EVALUATION OF THE EFFICACY OF BHUMYAMALAKYADI CHURNA IN

MADHUMEHA

(WITH SPECIAL REFERENCE TO ITS HYPOGLYCEMIC EFFECT)

Thesis submitted to the Rajiv Gandhi University of Health Sciences Karnataka,Bangalore

In partial fulfillment of regulations for the Award of the degree of

DOCTOR OF MEDICINE (AYURVEDA)

By

SHASHIDHAR. T. HOMBAL.

Guide Dr. Ch. Ranga Rao. M . D . (Ay u )

Professor and Head of the Department Post Graduate and Research Centre D.G.M.Ay.Medical College, Gadag.

Co-Guide

Dr. Siva Rama Prasad Ketamakka. M.D. (Ayu) Reader

Post Graduate and Research Centre D.G.M.Ay.Medical College, Gadag.

POST GRADUATE AND RESEARCH CENTRE DEPARTMENT OF KAYACHIKITSA

D.G.M.AY.MEDICAL COLLEGE GADAG.

LIST OF ILLUSTRATIONS

Sl. No. Figure Name Page No. 1. Photograph of Haritaki 56 2. Photograph of Bibhitaki 58 3. Photograph of Amalaki 60 4. Photograph of Pippali 62 5. Photograph of Guggulu 64 6. Photograph of Madhu 66 7. Photograph of Gomutra 68

List of Master Charts

Sl No Master Charts Page No

1. Demographic data 79

2. Data related to Personal history 80

3. Data related to Complaints 81

4. Data related to Associated Complaints 82

5. Data related to Upadravas 83

6 A. Data related to Objective Parameters 84

6 B. Data related to Objective Parameters 85

7 A. Data related to Lab Investigations 86

7 B. Data related to Lab Investigations 87

List of Figures

Sl No Figures Page No

1. Showing Age and Sex ratio 89

2. Showing the Religion incidence 90

3. Showing the Occupation incidence 91

4. Showing the Economical status incidence 92

5. Showing the Diet incidence 93

6. Showing the Family history incidence 94

7. Showing the Chronicity 95

8 Showing the body weight of Group A 103

9. Showing the body weight of Group B 103 10. Circumference of Udara of Group A 104 11. Circumference of Udara of Group B 104 12. Circumference of Spik of Group A 105 13. Circumference of Spik of Group B 105 14. Circumference of Sthana of Group A 106 15. Circumference of Sthana of Group B 106 16. Serum Cholesterol of Group A 107

17. Serum Cholesterol of Group B 107 18. Serum Triglyceride of Group A 108

19. Serum Triglyceride of Group B 108 20. Serum HDL Cholesterol of Group A 109 21. Serum HDL Cholesterol of Group B 109 22. Serum LDL Cholesterol of Group A 110 23. Serum HDL Cholesterol of Group B 110 24. Serum VLDL Cholesterol of Group A 111 25. Serum VLDL Cholesterol of Group B 111 26. Random Blood Sugar of Group A 112 27. Random Blood Sugar of Group B 112 28. Showing the Result 114

CONTENTS Page No.

1) INTRODUCTION 1

2) SHAREERA 9

3) NIDANA Hetu 19 Samprapti 25 Poorvarupa 30 Rupa 31 Bedha 40 Sadhyasadhyata 43

Upadrava 44

4) CHIKITSA 47 5) DRUG REVIEW 54 6) MATERIAL AND METHODS 71 7) OBSERVATION, ANALYSIS AND INTERPRETATION 79

8) CONCLUSION 115 9) SUMMERY 118

BIBLIOGRAPHY APPENDIX

Acknowledgement

ACKNOWLEDGEMENT

I am highly indebted to my guide, Dr Ch. Ranga Rao, H.O.D.

Department of Post Graduate and Research centre, sri D.G.M.Ayurvedic

Medical Col lege, Gadag for his valuable suggestions and guidance in

completing this work successful ly.

I am heart i ly thankful to Dr V.V.S.Shastr i . Under whose guidance

my work was started and he was the teacher who inspired me to take the

combinat ion of the drug mentioned in this thesis.

I am ever grateful to my Co-guide Dr. Siva Ram Prasad Ketamakka

who was a helping hand throughout the work and supported me in

completing the work in st ipulated t ime.

I am thankful to our Principal Dr G.B.Pati l for his support in

completing this work successful ly.

I am very much thankful to Mr. Nandakumar for his valuable help in

stat ist ical calculations.

I am thankful to Dr A.K.Panda and al l other staff of DGM col lege for

their help.

Acknowledgement

I acknowledge to our col lage l ibrar ian Mr V.M.Mundanamani and

his assistant Mr Sureban for support ing me by providing lot of books for

the study.

I am thankful to Mr Gir iachar Off icer National Information Centre

(NIC) Gadag, for giving me information about the work going on in

di f ferent parts of the world regarding this subject.

My personal thanks to Mr.N.N.Bhat and Mr C.S.Bhat who helped

me in understanding the Sanskri t versions.

I am thankful to Dr.(Mrs) M.D.Gojanur for support ing me by

referring the cases for tr ial.

I am thankful to my col leagues and fr iends who supported me in

cl inical tr ials and made the tr ial successful.

I am thankful to al l the pat ients who agreed to undergo the

treatment with the tr ial drug.

I am highly indebted to my beloved parents, who framed a proper

path for my carr ier.

Acknowledgement

I express my heartfel t grat i tude to al l my family members for their

constant help, love and care rendered during my study.

I am thankful to al l my teachers, from primary education to post

graduate education for helping me in bui lding up my carrier.

This l ist is incomplete without remembering my small sunny Kiran

(18 months) whose smile inspired and kept me cheerful throughout my

work.

I wish to thank al l the persons who have helped me directly and

indirect ly with apologies for my inabi l i ty to identi fy them individual ly.

Acknowledgement

ACKNOWLEDGEMENT

I am highly indebted to my guide, Dr Ch. Ranga Rao, H.O.D.

Department of Post Graduate and Research centre, sri D.G.M.Ayurvedic

Medical Col lege, Gadag for his valuable suggestions and guidance in

completing this work successful ly.

I am heart i ly thankful to Dr V.V.S.Shastr i . Under whose guidance

my work was started and he was the teacher who inspired me to take the

combinat ion of the drug mentioned in this thesis.

I am ever grateful to my Co-guide Dr. Siva Ram Prasad Ketamakka

who was a helping hand throughout the work and supported me in

completing the work in st ipulated t ime.

I am thankful to our Principal Dr G.B.Pati l for his support in

completing this work successful ly.

I am very much thankful to Mr. Nandakumar for his valuable help in

stat ist ical calculations.

I am thankful to Dr A.K.Panda and al l other staff of DGM col lege for

their help.

Acknowledgement

I acknowledge to our col lage l ibrar ian Mr V.M.Mundanamani and

his assistant Mr Sureban for support ing me by providing lot of books for

the study.

I am thankful to Mr Gir iachar Off icer National Information Centre

(NIC) Gadag, for giving me information about the work going on in

di f ferent parts of the world regarding this subject.

My personal thanks to Mr.N.N.Bhat and Mr C.S.Bhat who helped

me in understanding the Sanskri t versions.

I am thankful to Dr.(Mrs) M.D.Gojanur for support ing me by

referring the cases for tr ial.

I am thankful to my col leagues and fr iends who supported me in

cl inical tr ials and made the tr ial successful.

I am thankful to al l the pat ients who agreed to undergo the

treatment with the tr ial drug.

I am highly indebted to my beloved parents, who framed a proper

path for my carr ier.

Acknowledgement

I express my heartfel t grat i tude to al l my family members for their

constant help, love and care rendered during my study.

I am thankful to al l my teachers, from primary education to post

graduate education for helping me in bui lding up my carrier.

This l ist is incomplete without remembering my small sunny Kiran

(18 months) whose smile inspired and kept me cheerful throughout my

work.

I wish to thank al l the persons who have helped me directly and

indirect ly with apologies for my inabi l i ty to identi fy them individual ly.

Introduction 1

Madhumeha is emerging as the chronic non-communicable disease

of concern in developing countr ies. With changing environment,

urbanisat ion and al tered l i fe-style giving more comforts and sedentary l i fe

to human, simultaneously offer ing metabol ic diseases l ike Madhumeha.

Madhumeha is a disease in which certain pathological changes are

noticed in ur ine, the most important being the presence of sugar. Since

this disease is connected with the urinary system with the presence of

sugar in the urine, the comparison of Madhumeha with Diabetes Mell i tus

is just i f iable.

Madhumeha is also one of the identi f ied major cause of morbidi ty

and mortal i ty in India1. In further, Indians have high ethnic susceptibi l i ty

for developing Madhumeha at a younger age group. The disease usual ly

occurs after 30 years of age, seen more in male than in female.

Being a slow onset and often relat ively asymptomatic disease,

remains undiagnosed at onset, or even i f diagnosed is often ignored by

persons aff l icted with i t . In addit ion lack of awareness amongst health

professionals and inadequate health care faci l i t ies compound the problem

of Madhumeha related complications in our country2.

Introduction 2

The alarming rise in non – communicable diseases l ike Madhumeha

warrants immediate attent ion of the experts to develop and propose,

formulate, establ ish, not only effective treatment schedules, but also to

plan preventive measures against Madhumeha and control the morbidi ty

rate due to this disease. Ayurveda proposes a comfortable remedy as

pal l iat ive therapy.

ITHIHASA

There is precious information given by our Acharyas about al l the

aspects of the disease, which reveal the pathological aspects of disease

and make them easy to understand. They had a thorough knowledge of

the entire disease that can be observed in their l i terature. We can

observe the classical references which indicate the disease as one of the

dreadful and chronic. Our ancestors have tr ied to know about the

disease from various angles, which made them to think in many aspects

of the disease. By observat ion alone they have classif ied the disease

elaborately. Thus to understand the disease we have to know the subject

already exist ing since the days of Vedas which give valuable information

about the disease.

VEDIC PERIOD

Vedas are the oldest l i terature of civi l ization. Ayurveda is the

Upanga of Atharvan Veda. In Vedas we f ind two words “Asrava” and

Introduction 3

“Prameha”. In Atharvana Veda Asrava vyadhis are mentioned in which

Nasasrava, At imootra and Atisara are included3. The term Asrava i f

formed from “A – srava” means to f low.

In Atharvana Veda 6 / 44 / 3 “Visanaka” drug is indicated in vata

vyadhi. Kesava commenting on this, explained “Vatikruta nasani” as “

Vatikruta asravasya nasani”, means i t is indicated in Asrava vyadhis. In

the Manthra 2-3-1-3 of Atharvana Veda, the drugs emerged from valmika

are indicated in At isara, Atimootra and Nadivranam4.

This clearly indicates the prevalence of this disease with i ts

remedy in the Vedic period.

SAMHITA PERIOD

After Vedic period facts about Madhumeha were further explored by

Atreya which are recorded in “ Charaka Samhita” a complete treat ise of

medical sciences of i ts era. He explains various factors pertaining to

et iology, pathogenesis, complications and methods of treatment in detai l

in his treat ise. I t is a point of histor ical importance that the book

mentions the loss of sweet substance from urine5.

Charaka also mentioned in sutra sthana that the Madhumeha

occurs due to avri ta of Vayu6, and explains the mythological origin of

Introduction 4

Madhumeha in Nidana sthana7. During the destruction of Daksha’s as

sacri f ice, Gulma f i rst manifested in human being who f led in al l direct ions

due to the agitat ions in their body. Because of f leeing, swimming,

running, f ly ing, jumping etc. Pramehas and Kustas manifested themselves

in addit ion to the intake of Ghee.

Bhela samhita which is contemporary to Charaka samhita describes

the two types of Madhumeha i .e. prakruta prabhava (congenital) and

Swakruta (acquired)Prabhava8.

The most notable contribution of Sushruta was to devote a

separate chapter for the management of Madhumeha and he has tr ied

some specif ic preparations of minerals and vegitat ions. Further he has

also described in a separate chapter for the management of Carbuncles

which are the Upadravas of Madhumeha9.

After Sushruta, Vagbhata made great contribut ion to Indian

medicine. He simpl i f ied the exist ing knowledge and gave some new

preparat ions and ideas in the text. He classif ied two types of Madhumeha

on the basis of pathogenesis are Dhatukshayaja and Avaranaja10.

Artha shastra of kout i lya (321 – 296 BC) mentions a method to

induce Prameha in Human deal ing with the sense to injure the enemy.

Introduction 5

The spot obtained from burning chancl ion (krukalaka) and house l izard

(Gruha goul ika) together with the intestines of mott led frog (chitra bheka)

and honey, i f administered causes Prameha. This evidently points the

existence of Diabetogenic technique in the ancient t imes11.

MEDIEVAL PERIOD

This period of history of Indian medicine is known as a period of

commentators. Hence most of the books of this period are of col lections

and thoughts of previous authors, commentaries of previous books.

Madhavakara (9t h century A.D.) in his book Madhava nidana

compiled the thoughts of his earl ier authors without adding any thing new

to the knowledge on Madhumeha.

Gayadasa (11t h Century A.D.) commentator of Sushruta Samhita

elucidated that avi lata of urine in Prameha was due to the presence of

some components of dooshyas i .e. meda, mamsa etc12 .

Chakrapani, the commentator of Charaka samhita and the author of

Chakradatta, in the same period contr ibuted nothing signif icant with

reference to etiology of Prameha but recommended medicines and

regimen prescribed by Charaka and Sushruta and some of his own.

Introduction 6

Dalhana, another commentator of Sushruta samhita (12t h century)

contributed a myth that females do not suffer from Madhumeha13.

Sharangadara ( 13t h century AD) prescribed some new recipes for

the management of Prameha but did not contr ibute any thing in the f ield

of et iopathogenesis.

Bhavamishra (16t h century AD) contributed to the history of

Prameha by adding some new herbal and metal l ic preparat ions for the

management of Prameha14.

After Bhavamisra the development of Ayurveda is not so optimist ic

and had been stagnated. The concepts of ancient India regarding

Madhumeha are quite al ike with modern concepts. Descript ions of

Charaka, Sushruta show that even in that ancient t ime, Indian scholars

were famil iar with etiology, pathogenesis, symptomology and

complicat ions of Prameha, out standing being the knowledge of genetic

role in the etiopathogenesis. The regimen prescribed by them are useful

even in present era also, and these texts and their concepts do not

remain mearly as the histor ical mi le stones but have become the hope

of the Madhumeha cure at present sinerio.

Introduction 7

HISTORICAL MILESTONES.15

- Atharvana Veda is the oldest l i terature, which explains Madhumeha.

- In 2500 BC Eabers Papyrus ( Egypt ) wrote the f i rst cl inical

descript ion as “the disease without pain and melts the body” was

documented.

- In 600 BC Charaka (India) cl inical ly described Madhumeha and noted

role of heredity and Sweetness in ur ine.

- In 400 BC Sushruta (India) described same as that of Charaka.

- In 30 BC – 38 AD Celsus (Greece) gave some cl inical descript ion.

- In 1s t AD Aretaus (Greece) introduced the name as diabetes meaning

“to run through a pipe” .

- In 2nd AD Claudius Galenus proved that by consuming the drinks

which weakens the kidney wi l l al low the l iquids without change.

- In the same century Tchang Tchong king proved this as the disease of

thrust.

Introduction 8

- In 600 AD Aetius (Amida) treated this disease by using sedatives.

- In 980 – 1037 AD Avicenna ( Arab ) explained about Diabetic

Gangrene and put forward the question as “ is there any relat ion

between pancreas”

- In 1727 Brunner.J.C. ( Swiss ) removed the pancreas from the dogs

and found that they developed thirst and polyurea.

- In 1770 Thomas wi l l is ( England ) proved the di f ference between

Diabetes Mallets and Diabetes Insipidus.

- In 1775 Matheu Dobson Evaporated the specimen of ur ine of a

Diabetic patient and discovered a residue which was almost glucose.

- In 1782 Thomas Cawley recorded the disease.

- In 1788 Cawley (Engl ish) described pathology of pancreas.

- In 1815 M. Chevreul found out the presence of glucose in the urine.

Introduction 9

- In 1839 Bernard Naunyn studied the relat ion between the metabol ic

disturbance and pancreas.

- In 1841 Trommer found the test for urine glucose.

- In 1848 Claude Bernard proposed that the production of sugar in the

l iver is the reason for the r ise in the blood glucose Laval. He injured

the base of the fourth ventr ic le and proved the increase of blood sugar

level, he also proved when the blood sugar level is raised the sugar

starts f lowing out through urine. Even after the lowering of the blood

glucose level the urine contains glucose was the major discovery by

Claude Bernard.

- In 1845 Boucardet establ ished the relat ion between the Diabetes and

Pancreas.

- In 1850 Fehl ing found the test for testing the urine sugar.

- In 1867 Paul Langerhans (Germany) found islets of langerhans.

- In 1874 kusmal found the symptoms caused by increase in acitone in

the body.

Introduction 10

- In 1874 Oacar Minkowski found the acidosis.

- In 1886 Joshaf wan maring and Oscar Minkowski proved the

induct ion of diabetes by removing the Pancreas.

- In 1870 Clande Bernard ( France ) Noted sugar storage in l iver as

glucogon and elevated blood sugar in diabetes.

- In 1901 E.L.O.Pie proved the increase and decrease in the blood

glucose level is due to langerhans.

- In 1907 M.L Lane di f ferent iated and named the langerhans as two

types “alpha and beta“.

- In 1921 J.J.R.Macleod, Frederick . G . Banting and Charles.H. Best

(Toronto )discovered Insul in

- In 1926 H.C.Hagedorn mixed protimine to insul in and made i t to defuse

s lowly so that i t can act for longer t ime.

- In 1944 Von Noorden ( Vienna ) Bel ieved that l iver play a role in

diabetes.

Introduction 11

- In 1952 Sanger found the structure of the insul in.

- In 1954 A. Shef found Carbutamide was working as a hypoglycemic

agent. This was the f i rst oral hypoglycemic agent, but as i t had many

side effects i t was drown back from the market and a new drug similar

in the function of Carbutamide was introduced as Tobutamide which has

less side effects.

- In 1970 On words Merwin Gl iedman and other transplanted pancreas

culture of Is lets of cel ls of pancreas transplant of beta cel ls.

Even in 1999 also the research is going on throughout the world.

St i l l we are fai l ing to put ful l point to these milestones and newer aspects

of the disease are emerging out day by day.

Some of the latest research going throughout the country and abroad is given

below16,17.

- Toxicological Evaluat ion of Fenugreek seeds in Diabetic patients.

By Sharma R.D. at PG Dept, SN Medical col lege, Agra. –1996

- Consti tut ional study of pat ients of Diabetes Mell i tus vis-Avis

Madhumeha by R H Singh at Dept of Kayachiki tsa, B.H.U. 1996

Introduction 12

- Prognosis of Prameha on the Basis of Insul in level.

By Upadhyay at Dept of KC, I.M.S, B.H.U, Varnasi. 1996

- Diabetic foot ulcers treated the Ayurvedic way

By Ojha J K. at Dept of DG, B.H.U, Varnasi. – 1997

- Scope and use of Indigenous Herbal drugs in Madhumeha an Indian

Scenario. By Mukherjee.S K at C.D.R.I, Lucknow.- 1997

- Potential antidiabetic agents form plant sources. By R K Goyal at Dept

of Pharmacology, L M Col lege of Pharmacy, Ahmedabad.- 1997

-

- Evaluat ion of hypoglycemic act ivity of Tradit ional Herbal preparat ion

By Negam S A at Department of Pharmacology, NRC, Egypt. 1997.

