall victim to them. Here, the patient should be made to avoid all Kaphakara

ahara vihara either to prevent the occurrence or to cure the disease.

Nidana parivarjana in Dhatu kshaya janya Madhumehi190: Nidana parivarjana in

such Madhumehis is studied with special reference to Sahaja madhumeha. It lies entirely

on the Mata or Pita as to how best they act to prevent the occurrence of the disease in

them. They should avoid the Beeja, Beeja dhaga or Beeja bhaga avayava upatapa leading

to Madhumeharambhaka dosha dushti.

Apakarshana & Prakruti Vighatanana: The Apakarshana of Doshas are mainly done

through Samshodhana but only when Roga & Rogi bala are in Pravaravastha and when

either one or both are Avara, then it is done through Langhana and Langhana panchana,

which constitutes Samshamana chikitsa, in other words Prakruti vighatanana.

Apakarshana in Margavarana janya Madhumeha: Shodhana especially Vamana

should be preferred in a Madhumehi if the Dhatukshaya is minimum & there are Kapha

& Medodushti lakshanas. If there are Pittaja lakshanas & Dhatu kshaya does not render

76


the patient Durvirechya, then Virechana can be performed. Similarly, if the Anubandha

vata lakshanas are more and the patient is Samshodana arha then Basti can be performed.

Madhumeha is a Swedana anarha vyadhi191 but Niragni sweda in the form of

Vyayama is indicated. The selection of Yogas for Samshodhana & Snehana should be

selected as per the recipes prescribed in Kalpa sthana. After Shodhana, Shamana chikitsa

can be done by Kaphamedohara dravya.

Prakruti vighatana in Dhatu kshaya janya Madhumeha: Dhatu kshaya avastha is the

result of Beeja dushti in Sahaja madhumeha & due to a state of Atikarshita dhatus as a

result of continued Dhatu kshaya, which in fact is the progressed stage of Margavarana

janya madhumeha. Both the situations are considered Samshodhana anarha192. In such

cases, Samshamana chikitsa is advised, whereas Madhumeha in both these cases are

Asadhya and hence need not be treated. Notwithstanding this, the principles of chikitsa

for Vataja pramehas are for Vata anubandhadoshatva, which is still dependent on the

Kapha & Pitta doshas and not for Vvata anubandhya dosha janya madhumeha

characterized by Atishaya karshana of Dhatus. Hence Samshamana chikitsa should be

appropriately adopted in such patients.

AVASTHA ANUSARA CHIKITSA OF MADHUMEHA193:

Sushruta in the chapter of Prameha pidaka chikitsa has identified the stages of

Madhumeha & accordingly advised the treatment, which can be discussed as follows:

Stage I: Is the Poorvaroopa avastha where the Dosha dushya sammurchana has just

begun, the disease should be treated with Apatarpana, Vanaspathi kashaya and

Chagamootra. If left untreated, Madhumeha proceeds to the II stage.

77


Stage II: This is the Vyakta avastha of Madhumeha where, due to continued Madhura

ahara sevana, the Sweda, Mootra and Sleshma attain Madhura bhava & hence should be

treated with Ubhaya samshodhana i. e. Vamana, Virechana & Basti. If left untreated, the

disease progresses to stage III.

Stage III: In this stage, the Mamsa & Shonita undergo Pravruddha dushti causing

Shopha & other Upadravas and these should be appropriately treated as mentioned

accordingly, like Siramokshana in Shopha. If left untreated, the disease progresses to

stage IV.

Stage IV: In this stage, the Upadravas like Shopha would have attained Ativruddha

avastha, manifesting symptoms like Ruja & Vidaha, where Shastra chikitsa and

Vvranakriya should be performed. If neglected, the disease proceeds into Asadhya

avastha, which is the V & final stage.

Stage V: In the Asadhya avastha, the Upadravas become Mahantha & makes the disease

Asadhya, like here when the Pooya of Pidakas attain Abhyantaraprapti and become

Utsanga.

Analysis: Though explained as Prameha pidaka avastha chikitsa, description of stage

wise progression of the disease and the treatment has been done by Sushruta on the

pretext of explaining the Prameha pidaka chikitsa. This description seems to be Chikitsa

in case of Apathyanimittaja madhumeha, the course of this illness has been discussed

already under Samprapti & accordingly in the Poorvaroopavastha, Sushruta advises

Apatarpana & other Shamana dravyas as there is Alpadosha & Alpa dhatu dushti. Hence,

unless the need arises, Samshodhana is not the treatment of choice and as the Lakshanas

are predominantly due to Kapha, Kaphahara chikitsa should be done & this seems to be

78


the logic behind prescribing Apatarpana & Tikshna dravyas like Chaga mootra. Whereas

in Vyakta avastha there is Bahu dosha & a relatively Alpa dushti of dhatu like Medas &

Rakta which warrants Shodhana, accordingly Vamana, Virechana & Basti have been

advised as the Rogi is still Balavan & Sthoola & so, Shodanarha.

In the next stages, there is a progressive Dhatu kshaya & production of

Upadravas. The patient is Shodhana anarha & there is Vata pradhanyata. Hence, only

Shamana chikitsa & respective Upadrava chikitsa should be done. Sushruta has stressed

the importance of timely intervention in Madhumeha because in case of negligence, the

disease progresses involving Gambhira dhatus & the Upadravas pervade the entire body

making it Asadhya.

SANTARPANA APATARPANA CHIKITSA IN MADHUMEHA:

Madhumeha has been described as Santarpanotha vyadhi as well as

Apatarpanotha vyadhi. The former is Apathya nimittaja madhumeha & latter is Sahaja

madhumeha or Madhumeha due to Dhatu karshana due to long standing Prameha.

Accordingly, two forms of Madhumehis are encountered, one who is Sthoola & Balavan

for whom Apatarpana is the best & the other who is Krusha & Paridurbala for whom

Santarpana is the best.

I. Apatarpana chikitsa194: is done in the form of Langhana, Langhanapachana &

Doshavasechana.

a) Langhana this is done in Alpadoshavastha where only Upavasa, Pipasa, Maruta, Atapa

sevana, Rooksha udvartana, Pragadha vyayama, Nishi Jagarana & so on, which are

Kaphamedohara are helpful.

79


b) Langhanapachana: This is done in Madhyamadoshavastha where along with

Langhana, Ama pachana is done with Tikshna, Ushna dravyas.

c) Doshavasechana: This is done in Bahudoshavastha where the Shodhana of Doshas is

done from Ubhaya margas.

II. Santarpana Chikitsa: Laghusantarpana chikitsa is Prashastha for Krusha and

Durbala rogis195. The following can be administered in Madhumehi. a) Mantha b)

Kashaya c) Yava d) Churna e) Lehya f) Laghu Bhakshya. These formulations should be

prepared such that they cause Santarpana without causing Vriddhi of Kapha & Medas.

Among all these, Yava is considered as best for Madhumehi, which will be discussed in

the chapter of Pathya apathya.

Shreshta Aushadha prayoga in Madhumeha:

Shilajatu, Guggulu, Loharaja: These Dravyas are medicines par excellence in

Madhumeha, either in Krusha or Sthoola, as they are Virukshana & Chedaneeya, which is

good for Kapha, as well as Rasayana, which is good for Dhatukshaya & Vatavriddhi.

TREATMENT196

(A) Goals of treatment of diabetes:

Diabetes mellitus requires ongoing medical care as well as patient and family

education both to prevent acute illness and to reduce the risk of long term complications.

The therapeutic objective is to restore known metabolic derangements towards normal in

order to prevent and delay progression of diabetic complications. The management of

diabetes patient is not aimed solely at glycaemic control various aspects requiring

assessment and control. The aims of treatment have been varied according to an arbitrary

division of patients into three categories ranging from those in whom symptomatic relief

80


done seems the most appropriate or any attainable goal to those in whom an attempt at

maximal prophylaxis against future tissue damage seems desirable and possible

(B) Treatment regimens:

(i) Diet:

A well-balanced nutritious diet remains a fundamental element of therapy. In

obese patient with mild hyperglycemia the major goal of diet therapy is weight reduction

by caloric restriction.

1. Intake of protein and carbohydrate according to the recommendation of American

diabetes association.

2. Dietary fibres: Food such as oatmeal cereals and beans with relatively high soluble

fibre content as staple component of the diet in diabetes. These tend to retard nutrient

absorption rates so that glucose absorption is slower and hyperglycemia may be slightly

diminished high soluble fibre content in the diet may also ha favorable effect on blood

cholesterol levels.

3. Artificial sweeteners: Diabetes can use artificial sweetness like aspartame, sucralose,

acesulfame.

(ii) Oral anti diabetic agents: oral drugs are used to lower Blood glucose level by

achieving following goals.

1. Drugs that primarily stimulate insulin secretion.

2. Drugs that alter insulin action.

3. Drugs that principally affect absorption of glucose.

81


a) Sulphonylureas:

Mode of action: Stimulate production of insulin by increasing number of insulin

receptors.

Indications:

1) Maturity onset (Insulin dependent) diabetes of average wt. not controlled by diet.

2) Diabetes or normal weight stabilized on insulin dosage not more than 30 units per

day who have never been ketotic.

3) Failure to lose weight when this is indicated.

Contra-indications:

1) Juvenile diabetes. 2)Patients with ketosis. 3)Obese adult-onset uncontrolled

diabetics (Biguanides can be used). 4)Insulin taking diabetics. 5)Presence of

renal, hepatic or cardio respiratory disease or alcoholic abuse (because of

increased risk of lactic acidosis)

Adverse effects:

1) Hypoglycaemia: Most frequent with glibenclaimide also chlorpropamide. Increase

in hypoglycaemic effect if concomitant use of sulphonamides, salicylates,

phenylbutazone, Monoamine oxidase inhibitors.

2) Dyspepsia.

3) Skin rash including photosensitivity, rarely exfoliative dermatitis.

4) Facial flushing after ingestions of alcohol (mostly chlorpropamide)

5) Cholestatic Jaundice (chlorproppamide)

6) Blood dyscariasis (rare).

82


Drug Interactions With Sulphonylureas:

A) Increased hypoglycaemic action-beta-blockers, sulphonamides, phenylbutazone,

chloramphenicol, cyclophosphamide, salicylates, dicoumarol, and monoamine

oxidase inhibitors.

B) Decreased hypoglycaemic action-Adrenergic compounds, corticosteroids,

oestrogen containing oral contraceptives, thiazide, diuretics, and phenytoin.

Biguanides:

Mode of action: Major effect is to increase peripheral uptake of glucose and in large

doses to dealy or decrease intestinal absorption. Biguanides do not cause hypoglycaemia.

Indications:

1) Treatment of maturity onset, diabetic who failed to lose weight on diet.

2) In combination with sulphonylureas-To enchance the inadequate or failing effects

of sulphonylurea.

3) As an adjunct to insulin therapy in brittle diabetes whose blood sugar tends to

swing unpredictably, one who is prone to ketosis and who develops

hypoglycaemia with only slight overdose of insulin.

Adverse Effects:

1) Malaise, weakness, drowsiness. 2)Metallic taste in mouth, anorexia, nausea,

dyspepsia, diarrhoea. 3)Lactic acidosis. 4)Vitamin B12, malabsorption (after

prolonged treatment).

(iii) Insulin:

Insulin is indicated for type – 1 diabetic as well as for type - 2 diabetic patients

whose hyperglycemia does not respond to diet therapy either alone or combined with oral

83


hypoglycemic drugs. Insulin injections are very much necessary in severe conditions of

hyperglycemia.

There are various preparations are present depending upon their purity, solubility

and species (like Human / Bovine ).

Four principle types of insulin's are available.

1. Ultra - short acting with very rapid onset and short duration

2. Short acting with rapid onset of action

3. Intermediate acting

4. Long - action with slow onset of action.

The injection can be given with the help of syringes with half inched ultra fine

needles attached available in 1 ml, 0.5 ml, 0.3 ml and 0.25 ml sizes. For the injection any

part of the body covered by loose skin can be used such as abdomen, thigh, upper arms,

flanks and upper buttocks.

(iv) Insulin - like growth factor-1 (IGF - I) therapy

(v) Aspirin therapy

Steps in the management of diabetic patients:

(A) Diagnostic examination: All necessary examinations should be done for the

diagnosis including all systemic examinations and with the help of proper history.

(B) Patient education (Self management training): Since diabetes is a lifelong

disorder, education of the patient and the family is probably the most important

obligation of the physician who provides initial care.

Advice:

1. To check regular blood sugar level

84


2. Maintain diet control

The teaching curriculum should include explanations by the physician or the

nurse the nature of the diabetes and its potential, Acute and chronic hazards and how they

can be recognized early and prevented or treated.

(C) Self - monitoring of blood glucose.

Monitoring of blood glucose by patients has allowed greater flexibility in

management while achieving improved glycemic control.

Initial therapy:

Treatment must be individualized on the basis of the type of diabetes and specific

needs of each patient.

(1) The obese type 2 patient:

The most common type of diabetic patient is obese

A) Weight reduction 1.By means of use of prescribed diet and diet control 2.By

means of exercise to expand energy.

b. Hypoglycemic agents:

(2) The non-obese patient

Treatment mainly depends upon the blood glucose level.

a. Diet therapy: Diet with caloric content sufficient to maintain ideal weight

Restrictions of saturated fat and cholesterol are also strongly advised.

b. Oral hypoglycemic agents

Complication management: According to the complication and its severity.

