Virechana madhumeha pk006-gdg

By

Febin. K. Anto.

Dissertation Submitted to the Rajiv Gandhi University Of Health Sciences,Karnataka, Bangalore.

In partial fulfillment of the requirements for the degree of

AYURVEDA VACHASPATHI M.D. (PANCHAKARMA)

In

PANCHAKARMA

Under the guidance of

Dr. G. Purushothamacharyulu,M.D. (Ayu)

And co-guidance of

Dr. Shashidhar.H. Doddamani,M.D. (Ayu)

Post graduate department of Panchakarma, Shri D. G. Melmalagi Ayurvedic Medical College,

Gadag – 582103.

2005.

Clinical Evaluation of Virechana KarmaIn Madhumeha (NIDDM)

Ayurmitra

TAyComprehended

Rajiv Gandhi University Of Health Sciences, Karnataka, Bangalore.

DECLARATION BY THE CANDIDATE

hereby declare that this dissertation / thesis entitled “Clinical

Evaluation of Virechanakarma in madhumeha (NIDDM)” is a bonafide

and genuine research work carried out by me under the guidance of Dr. G.

Purushothamacharyulu, M.D. (Ayu), Professor and H.O.D, Post-graduate de-

partment of Panchakarma and co-guidance of Dr. Shashidhar. H. Doddamani,

M.D.(Ayu), Assistant Professor, Post graduate department of Panchakarma.

Date:Place: Febin. K. Anto.

I

CERTIFICATE BY THE GUIDE

This is to certify that the dissertation entitled “Clinical Evalua-

tion of Virechanakarma in madhumeha (NIDDM)” is a bonafide research

work done by Febin. K. Anto. in partial fulfillment of the requirement for the

degree of Ayurveda Vachaspathi. M.D. (Panchakarma).

Date:

Place: Dr. G. Purushothamacharyulu, M.D. (Ayu).

Professor & H.O.D

Post graduate department of Panchakarma.

ENDORSEMENT BY THE H.O.D AND PRINCIPAL OF

THE INSTITUTION

This is to certify that the dissertation entitled “Clinical Evalua-

tion of Virechanakarma in madhumeha (NIDDM)” is a bonafide research

work done by Febin. K. Anto. under the guidance of Dr.G.

Purushothamacharyulu, M.D. (Ayu), Professor and H.O.D, Postgraduate de-

partment of Panchakarma and co-guidance of Dr. Shashidhar.H. Doddamani,

M.D. (Ayu), Assistant Professor, Post graduate department of Panchakarma.

Dr. G. Purushothamacharyulu, M.D. (Ayu) Dr. G. B. Patil.

Professor & H.O.D, Principal.

Post graduate department of Panchakarma.

CERTIFICATE BY THE CO- GUIDE

This is to certify that the dissertation entitled “Clinical Evalu-

ation of Virechanakarma in madhumeha (NIDDM)” is a bonafide research

work done by Febin. K. Anto. in partial fulfillment of the requirement for

the degree of Ayurveda Vachaspathi. M.D. (Panchakarma).

Date: Dr. Shashidhar.H. Doddamani, M.D. (Ayu).

Place: Assistant Professor,

Post graduate Department of Panchakarma.

COPYRIGHT

Declaration by the candidate

I hereby declare that the Rajiv Gandhi University of Health

Sciences, Karnataka shall have the rights to preserve, use and dissemi-

nate this dissertation / thesis in print or electronic format for academic /

research purpose.

Date: Febin. K. Anto.

Place:

© Rajiv Gandhi University of Health Sciences, Karnataka.

I

Acknowledgement

“Many hands make light work”. This work carries some memories to express and record about some distinguished personalities with whom I had inspired during the course of this thesis.

I express my obligation to my honorable H.O.D and Guide Dr. G Purushothamacharyulu M.D (Ayu), in the P.G Department of Panchakarma, P.G.S&R, D.G.M.A.M.C, Gadag for his critical suggestions and expert guidance for the completion of this work.

I am extremely grateful and obliged to my co-guide Dr. Shashidhar.H.

Doddamani, Asst. Professor, P.G.S.&R, D.G.M.A.M.C, Gadag for his guidance and encouragement at every step of this work.

I express my deep gratitude to Dr .G.B Patil, Principal, D.G.M.A.M.C,

Gadag, for his encouragement as well as providing all necessary facilities for this research work.

I express my sincere gratitude to Dr.Shivaramudu M.D (Ayu), Assistant

Professor and Dr. Santhosh. N.Belavadi MD (Ayu), Lecturer for their sincere advices and assistance.

I express my sincere gratitude to Dr. V. Varadacharyulu M.D (Ayu), Dr.M.C.Patil M.D (Ayu), Dr. Mulgund M.D (Ayu), Dr. K.S.R Prasad M.D (Ayu), Dr. Dilip Kumar M.D (Ayu), Dr. R.V. Shetter M.D (Ayu), Dr. Kuber Sankh M.D (Ayu), Dr.G.Danappa Gowda M.D (Ayu) for their constant encouragement.

I also express my sincere gratitude to Dr.B.G.Swamy, Dr.V.M.Sajjan, Dr.U.V.Purad, Dr.Mallagowder, Dr.K.S.Paraddi, Dr.G.Yargeri, Dr.S.H.Radder and other undergraduate teachers for their support in the clinical work.

I thank to Shri. Nandakumar (Statistician), Dr. Arun Baburao Biradar ,

Shri. V.M. Mundinamani (Librarian), Shri. B.S. Tippanagoudar (lab technician), Shri. Basavaraj (X-Ray technician) and other hospital and office staff for their kind support in my study.

I express my sincere thanks to my colleagues and friends Dr. Satheesh. R.

Warrier, Dr. Subin Vaidyamadham, Dr. Renjith. P. Gopinath, Dr. Shajil. N, Dr. Shyju Ollakode, Dr. Sreenivasa Reddy, Dr. Hadimani, Dr. C. S. Hanumanta Gouda, Dr. Sankadal, Dr. Vanitha, Dr. Naveen, Dr. Santhosh. L. Y, Dr. Varsha. S. Kulkarni, Dr. P. Chandramouleeswaran, Dr. Uday Kumar, Dr. K. Krishnakumar, Dr. Ashwini Dev, Dr. Ratna Kumar, Dr. Jayaraj Basarigidad, Dr. Kendadamath, Dr. V. M. Hugar, Dr. Shyla. B, Dr. Suresh Hakkandi, Dr. Manjunath Akki, Dr. L. R. Biradar, Dr. Vijay Hiremath, and other post graduate scholars for their support.

II

I take this opportunity to remember my late ancestors Shri. Poulose Vaidyan, Shri. Francis Vaidyan and Shri. Pathrose Vaidyan whose lives have inspired me to take Ayurveda as my profession.

I acknowledge Mrs. Annam Poulose, Mr. Renil Anto, Mrs. Lidiya Renil,

Mr. Vinil Anto, Master. Andrews Renil for their inspiration and whole-hearted support. I also acknowledge Dr. Jose Kandamkulathy, Dr. Wilson Kandamkulathy, Dr. Davis Kandamkulathy, Mr. Wilson Kandamkulathy (Managing Director, Pathrose Vaidyan’s Kandamkulathy Vaidyasala), Dr. Rose Marry Wilson and Mr. Dipu Karuthedath for their inspiration and moral support.

I would like to mention the support and inspiration provided by Dr.

R.Ramabhadran, Director (ISM, Kerala) and Dr. P. S. Gopi, Retd. DMO (ISM, Kerala). I also acknowledge the support and inspiration provided by my teachers Dr. K.P. Muralidharan, Principal, S.J.S. Ayurveda College, Chennai, Dr. S. Swaminathan, H.O.D., Samhita & Siddhanta, S.J.S. College, Dr. S. Venugopal, Reader in Sanskrit, Dr. Vasudevareddy H.O.D. Shalya department and Dr. Ramdas Maganti, H.O.D., Kaya chikitsa, S.J.S. College.

I also thank Shri. C. S. Bhatt and family and Shri. Prasad and family for

the support and encouragement provided during my stay at Gadag.

I acknowledge my patients for their wholehearted consent to participate in this clinical trial. I express my thanks to all the persons who have helped me directly and indirectly with apologies for my inability to identify them individually.

Finally I dedicate this work to my respected parents Mr. Anto Kandamkulathy and Mrs. Rosily Anto, for their wholehearted inspiration and support to fulfill this dream.

Date : Signature of the candidate

Place : Febin. K. Anto.

III

ABSTRACT

Panchakarma is the popular term for shodhana chikitsa, among that virechana is

an important one. Virechana is the therapy by which the doshas are made to pass through

the adhomarga i.e. Gudamarga. In virechana the doshas even from the amasaya are taken

to the pakvashaya and they are removed through gudamarga.

In the treatment of Sthoola Madhumcha Virechana therapy has great importance

according to Ayurveda. In the modern system of medicine Madhumcha can be compaired

to diabetes mellitus. And it can be classified as insulin dependent, non insulin dependent,

malnutrition related and other types of diabetes mellitus associated with certain

conditions and syndromes. Among these non-insulin dependent diabetes mellitus

constitutes 85 % or more of all cases of diabetes. Diabetes has become the disease of the

masses. Over 20 million people are reported to be suffering from this “Sweet Disease”.

Between 1995 and 2005 India will have about 2-3 crore diabetic patients.

Even though the scientific world has conducted extensive studies but couldn’t

find a safe and effective therapy or medicine for this disease. In Ayurveda we can offer

several treatment modalities among that virechana therapy is a good, result oriented and

economical therapy which can control the blood sugar level and prevent further

complications without any side effects.

Virechana Karma is advised in Madhumeha patients having good body strength

and those who are sthoola in nature. The objective of this study was to assess the efficacy

of virechana in such patients. The study was designed as a prospective clinical trial and

30 patients were selected and given classical Virechana karma.

IV

The treatment contains the following steps.

01. Deepana pachana by Trikatu Choorna.

02. Shehapana by Thrikandakadyam Ghritam.

03. Abhyanga and mridu sweda by Moorchita tila taila and ushnajala snana.

04. Virechana by Vidanga Tanduladi choorna.

05. Samsarjana krama.

06. Follow-up for one month.

As a result of the proper administration of Virechana karma it was noted that, it

gives immediate and lasting results, both in sugar levels as well as in other complaints.

Among the 30 patients taken for the study, 17 patients (56.6%) responded good, 11

patients (36.6%), responded moderately and 2 patient’s (6.6%) response was poor. A

close perusal of observation and inference that can be drawn leads to the conclusions

such as, Virechana is an effective treatment in Sthoola Madhuneha and it also shows

lasting results. In mild and moderate type of Sthoola Madhumeha classical Virechana

alone is enough to control it. Even though only Virechana was administered in this study,

it was also noted that along with Virechana karma, administration of pathya ahara vihara

and shamanoushadis might help more. Also administration of repeated virechana may

give lasting results.

Key words –

Shodhana karma ; Virechana karma ; Sthoola Madhumeha ; Prameha ; Diabetes

mellitus ; Insulin resistance ; Obesity; Vidangatanduladi churna ; Thrikandakadyam

ghritam ; Blood sugar.

V

LIST OF ABBREVIATION USED

⇒ Ch. – Charaka Samhita.

⇒ G. R. – Good response.

⇒ M. R. – Moderate response.

⇒ P. R. – Poor response.

⇒ Su. – Sushruta Samhita.

⇒ Vag. – Ashtanga Hridaya.

VI

TABLE OF CONTENTS Chapters Page No.

1. Introduction 1-3

2. Objectives 4

3. Review of literature 5-72

4. Methodology 73-92

5. Results 93-123

6. Discussion 124-136

7. Conclusion 137

8. Summary 138-139

9. Bibliography 140-153

10. Annexure

VII

LIST OF TABLES Page No. Table No. 01. Historical milestones in the field of Diabetes mellitus. 8 Table No. 02. Showing the virechana yogyas. 12 Table No. 03. Showing the virechana ayogyas. 15 Table No. 04. showing the samyak snigdha lakshanas. 17 Table No. 05. Showing the virechana dravya jeeranoushadha and

ajeeranoushadha lakshanas. 19 Table No. 06. Showing the vega nirnaya. 20 Table No. 07. Showing the ayoga and atiyoga 21 Table No. 07a. Showing the samanya nidana of prameha. 43 Table No. 08. Showing the poorvaroopa of prameha 48 Table No. 08a. Showing are the Prameha according to the major classics. 60 Table No. 09. Showing the Vyavachedaka nidana. 67 Table No. 10. Upadravas of prameha according to Vagbhata and Sushruta

on dosha basis. 69 Table No. 11. Showing the properties of the ingredients of Trikatu churna 74 Table No. 12. Showing the properties of the ingredients of Thrikandya ghritam. 75 Table No. 13. Showing the properties of the ingredients of Moorchhita tila taila. 79 Table No. 14. Showing the properties of drugs used in Vidangataduladi churna. 80 Table No. 15. Showing the grades of the blood sugar level. 88 Table No. 16. Showing the demographic data. 94 Table No. 17. Showing the data related to disease. 95 Table No. 18. Showing the data of parameters. 96 Table No. 19. Showing the treatment protocol and observation. 97 Table No. 20. Showing the age group incidence and response. 98 Table No. 21. Showing the Sex group incidence and response. 99 Table No. 22. Showing the incidence of religion and response. 100 Table No. 23. Showing the incidence of occupation and response. 101 Table No. 24. Showing the Socioeconomic Status and response. 102 Table No. 25. Showing the food habits and response. 103 Table No. 26. Showing the chronicity and response. 104 Table No. 27. Showing the treatment history and response. 105 Table No. 28. Showing the family history and response. 106 Table No. 29. Showing the nature of koshta and response. 107 Table No. 30. Showing the Status of agni and response. 108 Table No. 31. Showing the nature of malapravritti in the patient and response. 109 Table No. 32. Showing the habits of the patient and response. 110 Table No. 33. Showing the prakriti of the patient and response. 111 Table No. 34. Showing the nidana status and response. 112 Table No. 35. Showing the days of deepana pachana and response. 113 Table No. 36. Showing the days of snehapana and response. 114 Table No. 37. Showing the incidence of samyak snigdha lakshanas and response. 115 Table No. 38. Showing the incidence of samyak virechana lakshanas and response.117 Table No. 39. Showing the number of vegas attained by patient and response. 119 Table No. 40. Showing the incidence of antaki and response. 120 Table No. 41. Showing the incidence of manaki and response. 121 Table No. 42. Showing the Overall assessment. 122 Table No. 43. Showing the Statistical results. 123

VIII

LIST OF FIGURES, PHOTOGRAPHS AND GRAPHS Title Page No.

1) Figure showing digestive system 26

2) Photo showing the drugs used in the study 73

3) Photo showing Vidangatanduladi churna and ingredients 80

4) Graph showing the age group incidence and response. 98

5) Graph showing the Sex group incidence and response. 99

6) Graph showing the incidence of religion and response. 100

7) Graph showing the incidence of occupation and response. 101

8) Graph showing the Socioeconomic Status and response. 102

9) Graph showing the food habits and response. 103

10) Graph showing the chronicity and response. 104

11) Graph showing the treatment history and response. 105

12) Graph showing the family history and response. 106

13) Graph showing the nature of koshta and response. 107

14) Graph showing the Status of agni and response. 108

15) Graph showing the nature of malapravritti in the patient and response. 109

16) Graph showing the habits of the patient and response. 110

17) Graph showing the prakriti of the patient and response. 111

18) Graph showing the nidana status and response. 112

19) Graph showing the days of deepana pachana and response. 113

20) Graph showing the days of snehapana and response. 114

21) Graph showing the incidence of samyak snigdha lakshanas and response. 115

22) Graph showing the incidence of samyak virechana lakshanas and response.117

23) Graph showing the number of vegas attained by patient and response. 119

24) Graph showing the incidence of antaki and response. 120

25) Graph showing the incidence of manaki and response. 121

26) Graph showing the Overall assessment. 122

“Clinical Evaluation of Virechana Karma In Madhumeha (NIDDM)”

Ayurveda the heritage of Indian civilization is not only a medical pathy but also a

full-fledged Science, consisting of all medical and allied branches essential to lead a

healthy life. Being a Science Ayurveda believes in supreme power. This concept is

essential to know the limitations of human efforts and to accept the existence of things

beyond the perception of our sense. Ayurveda considers the prime living principle i.e.

atma and the importance of which is now accepted by all.

The purpose of Ayurveda is to maintain health and to treat diseases, in order to

achieve the ultimate goal i.e. distraction from worldly things. Ayurveda is consisting of

two words ayu and veda. Ayu means life, which is a proper combination of body, mind,

sense organs and soul. Veda means knowledge.

Preservation of health and its maintenance are the main aim of Ayurveda. Its

attainment is due to personal, social and moral hygiene, which is very sophisticated and

highly developed. The regimens of day, night and seasons, if observed properly lead to

positive health. The disease is manifested when extrinsic factors provoke the bodily

doshas and this provocation is the stage proceed by accumulation and followed by

pacification and the provoked doshas are eliminated in fixed particular seasons by

emetics, purgatives etc. This application prohibits the recurrence of disease.

The Panchakarma therapy is an important part of Ayurveda. The procedures of

Panchakarma therapy have thrown new light on the management of diseases and have

provided effective weapons against many of them.

The Panchakarma therapy or five-fold purification procedures include, Vamana,

Virechana, Basthi, Nasya and Raktamokshana. This entire group of purification produces

is based up on promoting the body’s natural methods of elimination of unwanted

Introduction 1


substances. Thus the Panchakarma therapies of Ayurveda form a unique system of

therapy, which not only aims at physical correction and rehabilitation, but also aim at

imparting local medication and transdermal nourishment of the tissues.

Among the panchakarmas, virechana is an important one, which had great

importance. At the same time it is a highly effective therapy, which gives tremendous

results. It is a process by which the doshas are made to pass through the adhomarga i.e.

Guda.

Virechana is a specific treatment for pitta dosha, and pitta samsarga doshas. It is

also the treatment for kapha and vata doshas. In the process of virechana, the person will

not have that much amount of trouble and exhaustions as in normal purgation, as he has

been subjected to snehana, swedana etc.

Madhumeha is a disease known to mankind since vedic period. Ayurvedic

classics consider madhumeha among the twenty obstinate urinary disorders. The

development of modern science has revolutionized the approach to this disease and it’s

management.

Traditionally madhumeha is correlated with diabetes mellitus, which is known as

“Richman’s disease”, particularly because a person who is able to enjoy the pleasure of

life without any perceptible exercise is usually affected with this disease. The importance

of over nutrition is shown by the fact that, over the age of 40 some 80 percent of patients

developing diabetes are considerably over weight.

Obesity is considered to be a important risk factor for diabetes mellitus. In fact

Ayurveda considers sthoulya as a nidanarthakara roga for madhumeha.

Introduction 2


INCIDENCE AND PREVALENCE

Diabetes has become the disease of the masses. Over twenty million people are

reported to be suffering from this “sweet disease”. It is projected that by another twenty

years the number would rise to 60 million in India. In the past 16 years our population

has roughly doubled from about 68 million to the 1 billion mark and the number of

diabetics has increased by more than 7 fold. According to I.C.M.R. survey, it is

estimated that between 1995 and 2005, India will have about 2-3 crore diabetic patients.

Introduction 3


Need For Study :

The modern management of diabetes inspite of many advances still remains

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

acute and chronic complications, the fear of hypoglycemic episodes make it all the more

important to search out safe, effective and cheaper remedies. Such remedies could be

explored form the huge wealth of Ayurveda. Among that virechana is one of the jewel,

which gives tremendous results in many diseases including sthoola madhumeha.

Objectives :

Even though many research works are conducted on the effect of some indigenous

drugs on Madhumeha, only few have been conducted on samshodhana karma. So far only

less studies are conducted on the effect of virechana on sthoola madhumehi. So the

objective of this study is “Clinical evaluation of virechana karma in sthoola

madhumeha (NIDDM)” in order to evaluate its effect.

Objectives of the study 4


HISTORICAL REVIEW

Madhumeha is one of the ancient diseases and is as old as humanity and this

disease is well known to vedic period also.

Vedic Period :

Vedas are the oldest literature of civilization. Atharva veda is having close

relation to Ayurveda. In Vedas we find two words Asrava and Prameha. In Atharva

veda asrava vyadhis are mentioned in which nasasrava, atimootra and atisara are

included1. The term asrava is formed from A-Srava means to flow. Whitney (Atharva

veda translated and commented) interpreted this as “Flux” and Griffith (also translated

and commented) as “Morbid flow” 2.

In Koushika sutra of the Atharvanaveda we find reference of the work Prameha3.

In Atharvaveda 6/44/3 Visanaka drug is indicated in vatavyadhi. Kesava

commenting on this, explained “Vaikruta nasani” as “Vaikruta asravya nasani”,

means it is indicated in asrava vyadhis.

In the Manthra 23-1-3 of Atharvanaveda, the drugs emerged from valmika are

indicated in atisara, atimootra and nadivranam4.

This clearly indicates the prevalence of this disease with its remedy in the vedic

period.

Samhita Period :

It is a point of historical importance that Charaka samhita mentions the loss of

sweet substance from urine5.

Charaka also mentioned in sutrasthana that the Madhumeha occurs due to

avritatwa of vayu6.

Historical review 5


Charaka also mentioned the importance of ojus in Madhumeha samprapti7.

Bhela samhita which is contemporary to Charaka samhita describes the two types

of Madhumeha i.e. prakruta (congenital) and swakrita (acquired) 8.

The most notable contribution of Sushruta was to devote a separate chapter for the

management of Madhumeha and he mentioned some specific preparations of mineral and

vegetables. He has also given more importance to Shilajatu9. Further he also described a

separate chapter for the management of Carbuncles, which are the upadravas of

Madhumeha10.

After Sushruta, Vagbhata has given great contribution to Indian medicine. He

compiled the existing knowledge and added some new preparations and ideas to this

context. He mentioned two types of Madhumeha on the basis of pathogenesis, one is

Dhatukshayajanya and another is Avaranajanya11.

Arthashastra of Koutilya (321 – 296 BC) mentions a method to produce Prameha

in the section dealing with the means to injure the enemy. The spot obtained from

burning Chanclion (Krukalaka) and house lizard (Gruha Goulika) together with the

intestines of mottled frog (Chitra Bheka) and honey, if administered causes Prameha.

This evidently points the existence of diabetogenic technique in the ancient times12.

Medieval Period :

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

Madhavakara (9th century A.D.) in his book Madhava nidana compiled the

thoughts of his earlier authors without adding any thing new to the knowledge on

Madhumeha13.

Historical review 6


Gayadasa (11th Century A.D.) commentator of Sushruta samhita elucidated that

avilatva of urine in Prameha is due to the presence of some components of dooshya i.e.

meda, mamsa, etc14.

Dalhana, another commentator of Sushruta samhita (12th century) contributed a

myth that females do not suffer from Madhumeha15.

Sharangadhara (13th century A.D.) prescribed some new recipes for the

management of Prameha16.

Bhavamishra (16th century A.D) contributed to the history of prameha by adding

some new vegetables and metallic preparations for the management of prameha.

Ayurvedic physicians even three thousand years ago were aware of the extent to

which all the body tissues are involved in the pathogenesis of Prameha. Claims have been

made by China, Egypt and India as the home of discovery of this vast disease. But all

evidences points to the fact that, it is in ancient Sanskrit texts that the earliest reference

are found. These Sanskrit texts in turn were translated to Latin and became the source of

European medicine.

Three outstanding physicians of Ayurveda, Charaka, Sushruta and Vagbhata

better known as the Holy Triad made the earliest reference to diabetes as a “diseased

flow of urine” and “honey urine”. Charaka mentions that ants are attracted by Person’s

urine afflicted with this disease. Sushruta specifically mentions that the urine of the

diabetic person is sweet nature.

It seams, during this period no Greco-Roman physicians were acquainted with

symptoms of abnormal urine.

Historical review 7


Historical milestones in the field of Diabetes Mellitus

The relationship between the pancreas, an organ lying behind the upper intestines

and diabetes are firmly established by “Von Mering” and “Minkouski” in 1889. It was

on the mid night of July 30,1921, that a pancreatic extract produced in this manner was

injected to a depancreatised diabetic dog on the verge of coma and one hour later blood

sugar came down and urine sugar disappeared, Insulin was born!.

Table No.01. Historical milestones in the field of Diabetes mellitus17.

Sl. Invention Name Period

01. Clinical description document Eberus papyrus 1500 BC

02. Clinical description, noted sweetness in urine

and role of hereditary

Charaka 600 BC

03. Clinical description, noted sweetness in chine

and role of hereditary

Sushruta 400 BC

04. Clinical description Celsus 30 BC - 38 AD

05. Name diabetes Aretaus 30 - 90 AD

06. Introduce the term diarrhoea of urine Galan 132 - 201 AD

07. Evaporated specimen of Urine of patient and

discovered a residue which was almost

Glucose

Jaques Dubois

sylvanus

1478 – 1555

08. Dietary regulation for diabetes Arnatus

Luritanus

1511 – 1568

09. Role of heredity in diabetes Mortan Richard 1637 – 1698

10. Role of hereditary in diabetes Mortan Richard 1637 – 1698

Historical review 8


Sl. Invention Name Period

11. Removed pancreas from the dogs and found

that they developed thirst and polyurea

Burunner J.C. 1653 – 1727

12. First to add mellitus to diabetes Cellura William 1712 – 1790

13. First to separate diabetes incipidus from

mellitus

Johanu Frank 1745 – 1821

14. Described pathology of pancreas Cawley 1788

15. Liver’s role in diabetes Von Noorden 1858 – 1944

16. Described pancreatic Islets Langerhan paul 1969

17. Sugar storage in liver as glucagons and

elevated blood sugar in diabetes

Clande Bernad 1870

18. Experimental diabetes after removal of

pancreas

Von Mering and

Minkovasski

1889

19. Insulin almost discovered Zulger, Panlaski 1910 – 1920

20. Insulin from dog pancreas Banting and

Best

1921 - 1922

21. Transplant of beta cells Downwards

Mervin and

Gliedman

1970

22. Artificial pancreas Liebel selden 1974 - 1975

Historical review 9


VIRECHANA KARMA

Nirukti And Paribhasha

Virechana18 : - Virehana shabda is formed by the root “Rich” dhatu and “Vi”

upasasga. “Nich and “Lout” pratyaya are also take part in the derivation of the word

virechana.

“Visheshena rechateeti” “Vi + rich + Nich + Lyu.”

Virechana karma

Panchakarma is the popular term for shodhana chikitsa, and among that virechana

is an important one. Virechana is a process by which the doshas are made to pass through

the adhomarga i.e. Guda21. Its general meaning is to remove the doshas from the body,

but in Ayurveda removal of the doshas from the body trough guda is called as virechana.

Virechana is a specific therapy for pitta dosha and pitta samsarga doshas. It is

also the treatment for kapha in the pittasthana. Virechana is also useful in vata dosha as

sneha, sweda and mridu virechana are the main upakramas of vata dosha22.

Virechana karma In Major Classics

In the treatment of madhumeha virechana therapy has great importance. All the

Brihathrayies of Ayurveda has mentioned about Madhumeha and other classis like

Bhavaprakasha, Bhaishajya ratnavali, Yogaratnakara and Vangasena mentioned about

this disease and the importance of virechana in this condition23.