- Ant i diabet ic property of neem seed By Kannan J at Pharmacy Dept,

Faculty of tech and Engg, MS Universi ty of Boroda. Baroda 1997

- Hypoglycemic effect of Trigonel la foenum Leaf in Diabetic By A. Barry

at Dept of pathology and forensic Medicine, Universi ty of Basrah 1997.

Introduction 13

References

1 API Text book of Medicine pp 205

2 Diagnoses of Diabetes pp 2

3 Ayurveda I thisa pp 26

4 Ayurveda I thisa pp 29

5 Charaka Nidana 4 / 37

6 Charaka Sutra 17 / 78.

7 Charaka Nidana 8 / 11

8 Bhela Samhita Nidana sthana 6 / 1 – 4.

9 Sushruta Chiki tsa 12 / 16

10 Astanga .Hridaya.Nidana 10 / 8

11 Ardha Sastra of Kouti lya 16 / 179 / 1.

12 Su NI Naya Chandrika Commentory.6 / 6.

13 Nibandha sangraha on Su Ni 6 / 33

14 Bhava prakasha Madyama kanda 38 / 45 15 Sihimootra roga by A. Narayanappa.pp 4 16 Al l ied Ayurvedic Medical Research Abstracts (AAMRA) 17 Researches in Ayurveda 1997

Shareera 13

Charaka explained that the persons who take excess and heavy

food or food with sour and salty taste, new r ice, fresh wine and enjoy

long sleep wi l l increase, the kapha, pi t ta, meda and mamsa and obstructs

the Vata together with the ojus come down to the vast i and causes

Madhumeha1. By this i t can be seen that the vast i is involved in the

product ion of Madhumeha. In Madhumeha, Prabhoota mootrata is the

main lakshana. I t is a symptom of mootravaha srotodusti also2. Hence in

Madhumeha mootravaha srotodust i is present.

Charaka mentioned that Prameha occur whenever the Medas

(srotas) is vi t iated3. vr ikka and vapa are the moolas of Medovaha

Srotas4. So the involvement of vr ikkas is present in Madhumeha.

Thrishna is an important lakshana. The cause for tr ishna is Udakavaha

Srotodusti5. Talu and kloma are the moolas for Udakavaha srotas6.

Hence the involvement of Talu and Kloma are present in the product ion of

Madhumeha. Liver plays an important role in dhatuparinama. In

Madhumeha dhatuparinama alters because of the involvement of most of

the dhatus present in the pathogenesis. Hence the l iver is responsible in

the production of Madhumeha.

Thus i t can be said that the organs responsible for the product ion

of Madhumeha are -

Shareera 14

1. Taalu

2. Kloma

3. Vrikka

4. Vasti

5. Yakri t

But in ayurveda the knowledge of rachana and kriya of Madhumeha

are st i l l in controversy, but with the help of modern science the

Kriyatmaka vivechana can be discussed.

TALU

The classical texts in Ayurveda have given the brief descript ion

about Talu. I t is located above the kanta and becomes the base of the

siras as i t is evident from the del iberations in Bhela samhita. I t is the

moola for the Udakavaha srotas7. Charaka mentioned Talushosha and

pipasa wi l l exist i f Udakavaha Srotas is vi t iated8. Sushruta mentioned

nine Talugatha vyadhis9 . Charaka and Kashyapa stated that the union of

two bones forms Talu10.

KLOMA

Ayurveda acharyas stated that Kloma is the moola for Udakavaha

Srotas11. Al l acharyas mentioned this as one among the Kostangas12.

Shareera 15

Though there are many schools of thoughts regarding the anatomical

identi f ication, In Sushruta samhita i t is said that kloma is explained with

Yakri t which is located in the r ight side of the body13. Dalhana whi le

commenting on this said that i t is in the r ight side of body which is laying

down below the Yakri t and i t is also cal led as Ti lakam. Vagbhata says

that Kloma is located along with Yakri t in the r ight side of the body. I ts

combinat ion according to Sharangadhara samhita in Pit ta which is

agniroopa14. He has mentioned Agnashaya as i ts synonym. Adhamalla

whi le commenting on this says that i ts formation is with the sonitha ki t ta.

I t is in the r ight side and in contact with the l iver. He has also given

Ti lam as a synonym to Kloma15.

Charaka says that Talumoola and Kloma are the seats of

Udakavaha srotas. I f these srotases are vi t iated the pathological

changes i .e. shosha of above organs and thirst develops16. Chakrapani

whi le commenting on Kloma said that i t is a Pipasa sthana (thirst centre).

Sushruta also said as above and on injury to these srotases the

immediate death occurs besides polydipsia.

Based on the above descript ions i t is clear that Kloma in one

among the Kostangas and located adjacent to the Yakri t . The nearest

organs to the l iver are Gal lbladder and Pancreas. I t is also clear that

Shareera 16

only Pancreactomy causes the polydipsia and death so i t can be

considered as Kloma.

VRIKKAS

Vrikkas are two in number and are si tuated in Kosta. Al l acharyas

included vr ikkas in kostangas. In Dalhana commentary on Sushruta the

vr ikkas are described as two f leshy bodies, each si tuated on ei ther side

of spine and their shape as being l ike rounded bodies17. These are said

to be composed of the essence of the Rakta and Medas18. Sharangadara

whi le describing their function says that vr ikkas are said to be the

nourishers of the abdominal fat19. Adamalla whi le commenting on the

above states that vr ikkas are two rounded bodies in the abdomen which

are derived form the essence of the blood and fat and they originate form

fat. They are stated to be concerned with the nutr i t ion of the abdominal

fat. Ayruvedacharyas Charak, Dalhana, Chakrapani says vrikkas are two

in number and they are si tuated below the chest20.

VASTI

Embryological ly, Vasti is stated to be maternal contribut ion. I t is

stated to be derived form the essence of Rakta and kapha supported by

Pit ta in to which Vayu also enters21. Vast i has been included under

kostangas and Ashayas by al l acharyas. I t is stated to be one in

Shareera 17

number22. The term Vasti , Mutravasti , Vastipudaka, Mutrashaya and

Mutradhara seem to have been used as synonyms in Ayurvedic texts23.

Charaka whi le describing the locat ion of Vasti has stated that vasti

is si tuated in between the Sthoolaguda, Sevani, Sukravaha naadies and

Motravaha naadies24. According to Sushruta, Vast i is near to Nabhi, Kat i ,

Guda, Vankshana and Shepha. He further stated that vasti , Pourusha,

Vrushana and Guda are al l interrelated and si tuated in the pelvic cavity25.

According to Bhavamishra and Sharangadara, Vasti is located below the

Pakwashaya. Vagbhata says that i t is located inside the kat i26. Sushruta

states that i t is s ituated near the Garbhashaya in females27.

Regarding the shape and structure of the Vast i , Sushruta has

stated that i ts shape looks l ike that of “Alabu” and ful l of Siras and

Sanyus al l around. I t is stated to be Tanu twak i .e. a thin volved organ or

i ts coverings are thin and membranous. I t has one exit and l ies with i ts

mouth downwards28. Vagbhata has described i ts shape as Dhanur Vakra

i .e. bent l ike bow having one opening downwards and composed of l i t t le

muscles and blood. Adamalla described i ts shape as “Charmaka

Latwakara” that is l ike bag of leather. The Acharyas described i t to be

the storehouse of Mootra and seat of “Prana” being one of the important

marmas. Charaka says that i t is reservoir of mootra where al l the

Ambhuvaha Srotases ends. He also explained vasti as the moola of

Shareera 18

Mootravaha srotas. Sushruta stated that Mootraghata, Prameha, Sukra

doshas, Ashmari develops from Vasti only29.

YAKRIT

Since the Vedic period, the traces of gross anatomical knowledge

of Yakri t are avai lable. Sayana the commentator of Vedas whi le

commenting on the word Yakan coined in atharvana veda described that

Yakan is si tuated near the heart. The ward Yakan in his view means

Yakri t . Yakri t is described as one of the Matruja angas due to i ts

softness30 and i t is included in Kostangas. Yakri t in i ts embryonic stage

is formed by the shonitha. Yakri t is si tuated on the r ight side, below the

Hridaya31 and i t is the moola for the Raktavaha srotas32. Sushruta

mentioned Raktadharakala is present in Yakri t33.

SHAREERA KRIYA

Agni plays an important role in manifestation of Madhumeha hence

concept of Agni carr ies importance in the study of Madhumeha. Agni or

Jataragni is the main cause for every parinamas, or changes in the body.

Dahana (burning) and Paka (Chemical act ion) are the chief actions of

agni. I t spl i ts the Vi jateeya dravyas into sajateeya dravyas for easy

absorpt ion. The ingested food after reaching Amashaya enters the

digest ion by Antaragni. (Pachaka pit ta) in the presence of samana vayu

Shareera 19

and Kledaka kapha which effects the digest ion. The Ahara parinamakara

bhavas are Ushma, Vayu, Kleda, Sneha, and kala which are essential for

normal ahara pachana. The digestion and other metabol ism in the body

can be done only in presence of Agni.

The synonyms of Agni are kayagni, antaragni, kostagni,

audaryagni. There is no Agni other than Pitta, as i ts actions perform in

the l iving body is Paka or pachana. Acharyas mentioned 13 types of

agnis in the body. They are one Jataragni, f ive bhootagnis and seven

dhathwagnis. Samana vayu, which is located nearer to Jataragni moves

al l over the kosta, col lects the ingested food. Then separates prasada

and ki t ta bhagas of Ahara into Ahara rasa and mootra, pureesha

respectively.

According to the Ayurvedic physiology Bhutagnipaka fol lows

Jataragnipaka and i t completes the process of internal digestion, i t is

only after the complet ion of Bhootagnipaka the formation of ahara rasa is

possible. Dhatwagnipaka does not start t i l l the Bhootagnis completes i ts

process of digestion and supply the Sajaat iya nutrients to the

Dhatwagnis. But i t can be said that the si te of action of Bhootagnis starts

from the intestines t i l l the cel l membrane, the l iver being in between the

Bhutagnipaka that wi l l be predominant in i t . In the event of the fai lure of

the funct ion of Bhootagnis, the Dhatwagni wi l l not be in a posit ion to bui ld

Shareera 20

the respective dhatus. That is how the def icient function of Bhootagnis is

to be understood.

Agni assumes names of Vishamagni, Teekshnagni, Mandagni, and

Samagni according to doshic inf luence on i t .

Charaka says mandagni by i ts qual i t ies causes ajeerna and mala

sanchaya, thereby i t leads to several diseases. Mandagni vi t iates kapha,

kapha in turn vi t iates the other dhatus part icularly medo dhatu, and this

leads to Prameha. Hence the role of agni is to be considerable in the

study of Madhumeha.

Ayurveda has mentioned about the formation of Mootra and i ts

excret ion. Mootra has been described as the Drava Bhaga of the Kit ta

and i t is produced in Amapakvashaya, The l iquid port ion is said to

separated form the sol id fraction in the pakvashaya by the pureeshadhara

kala under the inf luence of Samana vayu, brought in to vasti and from

there i t is excreted by the Apanavata. Mootra is said to be an out come

of the digest ion of ingested food, and the seat of i ts production is

pakvashaya. Mootra is stated to be a mala derived form the food

ingested in four-fold manner. The l iquid port ion of ki t ta bhaga after

absorpt ion circulates in the body and i t is f inal ly carr ied to vrikkas by two

mutravaha dhamanis which divide in to innumerable branches forming the

mutravaha srotamsi through which i t oozes and there i t is named Mutra.

Shareera 21

From vrikkas, two Gavinis carry i t to vasti . Even though Vrikkas have

been mentioned in Ayurveda their relat ion with the formation of mootra

has not been clearly described. A deep study of Ayurveda classics

enl ightens to certain extent about mootropatt i . I f Vrikka, Gavini and

Medhra are considered as one system of srotas for the purpose of the

product ion and excretion of ur ine, I t remains stored in vast i t i l l is

excreted during mutra pravrutt i . I f so, there can be no di fference between

the views of Ayurveda and modern medicine.

MODERN ASPECT

Diabetes mell i tus is a chronic disease. I t results due to disturbance

in carbohydrate metabol ism and deficiency of Insul in34 secreted by the

Beta cel ls of Is lets of langerhans of pancreas, but hormones of pi tui tary

and adrenal glands are also int imately related to the development of

Diabetes State. Liver plays an important role in the metabol ism for

carbohydrate. I t stores glucose in the form of glycogen under the

inf luence of Insul in. Any alterat ion in this function leads to diabetes35.

So the involvement of organs in diabetes mell i tus are

- pi tui tary gland

- Pancreas.

- Adrenal gland

- Liver.

Shareera 22

PITUTARY GLAND36

This is a exceedingly important endocrine gland with a wide range

of functions including the control of the other endocrine glands and of

body growth.

This gland measures 1.5 cm in the coronal plane, 1 cm in the

sagital plane and 0.75 cm in vert ical form. I t l ies within the sel la Tarsica

of the sphenoid bone and posterio superior to the sphenoid air sinuses

below the optic chiasma. I t is f lattened ovoid lying in the hypophyseal

fossa (sel la Tarasica) and connected to the inferior surface of the

hypothalamic part of the brain by the infundibulum. Structural ly the gland

can be divided into two main parts

a) Anterior lobe which is composed of Adeno hypophyseas t issue.

b) Posterior lobe which is Neurohypophuyseas.

Posterior lobe of the hypophysis is the expanded inferior end of the

infundibulum and is developed from the brain. The anterior lobe is much

larger than the posterior lobe and consists of three parts, which part ly

surround that lobe and the infundibulum. The distal part forms most of

the anterior lobe. I t is separated form the posterior lobe by the thin sheet

of glandular t issues ( intermediate part) appl ied to the posterior lobe. The

infudibular part is a narrow upward projection of the distal part. The

Shareera 23

anterior lobe develops from the ectoderm and has only vascular

connection with the brain.

Anterior lobe is the master gland of endocrine system, because i t

produces proteotrophic hormones which effects the other ductless glands.

In these secretions two hormones are having direct action on

carbohydrate metabol ism. If any disturbance occurs i t leads to

Hyperglycemia or Hypoglycemia.

The hormones secreted are Growth hormone or somatotrophic

hormone (GH of STH ) and Adreno Cort ico Trophic Hormone (ACTH).

The pitui tary effect of STH on carbohydrate metabol ism is to st imulate i ts

storage. Administrat ion of growth hormone in animal or in man produces

hyperglycemia and glycosuria. So the growth hormone is diabetogenic

effect especial ly in man. The hormone is however increases the

glycogen content of cardiac muscle. Administrat ion of ACTH produces

simi lar effects as induced by growth hormone. Both STH and ACTH

increase gluconeogenesis and diminish the rate of oxidat ion of glucose.

Thus the anterior pi tui tary has a diabetogenic role.

GH (growth hormone) is also known as somatotropin, i ts pr incipal

function is to act on the skeleton and skeletal muscles, in part icular to

Shareera 24

increase their rate of growth and maintain their size once growth is

attained. GH causes cel ls to grow and mult iply by direct ly increasing the

rate at which amino acids enter cel ls and are bui l t up into proteins. GH is

considered to be a hormone of protein anabol ism since i t increases the

rate of protein synthesis. GH also promotes fat catabol ism that is i t

causes cel ls to switch from burning carbohydrates to burning fats for

energy released. At the same t ime GH accelerates the rate at which

glycogen stored in the l iver is converted into glucose and released in the

blood. Since the cel ls loosing fats for energy however they do not

consume as much glucose, the result is the increase in the blood sugar

level. A condit ion cal led hyperglycemia. This process is cal led

diabetogenic effect because it masks the elevated blood glucose level of

diabetes mell i tus. GH seems to produce many of i ts effects by convert ing

other factors in to growth promoting substance cal led soerto medians and

insul in l ike growth factors (IGF).

Other hormones can indirectly affect insul in production however for

instance GH raises blood glucose level and the r ise in glucose level

tr iggers insul in secret ion. ACTH by st imulat ing the secret ion of

glucocort icoids brings about hyperglycemia and also directly st imulates

the release of insul in GHIF (romatostatin) inhibi ts the secret ion of insul in.

One stimulus that inhibi ts GH secret ion is hyperglycemia high blood

sugar level. An abnormally high blood sugar level st imulates the

Shareera 25

hypothalamus to secrete the regulat ing factor GHIF (somatisat ion) GHIF

inhibi ts the release of GHAF and thus the secretion of GH. As a result

blood sugar level decreases.

PANCREAS37

The pancreas is a compound alveolar gland. I t has got both

endocrine and exocrine funct ions. I t l ies against the posterior abdominal

wal l behind peri toneum. The adult pancreas consists of a Head, Neck,

Body and Tai l . The whole organ is about 15 cm long with the r ight margin

of the head in contact with the descending part of the duodenum and the

tai l is in contact with the spleen. The disease diabetes mell i tus is

considered only to i ts endocrine secretion that is Insul in, so i t is more

important to go through i ts endocrine part.

ISLETS OF LANGERHANS

The islets of Langerhans are composed of various components that

are organized to form micro-organs. The mass of is lets within a pancreas

is dynamic and changes both with growth and development and with

functional chal lenges. As we learn more about the regulat ion of

di f ferent iat ion of is let cel l types, we also may learn how to enhance the

growth of is let cel ls, part icularly the beta cel ls.

Shareera 26

Is lets function both singly and in concert. Recent work has

revealed grater diversi ty in is lets than that previously recognized. There

is funct ional heterogeneity between islets and beta cel ls within the same

islet. Numerous peptides other than the four main is let hormones

( insul in, glucagon, somatostat in, and pancreat ic polypeptide) have been

immuno-local ized in is lets.

The islets of Langerhans are clusters of endocrine t issue scattered

throughout the exocrine pancreas. In the adult mammal, the is lets are 1

to 2% of the pancreat ic mass and thus comprise around 1gm of t issue in

the adult human. Islets are a complex mixture of cel ls and function both

separately as micro-organs and in concert as the endocrine pancreas.

Although the direct secret ion of insul in and glucagon form islets into the

portal vein has obvious advantages with respect to inf luence on hepatic

function. The islet mass is dynamic, adjusting to meet the changing

needs of the individual, whose size and level of activ i ty vary at di f ferent

stages of l i fe. When the islet mass cannot adjust to meet the demand,

diabetes results.

The pancreas of the adult human contains about 200 units, or 8mg,

of insul in. The size of an islet can range from only a few cel ls and less

than 40 micrometer in diameter to about 5000 cel ls and 400 micrometer

in diameter.

Shareera 27

GROWTH OF ISLET

The growth capacity of the beta cel l depends on the st imulus and

the abi l i ty of the cel l to recognize the st imulus as wel l as on the number

of beta cel ls that can enter the cel l cycle and undergo mitosis. There is

an increased incidence of polyploid beta cel ls in the diabetic human.

Although there may be numerous st imul i for beta-cel l growth, three major

st imul i are known. Glucose has been shown to st imulate modest growth

of ei ther neonatal or adult pancreat ic beta-cel ls in culture. Pregnancy

has been shown to cause both increased repl icat ion and mass of beta-

cel ls. As a paral lel f inding, in vi tro studies have shown that prolact in,

placental lactogen and growth hormone can st imulate repl icat ion of beta-

cel ls. Diabetes results only i f increased cel l loss or functional demands

cannot be met.

COMPONENTS OF THE ISLETS OF LANGERHANS

There are three major endocrine cel l types in is lets : the insul in

producing beta-cel l , the glucagon producing alpha-cel l , the somatostat in

producing delta-cel l .