85

Review of Literature Pathya Apathya

Pathya Apathya

General considerations on sthoola and krusha Madhumeha patients

Pathya differ from one set of patients to another like the difference of treatment in

them. In sthoola Madhumeha there is marga avarodha of vayu by vriddha kapha and

medas. Hence to rectify the imbalance of the dushyas and to reduce the amaroopi medas,

the patient should be advised to follow the following diet.

1) The diet which aims to wards the alleviation of kapha dosha and medodathu.

2) The diet which inhibits the vitiation of vayu.

3) The diet which gives strength to the body.

4) The diet which is having low caloric value and low glycemic index are to be

suggested to the patients.

Ahara:

In general, Ahara, which are Vatamedokara are Apathya in Madhumeha. In other words,

Madhumehi should be cautious about taking Ahara, which is Madhura rasa pradhana,

Guru and Abhishyandi.

It is advised to follow the general principles of food intake as laid down in Ashta

vidha ahara vidhi vishesha ayatanas with special emphasis on Matra. One should always

avoid Adhyashana, Vishamashana and Atimatra bhojana. In case of Sthoola Madhumehi,

Ushna, Tikshna, Lekhana, Virukshana and Chedaneeya aharas can be used liberally,

where as in Krusha Pramehi Laghu and Santarpana ahara, which is not Vatamedokara,

should be given; which means foods like Yava are ideal. Taila, Ghrita etc Snigdha

dravyas, which are basically Vatakara, can be used after Samskara so that they are

rendered Tarpaka as well as Vatamedohara qualities. Laghu, Tarpaka Pathya kalpana like

86


Yusha, Mantha, Yavagu, and Kashaya etc prepared from Kaphamedohara dravyas can be

used generously among the Pathya mentioned for Madhumeha. Tikta Rasa, Yava and

Madhu are seen to be indicated high in the priority lists of Ayurvedic classics.

Importance of Tikta rasa197,198

Madhumeha arambaka dosha is kapha, though the arambaka dosha is vayu here,

the vayu is in avrita avastha. Hence tikta rasa pradhana dravyas are beneficial. Tikta is

laghu and ruksha where as kapha is guru and snigdha.

Tikta rasa is having more laghu quality than other rasa likewise it is having very

less rukshata among kashaya, katu, and tikta rasa. Tikta rasa helps in decreasing kapha,

shareera kleda (through shoshana) and meda, which are known as the important factors

involved in Madhumeha. It helps in reducing factors involved in the Madhumeha it helps

in reducing the dravatwa of mootra. Dravatwa then leads to the decrease of saratwa hence

the frequency and quantity of mootra will be reduced thorough tikta rasa sevana.

Karavella, boomyamalaki, etc., are to be used.

Importance of yava199: yava is the best among the diets. In prameha yava is the diet of

choice, yava can be consumed in different modes of preparation yavana, yavamahada etc.

in chikitsa shastra it had been claimed that yava manda increases the quantity of mootra,

and yava kshara is known as mootrala. Hence a doubt arises whether yava is advisable in

Madhumeha. Infact yava is mootra vriddikaraka. To be precise it reduces, the dravaguna

of mootra and hence reduces frequency and quantity of urine. Along with these, yava is

rooksha and laghu and helps in bringing the vitiated kapha dosha to normalcy. Susruta

has termed yava as ‘atirooksha and prabhada mootra’ in actions, the person who is

87


affected by santharpanotha Madhumeha must perform vyayama, rooksha udvarthana,

ratri jagarana and others which will combat kapha and pitta.

Vihara200: Chankramana, Snana and Asana, four Kaya Viharas viz., Vyayama, Mrija,

Nishi gamana, and Jagarana are potent Vatamedohara viharas which can be performed in

increased magnitude by a Sthoola Madhumehi as he is Balavan. In a Krusha Madhumehi,

these should be advised depending on his Bala. If a Krusha rogi is unable to perform

Vyayama then only Mrija and Chankramana can be advised with some Vishama shareera

nyasa.

Among Viharas, Vyayama figures prominently in the classics as an effective

Vatamedohara vihara. Pragadha vyayama can be performed depending on one’s own

interest and knowledge. Vishama shareera nyasa can be performed by both Sthoola and

Krusha Pramehi in the form of Yogasanas but one should be careful while performing

these as they can be harmful if improperly performed. A regular and sustained exercise

regimen is beneficial.

Vyayama201: Any Karma or action of the body that produces Shareera ayasa is Vyayama.

Vyayama is Alasyahara, Sthoulya apakarshaka and causes Sthiratva, Laghuta and

Agnideepthi; the person becomes Klama, Pipasa, Ushna, Sheeta, Klesha-saha. Vyayama

should be performed to a man’s Ardhashakti. Otherwise, it can be harmful. Vyayama thus

is ideal in Madhumeha especially in Sthoola and Balavan.

Yogasana202: The severe diabetics can be advised to perform yogasana because in

yogasana both the body and mind gets steadiness without any physical exertion or stress.

88


Pranayama and Meditation: Breathing exercise and meditation techniques are also

proving as an effective panacea in stress management, thus acting synergistically in

Diabetic management. Meditative techniques like transcendental meditation of Maharshi

Mahesh Yogi, Sudarshana kriya of Pandit Sri Sri Ravishankar are popular innovations in

this field.

Vichara203, 204: Manas is among the adhistanas of Vyadhi. Rajas and Tamas are the dosha

of Manas, which get aggravated by Udeerana of Dharaneeya vega like Icha, Dwesha,

Moha, Krodha, Irshya, Mada, Matsarya and Shrama. The upaya for dharana of these vega

is by Indriya Nigraha. Due to Prajnaparadha, Rajo and Tamo dushti occur. This leads to

manifestation of Manasika roga. In milder forms of involvement of dosha leads to

hastening of development or aggravation of a Vyadhi. Hence Manasika dosha should be

balanced well by resorting to Jnana, Vignana, Atma Jnana etc. The Manasika dosha are

interrelated to Shareerika dosha. Tamoguna increases Kapha and Rajoguna increases

Vata and Pittta. Hence all these should be avoided. Rajo guna is the motivator of mind

into activity under normal circumstances. Hence mind should be motivated into Vyayama

and other activities, which help in reducing Vata and Medas.

APATHYA:

Apathya Vichara in Madhumeha has been summarised in table.

LIFE SYTLE MODIFICATION IN THERAPY OF DIABETES205:

Diet: Before the discovery of insulin(1921) the only treatment available for the diabetics

was diet therapy. This meant starvation and no carbohydrates. Over the past few decades

diet therapy has revolutionized. Present scientific concept is, as a diabetic, one can eat

normal diet and choose variety of food stuff available, provided the quality and quantity

89


is balanced and total calories are proportionate to ones ideal body weight. Diabetes is

modal disease where proper diet therapy can make wonders.

For type 1 diabetes neither diet nor exercise can be regarded as a primary modality of

treatment. In contrast, both are primary therapeutic options for management of type 2

diabetes. Their potential however is limited in most instances due to poor compliance.

Dietary management of diabetes should not only aim to achieve glycaemic control, but

also to normalise dislipidaemia, commonly associated with diabetes. The carbohydrate

content in the diet, the type of fat, quantity and type of protein has been altered from time

to time to meet these needs.

Carbohydrate content of the diet has to provide 50-60% of the calories and most of this is

to be in the form of complex carbohydrates with a high fibre content and low glycaemic

index. Fat content of the diet should provide 20-25% of the calories distributed in the

ratio of 1:1:1 among saturated, monosaturated and poly unsaturated fatty acids (PUFA).

PUFA content of less than 10% of the total calories and an EFA content of at least 3% of

the total calories is advisable with the n6/n3 ratio being less than 10. Protein intake

0.8g/kg is recommended, so as to contribute to 12-20% of the total calories. Vegetable

proteins are preferred due to their high fibre content and absence of saturated fat that is

present in animal proteins. A low fat diet also improves the lipid profile.

ALCOHOL:

Alcohol intake increases the risk of hypoglycaemia, may induce keto-acidosis, lactic

acidosis, and may contribute peripheral neuropathy. Alcohol is also an additional source

of calories, each ml provides 7k.cal and should therefore be avoided as per as possible.

90


CESSATION OF SMOKING:

Smoking in addition to being an independent risk factor for development of type 2

diabetes mellitus also contributes to the development and progression of the macro and

micro vascular complications of diabetes. Cigarette smoking is associated with an

adverse effect on the serum lipids and lipo-proteins. Increase in the platelet reactivity is

seen in hyper cholestrolaemic patients who smoke cigarettes. The effect of cigarette

smoking on the lipid profile is not limited only to smokers. A reduction in HDL

cholesterol levels is noted even in children passively exposed to cigarette smoke at home.

There is also evidence that smoking cessation reduces the risk of morbidity and mortality

from coronary artery disease.

EXERCISE:

Exercise constitutes the first step in the treatment of type 2 diabetes along with diet. It

improves the condition of a diabetic patient due to several factors. There is an increase in

the number of insulin receptors as well as the sensitivity of insulin receptors. In addition

there is an elevation of 2-3 DPG levels in the RBC and reduction in HbA1C. These

promote the delivery of oxygen to the peripheral tissues, which result in the improved

efficiency of the diabetic. The best form of exercises recommended to a diabetic is step

wise increase of aerobic exercise. On the other hand isometric exercise like weight lifting

sustained hand grip are to be avoided in diabetics as they increase arterial pressure.

YOGIC PRACTICES:

Recently several well planned studies have demonstrated the beneficial effects of yogic

practices in diabetics. Patients with diabetes demonstrated a significant fall in fasting and

91


post prandial blood sugar values and HbA1C with reduction in the requirements of oral

hypoglycemic agents and insulin. Patients with type 1 diabetes, with brittle diabetes

showed marked improvement with practice of yoga. There was a salutary affect on the

lipid profile with fall in serum cholesterol, triglycerides and HDL cholesterol fraction.

Certain asana have been identified as useful in the control of diabetes.

92


Table No. 10: Pathya in Sthoola Madhumehi206, 207, 208,209

Sl. No.

Ahara Sl. No.

Vihara

1)

2)

3)

4)

5)

6)

7)

8)

9)

10)

11)

12)

13)

14)

Vividha vyayama yoga

Niyuddha

Kreeda

Gajaturaga charya

Ratha charya

Padaticharya

Parikramana

Padaticharya

Astropastrabhyasa

Mrugaihi saha vaset

Apatarpana

Samshodhana

Pragada udvartana

Snana jalavasekaihi

Sl.

No.

Vichara

1)

2)

3)

4)

5)

6)

7)

8)

9)

10)

11)

12)

13)

14)

15)

16)

17)

18)

19)

20)

Patha

Haritaki & Madhu

Chitraka

Mridvek

Kapitha + Maricha + Madhu annapana

Ustra,Ashwa, khara pureesha churna

ashana

Shyamaka

Neevara

Amalaka

Tinduka

Ashmantaka phala

Mudgayusha

Triphala

Trikatu

Trimada

Draksharista

Yava Bhakshya

Arishta Kashaya Avalehya

Jangala Rasa

Shulya mamsa.

1) Chinta

93


Table No. 11: Pathya in Krusha Madhumehi208, 210, 211

Sl. No.

Ahara Sl. No.

Vihara

1)

2)

3)

4)

5)

6)

7)

Padratrana

Atapatrarahito

Brikshyashi

Gramaikatravasi

Krushet

Khanet Kupam

Shilonchavruthihi

Sl. No.