All the classics have given detailed description regarding Virechanakarma. In

Charaka samhita we can get the explanation of different virechana dravyas and kalpas in

kalpasthana and in sutrasthana. In siddhi sthana he explained the importance of

Virechana in different diseases, yogyas, ayogyas, siddhis, vyapats and pariharas etc. in

detail24.

Virechana karma


In Sushrutasamhita sutrasthana he gives explanation regarding adhobhagahara

dravyas in detail. Also in the sutrasthana he explains virechana pradhanani dravyas. In

chikitsasthana acharya gives information regarding method of application of virechana,

oushadha panavidhi, dosha nirharana karma, samyakyoga, atiyoga, vyapats, and their

chikitsa in detail25.

Vagbhata acharya in Ashtanga Hridaya Kalpasthana gives explanation of

virechana dravyas and their different kalpas. Apart from this in Sutrasthana, he gives

explanation of virechana vidhi, yogyas, ayogyas, etc. in detail26.

In the same way other acharyas like Yogaratnakara, Bhavaprakasha,

Sharangadhara, Vangasena, all gives explanations regarding Virechanakarma.

Types of Adhobhagahara Karma

Sharangadhara has explained 4 types of adhobhagahara karmas, they are27

01. Anulomana

02. Sramsana

03. Bhedana

04. Rechana

Among these, rechana karma expels pakva or apakva mala in drava form which is

considered as more good.

Virechana Dravyas

Virechana dravyas will have all the properties of vamana dravyas i.e., ushna,

teekshna, sookshma, yogavahi, vikashi etc. These drugs consisting of pritvi and jala

mahabhootas. Virechana dravyas have a specific property of removing the doshas from

the lower part of body i.e. Adhobhaga28.

Virechana karma


Virechana Vidhi

As a first step one has to observe whether the patient is fit for virechanakarma or

not. For this in classics criterias are given such as virechana yogyas, virechana ayogyas

etc. Those who are fit for virechana should only be given with virechana other wise it

will lead to lot of complications. At the same time one has to see whether the patient is

fit for snehana and swedana also, as they are the poorvakarmas of virechanakarma.

Table No. 02. Showing the Virechana Yogyas29.

Sl. Virechya Charaka Susruta Vagabata

01. Jwara + + +

02. Kushta + + +

03. Prameha + + +

04. Urdvaga raktapitta + + +

05. Bhagandara + + +

06. Arsha + + +

07. Pleeha dosha + + +

08. Gulma + + +

09. Arbuda + + -

10. Galaganda + + -

11. Grandhi + + +

12. Gara + + +

13. Vishoochika - + +

14. Alasaka + + -

15. Mootraaghhata + + +

16. Krimikoshta + + +

Virechana karma


17. Visarpa + + +

18. Pandu + + +

19. Sirashoola + + daha +

20. Parshva shoola + - -

21. Udaavartha + - -

22. Netra daha + + -

23. Aasya daha + + -

24. Hridroga + + -

25. Vyanga + - +

26. Neelika + - -

27. Aruchi + + -

28. Netrasrava + - -

29. Nasasrava + - -

30. Haleemaka + - +

31. Swasa + - +

32. Kasa + - +

33. Kamala + - +

34. Apachi + - +

35. Apasmara + - -

36. Unmada + - -

37. Vata rakta + + +

38. Yonidosha + + +

39. Retodosha + - +

40. Timira + + +

Virechana karma


41. Udara + + +

42. Avipaka + - -

43. Chardi + + +

44. Visphota + + +

45. Pakwashaya ruja - + +

46. Vibhanda - + +

47. Vidradhi - + +

48. Shvayadhu + + +

49. Shastra ksheena kshara agni dagdha - + -

50. Dushta Vrana - + +

51. Akshipaka - + -

52. Abhishyanda - + +

53. Kaacha - + +

54. Guda daha - + -

55. Medhra daha - + -

56. Nasa Karna daha - + -

57. Aanaha - + -

58. Shleepada - - -

59. Stanyadosha - - +

60. Hrullasa + - +

Virechana karma


Table No. 03. Showing the Virechana Ayogyas30.

Sl. Avirechya Charaka Susruta Vagbata

01. Subhaga + - -

02. Kshataguda + - +

03. Bhuktaanala + - -

04. Adhoga vaktapitta + + +

05. Langhita + - -

06. Durbalendriya + - -

07. Alpagni + + +

08. Niruda + - +

09. Kamadi vyagra + - -

10. Ajeerna + + +

11. Nava jwara + + +

12. Madatyaya + + +

13. Aadhmana + - +

14. Shalyardita + - +

15. Abhighata + - +

16. Atisnigdha + + +

17. Atirooksha + + +

18. Daruna Koshta + + -

19. Kshata ksheena + + +

20. Atisthoola + + +

21. Atiruksha + - +

Virechana karma


22. Bala, Vrudha + + +

23. Durbala + + +

24. Shranta + + -

25. Pipasita + + -

26. Karma, bhara Advahana + - -

27. Upavasita + + -

28. Maithunaprasakta + - -

29. Adhyayana Prasakta + - -

30. vyayama Prasakta + - -

31. Chinta prasakta + - -

32. Kshama + - -

33. Garbhini + + +

34. Nava prasuti - + +

35. Nava pratishyaya - + +

36. Rajayakshma - - -

37. Atisara - - -

38. Kshudhita + - +

39. Nitya dukhita - - +

40. Hrudrogi, Bhayabhoota - - +

Compared to other karmas like vamana, vasthi, nasya and raktamokshana,

virechana is less complicated and easy to administer, if administered in proper way.

Before the administration of virechana, the patient is made to undergo snehana and

swedana. Before the above two karmas i.e., snehana and swedana, deepana pachana

Virechana karma


should be administered in order to get niramata. After getting niramata patient should be

given shehana in arohana krama till he attains samyak snigdha lakshana, normally till 7

days. The sneha should be vyadyanuroopa and vyadyanukoola.

Table No. 04. Showing the Samyak Snigdha Lakshanas31.

Sl. Lakshanas Charaka Susruta Vagbata

01. Agnideepthi + + +

02. Snehodvega + - +

03. Asamhata varcha + + +

04. Anga laghava + + -

05. Gatra mardava + + -

06. Gatra snigdhata + +` +

07. Pureesha snigdhata + + +

08. Twak snigdhata - + -

09. Vatanuloma + - +

10. Adhomarga sneha srava - + +

11. Klama - + +

12. Shaithilya - + -

As a next step, patient should be given swedana till samyak swinna lakshanas.

After attaining swinnata, he should be given Virechana dravya. Before this a proper dose

and form should be fixed for the Virechana dravya and the total body condition should

also be assessed carefully in order to avoid further complications.

For Virechana dravya, uttama, madyama and alpamatras are mentioned, from that

one dose suitable to the patient should be selected. Also vaidya has to see whether any

Virechana karma


avirechya diseases are manifested in the patient during the day of the virechana. Both the

sneha used for the snehapana and the drug used for Virechana should be vyadhyanukoola

and vyadyanuroopa. Apart from the above factors like desha, kaala, bala, shareera, ahara

saatmya, satva, prakriti and vayaha should be considered32. Pradhana Karma in

Virechana vidhi consists of administration of Virechana dravya to till the stoppage of

virechana vegas.

The following ideas are necessarily kept in mind such as,

01. The administration of Virechana Yoga.

02. Deciding the Vegas.

03. Observation of the signs and Symptoms of samyak yoga, ayoga and atiyoga.

04. Examination of the patient who have undergone virechana therapy.

05. Vyapats if any, and their treatment.

Vagbhata Says, the patient has to take Virechana dravya just after kapha kala. As

soon as the drug meant to produce Virechana is administered, in some sensitive patients

there will be the sensation of nausea or vomiting. It is due to either bad taste of the drug

or due to utkleshana leading to anorexia. The properties of emetics and purgatives will

have stimulating properties. Hence the Purgatives may sometimes produce vomiting. As

soon as the patient drinks the purgative drug the patients face must be sprinkled with cold

water and the mouth should be washed with hot water.

The patient must also be made to lie on a bed and to allow him to take rest. A

little hot water must be given to the patient to drink so that the vega must come properly.

He must not allow touching even cold water up to last vega33.

Virechana karma


In a proper Virechana the patient passes mutra, purisha, pitta, kapha etc. in a

sequence. When there is no purgation, then instantaneously the hot water must be given

to drink and the hand must be made warm and sweda must be done on stomach. Vaidya

must observe the signs and symptoms of jeernoushadha and ajeernoushadha etc. that are

given in the following table34.

Table No. 05. Showing the Virechana dravya jeeranoushadha and ajeeranoushadha

lakshanas

Sl. Jeernoushadha Lakshana Ajeernoushadha lakshana

01. Vatanulomana Dourbalya

02. Swasthya Daha

03. Kshut Angasaada

04. Pipasa Bhrama

05. Mana prasannata Moorcha

06. Indriya prasannata

07. Shudha udgara, etc.

Here ajeernoushadha lakshanas indicates that the virechanoushadha undergone

pachana without doing its virechana effect.

Apart from the above lakshanas the hrit dosha lakshana also should be taken into

consideration. As told previously, in a proper virechana there will be expulsion of mala,

pitta and kapha in sequence i.e. “kaphantam virechanam”. After this only vata

nirgamana occurs. Also the appearance of dourbalyata and laghuta indicates that doshas

have properly gone out35.

Virechana karma


If ajeerna lakshanas are noted but ayoga of virechana happens, the patient should

never be given further dose of oushadha because it may lead to atiyoga. When the

oushadha undergone pachana and there is no hrit dosha lakshanas, then he should be

given food and again virechana oushadha should be administered on next day. Even then

virechana does not happen, after 10 days again virehana oushadha can be given after

proper snehana and swedana36.

Vega Nirnaya

For Veganirnaya the physician has to leave the first two three malayukta vegas

and then counting should be done. By observing the vegiki, maniki, antaki and laingiki

lakshanas, one has to decide whether virechana is pravara, madhyama or avara.

Table No.06. Showing the Virechana vega nirnaya37.

Sl. Vega vishaya Pravara Madhyama Avara

01. Vegiki lakshana 30 vega 20 vega 10 Vegas

02. Miniki lakshana 4 Prastha 3 Prastha 2 Prastha.

03. Antaki lakshana Kaphantam

04. Laigiki lakshana General signs and symptoms of virechana

A proper or well-performed Virechanakarma leads to samyak Virechana

lakshanas. i.e. 38,

Indriya prasannata.

Expulsion of vit, pitta, kapha and

vata in sequence.

Sroto shuddhi.

Vatanulomana.

Shareera laghuta.

Agnideepti

Absence of atiyoga and ayoga

virechana lakshanas.

Virechana karma


Like the knowledge of virechana samyak lakshanas, the knowledge of ayoga and

atiyoga lakshanas are also very essential39.

Table No. 07. Showing the Virechana ayoga and atiyoga laxanas.

Virechana ayoga lakshansa Virechana atiyoga lakshanas

Lakshanas Ch. Su. Vag. Lakshanas Ch. Su. Vag.

Kapha Praseka + + + Kapha Kshaya vikara + + -

Pitta Prakopa + + + Pitta kshaya vikara + - -

Vata Prakopa + - - Vata Kshaya vikaya + - -

Agni mandya + + - Anga marda + - _

Gaurava + + - Klama + - -

Pratishyaya + - + Vepathu + - _

Tandra + - _ Nidra + - -

Chardi + - - Dourbalya + - -

Aruchi + + + Tama pravesha + - -

Vata pratilomata + - - Unmada + - -

Daha - + + Hikka + - -

Hridaya Ashudhi - + + Moorcha - - -

Kukshi Ashudhi - + + Guda bhramsha - - -

Kandu - + + Shoola - + -

Vit sanga - -

+

+ Kapha pitta rahita, sweta, lohita udaka nissaranam

- - +

Mutra Sanga - + - Mamsa udaka srava - - +

Pidaka - - + Medo gandhavat srava

- - +

Virechana karma


Trishana - - +

Bhrama - - +

Netra Praveshana - - +

Ati vamana vyapat - - +

Rakta kshaya vikara + - -

Due to Kaphotklesha, aruchi and ajeernata, the virechanoushadha may produce

vamana. In such conditions, patient should be given snehana and swedana and again

oushadha should be given. Even then virechana is not possible, if oushadha is not satmya

to the patient and dravya is not producing any apriyata, once again oushadha can be given

for attaining Virechana40.

Soon after the samyak virechanakarma digestive power gets impaired. So the

peyadi samsarjana krama should be followed in order to bring back the normal agni41.

Except in the following conditions, in others peyadi samsarjana karma can be done.

They are,

Pitta kapha parisrava

Madatyaya

Vata pitta prakriti

In the above conditions tarpana can be administered.

Improper conduction of Virechana leads to the vyapats (complication) Like42,

Aadhmana

Jeevadana

Parikartika

Vibhrama

Parisrava

Stambha

Anga graha

Hrit graha

Klama

Virechana karma


Sushruta has given 15 vyapaths (complications) of Virechana43,

Vamana occurs with Virechana

dravya and vise versa

Shesha oushadatwam

Jeerna oushadhatwam

Aadhmana

Heena oushadha apahritatwam

Jeevadhana

Parikartika

Vata ruk

Parisrava

Ayoga

Pravahika

Atiyoga

Hridyopasarana

Vibandha

As seen above, acharyas have clearly mentioned the ayoga, atiyoga and vyapats in

detail and their treatment.

Mode of Action of Virechana Drugs

As explained earlier, the virechana dravyas have the properties like ushna,

teekshna, sookshma, vyavayi and vikashi gunas. The drug having these properties will

reach the heart by its potency and there by to the entire dhamanis. Also it reaches to big

small and minute srotases of the body. Due to the presence of ushna veerya, vishyandana

is produced; teekshna guna produces chedana of dosha samoohas and brings it to the

koshta. From there due to prithvi and jala mahabhoota gunas and also due to

adhobhagahara prabhava the doshas are get eliminated through guda marga. Both

virechana and vamana oushadha having the same properties, but virechana drugs

produces virechana and vamana drugs produces vamana only and it is only because of its

prabhava. Virechana dravyas produce uttejana in the sotases, dhamanies, koshta and

ultimately on hridaya kendra. Sushruta added sara guna along with the ushnadi gunas and

this sara guna is helpful in anulomana procedure44.

Virechana karma


Acharya Charaka says, the drugs acts not only due to its prabhava but also due to

it’s dravyatwa prabhava, gunatwa prabhava and both dravyatwa and gunatwa prabhava.

And the factors mentioned here may change based on conditions. The effect produced

due to above is called karma. The factor responsible for manifestation of effect is

veerya45.

Modern Concept of Purgatives46

The terms purgative, cathartic, laxative, and evacuant may be considered

synonymous. They are medicines that promote defecation largely by reducing the

viscosity of the contents of the lower colon.

Purgatives may be classified as:

01. Bulk purgatives.

02. Osmotic Purgatives.

03. Fecal softeners.

04. Stimulants.

01. Bulk purgatives :

These comprise indigestible vegetable fiber and hydrophilic colloids. Bulk

purgatives act by increasing the volume and lowering the viscosity of intestinal contents

to promote a large soft, solid stool. The substances thus encourage normal reflex bowel

activity, rendering it more effective and generally acting within 1-3 hours. Dietary fibers

are essentially the cell walls and supporting structures of vegetables and fruits.

Increasingly reference is made to non-starch polysaccharide (NSP), which refers to

carbohydrates that are not digestible by human enzymes and which can be assayed. NSP

comprises most of the fiber in our diet.

Virechana karma


02. Osmotic laxatives :

These are but little absorbed and increases the bulk and reduces viscosity of

intestinal contents to promote a fluid stool. Some inorganic salts retain water in the

intestinal lumen or, if given as hypertonic solution withdrawn it from the body. Lactulose

is a synthetic disaccharide, taken orally, it is unaffected by small intestinal disaccharides,

is not absorbable and this acts as an osmotic laxative.

03. Fecal softeners (emollient) :

The softening purposes of these agents are useful in the management of anal

fissures and hemorrhoids. In this the feces is softened by lowering the surface tension of

fluids in the bowel, which allows more water to remain in the feces.

04. Stimulant purgatives (contact laxatives) :

These increase intestinal motility by various mechanisms. They may cause

abdominal cramps and should not be used where there is intestinal obstruction.

After giving the explanation of virechana karma along with its modern aspects, it is

necessary to narrate the normal anatomical and physiological activities that are going on

in the stomach, small intestine, large intestine and rectum, which are given below.

Virechana karma


SHAREERA

Stomach 47

The stomach has the shape of an expanded “J”. The stomach performs 4 major

functions. Viz.

01. The bulk storage of the ingested food.

02. Disruption of chemical bonds in chemical materials through the action of acids

and enzymes.

03. Mechanical breakdown of ingested food.

04. Production of intrinsic factor, a glycoprotein whose presence in the digestive tract

is required for the absorption of the vitamin B12.

Regulation of Gastric phase –

The CNS, regulated by the short reflexes coordinated in the wall of stomach and

regulated by the digestive tract hormones can control the production of acids and

enzymes by the gastric mucous.

01. The cephahlic phase –

Function – Prepare stomach for arrival of food.

Duration – short. (minutes)

Mechanism – Neural via preganglionic fibers in vagus nerve and synapse in

submucosal plexus (by seeing, smell, taste or thoughts of food)

Actions – Primary – Increased volume of gastric juice by stimulating

mucous, enzyme and acid production.

Secondary – Stimulation of gastrin release by G cells.

Shareera 26


02. Gastric phase –

Enhance secretion started in cephalic phase, homogenizes and acidify the chyme.

It initiates the digestion of proteins by pepsin. Duration of the phase is long i.e. 3-4 hours.

Mechanism –

Neural – Short reflexes triggered by stimulation of stretch receptors as

stomach fills. There is also stimulation of chemo-receptors as PH increases.

Hormonal – Stimulation of gastrin release by G cells by

parasympathetic activity and presence of peptide and amino acids in chyme. Also the

release of histamine by mast cells as stomach fills. As a result there is an increased acid

and pepsinogen production, increased motility and initiation of mixing waves. The

mixing waves occur several times per minute and they gradually increase in intensity.

After an hour, the material with in the stomach is churning like the clothing in the

washing machine.

03. Intestinal phase –

The main function of this phase is controlled rate of chyme entry into duodenum.

The duration of this process is long. i.e. hours.

Mechanism –

Neural – short reflexes (entero-gastric reflex) triggered by the extension of

duodenum.

Hormonal –

Primary – Stimulation of CCK, GIP, and secretin release by presence of

acid, carbohydrate and lipids.

Shareera 27


Secondary – Release of gastrin stimulated by presence of undigested

proteins and peptides and finally there is feed back inhibition of gastric acid and

pepsinogen production, reduction of gastric motility.

The intestinal phase of gastric secretion begins when chyme starts to enter the

small intestine. The intestinal face generally starts after several hours of mixing

contractions, when the wave of contraction begins sweeping down the length of the

stomach. Each time the pylorus contracts, a small quantity of chyme squits through the

pyloric sphincter. The purpose of intestinal phase is to control the rate of gastric

emptying and ensure that the secretary, digestive functions of the small intestine can

proceed with reasonable efficacy. The arrival of chyme in the small intestine also triggers

other neural and hormonal events that co-ordinate the activities of intestinal tract,

pancreas, liver, and gall bladder.

Small Intestine48

The stomach is a holding tank where food is saturated with gastric juices and

exposed to stomach acids and the digestive effects of pepsin. These are the primary steps,

for most of the digestive and absorption functions occur in the small intestine, where the

products of digestion are absorbed.

The mucosa of the small intestine produces only a few of the enzymes involved.

The pancreas provides digestive enzymes as well as buffers that assist in the

neutralization of acidic chyme. The liver and the gall bladder provide bile, a solution that

contains additional buffers and bile salts, compounds that facilitates digestion and

absorption of lipids.

Shareera 28


The small intestine averages 6 m. in length and has a diameter ranging from 4 cm

at the stomach and about 2.5 cm at the junction to the large intestine. It accompanies all

abdominal regions except the right and left hypochondriac regions. It has 3 subdivisions.

duodenum, jejunum and ileum.

Intestinal Movements

After chyme has arrived in the duodenum weak peristaltic contractions move it

slowly towards the jejunum. These contractions are mesenteric reflexes not under CNS

control. Their effects are limited to with in a few centimeters of the site of the original

stimulus. These short reflexes are controlled by motor neurons in the submucosal and

mesenteric plexus. In addition, some of smooth muscle cells contract periodically even

without stimulation, establishing a basic contractile rhythm that then spreads from cell to

cell.

The stimulation of the parasympathetic system increases the sensitivity of these

mesenteric reflexes and accelerates both local peristalsis and segmentation. More

elaborate reflexes coordinate activities along the entire length of small intestine. Two

reflexes are triggered by the stimulation of the stretch receptors in the stomach as it fills.

The gastro-enteric reflexes stimulates motility and secretion along the entire length of the

small intestine, the gastro-ilial reflex triggers the relaxation of the iliocecal valve. The net

result is that, the materials pass form small intestine to the large intestine. Thus the

gastro-enteric and the gastro-ilial reflexes accelerate movements along with small

intestine, the opposite effect of the entero-gastric reflex. Hormones released by the

digestive tract can enhance or suppress reflex responses.

Shareera 29


Large Intestine 49

The horseshoe shaped large intestine begins at the end of the ilium and ends at the

anus. The large intestine lies inferior to the stomach and liver and almost completely

frames the small intestine. The major functions are –

01.Absorption of water and compactness of intestinal contents into faeces.

02. Absorption of important vitamins liberated by the bacterial action.

03. Storing of fecal material before defecation.

It has the following parts –

01. Caecum

02. Colon

03. Rectum

Movements of large intestine

The gastro-ilial and gastro-enteric reflexes move materials into the caecum at

mealtime. Movement form the caecum to the transverse colon occurs very slowly,

allowing hours for water absorption to convert the already thick material into a sludgy

paste. Peristaltic waves move material along the length of colon. Movements from the

transverse colon through the rest of the large intestine results form powerful peristaltic

contractions called “Mass movements” which occur a few times each day.

The stimulus is distention of the stomach and the duodenum and the commands

are relayed over the intestinal nerve plexus. The contractions force the fecal materials

into the rectum and produce the conscious urge to defecate.

Shareera 30


Defecation The rectal chamber is usually empty except when one of those powerful peristaltic

contractions forces fecal material out of the sigmoid colon. Distention of the rectal wall

then triggers the defecation reflex.

The defecation reflex involves two positive feed back loops both are triggered by

stretch receptor stimulation in the walls of the rectum. The first loop is a shorter reflex

that triggers a series of peristaltic contractions in the rectum that moves the feces towards

the anus. The second loop is a long reflex coordinated by the sacral parasympathetic

system. This reflex stimulates mass movements that push the fecal material to the rectum

from the descending colon and the sigmoid colon.

Rectal stretch receptors also trigger two reflexes important to the voluntary

control of defecation.

01. Visceral reflex –

Mediated by the parasympathetic innervations with in the pelvic nerves. This

reflex causes the relaxation of the internal anal sphincter, a smooth muscle sphincter that

controls the movements of the feces into the anorectal canal.

02. Somatic reflex –

That stimulates the immediate contraction of the external anal sphincter. The

elimination of the feces requires that both the internal and external anal sphincter to be

relaxed, but these reflexes open the internal sphincter and close the external sphincter.

The urge to defecate usually develops when rectal pressure reaches about 15 mm of Hg.

When it exceeds 55 mm of Hg external sphincter will relax and the defecation occurs.

Diabetes mellitus is a chronic disease due to the disordered carbohydrate

metabolism and results due to deficiency of insulin secreted by the beta cells of Islets of

Shareera 31


Langer Hans of pancreas. But the hormones of pituitary and adrenal glands are also

intimately related to the development of this state. Apart form this liver had its own role

in the manifestation of this disease, because it stores the glucose in the form of glycogen

under the influence of insulin. Any alteration in this leads to diabetes. So following are

the glands involved in the pathology of manifestation of the diabetes mellitus –

01. Pancreas

02. Pituitary

03. Adrenal

04. Liver

Pancreas50

The pancreas lines within the abdomino-pelvic cavity in the ‘J’ shaped loop

between the stomach and the small intestine. It is a slender, plane organ with a nodular

consistency. The adult pancreas is 20 –25 cm long and weights about 80 gms. The broad

head of the pancreas lines within the loop formed by the duodenum as it leaves the

pylorus. The slender body extends transversely towards the spleen and the tail is short

and bluntly rounded. The pancreas is retroperitonal and is firmly bound to the posterior

wall of abdominal cavity.

The surface of the pancreas has a lumby, lobular texture. A thin, transparent

connective tissue capsule wraps the entire organ. You can see the pancreatic lobules,

associated blood vessels and excretory ducts through the anterior capsule and the

overlying layer of peritoneum.

Arterial blood reaches the pancreas by way of branches of the splenic, superior

mesenteric and common hepatic arteries. The pancreatic arteries and Pancreaticoduodenal

arteries are the major branches from these vessels. Splenic vein and its branches drain the

pancreas.

Shareera 32


The pancreas is primarily an exocrine organ producing digestive enzymes and

buffers. The large pancreatic duct delivers these secretes to the duodenum. A small

accessory duct, or duct of Sanforini, may branch from the Pancreatic duct. The Pancreatic

duct extends within the attached mesentery to reach the duodenum, where it meats the

common bile duct from the liver and gall bladder.

The pancreas has two distinct functions, one endocrine and other exocrine. The

exocrine pancreas roughly 99 percent of the pancreatic volume consists of clusters of

gland cells, pancreatic acini, and their attached ducts. Together the gland and duct cells

secrete large quantities of an alkaline, enzyme rich fluid. This secretion reaches the

lumen of the digestive tract by traveling along a network of secretary ducts.

The endocrine pancreas consists of small groups of cells scattered among the

exocrine cells. The endocrine clusters are known as pancreatic Islets, or the Islets of

Langer Hans. Pancreatic islets account for only about 1 percent of the pancreatic cell

population. Nevertheless, a typical pancreas contains roughly 2 million pancreatic Islets.

Each Islet contains four different cell types.

01. Alpha cells –

Produce the hormone Glucagon. Glucagon raises blood glucose levels by

increasing the rates of glycogen break down and glucose release by the liver.

02. Beta cells –

Produce the hormone insulin. Insulin lowers blood glucose by increasing the rate

of glucose uptake and utilization by most body cells and increasing glycogen synthesis in

skeletal muscles and the liver. Beta cells also secrete amylin, a recently discovered

peptide hormone whose role is uncertain.

Shareera 33


03. Delta cells –

Produce a peptide hormone identical to somatostatin, a hypothalamic regulatory

hormone. Somatostatin produced in the pancreas suppresses glucagon and insulin release

by other islet cells and slows the rates of food absorption and enzyme secretion along the

digestive tract.

04. F cells –

Produce the hormone pancreatic polypeptide. It inhibits gallbladder contractions

and regulates the production of some pancreatic enzymes. It may help to control the rate

of nutrient absorption by the digestive tract.

Here focus is made on insulin and glucagon, the hormones responsible for the

regulation of blood glucose concentrations, which are given below. These hormones

interact to control blood glucose levels. When blood glucose levels rise, beta cells secrete

insulin, which then stimulates the transport of glucose across cell membranes. When

blood glucose levels decline, alpha cells secrete glucagon, which stimulates glucose

release by the liver.