Alpha-cell

The alpha cel ls are usual ly smaller and more columnar than the

beta cel ls and wel l granulated with granules 200 to 250 nm in diameter.

The granules are electron dense with narrow halo of less-dense material

Shareera 28

and a t ight ly f i t t ing granule-l imit ing membrane. There is l i t t le species of

variat ion.

Beta-cell

The beta cel ls are polyhedral, being trancated pyramids, and are

usual ly wel l granulated with secretary granules 250 to 350 nm in

diameter.

Delta-cell

The delta-cel ls are usual ly smaller than either alpha or beta cel ls,

are wel l granulated, and are often dendri t ic in shape. Within a delta cel l

the electron density of granules varies great ly. Each granule, 200 to 250

nm in diameter, contains material of homogenous moderate density that

f i l ls the granule-l imit ing membrane.

Table showing cel ls and their relat ive hormones

Cel l type Size of secretary granule (nm) % of cel ls Hormone

Beta 250 – 350 60 – 80 Insul in

Alfa 200 – 250 15 – 20 Glucagon

delta 200 - 250 5 – 10 somatostat in

MICROVASCULATURE

The islets are highly vascularized and has a direct arter iolar blood

supply. The fenestrae render these capi l laries highly permeable. The

Shareera 29

blood f low to the islets has been found to be disproport ionately large (10

to 20% of the pancreatic blood f low) for the 1 – 2% of pancreatic volume

. Factors regulat ing islet blood f low may effect is let hormone secretion.

High concentrations of glucose have been shown to enhance pancreat ic

blood f low and to preferent ial ly increase islet blood f low.

NERVES

The pancreas is innervated by sympathetic f ibers from the cel iac

gangl ion and by parasympathetic f ibers form the vagus nerve. These

parasympathetic f ibers synapse in small gangl ia dispersed in the

pancreas. They may act as pacemakers for the osci l lat ions in hormone

levels that occur without extr insic nervous connections, as in the isolated

perfused canine pancreas. Within the pancreas, nerve f ibers terminate in

perivascular, periacinar, and perinsular areas. Within the is lets the

nerves fol low the blood vessels and terminate within the pericapi l lary

space, within the capi l lary basement membrane, or closely apposed to

the endocrine cel ls38

Functions of these hormones :

INSULIN:

The insul in is hypoglycemic, ant i diabetic factor and the protein

bound hormone that regulates the blood glucose. I t also increases the

Shareera 30

oxidat ion of glucose to CO2 in the t issues and depresses

gluconeogenesis i .e. formation of glucose from the sources other than

carbohydrates.

Insul in increases combustion of sugar in the t issue and also helps

in the treatment of glucose in the cel ls. I t increases synthesis of

glycogen from sugar and lactate both in the l iver and muscle. This is

cal led the directive effect of insul in. Insul in promotes the uptake of

glucose inside the cel ls and the intercel lular phosphorylat ion of glucose

to glucose–6–phosphate. Glucose–6–phosphate i tsel f also appears to be

a specif ic activator of glycogen synthesis.

Insulin effect on protein metabolism:

I t prevents gluconeogenesis Glucose is normally formed from

proteins and l ipids in the l iver. In diabetes this process is enhanced.

High blood sugar level in diabetes is due to over product ion of glucose.

In the starving diabetes dextrose ni trogen ratio is fair ly constant. This

shows that both sugar and ni trogen are coming form the same source i .e.

proteins. When insul in is given both sugar and nitrogen excretion fai ls,

showing that formation of new glucose from proteins has been interfered.

Shareera 31

Insulin effect on fat metabolism:

I t prevents formation of ketone bodies (anti ketogenic). In advance

diabetes, excess ketone bodies are formed in l iver, due to incomplete

combustion of fatty acids. After the administrat ion of Insul in more sugars

burn and l iver glycogen increases displacing the l ipids. Hence l ipid

combustion is discouraged and ketosis disappears.

Insul in decreases the cholesteremia and l ipademia. I t also prevents

accumulation of excess l ipid in the l iver and breakdown of l ipid in

Adipose t issue.

GLUCOGON :-

The Alpha cel ls of the islets of Langerhans secrete Glucogon. I t is

a polypeptide hormone with 29 aminoacids having molecular weight of

3,485. This polypeptide has been completely synthesized. Glucogon

causes glycogenolysis in the l iver and antagonist to l iver by depriving the

action of Insul in.

The blood sugar level chief ly controls the secretary activi ty of

Alpha and Beta cel ls. Hyperglycemia st imulates the release of Insul in

where as, hypoglycemia wi l l release the glycogen. There is no good

evidence that a tropic hormone secreted by the pitui tary, directly

inf luences the secretary act ivi ty of the pancreatic is lets, through

secret ions derived form other endocrine glands for example, the adrenal

Shareera 32

gland have some effects. I f the is lets are completely removed or

extensively damaged, the lack of or reduced Insul in formation results in

hyperglycemia and the condit ion of diabetes mell i tus (Madhumeha).

Relat ively normal carbohydrates metabol ism can then be restored by

supplementat ion of insul in.

I t is necessary to point out however that though a def iciency of

insul in production and release may result in Diabetes, not al l cases of

Diabetes are due to a deficiency in Insul in product ion. Even pi tui tary,

Liver and Adrenals are also involved in this process. Cl inical syndromes

involving abnormal carbohydrate metabol ism and abnormal blood sugar

levels may result f rom either deficiency or excess product ion of Insul in

and Glycogen. The latter when injected result in an increase in blood

sugar. Excess production of insul in as in cases of Islet tumors results in

hypoglycemic and attains neurological changes, excess product ion of

Gastrin, acidi ty and peptic ulceration.

ADRENAL (SUPRA RENAL) GLANDS

The adrenal glands are si tuated on the upper poles of the kidneys.

Each gland weighs about 4 gm.

Microscopic structure - A dist inct connect ive t issue capsule surrounds

the parenchyma of the gland. Beneath the capsule the cortex is arranged

in 3 layers. They are -

Shareera 33

Zona Glomerulosa.

Zona Fasculata

Zona Reticularis

Zona Glomerulosa : - The outer layer which varies in thickness form

almost total absence to clusters of a dozen or more smal l cel ls is known

as Zona Glomerulosa. Zona Glomerulosa secretes mainly aldosterone

that is concerned with the salt and water balance and acts on the distal

convoluted tubule and col lecting ducts of the kidney. I t also secrets a

small amount of glucocort icoids and sex hormones.

Zona Fasculata : - inside the f i rst layer the cel ls are larger and form

more or less paral lel radial columns. They commonly contain fat droplets

which give them a spongy appearance. This region is known as a Zona

Fasculata. This layer secretes predominantly Glucocort icoide.

Zona Reticularis . : - Centre of the gland the regular arrangement of cel ls

of the Zona fasciculata is replaced by one of anastomosing cel l cords

forming the Zona Reticular is, which secretes sex hormones and a small

amount of Glucocort icoids but no Aldosterone.

The adrenal Medul la is chief ly composed of chromaff in cel ls

(phaeochromocytes) which ei ther secrete Adrenal ine or Nor- adrenal ine.

Shareera 34

LIVER :-

The l iver is the largest gland in the body. The greater part of the

Liver l ies under the covering of the r ibs and coastal cart i lage. The l iver

is a dark brown, highly vascular and soft organ that is commonly ruptured

or torn in abdominal injur ies. I t is approximately one f i f teenth of the body

weight in adult.

The l iver is determined by the surrounding organs i t retains the

shape of a blunt edge i t has two surfaces. Diaphragmatic surface

divisible into Superior, Anterio, posterior and right parts according to the

direct ion in which i f faces and visceral (posterior) surface faces

posterior ly and Inferiorly. Liver is divided into four lobes Right,

Quadrate, Caudate and Left lobes.

Functions of l iver in carbohydrate metabol ism are:-

1. Storage of Glycogen.

2. Conversion of Galactose and fructose into glucose.

3. Gluconeogenesis

4. Formation of many important chemical compounds from the

intermediate products of Carbohydrate Metabol ism.

Shareera 35

Liver is especial ly important for maintaining a normal blood glucose

concentration. For instance storage of glycogen al lows the l iver to

remove excess glucose from blood, store i t and then return i t in to the

blood when the blood glucose concentrat ion begins to fal l too low. This

is cal led the glucose buffer function of the l iver. As an example,

immediately after a meal containing large amounts of carbohydrates the

blood glucose concentrat ion raises about three t imes as much in the

person with a non functional l iver as in a person with a normal l iver.

Gluconeogenesis in the l iver is also concerned with maintaining a

normal blood glucose concentration for glucose neogenesis occurs to a

signif icant extent only when the glucose concentration begins to fal l

below normal. In such case large amounts of amino acids are converted

into glucose, there by helping to maintain a relat ively normal blood

glucose concentrat ion.

Shareera 36

SHAREERA

References

1 Charaka Nidana 4 / 4

2 Charaka Vimana 5 / 7

3 Ibid 5 / 7

4 Ibid 5 / 7

5 Ibid 5 / 7

6 Ibid 5 / 7

7 Sushruta Shareera 9 / 15

8 Charaka Vimana 5 / 7

9 Sushruta Nidana 16 / 42

10 Ibid 16 /45

11 Charaka Vimana 5 / 8

12 Charaka Shareera 7 /15

13 Sushruta Shareera 4 / 23

14 Sharangadara Poorva khanda 5 / 63

15 Adamalla on Sharngadhara 5 / 83

16 Charaka Vimana 5 / 8

17 Sushruta Nidana 7 / 18

18 Sushruta Shareera 4 / 30

19 Sharangadhara poorva khanda 5 / 40

20 Charaka Shareera 7 / 7

Shareera 37

21 Sushruta Shreera 4 / 26

22 Ibid 4 / 47

23 Charaka Shareera 9 / 4

24 Ibid 9 / 4

25 Sushruta Nidana 3 / 17,29

26 Astanga Hridaya Shareera 4 / 10

27 Sushruta Chikitsa 7 / 33

28 Sushruta Nidana 3 / 18

29 Ibid 3 /15

30 Sushruta Nidana 3 / 15

31 Dalhana on Su Sh 4 /23

32 Charaka Vimana 5 / 7

33 Sushruta Shareera 4 / 10

34 API Text of Medicine by Sanani pp 205

35 Ibid pp 204

36 Principles of Anatomy and Physiology by Gregfard Tortara

37 Joslin’s diabetes Mellitus. pp15

38 Ibid pp 216

Nidana 36

HETU

I t is bel ieved that Prameha is a hereditary disease and many

factors play an important in the product ion of the disease as a cl inical

enti ty. They are age, sex, diet, body weight, Infect ion, pregnancy, etc.

Emotional stress and trauma have also been considered as etiological

factors of Prameha. Charaka considers Madhumeha as one out of the four

veri t ies of vataja Pramehas1. He has also stated that al l factors that

increase Kapha are the causative factors of the Pramehas2. The general

et iological factors of Prameha as stated by Charaka are3 – “Addict ion to

the pleasures of lounging and sleeping, excessive use of curds, meat

juice of domestic, aquatic and wet land animals, mi lk or diary products,

newly harvested grains and drinks and products of jaggery".

The et iological factors as stated by Sushruta are simi lar to Charaka

and capable of vi t iat ing mainly the Kapha dosha. Sushruta states that al l

variet ies of Prameha, i f not properly treated and attended to at the onset,

may ult imately develop into Madhumeha4. Based on the etiology,

Sushruta has classif ied Prameha into two variet ies as sahaja and

apathya nimittaja. Apathya nimit taja is subdivided into two as Ahara

nimit taja and vihara nimit taja.

Nidana 37

1. Sahaja or Genetic origin.

Charaka4 and Susrata5 have evaluated that beeja dosha is also a

cause for Prameha. Further Sushruta has included Madhumeha in the

Adibala pravri t taja category of disease.

The term beeja has been considered as a sukra and shonitha5,

which correlates with the sperm and ovum of modern concepts. Beejas

are vi t iated with dosha (Vata especial ly responsible for division of cel ls

makes certain abnormali t ies in chromosomal galaxy of sperm or ovum)

are responsible for genesis of Prameha, In gross the organs which are

responsible for producing Prameha are ambuvaha srotas, mamsa, kleda,

kloma, mootravaha srotas. They are deformed since bir th and susceptible

to get Prameha, aggravated by nimit ta karana. This may be because of

the selective discriminative of these organs to develop Prameha. As a

result of defective beeja when Prameha is developed, then the person is

cal led as a Jatha Pramehi pat ient. Jata Pramehi6 has been considered as

a Kulaja vikara7. Few diseases included under this category are Kusta,

Arsha, Meha, Kshaya etc. Kulaja vikaras means the diseases, which are

carr ied from the former generat ion to the successive generat ion, and they

are of the defects in the genetic code.

Nidana 38

2. Apatya nimittaja

Apathya is the main cause for the disease. Apathya includes both

ahara and vihara. Al l acharyas have stressed the indulgence of

unwholesome food and vihara in the production of Prameha. Ahara and

vihara that increases kapha, medas and mootra lead to the genesis of

Prameha.

Charaka explains the Nidana8 as Amla, Lavana, Madhura Rasa and

Guru, Snigdha guna dravyas, Curd, Milk, Mamsa rasa of aquatic animals,

Fresh cereals. Guda and Guda vikara.aharas and Sitt ing idle, Excessive

sleep, Disl ike for walking, act ivi t ies and to take bath are the viharas for

Madhumeha.

Sushruta explains the Nidana9 as Madhura Rasa, Medhya, Snigdha,

Sheeta guna dravyas. Nava anna, Wine, Meat of animals l iv ing in marshy

lands and Guda as aaharaj hetus. Laziness, Day sleep, inactiveness as

viharaja hetus of Madhumeha.

Vagbhata explains the Nidana10 as Madhura, Amla, Lavana Rasa,

Guru, Snigdha, Sheeta, Picchi la Guna dravyas, Nava anna, Madhya,

Anupa Mamsa, Ikshu rasa, Guda and Guda vikara, Dadhi, Paya as ahara

Nidana 39

and Sit t ing for long t ime, Sexual intercourse, Sleeping excessively as

viharaja Nidana for Madhumeha.

Charaka has explained the vishista nidanas, of Prameha according

to their doshas, they are as fol low.

Kaphaja prameha nidana11.

Aharaja.

The frequent and excessive use of newly harvested rice

(Hayanaka), Yavaka, Chanaka, Uddalaka, Naisadha, Itkata,

Mukundaka, Mahavrihi , Promodaka and Sugandhaka grains.

The use of new blackgram and other pulses

The f lesh of domestic, land and aquatic animals.

Sugarcane juice, or the abundant use of mi lk, curds, ghee or sweet

and unripe art ic les.

Viharaja:

Avoidance of cleanl iness and exercise, excess indulgence in

sleeping, ly ing or sedentary habits, and al l factors which are l ikely

to increase kapha, Medas and mootra

The special morbid factor of the humor is excessive f luidi ty of

kapha.

Nidana 40

Pittaja prameha nidana12.

Aharaja:

The habitual use of ushna, amla, lavana, kshara and katu art ic les.

Adhyashana, Vishama ahara.

Viharaja:

Teekshna santapa sevana, Sharma , Krodha, Anxiety.

Vataja prameha nidana13.

Aharaja

The habitual use of rooksha, kashaya, katu, t ikta, laghu and sheeta

art ic les.

Viharaja:

Adhika Vyavaya and Vyayama, Excessive use of panchakarmas.

Vegadharana, Exessive indulgence in fasting, Atapa, Udvega,

Shoka, Abighata.

Nidana 41

Aetiology according to Modern concept

The cause of hyperglycemia can be divided into Heredity and

Acquired14,15.

Heredity

Posit ive family history may be obtained in around 40 % of patients

with NIDDM (Non Insul in Dependent Diabetes Mell i tus). Genes

responsible for this heret ic carriage of the disease are one for insul in

(Chromosome 11) insul in receptor (Chromosome 19) and glucose

transporter (Chromosome 1). But a defini te association of any of these

genes with cl inical NIDDM is yet to be establ ished.

Acquired and environmental factors.

Analysis of epidemiological data leads to identi f ication of aging,

obesity, composit ion of diet, physical inact ivi ty, stress and urbanisation

as environmental predisposing factors for NIDDM.

Nidana 42

SAMPRAPTI

The suppress ion or the inc idence of the d isease is dependent

upon the resul t o f the var ia t ions in the et io log ica l factors (n idana) .

In tens i ty o f the morb id factors (doshas) and suscept ib i l i ty o f the body–

elements (dushyas) . I f these three factors , main ly the et io log ica l

factors etc . , do not mutual ly assoc iate or suppor t , or i f do so af ter a

long lapse of t ime, or in a very mi ld form, e i ther there occurs no

mani festat ion of the d isease at a l l or the d isease takes a long per iod to

evolve, or appears ambulatory form. Under the contrary condi t ions, i t

g ives cont rary resul ts . Thus the d i f ferent causes of the modes of

inc idence la id down are suppressed in a l l d iseases16.

The samprapt i o f a d isease expla ins the method or process by

which the v i t ia ted doshas reach wi th the dushyas and produce the

anatomica l and phys io log ical changes in the target organs leading to

the express ion as a d isease. In terms of Kr iyakalas, the samprapt i

deals wi th the chaya, prakopa, prasara and Sthana samsraya of the

d isease-causing doshas, which leads to the dosha-dushya

sammurchana i .e . , the in teract ion between d is turbed funct ional factors

wi th the bas ic s t ructura l ent i t ies of the body.

Nidana 43

Charaka had c lear ly expla ined the samprapt i o f the Kaphaja

Prameha in the Prameha Nidana. Even though the d isease Prameha is

s ta ted to be due to the v i t ia t ion of the t r i -doshas, the spec i f ic morbi f ic

factors of the humor is excess ive f lu id i ty o f Kapha. The specia l

features of the suscept ib le body e lements(dushyas) are excess iveness

and demin ished v iscousness of Medas, Mamsa, Body f lu id (sareera

k leda) , Sukra, Rakta, Vasa, Maj ja , Las ika, Rasa and Ojus17.

When there is the s imul taneous congress of these three

patholog ica l condi t ions, the kapha is suddenly provoked s ince i t is

a l ready in chaya s tage. The v i t ia ted kapha quick ly spreads throughout

the body which is a l ready in degenerated condi t ion. In the path of i ts

c i rcu la t ion the kapha f i rs t encounters and mixes wi th the medas, owing

to the patholog ica l changes in the medas, v iz . , excess iveness and

d imin ished v iscousness and a lso owing to the great s imi lar i ty o f the

qual i t ies between the kapha and medas. Due to th is combinat ion of

v i t ia ted kapha and medas, the la t ter is v i t ia ted. The v i t ia ted kapha

coupled wi th the v i t ia ted medas now comes in contact wi th the sareera

k leda and mamsa which are in excess ive increase in the body. The

v i t ia ted body f lu id is changed in to ur ine. The or i f ices or pores of the

mootravahasrotas, represented by the k idneys and b ladder are in a

s ta te of d i la ta t ion due to the act ions of v i t ia ted medas and sareera

Nidana 44

kleda. The v i t ia ted kapha, upon reaching the mootravahasrotasas,

gets local ised there and thus develops the d isease ca l led Prameha 18.

The sareera- k leda combined wi th the kapha and the medas whi le

be ing conver ted in to ur ine on i ts ent rance in to the mootrasaya,

acqui res the fo l lowing ten patholog ica l character is t ics of Kapha. They

are unctuousness, heav iness, sweetness, denseness and s lowness.