Vichara

1)

2)

3)

4)

5)

6)

7)

8)

9)

10)

11)

12)

13)

14)

15)

16)

17)

18)

19)

20)

21)

Aviruddha annapana

Rasagandhavathi annapana

Hingu yukta yusha

Saindhava yukta yusha

Sarshapa yukta yusha

Mudgadi yusha & Odana

Mantha of all Dravyas mentioned as Pathya for Krusha

Kashaya

Yavadi churna

Lehya of Yavadi

Odana of Laghu tarpaka dravyas

Vatya of Laghu Tarpaka dravyas

Madya of Yavadi

Saktu of Yavadi

Apoopa of Yavadi

Vishkira mamsa

Pratuda mamsa

Yava churna soaked in Triphala Kwatha overnight, next day taken with Madhu & Saindhava

Yava saktu mixed with Haritaki, Amalaki etc. kwatha along with Guda, made into Apoopa

Purana shali odana

Tikta shakha odana

1)

2)

Muniriva samyatatma

Brahmarathamuddreth

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Table No. 12: Apathya Ahara, vihara, vichara212, 213, 214,215 Ahara Ahara Vihara

1) Picchila

2) Sheeta

3) Guru

4) Snigdha

5) Drava

6) Abhishyandi

7) Atipramana

8) Adhyashana

9) Virudhashana

10) Madhura

11) Amla lavana

12) Kaphakara

13) Medokara

14) Mootrakara

15) Sauvira

16) Tushodaka

17) Shakti

18) Maireya

19) Sura

20) Asava

21) Toya–Dushta

22) Paya

23) Taila

24) Ghrita

25) Ikshuvikara

26) Dadhivikara

27) Pistanna

28) Amlayavagu

29) Amlapanaka

30) Nava Madya

31) Gramya mamsa

32) Anupa mamsa

33) Matsya

34) Nava Hayanaka

35) Nava Yavaka

36) Nava Chinaka

37) Nava Uddalaka

38) Nava Naishadha

39) Nava Itkata

40) Nava Mukunda

41) Nava Mahavrihi

42) Nava Pramodaka

43) Nava Sugandhaka

44) Nava Kalaya

45) Masha

46) Tila

47) Palala

48) Dadhi

49) Nava Annapana

50) Kshara

51) Nishpava

52) Dushtambu

53) Kushmanda

54) Bhojanante

Jalapana

Souhitya

1) Divaswapna

2) Avyayama

3) Alasya

4) Mrija tyaga

5) Asana sukha

6) Anya slesha meda

mutra kriya

7) Snana tyaga

8) Chankramana Tyaga

9) Rakta Mokshana

10) Swedana

11) Dhoomapana

12) Mootravegadharana

13) Sheetala Jalasnana

14) Pushpa sugandha

15) Snehana

16) Dushtambu snana

17) Shareerika Ashrama

18) Vidhivarjita shayana

19) Vyavaya

Vichara 1. Bhaya

2. Krodha

3. Shoka

4. Alasya

5. Loulya

6. Mandotsaha

7. Abhyavaharyeshu

Grudhnus

8 Asatam Sanga

95

Drug Review Asanadi Kwatha

DRUG REVIEW

Drug plays a vital role in the management of the disease. Due to this reason; it has

been placed next to physician in the Chatushapada. The comprehensive knowledge of the

drug is very important to physician because without knowledge of the drug, the patient

can not be treated properly. It has been well said by Acharya Charaka ‘a drug that is

not understood perfectly is comparable to poison, weapon, fire and the thunderbolt;

while, the perfectly understood drug is comparable to ambrosia.

The best drug is that which cures the disease promptly and also preserves or sustains the

health of an individual.

ASANADI KWATHA:

Asanadi Kwatha is anubhuta yoga which is been prescribing in S.D.M. Ayurveda

hospital, Udupi, Karnataka Since 20 yrs. It contains 14 ingredients Properties of each

drug are mentioned in Table number 14. Most of these drugs have tikta, kashayarasa,

laghu, rooksha guna and katuvipaka.These are said to be kaphagna, mehagna, medogna

and mootrasangrahaneeya.

Tikta, kashayarasa, laghu, rooksha guna produces rookshana effect and they are

having opposite qualities to that of kapha and medas. Hence they act as mehagna and

kaphagna. When medas is reduced then the pressure on vapavahana is also diminished as

it is the moolasthana of medovahasrothas. Bahudravata will be present in Madhumeha.

Tikta, kashayarasa present in this yoga produces shoshana effect. Bahudravata will be

reduced by the absorption of excessive fluid from the body cells. when bahudravata

reaching basthi reduces then prabhoothamootrata, pratyatmalakshana of Prameha also

reduces. Pipasa which is dependent on prabhoothamootrata also subsides. Asanadi

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Kwatha reduces medas thereby Sthoulya and as it is mootrasangrahaneeya, absorbs

bahudrava and hence reduces polyuria, and polydipsia and thereby checks the

pathogenesis of Madhumeha. So, this kashaya considered to be Mehagna.

Ingredients217,218:

Table No.13: Ingredients of Asanadi Kwatha

Asana – 1 part Vibhitaki - 1part

Khadira – 1part Amalaki - 1part

Sariva - 1part Punarnava - 1part

Manjishta -1part Ashwaganda – 1part

Ushira - 1part Haridra – 1 part

Chandana - 1part Gokshura – 1 part

Haritaki - 1part Saptarangi - 2 part

Method Preparation: All the raw materials were procured and checked for genuinity

then dried and subjected to pulverization for the desired particle size viz. Kwatha churna.

1. ASANA ( Pterocarpus marsupium):

Chemical Composition : Tannin, kinotannic acid (70 to 80%) usually believed to be

identical with catechu tannic acid and distinct form gallo-tannic acid other constutents of

kino are pyrocatechin, gallic acid and gum.

97


Karma: Due to Rasa it acts against Kapha, Meda and Kleda. Due to Veerya it acts

against Vata. Bhavprakasa mentioned it as Mehaghna and Rasayana. It is also helpful in

blood disorders.

Pharmacological studies:

1. Extract of heart wood showed significant hypoglycemic action in fasting rabbits 3& 5

hrs. after oral administration (I.J.M.R,1967,55,166).

2. Alcoholic extract of stem significantly lowered blood sugar and improved glucose

tolerance of rabbits (J.Res.Ind.Med.1971, 6,205).

3. Administration of ethyl acetate extract for 14 consecutive days to rats produced

significant reduction in levels of triglycerides, total cholesterol and LDL (J. Nat. Prod

1993, 56, 989).

4. A flexible dose open trial was undertaken in 4 centers in India to evaluate the efficacy

of an ayurvedic drug asana in the management of newly diagnosed or untreated type 2

DM. By 12th week, control of blood sugar had been attain in 67 out of 97 patients

studied, and the dose at which control was attained was 2 g of the extract in about 73% of

the patients 3 g in about 16% and 4 g in 10% of patients. Mean HbA1c decreased

significantly (p<0.001) to 9.4%; no side effects were reported (Seshaiah, v.sundaram et

al, .1998).

2. SAPTARANGI (Salacia reticulate):

Chemical composition: Roots contain 1, 3 – diketones, fat, rubber, dulcitol, mangiferin,

phlobatannin, glycosidal tannins, leucopelargonidin.

Karma: Mutrasanghrahani, Madhumehara, Shothahara, Deepana, Anulomana,

Raktashodaka,

98



1. Roots have been used as an ant diabetic drug in the indigenous system of medicines

and clinical tests are said to have substantiated their efficacy. (The wealth of India, CSIR,

New Delhi).

2. Methanolic extract from the stems of Salacia chinensis (Hippocerateaceae) showed

potent anti-hyperglycemic effects in oral sucrose or maltose-loaded rats, inhibitory

effects on intestinal alpha-glucosidase, rat lens aldose reductase, formation of Amadori

compounds and advanced glycation end-products, nitric oxide production from

lipopolysaccharide-activated mouse peritoneal macrophage, and radical scavenging

activities.(Yoshikawa M et. al. Yakugaku Zasshi. 2003 Oct).

3. In a detailed study, the aqueous extract of the root bark showed a significant

hypoglycemic activity in the streptozotacin induced diabetes albino rats. The plasma

glucose concentration was determined at regular intervals following administration. The

drug was effective as a hypoglycemic agent at all doses tested (0.5g/kg, 1.0 g/kg and

5.0g/kg). The maximum decrease in plasma glucose was observed between 1-5hrs

following the administration of the drug. The maximum hypoglycemic activity of 30%

was observed 3hrs after administration. (Karunanayake, et al.1984).

3. HARIDRA (Curcuma longa):

Chemical composition: It contains 5-8% of volatile oil & yellow colouring matter-

Curcumin. In addition to this it contains Vit. A, Protein 6.3%, Fat 5.1%, Minerals 3.5% &

Carbohydrate 69.4%. Curcumin, curcuminoids, Germacrone, Tumerone, Curcumenol,

Turmeronol A & B, curlone, stigmasterol, beta tumerones, beta bisabolene, alpha

curcumene, Zingiberine, betasesquiphellandene, bisacurone, curcumene,

99


dehydrocuridione, procurdione, procurcumadiol, bis-acumol. The essential oil from the

rhizome contains d-a-phellandrene, d-sabinene, cineol, borneol, Zingiberene,

sequisterpenes (tumerones). The crystalline coloring matter, curcumin is diferuloyl

methane.

The antioxidant properties of curcuma powder are probably due to the phenolic

character of curcumin. (The wealth of India).

Karma: Shothahara, Vranaropana, Vranashodana, Kusthagana, Raktaprasadan,

Mutrasanghrahani..


1. In a research study administration of turmeric or curcumin to diabetic rats reduced the

blood sugar, Hb & HbA1c levels significantly. (ArunN, NaliniN. Plant Foods 2002)

2. Curcuma longa rhizome extracts showed blood glucose lowering activity in

experimental induced diabetic rats. After 3 & 6 hrs. Of curcuma injection (10 mg), 37.2%

& 54.5 % fall was observed respectively in glucose levels.(Tank R. et al, Indian Drugs

1990, V-27 (11), 587- 589)

4. Streptozotocin-induced diabetic rats were maintained on 0.5% curcumin containing

diet for 8 weeks. Blood cholesterol was lowered significantly by dietary curcumin in

these diabetic animals. Cholesterol decrease was exclusively from LDL-VLDL fraction.

Significant decrease in blood triglyceride and phospholipids was also brought about by

dietary curcumin in diabetic rats. (Babu PS, Srinivasan K. Mol Cell Biochem. 1997 Jan;

166(1-2):169-75.)

5. Curcumin from Curcuma longa was screened for neuroprotective activity .Oral

administration of curcumin to ethanol intoxicated rats revealed that the antioxidative and

100


hypo lipidaemic action of curcumin is-responsible for its protective role against ethanol

induced brain injury. (Rajakrishnan V, et.al. (Phytotherapy, 1999 Nov; 13(7):571-4])

4. KHADIRA (Acacia catechu)

Chemical Composition: Heart wood contains catechin, catechu tannic acid. Wood

contains 1-epicatechin, ± Afzelchin, gossypetin, procyanidin Ac, taxifolin.

Karma: Kapha-Pittahara, Medogna, Deepana, Dantya.


1. A flavoniod isolated from ethonolic extract of central wood of A. catechu showed

hypoglycaemic activity (chakravarthy et al., 1983)

2. Seeds exhibited marked hypoglycaemic activity in normal rats but not in alloxan

induced rats (I.J.M.R.1976).

5. SARIVA (Hemedismus Indicus):

Chemical Composition: Hyperoside, rutin, desinine, hexatriacontane, β-sitosterol;

hemidesminine, hemidesmin-1 and hemidesmin-2, P-methaxi salycilic aldehyde.

Karma: Tridoshara, Grahi.


1. A Saponin from it was found to have anti-inflammatory activity (ICMR, 1968-69)

2. It showed immunomodulator activity and immunosuppressant activity. It decreases the

phagocytosis in experimental studies (Atal et al., 1986).

6. MANJISHTA (Rubia cordifolia)

Chemical Composition: Antitumour cyclic hexapeptides, RA-V and RA-VII along with

RA-I-IV; anthraquin-ones munjistin, purpuroxanthin, rubiatriol, rubicoumaric acid, rubi

101


folic acid, pseudopurpurin, alizarin, M rubiadin, rubimallin, purpirin, xanthopurpurin,

ruberythric acid etc.

Karma: Kapha pitta hara, varnya, vishagna.


1. The blood purification effect of the partially purified fraction of the whole plant has

been studied on rabbit platelets. It inhibits the platelet aggregation-induced by PAF

(platelet aggravating factor) but not thrombin. It also inhibits the binding of 3H-PAF to

the platelets in the dose-dependent manner. Thus it appears that R.cordifolia inhibits

action of PAF at its receptor level either by its blocking or by desensitization (Tripati et

al., 1993).

2. Crude extract of R.cordifolia exhibited spasmolytic activity similar to that of verapamil

suggesting presence of calcium channel blocker like constituent(s) in this plant (Gilani et

al, .1994)

7. AMALAKI (Embilica officinalis)

Chemical Composition: Fruit contains gallic acid, tannic acid, sugars, albumin, cellulose

and minerals. The fruit is one of the richest natural sources of vitamin C, containing up to

720 mg/100g of fresh pulp and 921 mg/100cc of pressed juice. Other contents are as

follows: Moisture 81.20, protein 0.5, fat 0.1, minerals 0.7, fibre 3.4, carbohydrate 14.1,

calcium 0.05, phosphorus 0.02 % and iron 1.2 mg, nicotinic acid 0.2 mg per 100gms. of

fruit.

Karma: Daha prashamana, Chakshushya, Medhya, Rochana, Deepana, Anulomana,

Vrishya, Rasayana, Pramehagana..


102


1. Emblica fruit powder reduced blood sugar level in normal rabbits, as well as in

hyperglycemic rabbits proving the hypoglycaemic activity (Tripati et., 1979).

2. A clinical study on nisha amalaki churna in diabetes proves the efficacy of the

combination (Gopal Kumar et al; 1995 & Nagrjuna. Jan, 1983 p.105- 107)

3. hypo-lipidemec and anti atherosclerotic activity five groups of rabbits were studied for

16 weeks to determine the effect of emblica fruit and vit.c (6 mg/kg) on cholesterol

induced hypercholesterolemia and atherosclerosis. Both reduced the serum cholesterol

(Thakur & Mandal, 1984).

4. Amlaki Rasayana is said to have growth promoting effect. The drug has significant

effect on the levels of serum protein fractions, yet raises the total protein level.(Tewari

et.al; 1968).