Insulin

Insulin is a peptide hormone released by beta cells when glucose levels rise above

normal levels (70 to 110 m/c). Elevated levels of some amine acids, including arginine

and leucine, also stimulate insulin secretion. Insulin exerts its effects on cellular

metabolism in a series of steps that begins when insulin binds to receptor proteins on the

cell membrane. Binding heads to the activation of the receptor which functions as a

kinease and attaches phosphate groups to intracellular enzymes. Phosphorylation of

enzymes then produces Primary and secondary effects within the cell, the biochemical

details remain unresolved.

Shareera 34


One of the most important effects is the enhancement of glucose absorption and

utilization. Insulin receptors are present in most cell membranes. Such cells are called

insulin-dependent. However, cells in the brain and kidneys, cells in the lining of the

digestive tract, and red blood cells lack insulin receptors. These cells are called insulin

independent, because they can absorb and utilize glucose without insulin stimulation.

Effects of insulin on its target cells –

01. Acceleration of glucose up takes

This effect results from an increase in the number of glucose transport proteins in

the cell membrane. These proteins transport glucose into the cell by facilitated diffusion.

02. Acceleration of glucose utilization and enhanced ATP production

This effect occurs for two reasons –

(a) The rate of glucose use is proportional to its availability. when more

glucose enters the cells, more is used.

(b) Second messengers activate a key enzyme involved in the initial steps

of glycolysis.

03. Stimulation of glycogen formation (skeletal muscles and Liver cells)

When excess glucose enters these cells, it is stored in the form of glycogen.

04. Stimulation of amino acid absorption and protein synthesis

05. Stimulation of triglyceride formation in adipose tissues

Insulin stimulates the absorption of fatty acids and glycerol by adipocytes. The

adipose cells then store these components as triglycerides. Adipocytes also increase their

absorption of glucose; excess glucose is used in the synthesis of additional triglycerides.

As a whole (summary) insulin secreted when glucose is abundant and this

hormone stimulates glucose utilization to support growth and the establishment of

Shareera 35


carbohydrate (glycogen) and lipid (tryglyceride) reserves. The accelerated use of glucose

soon brings circulating glucose levels with in normal limits.

Glucagon

When glucose concentrations fall below normal, alpha cells release glucagons,

and energy reserves are mobilized. When glucagons binds to a receptor in the cell

membrane; it activates adenylate cyclase, and cAMP acts as a second messenger that

activates cytoplasmic enzymes. The primary effects of glucagons are –

01. Stimulation of glycogen breakdown in skeletal muscle and liver cells.

02. Stimulation of triglyceride breakdown in adipose tissues.

03. Stimulation of glucose production at the liver.

The liver cells absorb amino acids from blood steam, convert them to glucose,

and release the glucose into the circulation. This process of glucose synthesis in the liver

is called gluconeogenesis.

The results are a reduction in glucose use and the release of more glucose into the

blood steam consequently; blood glucose concentrations soon rise towards normal levels.

Pancreatic alpha cells and beta cells monitor blood glucose concentrations, and

the secretion of glucagon and insulin occur without endocrine or nervous instructions.

Yet, because the alpha cells and beta cells are very sensitive to changes in blood glucose

levels, any hormone that affects blood glucose concentrations will indirectly affect the

production of both insulin and glucagon. Insulin production is also influenced by

autonomic activity. Parasympathetic stimulation inhabits it.

Shareera 36


Pituitary Gland 51

This is an important ductless gland with lot of functions, including the control of

the other ductless glands and of body growth. This gland measures 1.5 cm in the coronal

plane, 1 cm in the sagittal plane and 0.75 cm in vertical form. It lies within the cella

tarsica of the sphenoid bone and the posterio-superior to the sphenoid air sinuses, below

the optic chiasma. It is flattened ovoid lying the hypophysial fossa and connected to the

inferior surface of the hypothalamic part of the brain by the infundibulum.

Structurally the gland can be divided into 2 main parts –

01. Anterior lobe – Which is composed of adenohypophyseas tissue.

02. Posterior lobe – Which is neurohypophyseas.

Posterior lobe of the hypophysis is the expanded 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 partly surrounds that lobe and the infundibulum. The distal

part forms most of the anterior lobe. It is separated from the posterior lobe by the thin

seat of glandular tissue applied to the posterior lobe. The infundibular part is a narrow

upward projection of the distal part. The anterior lobe develops from the ectoderm and

has only vascular connection with brain.

Anterior lobe is the master gland of the endocrine system, because it produces

protein tropic hormones, which affects the other ductless glands. In this secretions two

hormones are having direct action on carbohydrate metabolism. If any disturbance, which

leads to hyperglycemia or hypoglycemia. The two hormones are –

01. Growth Hormone or Somatotrophic hormone – (GH or STH)

02. Adrenocorticotrophic hormone (ACTH)

Shareera 37


The pituitary effect of STH on carbohydrate metabolism is to stimulate its

storage. Administration of growth hormone in the animal or in man produce

hyperglycemia and glycosuria. The high blood glucose level leads to its exhaustion and

atrophy. So the growth hormone has diabetogenic effect especially in man. The hormone

is however increase the glycogen content of cardiac muscles.

Administration of ACTH produces similar effects as induced by growth hormone.

Both STH and ACTH increase gluconeogenesis and diminish the rate of oxidation of

glucose. Thus the anterior pituitary has a diabetogenic role. GH is also known as

Somatotrophin and somatotrophic hormone causes cells to grow and multiply and it

increases the rate of protein synthesis. GH accelerates the rate at which glycogen stored

in the liver is converted to the glucose and released in the blood. GH raises blood glucose

level and the raise in the glucose, triggers insulin secretion. ACTH by stimulating

secretion of gluco-corticoids brings about hyperglycemia and also directly stimulates the

release of GHIF and inhibits the secretion of insulin. One stimulus that inhibits GH

secretion is hyperglycemia. An abnormally high blood sugar level stimulates the

hypothalamus to secret the regulating factor GHIF and it inhibits the release of GHAF

and thus the secretion of GH. As a result blood sugar level decreases.

Adrenal Gland 52

Adrenal glands are situated on the upper poles of the kidneys. Each gland weights

about 4 gms. A distinct connective tissue capsule surrounds the parenchyma of the gland.

Beneath the capsule the cortex is arranged in three layers –

01. Zona glomerulosa –

Secretes mainly aldeosterone and small amount of gluco-corticoids and sex

hormones.

Shareera 38


02. Zone fasciculata –

Secretes mainly gluco-corticoide.

03. Zona reticularis –

Secretes sex hormone and small amount of the glucocorticoids,

All the three zones of the adrenal gland can synthesis the gluco-corticoids. The

chief action of the gluco-corticoids is to increase glyconeogenesis in the liver and

stimulates formation of glycogen in the liver and muscles. The adrenal cortex also asserts

diabetogenic affects. Proteins are converted into carbohydrates i.e. glyconeogenesis occur

through the action of gluco-corticoids.

Therefore, constant production of carbohydrates and the insulin is required to

metabolize the excess of carbohydrates. The excessive glyconeogenesis exerts continued

strain upon the cells of Islets leads to hyperglycemia. When it is severe, causes damage to

beta cells and permanent insulin deficiency results. The adrenal action however depends

upon the action of anterior pituitary.

Liver 53

The liver is the largest gland in the body. The greater part of the liver lies under

the covering of the ribs and costal cartilage. The liver is a dark brown highly vascular soft

organ. It is approximately 1/50th of the body weight in the adults, but larger in the

newborn. The liver lies normally in the right hypochondrial and epigastric regions. The

surrounding organs determine the shape of the liver; it retains the shape of a blunt wedge.

It has two surfaces – diaphragmatic surface and visceral surface.

Lobes of liver –

The main lobes of liver right and left are demarcated form one another above and

in front by the falciform ligament and below and behind by the fissures for the

ligamentum teres and ligamentum venosum. The right lobe includes two subsidiary lobes.

Shareera 39


Important functions of liver with the special attention to carbohydrate metabolism

are -

01. Glycogen storage

02. Conversion of galactose and fructose in the glucose.

03. Gluconeogenesis

04. Formations of many important chemical components from the intermediate

products of carbohydrate metabolism.

The liver is especially important for maintaining a normal blood glucose

concentration. For instant storage of glycogen allows the liver to remove excess glucose

form blood, store it and return it to the blood when the blood glucose concentration

begins to fall too low. This is called Glucose buffer function of the liver.

Gluconeogenesis in the liver is also concerned with maintaining a normal blood glucose

concentration. Gluconeogenesis occurs to a significant extend only when the glucose

concentration begins to fall below normal. In such a case large amounts of amino acids

are converted into glucose, there by helping to maintain a relatively normal blood glucose

concentration.

Shareera 40


DISEASE REVIEW

Meha19 - It is a pum-Linga vachana formed by “Mih + Ghaj”

“Mehati Ksharati Shukratiranena iti”

Prameha : - It is also a masculin vachana formed by “Pra + Miha”

“Ksharane + Karane Khaj.”

It is a roga vishesha. Its paryayas are “Meha” as a mutra dosha by Raja Nighnatu

and as bahumutrata by Hemachandra. Diabetes is derived from a Greek word which

means “To siphon through” and mellitus a Latin word which means “Honey” 20.

Nidana

Nidana means the factor responsible for producing disease i.e. etiological

factors54.

According to this any factor, which has a tendency or capacity to produce disease

can be considered as Nidana. In classics only Charaka explains specific nidana for

madhumeha55.

Among the prameha nidanas that are mentioned in our classics samanya prameha

nidanas and kaphaj prameha nidanas can be considered as nidana for Madhumeha in

sthoola.

For all types of Prameha especially madhumeha, kapha dosha is the key factor,

and it can be established by Gangadhara’s version. In that he says, Gulma is caused by

vayu, raktapitta by pitta and madhumeha caused invariably due to the vitiation of kapha

dosha56.

In case of sthoola the madhumeha is due to doshavarana. And in this type of

doshavrita janya madhumeha, vataprakopa is due to avarana caused mainly by the

vitiation of kapha. If we take sthoulya here also kapha vardhaka factors are the main

factors behind57.

Disease Review 41


Though kapha is the arambhaka or main dosha in the samprapti of madhumeha,

pitta and vata also play an important role in complicating the disease58. It is worthwhile

to note the textual reference, that madhumeha will occur in due coarse, if Pramehas are

untreated and at the same time, it is better to note that madhumeha is a tridoshaja

vyadhi59.

In view of the above, all Prameha nidanas should be assessed clearly while

considering, the madhumeha. Hence the nidanas of various pramehas are discussed below

can be grouped under 2 main varieties60.

01.Sahaja (Hereditary)

02.Apathyaja (Acquired).

01. Sahaja (Hereditary Causes)

Charaka and Sushruta have agreed that beeja dosha is also a cause for

madhumeha. Sushruta has included madhumeha in the adibala pravritaja category of

disease. The term beeja has been considered as shukra and shonita61. If beejas are vitiated

with dosha responsible for causation of prameha, they will produce a jatha prameha

patient. Jatha pramehi has also been considered as a kulaja vikara. The diseases included

under this category are kushta, arsha, mehas, kshaya, etc.

02. APATHYAJA (ACQUIRED CAUSE)

Apathyaja causes of prameha can be further classified in to two groups

01. Samanya (General)

02. Vishesha (According to dosha)

Disease Review 42


Table No. 07a. Showing the Samanya Nidana of prameha61 –

Sl. Nidana Charaka Sushruta Vagbhata

Aaharaja Nidanas

01. Dadhi + - -

02. Gramya, oudaka mamsa + - -

03. Anupa mamsa + - +

04. Payaha + - +

05. Nava anna pana + - +

06. Guda Vikara + - +

07. Sheeta, Snigdha, Madhura

Madya sevana

- + -

08. Dravanna pana Sevanam - + -

09. Swadu, Amla, Lavana, Snigdha,

Pichila, Sheetala ahara.

- - +

10. Sura Sevana - - +

11. Ikshu rasam - - +

Viharaja Nidanas

12. Asya sukham + - -

13. Swapna sukham + - -

14. Diva swapnam - + -

15. Avyayamam - + -

16. Alasyam - + -

Disease Review 43


Kaphaja Prameha Nidana 63

AHARAJA NIDANAS

A. Rasa - Madhura padartha atisevana.

B. Guna - Drava taruna dravya atisevana.

C. Dravyas -

Dhanyas - Hayanaka, yavaka, navanna, cheena, uddalaka, naishada,

mukundaka, mahavrihi, pramodaka, sugandhaka, masha soopa added with ghrita.

Mamsa - Gramya, oudaka, anupa, mamsa rasa.

D. Others - Shakas, tila, pishtanna, payasa, krishara, vilepi, ikshu rasa, kshaudra,

mandaka, dadhi.

VIHARAJA NIDANAS

Vyayama varjana, adhika Nidra, shayana.

Asanasthaha.

Anya kapha meda mutra vridhikara viharas

Pittaja Prameha Nidana64

AHARAJA NIDANAS

A. Rasa - Amla, lavana, katu adhika sevana.

B. Guna - Ushna kshara adhika sevana.

C. Any - Ajeerna dravyas and vishamaharam.

VIHARAJA NIDANAS

Ati teekshna atapa sevana

Agni sevana.

Santapa

Shrama

Krodha.

Disease Review 44


Vataja Prameha Nidana65

AHARAJA NIDANAS

A. Rasa - Kashaya katu tikta ati sevana

B. Guna - Rooksha laghu sheeta ati sevana

C. Anya - Anashana

VIHARAJA NIDANAS

Vyavaya, ativyayama

Vamana, virechana, aasthapana,

shirovirechana ati upayoga

Vega sandharana

Abhighata

Atapa sevana

Udvega

Atishoka

Shonitatisekha

Ratri jagarana

Vishama shareera asana

Madhumeha Nidana 66

Only Charaka gives direct nidana or specific nidana responsible for the

production of Madhumeha, which can be narrated as follows –

Guru, snigdha, lavana rasatmaka

dravya atisevana

Navanna and pana

Atinidra

Asya sukham

Achinta

Avyayama

Asamshodhana

These factors contribute to the vikriti of the kapha, pitta, meda and mamsa. These

vitiated factors cause avarodha to normal vayu gati, which in turn carries the ojas to vasti

thus resulting in Madhumeha.

Disease Review 45


Sthoulya as a nidanarthakara Roga

Sushruta has stated that apthyanimittaja pramehi’s are sthoola67. Sthoulya is the

nidanarthakara roga for prameha. It is clear that samanya nidana of sthoulya and prameha

stimulates each other.

In sthoulya, the pathway of the vata gets obstructed by medas, as a result there

will be the vitiation of vayu, which in term stimulates the samana vayu resulting in the

aggravation of digestive fire and causes increased absorption of food and the individual

becomes heavy eater.

Etiology of Diabetas Mellitus68

A defective or deficient insulin secretary response, which translates in to impaired

carbohydrate use is a characteristic feature of diabetes mellitus and resulting in to

hyperglycemia.

Genetic Factors

Genetic factors are even more important than in type I diabetes. Among identical

twins, the concordance rate is 60% to 80%. In first-degree relatives with type II diabetes

the risk of developing disease is 20% to 40%.

The two main defects that characterize type II diabetes are

01. A derangement in beta cell secretion of Insulin.

02. A decreased response of peripheral tissues to respond to Insulin (Insulin

resistance).

Obesity

Among the initiating events, which are proposed for type II diabetes, obesity is an

extremely important environmental factor. Approximately 80% of type II diabetes is

obese.

Disease Review 46


Age

As the age advances the number of beta cells in pancreas, which produce insulin,

gets reduced. So the risks of diabetes increase with age especially after 40 years.

Sedentary Life

Some recent studies have indicated that people with sedentary life style are more

likely to have diabetes as compared to those who lead an active life. It is believed that

exercise and physical activity increase the effect of insulin on the cells.

Hereditary

The hereditary aspects of diabetes is well summarized in the following statement

by warren and Le Compte, when both the parents have diabetes, all the children may

expected to develop the disease, if they live long enough. When one parent has diabetes

and the other is diabetic carrier, 40% of their children may develop the disease. Where as,

if a diabetic or a carrier marries an individual who neither has diabetes nor a diabetic

carrier none of the children will have diabetes.

Obesity is mentioned as a major causative factor for diabetes Mellitus, as it causes

insulin resistance. In Ayurveda sthoulya is mentioned as a nidanarthakara roga of

prameha, and this prameha is included under santharpanajanya vyadhi.

Madhura, snigdhaadi bhojana are mentioned as nidanas for madhumeha. In

modern science over eating and sedentary lifestyles are the predisposing factors for

diabetes mellitus. This food articles and over eating causes obesity and which may cause

diabetes mellitus.

Disease Review 47


Poorva Roopa

The symptoms which are produced during the process of sthanasamshraya by

vitiated doshas are called as poorva roopa69.

Table No. 08. Showing the poorva roopas70.

Sl. Poorva roopa Charaka Sushruta Vagbhata

01. Kesha Jatilibhava + + -

02. Asya Madhuryata + - -

03. Kara, pada, Daha + + +

04. Kara, pada, Suptata + - -

05. Mukha, talu, gala, Kantha Shosha + - -

06. Pipasa + + +

07. Alasya + - -

08. Kaye Malam + - -

09. Paridaham + - -

10. Anga suptata + - -

11. Shatpada pipilikadhi shareera

Mootrabhi Saranam

+ - -

12. Visra shareera ganda + - -

13. Atinidra + - -

14. Tantra + + -

15. Snigdha, pichhila, guru, gatrata - + +

16. Madhura, Sukla, Mutrata - + -

17. Durgandha Swasa - + -

Disease Review 48


Sl. Poorva roopa Charaka Sushruta Vagbhata

18. Talu, gala, jihwa, danteshu Malotpatti - + +

19. Nakhaati vridhi - + +

20. Swedam - - +

21. Shareera daurgandha + - -

22. Keshaathi vridhi - - +

23. Sheeta priyatvam - - +

24. Mootre abhidhavanti Pipeelikascha + - -

25. Ghanangata - - +

26. Anga shithilatvam - - +

Madhavakara, Bhavaprakasha, Yogaratnakara and Bhela are also described the

poorva roopas, which are same as that of above description.

Roopa

Means symptoms of the actual manifestation of disease. At this stage dosha

dooshya Samoorchana would have been completed and the onset of the disease would

have been commenced. Madhavakara explains it as, when symptoms in the stage of

poorvaroopa become fully or clearly manifested they are called roopas. Roopa is the

prominent diagnostic key of a disease and hence thorough knowledge of the various

roopas of each disease is essential for a physician71.

Sushruta classified Prameha in to two types they are72,

01. Sahaja

02. Apathya nimittaja

He also explained the specific lakshanas of both the prameha as follows,

Disease Review 49


Sahaja

Sahaja pramehis are krisha, ruksha, alpashi, pipasa brusam (intense thirst) and

parisarana sheela (tendency for roaming).

Apathya Nimittaja

Apathya nimittaja pramehi’s are sthoola, snigdha, bhahwashi (polyphagia),

shayyasana sukhalu, and swapna sheela.

Clinical features of the Prameha may be divided in to 2 groups they are,

01. Samanya Lakshanas.

02. Vishesha Lakshanas.

Samanya Lakshanas73

Charaka has not described the general or samanya lakshanas of Prameha where as

Sushruta and Vagbhata have given the samanya lakshanas clearly.

They are –

01. Prabhoota mootrata

02. Avila moootrata

Vishesha Lakshanas

Charaka, Sushruta and Vagbhata mentioned the vishesha lakshanas.

Kaphaja Pramehas 74

01. Udaka meha : - The person passes clear urine, excessive in quantity, whitish,

cool, odourless and watery.

02. Ikshumeha : - The urine of person becomes sweat, cool slightly viscid, turbid and

resembling the juice of sugar cane.

03. Sandra meha : - The urine gets thickened if kept over night in a vessel.

Disease Review 50


04. Sandraprasada meha : - The character of urine manifests here partly dense and

partly clear after keeping in a vessel.

05. Shukla meha : - White urines are excreted here and appear as if mixed with flour,

and frequency of maturation takes place.

06. Shukra meha : - The person frequently passes urine, white, appears like shukra.

07. Sheeta meha : - The person excretes here large quantities of urine, which is

exceedingly sweet and cold.

08. Sikata meha : - The passing of urine is mixed with hard and small particles.

09. Shanair meha : - There is no force of urine during the time of passing, more over

person feels difficulty at the time of excretion.

10. Alalameha : - The urine is full of mucus threads is slim and viscid.

Pittaja Pramehas 75

01. Kshara meha : - The urine is alkali like in character.

02. Kala meha : - The provocation of pitta transforms the urine as warm and black in

colour.

03. Neela meha : - Passes urine of the colour of the wings of jaybird and is acidic in

reaction.

04. Lohita meha : - Urine smells like raw flesh and saltish warm and red.

05. Manjishta meha : - Person passes urine, which is profuse in quantity smells like

fresh meat.

06. Haridra meha : - Urine is of the colour of the colour of turneric water and is

pungent.

Disease Review 51


Vataja Pramehas76

01. Vasa meha : - Provoked vata passes urine mixed with or having the appearance

of fat.

02. Majja meha : - Discharges urine with majja frequently due to provoked vata.

03. Hasti meha : - Discharges frequently excusive amounts of urine like elephant.

04. Madhumeha : - Passes urine which is astringent and sweet in taste, yellowish and

whitish in colour Urine contains similar proportion of Honey.

Madhumeha Roopa77

Acharya Sushruta gives explanation regarding the lakshanas of Madhumeha, as

follows –

01. Gamanat sthananichati

02. Sthanat asananichati

03. Aasanat sayyamichati

04. Shayanat swapnamichati.

Apart from the above lakshanas urine similar to honey in colour and taste are also

attributed to Madhumeha78.

Clinical Features79

It is very difficult to sketch with brevity the diverse clinical presentation of

diabetes mellitus. Only a few characteristic patterns will be presented.

The type II (NIDDM) diabetes present with polyuria, polydipsia but unlike type I

diabetes patients are often older and frequently obese. Some times weakness or weight

loss also noted. Apart from these features others like, polyphagia, pruritis vulvae,

glycosuria, infections, delayed healing of wounds, impotency, are also noted.

Disease Review 52


Polyuria is due to the osmotic diuretic effect of glucose in kidney tubules. The

glycosuria induces an osmotic diuresis and thus polyuria, causing a profound loss of

water and electrolytes.

The obligatory renal water loss combined with the hyper osmolarity resulting

from the increased levels of glucose in the blood tends to deplete intracellular water,

triggering the osmoreceptors of the thirst centers of the brain. In this manner intense

thirst (polydipsia) appears.

The catabolism of proteins and fat tends to induce a negative energy balance,

which in turn leads to increasing appetite, i.e. polyphagia. Despite the increased appetite,

catabolic effects prevail, resulting in weight loss and muscle weakness. Frequently,

however the diagnosis made after routine blood or urine testing mainly in asymptomatic

persons.

Whenever the quantity of glucose entering the kidney tubules in the glomerular,

filtrate rises above approximately 225 mg/min, a significant proportion of the glucose

begins to spill in to the urine and when the quantity increases above about 325 mg/min

which is tubular maximum for glucose. All the excess, above this is lost in to urine

(Glycosuria).

A comparative study of madhumeha lakshanas with the Diabetes mellitus

explained in the modern science reveals a lot of similarities between them.

Prabhootaavilamootrata is considered as a prathyatma lakshana of Prameha. In

this the bahudrava kapha along with other dooshyas mainly kleda pradhana dooshyas in

the basti is the cause for prabhoota mootrata. The same reason has been given in modern

science for polyuria that the osmotic diuretic effect of glucose in the kidney tubules.

Disease Review 53


Glycosuria explained in the modern science can be taken as madhusama mootra.

The reason for this madhusama mootra is bahudrava kapha or ojus (Glucose) which is

excreted through moootra.

Pipasa or polydipsia mentioned in both sciences. Depletion of intracellular water

triggering the osmoreceptors of thirst center of brain and thirst is noted which is similar

to pipasa of Ayuredic science, here due to excessive loss of the urine; pipasa is noted.

Bahukankshata has been mentioned as a lakshana in apathya nimittaja

madhumeha, the same in modern science in terms of polyphagia.

In modern science the condition weakness is due to lack of glucose utilization,

loss of electrolyte and protein loss. In Ayurveda this same condition is due to aparipakwa

dhatus i.e., lack of proper nourishment of dhatus.

By considering the above similarities, we can come to a conclusion that

Madhumeha explained in Ayurvedic science and the diabetes mellitus mentioned in the

modern science are almost similar condition.

Samprapti

All the stages from the very contact of the body with hetus to the development of

the disease, including all its avasthas are together called the samprapti of disease. Every

fact connected with the process of disease at its various stages is considered in detail

under samprapti. Thus it is the entire pathogenesis, which takes place in the body under

the influence of etiological factors till the manifestation of disease80.

Acharya Charaka says, disease may manifest in various intensity or in different

ways based on the vikara vighata bhava and vikara vighata abhava i.e. based on nidana,

dosha, dooshya and their degree of vitiation disease may manifest on different ways.

Disease Review 54


When the equilibrium of these factors are disturbed or when they do not support each

other or when they are weak due to temporal factors then, either the disease does not

manifest it self or there is delay in manifestation or the disease is very mild or all its

symptoms are not properly manifested. From this we can conclude that manifestations of

diseases are based on the vikara vighata bhava and abhava81.

Even though acharya explained this in the context of Prameha, it is applicable to

all diseases.

Madhumeha Samprapti82

Only Charaka explains the direct Samprapti of madhumeha. Charaka explained

the relevance of avarana in the Samprapti or formation of Madhumeha. He explained this

in the “Keeyantaha Shiraseeya adhyaya” of Sutrasthana. On this context he explained

the nidanas, which are almost kapha and pitta vardaka.

Over use of Snigdha ahara, avyayama, etc. leads to provocation of kapha and pitta

intern causes increase in the quantity of meda and mamsa. Increased above factors

obstruct the path of vata leading to its provocation and thereby, leads ojas to basti causes

madhumeha roga. In this signs and symptoms of vata, pitta and kapha are manifested

frequently. They vanish at times and appear again. If neglected leads to further

compilations.

As explained earlier only Charaka explains the direct Samprapti of Madhumeha.

In classis, samanya Samprapti has also explained which is applicable to madhumeha also

as it is one among the 20 types of Prameha. Based on the both Symprapti, madhumeha

Samprapti can be explained in the following manner.

Disease Review 55


Due to nidana sevana kapha gets aggravated immediately, among three doshas

and here kapha that is vikruta and bahudrava in nature is due to agnimandya.

As rasa is the ashrayasthana of kapha and rasa is the aadya dhatu, the bahudrava

kapha vitiates rasa dhatu and travels all over body because of shithilata and

“Thanumaduryata noted”.

Here the Shareera shithilata is due to the formation of bahuabadha medas which is

formed due to nidana sevana and as a result there is no uttarottara dhatu pushti and leads

to shareera shaithilyata.

Bahudravata of shleshma also seen in this condition. As kapha is responsible for

shareera sthirata and when bahudravata or vitiation happens shareera shithilata results.