Then i t acqui res a spec ia l name accompanied wi th the qual i t ies of one

or more of the other condi t ions by which i t has been main ly modi f ied19.

The vit iated pitta produces Prameha by the same process as

described above20.

V i t ia ted Vata br ings about the mani festat ion of Vata ja Prameha

by the same process as descr ibed above. I f Vata by i ts rooksha qual i ty

changes the o jus which is natura l ly o f sweet taste, in to one of

ast r ingent taste and carr ies i t to the mootrasaya, then i t causes the

condi t ion ca l led Madhumeha21.

Charaka in Prameha Chik i tsa has expla ined the samprapt i in

br ie f 22. “ the Kapha, hav ing v i t ia ted the medas and mamsa dhatus and

the body f lu id , becomes loca l ised in the geni to-ur inary system and

causes Pramehas7 . The p i t ta, too, which is provoked by ushna dravyas

v i t ia t ing those very t issues, causes in the same manner o ther var ie t ies

Nidana 45

of Prameha. On the d iminut ion of the other two humors, the morb id

Vata draws in to the geni to – ur inary system the essent ia l dhatus, and

g ive r ise to the th i rd group of Pramehas. In every case the morb id

humor, hav ing reached the geni to-ur inary system, v i t ia tes the ur ine and

generates Pramehas corresponding to i ts spec i f ic nature” .

Sushruta has g iven more deta i ls about pathogenesis o f

Prameha 23. “ In a person who indulges in the mi thya ahara v ihara the

three doshas which are v i t ia ted and in an immature s tate jo in the

medas and t ravel to the mootrava srotas, gets loca l ised at the ent rance

of the vast i , when they are emi t ted through the urethra the d isease is

known as Prameha.

“The deranged kapha, in conjunct ion wi th the (morb id) p i t ta , vayu

and medas, g ives r ise to a l l kaphaja types of Prameha. The deranged

p i t ta , in conjunct ion wi th the deranged vayu, kapha, rakta and medas

produced the p i t ta ja ones; whi le the deranged vayu, in un ion wi th the

deranged kapha, p i t ta , medas, maj ja and vasa, engenders the types of

Vata ja Prameha” 24.

From the references c i ted above, the fo l lowing facts can be

e l ic i ted:

1 . The main dosha v i t ia ted in Prameha is kapha.

Nidana 46

2. But the other two doshas are a lso af fected and depending upon the

predominance of the s igns and symptoms of one par t icu lar

dosha, the d isease is named accord ing ly .

3 . The af fected dushyas are rasa, rakta, mamsa, medas, maj ja and

shukra. I t should be not iced that the asth i dhatu is not ment ioned

in the dushyas of th is d isease.

4 . In addi t ion shareera k leda, o jus, vasa and laseka are a lso af fected.

5 . Therefore i t is c lear ly understood that the dhatu par inama in

genera l is d is turbed.

6 . The v i t ia ted doshas get local ised in mootravaha srotas and d is turb

i ts normal funct ions, by d i la t ing i ts or f ices.

7 . The main s igns and symptoms v iz . Polyur ia and turb id i ty expresses

i tse l f the patholog ica l changes in the ur ine.v iz Mootravaha srotas

and vast i .

8 . The body- f lu id or shareera k leda is t ransformed in to a l iqu id mala

which is excreted as ur ine. S ince a l l the nut r ient e lements and

malas c i rcu la te a long wi th the rasarakta complex, i t is c lear that

there is a change in the composi t ion of the rasarakta complex.

9 . Because of th is change in the composi t ion of the rasarakta

complex, the d is turbance in the dhatu par inama can be eas i ly

understood.

Nidana 47

Charaka and vagbhata have descr ibed the pathogenesis of

Madhumeha as separate f rom Prameha. Vagbhata s tates that the

pathogenesis o f Madhumeha is o f two var ie t ies 25.

1 . The deplet ion of the dhatu leading to the v i t ia t ion of Vata

2. Obstruct ion to the normal c i rcu la t ion of Vata by the other doshas

leading to the v i t ia t ion of the former.

Th is par t icu lar in format ion leads us to inc lude that Madhumeha is

main ly due to the v i t ia t ion of Vata. Even accord ing to Charaka,

Madhumeha is enumerated as one of the Vata ja Pramehas. Vagbhata

has a lso s ta ted that any Prameha, i f not t reated and at tended to at the

outset , wi l l u l t imate ly develop in to Madhumeha. He has a lso c lear ly

s ta ted that there is an increase in the sweetness or sweet substances

in the body, which is expressed through the phys ica l qual i t ies of ur ine,

be ing the co lour and taste resembles honey 26.

A l l organs and par ts o f the body are made o f the i r u l t imate un i ts

or jeevaparamanus27. These innumerable jeevaparamanus or ce l ls o f

d i f ferent shareera avayavas are held together cemented to form

d i f ferent s t ructures and organs of the body. The substance that un i tes

and cements a ce l l w i th another for the format ion of var ious s t ructures

and organs is the in ter -ce l lu lar substance. By v i r tue of i ts v iscos i ty ,

smoothness, s l iminess and lubr icabi l i tuy, the in ter – ce l lu lar substance

Nidana 48

is cons idered s la ishmic in nature. Through th is in ter -ce l lu lar

substance pass the nut r ient mater ia l f rom capi l lar ies to ce l ls and the

metabol i tes pass in the reverse d i rect ion. In ter ference wi th i ts funct ion

leads u l t imate ly to the degenerat ion and decay of the ce l l and

consequent ly o f the s t ructures or dhatus of the body.

The physical and chemical characteristics of cell protoplasm in

general are parallel to those of the Kapha and the functions

ascribed to both are l ikewise. Therefore it can be seen that the

body structure including all the dhatus are completely made up of

kapha. Therefore kapha is that factor of the dosha-triad which not

only imparts strength to all dhatus but also prevents their decay and

degeneration28.

I f there is a disturbance in the nourishment of the cel ls, a

disturbance in the general dhatuparinama is surmised. Accordingly, there

can be a defic iency in the functions of kapha and also the sleshmika ojus

that is responsible for general immunity of the body.

The term kapha has been defined as “kapha the product of jala”29

and therefore there is no surprise to not ice that the body’s major

component is water. Since there is the vi t iat ion of kapha in Prameha, i t

can be easi ly understood the functions of shareera kleda or body-f luid.

Nidana 49

In the process of Ahara pachana the waste materials are separated

in two forms, one is l iquid and the another is sol id. The l iquid part is

absorbed from the kostha through the purishadharakala to be transformed

into urine and excreted through the mootrashaya30. The sara bhaga of

the food is ut i l ised by the respective dhatwagnis and the nutrients are

ut i l ised in the construct ion of the dhatus. This dhatwagni paka of

dhatuparinama also produces di f ferent ki t tas31. The ki t tas of the

dhatwagni paka which are ejected by cel ls wi l l natural ly enter into the

circulat ing rasa dhatu to be transported to their respect ive out lets. Since

i t has been stated that the shareera kleda, which is affected due to the

vi t iat ion of kapha, is changed into mootra32, i t is to be understood that

there is increased production of ki t ta bhaga in dhatwagni paka. I f there

is an increased product ion of ki t ta bhaga, i t can be easi ly summarised

that there is a decreased product ion of the prasadabhaga which is meant

for the construction of the dhatus or the organs of the body, leading to a

deficient repair and so degeneration of the body. The same thing has

been explained by the ancient scholars that in a Prameha patient, as

shareera saithi lyata.

The major port ion of the ki t ta bhaga, which is in a l iquid state, is

excreted by the mootravaha srotas. The normal function of mootravaha

srotas is to al low the ki t ta bhaga to pass through i ts pores and to prevent

the nutrient material from escaping out of the body. The vit iated kapha

upon reaching the mootravaha srotas gets local ised there and along with

Nidana 50

the vi t iated medas produces di latat ion of the pores of the mootravaha

srotas. Therefore, not only the substances that are to be excreted but

also some of the nutrient materials are also al lowed to pass through

these di lated pores.

According to Vagbhata, there is an increase in the sweetness or

sweet substances in the body of a Madhumeha pat ient33. This part icular

fact is noticed by the sweetness of the ur ine that can be observed and

recognised by attraction and assemblage of ants near the urine34. The

urine of a normal or healthy person is not sweet in taste. This sweetness

of the urine of a Madhumeha patient is due to the madhuradravya, which

is f i l tered by the mootravaha srotas from the rasarakta complex but could

not be reabsorbed completely during the paka or maturat ion of urine.

The madhuradravya is a natural component of the rasarakta

complex. Even though the ayurveda laid down that a person should

partake a food containing the six tastes, the major component of the

regular food is madhuradravya. Charaka considered cereals

(shukadhanya varga) as main source of food and the others l ike pulses,

legumes, meat, f ishes, frui ts, spices etc,. As support ing diet art ic les35.

The main const i tuent of al l cereals is carbohydrate, which are

madhuradravyas. Therefore the main product of the al imentary digestion

of these cereals to be absorbed into the blood is also a madhuradravya.

Nidana 51

Charaka also states that the madhurarasa confers bala or strength

on the Dhatus and ojus and that madhurarasa is compatible to the body36.

The madhurarasa therefore produces an increase in the body bulk i .e. i t

is the best in brimhanadravyas37. A substance which is having the

physiochemical qual i t ies / propert ies of Pridvhi and Ap is stated to be

Brimhana dravya38. I t should also be noted that substance of

madhurarasa is also having the qual i t ies of Pridhvi and Ap39. The Sharira

Bala is of two variet ies :

1) Vyayamashakti – the strength required to perform vigorous

physical work and

2) Vyadhikshamatwa shakti – the power to resist and overcome

forces or factors which bring about disease.

Vyayamashakti is dependent of wel l formed and i t confers the

Karmasadhana shakti on body. Vyadhikshamatwa is bestowed in the

normal functioning of Ojus, which is the essence of healthy Dhatus. Ojus

is also a madhuradravya. From the above the importance of the

madhuradravya for the nourishment and also strength of the body can be

clearly understood.

Nidana 52

Since i t is stated that the madhuradravya is excreted in the urine,

there can be only two causes for this excretion:

1) Excess of madhuradravya in the circulat ing rasarakta complex,

more than the amount required for the nourishment and strength

of the Dhatus and consequent overf lowing through mootravaha

srotases.

2) The increased release by the ori f ices of the mootravaha

srotases. I t has already been stated earl ier that these ori f ices of

the mootravaha srotases have been di lated due to the vi t iated

Tridoshas.

The dhatus of a Madhumeha pat ient are in a state of Saidhi lya40.

These indicate that the Dhatus are not being nourished in a proper

manner. But the madhuradravya, which is the main source of

nourishment and strength, is stated to be in excess in the Rasarakta

complex. I t is also a fact that al l the organs and parts of the body are

made up of their ul t imate units or Jeevaparamanus or cel ls. The

nourishment of these cel ls, which const i tute the Dhatus of the body, is

dependent upon the nutrients derived from the food freely entering into

them for their ut i l isation. I f there is an obstruction to the path or

entrance of these madhuradravyas into the cel ls, the Dhatus do not get

suff ic ient nutr i t ion and they’re by degenerate and decay. Because of this

obstruct ion entrance of the madhuradravyas into the cel l of the body

Nidana 53

interfered. There is an excess of such substances in the Rasarakta

complex developed in the body. The nourishment of the cel ls of the

dhatus is maintained by the ut i l isation of the respective nutrients by the

Dhatwagni. This dhatwagnipaka is possible only after the nutrients-

madhuradravya in this respect-enter the dhatus. Since there is an

obstruct ion to the entrance of the madhuradravya, the product of the

al imentary digest ion, into the Dhatus, we have to presume that there is a

deficiency in the function of the Bhutagnis.

Since the Dhatus are def iciently nourished due to the obstruction to

the entrance of the madhuradravya into the Dhatus, there wil l be deficient

formation and defect ive funct ioning of the Ojus, the essence of Dhatus.

Sushruta has already stated that Ojokshaya develops due to excessive

hunger41 – the hunger of the Dhatus for the madhuradravya in

Madhumeha patient. As stated earl ier, the vyadhikshamatwa of a person

is dependent on the normal functioning of the Ojus. Therefore in a

Madhumeha patient whose ojus is deficient ly formed, or vyadhikshamatwa

shakti is substandard. Therefore his body / dhatus are not capable of

resist ing the virulence of diseases especial ly of the Vaikarika krimi origin.

The Vaikarika krimi also thr ive to grow powerful in the presence of the

excessive madhuradravya. Not only the disease Madhumeha but also the

diseases due to vaikarika kr imis cause a hastening of the degeneration

and decay of the body.

Nidana 54

The important and ul t imate aim of a human being is to maintain the

l i fe as long as possible. Therefore when the madhuradravyas essential

for the maintenance of the l i fe are not al lowed to enter the Dhatus, the

body tr ies to deplete the store-houses of the madhuradravyas to be

ut i l ised by the body. In a healthy person, i f madhuradravyas are

consumed in excess of the requirement of the body, they are converted

into medas42,43.and stored for future use. Therefore, once the store-

house of the madhuradravyas are completely depleted, the medas and

other important dhatus (which contain protein mainly) are slowly

disintegrated for maintenance of l i fe. During this disintegrat ion of the

Dhatus which are mainly effected by the pachakamshas, the

products/metabol i tes, which are not capable of nourishing the body, some

t imes prove to be noxious producing several complicat ions l ike moorcha,

hr idgraha etc. One of the important condit ion due to this disintegrat ion of

medas is the dhatuja medovyapat with consequent development of

dhamaniprat ichaya44. Thus the knowledge of samprapti is important to

handle the Madhumeha patients.

Nidana 55

POORVARUPA

The prodormal symptomology of a disease has been described as

poorvaroopa. The knowledge of poorvaroopa has importance in early

management of patient and also in di f ferent ial diagnosis of disease so

that the disease is control led easi ly. The state of prodroma or poorvarupa

is expressed as when vi t iated doshas become local ised due to

srotovaigunya leading to the dosha-dushya-sammurchana. Kapha

predominant tr idoshas and dhatus along with ojus are chief ly effected in

Prameha. Thus poorvaroopa are very much varied in nature.

The fol lowing are the prodroma of Prameha.

1. Burning sensation of the palms of hands and the soles of the feet45,46,47.

2. Dryness in the mouth, palate and throat and thirst48.

3. Heaviness of the body49.

4. Coldness or sl iminess of the skin and l imbs, thermalgia and

numbness in the body50.

5. Smell l ike raw-meet in the body51.

6. Somnolence and continuous torpor and lassitude52.

7. Sweet taste in the mouth53,54.

8. Sl imy mucous deposit on the tongue, palate, pharynx and teeth55.

9. Increased excrement in the body, increased discharge from the

ori f ices in the body56,57.

Nidana 56

10. Sweetness and whiteness of urine58.

11. Attract ion of insects and ants to the body and urine59.

12. Matt ing of the hair and inordinate growth of the f inger and toe

nai ls60,61.

13. A bad smell ing breath and shortness of breath62.

Vagbhata has mentioned some more addit ional prodroma for Prameha.

1. Excessive perspirat ion63.

2. Laziness64.

3. Liking of cold comforts65.

From the above prodroma i t can be clearly seen that there is an

increased production of ki t ta bhaga in dhatu parinama as explained

earl ier.

Nidana 57

ROOPA

In the Roopa or actual manifestation of the disease, dosha dushya

sammurchana completes, and the onset of the disease wi l l be

commenced. The roopas may change from time to t ime and certain

symptoms may newly appear or some may disappear. Roopa is the

prominent diagnostic key, hence the knowledge of the various lakshanas

disease is essential for the benefi t of prognosis.

Cl inical features of the present disease Madhumeha are divided

into two groups

1. General features of Prameha

2. Special features of the Madhumeha.

Charaka has not described the general features of Prameha where

as Sushruta66 and Vagbhata67 have described the general features as

a. Avi la mootrata

b. Prabhoota mootrata.

Nidana 58

Specif ic Lakshanas of Madhumeha.

I t is one of the four Vataja Pramehas. The person with Madhumeha

passes urine which is astr ingent and sweet in taste, yel lowish or whit ish

in colour. The urine contains simi lar propert ies of Honey68,69,70.

Apart from the above lakshanas, Sushruta described typical lakshanas

for Madhumeha rogi71, that he desires –

1. To stay whi le walking.

2. To si t whi le staying

3. To take rest on bed whi le si t t ing

4. To go to sleep whi le taking rest.

Nidana 59

BHEDHA

Though Prameha is stated to be developed due to the vi t iat ion of

al l three doshas, the disease is mainly divided into three groups.

1. kaphaja Pramehas - which are again subdivided into 10 types72.

2. Pit taja Pramehas - which are again subdivided into 6 types73.

3. Vataja Pramehas - which are again subdivided into 4 types74.

Even though the three Ayurveda authori t ies Charaka, Sushruta and

Vagbhata agree the same number of Prameha in each group, there seems

to be di f ference in the nomenclature used by them. Increased quanti ty of

ur ine and increased turbidi ty in the urine are the main symptom in al l

Pramehas.

The name of each variety of Prameha is decided according to the

combinat ion of dosha and dushya, and the physical character

resemblance to the urine.

Nidana 60

kaphaja Pramehas according to Brihatrayees are

Charaka75 Sushruta76 Vagbhata77

Udaka Meha78 Udaka Meha79 Udaka Meha80

Ikshu Meha81 Ikshu Meha82 Ikshu Meha83

Sikata Meha84 Sikata Meha85 Sikata Meha86

Sanair Meha87 Sanair Meha88 Sanair Meha89

Sandra Meha90 Sandra Meha91 Sandra Meha92

Sukra Meha 93 Sukra Meha94 Sukra Meha95

Sandra prasad meha96 --- ---

Shukla Meha97 Pishta Meha98 Pishta Meha99

Sheeta Meha100 --- Sheeta Meha101

Alala Meha102 --- Alala Meha103

--- Sura Meha104 Sura

Meha105

--- Lavana Meha106 Lavana Meha107

--- Phena Meha108 ---

I t is not iced that there is a resemblance in the symptoms of

sandra prasada meha of Charaka and Sura meha of Vagbhata.

Nidana 61

Pit taja Pramehas according to Brihetraye

Charaka109 Sushruta110 Vagbhata111

Kshara Meha Kshara Meha Kshara Meha

Kala Meha --- Kala Meha

Neela Meha Neela Meha Neela Meha

Lohita Meha Shonita Meha Rakta Meha

Manj ishta Meha Manj ishta Meha Manj ista Meha

Haridra Meha Haridra Meha Haridra Meha

--- Amla Meha ---

There is resemblance in the symptoms of Lohita meha of charaka and

Shonitha meha and Rakta meha of Sushruta and Vagbhata respectively.

Vataja Pramehas according to Brihatraye

Charaka112 Sushruta113 Vagbhata114

Vasa Meha Vasa Meha Vasa Meha

Majja Meha --- Maj ja Meha

Hasti Meha Hasti Meha Hasti Meha

Madhu Meha Kshoudra Meha Madhu Meha

--- Sarpir Meha ---

There is a resemblance in the symptoms of Maj ja meha of Charaka

and the Sarpir meha of Sushruta.

Nidana 62

It is evident form the above table that Vagbhata closely fol lows

Charaka whi le Sushruta had a sl ight di f ferences.

MADHUMEHA:

Madhumeha can be sub classif ied mainly into two types.