5. Methanolic extract (75%) of Terminalia chebula, Terminalia bellerica, Emblica

officinalis and their combination named 'Triphala' are being used extensively in Indian

system of medicine. Oral administration of the extracts (100 mg/kg body weight) reduced

the blood sugar level in normal and in alloxan (120 mg/kg) diabetic rats significantly

within 4 hrs. Continued, daily administration of the drug produced a sustained effect.

(Sabu MC, Kuttan R. J Ethnopharmacol. 2002 July)

8. HARITAKI: (Terminalia chebula)

Chemical composition: Myrobalans contains astringent principles; tannin and a large

amount of gallic acid, lacilage. Major tannin constituents are chebulagic acid, chebulinic

acid & corilagin. Chebulinic acid when heated in water splits up into tannic acid and

gallic acid.

103


Karma: Vedanasthapana, Vranashodhana, Vranaropana, Deepana, Pachana, Krimighna,

Kusthaghna, Medhya, Chakshushya, Brimhaniya, Anulomana, Rasayana.


1. The fruits are laxative, stomachic, tonic. Main purgative ingredient of Triphala is T.

chebula, the other two only increasing the purgation activity of peristaltic movements

uniformly progressive. The purgative principle in the pericap of the fruit of T. chebula

has been found to be a glycoside which may be similar to sennoside. Chebulin possess

antispasmodic activity (The wealth of India Pg. No. 175, Vol. 10)

2. T. Chebula is found to possess hypoglycaemic activity on glucose induced

hyperglycaemia in rats (Tripati et. al; 1979).

3. Anti oxidant property of T. Chebula is reported (Fu Naiwu et.al; 1992)

4. Hypolipidimic action of ethyl acetate soluble fraction of the alcoholic extract of T.

Chebula stem in normal and trition-treated rats is reported (Kanna et.al; 1993)

9. VIBHITAKA (Terminalia bellerica):

Chemical Constituents: It contains gallotannic acid, β-sistesterol, resins, chebulagic

acid, glucose, galactose and fructose.

Karma: Anulomana, Bhedaniya, Shothahara, Kasaghna, Chakshushya.


1. T. bellerica showed significant activity against both gram positive and gram negative

bacteria. (Valsaraj et al; 1994).

2. A significant hepato protective effect was observed as evident from shortened

hexobarbitone “sleep time” and zaxozolamine “paralysis time” when compared with

CCL4 alone.(Anand et al; 1994).

104


10. USHIRA (Vetiveria zizanioidis):

Chemical Composition: A volatile essential oil, resin, colouring matter, a free acid, a

salt of lime, oxide of iron and woody matters.

Karma: Dahaprashaman, Trishnanigrahana, Stambhana, Swedapanyana,

Raktaprasadana,


1 .Khustineol exhibited juvenile hormone activity against mustered aphid(Lapaphis

Erysmi)-(Ind.J.Chem.1985,24B 496).

11. CHANDANA (Santalum album):

Chemical Constituents: Santalic acid, n-ocacosanol, plamitone.

Karma: dahaprashana, Varnya.

12. ASHWAGANDHA (Withamnia somnifera)

Chemical Constituents: Withaferin A, Withanon, Withanolide WS-1, Withanolide A-Y,

Somnitol etc.

Karma: vayasthapana, deepana, sothahara.

Pharmacological studies

1. Its powder provided significant relief from symptoms of anxiety neurosis besides a

quantitative reduction anxiety level (Singh et.al; 1977)

2. The immunomodulatory and immuno suppressive activity are established (Furmanowa

et.al; 2001).

13. PUNARNAVA (Boerhavia diffusa):

Chemical Constituents: Hentriacontane, β-sitosterol, oxalic acid, D-glucose,

punarnavoside, punarnavine-1,punarnavine-2, boeravinones A,B,Cetc.

105


Karma: sothahara, vayasthapana, deepana.


1. The administration of punarnava for a period of 3-6 months showed that the drug

desreased blood urea with a simultaneous increase in serum cholesterol and blood sugar.

This is attributed to the rasayana effect of the drug (Apparao et al., 1969)

2. The drug in the form of a powder on an aqueous decoction was found to be useful in

the treatment of nephritic syndrome in 22 patients. The drug compared well with known

drugs like corticosteroids. The drug induced diuresis in the patients. Besides relieve in

clinical edema, these patients also showed overall improvement, such as decrease in

albuminuria, rise in serum protein and fall in serum cholesterol level ( Singh & Udupa

1972d).

3. It produced 50% inhibition of lipid peroxidation at a concentration of 2.28 mg/dl and

1.84 mg/ml in Fe++ascorbate system. Through this the anti oxidant property of B.diffusa

is established.

4. The alkaloid fraction of B.diffusa root was found to posses restorative activity against

stress induced changes in plasma and adrenal cortisol levels. It also significantly

augmented the antibody production in stressed rats as compared to control (Mungantiwar

et al., 1997)

14. GOKSHURA (Tribulus terrestris )

Chemical Constituents:

Fruits - Chlorogenin, diosgenin, gigenin, rutin, rhamnose.

Roots – campesterol, β-sitosterol and stigmasterol, neotigogenin.

Karma: Vrushya, Mutrala, Rasayana.

106



1. Nephro protective activity - Nephro protective activity was evaluated in gentamicin-

induced nephro toxicity (80 mg/kg/day S.C) in male albino rats, NR-AG-I (containing

C.nurvala,T-terrestris, D. biflorus & shilajit) NR-AG-II (C.nurvala,T-terrestris, B.diffusa

S.officinarum &B.frondosa)

2. A new original preparation “Tribestan” has been obtained from T-Terrestris having a

stimulatory effect on sexual functions(Tomova, 1987).

107


Table No.14: Asanadi Kwatha - Rasa panchaka

S.no. Name L.Name Guna Rasa Virya Vipaka Doshgnata Rogagnata

1 Asana Pterocapus marsupium

Laghu, ruksha

Kashaya, Tikta sheeta katu Kapha

pitta hara Madhumeha, sthoulya,

2 Khadira Acasia catachu Laghu, ruksha

Tikta, katu kashaya

sheeta katu Kapha pittahara

Madhumeha kandu,kusta

3 Sariva Hemidismus indicus

Guru, Snigdha

Madhura Tikta sheeta Madhura Tridosara Prameha,jvar

a,kusta,vrana.

4 Manjista Rubia Cardifolia

Guru, ruksha

Madhura Tikta ushna Katu Kapha

pittahara

Prameha,mutrakrucchra, Kusta.

5 Ushira Vetiveria Zizanoides

Ruksha, laghu

Tikta, madhura sheeta Katu Kapha

pittahara trisna,mutrakrucchra,daha

6 Chandana Santalum album

Laghu, ruksha

Tikta, madhura sheeta Katu Kaphapitt

ahara prameha,dahajwara,trushna

7 Haritaki Terminalia Chebula

Laghu, Ruksha

Lavanavarjihtapancharasa

ushna Madhura Tridosara Prameha,vatarakta,kusta

8 Vibhitaki Terminalia Belarica

Ruksha, laghu Kashaya ushna Madhura Kapha

pittahara

Jwara,Kasa trushna,Shwasa.

9 Amalaki Emblica officinalis

Ruksa, laghu

Lavanavarjithapancharasa

sheeta Madhura Tridosara Prameha,Mutrakrucchra,kusta,netraroga

10 Punarnava Boveria diffusa Laghu, ruksha

MadhuraTikta kashaya

ushna Katu Kapha vatahara

pandu, swasa, hrudroga, sotha,

11 Aswaganda Withamnia Sominefera

Snigdha laghu

Tikta Katu kashaya

ushna Katu Vatakaphara

Mutagata, klibya,hridroga,nidranasa

12 Haridra Curcuma Longa

Ruksha laghu

Tikta katu ushna Katu Kaphavata

hara prameha,kusta,pandu

13 Gokshura Tribulus Terrestris

Guru, snigdha Madhura sheeta Madhura Vata

pittahara

Prameha, mutrakruchraklibya,kasa

14 Saptarangi Salacia Retituculata

Ruksha laghu

Tikta Kashaya ushna Katu Kapha

pittahara Prameha

108

Clinical Study Methodology

MATERIALS AND METHODS

A dissertation entitled “A clnical study on the effect of Asanadi Kwatha in Madhumeha”

was carried out on 20 patients who attended the OP & IP sections of SDM Ayurveda

Hospital, Udupi during April 2005 to December 2005.

Aim of study

1) To evaluate the effect of Asanadi Kwatha in Patients suffering from Sthoola &

Krusha Madhumeha.

2) To evaluate the effect of Asanadi Kwatha in NIDDM patients.

3) Comprehensive literary study on Madhumeha.

Source of Data: Patients of either sex between age group of 30 – 75 yrs who attended

IP & OP section of S.D.M. Ayurveda Hospital were selected

Selection of Patients:

Patients fulfilling above criteria were administered Asanadi Kwatha without interfering in

their routine dietary and physical activities.

Diagnostic Criteria:

Criteria – 1:

Patients presenting with Pratyatma Laxana of Madhumeha – Prabhoota & Avila

mootrata with Mootra or Tanu madhurya, with or without other Roopa were taken as

Madhumehi.

Criteria – 2:

F.B.S. 120mg/dl to 180 mg/dl

P.P.B.S. 160mg/dl to 300 mg/dl

109


Inclusion Criteria: Patients fulfilling the following conditions were included.

1) Patients between 30years to 75 yrs.

2) Sthoola & Krusha Madhumehi

3) Patients of Type 2 DM with fasting blood sugar greater than 120mg/dl & lesser

than 180 mg/dl & postprandial serum glucose level of more than 160mg/dl & less

than 300 mg/dl.

Exclusion Criteria: The following patients were excluded from the study

1) Patients below 30 yrs & above 75 years.

2) Jata Madhumehi

3) IDDM patients

4) Gestational diabetics.

5) DM secondary to drugs like corticosteroids or due to secondary disorders.

Investigations: The following investigations were done on a mandatory basis.

1. F.B.S 2. P.P.B.S 3. Urine Sugar

Research Design: A single blind clinical trial with pre & post test design was adopted.

Intervention: Intervention was done with Asanadi Kwatha 40 ml twice daily, before

food, for duration of 30days, with a follow up for every 7 days.

Asanadi Kwatha is prepared from Asanadi Kwatha churna and Jala, taken in the

proportion of 1:8 (40 grams of Asanadi Kwatha churna and 320 ml of water) Kashaya is

prepared by reducing up to chathurtha avashesha(80 ml). Obtained 80 ml of Asanadi

Kwatha is given in two divided doses i.e. 40 ml in two doses..

110


Assessment Criteria: Any change in the following symptoms were noted & taken for

assessment

(1) Fasting Blood sugar

(2) Post Prandial Blood Sugar

(3) Post Prandial Urine sugar

(4) Sweda Adhikya

Sweating after heavy work and fast movement or in hot weather - 0

Profuse sweating after moderate work and movement - 1

Sweating after little work and movement (stepping ladder etc.) - 2

Profuse sweating after little work and movement - 3

Sweating even at rest or in cold weather - 4

(5) Prabhoota Mootrata [Quantity {in liter}]

1.50 to 2.00 - 0

2.00 to 2.50 - 1

2.50 to 3.00 - 2

3.00 and onwards - 3

(6) Avila Mootrata (Turbid urine)

Crystal clear fluid - 0

Faintly cloudy or smoky (turbidity barely visible) - 1

Turbidity clearly present but newsprint -

easily read through test tube - 2

Newsprint not easily read through test tube - 3

Newsprint can not be seen through test tube - 4

111


(7) Sthoulya (Assessed according to body mass index in Kg/H in m2)

Undernourished (less than 20) - 1

Normal weight (18.5 to 24.9) - 0

Overweight (25.0 to 29.9) - 1

Obese (30.0 to 39.0) - 2

Morbid obesity (40 and above) - 3

(8) Dourbalya

Can do routine exercise/work - 0

Can do moderate exercise with hesistancy - 1

Can do mild exercise only, with difficulty - 2

Can not do mild exercise too - 3

(9) Suptata (Numbness & tingling sensation)

No Suptata - 0

Kara-pada-tala-Supti incontineous - 1

Kara-pada-tala- Supti contineous but not severe - 2

Kara-pada-tala- Supti contineous and severe - 3

(10) Daha (Burning sensation)

No daha - 0

Kara-pada-tala-daha/Supti incontineous - 1

Kara-pada-tala-daha/Supti contineous but not severe - 2

Kara-pada-tala- Daha contineous and severe - 3

112


(11) Bahvashitva (Polyphagia)

No Bahvashitva As usual - 0

Slightly increased (1 – 2 meals) - 1

Moderately increased (3 – 4 meals) - 2

Markedly increased (5 – 6 meals) - 3

(12) Trushna (Polydipsia)

Feeling of thirst 7 – 9 times/24 hours - 0

Feeling of thirst 9 - 11 times/24 hours - 1

Feeling of thirst 11 – 13 times/24 hours - 2

Feeling of thirst >13 times/24 hours - 3

113

Clinical study Observation

OBSERVATION

In the present study, 24 patients suffering from Madhumeha, fulfilling the inclusion

criteria were registered, out of which, 4 patients failed to complete the study for different

non-medical reasons. Following are the detailed descriptive statistical analysis of the

patients included in the study.