Further the buhudrava kapha vitiates medas and causes bahuabadha medas, which

is asamhata in nature. Apart from this bahudrava kapha condition, other factors like

nidanas like beeja dosha or kulaja dosha and in sthoulya condition also these abadha

medas is seen. As there is the medovaha srotodushti there is the occurrence of

sthanasamshraya between the kapha and medas as they are having same qualities. These

dosha dushya samoorchana causes obstruction in the path of vata and vitiates it. This vata

takes bahu drava kapha to all other dooshyas and vitiates them and further aggravation

leads to adhika kledata. Thus the increased kleda vitiates other dooshyas and moves, to

the basti and Madhumeha occurs.

Samprapti according to Modern83

Diabetes mellitus is characterized by glucose concentrations that are high enough

to over whelm the reapportion capabilities of the kidneys. Glucose appears in urine and

urine production generally become excessive. Other metabolic products, such as fatty

acids and other lipids are also present in abnormal concentrations.

Disease Review 56


While much has been learned in the recent years, the pathogenesis of type II

diabetes remains enigmatic. There is no evidence that autoimmune mechanisms are

involved in this. Life style clearly plays a role and clearly evident when obesity is

considered. Genetic factors are even more important than in type I diabetes.

The two metabolic defects that characterize type II diabetes are

01. Derangent on beta cell secretion of insulin.

02. Decreased response of peripheral tissues to respond to insulin (insulin resistance)

Deranged beta cell secretion of Insulin

In populations at risk for developing type II diabetes, a modest hyperinsulinemia

may be observed, attributed to beta cell hyper responsiveness to physiologic elevations in

blood glucose. With the development of overt disease, the pattern of insulin secretion

exhibits a subtle change. Early in the course of type II diabetes, insulin secretion appears

to be normal and plasma insulin levels are not reduced. However normal pattern of

insulin secretion is lost and the rapid first phase of insulin secretion triggered by glucose

is obtunded. Collectively this and other observations suggest derangements in beta cell

responses to hyperglycemia early in type 2 diabetes rather than deficiencies in insulin

synthesis.

A mild to moderate deficiency of insulin develops later in the course of type II

diabetes that is less severe than the- type I. The reason for this is not clearly known but

irreversible beta cell damage appears to be present. According to one view, all the

somatic cells of predisposing individual including pancreatic beta cells are genetically

vulnerable to injury, leading to accelerated cell turnover and premature aging and finally

to reduction in beta-cells mass. Chronic hyperglycemia may exhaust the ability of beta

cells to function (called glucose toxicity), as a consequence of persistent beta cell

stimulation.

Disease Review 57


Insulin Resistance

Insulin deficiency is present in the course, of type II diabetes. Reduced

responsiveness of peripheral tissues i.e. insulin resistance, is a major factor in the

development of type II diabetes. In obesity it is very much prominent or clear. The

molecular basis of insulin resistance is not clear. There may be a decrease in the number

of insulin receptors and more important post receptor signaling by insulin is impaired.

Also the insulin resistance leads to,

01. The inability of circulating insulin to properly direct the disposition of glucose.

02. A more persistent hyperglycemia.

03. More Prolonged stimulation of the pancreatic beta cell.

Obesity

Obesity is an extremely important environmental factor in the formation of type II

diabetes.

Approximately 80% of type II debates are obese. In this, the impaired binding is a

result of decrease in the number of insulin receptors.

Amylin

Among the pathological changes, which are happening in type II diabetes, the

most consistent of these changes is probably deposition of amyloid, which is

accompanied by atrophy of the normal tissue, particularly Islet epithelial cells. In more

advanced lesions, the Islet is more or less converted to amyloid and the reduction in the

number of insulin secreting cell is more pronounced than that of glucagons-secreting

cells. Heavy deposition of amyloid itself is rare without diabetes.

Disease Review 58


Acharyas have given importance to the medovaha srotas in the pathogenesis of

madhumeha. In classics it is mentioned that vapavahana is the moola sthana of medovaha

srotas, and which can be considered as pancreas. But there is no much description in

Ayurvedic classics regarding vapavahana. Charaka has explained that the vapavahana is

an udarasthaanga and he also says, it is having the shape of taila varti. So on the basis of

this physio-anatomical similarity, we can co-relate the vapavahana with pancreas. But

kloma also considered as pancreas by some acharyas. As pipasa mentioned as a kloma

vikriti lakshana, which is the main characteristics of the madhumeha, here it can also co-

relate with the pancreas.

Insulin resistance and relative insulin deficiency are the major step in the

pathogenesis of the diabetes mellitus on obese individuals. If the pancreas is healthy and

if it secretes sufficient insulin even this obese people will also won’t get diabetes

mellitus. There is no explanation regarding insulin resistance in Ayurveda. Even though

in some recent literary works medodhatwagni is correlated with insulin. But, no proves

are available for exact co-relation. If we see the pathology, we can see that the concept of

agni plays a great role i.e. agni mandya is considered to play key role in the formation of

aparipakwa dosha and dushyas which is the main defect behind madhumeha.

In normal state sthiratwa, dardya, utasaha, vrishada, buddhi, etc are contributed by

kapha, which is also known as bala or oja. By seeing this we can co-relate this kapha with

glucose. In madhumeha the kapha which is vitiated and which is in bahudravata form

travels all over the body in rasa produces tanu madhuryata, which can be taken as

hyperglycemia i.e. increased blood glucose condition.

Disease Review 59


Also in the Samprapti we can see the word basti. In Ayurveda it has been used in

different contexts in different meaning i.e. as bladder, whole urinary tract and also

kidney. Sushrutaacharya says nabhi prishta madhyaha basti. Anatomically kidney and

ureters are situated in this region. Also he says, the term “Bastau” which indicates the

plural sense i.e. two kidneys.

So, here an attempt is made to co-relate the pathogenic factors mentioned in

Ayurveda and in modern science. To prove the above ideas correctly, further studies are

needed.

Bheda

Though prameha is stated to be a condition due to the vitiation of all three doshas,

the disease is mainly divided in to 3 groups84 –

01. Kaphaja Pramehas - 10 in number.

02. Pittaja Pramehas - 6 in number.

03. Vataja Pramehas - 4 in number.

Even though the three Ayurvedic authorities Charaka, Sushruta and Vagbhata

agree the same number of pramehas in each group, they seems to be different in the

nomenclature used by them.

Table No. 08a. Showing are the Pramehas according to the major classics85,86,87..

No. Charaka Sushruta Vagbhat

Kaphaja Prameha (10)

01. Udaka Meha Udaka Meha Udaka Meha

02. Ikshu Meha Ikshu Meha Ikshu Meha

03. Sikata Meha Sikata Meha Sikata Meha

Disease Review 60


04. Sanair Meha Shanair Meha Shanair Meha

05. Sandra Meha Sandra Meha Sandra Meha

06. Shukra Meha Shukra Meha Shukra Meha

07. Sandra Prasada Meha -- --

08. Shukla meha Pishta Meha Pishta Meha

09. Sheeta meha -- Sheeta Meha

10. Aalala Meha -- Aalala Meha

11. -- Sura Meha Sura Meha

12. -- Lavana Meha Lavana Meha

13. -- Phena Meha --

Pittaj Prameha (06)

01. Kshara Meha Kshara Meha Kshara meha

02. Kala Meha -- Kala meha

03. Neela Meha Neela Meha Neela Meha

04. Lohita Meha Shonita Meha Rakta Meha

05. Manjishta Meha Manjishta Meha Manjishta Meha

06. Haridra Meha Haridra Meha Haridra Meha

07. -- Amla Meha --

Vataja Meha (04)

01. Vasa Meha Vasa Meha Vasa Meha

02. Majja Meha -- Majja Meha

03. Hasti Meha Hasti Meha Hasti Meha

04. Madhu Meha Kshaudra Meha Madhu Meha

05. -- Sarpir Meha --

Disease Review 61


Apart from the above classifications, the following types of classification can also

be given, such as,

I. Based on hetu bheda88

01. Sahaja

02. Apathya nimittaja

II. Based on chikitsa89

01. Sthoola - balavan

02. Krusha – durbala

III. Based on samprapti90

01. Dhatukshayajanya

02. Doshavruttajanya

Vagbhata explains that, avritajanya madhumeha is kashta sadhya and

dhatukshayajanya as asadya.

Classification Of Diabetes Mellitus91

I) Primary diabetes

(i) Type I Insulin dependent diabetes Mellitus (IDDM)

(ii) Type II Non-Insulin dependent diabetes Mellitus (NIDDM)

Under this type II again 2 types can be seen

01. Non obese NIDDM

02. Obese NIDDM

Genetic defects of beta cell function including maturity on set diabetes of young

known as MODY (1,2,3).

Disease Review 62


II) Secondary Diabetes

01. Pancreatic Pathology

(a) Pancreatitis (b) Haemochromatosis

(c) Neoplastic disease (d) Pancreactectomy

(e) Cystic fibrosis.

02. Iaotrogenic

(a) Corticosteroid (b) Thiazide diuretics

(c) Phenytoin.

03. Endocrine disease Induced

(a) Cushing’s Syndrome (b) Acromegaly

(c) Thyrotoxicosis (d) Phaeochromocytoma

(e) Glucogonoma.

04. Liver disease

05. Excess endogenous production of hormonal antagonists to insulin

(a) Growth hormone (Acromegaly)

(b) Glucocorticoids (Cushing’s syndrome)

(c) Thyroid hormones (Hyperthyroidism)

(d) Catecholaminus (Phalochromocytma)

(e) Human placental lactogen (Pregnancy)

(f) Glucagon (Glucagonoma)

(g) Counter regulatory hormones (Severe burns, trauma).

06. Gestational diabetes mellitus

Disease Review 63


Kulaja dosha and beeja dosha have been mentioned in the causative factors of

sahaja Prameha. Such patients are said to be weak, emaciated, suffering from thirst, loss

of appetite and are required to be treated with a nourishing diet.

In diabetes also genetic and hereditary factors are mentioned as causative factor.

In such patients, weakness and emaciation are noted. They are also asthenic. The above-

mentioned patients are juvenile diabetics and require a nourishing diet. There for sahaja

prameha and Juvenile diabetes may be correlated.

Apathya nimittaja Madhumeha explained on Ayurveda, in such patient’s

atikshudha, atinidra and aalasya are noted. And it is caused due to over intake of

madhura snigdha aahara and vihara which favours kapha-medovriddhi Maturity onset

diabetes tend to over eat and are lazy in nature, even though age factor is not mentioned

in Ayurveda while explaining chikitsa in Ayurveda, acharya have explained sthoola and

krisha classification. The same type of classification can be seen in Modern Science as

obese and non-obese type.

Apart from the above, doshika type of classification is widely explained in

Ayurveda. But detailed explanation of sthoola and krisha types explained above is not

available in classics.

Sadhyaasadhyata

The physician who knows the difference between curable and incurable disease

and begins treatment in time with a thorough knowledge of the case, succeeds in his

efforts without any doubt. Those who lack the above knowledge invariably suffer loss of

income and fame. Like other diseases, the knowledge of Sadhyaasadhyata is very

important in case of madhumeha. The sadhyaasadhyata or prognosis should be assessed

Disease Review 64


based on the following factors such as hetu, poorvaroopa, roopa, dosha, dooshya, prakriti,

kala, desha upadrava, sarvoushadhakshamata, Chatushpada, etc.

As discussed earlier, Prameha is commonly classified is to three verities92.

01. Kaphaja Prameha -10 in number.

02. Pittaja Prameha - 6 in number.

03. Vataja Prameha - 4 in number.

Among the above 3 verities kaphaja types are considered as curable (sadhya),

because, the meda having homogenous properties is affected and the kapha is dominant.

Both these factors are amendable to the same type of treatment93.

The Six-pittaja pramehas are only yapya. Because the dosha involved are mainly

pitta and when it associates with kapha-medas leads to antagonism in the treatment. The

main reason for this yapyata is contradiction in the treatment due to opposite treatment

involvement among pitta and meda94.

The four verities of vataja prameha due to vitiation of vata are known to be

incurable or asadhya, because of their seriousness and also due to the contradiction

involved in the treatment95.

The factors that are considered as pathya for vayu is an apathya for meda. So

due to virudhopakrama or contradiction in treatment, vataja prameha is considered as

asadhya.

As madhumeha is a variety of vataja prameha, it is also considered as asadya.

But Vagbhata and Charaka acharya termed avruttajanya madhumeha as kruchra sadhya

vyadhi96.

Disease Review 65


Apart from the above considerations following situation should also be taken in

to consideration.

01. The Kaphaja and pittaja groups of prameha, if they are developed after full

expression of poorvaroopas, they are asadhya97.

02. Kaphaja prameha gradually develop in to pittaja prameha and they both

transform in to vataja prameha, which are incurable98.

03. If kaphaja prameha gradually turns in to pittaja prameha these are yapya.

04. Even the pittaja pramehas are curable if there is no severe vitiation of medas.

05. The patients who are pramehi right from birth (Jata pramehi) and those who have

prameha due to beeja dosha are treated as asadhya99.

06. All the prameha if untreated or neglected, it ends in madhumeha in their due

course and it is considered as asadhya.

07. It is stated that prameha patent suffering with pidakas and complications like

hridgraha, then he should be considered as madhumeha rogi and this type of

madhumeha is incurable100.

Basavaraja a 16th century physician of Andra Pradesh has mentioned a test for

urine for finding the prognosis of each dosha group. The urine of a prameha patient is to

be collected in a wide mouthed vessel and boiled on a mild flame till evaporation. The

incurability of the disease depends up on the amount of residue. A vataja Prameha is

considered as incurable if the residue is 1/5th of the volume of urine taken for test. Pittaja

prameha is incurable if the residue is ¼th and kaphaja prameha is incurable if the residue

is 1/9th. 101

Disease Review 66


Vyavachedaka Nidana

Vyavachedaka nidana or differential diagnosis helps a physician to establish

accurate diagnosis of the disease. This is a method to diagnose the particular disease by

comparing its signs and symptoms with other diseases.

Prabhoota mootrata and Avila mootrata are the lakshanas, which will manifests in

all the 20 varieties of pramehas. So as to distinguish madhumeha from other pramehas

the study of them should be made.

In Ayurveda the acharyas mentioned 20 types of pramehas and among that

madhumeha is the one. Detailed descriptions regarding the each type along with its

characteristics are already discussed.

As sthoola madhumeha is considered as apathya nimittaja variety of pramehas,

sahaja prameha has to be differentiated form this102.

Table No. 09. Showing the Vyavachedaka nidana.

Apathyanimittaja Sahaja

Nidana Lakshanas

Mithyaahara and vihara

Snigdha

Bahuashee

Sthoola

Shayyasana

Swapna sheela

Beeja dosha

Rooksha

Alpashee

Krisha

Paribhramana sheela

Disease Review 67


Upadrava

Upadrava is a disease produced after the manifestation of the original disease and

depends on that disease irrespective of whether upadrava is major or minor103.

After the occurrence of the original disease the dosha or doshas are further

vitiated owing to abnormal ahara, vihara etc, thus leading to a secondary disease or

complication which is known as an upadrava in Ayurveda.

Acharya Charaka has described the upadrava of prameha in general where as

Sushruta and Vagbhata have mentioned updravas separately for each doshic group.

General upadvas of prameha according to Charaka 104

01. Trishna

02. Dourbalya

03. Arochaka

04. Avipaka

05. Vidradhi

06. Jwara

07. Pidaka

08. Atisara

09. Daha

10. Puti mamsa

11. Alaji

Disease Review 68


Classification

Table No. 10.Upadravas of prameha according to Vagbhata and Sushruta on dosha

basis105.

No. Upadrava Vagbhata Sushruta

Kaphaja prameha updravas

01. Aalasyam - +

02. Pratishyaya + +

03. Shaithilya - +

04. Aruchi + +

05. Avipaka + +

06. Kapha Prasekam - +

07. Chardi + +

08. Nidra + +

09. Kasa + +

10. Swasa - +

Pittaja prameha upadravas

01. Vrishana vedana + +

02. Vasti shoola + +

03. Medhra todha + +

04. Hrit shoola - +

05. Amlodgara + +

06. Jwara + +

07. Atisara - +

Disease review 69


08. Arochaka - +

09. Daha + +

10. Moorcha + +

11. Pipasa - +

12. Nidranasha - +

13. Pandu roga - +

14. Trishna + -

15. Peeta mootra netra twak - +

Vataja prameha Upadravas

01. Hrid graha + +

02. Loulya + +

03. Anidra + +

04. Sthambha - +

05. Kampa - +

06. Shoola + +

07. Badda pureeshatwam - +

08. Udavarta + -

09. Kanthagraha + -

10. Sosha + -

11. Kasa + -

12. Swasa + -

Madhavakara and Bhavamishra also mentioned the same in Vagbhata way.

Disease review 70


Prameha Pidaka

Charka in his Suthrasthana explained special Samprapti for madhumeha and he

explains that the lakshanas manifest and vanish at times. He also states that if neglected,

this disease causes serious types of pidakas in subcutaneous, muscular area, vital parts

and joints of the body. Hence pidaka can be termed as upadrava of madhumeha106.

There are different opinions among the acharyas regarding the number of pidakas

as follows. 107,108,109.

No. Charaka Sushruta Vagbhata

01. Sharavika Sharavika Sharavika

02. Kachapika Kachaptka Kachapika

03. Jalini Jalini Jalini

04. Sarshapika Sarshapika Sarshapika

05. Alaji Alaji Alaji

06. Vinata Vinata Vinata

07. Vidradi Vidhradi Vidhradi

08. - Masurika Kuluttika

09. - Putrini Putrini

10. - Vidarika Vidarika

Complications Of Diabetes110

01. Hypoglycemia

02. Diabetic ketoacidosis

03. Non-ketotic hyperosmolar diabetic coma

04. Diabetic macro angiopathy etc.

Disease review 71


Long-term complications of Diabetes are,

01. Diabetic Nephropathy.

02. Diabetic Retinopathy.

03. Diabetic Neuropathy.

04. Diabetic foot etc.

Same of the upadravas of Ayurveda can be correlated to some of the

complications of modern science. For eg. trishana, bhrama, shoola, tamapravesha, shwasa

can be correlated to Diabetic ketoacidosis, in which thirst, weakness, blurring vision,

abdominal pain, airhunger, etc are seen. Above conditions are seen in hypoglycemic

condition also.

Reticulopathy, a type of diabetic neuropathy is a sensory syndrome in which, pain

occurs over the distribution of one or more spinal nerves usually in chest wall or

abdomen. It mimics acute surgical abdomen. Shoola (Udarashoola) explained in

Ayurveda can be correlated to this.

Disease review 72

Nidana sevana

Vikrita bahudrava kapha (Shleshma)

Travels all over the body because of shareera shithilata

Medodhatwagni mandya

Vitiation of medovaha srotas

Bahu abaddha medas

Dosha dushya sammurchhana

Bahudrava shleshma with bahu abadhha meda

Vitiation of other dooshyas

Adhika kledata of dhatus

Basthi

MADHUMEHA

Beeja dosha

Sthoulya

Shleshma, pitta, meda, mamsa,

ativriddhi

Obstruction to vata due to

aavarana by vitiated kapha,

pitta and meda.

Squeezing of ojus

MADHUMEHA SAMPRAPTI

Genetic predispostion Envirnoment

Multi genetic defecets Obesity

Primary beta-cell defect Peripheral tissue insulin resistance

Deranged insulin Secretion Inadequate glucose utilization

Hyperglycemia

Beta cells exhaustion

Type II diabetes

PATHOLOGY OF TYPES II DIABETES


CHIKITSA

Chikitsa paribhasha

The term chikitsa is derived from the root “Kit rogapanayane” according to

Shabda stoma mahanidhi,

According to Amarakosha chikitsa is “Ruk Pratikriya”.

So the ultimate aim of chikitsa is “Swasthasya Swasthya Rakshanam and

Aaturasya roga nivaranam”.

Acharya Charaka while explaining the line of treatment, or chikitsa sootra

explains 2 varieties of pramehis. They are as follows111.

01. Sthoola - balavan

02. Krusha - durabala.

For above two types, two different line of treatments are explained. Among these

two, the first one is the sthoola-balavan and having doshabaladhikya should be given with

samshodhana therapies, and the second one i.e. Krusha-durbala should be treated with

samshamana therapies. Vagbhata also says that, the pramehis those who are having good

bala should be administered with shodhana kriyas.

Sushruta acharya mentions 2 types of pramehis. They are112

01. Sahaja Pramehi

02. Apathya Nimittaja Pramehi.

Among there, sahaja prameha is due to beeja dosha and such patient are krusha in

nature. They should be treated with shamana oushadhas and annapanas, which are treated

with pramehahara oushadhis.

Chikitsa I 72


The apathya nimttaja sthoola pramehi should be given apatarpana chikitsa. After

the completion of samshodhana kriya, the patient is to be subjected to santarpana Kriya.

Again Charaka described the special chikitsa for each type of prameha i.e.

kaphaja, pittaja and vataja. Proper vamana kriya and langhana kriya administered at

proper time cures kaphaja prameha. The virechana kriya, the santarpana kriya and

samshamana kriyas cures the pittaja variety of prameha113. Even though the vataja

pramehas are stated to be incurable, the duty of a physician is to help the patient to live

longer by preventing the complications. So the vataja prameha should also be treated

accordingly.

Shamana chikitsa is indicated for a prameha patient who is not eligible for

shodhana chikitsa and also the patient who has completed the shodhana karma

successfully.

Many verities of decoctions, choornas and lehyas have been described for the

treatment of the twenty varieties of prameha by all Ayurvedic authorities.

Sushruta has separately devoted one chapter for the treatment of madhumeha114.

In that he has prescribed shilajatu, makshika and tuvarka exclusively in the

treatment of Madhumeha.

Treatment In Kriyakalas

Sushruta has explained prameha chikitsa based kriyakalas115. In the poorvaroopa

condition (Sthana samsrayam),

Vanaspati kashaya, basthi mootra, etc should be administered. If the above kriyas

are not done and if the person continues madhurahara sevana, his urine, sweat and

shleshma become sweet and the prameha lakshanas become clear i.e, vyakta stage.

Chikitsa II 72


In this condition urdwa, adha, shodhana should be done. If it is not done the

doshas become pravridha and vitiates mamsa, shonita and causes shopha. In this stage

shopha chikitsa and sira moksha should be done i.e. bheda stage. If this condition is left

untreated the shopha becomes big with increased pain and in this condition shastra kriya

should be done and also vranakriyaopaseva.

In this condition also, the treatment is not adopted the condition become asadhya.

Pathyaapathya

The term pathya means that which is compatible to health and apathyam is that

which is incompatible to health116.

It has already been stated that the main etiology of madhumeha is excessive

indulgence of guru, snigdha, amla, lavana padarthas and by using new food grain and

drinks. Because of this, for a madhumeha patient of recent origin dietary control is the

main one. The principal diet of the patient should be yavadhanya or barley117.

The patient should be given mantha, kashayas and linctuses made of the powder

of barley and the food, which is easily digestible. Cooked barley mixed with snigdha

dravya, saktu and apoopa made of barley mixed with the soups of the flesh of the birds of

vishkira and pratuda group and also the meat juice of jangala animals should be given as

diet. The patient should be given cooked old rice with the soup of green-gram and other

pulses and bitter vegetables. A patient suffering from kaphaja prameha should eat various

preparations of barley mixed with honey118.

The barley steeped over night in the decoction of triphala and taken with honey

and seedhu wine is the best nutrient diet for prameha patient. The patient should use

barley soaked in the various decoctions prescribed for the cure of the kaphaja prameha.

Chikitsa III 72


Patient should use various eatables prepared of barley which have been previously give to

donkeys, horses, cows, swans and deer and excreted by them in their dung, should be

used119. Patient should drink water prepared with kusha, darba or madhukam or triphala

kashayam or seedu madya. The man who habituated to roasted barely, dry baked barley,

barley powder, green-gram and amalaki, does not get prameha, switra, mootrakrichra and

kaphaja kushta120.

Pathya Viharas

Prameha can be controlled by vyayama, udvartana, snana, jalasechana and lepas

with twak, ela, agaru, chandana, etc.

Sushruta explains wrestling, active sports, riding on a horse or elephant, long

walking, javelin throwing, etc. as good viharas in prameha. He also suggested a walk of

hundred yojanas simply without paricharakas, shoe and umbrella. A rich man suffering

from prameha should live by taking amalaki, kapitta, tinduka and mantaka and live along

with deer. He should walk with cow and should take mala mootra of cows as diet121. A

weak and emaciated patient should not be advised any physical exercise.

Pathya according to Yogaratnakara122

Shalidhanya, patola, tanduliyaka, vastuka, mudga, yoosha, apakva kadaliphalam,

kodrava, godhuma, kulattha, tikta shakha like klaravellaka, jangala mamsa rasa,

saindhava and maricha, etc.

Apathya Aharas

Navanna, dadhi, souvirakam, sura, shuktam, kshara, ghrita, ikshurasa vikaras,

pishtanna, anoopa mamsam, doomapanam, swedanam, raktamoksham, mootra vega

dharana, diwaswapnam and sadaasana.

Chikitsa IV 72


DRUG REVIEW

After describing the details regarding various aspects of virechana karma and

madhumeha, it is necessary to go through the details of treatment adopted in the present

study. The treatment adopted is virechana karma and for this, as a poorva karma deepana

pachana, arohana snehapana and swedana are necessary. For this purposes the following

yogas are used –

01. Deepana pachana – Trikattu churna123.

02. Snehapana – Thrikantakadyam ghritam124.

03. Abhynaga and swedwa – Moorchita tila taila and ushnajala snana 125

04. Virechana – Vidanga tanduladi churna126.

The drugs used to prepare the above yogas along with its properties are given

below –

Study plan 73


Table No. 11. Showing the properties of the ingredients of Trikatu churna

Sl. San.

Name

Latin

Name

Family Rasa Guna Veerya Vipaka Doshaghnata Karma

01. Pippali127 Piper

longum

Piperaceae Katu Laghu,

snigdha,

teekshna

Anushna

sheeta

Madhura Kapha-vata Anulomana, Pachana,

Yakrit pleeha

vikaraghnam

02. Marich128 Piper

nigrum


teekshna

Ushna Katu Vata-kapha Deepana-pachana,

yakritottejaka,

vatanulomana

03. Shunthi129 Zinziber

officinali

Zinziberaceae katu Laghu,

snigdha

Ushna Madhura Kapha-vata Agni deepana,

pachana,

vatanulomana

Study plan 74


Table No. 12. Showing the properties of the ingredients of Thrikantakadyam ghritam.

Sl. San. Name Latin Name Family Rasa Guna Veerya Vipaka Doshaghnata Karma

01. Manjishta130 Rubi cordifolia Rubiacea Kashaya,

tikta,

madhura

Guru,

ruksha

Ushna Katu Kapha, Pitta Pramehahara,

deepana,

pachana, balya,

jwaraghna, rakta

shodhaka

02. Musta131 Cyprus

rotandus

Cyperaceae Tikta Laghu,

ruksha

Sheeta Katu Kapha, Pitta Kledahara,

deepana,

pachana, rakta

prasadana,

mutrala,

trishnahara

03. Patola132 Trichocanthes

dioica

Cucurbitaceae Tikta Laghu,

ruksha

Ushna Katu Tridosha Deepana,

pachana,

anulomana,

rakta shodhaka,

virechana,

trishnanigrahana

Study plan 75



04. Ativisha133 Aconitum

heterophyllum

Cucurbitaceae Tikta Laghu Ushna Katu Tridosha Medohara, kaphahara, ajeernaghnam vrishya, raktashodhaka

05. Gokshura134 Tribulus

terrestris

Zygophyllaceae Madhura Guru,

snigdha

Sheeta Madhura Tridosha Anulomana,

mutrala,

pleehaghna

06. Haridra135 Curcuma longa Sciataminae Tikta,

katu

Ruksha,

laghu

Ushna Katu Tridosha Amahara, mutra

virajaneeya,

pramehahara,

raktaprasadana

07. Lodhra136 Symplocos

racemosa

Symplocaceae Kashaya Ruksha,

laghu

Sheeta Katu Kapha, pitta Shophahara,

raktavikara

prashamana,

kushtaghna.