Type one a) Kulaja or Sahaja (Hereditary)

b) Doshaja or Apathya nimit taja ( acquired)

Type two a) Dhatu kshaya janya Madhumeha115

b) Doshavruta janya Madhumeha

Charaka has divided the Madhumeha pat ients into two veri t ies basing

on the l ine of treatment aspect116.

1. Sthoola (stout or strong)

2. Krisha (emaciated or week)

Sushruta accepts Sahaja rogi as krisha and the Apathya nimitaaja rogi

as sthoola rogi in his classif icat ion.

.

Nidana 63

SADHYASADHYATA

As discussed earl ier, Prameha is classif ied in to three veriet ies i .e.

1. Kaphaja Pramehas - 10

2. Pittaja Pramehas - 6

3. Vataja Pramehas - 4

The ten kaphaja Pramehas are said to be sadhya (curable)117,118. Because

a. The medas having homogenous propert ies is effected

b. The kapha is dominant

c. Both these factors are amendable to the same type of treatment.

The six pit taja Pramehas are only Yapya (pal l iable )119,120 owing to the

proximity of the seat of the vi t iated doshas and that of the Medas and

owing to the antagonism involved in their treatment.

The four variet ies of Vataja Prameha due to the vi t iat ion of Vata

are known to be incurable121,122 because of their seriousness and also

because of the contradict ion involved in their treatment.

Vagbhata adds to the above :

a. The kaphaja and Pit taja groups of Prameha i f they are

developed after ful l expression of prodroma to are incurable123.

Nidana 64

b. Kaphaja Pramehas gradual ly develops into pi t taja Pramehas and

they both transforms into Vataja Pramehas that are incurable.

c. I f kaphaja Pramehas gradual ly turns into pi t taja Pramehas these

are yapya.

d. Even the pit taja Pramehas are curable i f there is no severe

vi t iat ion of medas124, even this is appl icable for Vataja mehas.

Charaka has stated that this disease is relapsing in nature.

Though certain varieties are stated to be curable they appear to be

so only for certain period and relapse is definite.

Madhumeha, which is a veri ty of Vataja Prameha, is also to be

considered, as incurable but with specif ic l ine of treatment these can be

pal l iable.

Jata pramehi or Beeja doshaja are incurable due to leenata of dosha

and as they themselves makes inf luence of prakrit i of pat ient.

Sushruta stated that i f Prameha patient suffering with pidikas and

complicat ions l ike Hridgraha, then he should be considered as

incurable125.

Interestingly Basavrajeeyum 16t h century Ayurvedic text from Andra

pradesh, has mentioned a test for urine to know the prognosis of each

dosha group. The urine of a Prameha patient has to be col lected in a

wide mouthed vessel and boi led on a mild f lame t i l l evaporat ion. The

incurabi l i ty of the disease depends upon the amount of residue. A Vataja

Nidana 65

Prameha is considered incurable i f the residue is 1/5t h of the volume of

ur ine taken for the test. Pittaja Prameha is incurable i f the residue is

1/7t h and kaphaja Prameha is incurable i f the residue is 1/9t h of the

volume of ur ine in the test126.

Nidana 66

VYAVACHEDAKA NIDANA

I t was stated that cordinal signs of Madhumeha are

Bahumootrata and Avilamootrata127. The bahumootrata is noticed as

a symptom in many diseases. But the combination of bahumootrata

and Avilamootrata is noticed in Prameha only.

Urine is stated to be Madhura in the fol lowing variet ies of

Pramehas.

Ikshumeha128 – Due to kapha the patients pass the urine which is

sweet, cold, st icky and l ike a sugarcane juice.

Sheetha meha129 - Due to kapha the patient passes the urine which is

cold, sweet and frequency of the urination is increased.

Madhumeha130 - Due to Vata prokopa urine of the patient wi l l be

kashya, madhura, pandu and ruksha.

The chief physical qual i t ies of the urine of Madhumeha patient are

the colour and the taste resembling honey. Sushruta stated that a pat ient

who is suffer ing from pidikas, hridgraha, and other complicat ions in

addit ion to the other characterist ics of ur ine should be considered as

Madhumeha patient.

Nidana 67

Vagbhata stated that mootra madhuryata is not diagnost ic lakshana

of Madhumeha, but i f the patient is having shareera madhuryata, then i t

is considered as Madhumeha131. I t is observed that the urine and body are

attracted by the ants. No specif ic test for the Madhumeha patient has not

been ascribed in any Ayurvedic classics. Here the attract ion of ants to

the body is an indicat ion of the presence of the madhuryata in the body

i .e. Rasa and Rakta. Since these two dhatus exist in the superf ic ial parts

of the body in abundance as such the ants are natural ly attracted towards

twak. The madhuryata corresponds to the raised blood sugar levels in

Madhumeha (diabetes mell i tus).

Nidana 68

UPADRAVA

Upadrava is a disease produced after the manifestation of the

original disease and depends on this disease irrespective of whether

upadrava is major or minor132. After the occurrence of the original

disease the dosha or doshas are further vi t iated owing to abnormal

ahara, vihar etc., thus leading to a secondary disease or complicat ion

which is known as an upadrava.

If al l the Pramehas are not treated properly and attended, they

may ult imately develop into Madhumeha. Madhumeha is considered

to be one of the 20 Pramehas by Charaka. Apart form this Charaka

has described the upadravas of Prameha in general. Where as

Sushruta and Vagbhata have mentioned upadravas separately for

each doshic group.

The general upadravas of Pramehas according to Charaka are

as fol lows133. Trishna, Atisara, Jwara, Daha, Dourabalya,

Arochaka, Avipaka, Puti mamsa, Pidika , Alaji, Vidradhi.

Charaka mentioned the upadravas (complications) of

Madhumeha as134 Trishna, Shwasa, Mamsa kotha, Moha, Hikka,

Mada, Jwara, Visarpa among them many of upadravas are seen in

patients, they have been explained under the heading of

observation.

Nidana 69

References 1 Charaka Nidana 4 / 44

2 Ibid 4 / 5

3 Ibid 4 / 5

4 Sushruta Nidana 6 / 30

5 Chakrapani on Ch su 3 / 17

6 Charaka Chiki tsa 6 / 57

7 Ibid 6 / 57

8 Charaka Nidana 4 / 5

9 Sushruta Nidana 6 / 3

10 Astanga Sangraha Nidana 10 / 3

11 Charaka Nidana 4 / 5

12 Ibid 4 / 23

13 Ibid 4 / 36

14 API Text Book of Medicine. pp 205

15 Josl in’s Diabetes Mell i tus pp 240 16 Charaka Nidana 4 / 4

17 Ibid 4 / 7

18 Ibid 4 / 8

19 Ibid 4 / 9

20 Ibid 4 / 5

21 Ibid 4 / 37

Nidana 70

22 Charaka Chiki tsa 6 / 5,6

23 Sushruta Nidana 6 / 4

24 Ibid 6 / 4

25 Astanga hridhya Nidana 10 / 8

26 Ibid 10 / 8

27 Chharaka Shareera 7 / 17

28 Diabetes and treatment by VVS Sastri pp18

29 Sabdastoma Mahanidhi

30 Astanga hridhya sutra 3 / 61

31 Chakrapani on Ch Chi 15 / 15

32 Charaka Nidana 4 / 8

33 Astanga hridhya Nidana 10 / 20,21

34 Charaka Nidana 4 / 47

35 Charaka sutra 27 / 28

36 Ibid 26 / 43

37 Asthanga hridhaya sutra 10 / 7,8

38 Hemadri on Ah su 14 / 3

39 Astanga Hridhaya sutra 10 / 1

40 Charaka Nidana 4 / 8

41 Sushruta Sutra 15 / 23

42 Charaka sutra 26 / 43

Nidana 71

43 Astanga Hridhya sutra 10 / 9

44 Dhamanipratichaya by VVS Sastr i .pp 69

45 Sushruta Nidana 6 / 5

46 Charaka Nidana 4 / 47 47 Astanga Sangraha Nidana 10 / 7 48 Sushruta Nidana 6 / 5

49 Ibid 6 / 5

50 Charaka Nidana 4 / 47

51 Ibid 4 / 47

52 Ibid 4 / 47

53 Ibid 4 / 47

54 Astanga Sangraha Nidana 10 / 7 55 Sushruta Nidana 6 / 5

56 Charaka Nidana 4 / 47

57 Astanga Sangraha Nidana 10 / 7 58 Sushruta Nidana 6 / 5

59 Charaka Nidana 4 / 47

60 Sushruta Nidana 6 / 5

61 Charaka Nidana 4 / 47 62 Sushruta Nidana 6 / 5

63 Astanga Sangraha Nidana 10 / 7

64 Ibid 10 / 7

65 Ibid 10 / 7

Nidana 72

66 Sushruta Nidana 6 / 6

67 Astanga Hridhya Nidana 10 / 7

68 Astanga Sangraha Nidana 10 / 8

69 Charaka Nidana 4 / 44 70 Sushruta Nidana 6 / 14 71 Sushruta Nidana 6 / 28

72 Charaka Nidana 4 / 11

73 Ibid 4 / 24

74 Ibid 4 / 38

75 Ibid 4 / 4

76 Sushruta Nidana 6 / 5

77 Astanga Sangraha Nidana 10 / 8

78 Charaka Nidana 4 / 13

79 Sushruta Nidana 6 / 12

80 Astanga Sangraha Nidana 10 / 8

81 Charaka Nidana 4 / 14

82 Sushruta Nidana 6 / 12

83 Astanga Sangraha Nidana 10 / 8

84 Charaka Nidana 4 / 20

85 Sushruta Nidana 6 / 12

86 Astanga Sangraha Nidana 10 / 8

87 Charaka Nidana 4 / 21

88 Sushruta Nidana 6 / 12

Nidana 73

89 Astanga Sangraha Nidana 10 / 8

90 Charaka Nidana 4 / 15

91 Sushruta Nidana 6 / 12

92 Astanga Sangraha Nidana 10 / 8

93 Charaka Nidana 4 / 18

94 Sushruta Nidana 6 / 12

95 Astanga Sangraha Nidana 10 / 8

96 Charaka Nidana 4 / 16

97 Ibid 4 / 17

98 Sushruta Nidana 6 / 12

99 Astanga Sangraha Nidana 10 / 8

100 Charaka Nidana 4 / 19

101 Astanga Sangraha Nidana 10 / 8

102 Charaka Nidana 4 / 22

103 Astanga Sangraha Nidana 10 / 8

104 Sushruta Nidana 6 / 12

105 Astanga Sangraha Nidana 10 / 8

106 Sushruta Nidana 6 / 12

107 Astanga Sangraha Nidana 10 / 8

108 Sushruta Nidana 6 / 12

109 Charaka Nidana 4 / 18

110 Sushruta Nidana 6 / 13

111 Astanga Sangraha Nidana 10 / 8

Nidana 74

112 Charaka Nidana 4 / 28

113 Sushruta Nidana 6 / 41

114 Astanga Sangraha 10 / 8

115 Astanga hridhya Nidana 10 / 18

116 Charaka Chikitsa 6 / 15

117 Ibid 6 / 7

118 Sangraha Nidana 10 / 5 119 Astanga Sangraha Nidana 10 / 5

120 Charaka Nidana 4 / 27 121 Astanga Sangraha Nidana 10 / 5

122 Charaka Nidana 4 / 38 123 Astanga Sangraha Nidana 10 / 41

124 Astanga Sangraha Nidana 10 / 17

125 Sushruta Nidana 6 / 27

126 Basavarajeeyam 9 / 30

127 Astanga hridhya Nidana 10 / 7

128 Charaka Nidana 4 / 14

129 Ibid 4 / 19

130 Ibid 4 / 44

131 Astanga hridhya Nidana 10 / 21

132 Charaka Chikitsa 21 / 40 133 Charaka Nidana 4 / 42 134 Charaka sutra 17 / 109

Drug Review 72

The treatment of Madhumeha with herbal drugs is wel l known

since the t ime of Charaka and Sushruta. Even today the herbal drugs

carry equal importance because of their effect ive and safe action. The

fol lowing drugs are selected for the tr ial after keenly observing the

pathophysiology of the disease according to Modern and Ayurvedic

science. Propert ies and act ions of Madhunashini , Bringaraj,

Bhumyamalaki and Eranda when combined, are found very much

suitable for treat ing Madhumeha. Al l these drugs are abundantly

avai lable and very effect ive. As Madhumeha is asadhya i t can be made

yapya with proper and continues treatment, patients have to consume

the drug for long periods, thus an economical and effective remedy

can be offered for the patients suffering from Madhumeha.

Individual drug used in Bhumyamalakyadi churna is explained

below.

Drug Review 73

MADHUNASANI1,2,3

Sanskri t - Madhunasani

Hindi - Gudamar

Kannada - kadachigana bal l i

Engl ish - Smal l Indian Ipecacuanha

Latin - Gymnema sylvestre

Family - Asclepiadaceae

Synonyms4 - Anyada, Chakrashreni, Meshashrangi, Meshaval l i ,

Sarpadanshtr ika.

Distribution5 -

A cl imbing plant common in Central and Southern India, on the

Western Ghats and in the Goa terri tory.

Parts used -

Dr ied panchanga of the plant is used.

Brief description6 -

A large woody much-branched cl imber running over the tops of

high trees. Leaves 3.2–5 by 1.3–3.2 cm., ovate, el l ipt ic. Base

rounded, petioles 6–13 mm. Long, pubescent. Flowers in pedunculate,

densely pubescent, shorter than the petioles, pedicels 3 – 13 mm long,

corol la yel low, 4 –5 mm.. fol l ic les 6.3 – 7.5 by 0.8 cm., trerete, r igid.

Seeds 1.3cm long, narrowly ovoid, f lat with a thin broad marginal wing,

brown, glabrous.

Drug Review 74

Pharmacological properties7 –

Guna – Laghu, Ruksha.

Rasa – Kashaya, t ikta.

Vipaka – Katu.

Veerya – Ushna.

Doshaghnata – Kapha vata hara.

Chemical composition –

Gymnemic acid, Quercitol , calcium oxalate, carbonic acid,

Phosphoric acid, Ferr ic oxide, Manganese, some tartar ic acid etc.

The sweetness - suppressing polypeptide gurmarin isolated

form the leaves consists of 35 amino acid residues including three

intramolecular disulf ide bonds. Herein, the total chemical synthesis of

grumarin was done and gurmarin being 1.9% based on the start ing

amino acid resin8.

The sweetness - suppressing polypeptide gurmarin has been

isolated form the leaves of Gymnema sylvestre and consists of 35

amino acid residues including three intramolecular disulf ide bonds.

The primary structure has already been determined. The posi t ions of

the disulf ide bonds were located, by a combinat ion of mass

spectrometr ic analysis and swquencing of cystine-containing peptides

obtained bythermolysin – catalyzed hydrolysis of grumarin to be cys3-

cys18, cys10-cts23, and cys17- csy339.

Drug Review 75

Actions concerned to disease –

The powdered leaves were found to have an oxidise act ion on

glucose solut ion and glycolysis occurred which reduced the strength of

the glucose solut ion from 2.3 to 0.66 % in 29 hours10. Drug acts

indirect ly through stimulation in insul in secretion of the pancreas, as i t

has no direct action on the carbohydrate metabol ism11.

Destroys glycosuria and other urinary disorders12.

The leaves cause hypoglycemia which sets in soon after the

administrat ion of the drug whether by mouth or by inject ion, lasts for a

variable t ime, is not necessari ly proport ionate to the dose and in never

excessive. They do not contain any water soluble or alcohol soluble

substance which destroys glucose in vi tro; nor do they yield any

chemical body resembling insul in. The drug has no direct act ion in

carbohydrate metabol ism, and acts indirect ly through st imulation of

insul in secret ion of the pancreas.

Kapha medo hara, Meha hara, sarva Meha hara13,

Extracts of gymnemic acids, which wre taken form gymnema

sylverstre ware tested for their act ion on blood glucose. The

conclusion of the study was gymnemic acids suppress the elevat ion of

blood glucose level by inhibi t ing glucose uptake in the intestine14.

Drug Review 76

Gymnemic acid inhibi tes smooth muscle from uptaking the

glucose, which is the energy source of the muscle15.

Intravenous injection of gurmarin did not cause any signif icant

effect on taste responses at al l . These results suggest that gurmarin

acts on the apical side of the taste cel l . Possibly by binding to the

sweet taste receptor protein16.

Drug Review 77

BHRINGARAJ17, 18,19

Sanskri t - BRINGARAJ

Hindi - Bringra

Kannada - kadiggaraga

Latin - Ecl ipta alba Hassk.

Family - Compositae20

Synonyms - Angaraka, Bhringa, Ekaraja, Ni lapushpa, Shyamala.

Distribtuion21 -

Bangal, Burma, Malay peninsula, Central India, Punjab,

W.Rajputana, Peninsular India, Ceylon. (IMP 1361)

Parts used - Dried panchanga of the plant is used.

Brief discription22 -

I t is annual, erect or prostrate, branched. Oftern rooting at the

nodes; stem and branches str igose with appressed white hairs.

Leaves are sessile, 2.5 – 7.5 cm. Long, variable in breadth, usual ly

oblong – lanceolate, subentire, acute or sub acute, sparsely str igose

with appressed hairs on both sides, base tapering. Flower Heads are 6

– 8 mm. Diam., soli tary or two together on unequal axi l lary peduncles.

Ray f lowers are l igulate, l igule smal l, spreading, white. Disk f lowers

are tubular, corol las often 4 toothed. Achenes cuneate, compressed

and with a narrow wing.

Drug Review 78

Pharmacological properties23 –

Guna – Laghu, Ruksha.

Rasa – katu, t ikta.

Vipaka – katu.

Veerya – ushna.

Doshaghnata – kapha vata shamak.

Chemical composition24 –

Alkaloid ecl ipt ine, Resin, Ecl ipt ine, Wedelolactone,

Actions concerned to disease –

Pr incipal ly used in Liver enlargements, used in jaundice,

scalding of urine25,Used in derangement’s of the l iver26

Drug Review 79

BHUMYAMALAKI27,28,29

Sanskrit - BHUMYAMALAKI

Hindhi - Bhuie amla

Kannada - Guggri kasa

Latin - Phyl lanthus urinaria Linn.

Family - Euphorbiaceae.

Synonyms30 - Hajata, Bahupatra, Bahuphala, Charat i

Dalasparshini .

Distribtuion31 -

Tropics general ly, al l over India.

Parts used -

Dried panchanga of the plant is used.

Brief discription32 -

Annual, 30 – 60 cm high, glabrous, Stems erect, s l ightly

branched; leaf bearing branchlets short, f lat tened or sl ight ly winged.

Leaves closely placed, sessi le, 6 – 13 by 2.5 – 6 mm, oblong,

rounded, apiculate at the apex, pale beneath, glabrous, base rounded,

st ipules pelate, very acute,. Flowers minute, axi l lary, sol i tary,

yel lowish. Sepals 0.8 – 1 mm. Long, oblong. Rounded, not enlarged in

frui t . Capsules 3 mm. Diam., globose, scarcely lobed, echinate.

Seeds 1.5 mm. Long, 3 – gonous, rounded on the back, transversely

furrowed. ( imp 2223)

Drug Review 80

Pharmacological properties33 –

Guna – Laghu, Ruksha.

Rasa – kashaya, t ikta, Madhura.

Vipaka –. Madhura.

Veerya – Sheeta.