Total patients registered for the study : 25

Completed : 20

Drop outs (LAMA) : 5

Observations

1. Age Incidence: The majority of the patients (50 %) were reported in the age group of

51 – 60 years followed by 35% in the age group of 61 - 70 years, 15% in the age group of

41 – 50 years (Table15 & Graph 1).

2. Sex Incidence: Equal incidence of Madhumeha was found in either sex

(Table16 & Graph 2)

3. Marital status incidence: 100% patients were married. None was unmarried. (Table

17& Gaph 3)

4. Educational status incidence: 30% of the patients were educated up to Middle

school. While 20% completed primary school, 20% were completed high school. 15%

uneducated and 15% Graduated (table18 & Graph 4)

5. Religion incidence: Maximum number of patients i.e. 70% were Hindus, 20% patients

were Christians and 10% patients were Muslims(table19 & Graph5)

114


6. Socio-Economic status incidence: It is observed that maximum patient belongs to

middle class i.e. 45%, followed by upper middle 30%, lower middle 10% poor 10%. And

rich were 5 %.( Table20 & Graph 6)

7. Occupational Incidence: Most of the patients were habituated to a sedentary life style

i.e. 40%, moderate workers were 35%. While the remaining 25% were accustomed to

performing heavy work (Table 21 & Graph 7)

8. Incidence of Addictions: Data depicts that maximum number of patients i.e. 45%

were taking tea/coffee, however 40% of the patients were Smokers, 10% of the patients

were addicted to alcohol and 5% had habit of chewing tobacco. (Table22 & Graph 8).

9. Incidence of Dietary Habits: 80% of the patients were accustomed to mixed type of

diet while 20% were Vegetarians (Table23 & Graph 9).

10. Incidence of Deha Prakruti: A predominance of Pittakapha prakruti was observed

in the patients with 45% followed by Vatakapha 35% and 15% of Vatapittala, 5% of

Kaphavatala prakruti (Table 24 & Graph 10).

11. Incidence of Sara: 65% of the patients were of Madhyama Sara while 25% were of

Avara Sara, 10% were of pravar sara observed (Table25 & Graph 11).

12. Incidence in Samhanana: Patients of Madhyama Samhanana were 80% while those

of Pravara Samhanana were 20% (Table26 & Graph 12).

13. Incidence of Satva: Satva analysis of the patients revealed 50% of Madhyama a

Satva, 30% of Pravar Satva remaining of avara satva (table 27 & graph 13).

115


14. Incidence of Rasa Satmya: 55% of the patients were Sarvarasa Satmya while 45%

were Madhyama Rasa Satmya i.e. accustomed to more than one Rasa (Table28 &

Graph14).

15. Incidence of Agni: Teekshna Agni was observed in 55% of the patients, Vishama

Agni in 25% and Manda Agni in 20% (Table29 & Graph 15).

16. Incidence of Bala: 70% of the patients were of Madhyama Bala, 20 % of Avara Bala

and 10% of Pravara Bala (Table30 & Graph 16).

17. Incidence of Family History: Majority of the patients were not having any family

history (Table31 & Graph 17).

116

Clinical Study Observation

OBSERVATION

Table 15: Age Incidence

Age group No. of Pts %

31 – 40 0 0 41 – 50 3 15 51 – 60 10 50 61 – 70 7 35

Graph 1: Age Incidence (in %)

Table 16: Sex incidence

0

20

40

60

31 - 40 41 - 50 51 - 60 61 - 70

AGE INCIDENCE

No of Pts

Sex No. of Pts % Male 10 50

Female 10 50

Graph 2: Sex incidence (in %)

0

20

40

60

M ale Female

SEX INCIDENCE

No of Pts (%)

117


Table 17: Marital Status Status No. of pts %

Single 0 0

Married 20 100

Graph 3: Marital Status (in%)

020406080

100

Single M arried

MARITAL STATUS

No of pts (%)

Table 18: Educational status

Education No of Pts % U 3 15 PS 4 20 MS 6 30 HS 4 20 G 3 15

118


Graph 4: Educational status (in %)

0

10

20

30

U PS M S HS G

EDUCATIONAL STATUS

No of Pts in %

Table 19: Religion Incidence

Religion No of Pts %

Hindu 14 70

Muslim 2 10

Christian 4 20

Graph 5: Religion Incidence (in %)

0

20

40

60

80

Hindu M uslim Christian

RELIGION INCIDENCE

No of Pts (%)

Table 20: Socio - Economic Status

Status No of Pts % VP 0 0 P 2 10

LM 2 10 M 9 45

UM 6 30 R 1 5

119


Graph 6: Socio - Economic Status (in %)

0

20

40

60

VP P LM M UM R

SOCIOECONOMIC STATUS OF PATIENTS

No of Pts in %

Table 21: Occupational Incidence

Occupation No of Pts %

HW 5 25

MW 7 35

SW 8 40

Graph 7: Occupational Incidence (in %)

0

10

20

30

40

HW M W SW

OCCUPATIONAL INCIDENCE

No of Pts (%)

Table 22: Incidence of Addictions

Habits No of Pts in% SM 8 40 TB 1 5 SN 0 0 AL 2 10 T/C 9 45

120


Graph 8: Incidence of Addictions (in %)

01020304050

Sm Tb Sn Al T/C

ADDICTIONS

No of Pts in %

Table 23: Dietary Habits

Diet No of Pts %

Veg 4 20

Mixed 16 80

Graph 9: Dietary Habits (in %)

020406080

Veg M ixed

DIETARY HABITS

No of Pts in %

Table 24: Deha Prakruti

Prakruti No. of Pts % VP 3 15 PV 0 0 VK 7 35 KV 1 5 PK 9 45 KP 0 0 T 0 0

121


Graph 10: Deha Prakruti (in %)

01020304050

VP PV VK KV PK KP T

PRAKRUTITAHA INCIDENCE

No of Pts in %

Table 25: Sara incidence (in %)

Saratah No. of Pts %

Pravara 2 10

Madyama 13 65

Avara 5 25

Graph 11: Sara incidence

0

20

40

60

80

Pravara M adyama Avara

SARATAHA INCIDENCE

No of Pts in %

Table 26: Samhanana (in %)

Samhanan No. of Pts %

Pravara 4 20

Madhyam 16 80

Avara 0 0

122


Graph 12: Samhanana (in %)

0

20

40

60

80

Pravara M adhyam Avara

SAMHANANA OF THE PATIENTS

No of Pts in %

Table 27: Satva incidence

Satva No of Pts %

Pravara 6 30

Madhyam 10 50

Avara 4 20

Graph 13: Satva incidence (in %)

0

20

40

60


SATVATAHA INCIDENCE

No of Pts in %

Table 28: Rasa Satmyata

Rasa No of Pts % Sarva 11 55

Madyama 9 45 Avara 0 0

123


Graph 14: Rasa Satmyata (in %)

0

20

40

60


RASA SATMYA INCIDENCE

No of Pts in %

Table 29: Status of Agni Agni No of Pts %

Teekshna 11 55

Sama 0 0

Vishama 5 25

Manda 4 20

Graph 15: Status of Agni (in %)

0

20

40

60

TeekshnaSama VishamaM anda

AGNI PRADHANYATA

No of Pts in %

Table 30: Bala incidence

Bala No of Pts %

Pravara 2 10

Madhyam 14 70

Avara 4 20

124


Graph 16: Bala incidence (in %)

0

20

40

60

80

Pravara M adyama Avara

BALA INCIDENCE

No of Pts (%)

Table 31: Family History

Relation No. of Pts % First degree 4 20

Second degree

0 0

No history 16 80

Graph 17: Family History (in %)

020406080

firstdegree

seconddegree

Nohistory

Family history

No.of Pts in %

125

Clinical study Results

RESULTS

1. Effect on Prabootha mutrata: The mean score of Prabhoota Mutrata which was

1.155±0.686 before treatment came down to 0.750±0.786 after treatment. Statistical

analysis of this data proved to be highly significant, ruling out the possibility of chance.

(P=<0.001) (Table 32 & Graph 18).

2. Effect on Avila mutrata: The mean Avila Mutrata of urine which was 1.050±0.887

before treatment reduced to 0.200±410 after treatment statistical analasis of data proved

to be significant at P<0.001 (Table 33 & Graph 19).

3. Effect on Karapada daha: Before treatment the mean score of Karapada daha was

1.3±0.733 and after treatment it was 0.5±0.224 indicating that there was a significant

improvement. This result is highly significant at P<0.001 (Table 34 & Graph 20).

4. Effect on Kara pada suptata: Improvement was seen in this symptom with a

reduction in the mean score from 0.90±0.852 to 0.150±0.366 which is statistically

significant at P<0.001 (Table 35 & Graph 21).

5. Effect on Bahu ashee: There was no statistically significant change in the

symptomatology with the mean scores being 1.250±0.716 and 1.050±0.686 pre and post

treatment respectively (Table 36 & Graph 22).

6. Effect on Trushna: The mean score of Trushna before treatment was 1.10±0.788

treatment and this reduced to 0.050±0.224 following the treatment which indicates that

the difference is highly significant statistically, ruling out the possibility of chance.

(P<0.001) (Table 37 & Graph 23)

126

Clinical study Results

7. Effect of Ati sweda: The mean score for Sweda adhikya which was 1.150±0.745

before treatment came down to 0.1±0.308 after the treatment. This difference is highly

significant statistically. (P=<0.001) (Table 38 & Graph 24).

8. Effect on Daurbalya: The mean score was 1.4±0.598 before treatment and 0.2±0.410

after treatment. This is statistically highly significant at P<0.001 and rules out the

possibility of the change having occurred by chance (Table 39 & Graph 25).

9. Effect on Sthoulya: The mean scores remained the same, thus indicating that a

difference does not exist to obtain a descriptive statistical analysis of significance (table

40 & Graph 26)

10. Effect on FBS: The mean FBS score before treatment was 136.7±22.49 and after

treatment 117.7±25.84 this is statistically highly significant at P<0.001 (Table 41 &

Graph 27).

11. Effect on PPBS: The mean scores of PPBS reduced from 228.15±49.62 to

194.25±47.94 following the treatment. This result was found to be highly significant at

P=<0.001 (table 42 & Graph 28).

12. Effect on Urine sugar: The mean PPUS values showed a decrease from 0.5±0.513 to

0.05±0.224. This change was significant statistically. (P<0.001) (Table 43 & Graph 29)

127

Clinical Study Results

RESULTS TABLE

Table 32: Effect on Prabhoota Mootrata

Mean Difference in Means Paired ‘t’ Test

BT AT S.D. S.E.M ‘t’ P 1.1550±0.686 0.750±0.786 0.800 0.616 0.138 5.582 <0.001

Graph 18: Effect on Prabhoota Mootrata

1.155

0.75

0

0.5

1

1.5

Mea

n

Effect on Prabuta mutrata

BTAT

Table 33: Effect on Avila mutrata


BT AT S.D. S.E.M ‘t’ P 1.050±0.887

0.200±0.410 0.850 0.745 0.167 5.101 <0.001

Graph 19: Effect on Avila mutrata

1.05

0.2

0

0.5

1

1.5

Mea

n

Effect on Avila Mutrata

BTAT

128


Table 34: Effect on Karapada Daha

Graph 20: Effect on Karapada Daha


BT AT S.D. S.E.M ‘t’ P 1.300±0.733

0.0500±0.224 1.250 0.716 0.160 7.804 <0.001

1.3

0.5

0

0.5

1

1.5

Mea

n

Effect on Karapada daha

BTAT

Table 35: Effect on Karapada Suptata

Graph 21: Effect on Karapada Suptata


BT AT S.D. S.E.M ‘t’ P 0.900±0.852

0.150±0.366 0.750 0.716 0.160 4.682 <0.001

0.9

0.15

0

0.5

1

Mea

n

Effect on Karapada suptata

BTAT

129


Table 36: Effect on Bahu Ashee


BT AT S.D. S.E.M ‘t’ P 1.250±0.716

1.050±0.686 0.200 0.410 0.0918 2.179 = 0.42

Graph 22: Effect on Bahu Ashee

1.25

1.05

0.9

1

1.11.2

1.3

Mea

n

Effect on Bahu Ashee

BTAT

Table 37: Effect on Trushna


BT AT S.D. S.E.M ‘t’ P 1.100±0.788

0.0500±0.224 1.050 0.759 0.170 6.185 <0.001

Graph 23: Effect on Trushna

1.1

0.05

0

0.5

1

1.5

Mea

n

Effect on Trushna

BTAT

130


Table 38: Effect on Ati sweda


BT AT S.D. S.E.M ‘t’ P 1.150±0.745

0.100±0.308 1.050 0.686 0.153 6.842 <0.001

Graph 24: Effect on Ati sweda

1.15

1

0.9

1

1.1

1.2

Mea

n

Effect on Atisweda

BTAT

Table 39: Effect on Daurbalya


BT AT S.D. S.E.M ‘t’ P 1.400±0.598

0.200±0.410 1.200 0.523 0.117 10.258 <0.001

Graph 25: Effect on Daurbalya

1.4

0.2

0

0.5

1

1.5

Mea

n

Effect on Dourbalya

BTAT

131


Table 40. Effect on Sthoulya


BT AT S.D. S.E.M ‘t’ P 0.750±0.716

0.750±0.716 0.000 0.000 0.000 0.000 =1.000

Graph 26. Effect on Sthoulya

0.75 0.75

0

0.5

1

Mea

n

Effect on sthoulya

BTAT

Table 41: Effect on FBS


BT AT S.D. S.E.M ‘t’ P 136.7±22.49

117.7±25.84 19.0 13.123 2.934 6.475 <0.001

Graph 27: Effect on FBS

136.7

117.7

100110

120130

140

Mea

n

Effect on FBS

BTAT

132


Table 42: Effect on PPBS


BT AT S.D. S.E.M ‘t’ P 228.15±49.62

194.25±47.94 33.900 19.963 4.464 7.594 <0.001

Graph 28: Effect on PPBS

228.15

194.25

160

180

200

220

240

Mea

n

Effect on PPBS

BTAT

Table 43: Effect on Urine Sugar


BT AT S.D. S.E.M ‘t’ P 0.500±0.513

0.0500±0.224 0.450 0.510 0.114 3.943 <0.001

Graph 29: Effect on Urine Sugar

0.5

0.05

0

0.2

0.4

0.6

Mea

n

Effect on Urine Sugar

BTAT

133

Clinical study Discussion

DISCUSSION

Madhumeha is a widely evidential disease since ancient age till today and

evidence is increasing day by day with lips and bounce with their complications and

complexes. Diabetes mellitus is similar to Madhumeha which is a subtype of Vataja

Prameha.