08. Vacha137 Acorus

calamus

Araceae Tikta,

katu

Laghu,

teekshna,

sara

Ushna Katu Kapha, vata Medohara,

anulomana,

mutrajanana,

reducesrakta

bhara

Study plan 76



09. Arjuna138 Terminalia

arjuna

Combertaceae Kashaya Laghu,

ruksha

Sheeta Katu Kapha, pitta Hridya,

medohara,

pramehahara,

mutradoshahara

10. Padmaka139 Prunus

cirasoidus

Rosaceae Kashaya,

tikta

Laghu,

snigdha

Sheeta Katu Tridosha Hridya,

medohara,

antipruritic,

ashmarighna

11. Arishta140 Azadirachta

indica

Meliaceae Tikta,

kashaya

Laghu Sheeta Katu Kapha, pitta Pramehahara,

anulomana,

kushtaghna

12. Chandana141 Santalum alba Santalacae Tikta,

madhura

Laghu,

ruksha

Sheeta Katu Pitta, kapha Basti shodhaka,

rakta vikarahara,

yakrit uttejaka

13. Agaru142 Aquilaria

agallocta

Thymelecea Katu,

tikta

Laghu,

rooksha,

teekshna

Ushna Katu Kapha vata Mutrashaya

shithila nashana,

anulomana,

rakta shodhaka,

shoshahara,

Study plan 77



14. Deepyaka

(Ajamoda)

143

Carum

roxburghianum

Umbellifere Katu,tikta Laghu,

rooksha,

teekshna

Ushna Katu Kapha-vata Mutra

pravartaka,

deepana, vidahi,

hridayottejaka

15. Bhallataka144 Semacarpus

anacardium

Anacardiaceae Madhura,

kashaya

Laghu,

snigdha,

teekshna,

ushna

Ushna Madhura Tridosha Deepana,

pachana,

yakrittotejaka,

hridayottejaka,

nadibalaprada.

16. Khadira145 Acacia catechu Legumineseae Tikta,

kashaya

Laghu,

ruksha

Sheeta Katu Kapha, pitta Pramehaghna,

Kushtaghna,

Medohara

Study plan 78


Table No. 13. Showing the properties of the ingredients of Moorchita tila taila.

Sl. Sankrit

name

Latin name Family Rasa Guna Veerya Vipaka Doshaghnata Karma

01. Tila taila Sesamum

indicum

Pedaliaceae Madhura,

kashaya,

tikta

Sookshma,

vyavayi,

vikashi,

vishada,

guru, sara,

teekshna,

hima

sparsha

Ushna Madhura Tridoshaghna Deepana,

pachana,

pramehahara,

vrinahara,

mamsadhatu

pushtikara,

keshya, netrya.

Study plan 79


Table No.14. Showing the properties of drugs used in Vidangatanduladi churna.

Sl. Sankrit

name


01. Vidanga

146

Embelia

ribes

Myrsinacae Katu,

kashaya

Laghu,

rookhsa,

teekshna

Ushna Katu Vata kapha Medohara,

Kushtaghna,

anuloma,

deepana,

pachana

02. Amalaki

147

Emblica

officinalis

Euphorbiaceae Pancharasa

amla

pradhana

Guru,

sheeta,

rooksha

Sheeta Madhura Tidosha Anulomana,

pramehaghna

03. Vibhitaki

148

Terminalia

bellerica

Combertaceae Kashaya Laghu,

ruksha

Ushna Madhura Tridosha Anulomana,

virechaka

04. Haritaki

149

Terminalia

chabula

Combertaceae Pancharasa lavana varjita

Laghu, rooksha

Ushna Madhura Tridosha Vibandhaghna, pachana, yakritpleehottejaka

Study plan 80


Study plan 81

Sl. Sankrit

name


05. Pippali150 Piper

longum


snigdha,

teekshna

Anushnas

heeta

Madhura Kapha vata Virechaka,

pachana,

yakritpleehottej

aka

06. Trivrit151 Operculina

turpentum

Convoluaceae Katu, tikta,

madhura,

kashaya

Laghu,

rooksha,

teekshna

Ushna Katu Kapha pitta Virechaka,

medohara

07. Yavaskha

ra152

Horadeum

velgar ash

Katu Laghu,

snigdha,

sookshma

Ushna Katu Kapha vata Kaphavata roga,

pleehodara,

shukra-

shleshma-

vibandhahara,

mutraghatahara,

mootrakrichhrah

ara


Chemical composition of virechana drugs

Vidanga – Embelia ribes153

Part used –

Berries, leaves and rook bark.

Chemical composition –

Contains embelic acid, a volatile and fixed oil, colouring matter, tannin, a resinoid

body acid and an alkaloid called christembine. Crystalline compounds of embolic acid

with soda, potash and ammonia are obtained. Berries contain vidangin.

Embolic acid contains the following derivations,

01. A monoacetyl derivative.

02. A monosemicarbazone

03. A dihydrazone

04. An oxime

05. A di-semicarbazone.

Action –

Fruits or dried berries are carminative, antihelminthic, stimulant and alterative.

Pulp is purgative. Fresh juice is cooling, diuretic and laxative.

Amalaki – Emblica officinalis 154

Parts used –

Dried fruits, nut or seed, leaves, root, bark, and flowers.


Fruits contain tannic acid, albumin, cellulose, calcium, etc. it contains vitamin C

in large amount. Also contains protein, carbohydrate, red phosphorus, iron and nicotinic

acid. Seeds contain yellow oil.

Study plan 82


Action –

Fresh fruit is refrigerant, diuretic and laxative. Green fruit is exceedingly acid.

Fruit is also carminative and stomachic. Dried fruit is sour and astringent. Flowers are

cooling and aperient. Bark is astringent.

Haritaki – Teminalia chebula155

Parts used – Dried fruits, immature fruits, myrobalans, and mature fruit. Mostly

outer skin of fruit.


Myrobalans contain astringent principles, tannin and a large amount of gallic acid,

lucilage, a brown yellow colouring matter, chebulic acid which when heated in water

splits up in to tannic and gallic acids.

Actions –

Myrobalans are safe and affective. Purgative, astringent and alterative. Unripe

fruits are more purgative and the ripe are astringent. Rangari harade are alternative,

stomachic, laxative and tonic. Suvari harade is a valuable purgative. Bala harade is a mild

and safe aperient and antibilious, through astringent. Ripe fruit is considered as purgative

removing bile and phlegm and to adjust bile.

Vibhitaki – Termianlia bellerica156

Part used – Fruits.


Beleric myrobalans consist of gallo-tannic acid, colouring matter, resins and

greenish yellow oil.

Study plan 83


Action –

Astringent tonic, expectorant and laxative.

Pippali – Piper longum 157

Parts used –

Immature berries (i.e. dried unripe fruits or fruiting spikes) dried in the sun and

stems (roots).

Chemical constituents –

Resin, volatile oil, starch, gum, fatty oil, inorganic matter and an alkaloid,

piperine 1-2 p.c.

Action –

Infusion is stimulant, carminative and alternative tonic more powerful than black

pepper, also aphrodisiac, diuretic, vermifuge and emmenagogue. Root is stimulant.

Trivrit – Operculina turpentum 158

Part used – Root bark.


Resin, volatile oil, starch, gum, fatty oil, inorganic matter and resin piperine 1-

2%. Also contain resin, albumin, iron, lignanine and some salts.

Action –

Root bark contains turpethine, which causes purgation.

Study plan 84


Yavakshara – Hordeum vulgare ash. 159

Part used –

Ash. Ripped barley plants should be cut, dried, and then burnt to ashes and the

alkaline material, obtained form that ash by kshara vidhi, is known as yavakshara. For

burning, spikes or whole plant may be taken.


Mainly contain potassium chloride 50.8%, potassium sulphate 20.2%, potassium

bicarbonate 12.6% and potassium carbonate 6.8%. Thus it is a mixture of potassium salts.

Study plan 85


Research approach

In this work, the aim was to evaluate the efficacy of virechana karma clinically in

Madhumeha roga.

After the completion of the full treatment the results were assessed by comparing

the before treatment data with the after treatment data.

Source of data

Patients suffering form madhumeha were selected from P.G. S. & R., Department

of Panchakarma O.P.D. of D.G.M. Ayurvedic Medical College and hospital, Gadag by

preset inclusion and exclusion criteria.

Study design

The study was done in a single group. Prospective clinical trial.

The treatment modality used in this clinical study was virechana karma, which

included deepana-pachana with trikatu choorna, snehapana with thrikantakadym ghritam,

abhyanga sweda with moorchhita tila taila and ushna jala snana. Virechana using

Vidanga tanduladi choorna, which was followed by samsarjana karma and follow – up

for one month. During the follow-up period patients were given placebo capsules.

Sample size

A minimum of 30 patients were taken for study. All the patients received classical

virechana karma.

Inclusion criteria

Patients satisfying the following criteria were taken for study. They are –

The patients between the age group of 35 to 60 years.

Non-complicated NIDDM.

Study plan 86


Patients having the clinical features of madhumeha.

Irrespective of sex.

Madhumeha patients having good body strength, sthoola and also fit for virechana

karma.

Exclusion criteria

If any of the following conditions were noted, such patients were excluded form

the present study. They are –

Insulin dependant diabetes mellitus.

Patients complicated with other systemic disorders.

Patients less than 35 and above 60 years of age.

Patients with diabetic complications.

Plan of study

Selected patients were given virechana karma.

A. Deepana-pachana – Deepana pachana till nirama laskhanas appears. For this the

drug administered was trikatu choorna, 3 gms 3 times a day before food.

B. Snehapana – For snehapana thrikantakadyam ghrita was selected. After attaining

appropriate niramata, the snehapana was started with hrasveeyasi matra i.e. 30 ml

and gradually increased to 3 or 4 days. It is mentioned in classics that for

madhumeha rogis, less sneha is enough, as kaphotklesha is already there.

C. Abhynaga and sweda – As sweda is contraindicated in Madhumeha, the patients

were administered with abhynaga and ushna jala snana. For abhynaga moorchita

tila taila was used.

Study plan 87


D. Virechana karma – On fourth day the patients were given with virechana yoga

after assessing status of patient’s koshta, bala, etc. The medicine used was

Vidanga tanduladi choorna.

E. Samsarjana karma – Samsarjana karma was performed depending upon the

shuddhi.

F. Follow up – Follow up for one month. During this period of follow up the patient

was advised to follow the diet, which he had followed prior to our study.

Investigations and Selection of Patients

Objective parameters

The following investigations were done prior to the study.

01. Blood – FBS, PPBS.

02. Urine – Urine sugar.

After interpretation of the laboratory investigations, mild and moderate types of

patients were taken for study. Mild and moderate criteria’s are given here.

Table No. 15. Showing the grades of the blood sugar level. 160

Sl. Level FBS RBS PPBS Urine

sugar

01. Normal 70-120 mg/dl. 120-180 120-180 Nil

02. Mild 121-170 mg/dl. 181-230 181-230 0.5%

03. Moderate 171-220 mg/dl. 231-280 231-280 1.0-1.5 %

04. Severe 221-mg/dl and

above

281 mg/dl and

above

281 mg/ dl and

above

2% and

above

Study plan 88


Subjective parameters

Apart form the above parameters; the following parameters were also taken for

assessing the patient. They are –

01. Prabhuta mutrata

02. Kshudadhikya

03. Pipasadhikya

04. Karapada daha

05. Ati sweda

Method of Assessment and grading

The assessment of results by observing the severity of symptomatology as well as

the laboratory investigations.

The severity of the symptoms, urine sugar, fasting blood sugar and post prandial

blood sugar were assessed before the treatment, after snehapana, after virechana, after

15th and 30th day of follow up.

Grading of parameters

The results were evaluated by observing subjective and objective parameters by

grading method. The grading was done in the following manner.

01. Prabhuta mutrata –

Grade 0 – 2-3 times / day, 0-1 times / night.



Grade 3 – > 7 times / day, > 5 times / night.

02. Pipasadhikya –

Study plan 89


Grade 0 – Normal.

Grade 1 – Slightly increased.

Grade 2 – Severely increased.

03. Kshudhadhikya –

Grade 0 – Normal.

Grade 1 – Increased, but can tolerate.

Grade 2 – Increased, but can’t tolerate without consuming food.

04. Kara pada daha –

Grade 0 – Absent.

Grade 1 – Slightly present.

Grade 2 – Present.

05. Ati sweda –

Grade 0 – Absent.

Grade 1 – Present.

06. F.B.S. –

FBS levels,

Grade 0 - 120 and below

Grade 1 - 121-140

Grade 2 - 141-160

Grade 3 - 161-180

Grade 4 - 181-200

Grade 5 - 201-220

07. PPBS (Post prandial Sugar) –

Study plan 90


PPBS levels –

Grade 0 - 180 and below

Grade 1 - 181-200

Grade 2 - 201-220

Grade 3 - 221-240

Grade 4 - 241-260

Grade 5 - 261-280

08. Urine sugar –

Urine sugar -

Grade 0 - Nil

Grade 1 - 0.5

Grade 2 - 1.0 - 1.5

Study plan 91


Overall Assessment –

The overall assessment of the study was performed by considering all the

parameters of assessment and for that following method of overall grading was used.

01. Good response - Patients with 60% and above results, by

considering all subjective and objective

parameters.

02. Moderate response - Patients with 30% to 59% results, by

considering all subjective and objective parameters.

03. Poor response - Patient with 1% to 29% of results by

considering all subjective and objective

parameters.

04. No response - Patients with no change after considering all

subjects and objective parameters.

Study plan 92


In the present clinical study subjective and objective changes were

considered for the assessment of Ayurvedic management of Sthoola madhumeha with

classical virechana karma. Thirty patients were selected and were administered with

virechana. All the patients were assessed before and after the treatment. Both subjective

and objective changes were recorded according to the guidelines of proforma of case

sheet.

The data were collected as follows: -

1. Demographic data

2. Data related to etiological factors, type, duration, etc.

3. Data related to incidence of disease and response to treatment.

4. Data related to subjective and objective parameters before and after treatment.

5. Statistical analysis and assessment for response.

Results 93


Table No. 20 Showing the age group incidence and response.

Sl.

NO

Age

Groups

No. of

Pts.

% GR % MR % PR %

01. 35-39 5 16 3 60 2 40 - -

02. 40-44 3 10 3 100 - - - -

03. 45-49 7 23 4 57 2 28.5 1 14.2

04. 50-54 6 20 3 50 3 50 - -

05. 55-59 7 23 2 28 4 57 1 14.2

06. 60-64 2 6.6 2 100 - - - -

Among age group 35-39 it contains 5 patients i.e. (16%) and in that 3 patients

responded good (60%), and 2 patients responded moderately (40%). 40-44 age group includes 3 patients i.e. 10% and in that all 3 patients responded good.

Age group 45-49 includes 7 patients i.e. 23% and in that 4 patients (57%) responded god, 2 patient (28.5%) responded moderately and 1 patient’s response was poor (14.2%) Age group 50-54 includes 6 patients i.e. 20%. In that 3 patients responded good and 3 patents moderately i.e. each 50%. 55-59 age group contains 7 patients i.e. 23% is in that 2 patients responded good (28.6%), 4 patients responded moderately (57%) and 1 patient response was poor (14.2%).

Last 60-64 age group includes 2 patients i.e. 6.6% and in that all 2 patents responded good (100%). Figure No. 04.

Age group inc ide nc e & re s pons e

5

3

76

7

23 3

43

2 22

0

23

4

00 01

01

0012345678

35-39 40-44 45-49 50-54 55-59 60-64

A g e g r o u p

No.

of P

t.'s

No. of Pt.'s GR MR PR

Results 94


Table No. 21. Showing the Sex group incidence and response.

Sl.No Sex No. of

Pts.

% GR % MR % PR %

01. Male 22 73.33 12 54.5 9 40.9 1 4.5

02. Female 8 26.66 5 62.5 2 25 1 12.5

Out of 30 patients, 22 were males (73.33%) and 8 were females (26.66%). Among

males 12 patients (54.5%) responded good, 9 patients (40.4%) responded moderately and

1 patient’s (4.5%), response was poor.

Among females 5 patients responded good (62.5%), 2 patients responded

moderately (25%) and 1 patient’s (12.5%) response was poor.

Figure No. 05.

Sex inc idence & response22

8

12

5

9

21 10

5

10

15

20

25

Male FemaleSe x

No.

of P

t.'s

No. of pt's . GR MR PR

Results 95


Table No. 22. Showing the incidence of religion and response.

Sl.

No

Religion No. of pts. % GR % MR % PR %

01 Hindu 25 83.33 14 56 9 36 2 8

02 Muslim 4 13.33 3 75 1 25 - -

03 Christian 1 3.33 - - 1 100% - -

04 Others 0 0% - - - - - -

In religion 25 patients were hindu (83.33%), 4 patients were muslim (13.33%)

and 1 patient was Christian (3.33%). Among the hindus, 14 patients (56%) responded

good, 9 patients (36%) responded moderately and 2 patients (8%) response was poor. The

only one Christian patient responded moderately (100%).

Figure No. 06.

Religion incidence & response25

41 0

14

30 0

9

1 1 02

0 0 00

5

10

15

20

25

30

Hindu Musilin Christain Others Religion

No.

of P

t.;s


Results 96


Table No. 23 Showing the incidence of occupation and response.

Sl.

No

Occupation No. of Pts % GR % MR % PR %

01 Sedentary 17 56.66 10 58.8 6 35.2 1 5.8

02 Active 0 0 - - - - - -

03 Labor 13 43.33 7 53.8 5 38.4 1 7.6

04 Others 0 0 - - - - - -

In occupation status, 17 patients were sedentary (56.66%), and 13 patients were

labors (43.33%).

Among the sedentary category 10 patients (58.8%) responded good, 6 patients

(35.2%) responded moderately and 1 patient’s (5.8%) response was poor.

Among labors 7 patients responded good (53.8%), 5 patients (38.4%) responded

moderately, and 1 patient (7.6%) response was poor.

Figure No. 07.

Occuaption incidence & response17

0

13

0

10

0

7

0

6

0

5

01 0 1 00

5

10

15

20

Sedentary Active Labor Others

Occupation

No.

of P

t.'s


Results 97


Table No. 24 Showing the Socioeconomic Status and response.

Sl. Eco. Status No.

of

Pts.

% Goo

d

% Mod. % Poo

r

%

01. Poor 1 3.33 1 100 - -

02. Middle 6 20 3 50 3 50 - -

03. Upper

middle

13 43.33 8 61.5 4 30.7 1 7.6

04. High class 10 33.33 6 60 3 30 1 10

Among 30 patients 1 patient was poor (3.33%) and that patient responded

moderately.

6 patients (20%) were middle class, among them 3 patients (50%) response was

good and remaining 3 patients (50%) responded moderately.

13 patients were upper middle class and in that 8 patients (61.5%) responded

good, 4 patients (30.7%) responded moderately and 1 patient’s (7.6%) response was poor.

Among 10 high-class patient (33.33%). 6 Patients (60%) responded good, 3

patients (30%) responded moderately and one patient (10%) response was poor.

Figure No. 08.

Socio-economical status & response

1

6

1310

3

86

13 4 3

0 0 1 10

5

10

15

Poor Middle Upper middle High classEconomical satus

No.

of P

t.'s

No. of Pts. Good Mod. Poor

Results 98


Table No. 25. Showing the food habits and response.

Sl. Diet No. of pts. % GR % MR % PR %

01. Veg. 15 50 11 73.3 3 20 1 6.6

02. Mixed 15 50 6 40 8 53.3 1 6.6

Among 30 patients, 15 patients were vegetarians (50%) and remaining 15 patients

(50%) used to consume mixed food. Among vegetarian 11 patients (73.3%) responded

good, 3 patients (20%) responded moderately and I patient’s reponse was poor.

Among patients consuming mixed diet, 6 patients (40%) responded good, 8

patients (53.3%) responded moderately and 1 patient’s (6.6%) response was poor.

Figure No. 09.

Food habits & response15 15

11

6

3

8

1 102468

10121416

Veg. Mixed

Food habit

No.

of P

t.'s

No. of pts. GR MR PR

Results 99


Table No. 26. Showing the chronicity and response.

Sl. Duration No. of

pts.

% GR % MR. % PR %

01. Newly diagnosed 8 26.6 5 62.5 3 37.5 - -

02. Below 1 yr. 3 10.0 2 66.6 1 33.3 1 -

03. 1-2 yrs. 16 53.33 9 56.2 6 37.5 1 6.2

04. More than 2 yrs. 3 10.0 1 33.3 1 33.3 1 33.3

Among 30 patients, 8 patients (26.66%) were newly diagnosed. In that category, 5

patients (62.5%) responded good and 3 patients (37.5%) responded moderately.

In the below 1 year group which contains 3 patients (10%) and in that 2 patients

(66.6%) responded good and 1 patient’s response was moderate (33.3%).

In the 1-2 year group contains 16 patients (53.33%). Among them 9 patients

(56.2%) responded good, 6 patients (37.5%) responded moderately and 1 patient’s

(6.26%) response was poor.

More than 2 year group contains 3 patients (10%) and in that 3 patients responded

good, moderate and poor respectively i.e. (33.3%) each.

Figure No. 10.

Chron icity & re sponse

8

3

16

35

2

9

13

1

6

10 0 1 10

5

10

15

20

N D <1yr. 1 -2 yrs . >2yrs .Chronic ity

No.

of P

t.'

N o. o f Pts GR MR PR

Results 100


Table No. 27. Showing the treatment history and response.

Sl. Treatment history No. of

pts.

% GR % MR. % PR %

01. Allopathic treatment 20 66.66 11 55 7 35 2 10

02. Ayurvedic treatment 2 6.66 1 50 1 50 - -

03. Both 0 0 - - - - - -

04. No history 8 26.66 5 62.5 3 37.5 - -

Among 30 patients, 20 patients (66.66%) had undergone allopathic treatment, 2

patients (6.66%) had taken Ayurvedic treatment an 8 patients (26.66%) had no treatment

history.

Among the patients those who had taken allopathic treatment, 11 patients (55%)

responded good, 7 patients (35%) responded moderately and 2 patients (10%) responded

poorly.

In Ayurvedic treatment group, 1 patient’s (50%) responded good and 1 patient’s

(50%) responded moderately.

In the no treatment history group 5 patients (62.5%) responded good and 3 patients

(37.5%) responded moderately.

Figure No. 11.

Treatment history & response

20

20

811

1 0

57

1 032

0 0 00

5

10

15

20

25

Allo.treat Ayu.treat Both No hist.

Treatment

No.

of P

t.'s

No. of GR MR. PR

Results 101


Table No. 28. Showing the family history and response.

Sl. Family history No. of

pts.

% GR % MR % PR %

01. Present 15 50 8 53.3 7 46.6 - -

02. Absent 15 50 10 66.6 3 20 2 13.3

Among 30 patients, 15 patients (50%) had family history and in that 8 patients

(53.3%) responded good and 17 patients responded moderately.

Other 15 patients (50%) had no family history and in that 10 patients (66.6%)

responded good, 3 patients (20%) responded moderately an 2 patients (13.3%) response

was poor.

Figure No. 12.

Family history & response15 15

810

7

3

02

02468

10121416

Present Absent

Family history

No.

of P

t.'s

No. of GR MR. PR

Results 102


Table No. 29. Showing the nature of koshta and response.

Sl. Koshta No. of

pts.

% GR % MR. % PR %

01. Mrudu 2 6.66 1 50 1 50 - -

02. Madhyama 27 30 16 29.2 9 33.3 2 7.4

03. Krura 1 3.33 1 100 6 100 1 6.2

Among 30 patients, 2 patients (6.66%) had mrudu koshta, 27 patient had (30%),

madhyama koshta and 1 patient’s had krura koshta.

In mrudu koshta patients, 1 patient’s (50%) response was good and 1 patient

responded moderately.

Among madhyma koshta patients, 16 patients (30%) responded good, 2 patients

(33.3%) responded moderately and 2 patients (7.4%) responded poorly.

1 krura koshta patient (100%) responded good.

Figure No. 13.

Nature of koshta & response

2

27

11

16

11

96

0 2 10

5

10

15

20

25

30

Mrudu Madhyama Krura

Koshta

No.

of P

t.'s

No. of GR MR. PR

Results 103


Table No. 30. Showing the Status of agni and response.

Sl. Agni No. of

pts.

% GR % MR. % PR %

01. Manda 1 3.33 1 100 - - - -

02. Teekshna 21 70 9 42.8 10 47.6 2 9.52

03. Sama 8 26.66 8 100 - - - -

04. Vishama 0 0 - - - - - -

Among 30 patients 21 patients (70%) had teeskhna agni and in that 9 patients

(42.8%) responded good. 10 patients (47.6%) responded moderately and 2 patient’s


Only one patient had (33.33%). manda agni and he responded good. 8 patients

(26.66%) had sama agni and in them all 8 patients (100%) responded good.

Figure No. 14.

Nature of agni & response

1

21

8

01

9 8

00

10

0 00 2 0 005

10152025

Manda Teekshna Sama Vishama Agni

No.

of P

t.'s

No. of GR MR. PR

Results 104


Table No. 31. Showing the nature of malapravritti in the patient and response

Sl. Malapravritti No. of

pts.

% GR % MR. % PR %

01. Free 16 53.55 10 62.5 6 37.5 - -

02. Constipation 14 46.66 7 50 5 35.7 2 14.2

Among 30 patients, 16 patients (53.33%) had free bowel and in that 10 patients

(62.5%) responded good and 6 patients (37.5%) responded moderately.

16 patients had constipation (46.66%) and in that 7 patients (50%) responded

good, 5 patients (35.7%) responded moderately and 2 patients (14.2%) response was

poor.

Figure No. 15.

Nature of Malapravritti

1614

1076 5

02

0

5

10

15

20

Free Constipation

Malapravritti

No.

of P

t.'

No. of GR MR. PR

Results 105


Table No. 32. Showing the habits of the patient and response.

Sl. Habits No. of

pts.

% GR % MR. % PR %

01. Smoking 17 36.6 6 54.5 4 36.6 1 9

02. Alcohol 12 40 9 75 2 16.6 1 8.3

03. Tobacco 2 6.66 1 50 1 50 - -

04. Alc. + Smk. 7 23.33 5 71.4 1 14.2 1 14.2

05. No habits 12 40 6 50 5 41.6 1 8.3

Among 30 patients, 11 patients (36.6%) had the habit of smoking and in them, 6 patients (54.5%) responded good, 4 patients (36.3%) responded moderately and 1 patient’s (9.0%) response was poor.