Doshaghnata – Kapha Pit ta shamak. (DGV 640)

Chemical composition34 –

Acrid, sour, cooling, bit ter, sweetish; alexipharmic components

are present

Actions concerned to disease –

Useful in thirst, urinary discharges35. in jaundice36,and i t is l iver

st imulant, thrust control ler37, i t is best for urinary disorders especial ly

Prameha, controls Daha38

Drug Review 81

ERANDA39,40,41

Sanskri t - ERANDA

Hindhi - Endi

Kannada - Audala

Latin - Ricinus communis Linn.

Family - Euphorbiaceae.

Synonyms42 - Gandharva hasthah, Panchangulam, Vatari ,

Eranda.

Distribution43 -

This plant is common and quite wi ld in the jungles in India, I t is

cult ivated throughout India, chiefly in the Tamil nadu, Bengal and

Maharastra Presidencies. And also widely cult ivated in tropical

countries.

Part used -

Leaves.

Brief description44 -

Eranda is eka varshika or bahuvarshayu gulma or vr ikshaka

which grows up to 17feet. Leaves are green 30 – 60 cm in diameter

with 5 – 10 projections. leaf stem wil l be 4 – 12 inch long and tublar.

Flowers are unisexual, male f lowers are above and the females are

Drug Review 82

below in the plant. Frui t is thorny and 1 – 3 cms in diameter. Seeds

are oval, shiny, mult icolored and hard, which yields oi l .

Pharmacological properties45 –

Guna – Snigdha, Tikshna, Sukshma.

Rasa – kashaya, Madhura.

Vipaka –. Madhura.

Veerya – Ushna.

Doshaghnata – Kapha vata shamak.

Chemical composition46 –

Fixed oi l 45 to 52 %, Ricinine, proteins 20 pc., starch, mucilage,

and ash 10pc.,

Actions concerned to disease –

Leaves are useful in “vata” and “kapha” diseases, used in l iver

troubles47, especial ly enlarged Liver and Mutravishodaka48,

Drug Review 83

REFERENCE

1 The Indian Materia medica pp 596 2 Indian Medicinal Plants pp 1625 3 Bhava prakasha Guduchadi verga pp 443 4 Indian Medicinal Plants pp 1627 5 Indian Medicinal Plants pp 1625 6 Indian Medicinal Plants pp 1625 7 Bhava prakasha pp 444 8 by Tonosaki K at Central Reseach Laborator ies, Aj inomoto Co., Inc.

Kawasaki, Japan. In 1996 9 by Ota M at Central Research Laboratories Aj inomoto Co , Inc,

Kawasaki, Japan in 1995 10 The Indian Materia medica pp 598 11 The Indian Materia medica pp 598 12 The Indian Materia medica pp 598 13 Sushruta Sutrasthana 38 / 13, 74 14 by Tanaka K at Division of veterinary pharmacology, Nippon veterinary and

animal science university, Tokyo. Japan. In 1997 15 by Nakajyo S at Division of veterinary pharmacology, Nippon veterinary and

animal science university, Tokyo. Japan. In 1996 16 by Imoto T at Department of physiology, Faculty of Medicine, Tottor i

University, Yonago, Japan. In 1995 17 The Indian Materica Medica pp 469 18 Indian Medicinal Plants pp 1361 19 Bhava Prakasha, Gudchadi varga – pp 429 20 Indian Medicinal Plants pp 1363 21 Indian Medicinal Plants pp 1361 22 Indian Medicinal Plants pp 1361 23 Bhava Prakasha, Gudchadi varga – pp 430 24 The Indian Materica Medica pp 469 25 Indian Medicinal Plants pp 1361 26 The Indian Materica Medica pp 469 27 Indian Medicinal Plants pp 2223

Drug Review 84

28 The Indian Materica Medica pp 949 29 Bhava Prakasha, Gudchadi varga – pp 460 30 Indian Medicinal Plants pp 2223 31 Indian Medicinal Plants pp 2223 32 Indian Medicinal Plants pp 2223 33 Bhava Prakasha, Gudchadi varga – pp 460 34 Indian Medicinal Plants pp 2223 35 Indian Medicinal Plants pp 2223 36 The Indian Materica Medica pp 949 37 Bhava Prakasha, Gudchadi varga – pp 460 38 Raja Niguntu pp 263 39 Bhava Prakasha, Gudchadi varga – pp 299 40 The Indian Materica Medica pp1065 41 Indian Medicinal Plants pp 2275 42 The Indian Materica Medica pp1065 43 The Indian Materica Medica pp1065 44 The Indian Materica Medica pp1065 45 Bhava Prakasha, Gudchadi varga – pp 299 46 The Indian Materica Medica pp1065 47 Indian Medicinal Plants pp 2275 48 Bhava Prakasha, Gudchadi varga – pp 299

Chikitsa 69

The term Chiki tsa is derived form the root “KIT ROGAPANAYANE”1.

According to Amaarkosha Chikitsa is Ruk Pratikr iya. Chikitsa is the

process by which the doshas and dhatus are brought into normalcy.

Madhumeha is a chronic relapsing disease and may also develop as a

hereditary disease. Madhumeha patients are divided in two variet ies.

1. Sthula and 2. Krisa

Sthula patients are capable of withstanding the shodhana karma and

the krisa patients are incapable of withstanding i t . Therefore a sthula

patient has to be treated with the sodhana chiki tsa and drisha with

pal iat ive treatment.

For every Shodhana chiki tsa the pat ient should undergo poorva

karma. But the Madhumeha patient is prohibi ted from undergoing sweda

karma 3. In sthula patient after complet ion of sneha karma the doshas

should be el iminated by urdhava and adhosodhana as Vamana and

Virechana respect ively.

After the completion of the Sodhana karma the pat ient has to be

subjected for samsarjana krama. Even though the madhumeha is

santarpana janya roga, the pat ient should not be subjected to Apatarpana

kriya, because i t may result in to Gulma, Kshaya, Mehana shoola, vasti

Chikitsa 70

shoola and Mootra graha. The Brimhana chiki tsa should be carried out

considering the strength of the jataragni of the individual pat ient4. A krisa

or emaciated, and Durbala or weak pat ient who is not capable of

withstanding the shodhana karma requires Bhrimhana chiki tsa5.

Even though the vataja Pramehas are stated to be incurable the duty

of physician is to treat the pat ient and prevent the future complicat ions.

Therefore vataja Prameha should be treated.

SHAMSAMANA CHIKITSA

Shamana chiki tsa is indicated for a Prameha patient who is not

el igible for shodhana chiki tsa, and also the patient who has completed the

shodana karma.

Many variet ies of decoctions, choornas and lehyas have been

described for the treatment of the twenty variet ies of Pramehas by al l

Ayurvedic authori t ies. Vyayam, udvarthana, snana, jala sechana and the

lepas with Twak, Ela, Agar and chandana are useful in Prameha patient6.

Avoiding the causative factors (Nidana) is also a treatment7. In our

tr ial we have used only shamana therapy, which has yield a very

signif icant result.

Chikitsa 71

The pat ient of prameha who is not f i t for evacuation should be

subjected to pacif icatory management for al leviat ion of the disease such

as mantha (churned drink), extracts, l inctus made of barley powder and

l ight edibles. He should eat rough food art ic les such as boi led barley,

barley cakes, f lour of parched grains and apupa with palatable meat -

soup of wi ld birds part icularly gal l inaceous and peckers. He should take

old shal i r ice with soup of mudga etc. and bit ter vegetables added with oi l

of dant i and ingudi or l inseed and mustard. In cereals, he should use

shashtika and wi ld r ice. The diet of the patient of prameha should consist

mainly of barley. One suffering form kaphaja prameha should eat various

preparat ions of barley added with honey. Barley grain dipped in decoction

of tr iphala for the whole night make a saturat ing food taken with honey.

The patient may also take them regularly mixed with vinegar for al leviat ion

of Prameha. He should use f lour of parched grains, bolus, parched grains

and other various edibles made of barley impregnated with deccoctions of

durgs prescribed in kaphaja prameha. Various preparat ions of barley

mixed with the meat of ass, horse, bul l , swan and spotted deer should be

prescribed. The seeds of bamboo and wheat may also be used in forms

simi lar to those of barley8.

Chikitsa 72

REFERENCE

1 Shabda Sthoma Mahanidhi

3 Charaka Sutra 14 / 16

4 Charaka Chikitsa 6 / 16,17

5 Ibid 6 / 15

6 Ibid 6 / 48

7 Ibid 6 / 51

8 Ibid 6 / 18 – 24.

Materials & Methods 83

MATERIAL AND METHODS

Materials -

a. Materials for literary search.

Literary search is done from classical Ayurvedic texts, Modern

texts, Medlar search and updated through journals.

b. Materials for clinical study.

Bhumyamalakyadi churna, composed of

Madhunashini

Eranda

Bhumyamalaki

Bhringaraj

is taken for the cl inical tr ial .

Collection of Drugs: -

Al l the drugs were personally col lected from Kapat hi l ls, and were

conf irmed their identi ty by the Botanist.

Method of Preparation: -

Panchangas of above said drugs were cleaned thoroughly by

running water to take out physical impuri t ies and dried in the shade. The

dried herbs were powdered separately in the pulval iser to get a f ine

powder.

Materials & Methods 84

Again the wet drugs are col lected, to extract swarasa, which is

ut i l ised for giving bhavana to the corresponding herb powders to increase

their potency. These powders are mixed in proport ions and f i l led in

500mg capsules for easy palatabi l i ty for the patient.

CLINICAL TRIAL

Methods :

Selection of Sample

Pat ients suffer ing from Madhumeha are selected from the

Post Graduate And Research Centre OPD/IPD of D.G.M. Ayurvedic

Col lege Hospital and medical camp organised exclusively for

Madhumeha patients at Post Graduate And Research Centre of

D.G.M. Ayurvedic col lege Hospital , Gadag.

Inclusive criteria -

- Pat ients between the age of 25 to 65 years

- Irrespective of sex

- Less than 5 years chronici ty.

Exclusive criteria -

- Pat ients having known organic lesions.

- Insul in dependent

Materials & Methods 85

Laboratory Investigations

The selected pat ients were subjected to fol lowing laboratory

investigat ions

Fast ing blood sugar

Post partal blood sugar

Urine sugar

Serum cholesterol

Diagnostic Criteria

Diagnosis was made on the basis of subject ive parameters

mentioned in the classics and object ive ( lab invest igations) parameters.

Table showing the normal values of objective parameters.

Lab investigat ions Normal values

Fasting blood sugar 80 –120 mg%

Post partal blood sugar 110 – 140 mg%

Serum Cholesterol 120 – 250 mg%

Urine sugar Ni l

Materials & Methods 86

Lab investigation methods

1. Blood Glucose

Blood glucose is determined by using Gluzyme Glucose reagent

set.

Procedure – blood is col lected in a ster i l ized container. Serum is

separated form the cel ls at the earl iest possible t ime (within 30 min), then

the blood is mixed with the reagent (working solution) and heated at

37°C. for 15 min. and then observed in colorimeter under 520 nm.

pipett ing scheme

Blank Standard Test

Working enzyme reagent (ml) 3.0 3.0 3.0

Dist i l led water (ml) 0.025 - -

Standard (ml) - 0.025 -

Sample (ml) - - 0.025

Calculation

Glucose in mg/dl = Absorbance of sample X 100 Absorbance of standard

and the result is recorded in the case sheet.

2. Urine sugar

Urine is col lected in a test tube and mixed with 5ml of Benedicts

solution and heated t i l l i t boi ls, i t is al lowed to cool to room temperature

and then the colour change is noted.

Materials & Methods 87

3. Serum Cholesterol

Modif ied Al lain’s method Cholesterol ki t is used for measuring the

cholesterol level. blood is col lected in a ster i l ized container. Serum is

separated form the cel ls and mixed with the working reagent and by

using the colorimeter (green f i l ter) the cholesterol was estimated.

pipett ing scheme

Blank Standard Test

Working enzyme reagent (ml) 1.0 1.0 1.0

Dist i l led water (ml) 0.01 - -

Cholesterol Standard (ml) - 0.01 -

Sample (ml) - - 0.01

Calculation -

Total Cholesterol in mg% = A of (T) x 200 A of (S)

Study design -

Prospective cl inical trai l .

Sample size -

30 patients are subjected for the study. They are grouped as

A) Hyperglycemic and Hypol ipidimic

B) Hyperglycemic and Hyperl ipidimic

Materials & Methods 88

In each group 15 patients are included on the bases of lab

investigat ions.

Posology - 3gms / 24 hours in divided dose

Duration of treatment -

Durat ion of the study was 30 days from the day of ini t iat ion of

“Bhumyamalakyadi Churna”.

Follow up –

Al l the patients were asked to report every Partnight fol lowup.

Diet -

Pat ients were asked to take regular bl ind diet as far as possible.

-

Criteria for assessment of treatment –

Results of the treatment were assessed on the bases of di f ferences

between the base l ine data and assessment data. The lab investigat ion

variables were subjected for stat ist ical analysis by applying student ‘ t ’

test and paired ‘ t ’ test.

Observation, Analysis & Interpretation 89

Thirty patients are selected for the cl inical study and grouped into

group A and B each of f i f teen. The data col lected is as fol lows –

Demographic data

Master chart - 1

Sl No

OPD No

Date of Initiation

Name A Yrs

S Rl

O E S

Dt F H

F O

Gr Result

1 4477 06/07/99 TRR 58 M 1 2 2 M P 1 B Relieved 2 7510 24/08/99 SRT 43 M 1 1 3 M M 2 A Palliative 3 11186 27/10/99 PNY 50 M 1 1 1 V N 2 B Relieved 4 11187 27/10/99 GHK 62 M 1 1 2 V N 2 A Palliative 5 11188 27/10/99 HBG 40 M 1 1 3 V P 2 B Palliative 6 11189 27/10/99 MBL 42 M 1 1 3 V M 2 A Relieved 7 11191 27/10/99 IPM 48 M 1 1 2 V P 2 B Not responded 8 11192 27/10/99 VMV 59 M 1 2 2 V P 2 A Relieved 9 11193 27/10/99 MBK 64 M 1 1 2 V P 2 A Relieved 10 11194 27/10/99 MKJ 48 M 1 1 2 V P 1 B Not responded 11 11198 27/10/99 NTB 40 F 1 1 4 M N 1 B Relieved 12 11199 27/10/99 CNS 62 M 1 1 4 V P 2 A Relieved 13 11201 27/10/99 SSB 39 M 1 2 3 M M 1 B Not responded 14 11202 27/10/99 CBG 52 M 1 1 4 M N 2 A Palliative 15 11330 27/10/99 RPA 56 M 1 3 1 V N 1 A Palliative 16 11346 27/10/99 AAB 38 F 2 2 3 M P 1 B Relieved 17 11397 28/10/99 CSP 57 M 1 2 4 V P 2 B Palliative 18 11456 28/10/99 ASN 49 F 1 1 3 V P 1 B Relieved 19 11627 01/11/99 PHW 58 F 1 1 3 M N 2 B Not responded 20 11686 02/11/99 BSM 54 M 1 2 4 M P 2 A Palliative 21 11689 02/11/99 GTH 60 F 1 1 4 V N 2 B Palliative 22 11709 03/11/99 NKB 45 M 1 1 3 M P 1 A Palliative 23 11820 04/11/99 SFN 50 M 1 1 4 M P 2 A Relieved 24 11891 04/11/99 TVR 47 M 1 1 3 M M 1 B Relieved 25 11895 07/11/99 PSB 39 F 1 1 4 V M 2 A Palliative 26 11919 08/11/99 MSA 43 F 1 1 3 V P 2 B Relieved 27 12044 11/11/99 AKJ 36 M 1 1 4 V P 2 A Not responded 28 12335 11/11/99 MNR 48 M 1 1 4 M M 2 A Relieved 29 12357 16/11/99 SSM 39 M 1 1 4 V M 2 B Relieved 30 12633 21/11/99 MSB 61 M 1 1 4 V P 2 A Relieved

AY – Age in Yea rs, S – Sex (M – Male, F – Female), Rl - Religion (1- Hindu, 2 - Muslim, 3 - others), O - Occupation (1 - Sedentary, 2 - Active, 3 - Labor), ES - Economical status (1= 0-1Lack,2=1-2 L,3=2-3 L,4=3 L & above), Dt - Diet (v - vegetarian, M - mixed) FH – Family history (P- Paternal, M – Maternal,N – nil), FO – Fresh / Old (1 - Fresh, 2 – Old ) Gr – Group ( A – Hyperglycemic & Hypolipidimic, B - Hyperglycemic & Hyperlipidimic),

Observation, Analysis & Interpretation 90

Master Chart 2

Complaints

1 2 3 4 5 6 Sl No

B A B A B A B A B A B A

Result

1 + + + - + - + + - - + - Relieved 2 + - + - + - - - + - + - Palliative 3 + - + - + - - - - - + - Relieved 4 + - + - + - + - + + + + Palliative 5 + + + + + - + + + - + + Palliative 6 + + + - + - - - - - + - Relieved 7 + - + - + - - - - - + - Not responded 8 + - + - + - - - + + + - Relieved 9 + - + - - - - - - - + - Relieved 10 + + + + + - - - + - + + Not responded 11 + - + - + - - - + + + - Relieved 12 + - + - + - - - - - + - Relieved 13 + + + - - - - - + + + - Not responded 14 + + + - + - - - + - + + Palliative 15 + + + - + - - - - - + + Palliative 16 + - + - - - - - - - + - Relieved 17 + + + - + - - - + + + + Palliative 18 + - + - - - + + - - + - Relieved 19 + - + - + - + + + - + - Not responded 20 + - + - + - - - - - + - Palliative 21 + + + - + - - - + - + - Palliative 22 + - + - + - + + + + + - Palliative 23 + - + - + - - - - - + - Relieved 24 + - + - + - - - + + + - Relieved 25 + + + - + - + + - - + + Palliative 26 + + + - + - - - + + + - Relieved 27 + + + - + - - - - - + + Not responded 28 + - + - + - - - + - + - Relieved

29 + - + - + - - - - - + - Relieved 30 + - + - + + - - + + + - Relieved

Complaints (1=Prabhoota Mootrata,2=Avil Mootrata,3=Ashaktata,4=Shareera bhara hani,5=Jangha mansa graha,

6 = Madhura mootrata, B – Before treatment, A – After treatment)

Observation, Analysis & Interpretation 91

Master chart - 3

Personal history Sl No 1 2 3 4 5 6 7 8 9 10 11 12 13 14

Result

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

1 . Madhura , 2 . Shee ta , 3 .Sn igdha , 4 .Guda , 5 . Navanna , 6 .Mamsa, 7 . Dugdha, 8 .Dah i ,

9 .Gudav ik r i t i , 10 .Dugdhav ik r i t i , 11 .Avyayama, 12 .D iwaswapna , 13 .Swapnasukham,

14 Man is ika ch in ta .

Observation, Analysis & Interpretation 92

Master Chart – 4 POORVAROOPA poorvaroopa

B – Before treatment, A – After treatment. 1 – Dantadeenam malatavam, 2 – Pada daha, 3 – Panidaha, 4 – Deha chikkanata, 5 – Shareera durgandha, 6 – Mukha madhurata, 7 – Talu klomashosha, 8 – Kesha jatilata, 9 – Nakha vriddhi, 10 – Alasya, 11 – Trishna, 12 – Maldhikyata in bahya chidra, 13 – Swedadhikya, 14 – Shitaiccha, 15 – Swasa, 16 – Mutramadhurata, 17 – Mutrashuklata.