Madhumeha is a disease in which the patient voids excessive quantity of urine

having concordance with Madhu i.e. of Kashaya and Madhura taste, Ruksha texture and

honey like color. In Madhumeha, mainly the Vata and Kapha are predominant though the

disease is Tridoshakopanimittaja. The Vata may be provoked either directly by its

etiological factors or by the Avarana of its path by Kapha, Pitta or other Dushyas. So,

Vagbhata has classified the Madhumeha into two categories i.e. Dhatuapakarshanajanya

Madhumeha and Avarnajanya Madhumeha. Avaranajanya pathogenesis occurs due to

etiological factors mainly concordant with Kapha and Pitta, but the vitiation of Vata

occurs due to Avarana. Dhatuapakarshanajanya pathology occurs due to depletion of

Dhatus, because of the Vata vitiating etiological factors. Acharya Charaka has classified

Madhumeha into Santarpanajanya and Apatarpanajanya. The Apatarpanajanya

Madhumeha can be correlated with Dhatuapakarshanajanya Madhumeha, while the

Santarpanajanya Madhumeha correlates with Avaranajanya Madhuemeha. Therefore, this

disease may be caused both by the under nutrition as well as by over nutrition. The first

type of Madhumeha is considered to be Asadhya and no specific remedy is recommended

for this. But, the later type has been told as Krichhra Sadhya and can be cured with

extensive measurements.

134


The main pathophysiology behind Diabetes mellitus is the disturbed metabolism

of the carbohydrates, fats and proteins due to either absolute or relative lack of Insulin.

The Diabetes mellitus has been broadly classified as type 1 and type 2. The type 1

Diabetes mellitus patients are usually asthenic in body constitution and suffer from it in

the early years of life, while the type 2 Diabetes mellitus patients are usually obese and

suffer from it in their 40’s. The type 2 Diabetes mellitus patients can be managed easily

by hypoglycemic drugs whereas in type 1 Diabetes mellitus patients besides

hypoglycemic drugs, the Insulin therapy is obscure. So, the type 1 Diabetes mellitus is

nearer to Dhatuapakarshanajanya Madhumeha while the type 2 Diabetes mellitus

resembles to Avaranajanya Madhumeha.

The detailed study of Madhumeha according to Ayurvedic classics and modern

medicine unveils the following facts.

Madhumeha = madhusamam Diabetes Mellitus = honey urine

Beeja, Beejabhaga & Beejabhaga avayava

upatapa leading to Madhumeharambhaka dosha

dushti in Sahaja Madhumeha

Genetic susceptibility in the 6th Chromosome

leading to IDDM

Kulaja vikara Familial inheritance more in IDDM

Kaphamedokara ahara vihara sevana,

Avyayama and Chinta tyaga

Over eating and under activity

Ksheera, dadhi as Kaphakara ahara Bovine albumin

Vikara vighata abhava and Sahaja asatmya Auto immunity

Sthoulya upadrava Obesity leading to NIDDM

Anashana

Malnutrition in infancy predisposes to IDDM

135


Two kinds of madhumehis- Sthoola & Krusha

have been identified clearly

Obese people are more predisposed to develop

the disease especially the NIDDM and the

non-obese people also prone foe for DM

Prabhoota Mootrata Polyuria

Bahvashee Polyphagia

Trushna Polydipsia

Alasya Lassitude

Sthoulya (Margavarana janya) Rapid wt. gain (especially in NIDDM)

Krusha (Sahaja) Rapid weight loss in IDDM

Mootra madhurya Glycosuria

Tanu madhurya Hyperglycaemia

Kampa, Bhrama, Tamah ,Loulya upadravas

Hypoglycemia: Sweating, nervousness,

tremor, hunger, confusion, abnormal

behaviour and loss of consciousness

Bhrama,Tamah, Moorccha,

Shoola,Chardi,Jwara Shwasa, Pipasa, Udavarta

Upadravas

Ketoacidosis & hyper-osmolar

coma:Anorexia, vomiting, abdominal pain,

loss of consciousness, Kussmaul’s respiration.

Coma

Suptata

Neuropathies: Numbness, paraesthesia, pain,

abnormal gait.

Arochaka, Avipaka, Amlika, Atisara,Shoola,

Udavarta, Baddha pureeshata

Constipation, diarrhoea, dysphagia and other

GI symptoms

Though, the discovery of Insulin and other hypoglycemic drugs is a great

achievement of modern medical science but the hazardous side effects of hypoglycemic

after long term use are incurable and hence an ideal therapy is still obscure. “Diabetes

mellitus” being a hereditary disease is spreading from generations to generation. The

136


changing lifestyle, lack of exercise, fast food and stress are also major reasons for the

new patients and for the enhancement of the disease in old once. Unfortunately, these

causative factors remain hidden and are ignored at management level. The Ayurvedic

scientists are trying to find out the best herbal hypoglycemic drugs

In the pathogenesis of the Avaranajanya Madhumeha, the Kapha and Pitta are the

main Dosha, whereas the most important Dushyas are Meda and Kleda. In Madhumeha,

the Dhatukshaya is also predominant. So, in its management such drugs have to be

selected which are against Meda and Kleda as well as have the Rasayana effect. Asanadi

Kwatha is anubhoota yoga, which is been priscribing in S.D.M Ayurvedic Hospital,

Udupi, Karnataka since 20 yrs. The most of the drugs of asanadi Kwatha are mentioned

in Prameha adhyaya either in Charaka or Susrutha. This preparation conatians fourteen

drugs. They are Asana, Saptarangi, Khadira, Sariva Manjiashta, Ushira, Chandana,

Haritaki, Vibhitaki, Amalaki, Punarnava, Ashwaganda, Haridra, Gokshura these drugs

possess hypoglycemic, Neuroprotective, Nephroprotective Medoghna,

Mootrasangrahaniya, Rasayana, Deepana and Pachana properties.

While deciding the inclusion criteria, the terms Sthoola & Krusha madhumehi

have been used in a much broader sense than to mean only the abnormal states conveyed

by them. In other words, the word Sthoola covers patients from normal to obese & the

term Krusha covers patients who were normal to under weight. The terms Madhumeha &

Prameha have been used as synonyms throughout the study. Patients who attended the

O.P & I.P section of S.D.M Ayurveda hospital were selected randomly, irrespective of

the sexes, fulfilling all the criteria for inclusion & exclusion. Freshly diagnosed cases and

cases that were not on allopathic medicines were taken for the study. The range of fasting

137


& postprandial blood sugar was fixed between 120 mg/dl -180 mg/dl & 160mg/dl to 300

mg/dl respectively considering the safe limits of the disease. This was done to avoid

putting the patient into the risk of developing complications as in the case of higher sugar

values. Pre and post test design was planned and the patients were asked to take 40ml of

Asanadi Kwatha before food twice daily. Asanadi Kwatha is prepared from Asanadi

Kwatha churna and water in the proportion of 1:8( as most of the drugs are madyama

dravya) i.e. 40 grams of Asanadi Kwatha churna and 320 ml of water it has to be boiled

and reduced to ¼ i.e. 80 ml( 40 ml in two divided doses) FBS, PPBS and urine sugar

were conducted on a mandatory basis. Facilities for glycosylated haemoglobin test were

unavailable in the patients’ accessible area. The cost involved for performing glucose

tolerance test along with serum glucose level was unaffordable for the patient,

The Pratyatma lakshana of Madhumeha including Tanu madhuryata & Mutra

madhuryata along with other most common symptoms were taken for assessment. This

included the W.H.O. approved American Diabetic Association diagnostic criteria. The

symptoms were graded and scored.

Maximum number of patients belonged to the age group of 51-70 yrs. which

supports the view that the prevalence of Type 2 DM is more in the middle to old age.

There was an equal distribution of the disease in both the sexes, nothing specific can be

derived from this. This may be due to the demographic facts. Hindus were 65%, which

again indicative of demographic situation of this region. More number of patients was

from middle to upper middle class; this finding reflects the pattern of patients coming to

the hospital of this institute according to their socio-economic conditions and also the

increasing substantial sedentary habits among them. The incidence was also more in

138


people who were involved in professions, who did not involve much physical work like

business executives, shop owners, hotel cashiers & so on. Observation of addiction in the

present study revealed that Maximum number of patients i.e. 45% were addicted to

Tea/Coffee followed by Beedi/Cigarette smoking 40%, 10% patients were addicted to

alcohol and Tobacco chewing 5%. All these addictions decreased the natural immunity

and also provoke the Vata to manifest the disease Madhumeha earlier and with severity.

Majority of the patients i.e.50% were suffering from the disease for 1 – 3 years. Only

20% of the patients confirmed the family history of Madhumeha which reflects the fact

that a familial trait is associated with the disease, while the others, either were not aware

of it or clearly ruled out any family history of Madhumeha. This gives a hint that, the

development of Madhumeha is not totally familial. Majority of patients were of pitta

Kapha prakruti. None were of Pitta Vata & Kapha Pitta prakruti. Majority of the patients

were of Madhyama to Avara Sara, which indicates the involvement of Dhatus in

Madhumeha. On treatment with Asanadi Kwatha, the following results were observed on

the subjective symptoms.

1) Effect on Prabhoota mootrata: Mild to severe Prabhoota mootrata(both in terms of

quantity and frequency) was seen in 100% of patients, 69.2% relief was observed in

Prabhuta Mutrata at statistically highly significant level (P<0.001), This relief in Prabhuta

Mutrata may be due to the Mutrasanghrahani action of Asana, Haridra and Saptarangi,

and due to Kashaya Rasa of Asana & Saptarangi which exerts Stambhana action. It may

be possible that drug has acted upon Apana Vayu and corrected its vitiation.

139


2) Effect on Avila mootrata: In majority of patients Avila mutrata was observed, 80%

improvement was seen in avila mutrata, this may be the combined effect of asanadi

Kwatha drugs.

3) Effect on Trushna: Mild to severe Trushna was seen in 100% of the patients and mild

to maximum improvement was seen in 90% of the patients indicating that Asanadi

Kwatha has good effect on the symptom Trushna. The relief in Trushna may be because

most of the drugs are Kapha- Pitta Shamaka and also due to Trishnanigrahana action of

Ushira and Chandana.

4) Effect on Sthoulya: 15% patients were obese, 40% of patients were overweight for

their age and height. The rest had normal weight. But reduction in weight was not

observed. It is however interesting to note that majority of patients were not obese.

Almost 70% of the patients had an adipose abdomen, which corroborates the fact that

Indians have inherited condition called central adiposity (i.e. for a given body mass index

Indians have a higher amount of fat than other races). There have been strong evidences

implicating this condition for the development of DM (Ramachandran – Diabetic

research center, Chennai).

5) Effect on Sweda adhikya: Mild to severe Sweda adhikya was seen in 75% of patients

and 90% of improvement was observed. Vitiation of Pitta Dosha causes Sweda-

Atipravriti. Most of the ingredients of the Asanadi Kwatha are Kapha –Pitta Shamaka and

Sheeta Virya. Ushira having the action of Swedapanyana and Asana having Kashaya

Rasa and Stambhana action might have checked the excessive sweating.

6) Effect on Daurbalya: Mild to severe Dourbalya was seen in 100% of the patients and

moderate to maximum improvement was seen in 100% of patients. Rasayana &

140


antioxidant properties of the ingredients of Asanadi Kwatha prevent the Dhatu depletion.

The Pramehagna properties of the ingredients of Asanadi Kwatha may facilitate entry of

glucose inside the cell for utilization, thus providing energy to the cells and the patient

gets relief in Daurbalya.