12 patients (40%) had the habit of drinking alcohol and in them 12 patients (75%)

responded good, 2 patients (16.6%), responded moderately and 1 patient’s (8.37%)

response was poor.

2 patients (6.66%) had the habit of tobacco chewing and they responded good and

moderate respectively (50%) each.

7 patients (23.33%) had the habit of alcohol and smoking and in them 5 patients

(71.4%) responded good 1 patient’s (14.2%) responded moderately and remaining 1

(14.2%) responded poorly.

In the no habit group 6 patients (50%) responded good, 5 patients (46.6%)

responded moderately and 1 patient’s (8.3%0 response was poor.

Figure No. 16.

Habits & response17

12

2

7

12

69

1

5 64

2 1 1

5

1 1 0 1 102468

1012141618

Smoking Alcohol Tobacco Alc. + Smk. No habits

Habits

No.

of P

t.'s

No. of GR MR. PR

Results 106


Table No. 33. Showing the prakriti of the patient and response.

Sl. Prakriti No. of

pts.

% GR % MR. % PR %

01. Kapha-pitta 15 50 9 60 5 33.3 1 6.6

02. Kapha-vata 15 50 8 53.3 6 40 1 6.6

03. Vata-pitta 0 0 - - - - - -

Among 30 patients, 15 patients (50%) each came under kapha pitta and kapha-

vata prakrities.

In first group 9 patients (60%) responded good, 5 patients (33.3%) responded

moderately and 1 patient’s (6.6%) response was poor.

Among kapha-vata prakriti patients, 8 patients (53.3%) responded good, 6

patients (40%) responded moderately and 1 patient’s (6.6%) response was poor.

Figure No. 17.

Prakriti incidence & response15 15

0

9 8

0

5 6

01 1 002468

10121416

Kapha-pitta Kapha-vata Vata-pittaPrakriti

No.

of P

t.'s

No. of GR MR. PR

Results 107


Table No. 34. Showing the Nidana status and response.

Sl. Nidana No. of pts.

% GR % MR. % PR %

01. Snigdha 30 100 17 56.6 11 36.6 2 6.6

02. Guru ahara 30 100 17 56.6 11 36.6 2 6.6

03. Asya sukha 27 90 15 55.5 10 37 2 7.4

04. Swapna sukha 25 83.3 12 48 11 44 2 8

05. Alpavyayama 26 86.6 14 53.8 10 38.4 2 7.6

06. Alpa chinta 12 40 8 66.6 4 33.3 - -

Among 30 patients, all of them used to indulge in general aharaja nidanas, like snigdha atyupayoga (100%) and guru ahara atyupayoga (100%). Among them 17 patients (56.6%) responded good, 11 patients (36.6%) responded moderately and 2 patients (6.6%) response was poor.

27 patients (90%) used to indulge in the vihara asyasukham and in that 15 patients (55.5%) respomded good, 10 patients (37%) responded moderately and 2 patients (7.4%) responded poorly.

25 patients (83.3%) indulge in more swapna sukham vihara and in that 12 patients (48%) responded good, 11 patients (44%) responded moderately and 2 patients (8%) responded poorly.

26 patients (86.6%) indulge in alpavyayama and in that 14 patients (53.8%) responded good, 10 patients (38.4) responded moderately and 2 patients (8%) responded poorly.

12 patients (40%) indulge in alpachinta and in that 8 patients (66.6%) responded good, 4 patients (33.3%) responded moderately. Figure No. 18.

Nida na incide nce & re sponse30 30

27 25 26

1217 17 15

12 148

11 11 10 11 1042 2 2 2 2 0

05

101520253035

Sng Guru A sya Sw apna A l v ya A l chi

Nida na

No.

of p

t.'s

No. of GR M R. PR

Results 108


Table No. 35. Showing the days of deepana pachana and response.

Sl. Deepana pachana No. of

pts.

% GR % MR. % PR %

01. Up to 3 days 18 60 11 61.1 6 33.3 1 5.5

02. 4 days 12 40 6 50 5 41.6 1 8.3

Among 30 patients (60%), 18 patients were given deepana pachana for 3 days. In

that 11 patients (61.1%) responded good, 6 patients (33.3%), responded moderately and 1

patient’s (8.3%) response was poor.

12 patients (40%), took deepana pachana for 4 days. In that 6 patients (50%)

responded good, 5 patients (41.6%0 responded moderately and 1 patient’s (8.3%)

response was poor.

Figure No. 19.

Da ys of De e pa na -pa cha na & re sponse18

1211

66 5

1 10

5

10

15

20

Up to 3 days 4 days

D ays

No.

of P

t.'s

No. of GR M R. PR

Results 109


Table No. 36. Showing the days of snehapana and response.

Sl. Snehapana No. of

pts.

% GR % MR. % PR %

01. Up to 3 days 21 70 12 57.14 8 38.09 1 4.76

02. More than 3 days 9 30 5 55.5 3 33.3 1 11.11

Among 30 patients 21 patients (57.14) received snehapana for 3 days and in that

12 patients (57.14) responded good, 8 patients (38.09) responded moderately and 1

patient’s (7.6%) responded poorly.

9 patients (30%) received snehapana for 4 days in that, 5 patients responded good

(55.55%), 3 patients (33.3%) responded moderately and 1 patient (11.11%) responded

poor.

Figure No. 20.

Da ys of S ne ha pa na & re sponse

21

912

58

31 1

0

5

10

15

20

25

Up to 3 day s More than 3 day s

Da ys

No.

of P

t.'s

No. of G R M R. P R

Results 110


Table No. 37. Showing the incidence of samyak snigdha lakshanas and response.

Sl. Samyak snigdha lashana No. of

pts.

% GR % MR. % PR %

01. Vatanulomana 26 86 14 53.8 10 38.4 2 7.6

02. Agni deepti 30 100 17 56.6 11 36.6 2 6.6

03. Purisha snigdhata 30 100 17 56.6 11 36.6 2 6.6

04. Asamhat varcha 26 86 14 53.8 10 38.4 2 7.6

05. Twak snigdhata 28 93 16 57.1 10 35.7 2 7.1

06. Anga laghuta 20 66.6 11 55 7 35 2 10

07. Gatra mardava 24 80 12 50 11 45 1 4.1

08. Klama 29 96.6 17 58.6 10 41.6 2 6.8

09. Shaithilya 10 33.3 6 60 4 40 0 -

Among 30 patients 26 patients (86%) showed vatanulomata. In that 14 patients

(58.8%) responded good, 10 patients (38.4%) responded moderately and 2 patients


All patients (100%) showed agni deepti. In that 17 patients (56.6%) responded

good, 11 patients (36.6%) responded moderately and 2 patients (6.6%) responded poorly.

All patients (100%) showed purisha snigdhata and in that 17 patients (56.6%)

responded good, 11 patients (36.6%) responded moderately and 2 patients (6.6%)

responded poorly.

Results 111


26 patients (86%) showed asamahat varcha in that 14 patients (53.8%) responded

good, 10 patients (38.4%) responded moderately and 2 patients (7.%) responded poorly.

28 patients (93%) showed twak snigdhata. In that 16 patients (57.1%) responded

good, 10 patients (35.7%0 responded moderately and 2 patients (7.1%) responded poorly.

20 patients (66.6%) showed anga laghuta and in that 11 patients (55%) responded

good, 7 patients (35%) responded moderately and 2 patients (10%) responded poorly.

24 patients (80%) showed gatra mardava and in that 12 patients (50%) responded

good, 11 patients (45%) responded moderately and 1 patient (4.1%) responded poorly.

29 patients (96.6%) showed klama and in that 17 patients (58.6%) responded


10 patients (33.3%) showed shaithilya and in that 6 patients (60%) responded

good and 4 patients (40%) responded moderately.

Figure No. 21.

Indence of samyak snigdha lakshana & response

26

30 30

2628

20

24

29

10

14

17 17

1416

11 12

17

6

10 11 11 10 10

7

11 10

42 2 2 2 2 2 1 2

00

5

10

15

20

25

30

35

VA AD PS AV TS AL GM Kl Sh

Samyka snigdha lakshana

No.

of p

ts.

No. of pts. GR MR. PR

Results 112


Table No. 38. Showing the incidence of samyak virechana lakshanas and response.

Sl. Samyak virechana lakshanas No. of

pts.

% GR % MR. % PR %

01. Indriya prasannata 25 83.3 14 56 10 40 1 4

02. Sroto shuddhi 28 93.3 15 53.5 11 39.2 2 7.1

03. Agni deepti 24 80 14 58.3 9 37.5 1 4.1

04. Exp. Vit pitta, kapha, vata 30 100 17 56.6 11 36.6 2 6.6

05. Vatanulomana 24 80 14 58.3 8 33.3 2 8.3

06. Absence of ayoga and atoyoga 27 90 14 51.8 11 40.7 2 7.4

07. Shareera laghuta 25 83.3 16 64 7 28 2 8

Among 30 patients 25 patients (83.3%) showed indriya prasannata in that 14

patients (56%) responded good, 10 patients (40%) responded moderately and 1 patient

(4%) responded poorly.

28 patients (93.3%) showed sroto shuddhi and in that 15 patients (53.3%)


responded poorly.

24 patients (80%) showed agni deepti and in that 14 patients (58.3) responded

good, 9 patients (37.5) responded moderately and 1 patient (4.1%) responded poorly.

All patients (100%) passed vit, pitta, kapha, and vata in sequence and in that 17

patients (56.6%) responded good. 11 patients (36.6%) responded moderately and 2

patients (6.6%) responded poorly.

Results 113


24 patients (80%) showed vatanulomana in that 14 patients (58.3%) responded


27 patients (90%) showed no atiyoga and ayoga and in that 14 patients (51.8%)


responded poorly.

25 patients (83%) showed shareera laghuta in that 16 patients (64%) responded

good, 7 patients (28%) responded moderately and 2 patients (8%) responded poorly.

Figure No. 22.

25

1410

1

28

1511

2

24

14

9

1

30

17

11

2

24

14

8

2

27

1411

2

25

16

7

20

5

10

15

20

25

30

No.of

pts.

IP SS AD Ex.V.P.K VA AAA SL

Samyak virechana lakshanas

Incidence of samyak lakshanas of virechana & response

No. of GR MR. PR

Results 114


Table No. 39. Showing the number of Vegas attained by patient and response.

Sl. Vega No. of

pts.

% GR % MR. % PR %

01. 5-10 3 10 2 66.6 1 33.3 - -

02. 11-15 13 43.3 6 46.15 6 46.15 1 7.6

03. 16-20 14 46.6 9 64.2 4 28.5 1 7.14

Among 30 patients 3 patients (10%) comes under 5-10 vegas group, and in that 2

patients (66.6%) responded good and 1 patient’s (33.3%) responded moderately.

Among the 13 patients on 11-15 vega group (43.3%), 6 patients, (46.15%)

responded good, 6 patients (46.15%), responded moderately and 1 patient’s response was

poor.

Among the 14 patients (46.6%) in 16-20 group, 9 patients (64.2%) responded

good, 4 patients (28.5%), responded moderately and 1 patient’s response (7.14%) was

poor.

Figure No. 23.

No. of vegas & response

3

13 14

2

6

9

1

64

0 1 102468

10121416

5 - 10 vega 11 - 15 vega 16 - 20 vegaVegas

No.

of P

t.'s

No. of GR MR. PR

Results 115


Table No. 40. Showing the incidence of Antaki and response.

Sl. Antaki No. of

pts.

% GR % MR. % PR %

01. Kaphantam observed`` 30 100 17 56.6 11 36.6 2 6.6

02. Kaphantam not observed - - - - - - - -

Among 30 Patients (100 %), all Patients (100 %) attained Kaphantham

Virechanam. In that 17 patients (56.6 %) responded good, 11 Patients (36.6 %)

responded moderately and 2 Patients (6.6%) responded poorly.

Figure No. 24.

Incidence of antaki vega & response

30

0

17

0

11

02

00

5

10

15

20

25

30

35

K.O. K.nO.

Antaki vega

No.

of p

ts.

No. of GR MR. PR

Results 116


Table No. 41. Showing the incidence of manaki and response.

Sl. Manaki No. of

pts.

% GR % MR. % PR %

01. 2000 ml & below 7 23.23 3 42.8 3 42.8 1 14.2

02. Above 2000 ml 23 76.6 14 60.8 8 34.7 1 4.3

Among 30 Patients 7 Patients (23.3 %) passed Vegas of 2000 ml and below,in

that 3 Patients (42.8 %) responded good, 3 Patients ( 42.8 %) responded moderately and

1 Patient (14.4 %) responded poorly

23 Patients (76.6 %) passed Vegas of above 2000ml, in that 14 patients (60.8

%)responded good, 8 Patients (34.7 %) responded moderately and 1 Patient (4.3 %)

responded poorly.

Figure No. 25.

73 3

1

23

14

8

10

5

10

15

20

25

No.of

pts.

2000 ml & below Above 2000 ml

Manaki

Incidence of manaki & response

No. of GR MR. PR

Results 117


Table No. 42. Showing the Overall assessment.

Sl. Assessment No. of pts. %

01. Good response 17 56.6

02. Moderate response 11 36.6

03. Poor response 2 6.6

04. No response 0 0

Among the 30 Patients, 17 Patients (56.6 %) responded good, 11 Patients (36.6

%) responded moderately and 2 Patient’s (6.6 %) response was poor.

Figure No. 26.

Assessment of results

GR56%

MR37%

NR0%

PR7%

GR MR PR NR

Results 118

Table No. 16. Showing the demographic data. Sex Religion Occupation Socioeconomic status Diet Duration Sl.

No. OPD No.

Age (yrs) M F H M C O S A L O P M UM HC V M ND < 1 1-2 > 2

01. 3909 60 + - + - - - + - - - - - + - + - + - - - 02. 3847 35 + - + - - - - - + - - + - - + - - - + - 03. 3912 35 - + + - - - + - - - - - + - + - + - - - 04. 3951 43 + - + - - - + - - - - - - + + - - - + - 05. 3010 58 + - - + - - + - - - - - - + - + - - + - 06. 4004 36 + - + - - - - - + - - - - + - + + - - - 07. 4030 60 + - + - - - + - - - - + - - + - - - - + 08. 4019 49 + - + - - - - - + - - - + - + - - - + - 09. 4000 53 + - + - - - + - - - - + - - + - - - + - 10. 4667 53 + - + - - - + - - - - - + - - + - - - + 11. 087 38 + - + - - - - - + - - - - + - + + - - - 12. 041 43 + - + - - - - - + - - + - - - + - - + - 13. 090 37 + - - + - - - - + - - - - + - + - + - - 14. 042 40 + - + - - - - - + - - - + - - + - - + - 15. 0578 52 + - + - - - + - - - - - - + + - - - + - 16. 047 52 + - - + - - - - + - - - + - - + + - - - 17. 060 54 - + + - - - + - - - - - + - + - - + - - 18. 0891 58 - + + - - - + - - - - - - + + - - - + - 19. 0844 48 - + + - - - + - - - - - + - + - - - + - 20. 0922 47 + - + - - - - - + - - - - + - + - - + - 21. 1095 59 - + + - - - + - - - - - + - + - - - - + 22. 1179 42 + - + - - - - - + - + - - - - + - - + - 23. 2481 47 - + + - - - - - + - - + - - + - - - + - 24. 1304 52 - + + - - - + - - - - + - - - + + - - - 25. 1332 57 - + + - - - + - - - - - + - + - - - + - 26. 1317 58 + - + - - - + - - - - - - + - + - - + - 27. 073 55 + - + - - - + - - - - - + - + - - - + - 28. 1301 59 + - + - - - - - + - - - + - - + - + - - 29. 1023 49 + - - - + - - - + - - - + - - + + - - - 30. 089 54 + - - + - - + - - - - - - + - + + - - -

M – Male; F- Female; H- Hindu; M- Muslim; C – Christian; O – Others; S – Sedentary; A – Active; L – Labor; O – Others; P- Poor; M – Middle class; Um – Upper middle class; HC – High class; V- Vegetarian; M – Mixed; ND – Newly diagnosed; < 1 – Below 1 year; 1-2 – 1-2 years; > 2 – More than 2 years.

94

Table No. 17. Showing the data related to disease. Family history Family

history Koshta Agni Bowel Habits Prakriti Sl.

No. OPD No.

Al Ay No Du P A Mr Ma Kr M T S F C S A T No KP KV VP 01. 3909 - - + - + - - + - - - + - + - + - - + - - 02. 3847 + - - 2 y + - - + - - + - + - + - - - - + - 03. 3912 - - + - + - - + - - + - + - - - - + + - - 04. 3951 + - - 1 y + - - + - - - + + - - + - - - + - 05. 3010 + - - 1 ½ y + - - + - - + - - + - - - + + - - 06. 4004 - - + - + - + - - - - + + - + + - - - + - 07. 4030 + - - 3 y + - - + - - + - - + - - + - - + - 08. 4019 + - - 1 y - + - + - - - + + - + + - - + - - 09. 4000 + - - 1 y + - - + - - + - - + - - + - - + - 10. 4667 + - - 2 ½ y + - - + - - + - - + - - - + - + - 11. 087 - - + - + - - + - - + - + - + - - - + - - 12. 041 + - - 8 m - + - + - - - + + - + + - - + - - 13. 090 + - - 5 m - + - + - - + - + - + + - - + - - 14. 042 + - - 1 y - + - + - - - + + - + + - - + - - 15. 0578 + - - 1 ½ y + - - + - - + - - + + - - - - - - 16. 047 - - + - - + - + - - - + + - - + - - + + - 17. 060 + - - 9 m - + - + - - + - + - - - - + + + - 18. 0891 + - - 1 y + - - + - - + - + - - - - + + + - 19. 0844 + - - 1 y - + - + - - + - - + - - - + - - - 20. 0922 + - - 1 ½ y - + - + - - + - - + + + - - - - - 21. 1095 + - - 3 y - + - + - - + - - + - - - + + + - 22. 1179 + - - 1 ½ + - - + - - + - - + - + - - - - - 23. 2481 - + - 8 m - + - + - - + - - + - - - + - - - 24. 1304 - - + - + - - + - - + - + - - - - + - - - 25. 1332 + - - 1 ½ y - + - + - - + - + - - - - + + + - 26. 1317 + - - 2 y - + - + - - + + - + - - - + - - - 27. 073 + - - 8 m - + - + - - + - - + - + - - - - - 28. 1301 - + - 2 m + - - + - - + - + - + + - - + + - 29. 1023 - - + - - + - - - - - - + - + - - - + + - 30. 089 - - + - - + + - + + - - - + - - - + - - -

Al – Allopathy; Ay – Ayurveda; No. – No history; Du. – Duration; P – Present; A – Absent; Mr. – Mridu; Ma. – Madhyama; Kr. – Krura; M. – Manda; T. Teekshna; S. – Sama; F – Free; C. – Constipation; S. – Smoking; A. – Alcohol; T. – Tobacco; N. – No habits; KP. – Kapha-pitta; KV – Kapha-vata; VP – Vata-pitta.

95

Table No. 18. Showing the data of parameters. Prabhoota

mutrata Pipasadhikya Kshudadhikya Karapadadaha Ati Sweda FBS PPBS Urine sugar Body weight Sl. OPD

NO. BT AV AF BT AV AF BT AV AF BT AV AF BT AV AF BT AV AF BT AV AF BT AV AF BT AV AF

01. 3909 1 0 0 2 0 0 1 0 0 1 0 0 0 0 0 131 85 93 213 125 140 .5 0 0.0 78 76 74 02. 3847 3 1 1 2 1 1 2 1 1 1 1 1 1 0 0 180 127 140 260 227 240 1.5 1 .5 86.5 85 83 03. 3912 2 0 0 1 0 0 2 1 1 2 1 1 0 0 0 132 85 92 212 170 177 .5 0 .5 58 57 54 04. 3951 2 0 0 2 1 1 2 0 0 1 0 0 0 0 0 106 81 94 210 182 192 .5 .5 0 68 67.5 66.5 05. 3010 2 1 1 2 1 1 2 1 1 0 0 0 1 0 0 188 146 156 270 200 212 1.5 .5 .5 56 85 84 06. 4004 3 1 1 1 0 0 2 0 0 1 0 0 1 0 0 170 110 120 260 202 207 1.5 .5 1 74 73 70 07. 4030 3 1 1 2 1 1 2 0 0 1 0 0 1 0 0 152 117 129 242 208 230 1.5 .5 1 86 85 83 08. 4019 2 0 1 1 0 0 2 0 1 1 0 0 1 1 1 142 106 114 248 181 194 1.5 .5 .5 67 67 65 09. 4000 3 1 2 2 0 1 1 0 1 1 0 0 0 0 0 160 124 133 252 190 200 1.5 .5 1 71 70 67 10. 4667 2 1 1 1 0 1 2 0 1 0 0 0 1 0 1 139 98 110 222 180 192 1 .5 .5 84 82 82 11. 087 2 0 1 2 1 1 1 1 1 2 1 1 1 0 0 140 79 88 245 171 184 1 .5 .5 76 74 71 12. 041 2 0 1 2 1 1 2 1 1 1 0 0 1 0 0 140 79 89 234 170 183 1 .5 .5 84 84 82 13. 090 3 1 1 1 0 0 2 1 1 1 0 0 1 0 0 160 111 120 258 190 205 1.5 .5 1 86 85 84 14. 042 2 1 1 1 0 0 2 1 1 1 1 1 1 0 0 132 71 80 208 141 153 1 0 .5 74 72 72 15. 0578 2 0 1 1 0 0 2 0 1 1 0 1 1 0 0 156 106 120 230 170 182 1.5 .5 .5 69 68 65 16. 047 2 1 1 1 0 0 2 0 1 1 0 0 1 0 1 127 75 86 201 151 168 1 .5 .5 68 67 66 17. 060 3 1 1 1 0 0 2 0 0 1 0 0 0 0 0 141 102 116 222 157 165 1 .5 .5 72 71 69 18. 0891 2 1 1 1 0 0 2 0 1 0 0 0 1 0 0 150 120 123 240 202 215 1.5 .5 .5 58 57 55 19. 0844 2 0 0 2 1 1 1 0 0 2 1 1 1 0 0 126 81 97 187 118 134 .5 0 0 57 57 55.5 20. 0922 2 1 1 2 2 2 2 2 2 1 0 0 1 0 1 149 151 160 220 220 230 1 1 1 72 78 77 21. 1095 2 1 1 1 0 1 2 1 1 0 0 0 0 0 0 166 140 148 242 118 222 .5 0 .5 76 65 64 22. 1179 2 0 0 2 1 1 2 1 1 2 0 0 1 1 1 160 126 134 257 211 223 1.5 .5 1 68 67 65 23. 2481 2 1 1 2 1 1 1 0 0 2 1 1 1 0 0 160 132 139 223 177 189 1 .5 .5 57 56 53 24. 1304 2 0 1 2 0 1 1 0 1 0 0 0 1 0 1 145 88 98 189 117 134 .5 0 0 59 58 56 25. 1332 3 1 2 2 1 1 2 1 1 2 0 2 0 0 0 151 130 139 240 210 221 1.5 .5 .5 60 59 58 26. 1317 3 1 1 2 0 1 2 1 1 2 1 1 1 0 1 170 139 150 260 219 233 1.5 1 1 64 63 60 27. 073 3 1 1 2 1 1 1 0 0 2 0 1 0 0 0 149 81 89 230 154 164 1 .5 .5 92 90 88 28. 1301 2 1 1 2 0 1 1 1 1 2 0 1 1 0 1 129 72 79 215 150 160 1.5 .5 1 85 84 82 29. 1023 3 1 1 2 0 1 2 1 1 0 0 0 1 0 0 126 68 78 235 180 186 1 .5 1 67 66 64 30. 089 2 0 1 2 0 2 2 1 1 2 1 1 0 0 0 111 80 89 200 150 157 .5 0.0 0 78 78 78

BT – Before treatment; AV – After virechana; AF – After follow-up.

96

Table No.19. Showing the treatment protocol and observation. Deepana pachana

Snehapana – details Virechana details Sl. No.

OPD No.

3 D 4 D 1 D 2 D 3 D 4 D T N3 N4 Dose TiA 1 V L V A B C KA NKA B2000 A2000 01. 3909 + - 30 ml 60 ml 90 ml 120 ml 300 - + 12 gr 7 am 8.30 11.00 - + - + - - + 02. 3847 - + 30 ml 60 ml 90 ml 120 ml 300 - + 12 gr 7 am 8.30 11.15 - + - + - + - 03. 3912 - + 30 ml 60 ml 90 ml 120 ml 300 - + 10 gr 7 am 9.00 11.45 + - - + - - + 04. 3951 - + 30 ml 60 ml 90 ml 120 ml 300 - + 15 gr 7 am 8.45 11.45 - - + + - + - 05. 3010 - + 30 ml 60 ml 90 ml 120 ml 300 - + 15 gr 7 am 8.00 11.30 + - - + - - + 06. 4004 + - 30 ml 60 ml 90 ml 120 ml 300 - + 15 gr 7 am 9.00 12.00 + - - + - - + 07. 4030 + - 30 ml 60 ml 90 ml - 180 - + 15 gr 7 am 9.00 1.30 + - - + - - + 08. 4019 + - 30 ml 60 ml 90 ml 120 ml 300 + - 15 gr 7 am 8.30 12.30 + - - + - - + 09. 4000 + - 30 ml 60 ml 90 ml - 180 - + 15 gr 7 am 8.30 12.30 - + - + - + - 10. 4667 + - 30 ml 60 ml 90 ml - 180 + - 12 gr 7 am 9.00 11.30 - + - + - - + 11. 087 + - 30 ml 60 ml 90 ml - 180 + - 15 gr 7 am 9.00 12.00 + - - + - - + 12. 041 + - 30 ml 60 ml 90 ml - 180 + - 15 gr 7 am 9.00 2.30 + - - + - - + 13. 090 + - 30 ml 60 ml 90 ml - 180 + - 12 gr 7 am 8.30 12.30 + - - + - - + 14. 042 + - 30 ml 60 ml 90 ml - 180 + - 1v gr 7 am 9.45 12.00 - + - + - + - 15. 0578 + - 30 ml 60 ml 90 ml - 180 + - 15 gr 7 am 9.30 11.30 + - - + - - + 16. 047 + - 30 ml 60 ml 90 ml - 180 + - 15 gr 7 am 9.00 12.00 - + - + - - + 17. 060 + - 30 ml 60 ml 90 ml - 180 + - 15 gr 7 am 8.30 12.30 - + - + - - + 18. 0891 - + 30 ml 60 ml 90 ml - 180 + - 15 gr 7 am 9.00 12.40 + - - + - - + 19. 0844 - + 30 ml 60 ml 90 ml - 180 - + 15 gr 7 am 9.00 12.00 + - - + - - + 20. 0922 + - 30 ml 60 ml 90 ml 120 ml 300 - + 15 gr 7 am 8.45 2.30 + - - + - - + 21. 1095 - + 30 ml 60 ml 90 ml - 180 + - 12 gr 7 am 9.00 12.00 - + - + - + - 22. 1179 + - 30 ml 60 ml 90 ml - 180 + - 15 gr 7 am 10.00 1.00 - + - + - - + 23. 2481 - + 30 ml 60 ml 90 ml - 180 + - 12 gr 7 am 9.30 12.00 - + - + - - + 24. 1304 + - 30 ml 60 ml 90 ml - 180 + - 15 gr 7 am 9.30 1.00 + - - + - - + 25. 1332 - + 30 ml 60 ml 90 ml - 180 + - 15 gr 7 am 9.00 11.45 - + - + - - + 26. 1317 + - 30 ml 60 ml 90 ml - 180 + - 15 gr 7 am 9.45 12.30 - + - + - - + 27. 073 - + 30 ml 60 ml 90 ml - 180 + - 12 gr 7 am 8.45 12.30 - + - + - + 28. 1301 - + 30 ml 60 ml 90 ml - 180 + - 15 gr 7 am 9.00 12.40 + - - + - - + 29. 1023 - + 30 ml 60 ml 90 ml 120 ml 300 - + 12 gr 7 am 8.30 1.00 - - + + - + - 30. 089 + - 30 ml 60 ml 90 ml - 180 + - 15 gr 7 am 9.30 12.30 - - + + - + -

3 D – 3 Days; 4 D – 4 Days; 1 D – 1 Day; 2 D – 2 Days; 3 D – 3 Days; 4 D – 4 Days; T – Total dose; N 3 – No. of patients taken sneha for 3 days; N 4 – No. of patients taken sneha for 4 days; TiA – Time of administration; 1 V – First vega; LV – Last vega; A – Grade A in which patient had passed 15-20 vegas; B – Grade B in which patients had passed 10-15 vegas; C – Group C in which patient had passed 5-10 vegas. KA – Kaphantam observed; NKA – No kaphantama observed; B2000 – The mana of 2000 ml and below; A2000 – The mana of above 2000 ml.