Observation, Analysis & Interpretation 93

Master Chart – 5 SROTAS

Udakavaha Medovaha Mamsavaha Mootravaha 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18

B A B A B A B A B A B A B A B A B A B A B A B A B A B A B A B A B A B A 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 + - + - + - + - + - - - - - - - + - - - - - - - - - - - - - + - - - - -

B – Before treatment, A – After treatment. 1 – Jihwa shosha, 2 – Talu shosha, 3 – Osta shosha, 4 – Kloma shosha, 5 – Prawridha pipasa, 6 – Sweda, 7 – Snigdhanagata, 8 – Sthula shophata, 9 – Pipasa, 10 – Arbuda, 11 – Arsha, 12 – Mamsa shosha, 13 – Shira granthi, 14 – Alpalpa mootrata, 15 – Mootra rodha, 16 – Adhika mootra, 17 – Sashoola mootra, 18 – Basti stabhadata.

Observation, Analysis & Interpretation 94

Master Chart – 6 Upadravas

Upadravas 1 2 3 4 5 6 7 8 9

Sl N B A B A B A B A B A B A B A B A B A

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

1 – Prameha pidika, 2 – Atisara, 3 – Jwara, 4 – Daha, 5 – Arochaka, 6 – avipaka

7 – Chardi, 8 – Kasa, 9 – Pratishyaya

Observation, Analysis & Interpretation 95

Master chart 7 - A

Lab Investigation FBS mg/dl PPBS mg/dl US % SC mg%

Sl N B A Dif B A Dif B A Dif B A Dif

Result

2 238 113 125 293 148 145 1.5 00 1.5 180 178 2 Palliative 4 213 094 119 500 165 340 02 0.5 1.5 150 150 0 Palliative 6 272 116 156 486 134 322 1.5 00 1.5 232 230 2 Relieved 8 200 126 074 366 131 235 1.5 00 1.5 203 194 9 Relieved 9 265 098 167 350 120 230 01 00 01 128 128 0 Relieved

12 216 124 092 289 130 159 01 00 01 140 136 4 Relieved 14 183 090 093 380 184 196 01 0.5 0.5 154 149 5 Palliative 15 127 102 025 227 153 075 01 0.5 0.5 160 154 6 Palliative 20 197 092 105 234 150 084 0.5 00 0.5 160 160 0 Palliative 22 119 082 037 231 146 085 0.5 00 0.5 210 203 7 Palliative 23 178 112 066 230 136 094 0.5 00 0.5 190 187 3 Relieved 25 296 118 188 341 162 179 1.5 0.5 01 188 182 6 Palliative 27 297 143 154 428 180 248 02 0.5 1.5 212 208 4 Not responded 28 140 103 037 210 132 078 01 00 01 183 181 2 Relieved 30 206 102 104 263 142 121 1.5 00 1.5 168 166 2 Relieved

Master chart 7 - B

Lab Investigation FBS mg/dl PPBS mg/dl US % SC mg%

Sl N B A Dif B A Dif B A Dif B A Dif

Result

1 264 117 107 326 136 150 1.5 00 1.5 353 350 3 Relieved 3 107 097 010 157 132 025 0.5 00 0.5 346 341 5 Relieved 5 290 110 180 488 196 292 02 0.5 1.5 324 321 3 Palliative 7 310 142 168 427 136 291 02 00 02 296 292 4 Not responded

10 190 146 044 279 215 064 01 01 00 340 337 3 Not responded 11 122 096 026 155 114 041 0.5 00 0.5 311 306 5 Relieved 13 392 130 262 502 152 350 02 00 1.5 322 320 2 Not responded 16 180 090 090 240 130 110 1.5 00 1.5 311 302 9 Relieved 17 293 104 189 380 156 224 1.5 0.5 01 340 335 5 Palliative 18 160 111 049 182 128 054 0.5 00 0.5 378 374 4 Relieved 19 202 134 068 264 204 060 01 00 01 409 403 6 Not responded 21 160 117 043 208 131 077 02 0.5 1.5 281 279 2 Palliative 24 155 106 049 312 148 164 1.5 00 1.5 286 285 1 Relieved 26 271 117 162 324 151 173 1.5 00 01 406 405 1 Relieved 29 192 095 097 280 127 153 1.5 00 1.5 313 310 3 Relieved

B – Before Treatment, A – After Treatment,.FBS – Fasting blood sugar, PLBS – Post lunch blood sugar, US – Urine sugar, SC – Serum Cholesterol,

1. Distribution of patients by age

Observation, Analysis & Interpretation 96

Age No of patients Percentage Responded Percentage

36 – 45 11 37% 10 91%

46 – 55 9 30% 6 67%

56 - 65 10 33% 9 90%

Largest incidences are found in the age group of 36 – 45. I t

shows middle-aged people are more prone to get into this

condit ion.

3. Distribution of patients by sex

sex No of patients Percentage Responded Percentage

Male 23 77% 20 87%

Female 7 23% 5 71%

This data shows among 30 pat ients 23 (77%) are male and

only 7 (23%) are female. This indicates the incidence of

Madhumeha is more in male.

Graphic representat ion of age and sex is shown in f igure 1

Observation, Analysis & Interpretation 97

3. Distribution of patients by religion

Rel igion

No of patients Percentage Responded Percentage

Hindu 29 97% 24 83%

Musl im 1 3% 1 100%

Others 0 0% 0 0%

Figure 1 Showing Age and Sex ratio

0

1

2

3

4

5

6

7

8

9

Sex

Num

ber o

f Pat

ient

s

36 - 45 7 4

46 - 55 8 1

56 - 65 7 3

Male Female

Observation, Analysis & Interpretation 98

The data shows among 30 pat ients 29 (97%) belongs to Hindu,

1 (3%) belongs to Musl im. I t dose not mean that Hindus are more

prone for this disease. This may be due to the area from where

sampling is being done.

4. Distribution of patients by Occupation.

Occupation No of patients Percentage Responded Percentage

Sedentary 23 77% 19 83%

Active 6 20% 5 83%

Labour 1 3% 1 100%

The data shows among 30 pat ients 23 (77%) belong to sedentary

occupation group, 6 (20%) belong to act ive occupation group and 1 (3%)

Figure no 2 Showing the Religion incidence

Hindu97%

Others0%

Muslim3%

Observation, Analysis & Interpretation 99

incidence witnessed from labour group. This shows sedentary work or

less laborious work might have more susceptibi l i ty to the disease.

5. Distribution of patients by Economical status

Income @ No of patients Percentage Responded %

under –1 lakh 2 7% 2 100

1 – 2 lakh 5 17% 4 80

2 – 3 lakh 10 33% 9 90

3 lakh and above 13 43% 10 77

This data shows out of 30 patients, 13 (43%) belong to 3 lakh

and above category, 10 (33%) belong to 2 – 3 lakh category, 5

(17%) belong to 1 – 2 lakh, 2 (7%) belong to under 1 lakh group. I t

c learly indicates the incidence of the disease is more in higher

economical class of people, because of high calor ic diet in take

and less ut i l i ty of i t . Diagrammatic representat ion of occupation

and economical status is shown in f igure No 3

Observation, Analysis & Interpretation 100

Figure No 3 Showing the incidence of Economical status and occupation

0

2

4

6

8

10

12

Income per @

Num

ber o

f pat

ient

s

Sedentary 1 4 8 10

Active 0 2 2 2

Labour 1 0 0 0

0 - 1 Lack 1 - 2 Lacks 2 - 3 Lacks 3 Lacks and above

Observation, Analysis & Interpretation 101

6. Distribution of patients by Diet

Diet Number of pat ients Percentage

Vegetarian 20 67%

Mixed 10 33%

This data shows 20 (67%) of the patients are vegetarians and 10

(33%) are having mixed (both veg and nonveg) food habits. This may be

because of more number of pat ients selected from Hindu rel igion.

Figure no 4 Showing the incidence of Diet

Veg67%

Mixed33%

Observation, Analysis & Interpretation 102

7. Distribution of patients by Family history

Family History Number of pat ients Percentage

Paternal 15 50%

Maternal 6 20%

Without F History 9 30%

Maximum patients i .e. 21 (70%) had a family history. Among them

15 (50%) had paternal and 6 (20%) had maternal history.

Figure no 5Showing the incidence of Family History

Maternal20%

Non30%

Paternal50%

Observation, Analysis & Interpretation 103

Data related to Result

Total

Result No of patients Percentage

Rel ieved 15 50%

pal l iat ive 10 33%

Not responded 5 17%

Group A

Result No of patients Percentage

Rel ieved 7 46%

pal l iat ive 7 46%

Not responded 1 6%

Group B

Result No of patients Percentage

Rel ieved 3 20%

pal l iat ive 8 53%

Not responded 4 26%

By the above data we can observe the effect of the medicine is

signif icant, and is working better on group A pat ients than in Group B.

Graphical representat ion of i t is given in f ig No 6.

Observation, Analysis & Interpretation 104

Figure No 6 Showing the Results

0

2

4

6

8

10

12

14

16

Result

Num

ber o

f pat

ient

s

Total 15 10 5

Group A 7 7 1

Group B 3 8 4

Relived Palliative Not responded

Observation, Analysis & Interpretation 105

Data of Personal history

To asses the nidanas of the disease, detai led personal history is

taken with more concentrat ion drawn towards ahara and vihara of the

patient.

Data pertaining to

a. Ahara

Ahara No of patients Percentage

Madhura 29 97%

Sheeta 28 94%

Snigdha 28 94%

Guda 30 100%

Navanna 27 90%

Mamsa 20 67%

Dugdha 28 94%

Dahi 30 100%

Gudavikri t i 30 100%

Dugdha vikri t i 29 97%

Data revels that more than 90% of the patients are habituated for

the food, which are said to be the nidana of the Madhumeha.

b. Vihara

Vihara No of patients Percentage

Avyayama 26 87%

Diwaswapna 29 97%

swapnasukham 22 73%

87% of the pat ients have lack of physical exercise, 97% of the

patients have the habit of Diwaswapna and 73% of the pat ients have

Observation, Analysis & Interpretation 106

swapnasukham , these factors intensif ies the disease along with aharaja

karana.

c. Manasika

Chinta No of patients Percentage

Present 8 27%

Absent 22 73%

73% of the pat ients are leading happy l i fe without much worr ies,

which is one of the causative factor for Madhumeha.

Observation, Analysis & Interpretation 107

Data related to the disease.

a. Roopas

This table shows the number of patients having part icular complaint

and i ts rel ief after the treatment.

Complaints No of patients % Rel ieve

d

% Sig

Prabhoota Mootrata 30 100 18 60 S

Avi la Mootrata 30 100 28 93 HS

Ashaktata 26 87 25 96 HS

Shareeara Bhara hani 8 27 2 25 NS

Jangha mamsa graha 16 53 9 56 S

Madhura mootrata 30 100 22 73 S

Key Note; Sin–significance, S–significance, HS-Highly significance, NS–Not significance

Prabhoota mootrata, Avi la Mootrata and Madhura mootrata are

found in al l the pat ients and among them 60% , 93% and 73% of the

patients are Rel ieved form the symptom respectively. 87% of the patients

complained of Ashaktata and 96% of them were rel ieved from this

complaint. 53% of the patients had Jangha mamsa graha and 56% of

them are Rel ieved. Shareeara bharahani was complained by 27% of the

patients.

Observation, Analysis & Interpretation 108

b. Poorvaroopa.

The master chart of poorvaroopa is given in Master chart 4 and

analysis is as under.

Associated Complaints No of patients % Rel ieved %

Dantadeenam malatavam 17 57% 15 86%

Pada daha 25 84% 19 76%

Panidaha 24 80% 20 85%

Deha chikkanata 23 77% 21 91%

Shareera durgandha 23 77% 22 95%

Mukha madhurata 19 63% 16 85%

Talu klomashosha 29 97% 24 82%

Kesha jatilata 15 50% 9 60%

Nakha vriddhi 23 77% 13 56%

Alasya 28 93% 26 93%

Trishna 30 100% 27 90%

Maldhikyata 12 40% 9 75%

Swedadhikya 27 90% 25 92%

Shitaiccha 19 63% 16 84%

Swasa 7 23% 5 71%

Mutramadhurata 21 70% 20 95%

Mutrashuklata 19 63% 17 85%

This data justi f ies the statement “poorvaroopas are seen along with

roopas of the disease” more than 70% of the patients are having poorva

roopa as complaint even after the manifestation of the disease which can

be said as di f f icul ty to treat but 82% of them are rel ieved from the

complaints after the treatment.

c. Srotas

Observation, Analysis & Interpretation 109

Four srotases viz Udakavaha Medovaha Mamsavaha Mutravaha

which are in concern are discussed in Master chart 5

Udakavaha Srotas

Udakavaha No of patients % Rel ieved %

Jihwa shosha 30 100 30 100

Talu shosha 30 100 30 100

Osta shosha 29 97 29 100

Kloma shosha 29 97 29 100

Prowridha pipasa 30 100 30 100

Al l the pat ients suffer ing from the udakavaha srotodusti were

Rel ieved to ful l extent on gett ing this treatment.

Medovaha Srotas

Medovaha No of patients % Rel ieved %

Sweda 17 57 14 82

Snigdhangata 12 40 0 00

Sthula shophata 8 27 0 00

Pipasa 30 100 28 93

Pat ients suffer ing form medovaha srotodust i is analysed above

which indicate the grater success in treat ing the medovaha srotodust i

also.

Observation, Analysis & Interpretation 110

Mamsavaha Srotas

Mamsavaha No of patients % Rel ieved %

Aubuda 1 3 0 00

Arsha 7 23 0 00

Mamsa shosha 1 3 1 100

Shira granthi 2 7 0 00

Involvement of Mamsavaha srotas is seen in very less patients

compared with other srotases.

Mootravaha Srotas

Mootravaha No of patients % Rel ieved %

Alpalpa motrata 00 0 00 00

Mootra rodha 00 0 00 00

Adhika mootra 30 100 28 93

Sashoola mootra 02 7 02 100

Bast i s tabdhata 00 0 00 00

The main symptom in this srotodusti observed was Adhika mootrata

that was Rel ieved in 93% of the patients.

Observation, Analysis & Interpretation 111

d. Upadravas

Detai led Master chart of upadravas is given in master chart 6

Complaints No of patients % Rel ieved %

Prameha pidika 4 13 3 75

At isara 2 7 2 100

Jwara 2 7 2 100

Daha 19 63 16 84

Arochaka 14 47 12 86

Avipaka 6 20 6 100

Chardi 3 10 3 100

Kasa 2 7 1 50

pratishyaya 4 13 4 100

Data revi les 63% of the pat ients were suffer ing from Daha, 84% of

them were Rel ieved among them. 47% of the pat ients were complaining

of Arochaka, among them 86% of the patients were Rel ieved from this

complicat ion after the treatment of madhumeha.13% of the pat ients had

prameha pidika which is Rel ieved in 75% . Other minor complicat ions

were also reported and Rel ieved to a grater extent as shown in the table.

Observation, Analysis & Interpretation 112

e. Laboratory investigations.

The f igures of lab investigat ions are shown below.

Observation, Analysis & Interpretation 113

Figure No. 8Fasting Blood Sugar of Group - B

0

50

100

150

200

250

300

350

400

450

Patient Sl No

F.B

.S. i

n m

g/dl

Before 264 107 290 310 190 122 392 180 293 160 202 160 155 271 192

After 117 97 110 142 146 96 130 90 104 111 134 117 106 117 95

1 3 5 7 10 11 13 16 17 18 19 21 24 26 29

Figure No. 7Fasting Blood Sugar of Group A

0

50

100

150

200

250

300

350

Patient Sl No

F.B

.S. i

n m

g/dl

Before 238 213 272 200 265 216 183 127 197 119 178 296 297 140 206

After 113 94 116 126 98 124 90 102 92 82 112 118 143 103 102

2 4 6 8 9 12 14 15 20 22 23 25 27 28 30

Observation, Analysis & Interpretation 114

Figure No. 9Post partal Blood Sugar of Group - A

0

100

200

300

400

500

600

Patient Sl No

P.P

.B.S

. in

mg/

dl

Before 293 500 486 366 350 289 380 227 234 231 230 341 428 210 263

After 148 165 134 131 120 130 184 153 150 146 136 162 180 132 142

2 4 6 8 9 12 14 15 20 22 23 25 27 28 30

Figure No. 10Post partal Blood Sugar of Group - B

0

100

200

300

400

500

600

Patient Sl No

P.P

.B.S

. in

mg/

dl

Before 326 157 488 427 279 155 502 240 380 182 264 208 312 324 280

After 136 132 196 136 215 114 152 130 156 128 204 131 148 151 127

1 3 5 7 10 11 13 16 17 18 19 21 24 26 29

Observation, Analysis & Interpretation 115

Figure No. 11Urine Sugar of Group A

0

0.5

1

1.5

2

2.5

Patient Sl No

Urin

e S

ugar

in %

Before 1.5 2 1.5 1.5 1 1 1 1 0.5 0.5 0.5 1.5 2 1 1.5

After 0 0.5 0 0 0 0 0.5 0.5 0 0 0 0.5 0.5 0 0

2 4 6 8 9 12 14 15 20 22 23 25 27 28 30

Figure No 12Urine Sugar of Group - B

0

0.5

1

1.5

2

2.5

Patient Sl No

Urin

e S

ugar

in %

l

Before 1.5 0.5 2 2 1 0.5 2 1.5 1.5 0.5 1 2 1.5 1.5 1.5

After 0 0 0.5 0 1 0 0 0 0.5 0 0 0.5 0 0 0

1 3 5 7 10 11 13 16 17 18 19 21 24 26 29

Observation, Analysis & Interpretation 116

Figure No. 13Serum Cholesterol of Group - A

0

50

100

150

200

250

Patient Sl No

in m

g / d

l

Before 180 150 232 203 128 140 154 160 160 210 190 188 212 183 168

After 178 150 230 194 128 136 149 154 160 203 187 182 208 181 166

2 4 6 8 9 12 14 15 20 22 23 25 27 28 30

Figure No. 14Serum Cholestroel of Group - B

0

50

100

150

200

250

300

350

400

450

Patient Sl No

in m

g / d

l

Before 353 346 324 296 340 311 322 311 340 378 409 281 286 406 313

After 350 341 321 292 337 306 320 302 335 374 403 279 285 405 310

1 3 5 7 10 11 13 16 17 18 19 21 24 26 29

Observation, Analysis & Interpretation 117

Analysis of the objective parameters (master chart 7 – A and 7 – B,

Figure No 7 to 14 ) are given below with the help of stat ist ical calculation

and i ts signif icance. The calculat ion is done by using student ‘ t ’ test and

paired ‘ t ’ test

Test of significance

Objectives Group Mean S.D. S.E. P.S.E t -value p-value Remark

Before 209.80 56.549 14.600 Fasting blood sugar A After 107.66 16.162 4.1730 15.18 6.726 P< 0.001 Highly

significant Before 219.20 80.109 20.684 Fasting

blood sugar B After 114.13 17.381 4.4879 21.16 4.964 P< 0.001 Highly significant

Before 321.87 95.517 24.662 Post partal blood sugar A After 147.53 18.638 4.8125 25.12 6.938 P< 0.001 Highly

significant Before 308.27 103.52 26.730 Post partal

blood sugar B After 150.40 30.572 7.8938 27.87 5.664 P< 0.001 Highly significant

Before 177.53 29.130 7.5200 Serum Cholesterol A After 173.60 28.250 7.2900 10.47 0.3752 P > 0.05 Not

significant Before 328.00 39.740 10.260 Serum

Cholesterol B After 323.40 40.740 10.450 14.64 0.3141 P > 0.05 Not significant

Before 1.2 0.4900 0.1272 Urine sugar A After 0.16 0.2400 0.0629 0.141 7.326 P< 001 Highly

significant Before 1.36 0.5400 0.1419 Urine

sugar B After 0.2 0.2500 0.0654 0.156 7.419 P< 001 Highly significant

The calculation is done by using student ‘ t ’ test and paired ‘ t ’

test. By observing al l the data above and the calculat ions of their

s ignif icance we can conclude that the drug is having a very good act ion on

blood glucose levels, as well as on the urine sugar levels.