7) Effect on Kara pada daha: Mild to severe Kara pada daha was seen in 85% of the

patients & moderate to good improvement was seen in 95% of the patients. Relief in kara

pada daha may be due to most of the drugs are Pitta Kapha Shamaka and Sheeta Virya

and also Raktaprasadan Karma of Haridra, Manjishta and Dahaprashaman action of

Ushira. Neuroprotective effect of Haridra, Ashwagandha, haritaki might have also

provided the relief in this manifestation.

8) Effect of Karapada Suptata: 60% of the patients had mild to severe Karapada

Suptata & mild to maximum improvement was seen in 80% of them. Raktaprasadana

Karma of Haridra, Manjishta. and anti diabetic action of Saptarangi and Asana may have

provided the relief in Kara-Pada Suptata. Neuroprotective effect of ashwaganda, Haritaki

Haridra, may also have provided relief in this manifestation.

9) Effect on Bahvashi: Mild to moderate Bahvashitva was seen in 80% of the patients

16% improvement was observed. As most of the drugs are Pitta–Kapha Shamaka, this

may be the reason for the relief in Kshudha Adhika

The following were the changes observed in the objective symptoms after

treatment:

1) Effect on Fasting Blood sugar (FBS): The mean FBS score before treatment

was 136.7and after treatment 117.7This is statistically highly significant at

P<0.001.

141


2) Effect on Post Prandial Blood Sugar (PPBS): The mean difference between before

& after treatment is 33.9. Relief in PPBS was at statistically significant level (P<0.01).

Effect on FBS & PPBS may be due to the Pramehagana action of various

ingredients in Asanadi Kwatha like Asana, Saptarangi, Amalaki, Haridra, Khadira,

Haritaki are the Mehagana drugs due to which both FBS & PPBS have reduced. In

modern science, clinical & experimental studies depict that Asana, Saptarangi, Amalaki,

Haridra, Kadira, Haritaki possess anti diabetic action. It was found that in borderline

cases, the sugar levels came to normal, but in cases with sugar levels near the upper limit

of the range, it did not return to the normal limits. This may give a hint about a probable

requirement of an extension in the duration of treatment.

3) Effect on Urine Sugar: The mean difference in the before treatment & after treatment

was 0.45 this relief obtained could be due to the Mehagna property of the ingredients of

Asanadi Kwatha.

It was observed that the symptoms that were mild returned back to normal after

one month of treatment but those that were moderate came down to mild & severe

symptoms reduced to a moderate intensity. Moreover, the severity & number of

symptoms seemed to be directly proportional to the increase in the serum glucose levels

because we found that patients with blood glucose levels at the upper limit of the range

usually presented with moderate to severe symptoms than those at the lower limit of the

range. Even the number of symptoms varied in the same manner.

Most of the Asanadi Kwatha drugs have Tikta, kashaya rasa, laghu, rooksha guna and

katu vipaka. These are said to be kaphagna, Mehagna, Medogna and

Mootrasangrahaneeya.

142


Tikta, kashayarasa, laghu, rooksha guna produces rookshana effect and

they are having opposite qualities to that of kapha and Medas. Both Medas and Kapha

being the main entity of the Samprapti, thus by breaking the Samprapti (correcting the

vitiation of Medas and Kapha) treats the disease. Hence they act as Mehagna and

kaphagna. When medas is reduced then the pressure on vapavahana is also diminished as

it is the moolasthana of medovahasrothas.

Bahudravata will be present in Madhumeha. Tikta, kashayarasa present in

this yoga produces shoshana effect. Bahudravata will be reduced by the absorption of

excessive fluid from the body cells. When bahudravata reaching basthi reduces then

prabhoothamootrata, pratyatmalakshana of Madhumeha also reduces. Pipasa which is

dependent on prabhoothamootrata also subsides. Asanadi kashaya reduces medas

thereby Sthoulya and as it is mootrasangrahaneeya, absorbs bahudrava and hence reduces

polyuria, and polydipsia and thereby checks the pathogenesis of Madhumeha.

In summary, it can be said that the present study shows Significant remission in

Signs & symptoms of illness Madhumeha vis–a-vis DM corroborated with definite

reduction in blood sugar levels. Though there is significant reduction the normal values

of sugar were not achieved by the period of one month and therefore it is imperative that

diet and exercise will help in management of the disease.

143

EFFECT OF TREATMENT

Table No 58: Effect on Kandu

Kandu (mean score) Difference in Means

% Paired ‘t’ Test

BT (±SD) AT (±SD) S.D. S.E.M ‘t’ P 1.450

(± 1.099) 0.000

(± 0.000)

1.450

100

1.099 0.246

5.900 P<0.001

On Kandu (mild to moderate) drastic improvement was seen by the effect of

PTGG and CHCD, i.e. before the treatment the mean score was 1.45 and reduced to 0

after the treatment and this change that occurred with the treatment, is statistically

significant (P<0.001). Further details with standard deviation, standard error of Mean, ‘t’

value, P values are given above in the table.

Table No 59: Effect on Erythema

Erythema (mean score)

Difference in Means


BT (±SD) AT (±SD) S.D. S.E.M ‘t’ P 3.000

(± 0.562) 0.750

(± 0.786)

2.250

75 0.851 0.190 11.828 P<0.001

Statistically it was observed that the mean score in erythema before the treatment

was 3.00 which reduced to 0.75 after the treatment. This remission of the symptom after

the treatment is statistically significant (P=<0.001). Particulars of statistics are given

above.

Fig No 36 Effect on Kandu and Erythema

1.45

0

3

0.75

0

0.5

1

1.5

2

2.5

3

Kandu Erythema

BT

AT

Table No 60: Effect on Scaling:

Scaling (mean score)

Difference in Means


BT (±SD) AT(±SD) S.D. S.E.M ‘t’ P 2.550

(± 0.887) 0.250

(± 0.444)

2.300

90.19 0.923 0.206

11.139 P<0.001

Statistical analysis revealed that the mean score of Scaling was 2.550 before the

treatment was reduced to 0.250 after the treatment and this change that occurred with the

treatment is statistically significant (P = <0.001). Further details with standard deviation,

standard error of mean, ‘t’ value, and P values are given above.

Table No 61: Effect on Shyava ,Raktakrishna varna

Shyava Varna (mean score)

Difference in Means


BT(±SD) AT(±SD) S.D. S.E.M ‘t’ P 2.900

(± 0.641) 1.250

(± 0.851)

1.650

56.89 0.933 0.209

7.906 P<0.001

Statistical analysis revealed that the mean score of Shyava,Rakta Krishna

varna was 2.900 before the treatment was reduced to 1.250 after the treatment and this

change that occurred with the treatment is statistically significant (P = <0.001). Further

details with standarddeviation, standard error of mean, ‘t’ value, and P values are given

above.

Fig No. 37 Effect on Scaling and Shyava ,Raktakrishna varna

0

0.5

1

1.5

2

2.5

3

Scaling Shyavata

BTAT

Table No 62: Effect on Kinakhara sparsha

Kinakharasparsha (mean score)

Difference in Means



(± 0.553) 0.500

(± 0.688)

1.600

76.19 0.598 0.134 11.961 P<0.001

Statistical analysis revealed that the mean score of Kinakhara sparsha was 2.100

before the treatment was reduced to 0.500 after the treatment and this change that

occurred with the treatment is statistically significant (P = <0.001). Further details with

standard deviation, standard error of mean, ‘t’ value, and P values are given above.

Table No 63: Effect on Rookshata:

Rookshata (mean score)

Difference in Means



(± 0.671) 0.350

(± 0.587)

1.800

83.72 0.768 0.172 10.485 P<0.001

Statistical analysis revealed that the mean score of Rookshata was 2.150 before the



standard error of mean, ‘t’ value, and P values are given above

Fig No. 38 Effect on Kinakhara sparsha and Rookshata

2.1

0.5

2.15

0.35

0

0.5

1

1.5

2

2.5

Kinakhar Rooksha

BTAT

Table No 64: Effect on Vritta

Vritta (mean score) Difference in Means



(± 0.999) 1.100

(± 1.071)

1.850

62.71 1.268 0.284 6.525 P<0.001

Statistical analysis revealed that the mean score of Vritta was 2.950 before the




Table No 65: Effect on Ghana

Ghana (mean score) Difference in Means

& Paired ‘t’ Test


(± 0.968) 1.000

(± 1.124)

1.100

52.38 1.071 0.240 4.593 P<0.001

Statistical analysis revealed that the mean score of Ghana was 2.110 before the




Fig No 39 Effect on Vritta and Ghana

2.95

1.1

2.1

1

0

0.5

1

1.5

2

2.5

3

Vritta Ghana

BTAT

Table No 66: Effect on Nakhadushti

Nakhadushti (mean score)

Difference in Means



(± 1.146) 0.450

(± 1.146)

0.000

0 0.000 0.000 0.000 P=1.000


treatment was remained same as 0.450 after the treatment and this change that occurred

with the treatment is statistically not significant (P =1.000). Further details with standard

deviation, standard error of mean, ‘t’ value, and P values are given above.

Table No 67: Changes in PASI scoring

PASI (mean score)

Difference in Means



(±12.471) 4.070

(± 5.857)

11.670

74.14 9.024 2.018 5.783 P<0.001

Statistical analysis revealed that the mean score of PASI was 15.740 before the




Fig No 40. Effect on Nakhadushti PASI scoring

0.45 0.45

15.74

4.07

02468

10121416

N.Dushti PASI

BTAT

Table No 68: Effect on Auspitz sign

Auspitz

(mean score) Difference in Means



(± 0.366) 0.150

(± 0.366)

0.700

85.35 0.470 0.105 6.658 P<0.001

Statistical analysis revealed that the mean score of Auspitz sign was 0.850 before

the treatment was reduced to 0.150 after the treatment and this change that occurred with

the treatment is statistically significant (P = <0.001). Further details with standard


Table No 69: Effect on Candlegreece sign

Candlegreece sign (mean score)

Difference in Means



(± 0.224) 0.250

(± 0.444)

0.700

73.68 0.470 0.105 6.658 P<0.001

Statistical analysis revealed that the mean score of Candlegreace sign was 0.950

before the treatment was reduced to 0.250 after the treatment and this change that

occurred with the treatment is statistically significant (P = <0.001). Further details with

standard deviation, standard error of mean, ‘t’ value, and P values are given above.

Fig No. 41 Effect on Auspitz sign and Candlegreece sign

0

0.2

0.4

0.6

0.8

1

Auspitz C.Greece

BTAT

Table No70: Effect on Koebners phenomena:

Koebners phenomena

(mean score)

Difference in Means



(± 0.410) 0.200

(± 0.410)

0.000

0 0.000 0.000 0.000 P=1.000


treatment was remained same as 0.200 after the treatment and this change that occurred

with the treatment is statistically not significant (P =1.000). Further details with standard


Fig No 42 Effect on Koebners phenomena

0.2 0.2

0

0.05

0.1

0.15

0.2

Koe.Phen

BTAT

Summary

SUMMARY

The frame of the dissertation work entitled "A Clinical Study on the

Asanadi qwatha in management of Madhumeha” is designed in following Aims &

objectives

1) To do a comprehensive literary study on Madhumeha

2) To evaluate the effect of Asanadi kwatha in Sthoola & Krusha Madhumehis.

3) To evaluate the effect of Asanadi kwatha in type 2 diabetes mellitus patients

The whole topic is elaborated in four parts and is named as Review of literature.

Methodology, Discussion and Conclusion.

Review of literature contains Prologue, Historical review, conceptual study, Drug

review.

In prologue, gravity of the problem and previous works on this study has been mentioned.

Conceptual Study:

Historical glimpses with regards to disease Madhumeha (Diabetes mellitus) traces the

various developments right from the Vedic period up to the modern era.

The disease Madhumeha has been dealt from both the Ayurvedic point of view as well as

modern point of view. Its Nirukti & paribasha, Nidana, Purvarupa, Rupa, Samprapti,

Sadhya-Asadhyadta, Upadrava, Arishta lakshana, Chikitsa and Pathya-Apathya have

been described in an elaborative manner. The disease review from the modern point of

view deals with definition, aetiology, prediabetic state, clinical features, pathogenesis,

complications, treatment and life style management of Diabetes mellitus.

146

Summary

Drug study:

In the drug study individual drugs of Asanadi qwatha have been described in

detail with latest possible research information. The Asanadi qwatha contains fourteen

herbs viz. Asana, Saptarangi, Khadira, Sariva, Manjishta, Ushira, Chandana, Harithaki,

Vibhitaki, Amalaki, Punarnava, Ashwagandha, Haridra. and Gokshura.

Methodology:

The second part comprises of Aims & objectives, Material and methods which includes

inclusion criteria, exclusion criteria, diagnostic criteria, assessment criteria, laboratory

investigations, There after observations and results of the therapy has been discussed.

Materials and Method:

25 patients of Madhumeha were registered in this study out of which total 20

patients completed treatment.

Asanadi qwatha was given in the dose of 40 ml twice daily before meals with

water for 30 days with out altering their routine dietary and physical activities.

Observations:

The maximum no. of patients i.e. 50% were from the age group of 51 to 70 years,

maximum no. of patients were urban inhabitants (65%), Max. were sedentary i.e. 40%,

Maximum number of patients i.e. 80% of this series were non-vegetarian, 80 % patients

were taking Madhura Rasa dominant diet, 45% were addicted to Tea/Coffee.