97


Statistical results

Table No. 43. Showing the Statistical results.

Sl. Parameters Mean S.D. S.E. t-value p-value Remarks

01. Prabhoota mutrata 1.633 0.49 0.089 18.348 < 0.001 H.S.

02. Kshuda adhikya 1.1 0.481 0.087 12.643 < 0.001 H.S.

03. Pipasa adhikya 1.266 0.521 0.95 13.326 < 0.001 H.S.

04. Karapada daha 0.9 0.481 0.087 10.344 < 0.001 H.S.

05. Ati Sweda 0.66 0.479 0.087 7.742 < 0.001 H.S.

06. Post Prandial Blood Sugar 41.433 18.329 3.346 12.382 < 0.001 H.S

07. Fasting Blood Sugar 29.8333 22.696 4.143 7.079 < 0.001 H.S

08. Urine sugar 0.55 0.3037 0.055 10.00 < 0.001 H.S.S

09. Body weight 3.7 1.95 0.356 10.39 < 0.001 H.S.

Statistical conclusion

01. All the subjective parameters shows highly significance, specially the parameter

prabhootra mutrata, as p value is 0.001.

02. The parameters kshudadhikya pipasadhikya, atisweda and karapadadaha shows

highly significance as p value is 0.001.

03. The mean effect of atisweda before and after treatment is low as compared with

other parameters.

04. The objective parameters FBS, PPBS, Urine sugar, and body weight also shows

highly significant, as p value is 0.001.

05. The mean affect of PPBS before and after treatment is more and also there is a

much variation in PPBS.

06. The mean and variants is more in the parameter FBS. There is a least variation in

urine sugar as compared to others, (By Comparing S.D)

These are form the above mentioned table using paired t test.

Results 123


Virechana is one of the purificatory therapy among panchakarmas. In the present

study, the first point to be discussed is how virechana is helpful in sthooola Madhumehi.

Mode of action of Virechana in sthoola madhumehi

In the classics samshodhana, shamanaushadhis and also pathyahara viharas are

mentioned for sthoola modhumehi from that, classical virechana karma was taken here

for the study.

Among samshodhana, vamana is indicated for kaphaja Prameha, but

contraindicated in sthoulya. But virechana is indicated for both sthoulya and Prameha.

The factors which helps in the pacification of sthoola Madhumeha by virechana

are,

01. Elimination of doshas along with mala.

02. Madhumeha is a kledajanya vyadhi, even though other doshas are involved in the

Samprapthi of this disease, kapha is the main factor especially along with medas,

mamsa and pitta. Virechana expels excess amount of vitiated kleda, malas and

doshas from the body, which is very much helpful to clear or check the

dhadhuparinama and there by helps in the reduction or pacification of the disease.

03. Excretion of pitta (bile) takes place, as a result fat metabolism is checked and

hence undigested and unutilized fat will be excreted out.

04. Restriction of diet during snehapana, virechana and samsarjana krama helps or

brings about mobilization of fat from its deposits.

05. In the treatment of sthoolamehi reduction of weight is also have a role. Above

mentioned factors are very much helpful in the reduction of weight, when there

is reduction of weight, then insulin resistance will be reduced and as a result

relative insulin deficiency will also get corrected.

Summary 124


06. Obesity is an extremely important environmental factor in the formation of type –

2 diabetes. Approximately 80% of type 2 diabetes are obese. In this impaired

binding is a result of decrease in the number of insulin receptors. Virechana

therapy diminishes the insulin resistance by the reduction of weight and there by

reduces the stress on beta cells.

07. Among the pathological changes which are happening in type 2 diabetes the most

consistent of these changes is probably deposit of amyloid which is accompanied

by atrophy of the normal tissue particularly Islets of epithelial cells. These

amyloids are fibrillar proteins in various organs and tissues, in such that vital

functions are compromised.

The associated disease state may be inflammatory, hereditary or

neoplastic and deposition can be local, generalized or systemic. In more

advanced lesions, the Islets are more or less converted to amyloid and the

reduction in the number of insulin secreting cells are more propounded than that

of glucagon secreting cells.

Heavy deposition of amyloids itself are rare without diabetes. The amyloids are

fat soluble and when snehapana and Swedana are administered in the patient, these

amyloids get dissolved in snehana, as a result of Swedana it moves to koshta and get

eliminated by virechana karma.

Above said factors may be the reason why virechana is effective in sthoola

madhumehi.

Summary 125


Madhumeha v/s diabetes mellitus:

Madhumeha is a disease Known to mankind since Vedic period. Ayurvedic

classics consider madhumeha among the twenty obstinate urinary disorders. At the same

time it is also explained that, when prameha are left untreated, it leads to the condition

called Madhumeha. So Madhumeha can also be considered as an advanced condition or

stage of prameha apart from the 20- types and also Prameha is a Nidanarthakara roga of

Madhumeha.

Traditionally, Madhumeha has been equated with diabetes mellitus. Madhumeha

is a disease in which certain pathological changes in urine are noted along with some

other changes, the most important being the presence of sugar (mootra madhuryata).

Since the disease is connected with the urinary system with the presence of sugar in

urine. Apart from this, tanu madhuryata also mentioned, which can be taken as blood

sugar. Like this the equation of Madhumeha with diabetes mellitus is justifiable.

Also in view of the similarity in signs and symptoms Madhumeha has been

equated, with diabetes. Among them, some correlations are given below.

Obesity is mentioned as a major causative factor for diabetes mellitus, as it cause,

insulin resistance. In Ayurveda Sthoulya is mentioned as a nidanarthakara roga for

Madhumeha and is included under santarpanajanya vyadhi.

Madhura, snigdha bhojana are mentioned as nidanas for madhumeha. In modern

science over eating and sedentary life styles are the predisposing factor for diabetes

mellitus. Those food articles and overeating, causes obesity and which may cause

Diabetes mellitus.

Summary 126


Prabhoota avila mootrata is considered as a pratyatma lakshana of madhumeha.

In this the bahudrava kapha along with other dooshyas mainly kleda pradhana dooshyas

in the basti is the cause for prabhoota avila mootrata. The same reason has been given in

modern science for Polyurea that is the osmotic diuretic effect of glucose in the kidney

tubules.

Glycosuria explained in the modern science can be taken as madhusama mootra.

The reason for this Madhusama mootra is bahudrava kapha or ojus, which is excreted

through mootra.

Pipasa or polydipsia mentioned in both sciences. Depletion of intracellular water

triggering the more receptors of thirst center of brain and thirst is noted, which is similar

to pipasa of Ayurvedic Science and here due to excessive loss of the urine, pipasa is

noted.

In modern science the condition weakness is due to lack of glucose utilization,

loss of electrolyte and protein loss. In Ayurveda this same condition is due to aparipakwa,

dhatus i.e., lack of proper nourishment of dhatus.

Kulaja dosha and beeja dosha have been mentioned in the causative factors of

Sahaja Prameha. Such patients are said to be weak, emaciated, suffering from thirst, loss

of appetite and are required to be treated with a nourishing diet.

In diabetes also genetic and hereditary factors are mentioned as causative factors.

In such patients weakness and emaciation are noted. The above-mentioned patients are

Juvenile diabetics and require a nourishing diet. Therefore Sahaja Pramehi and Juvenile

diabetes may be correlated.

Summary 127


Apathyanimittaja Madhumeha explained on Ayurveda, in such patients,

atikshudha, atinidra and aalasya are noted. And it is caused due to over intake of

madhura snigdha ahara and vihara which favours kapha medovridhi. Maturity onset

diabetes tend to over eat and are lazy in nature, even though age factor is not mentioned

in Ayurveda, while explaining chikitsa acharya have explained sthoola and krisha

classification. The same type of classification can be seen in modern science as obese

and non-obese type.

Upadravas of Ayurveda can be correlated to some of the complications of modern

science. For eg. Trishna, bhrama, shoola, tama pravesha, shwasa can be correlated to

diabetic Ketoacidosis, in which thirst, weakness, blurred vision, abdominal pain, air

hunger etc are seen.

Insulin resistance and relative insulin deficiency are the major step in the

pathogenesis of the diabetes mellitus on obese indviduals. There is no explanation

regarding insulin resistance in Ayurveda. Even though in some recent literary works,

medodhatwagni is correlated with insulin. But no proves are available for exact

correlation.

In the normal state sthiratwa, dardya, utsaha, vrishata, budhi, etc are contributed

by kapha, which is also known as bala or oja. By seeing this, we can correlate this kapha

with glucose. In madhumeha, the kapha, which is vitiated and which is in bahudravata

form travels all over the body in rasa produces tanu madhuryata, which can be taken as

hyperglycemia, i.e. increased blood glucose condition.

Summary 128


By considering the above similarities we can come to a conclusion that

madhumeha explained in Ayurvedic science and the diabetes mellitus mentioned in the

modern science are almost similar condition.

Discussion On Inclusion And Exclusion Criteria And Diagnosis

Mild and moderate type of obese NIDDM cases are taken for the study. Because

of the same reason, complications are very rarely observed during the treatment period in

patients.

For the mild, moderate sugar level selection, gradings were given and the patient

selection was mainly based on that criteria. Apart from this, other inclusive and exclusive

criterias are explained, which are explained in the exclusion and inclusion criterias. The

main idea behind the exclusion and inclusion of particular cases are to avoid

complications. For example insulin dependency and even patients who have developed

complications were excluded from the study, because of lack of emergency treatment.

For the diagnosis of patient, mainly mootramadhuryata and tanumadhuryata are

taken which are confirmed by blood and urine sugar examination. Apart from these

factors, patients who are sthoola and having prabhoota mootra Pravruti with other

associated symptoms of madhumeha are selected. Sushruta had given the explanation

that, if a patient had praboota mootrapravruti along with half of poorvaroopas, then we

can consider him as a madhumeha rogi.

Summary 129


Discussion On Observation

All the cases were reported to DGM Ayurveda medical college hospital, post

graduation department. Special medical camps were also conducted in the college for

selecting the patient. 42 cases were registered and from that 30 cases were selected for

the study. Observed features in the patients during the study were recorded in the case

sheets and these observations were analyzed and tabulated after completion of clinical

study. These observational findings are discussed below.

Age

Risk of diabetes increases as age advances; because of decrease in beta cells

especially after 40 years. It is also a recorded fact that, the NIDDM occurs only after 3rd

decade of life. In this study, above factors were proved, as all the patients were between

the age group of 30 to 60. And also it is noted that maximum number of patients; were

between the age of 40 to 60 Years.

Sex

Acharya Sushruta had said that women won’t get Madhumeha; because their body

gets cleaned every month by the raja pravrutti. But it is considered as a controversial

dialogue as women also getting madhumeha and they are also at high risk of getting

diabetes compared to men after 30 Years. From Sushruta’s statement we an understand

the importance of shodhana. But in this study male patients were more compared to

females i.e. 22 male patients and 8 female patients.

Summary 130


Food Habits

In the manifestation of madhumeha, food habits had great importance. If we

check the nidana aspects we can see the importance of food habits. At the same time lot

of foods are also mentioned which are helpful in controlling madhumeha.

In the present study 15 Patients were vegetarians and 15 patients were non

vegetarians (mixed). From these we can see that high calorie intake is the main risk

factor for diabetes and sthoulya. Food items which increase the sleshma, medas and

mamsa are the main reason behind madhumeha. In the same way sthoulya also having the

same type of aharaja nidna.

Religion

In the present study majority of the patients were hindus (25%), but it does not

mean that hindus are more prone to this disease. This may be due to the method of

sampling. The patients were selected incidentally.

Occupation

Maximum number of patients were with sedentary type of occupations. In

sedentary type of occupations physical activities are very less and in both Ayurveda and

modern science, it is clearly mentioned that people with sedentary life styles are more

prone to diabetes mellitus or Madhumeha.

Socioeconomic Status

In the present study majority of the patients belongs to upper middle and high

class. In these classes, the people indulge in very less activities and ultimately with

sedentary life styles and such persons are more prone to diabetes.

Summary 131


Family History

In the present study 15 patients had family history and rest of the 15 the patients

had no family history of madhumeha. It is a well-proven factor that family history had a

main role in the manifestation of sthoola madhumeha.

Chronicity

In the present study only mild and moderate type of diabetes mellitus were taken

for the study and in this study 8 patients were newly diagnosed. In the remaining patients,

16 patients were suffering from this disease since 1-2 years, 3 patients below 1 year and 3

patients were there in the above 2 years category. As it is a chronic, relapsing type of

disease, only mild and moderate types of cases were taken for the study.

Deha Prakriti

Even though madhumeha is a disease with the involvement of 3 doshas, it is

mainly a disease of kaphaja origin. In the present study 15 patients were with kapha pitta

prakriti and 15 patients were with kapha vata Prakriti. From this we can understand the

involvement of Kapha as a main dosha in the manifestation of madhumeha.

Agni

Majority of the patients (21 patients) were with teekshna agni followed by

Samagni (8 patients) and mandagni (1 patient). Presence of teekshnaagni patients in

majority may be due to the disease process and in sthoulya also teekshnaagni is a

characteristic feature.

Summary 132


Nidanas

Most of the nidanas mentioned in the classics were elicited in this study. Among

general nidanas, all patients used to take snigdha aharas and guru aharas excessively.

Among the viharas, asya sukham (27 patients), swapna sukham (25 patients), alpa

vyayama (26 patients) and alpa chinta (12 patients) were also noted. From this we can see

that snigdhadi ahara dravyas and asya sukhadi viharas had key role among the nidanas.

Basavaraja a 16th century physician of Andhrapradesh has included the excessive

indulgence in alcoholic beverages as one of the nidana of prameha roga. In the present

study 18 patients had the habit of taking alcoholic drinks.

Lakshanas

In all the patients prabhoota mootrata was noted. Other symptoms like

pipasadhikya, kshudadhikya, karapada daha, atisweda, etc. were also seen in most of the

patients. Gayadasa says kara pada daha is due to prabhava of roga and other symptoms

like snigdha pichila guruta and madhurata shukla mootrata are due to kapha only.

Regarding other symptoms discussions were done already.

Deepana pachana

Done for a period of maximum 4 days. The medicine used were Trikatu churna

and is deepana pachana in property.

Snehapana

After the niramata by deepana pachana, senhapana was started with 30 ml and

increased 3 or 4 days in increasing doses. In the present clinical study maximum dose

given in a patient was 300 ml and a minimum of 180 ml.

Summary 133


Like the other cases, in madhumeha snehapana is not needed for more days. The

same explanation is given in classics that in madhumeha, less snehana is enough, as

kaphotklesha is already there.

Abhyanga and Sweda

For abhyanga moorchita tila taila was used and for swedana ushna jala snana was

performed. In madhumeha swedana is contraindicated. Even though swedna is

contraindicated, in classics, it is mentioned that, if necessary, we can do mridu swedana.

So, here mridu Sweda was performed i.e. Ushna jala snana.

Virechana

Virechana dravyas were administered just after kapha kala. Before the

administration, observations like pulse, B.P., respiratory rate and temperature were noted.

All these were also noted during and after the completion of virechana karma, because

there may be variations in that readings, during virechana. So, one has to observe whether

it is in normal limits or not. Parameters like vegiki, manaki, antaki and laingiki were also

noted by intorogation with patient. In the present study 13 patients passed Vegas between

10-15, 14 patients passed in between the 15-20 vegas and 3 patients passed between 5-10

vegas. In classics it is mentioned that in uttama shodhana 30 vegas, in madhyama

shodhana 20 vegas and in avara 10 vegas noted. So in this study majority of the patients

got madhyama shodhana. In the present day and in the present health condition

madhyama shodhana can be considered as good shodhana.

Summary 134


Discussion On Treatment And Results

Samshodhana has been given more importance in our classics. And it gives long

standing effect. In madhumeha samshodhana is advised especially for sthoola and

balavan in order to correct agni and to reduce the kleda and medas, which are increased

in the disease process of madhumeha.

In the present study it was noted that virechana had immediate and long standing

effect. During the follow-up period only placebo capsules were given in order to know

the long standing effect of virechana. It was noted that the increase of sugar levels were

gradual and other symptoms were very minute. It was also a notable point that out of 30

patients 8 patients were newly diagnosed in our college, 16 patients were suffering from

madhumeha since 1-2 years, 3 patients below 1 year and only 3 patients were suffering

form this disease since 2 or more than 2 years.

In this present study 42 patients were registered, and in that 4 patients were not

satisfying the criteria of study, 3 patients were not able to come for follow up and 5

patients discontinued the treatment before virechana karma.

The result of the study confirmed that virechana is highly effective in sthoola

madhumeha. As explained, the study was a single grouped and prospective clinical trial.

And the group showed remarkable reduction in the symptoms as well as in blood sugar

levels. Body weight of the patient was also observed before and after the study and in that

also reduction was noted, which was statistically significant. (As p-value less than 0.05).

From this we can assume that virechana corrects the agni and reduces kleda and

medas which are increased in this condition. Modern science also agreed the factor that,

obesity leads to insulin resistance.

Summary 135


In this study all parameters showed marked response. Among the subjective

parameters prabhoota mootrata showed maximum significance compaired to others (p-

value 0.001). The mean effect of atisweda , before and after the treatment was low as

compaired to others. Even then it was statistically significant.

Objective parameters showed high significance. Among them PPBS and FBS

showed more mean variation in before and after treatments as compaired to urine sugar.

Summary 136

A close perusal of the observation and inference that can be drawn leads to the

following conclusions –

01. Virechana is an effective treatment in sthoola madhumeha. And it also shows

lasting results.

02. In mild and moderate type of sthoola madhumeha classical virechana alone is

enough to control it.

03. Along with virechana karma, administration of pathya ahara viharas may give

more effect.

04. In order to reduce the over weight of patient and to bring down the madhumeha

condition to normalcy, repeated virechana at specific intervals should be adopted,

keeping in mind that bala of the patient does not deteriorate. This would help in

obtaining positive results in the management of madhumeha.

05. Even though severe cases were not there in this study, it can be assessed that, in

severe cases of madhumeha reapeated virechana, intake of shamanoushadhis and

pathya ahara viharas are essential to control the condition.

Suggestions For The Future Study

01. Study on large sample.

02. Study on repeated virechana in madhumeha.

137


The Panchakarma therapy is an important part of Ayurveda. The procedures of

Panchakarma therapy have thrown new light on the management of disease and have

provided effective weapons against them. The entire group of purification procedures is

based up on promoting the body’s natural methods of elimination of unwanted

substances. Among the Panchakarmas, the virechana is an important one, which had great

importance and at the same time it is highly effective therapy. It is a process by which

the doshas are made to pass through the adhomarga i.e. guda. Virechana is a specific

treatment for pitta dosha, and pitta samsarga doshas. It is also the treatment for kapha and

vata doshas. In the process of virechana, the person will not have that much amount of

trouble and exhaustion as in normal purgation, as he has been subjected to snehana,

swedana, etc.

Management of madhumeha is perhaps one of the most important and interesting

subject in clinical practice considering its high prevalence as well as profound impact the

treatment has on long term morbidity and mortality of the patient. Increasing urbanization

industrialization and changing life styles seems to be contributing to increasing

prevalence of sthoola madhumeha.

Like the disease, the treatment also is a prolonged one. Since the patient of

madhumeha have been divided in to the sthoola and krisha varities, the separate methods

of treatments are mentioned in classics, and from that virechana therapy was taken as a

choice of treatment in the present study and is adopted in sthoola madhumeha patients.

So, the objectives of this study was, Evaluate the efficacy of virechana karma in

madhumeha (NIDDM)

The present work covered the following areas-

Summary 138


01. Introductory part regarding the present work and the objectives.

02. Historical aspect of virechana, madhumeha and also the mile stones in the field of

diabetes mellitus.

03. Virechana karma in detail along with its modern concepts, anatomical and

physiological aspects.

04. Modern description regarding the diabetes mellitus along with the physiological

and anatomical descriptions of glands involved in it.

05. Nidana panchakas of madhumeha, simultaneously explanation of dibetes mellitus

in modern counterpart has been done along with the comparison and description

in the same context.

06. Description regarding the materials and methods used in the present study.

07. Observations of the present study, results, discussion, summery, conclusion and

finally bibliography and references.

The study was conducted in a single group and all the patients received classical

virechana.

The effect of the therapy was assessed statistically by using paired t-test.

It was found that virechana shows long term effect. But, it was also noted that due

to food and activities of the patient there is gradual variation in sugar levels after

virechana. So after virechana if the person follows strict diet, sugar levels and other

associated complaints can be controlled.

Summary 139

1. Shastry. VVS, Ayurveda Prabandhavali Diabetes and treatment (vol. 6) chapter 1. Kottakkal: Arya Vaidya Shala Publications; 1993. p. 10.

2. Raghunath Dr, History of Diabetes from Remote to Recent times chapter 2.

Nagpur: Baidyanath Ayurveda Bhavan Ltd; 1985. p. 56.

3. Raghunath Dr, History of Diabetes from Remote to Recent times chapter 2. Nagpur: Baidyanath Ayurveda Bhavan Ltd; 1985. p. 58.

4. Raghunath Dr, History of Diabetes from Remote to Recent times chapter 2.

Nagpur: Baidyanath Ayurveda Bhavan Ltd; 1985. p. 62.

5. Agnivesa, Charakasamhitha Nidanasthana chapter 4 sloka 37. 4th ed. Varanasi: Chaukhambha Kasi Sanskrit Sansthan; 1994. p. 215. (Kasi Sanskrit series 228).

6. Agnivesa, Charaka samhitha Sutrasthana chapter 17 sloka 78. 4th ed. Varanasi:

Chaukhambha kasi Sanskrit series; 1994. p. 103. (Krishnadas academic series; vol 4).


Chaukhambha Kasi Sanskrit Sansthan; 1994. p. 103. (Krishnadas academic series vol 4).

8. Bhelacharya, Bhela Samhita Nidanasthana chapter 6 sloka1-4. 1st ed.Girija Dayal

Sukla ,editor. Varanasi: Chaukhambha Vidya Bhavan; 1959. p. 65.

9. Sushrutha, Sushruthasamhitha Chikitsasthana chapter 13. Varanasi: Krishnadas Academy; 1980.p.456. (Krishnadas academic series vol 51).

10. Sushrutha, Sushruthasamhitha Chikitsasthana chapter 12. Varanasi: Krishnadas

Academy; 1980. p. 450. (Krishnadas academic series; vol 51).

11. Vagbhata, Ashtangahridaya Nidanasthana chapter 10 sloka 18. Varanasi: Krishnadas Academy; 1982. p.504. (Krishnadas Ayurvedic series 4).

12. Koutilya, Arthashastra Chapter 16 sloka 179. Varanasi: Chaukhambha Sanskrit

Sansthan: 1978.

13. Madhavakara, Madhavanidana Madhukosha chapter 33 sloka1-32 Varanasi: Chaukhambha Surbharathi Prakashan; 1998.p.38. (Chaukhambha Ayurvijnana Granthamala 46).

14. Sushrutha, Sushruthasamhitha Nidanasthana Nyayachandrika Commentary

chapter 6 sloka 6. Varanasi: Krishnadas Academy; 1980. p. 290. (Krishnadas Ayurveda series 51).

Bibliographic references 140

15. Sushrutha, Sushruthasamhitha Nidanasthana Nibandha samgraha commentary chapter 6 sloka 3. p.290. Varanasi: Krishnadas Academy; 1980. p. 268. (Krishnadas Ayurveda series 51).

16. Bhavamishra, Bhavaprakasha Utharakhanda chapter 38 sloka 4. 5th ed. Varanasi:

Chaukhambha Orientalia; 1988. p. 367. (Chaukhambha Sanskrit series 130).

17. Raghunath Dr, History of Diabetes from Remote to Recent times chapter 3 Nagpur: Baidyanath Ayurveda Bhavan Ltd; 1985. p. 70.

18. Raja Radhakantha Deva Bahadur, Shabdakalpadruma vol 4, 3rd ed.

Varanasi:Chaukambha Sanskrit Series; p. 255.(Chaukambha Samskrita Granthamala-93).

19. Raja Radhakantha Deva Bahadur, Shabdakalpadruma vol 3, 3rd ed. Varanasi:

Chaukambha Sanskrit Series; p. 421.(Chaukambha Samskrita Granthamala-93).

20. Kahn Ronald C MD, Weir GC, Joslin’s Diabetes Mellitus. Chapter 1. 13th ed. USA. Lea & Febiger; 1994.p. 36.

21. Agnivesa, Charaka samhitha Kalpasthana chapter 1 sloka 4. 4th ed. Varanasi:

Chaukhambha kasi Sanskrit series; 1994. p. 651. (Krishnadas academic series vol 4).

22. Vagbhata, Ashtangahridaya Sutrasthana chapter 13 sloka 4-11. Varanasi:

Krishnadas Academy; 1982. p. 211-213. (Krishnadas Academic series 4).

23. Agnivesa, Charaka samhitha Chikitsasthana chapter 6 sloka 15. 4th ed. Varanasi: Chaukhambha kasi Sanskrit series; 1994. p. 446. (Krishnadas academic series vol 4).

Vagbhata, Ashtangahridaya Chikitsasthana chapter 12 sloka 3. Varanasi: Krishnadas Academy; 1982. p. 678. (Krishnadas Academic series 4). Bhavamishra, Bhavaprakasha Uttarakhanda chapter 38 sloka 44. 5th ed. Varanasi: Chaukhambha Orientalia; 1988. p. 367. (Chaukhambha Sanskrit series 130). Yogaratnakara Uttarardha Prameha chikitsaprakarana. Vaidya Lakshmipatisastry, editor. Varanasi: Chaukhambha Sanskrit Sansthan; 1988. p. 82-96. (Kasi Sanskrit series 160).