Observation, Analysis & Interpretation 118

f . Result:

The over al l result of the study included group A and B as shown in

the f igure no 6 are summersied as below.

The total patients taken for the study are 30, 15 in each group.

Result No of patients Group A No of patients Group B

Rel ieved 7 3

pal l iat ive 7 8

Not responded 1 4

Group A Not responded

3%

Group B Relived10%

Group A palliative

23%

Group B Not responded

13%

Group B palliative

28%

Group A Relived23%

Conclusion 118

In the present tr ial 30 cases were taken for the study. The tr ial

drug, “Bhumamalakidi churna” had a very good effect on al l the pat ients,

not only by regulat ing their blood glucose levels down but also by

rel ieving them from the signs and symptoms. Especial ly al l the patients

were sat isf ied because of reduced frequency of mituration and burning

sensation of hands and feet.

Even though the combinat ion of t r ial drug is not mentioned in the

classics of Ayurveda, we have combined i t by observing the

pathophysiology of the disease and the actions of the individual drugs,

viz Madhu nasani as an establ ished hypoglycemic agent, Bhumamalaki

and Bhranjraja are good l iver correctors as the l iver is the main organ

involved in glucose metabol ism. Eranda is included in the combination

because of i ts establ ished vata hara effect, as Madhumeha is a vataja

prameha,. After col lecting the herbs personal ly identi f ied by Botanist and,

they were processed as the tr ial drug.

One pat ient (Sl No 1, OPD No 4477 ) approached our PG Hospital

for chronic (one and half month duration) non heal ing ulcers, he was

detected as a diabetic, he was the f i rst patient for our tr ial , even though

the ulcers were big enough (as shown in the photo graph 5 ) we took

bold steps to treat him with our tr ial drug (without any al lopathic drug),

When the patient reported at regular intervals of 15 days, the changes in

the ulcers are noted as (photograph 6 ), and after 31 days the ulcer was

Conclusion 119

ful ly disappeared (photograph 7 ). A camp was set up on 25 – 10 – 99 to

screen the pat ients for the tr ial . We screened 46 pat ients and 18

patients were selected among them.

By the observat ion of the laboratory reports of the pat ients we can

assume the tr ial drug “Bhumamalakadi churna” is highly effect ive on

the NIDDM (Non Insul in Dependent Diabetes Mell i tus ) pat ients. Two

patients other than that of the tr ial patients who were on insul in therapy

were also given the tr ial drug out of interest to know the effect on the

insul in dependent pat ients, even these two patients responded wel l . The

task for these two patients was dif f icult and r isky so i t was done under

close observation and even though the insul in was slowly reduced (2

units per day) the blood sugar level were reduced. This tr ial of these two

patients out of st ipulated inclusive cri ter ia has shown signif icance of

result .

By the assesment of parameters, i t is confirmed that the eff icacy of

tr ial drug “Bhumamalakadi churna´is one of the best al ternate therapy for

the patients of NIDDM. I t has shown remarkable results over the patients

within 30 days. Prolonged use of the medicine doesn’t have any side

effects and further at an economical price the pal l iat ion is possible.

Summary 120

This thesis enti t led “EVALUATION OF THE EFFECT OF

BHUMYAMALAKYADI CHURNA IN MADHUMEHA (With special reference to

i ts hypoglycemic effect)” is summarised as fol lows.

- Madhumeha is one out of the 20 variet ies of Pramehas. I t is Vata

predominant there by considered under vataja mehas. Madhumeha is a

yapya vyadhi.

- I ts treatment is to be a vatahara, kaphahara, and dusta medohara

along with i ts action over mootravaha srotas.

- The present drug selected is having i ts effect over Vata, kapha and

medas. Moreover i ts pharmacological action is over the l iver, in the

process of neoglucogenises as a part of glucose metabol ism in the

body. Secondly i t acts over the Vata, specif ical ly pacifying Vata and

i ts involvement in the disease. Hypoglycemic act ion of

“BHUMYAMALAKYADI CHURNA” is remarkable.

- The classical aff i rmed pathogenesis, as the involvement of medas with

i ts classical signs and symptoms in Madhumeha are stand st i l l even in

21s t century. The pratyatmaniyata lakshana of Madhumeha are

Prabhutamootrata and Avi la mootrata along with ashaktata.

Summary 121

- The cl inical study of the ent i t led thesis “ EVALUATION OF THE EFFECT

OF BHUMYAMALAKYADI CHURNA IN MADHUMEHA (With special

reference to i ts hypoglycemic effect)” have studied over 30 patients in

two groups A ) Hyperglycemic and Hypolipidimic

B ) Hyperglycemic and Hyperl ipidimic.

- Observation of the signs and symptoms, sex, age, incidence, and

results are explained in tubular and graphic forms.

- Results of the treatment were assessed on the bases of di f ferences

between the base l ine data and assessment data . The lab

investigat ion variables were subjected for stat ist ical analysis by

applying student ‘ t ’ test and paired ‘ t ’ test.

- The subjective and objective parameters under stat ist ical viabi l i ty

have shown high signif icance rate with respect to both groups. In

Hyperglycemic and Hypol ipidimic group, 46% of the patient are

rel ieved, 46% are in pal l iat ive group and only 6% of the patients are

not responded. Similarly in Hyperglycemic and Hyperl ipidimic group,

20% of the patients are rel ieved, 53% pal l iat ive and 26% are not

responded. This data reveals the effect of Bhumyamalakyadi churna

highly signif icant. Not responded dosent mean their blood sugar did

not decrease but i t was not up to the mark.

Bibliography

BIBLIOGRAPHY

Charak Samhita Poorvardha

By Vaidya Satyanaryana Shastri . 1s t edit ion 1962

Publ ished by Chowkhamba Vidya Bhavan. Varanasi.

Charak Samhita Uttarardha

By Vaidya Satyanaryana Shastr i . 1s t edit ion 1962

Publ ished by Chowkhamba Vidya Bhavan. Varanasi.

Sushruta Samhita Poorvardha

By Kaviraja Ambikadutta shastr i . 8t h edit ion

Publ ished by Chowkhamba Sanskri t Sansthan, Varanasi.

Sushruta Samhita Uttarardha

By Kaviraja Ambikadutta shastr i . 8t h edit ion

Publ ished by Chowkhamba Sanskri t Sansthan, Varanasi

Astanga Samgraha of Vagbhata

By Prof K.R.Srikantha Murthy. 1s t edit ion 1996

Published by Chowkhamba Oriental ia, Varanasi.

Astanga Hridaya with commentaries of Arunadatta and Hemadri

By Harisastry paradakar Vaidya, 1939

Published by Nirnaya sagar press Bombay.

Bhavaprakasa

By Sri Brahmasankara Misra. 4t h edit ion 1984

Published by Chowkhamba Sanskri t Sansthan, Varanasi.

Bibliography

Madhava Nidana with Madhukosha sanskri t vyakarna.

By Acharya Sri Narindranath shastr i . 1s t edit ion 1989

Publ ished by Moti lal Banarasidas, Varnasi.

Rajanighantu

By Pandit Narahari . 2nd edit ion 1998

Publ ished by Krishnadas Academy, Varansai.

Bhela Samhita

By Gir i ja Dayal Shukla, 1959

Publ ished by Chowkhamba publ ication, Varnasi.

Essentials of Basic Ayurveda Concepts.

By Prof Dr. V.V.S.Sastri . 1999

Publ ished by Publ ication Division, PGARC,

DGM Ay Medical Col lege, Gadag

Josl in’s Diabetes Mell i tus.

By C. Ronald Kahn. 13t h edit ion 1994

Published by Lea and Febiger, A Waverly company, London.

API Text book of Medicine.

By G.S.Sainani 5t h edit ion 1992

Published by Associat ion of Physicians of India, Bombay.

Indian Materia Medica

by K.M.Nadkarni. Vol 1 - 2 2nd edit ion 1982

Publ ished by Popular Prakashan Bombay

Bibliography

Indian Medicinal Plants

by Kirt ikar & Basu Vol 1 - 3 2n d edit ion 1975

Shareera kriya vi jnanam

By M. Ramasundar Rao 2n d edit ion 1994

Publ ished by M. Madhava, Metro Printers, Vi jayawada.

Chakradatta

By Priyavrat Sharma. 2n d edit ion 1998

Publ ished by Chowkhamba Oriental ia, Varanasi.

Researches in Ayurveda

By Dr. M.S.Baghel. 1s t edit ion 1997

Published by Mridu Ayruvedic Publ icat ion and Sales. Jamnagar.

Cunninghama Manual of Pratactical Anatomy Vol 1 to 3

Publ ished at Great Bri tain, Oxford Universi ty Press.

Dorland’s Pocket Medical Dict ionary.

By Douglas M. Anderson. 24t h edit ion 1989

Publ ished by Oxford & IBH publ ishing Co. Pvt. Ltd. Bombay.

Human Physiology

By Dr C.C.Chatter jee 11t h edit ion 1992

Publ ished by Medical Al l ide Agency. Calcutta.

Digestion and Metabol ism in Ayurveda,

By C.Dwarkanath,

Published by Baidyanath Publ ications, Calcutta.

Bibliography

Davidsons Principles and Practice of medicine,

by John Maclod 1992

Publ ished by Pitman press, Great Bri tain.

Gray’s Anatomy

by Henry Gray 1973

Publ ished by Longman group Ltd.

Introduct ion to Kayachiktsa,

by C. Dwarkanath,

Publ ished by Chowkamba offest press, Varanasi.

Kashyapa Samhita,

by Vridha Jeevaka, 1953

Publ ished by Chowkhamba Vidya Bhavan. Varanasi

Principles of Internal Medicine

by T.R. Harr ison and Co. 1962

A Hand book on Endocrine disorders

by Natoobhai. J. Shah 2n d edit ion 1962

publ ished by Unichem Laboratories, Bombay.

Review of medical Physiology

by Wil lam. F. Ganong, 11t h edit ion 1983

Publ ished by Lange Medical publ icat ions, Maruzen.

The Ayurveda Encyclopedia

by Swami Sada shiva Tirtha. 1s t edit ion 1998

Publ ished by Indian books centre, Delhi. Your Guide to Health

Bibliography

By Cl i f ford R. Anderson. 10t h edit ion 1999

Publ ished by G.S.Robert Cl ive, Pune.

Yogaratnakara with Vaidyaprabha hindi commentary

By Dr Indradev Tripathi 1s t edit ion 1998

Publ ished by krishnadas Academy, Varanasi.

Nidana Chiki tsa Hastamalaka

By Ranaji t Roy Desai. 1s t edit ion 1978

Publ ished by Baidyanath Ayurveda bhavan, Nagapur.

Cl inical Methods in Ayurveda

By K.R. Srikantamurthy. 2n d edit ion 1996

Publ ished by Chaukhambha Oriental ia, Varanasi.

From Fat to Fi t

By Dr D.R.Gala. 1s t edit ion 1998

Publ ished by Navneet Publ icat ions Ltd, Gujarat.

Schafer’s essentials of Histology

By Schafers 16t h edit ion 1954

Publ ished by Orient longmans l td.

CASE SHEET FOR “MADHUMEHA”

POST GRADUATE AND RESEARCH CENTERE,(KAYACHIKITSA) SHRI. D.G.M.AYURVEDIC MEDICAL COLLEGE, GADAG.

Guide : Dr.V.V.S.Sastri, Dr Shashidhar.T.Hombal. D.Ay.M.(BHU) M.D. Scholar Co-guide : Dr. Shivarama Prasad Kethamakka. M.A.(Astro),M.D.(Ay) 1. Name of the Patient Sl.No. 2. Father’s/Husband’s Name OPD No 3. Age - Years IPD No 4. Sex - M F Bed No 5. Religion Hindu Muslim Christian Sikh Date of Schedule initiation Date of Schedule completion 6. Occupation - Sedentary Active Labour 7. Economical status Poor Middle class Higher middle class Higher class 8.Diet - Veg Mixed 9. Address Pin 10. Selection Included Group A Hyperglycemic & Hypolipidimic

Excluded B Hyperglycemic & Hyperlipidimic 11. Result Relived Palliative Not responded Discontinued

12. Chief complaints with duration.

Duration No

Complaints < 1 Yr 1Yr 2 Yrs 3 Yrs 4Yrs 5Yrs

After Treatment

1 Prabhoota mootrata 2 Avila mootrata 3 Ashaktata 4 Shareera bhara hani 5 Jangaha mamsa graha 6 Mootra madhuryata 13. History of present illness : Disease was detected

As accidental In regular check up By suspicion

14. Family history 15. Personal History.

a. Ahara

Madhura Sheeta Snigdha

Guda Dugdha Nava anna Dahi

Gramya Guda vikriti Audaka Dugdha vikriti

Mamsa

Anupa b. Vihara

Avyayama Diwaswapna Swapnasukham

c. Manishika- Chinta. Yes No

16. Samanaya Pareeksha.

a. Pulse b. Blood pressure c. Temprature d. Height e. Respitation f. Weight

Patient. Brother Sister

Brother Father Mother

Grandfather Grandmother

Sister Sister Brother

Grandfather Grandmother

17. Poorvaroopa.

Lakshanas B A Lakshanas B A Dantadeenam Malatvam Trishna Pada daha Maldhikyata in bahya chidra Pani daha Swedadhikya Deha chikkanata Sheeta iccha Shareera durgandha Swasa Mukha madhurta Mutra madhurata Talu kloma shosha Mutra shuklata Kesh jatilata Tandra Nakha vriddhi Nidra Alasya Shitalangata

18. Roopa.

Lakshanas Before treatment After treatment Prabhoota mootrata Avila mootrata Madhura mootrata

19. Sroto Pareeksha

A – Udakavaha B - Mootravaha

Lakshanas B A Lakshanas B A Jihwa shosha Alpalpa mootrata Talu shosha Mootara rodha Osta shosha Adhika mootra Kloma shosha Sashoola mootra Prawridha pipasa Basti stabdhata C - Mamsavaha

D - Medovaha

Lakshanas B A Lakshanas B A Arbuda Sweda Arsha Snighanagata Mamsa shosha Sthulashophata Shira granthi

Pipasa

20. Upashaya / Anupashaya

Upashaya Anupashaya Shita iccha Ushna Madhurrahit ahara Madhuara ahara vyayama

Diwa swapana

21. Upadravas

Lakshanas B A Lakshanas B A Prameha pidika Avipaka Atisara Chardi Jwara Kasa Daha pratishyaya Arochaka

Other

22. Lab investigations a Urine

Test Before After Sugar

b. Blood.

Test Before After Fasting blood sugar Post partal blood sugar Serum cholesterol

Signature of supervisor signature of scholar.

WEL COME

““Evaluation of the efficacy ofEvaluation of the efficacy ofBhumyamalakyadi churnaBhumyamalakyadi churna inin

madhumehamadhumeha””(with special reference to its hypoglycemic effect)(with special reference to its hypoglycemic effect)

NIRUKTI

“ prachuram varamvaram va mehati mootratyagam karoti yasmin roge sa prameha”

Madhumeha = Madhu + Meha

Madhu = Honey

Meha = Urination

NIDANA

Asya sukham Swapna sukham dadhini gramyodakanuparasa payamsi |

Navanna panam gudavaikratam cha prameha hetu kaphakrut survam ||

Cha Chi 6/4M.N. 33/1

DOSHA DUSHYA

Kapha sapitta pawanascha dosha medhoassrasukrambhuvasalasika |Majja rasouja pishitum cha dushya pramehinam vimshathireva meha||

Cha Chi 6/8M.N. 33/41

SAMPRAPTI

Medascha mamsacha shareerajam cha kledam kaphovastigatam pradushya |

Karoti mehan samoodernamusnisthaneva pittam paridushya chapi ||

Kshineshu dosheshwavakrushya vasthou dathun pramehananila karoti |

Cha Chi 6/5

SAMPRAPTI TALIKA

Favorable combination of Nidana, Dosha & Dushya.

Kapha immediately aggravates.

Aggravated kapha spreads all over the body.

First mixes with medas.

Vitiated kapha with vitiated medas mixes with mamsa and shareera kleda

Vitiation of mamsa provides manifestation of putrified carbuncles = pidika.

The liquefied dhatus further vitiate and transfer into urine.

Prabhoota mutrata & avila mutrata.

PRAMEHA

PURVA RUPA

Dhanthadinam maladythwam pragrupam panipadhayoho |

Daha chikkanatha dehe trut swadyasyam cha jayate ||

M.N. 33/5

LAKSHANA

Samanyam lakshanam tesham prabootavilamootrata |

M.N. 33/6

BHEDA

Doshadushyavisheshapi tatsamyoga visheshatha |

Mutravarnadi bhedena bhedo meheshu kalpyate ||

M.N.33/6

KAPHAJA = 10PITTAJA = 06VATAJA = 04TOTAL = 20 Types

CHIKITSA

Madhunashini (Gymnema sylvestre)Eranda (Ricinus communis Linn.)Bhumyamalaki (Phyllanthus urinaria Linn)Bhringaraj (Eclipta alba)

SADYASADHYATA

Sadhya kaphota dasha pittaja shat yapya na sadhya pavanachatuska |

Samakriyatwathdwishamakriyathwath mahatyatwacha yathakramam ||

Chi Chi 6/7.

Showing the Results

0

2

4

6

8

10

12

14

16

Result

Num

ber o

f patients

Total 15 10 5

Group A 7 7 1

Group B 3 8 4

Relived Palliative Not responded

DISSERTATION REPORT

Test of significance

ObjectivesGroup

Mean S.D. S.E. P.S.E t -value p-value Remark

Fasting blood sugar

A Before 209.80 56.549 14.600 15.18 6.726 P< 0.001 Highly significant

After 107.66 16.162 4.1730

Fasting blood sugar

B Before 219.20 80.109 20.684 21.16 4.964 P< 0.001 Highly significant

After 114.13 17.381 4.4879

Post partalblood sugar

A Before 321.87 95.517 24.662 25.12 6.938 P< 0.001 Highly significant

After 147.53 18.638 4.8125

Post partalblood sugar

B Before 308.27 103.52 26.730 27.87 5.664 P< 0.001 Highly significant

After 150.40 30.572 7.8938

Serum Cholesterol

A Before 177.53 29.130 7.5200 10.47 0.3752 P > 0.05 Notsignificant

After 173.60 28.250 7.2900

Serum Cholesterol

B Before 328.00 39.740 10.260 14.64 0.3141 P > 0.05 Not significant

After 323.40 40.740 10.450

Urine sugar

A Before 1.2 0.4900 0.1272 0.141 7.326 P< 001 Highly significant

After 0.16 0.2400 0.0629

Urine sugar

B Before 1.36 0.5400 0.1419 0.156 7.419 P< 001 Highly significant

After 0.2 0.2500 0.0654

RESULTS

Group A Relived

Group A palliative Group A Not

responded

Group B Relived

Group B palliative

Group B Not responded

CONCLUSION

The trial drug, “Bhumymalakyadi churna” had a very good effect on all the patients, not only by regulating their blood glucose levels but also by relieving them from the signs and symptoms.

Thank you