Maximum number of patients i.e. 80% confirmed that they were not having any

family history of Madhumeha

The maximum number of the patients i.e. 50 % were suffering from the disease

for last 1 – 3 years, Maximum no. of patients i.e. 45% were having Pittaja-Kapha prakriti.

147

Summary

The maximum number of patients were normal weight i.e; 45 % and 15% were

obese. Vyayama Shakti was found Avara in 65% patients,

The maximum number of patients i.e.; 50% were found to have Pravara

Abhyavaharana Shakti and Maximum i.e.; 55% patients were having Krura Koshtha,

majority i.e. 50 % of the patients were having Tikshnagni, 60% patients were having

normal systolic blood pressure, 55% patients were having normal diastolic blood

pressure.

The prominent Nidanas reported were Guru Ahara (70%), Madhura Ahara

(80%), Snigdha Ahara (65%), Katu-Tikta Ahara Sevana was found in 35% patients.

Avyayama was found in 75% patients, while Chinta was found in 45% patients. Drava

Ahara (50%), Diwaswapna (80%), Asya Sukha (75%).

The following were the changes observed in the subjective symptoms after

treatment:

1) Effect on Prabhoota mootrata: Mild to severe Prabhoota mootrata(both in terms of

quantity and frequency) was seen in 100% of patients, 69.2% relief was observed in

Prabhuta Mutrata at statistically highly significant level (P<0.001),

2) Effect on Avila mootrata: In majority of patients Avila mutrata was observed, 80%

improvement was seen in avila mutrata.

3) Effect on Trushna: Mild to severe Trushna was seen in 100% of the patients and mild

to maximum improvement was seen in 90% of the patients.

4) Effect on Sthoulya: 15% patients were obese, 40% of patients were overweight for

their age and height. The rest had normal weight. But reduction in weight was not

observed.

148

Summary

5) Effect on Sweda adhikya: Mild to severe Sweda adhikya was seen in 75% of patients

and 90% of improvement was observed.

6) Effect on Daurbalya: Mild to severe Dourbalya was seen in 100% of the patients and

moderate to maximum improvement was seen in 100% of patients.

7) Effect on Kara pada daha: Mild to severe Kara pada daha was seen in 85% of the

patients & moderate to good improvement was seen in 95% of the patients.

8) Effect of Karapada Suptata: 60% of the patients had mild to severe Karapada Suptata

& mild to maximum improvement was seen in 80% of them.

9) Effect on Bahvashi: Mild to moderate Bahvashitva was seen in 80% of the patients

16% improvement was observed.

The following were the changes observed in the objective symptoms after

treatment:

1) Effect on Fasting Blood sugar (FBS): The mean FBS score before treatment

was 136.7and after treatment 117.7. This is statistically highly significant at

P<0.001.

2) Effect on Post Prandial Blood Sugar (PPBS): The mean difference between before &

after treatment is 33.9. Relief in PPBS was at statistically significant level (P<0.01).

3) Effect on Urine Sugar: The mean difference in the before treatment & after treatment

was 0.45.

149

Summary

Discussion

This section deals with the discussion based on the clinical study. Critical

discussion with probable reasoning and lastly overall effect of therapy have been

presented

Conclusions

The last section deals with the Summary and Conclusions drawn from the present

study.

150

DEPARTMENT OF KAYA CHIKITSA

S. D. M. COLLEGE OF AYURVEDA, UDUPI.

CASE PROFORMA FOR CLINICAL STUDY ON MADHUMEHA

I. ATURA VIVARA

1. Atura Nama : 10. Antah Kramanka :

2. Linga : M / F 11.Bahi Kramanka :

3. Vaya : ___ years. 12. Shayyagara Kramanka

4. Vaivahika Vruttanta : M / UM / W / D 13. Shayya Kramanka :

5. Vrutti : 14.Pravesha Dinanka :

6. Jati : H / M / C / J / Si 15.Nirgamana Dinanka :

7. Saksharata : UE / PS / MS / HS / GR / PG 16.Vilasa :

8. Samajika Sthithi : VP / P / LM / M / UM / R 17.Phone :

9. Dinanka : 18.E-mail :

II. VEDANA SAMUCHRAYAM

A. PRADHANA VEDANA :

1) Mootra Sambandhi :

*Frequency __times / day, __times / night.

*Color : ________since __days.

*Density : Milky White / Buffy / Turbid / Clear since ____ days.

* Amount (approx)_________ ml/24 hours since ____ days.

* Discomfort during urination __________ since ____ days.

* Urge for micturition after drinking water Yes / No.

2) PIPASA SAMBANDHI - has observed increased feeling of thirst

Yes Since___days / No

3) AHARA ABHYAVAHARANA SAMBHANDHI- has observed unusual

increase of appetite. Yes Since __Days / No

4) SWEDA SAMBHANDHI - has observed unusual increase of sweat & body odour.

Yes Since ___Days / No

5) ANYA

B) ANUBANDHA VEDANA :

III. VEDANA VRUTTANTA

IV. POORVA VYADHI CHIKITSA VRUTTANTA

V. KOUTUMBIKA VRUTTANTA

Relative Dead / Alive Health status Treatment history

VI. VYAKTHIGATA VRUTTANTA :

1. AHARA SAMBANDHI VRUTTANTA : Veg / Mixed

AHARA : frequency of intake / day ________

(SARVAGRAHA)

PARIGRAHA (Approximate amount of intake per meal)

Staple : Amount / day in gram /cal

Rice / Wheat / Ragi / Bread products

Bengal gram (toor dal) / Black gram (urad dal) / Green gram (moong dal) / Horse gram /

Chanaka / Others

Vegetables : Amount / day in grams / cal

Green leafy / Stem / Roots tuber / Rhizome / Others.

Fruits : Amount /day / week in grams / cal

Banana / Grape / Apple / Chikku / Pineapple / Mango / Others

Milk & Dairy products : Amount /day / week in grams / cal

Milk/Curds/Butter/Ghee/Butter milk/Others

Sugar & its products : Amount /day / week in grams / cal

Sugar/Jaggery/Chocolate

Desserts : Amount /day / week in grams /cal

Milk / Cream preparations / Ghee butter preparations / Dalda / Vanaspathi preparation

Curd preparation / Ice cream / fruit salads / Pastries / wafers / cakes

Deep fried food stuffs : Amount / day / week in grams / cal

Vada / Bonda / Pakoda / Bajji / Other fried snacks

Oils : Amount /day / week in grams / cal

Sunflower/Coconut/Ground nut /Dalda/Vanaspathi/Ghee/Mustard/Others

Meat : Amount /day / week / months in grams / cal

Chicken/Mutton/Pork/Beef/Sea food/Egg/Others

Beverages : Amount /day / week in grams / cal

Tea/Coffee/Alcohol

2. VIHARA SAMBANDHI VRUTTANTA

Sleep : ___Hours / day : ___ Hours / night :

Disturbed : Due to

Exercise: Type No exercise

Hours _______ per day _______ hours / week

Stress: Type Relieving factors

Aggravating factors Days/year of exposure

No stress

Samshodhana: Undergone Yes / No

Type of profession: Sedentary / Involves physical strain

involves mental strain / Both. Since ________ Years .

Relaxation (Apart from day / night sleep) : Prayer / Meditation / Others.

Recreation / Entertainment : Television / Indoor games / Outdoor games

Sexual intercourse: __________ times / week

1. Mala : ________ times daily regular / irregular

2. Mootra : ________ times daily

3. Madakari Dravya Abhyasa : Smoking ___ / day : since __years

Alcohol __ ml / day : since __ years

Tobacco chewing : since __ years

Tobacco snuff : since __ year

4. Anya Abhyasa :

VII. RAJO SAMBANDHI VRUTTANTA :

1. Menstruating / attained menopause at ________ years of age.

2. Menstrual cycle :

3. History of : Udavartini/Asrugdara/ Shwethapradar / Anya YonigataVikara

4. P ____ G _____ L ____ D ____

5. History of infertility : primary / secondary

VIII MANASIKA VRUTTANTA:

IX. VITAL SIGNS

I VISIT

II

VISIT

III

VISIT

IV

VISIT

1. Pulse (Nadi) / Min

2. BP ___ mmHg

3. Temperature oF

4. Heart rate / Min

5. Respiratory rate / Min

X. GENERAL PHYSICAL EXAMINATION

Built and Nourishment : __Wt __ Ht

Pallor / Edema / Nail changes / Cyanosis / Icterus / Lymphadenopathy / Neck

XI. SYSTEMIC EXAMINATION

RESPIRATORY SYSTEM :

GASTRO INTESTINAL SYSTEM :

CARDIOVASCULAR SYSTEM :

GENITOURINARY SYSTEM :

CENTRAL NERVOUS SYSTEM :

LOCOMOTOR SYSTEM :

Examination of the limbs : Pulses / Ulcer ( if any)

XII SROTO PAREEKSHA :

• Pranavaha Srotas :

• Udakavaha Srotas :

• Annavaha Srotas :

• Rasavaha Srotas :

• Raktavaha Srotas :

• Mamsavaha Srotas :

• Medavaha Srotas :

• Astivaha Srotas :

• Majjavaha Srotas:

• Shukravaha Srotas:

• Mootravaha Srotas :

• Pureeshavaha Srotas:

• Swedavaha Srotas :

XIII. ROOPA SANKALANA

A. ROOPA (SAMANYA)

1. Sweda adhikya

2. Anga Gandha

3. Anga Shaithilya

4. Anga Sada

5. Hridayopadeha

6. Netropadeha

7. Jihwopadeha

8. Sravanopadeha

9. Taluni malotpatti

10. Danteshu malotpatti

11. Ghanangata

12. Keshativruddhi

13. Keshajatellabhava

14. Nakhativruddhi

15. Sheetapriyatwam

16. Gala shosha

17. Talu shosha

18. Asya madhurya

19. Karadaha

20. Padadaha

21. Mootrapipilikabhisarana

22. Shuklamootrata

23. Snigdha gatrata

24. Picchila gatrata

25. Guru gatrata

26. Pipasa

27. Shwasa dourgandhya

28. Tandra

29. Kara suptata

30. Pada suptata

31. Anga suptata

32. Alasya

33. Mukha shosha

34. Kaya chidresha upadeha

35. Sarvakala nidra

36. Pipilika shareerabhesarana

B. VISHESHA ROOPA

1. Prabhoota mootrala

2. Avila mootrata

3. Sthoulya

4. Bahu ashee

5. Snighdhangata

6. Shayyasanaswapnasheela

(activity)

7. Krushatra

8. Alpashee

9. Rookshata

10. Paribramanasheela

11. Mutra madhurya

(urine sugar)

12. Mutra kashaya varna

13. Mutra pandu varna

14. Tanu madhurya

(FBS PPBS)

C. UPADRAVA

1. Trushna

2. Daha

3. Atisara

4. Dourbalya

5. Arochaka

6. Avipaka

7. Alagi vidradi

adipootimamsapidaka

8. Udavarta

9. Kampa

10. Hridgraha

11. Shoola

12. Nidranasha

13. Shosha

14. Kasa

15. Sthambha

16. Badha purishatra

D. COMPLICATIONS

1. Retinopathy

2. Nephropathy

3. Neuropathy

4. Atherosclerosis

5. Peripheral ischemia

6. Diabetic hand

7. Diabetic foot

8. Cerebrovascular accidents

9. Ischemic heart disease

10. Gangrene

11. Carbuncles

12. Skin changes

XiV. INVESTIGATION :

A. BLOOD I II III IV

1) FBS mg/dl

2) PPBS mg/dl

3) RBS mg/dl

4) Urine Sugar

B. ROUTINE

HAEMATOLOGY I Visit II Visit III Visit IV Visit

Total WBC Count

(cells/cumm)

Lymphocytes

Monocytes

Neutrophils

Eosionophils

Basophils

Hb%

ESR (in mm/I hour)

E. OTHER INVESTIGATIONS

XV. SAMPRAPTI GHATAKA

DOSHA :

DUSHYA :

SROTAS :

SROTODUSTI LAKSHANA :

AGNI :

AMA :

UDBHAVA STHANA :

SANCHARA STHANA :

ADHISHTANA :

VYAKTA STHANA :

ROGA MARGA :

XVI. UPASHAYA ANUPASHAYA :

XVII. VYADHI :

XVIII. PRAKARA :

XIX. SADYASADYATA :

XX. CHIKITSA :

STHOOLA KRUSHA

XXI. FOLLOW UP ASSESSMENT CRITERIA (FORTNIGHTLY CHECK UP)

I Visit II Visit III Visit IV Visit V Visit VI VisitSubsequent

Visits

1. Prabhoola Mootrata

2. Avila Mootrala

3. Thrushna

4. Sthoulya

5. Sweda adhikya

6. Dourbalya

7. Karapada daha

8. Karapada suptata

9. Tingling sensation

10. Bahu ashee

11. FBS

12. PPBS

13. GHb (if done)

14. GTT (if done)

15. Urine sugar

VIKRITI :

HETU :

ROGI BALA :

LINGA :

DESHA :

ROGA BALA :

PRAKRUTI :

KALA :

CHIKITSA : ASANADI KWATHA 40 ml BD.

Bibliography

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