24. Agnivesa, Charaka samhitha Sutrasthana chapter 2 sloka 9. 4th ed. Varanasi: Chaukhambha kasi Sanskrit series; 1994. p. 24. (Krishnadas academic series vol 4).

Agnivesa, Charaka samhitha Kalpasthana chapter 7,12. 4th ed. Varanasi: Chaukhambha kasi Sanskrit series; 1994.p.362-366, 370-376. (Krishnadas academic series vol 4).


Agnivesa, Charaka samhitha Sidhisthana chapter 6. 4th ed. Varanasi: Chaukhambha kasi Sanskrit series; 1994.p703-708. (Krishnadas academic series vol 4).

25. Sushrutha, Sushruthasamhitha Sutrasthana chapter 44. Varanasi: Krishnadas Academy; 1980.p.186-189. (Krishnadas Ayurveda series 51).

Sushrutha, Sushruthasamhitha Chikitsasthana chapter 33,34 Varanasi: Krishnadas Academy; 1980.p.514-524. (Krishnadas Ayurveda series 51).

26. Vagbhata, Ashtangahridaya Sutrasthana chapter 15,18. Varanasi: Krishnadas Academy; 1982.p.229-240,260-270. (Krishnadas academic series 4).

Vagbhata, Ashtangahridaya Kalpasthana chapter 2,3 Varanasi: Krishnadas Academy; 1982.p.741-748,748-752. (Krishnadas academic series 4).

27. Sharangadhara, Sarngadhara samhitha Poorvakhanda chapter 4 sloka 3-6. 3rd ed. Varanasi: Chaukhambha Orientalia; 1983. p. 35-36. (Jaikrishnadas Ayu. Granthamala 53).

28. Agnivesa, Charaka samhitha Kalpasthana chapter 1 sloka 5. 4th ed. Varanasi:


29. Agnivesa, Charaka samhitha Sidhisthana chapter 2 sloka 13. 4th ed. Varanasi:


Sushrutha, Sushruthasamhitha Chikitsasthana chapter 33 sloka 32. Varanasi: Krishnadas Academy; 1980. p. 519. (Krishnadas Ayurveda series 51)

Vagbhata, Ashtangahridaya Sutrasthana chapter 18 sloka 10. Varanasi: Krishnadas Academy; 1982. p. 261. (Krishnadas academic series 4).

30. Agnivesa, Charaka samhitha Sidhisthana chapter 2 sloka 11. 4th ed. Varanasi: Chaukhambha Kasi Sanskrit series; 1994. p. 688. (Krishnadas academic series vol 4).

Sushrutha, Sushruthasamhitha Chikitsasthana chapter 33 sloka 34. Varanasi: Krishnadas Academy; 1980. p. 519. (Krishnadas Ayurveda series 51). Vagbhata, Ashtangahridaya Sutrasthana chapter 18 sloka 7. Varanasi: Krishnadas Academy; 1982. p. 261. (Krishnadas academic series 4).

31. Vagbhata, Ashtangahridaya Sutrasthana chapter 16 sloka 17,18,19,. Varanasi: Krishnadas Academy; 1982. p. 247- 249. (Krishnadas Academic series 4).



33. Sushrutha, Sushruthasamhitha Chikitsasthana chapter 33 sloka 22. Varanasi:

Krishnadas Academy; 1980. p. 518. (Krishnadas Ayurveda series 51).


34. Agnivesa, Charaka samhitha Sidhisthana chapter 6 sloka 26-27. 4th ed. Varanasi: Chaukhambha Kasi Sanskrit series; 1994. p. 705. (Krishnadas academic series vol 4).


Chaukhambha Kasi Sanskrit series; 1994. p. 705. (Krishnadas academic series vol 4).

36. Vagbhata, Ashtangahridaya Sutrasthana chapter 18 sloka 37. Varanasi:

Krishnadas Academy; 1982. p. 247, 167. (Krishnadas academic series 4).




39. Agnivesa, Charaka samhitha Sidhisthana chapter 1 sloka 18-19. 4th ed. Varanasi:


Sushrutha, Sushruthasamhitha Chikitsasthana chapter 33 sloka 24. Varanasi: Krishnadas Academy; 1980. p. 518. (Krishnadas Ayurveda series 51). Vagbhata, Ashtangahridaya Sutrasthana chapter 18 sloka 39-40. Varanasi: Krishnadas Academy; 1982. p. 268. (Krishnadas Academic series 4).

40. Agnivesa, Charaka samhitha Sidhisthana chapter 6 sloka 31-32. 4th ed. Varanasi:

Chaukhambha Kasi Sanskrit series; 1994. p. 706. (Krishnadas academic series; vol 4).

41. Vagbhata, Ashtangahridaya Sutrasthana chapter 18 sloka 42-45. Varanasi:

Krishnadas Academy; 1982. p. 267. (Krishnadas academic series 4).




44. Agnivesa, Charaka samhitha Sutrasthana chapter 26 sloka 67. 4th ed. Varanasi: Chaukhambha Kasi Sanskrit series; 1994. p. 141. (Krishnadas academic series vol 4).



46. Dr. Laurence, Clinical Pharmacology chapter 33. 8th ed. London: Churchil

Livingstone; 1997. p. 579-583.

47. Martini.F.H, Fundamentals of Anatomy and Physiology chapter 24. 4th ed. New Jersey: Prentice Hall Inc. Simon & Schuster; 1998. p. 877-878.

48. Martini.F.H, Fundamentals of Anatomy and Physiology chapter 24. 4th ed. New

Jersey: Prentice Hall Inc. Simon & Schuster; 1998. p. 884-885.








54. Madhavakara, Madhavanidana chapter 1 sloka 5. Varanasi: Chaukhambha

Surbharathi Prakashan; 1998. p. 16. (Chaukhambha Ayurvijnana Granthamala 46).



56. Agnivesa, Charaka samhitha Nidanasthana chapter 04 sloka 3. 4th ed. Varanasi:




58. Sushrutha, Sushruthasamhitha Nidanasthana chapter 6 sloka 27. Varanasi:



59. Agnivesa, Charaka samhitha Nidanasthana chapter 04 sloka 3. 4th ed. Varanasi: Chaukhambha Kasi Sanskrit series; 1994. p. 211. (Krishnadas academic series vol 4).



61. Agnivesa, Charaka samhitha Shareerasthana chapter 3 sloka 17. 4th ed. Varanasi: Chaukhambha Kasi Sanskrit series; 1994. p. 350. (Krishnadas academic series vol 4).

62. Agnivesa, Charaka samhitha Chikitsasthana chapter 6 sloka 4. 4th ed. Varanasi:


Sushrutha, Sushruthasamhitha Nidanaasthana chapter 6 sloka 3. Varanasi: Krishnadas Academy; 1980. p. 289. (Krishnadas Ayurveda series 51). Vagbhata, Ashtangahridaya Nidanasthana chapter 10 sloka 3. Varanasi: Krishnadas Academy; 1982. p. 502. (Krishnadas academic series 4).











68. Cotran SR, Pathologic Basis of Disease chapter 20. 6th ed. Philadelphia: Saunders; 2003. p. 913.

Davidson Stanley Sir, Principles and Practice of Medicine chapter 12. CRW Edwards ,editor. London: Churchill Livingston 1995. p. 728.





Sushrutha, Sushruthasamhitha Chikitsasthana chapter 6 sloka 5. Varanasi: Krishnadas Academy; 1980. p. 290. (Krishnadas Ayurveda series 51). Vagbhata, Ashtangahridaya Nidanasthana chapter 10 sloka 38. Varanasi: Krishnadas Academy; 1982. p. 505. (Krishnadas academic series 4).

71. Madhavakara, Madhavanidana chapter 1 sloka 7. Varanasi: Chaukhambha Surbharathi Prakashan; 1998. p. 39. (Chaukhambha Ayurvijnana Granthamala 46).



73. Vagbhata, Ashtangahridaya Nidanasthana chapter 10 sloka 7. Varanasi: Krishnadas Academy; 1982. p. 502. (Krishnadas academic series 4).

Sushrutha, Sushruthasamhitha Chikiitsasthana chapter 6 sloka 6. Varanasi: Krishnadas Academy; 1980. p. 290. (Krishnadas Ayurveda series 51).

74. Agnivesa, Charaka samhitha Nidanasthana chapter 04 sloka 13-22. 4th ed. Varanasi: Chaukhambha Kasi Sanskrit series; 1994. p. 214. (Krishnadas academic series vol 4).

75. Agnivesa, Charaka samhitha Nidanasthana chapter 04 sloka 29-34. 4th ed.

Varanasi: Chaukhambha Kasi Sanskrit series; 1994. p. 214. (Krishnadas academic series vol 4).



77. Sushrutha, Sushruthasamhitha Nidanasthana chapter 6 sloka 25. Varanasi:


78. Vagbhata, Ashtangahridaya Nidanasthana chapter 10 sloka 18. Varanasi: Krishnadas Academy; 1982. p. 504. (Krishnadas Academic series 4).

79. Cotran SR, Pathologic Basis of Disease chapter 20. 6th ed. Philadelphia: Saunders;

2003. p. 913-916.

80. Madhavakara, Madhavanidana chapter 1 sloka 10. Varanasi: Chaukhambha Surbharathi Prakashan; 1998. p. 58. (Chaukhambha Ayurvijnana Granthamala 46).



82. Agnivesa, Charaka samhitha Sutrasthana chapter 17 sloka 78-79. 4th ed.

Varanasi: Chaukhambha Kasi Sanskrit series; 1994. p. 203. (Krishnadas academic series; vol 4).

Agnivesa, Charaka samhitha Chikitsasthana chapter 6 sloka 5. 4th ed. Varanasi: Chaukhambha Kasi Sanskrit series; 1994. p. 444. (Krishnadas academic series vol 4).






Agnivesa, Charaka samhitha Nidanasthana chapter 4 sloka 29-34. 4th ed. Varanasi: Chaukhambha Kasi Sanskrit series; 1994. p. 214. (Krishnadas academic series vol 4). Agnivesa, Charaka samhitha Nidanasthana chapter 4 sloka 41-44. 4th ed. Varanasi: Chaukhambha Kasi Sanskrit series; 1994. p. 215. (Krishnadas academic series vol 4).

86. Sushrutha, Sushrutha samhitha Nidanasthana chapter 6 sloka 10-12. Varanasi: Krishnadas Academy; 1980. p. 291. (Krishnadas Ayurveda series 51).

87. Vagbhata, Ashtangahridaya Nidanasthana chapter 10 sloka 13-19. Varanasi:

Krishnadas Academy; 1982. p. 503-504. (Krishnadas academic series 4).

88. Sushrutha, Sushrutha samhitha Chikitsasthana chapter 11 sloka 3. Varanasi: Krishnadas Academy; 1980. p. 451. (Krishnadas Ayurveda series 51).

89. Agnivesa, Charaka samhitha Chikitsasthana chapter 6 sloka 15-16. 4th ed.


90. Vagbhata, Ashtangahridaya Nidanasthana chapter 10 sloka 18. Varanasi:




Davidson Stanley Sir, Principles and Practice of Medicine chapter 12. CRW Edwards, editor. London: Churchill Livingston 1995. p. 725.

92. Agnivesa, Charaka samhitha Chikitsasthana chapter 6 sloka 7. 4th ed. Varanasi: Chaukhambha Kasi Sanskrit series; 1994. p. 445. (Krishnadas academic series vol 4).









97. Vagbhata, Ashtangahridaya Nidanasthana chapter 10 sloka 41. Varanasi: Krishnadas Academy; 1982. p. 506. (Krishnadas academic series 4).



99. Yogaratnakara – Pramehachikitsa Vaidya Lakshmipatisastry,editor. Varanasi: Chaukhambha Sanskrit Sansthan; 1988. p. 82. (Kasi Sanskrit series 160).

100. Sushrutha, Sushrutha samhitha Nidanasthana chapter 6 sloka 24. Varanasi:


101. Vaidya Basavaraja, Basavarajeeya 9th prakarana. Varanasi: Chaukhambha vidya Bhavana; p. 156.

102. Sushrutha, Sushrutha samhitha Chikitsasthana chapter 11 sloka 3. Varanasi: Krishnadas Academy; 1980. p. 451. (Krishnadas Ayurveda series 51).

103. Agnivesa, Charaka samhitha Chikitsasthana chapter 21 sloka 40. 4th ed.





105. Vagbhata, Ashtangahridaya Nidanasthana chapter 6 sloka 22-24. Varanasi:

Krishnadas Academy; 1982. p. 504. (Krishnadas academic series 4). Sushrutha, Sushrutha samhitha Nidanasthana chapter 6 sloka 13. Varanasi: Krishnadas Academy; 1980. p. 291. (Krishnadas Ayurveda series 51).

106. Agnivesa, Charaka samhitha Sutrasthana chapter 17 sloka 78-82. 4th ed. Varanasi: Chaukhambha Kasi Sanskrit series; 1994. p. 103. (Krishnadas academic series vol 4).

107. Agnivesa, Charaka samhitha Sutrasthana chapter 17 sloka 105-106. 4th ed.


108. Sushrutha, Sushrutha samhitha Nidanasthana chapter 6 sloka 14. Varanasi: Krishnadas Academy; 1980. p. 292. (Krishnadas Ayurveda series 51). 109. Vagbhata, Ashtangahridaya Nidanasthana chapter 10 sloka 24. Varanasi: Krishnadas Academy; 1982. p. 504. (Krishnadas academic series 4). 110. Cotran SR, Pathologic Basis of Disease chapter 20. 6th ed. Philadelphia: Saunders; 2003. p. 913.

Davidson Stanley Sir, Principles and Practice of Medicine chapter 12. CRW Edwards, editor. London: Churchill Livingston 1995. p. 754-757.

111. Agnivesa, Charaka samhitha Chikitsasthana chapter 6 sloka 7-8. 4th ed. Varanasi: Chaukhambha Kasi Sanskrit series; 1994. p. 445. (Krishnadas academic series vol 4).

112. Sushrutha, Sushrutha samhitha Nidanasthana chapter 11 sloka 3. Varanasi: Krishnadas Academy; 1980. p. 451. (Krishnadas Ayurveda series 51). 113. Agnivesa, Charaka samhitha Chikitsasthana chapter 6 sloka 25. 4th ed. Varanasi:


114. Sushrutha, Sushrutha samhitha Nidanasthana chapter 13. Varanasi: Krishnadas Academy; 1980. p. 451. (Krishnadas Ayurveda series 51). 115. Sushrutha, Sushrutha samhitha Chikitsasthana chapter 12 sloka 4-5. Varanasi: Krishnadas Academy; 1980. p. 454. (Krishnadas Ayurveda series 51).






119. Agnivesa, Charaka samhitha Chikitsasthana chapter 6 sloka 24. 4th ed. Varanasi: Chaukhambha Kasi Sanskrit series; 1994. p. 446. (Krishnadas academic series; vol 4).


121. Sushrutha, Sushrutha samhitha Chikitsasthana chapter 11 sloka 12. Varanasi: Krishnadas Academy; 1980. p. 453. (Krishnadas Ayurveda series 51). 122. Yogaratnakara Prameha chikitsa prakarana shloka 2-4. Vaidya

Lakshmipatisastry ,editor. Varanasi: Chaukhambha Sanskrit Sansthan; 1988. p. 35, 36. (Kasi Sanskrit series 160).

123. Vagbhata, Ashtangahridaya Suthrasthana chapter 6 sloka 164. Varanasi: Krishnadas Academy; 1982. p. 119. (Krishnadas academic series 4).

Nadkarni KM Dr, Indian Materia Medica vol 1. 3rd ed. Bombay: Popular prakashan; 1983. p. 1308.

Nadkarni KM Dr, Indian Materia Medica vol 1. 3rd ed. Bombay: Popular prakashan; 1983. p. 969. Nadkarni KM Dr, Indian Materia Medica vol 1. 3rd ed. Bombay: Popular prakashan; 1983. p.985.

124. Vagbhata, Ashtangahridaya Chikitsasthana chapter 12 sloka 27-28. Varanasi: Krishnadas Academy; 1982. p. 679. (Krishnadas academic series 4). 125. Govindadasa, Bhaishajyaratnavali Jwarachikitsa prakarana. 7th ed. Kaviraj

Ambikadatta Shastri editor. Varanasi: Chaukhambha Orientalia; 1983. p. 130. (Kasi Sanskrit series 152). Sushrutha, Sushruthasamhitha Chikitsasthana chapter 32 sloka 27. Varanasi: Krishnadas Academy; 1980. p. 512. (Krishnadas Ayurveda series 51).


126. Vagbhata, Ashtangahridaya Kalpasthana chapter 2 sloka 15-16. Varanasi: Krishnadas Academy; 1982. p. 743. (Krishnadas academic series 4). 127. Gogte. VM, Ayurvedic Pharmacology. Bombay: Bharatheeya Vidya Bhavan;

2000. p . 424. 128. Gogte. VM, Ayurvedic Pharmacology. Bombay: Bharatheeya Vidya Bhavan;

2000. p . 459.

129. Gogte. VM, Ayurvedic Pharmacology. Bombay: Bharatheeya Vidya Bhavan; 2000. p . 313.

130. Gogte. VM, Ayurvedic Pharmacology. Bombay: Bharatheeya Vidya Bhavan;

2000. p . 464.



2000. p . 415.



2000. p . 361.



2000. p . 477.



2000. p . 299.



2000. p . 409.




2000. p . 288, 574.



2000. p . 444.

145. Gogte. VM, Ayurvedic Pharmacology. Bombay: Bharatheeya Vidya Bhavan; 2000. p . 245,547.


2000. p . 487.



2000. p . 438.



2000. p . 424.


152. Vaidya Yadavji Trikamji Acharya, Rasamrita Lavana kshara vignaneeya,

chapter 2. Varanasi: Chaukhamba Sanskrita Bhavan; 1998. p. 137.(Chaukambha Sanskit Bhavan Series 2) Agnivesa, Charaka samhitha Sutrasthana chapter 27. 4th ed. Varanasi: Chaukhambha Kasi Sanskrit series; 1994. (Krishnadas academic series vol 4). Sushrutha, Sushrutha samhitha Sutrasthana chapter 46. Varanasi: Krishnadas Academy; 1980. (Krishnadas Ayurveda series 51).

153. Nadkarni KM Dr, Indian Materia Medica vol 1. 3rd ed. Bombay: Popular prakashan; 1976. p. 478. 154. Nadkarni KM Dr, Indian Materia Medica vol 1. 3rd ed. Bombay: Popular prakashan; 1976. p. 1208.


155. Nadkarni KM Dr, Indian Materia Medica vol 1. 3rd ed. Bombay: Popular prakashan; 1976. p. 1202. 156. Nadkarni KM Dr, Indian Materia Medica vol 1. 3rd ed. Bombay: Popular prakashan; 1976. p. 480. 157. Nadkarni KM Dr, Indian Materia Medica vol 1. 3rd ed. Bombay: Popular prakashan; 1976. p. 985. 158. Nadkarni KM Dr, Indian Materia Medica vol 1. 3rd ed. Bombay: Popular

prakashan; 1976. p. 1015.

159. Rasamrita Lavana kshara vignaneeya, chapter 2. Varanasi: Chaukhamba Sanskrita Bhavan. p. 137.(Chaukambha Sanskrit Bhavan series 2).

160. Goud Kiran Dr, Effect of Salasaradigana basti in Sthoola Madhumehi (Un

published doctoral dissertation). Bangalore: Rajiv Gandhi University of Health Sciences; 1999.


SPECIAL CASESHEET FOR MADHUMEHA

Post Graduate Studies And Research Center (Panchakarma) Shree DGM Ayurvedic Medical College, Gadag.

Guide : Dr. G.Purushothamacharyalu, PG Scholar : MD (Ayu) Febin.K.Anto

Co- Guide : Dr. Shashidhar.H. Doddamani. MD (Ayu) 1. Name of the patient : Sl. No : 2. Father’s / Husband’s Name : OPD No : 3. Age : IPD No : 4. Sex : 5. Religion :

M F

Hindu Muslim Christian Others

Poor Middle Upper middle class High class

Sedentary Active Labor Others 6. Occupation : 7. Economical Status : 8. Diet : 9. Address :_____________________________ Phone No : ____________________________ Email ID :

_____________________________ Pin

Veg Mixed

10. Date of Schedule Initiation :

Date of Schedule Completion :

11. Result : 12. Consent : I here by agree that, I have been fully educated with the disease and

Good Response Moderate Response

Poor Response

No Response

treatment, here by satisfied whole heartedly, and accept the medical trial over

me

Investigator’s Signature Patient’s Signature

13. COMPLAINTS WITH DURATION :-

Chief Complaints P/A Duration Prabhuta Mutrata Kshudadhikya Ati Sweda Pipasadhikya Karapada daha Other complaints P/A Duration Anga Saidhilyam Sareera ghanatwam Seeta Priyatwam Hrut-Netra-Jihwa Shravana upadeha Shareeradurgandha Chikkanata dehe

14. HISTORY OF PRESENT ILLNESS :- >Appearance of similar complaints before :

Yes No Incidental Gradual Hereditary >Onset : 15. HISTORY OF PAST ILLNESS Hypertension Jaundice Cardiac disorders Asthma T.B Others : 16. TREATMENT HISTORY :- Modern Medicine :- Yes No If Yes :- Duration Drug Ayurvedic medicine :- Yes No If Yes :-

Drug

Duration Relief with previous

Yes No Duration of relief

treatment :- 17. FAMILY HISTORY :- Present Absent

Father Mother Brother

Spouse Children Sister

Others

18. PERSONAL HISTORY

Mrudu Madhya Kroora Koshta

Veg Mixed Diet Poor Moderate Good Appetite Bowels Free Constipated Urine Normal Abnormal

Day Night

Number of times

Sleep Normal Loss More Disturbed

Habit Smoking Alcohol Tobacco

chewing No

Habits

Duration Of Habits :-

Menstrual Cycle Regular Irregular Menopause

19. ASHTASTHANA PAREKSHA a. Nadee Dosha Gati Poornata Spandana Kathinya

b. Mootra :

c. Malam : Constipation Loose Normal d. Jihwa : e. Sabdam : f. Sparsham : g. Drink :

Sthoola Krisha h. Akrithi :

20. GENERAL EXAMINATION : - Appearance

Healthy Unwell Nutrition

Obese Moderate Poor

Orientation Good Poor

Memory Normal Medium Poor

Height in cms:- Weight in kg :- BMI :- Temperature in degree Farenheit:- Pulse Rate:- Heart rate:- Respiratory Rate:- Bloodpressure:- mmHg. 21. DASAVIDHA PAREEKSHA :-

A) Prakruthi Vata Pitha Kapha Vatapitha Vatakapha Pithakapha Sannipatha

B) Vikruthi

Hetu

Dosha

Dushya

Bala

Prakruthi

Desa

Kala

Linga

C) Sara

Pravara Madhyama Avara

D) Samhanana Susamhatha Madhyasamhata Asamhata

E) Pramana Sama Heena Adhika

F) Satmya Ekarasa Sarvarasa Vyamishra Rooksha satmya Snigdha satmya

G) Satva Pravara Madhya Avara

H) Ahara shakthi

Abhyavahara Pravara Madhyama Avara

Jaranashakti Pravana Madhyama Avara

Pravara Madhyama Avara I) Vyayama shakthi

Bala Madhya Vruddha J) Vayaha

22. SROTOPAREEKSHA :-

Srotas Observed Lakshanas

Pranavaha

Annavaha

Udakavaha

Rasavaha

Rakthavaha

Mamsavaha

Medovaha

Asthivaha

Majjavaha

Shukravaha

Pureshavaha

Mutravaha

Swedovaha

Arthavavaha

23. NIDANA PANCHAKA :-

a. Nidana > General :-

Ahara

Snigdhaahara Atyupayoga Guru Ahara Atyupayoga Vihara

Asyasukham Swapnasukham Alpavyayamam Alpachintha

> Vataja Nidana :-

Ahara

Ruksha Atyupayoga Katu Atyupayoga Kashaya Atyupayoga Tiktha Atyupayoga

Vihara Vamana Atiprayoga Virechana Atiprayoga Basthi Atiprayoga Atimaithunasheela Ativyayamasheela Atyupavasasheela Rakthamokshana Atiprayoga Vegadharanasheela

> Pithaja Nidana :-

Ahara Ushna Atyupayoga Amla Atyupayoga Lavana Atyupayoga Katu Atyupayoga Vishamaaharasevana Ajeernaaharasevana

Vihara Teekshna Atapasevana Atishrama

> Kaphaja Nidana :-

Ahara Gramyamamsa Atyupayoga Anupamamsa Atyupayoga Oudakamamsa Atyupayoga Sakaahara Atypayoga Ksheera Atyupayoga Dadhi Atypayoga

Vihara

Avyayama Divaswapnam Aasanasheela

b. Poorva roopa : c. Roopa :

d. Upashaya / Anupashaya : e. Samprapthi

24. OTHER INVESTIGATIONS. Blood-Hb- TC- DC- ESR- SERUM CHOLESTROL- 25. TREATMENT PROTOCOL :-

Procedure Day Dose Observations

Deepanana Pachana (By Trikatuchurna)

Snehapana (By Trikandakadyam Gritham) :- OBSERVATION OF JEERYAMANA LAKSHANAS

Lakshanas I II III IV V VI VIIShiroruja Bhrama Lalasrava Murcha Angasada Klama Trishna Daha Arati

SNEHA JEERNA LAKSHANAS

Lakshanas I II III IV V VI VII Jeeryamanalakshana Prashamana

Vatanulomana Kshudha pravrutti Trisha pravrutti Udgara shuddhi Shareeralaghutha Utsaaha

OBSERVATION OF SAMYAK SNIGDHA LAKSHANAS

Lakshanas I II III IV V VI VII Vatanulomana Agnideepti Purisha snigdhata Asamhata Varchas Twak snigdhata Anga laghava Gatra mardhava Klama Shaithilya

Abhyanga & Mruduswedana :-

Day 1 Day 2 Day 3 Day 4 Pradhanakarma :- Poorva Nireekshana :

Nidra :- Malavegotsarga :- Jeernaahara :- Mangalacharana :-

Tatkaleena Nireekshana : > Virechanayoga Dose : gms. > Time of first Vega : > Time of last Vega : > Total No. of Vegas :

Vital Data :

Observation Before Virechana

During Virechana

After Virechana

Pulse Blood Pressure Respiratory Rate Temperature

Virechanakarma Parimana :

Laingiki Maaniki Vaigiki Aanthiki

Day 1

Day 2

Day 3

Day 4

Day 5

Day 6

Samsarjana karma

Day 7

26. ASSESSMENT OF RESULTS A. Subjective Parameters

Symptoms Before

treatmentAfter

SnehapanaAfter

Virechana15th day of follow-up

30th day of follow-

up Prabhuthamutratha Kshudadhikya Pipasadhikya Karapada daha Ati Sweda

B. Objective Parameters

Investigation Before treatment

After Snehana

After Virechana

15th day of

follow-up

30th day of follow-

up F.B.S

PPBS

Urine sugar

Body Weight

27. INVESTIGATORS NOTE :- Signature of Co-Guide Signature of Guide

SCORE-SHEET A) Prabhuthamutratha : Grade O - 2-3 times/day time ; 0-1 times/night Grade 1 - 4-5 times/day time ; 2-3 times/night Grade 2 - 6-7 times/day time ; 4-5 times/night Grade 3 - > 7 times/day time ; >5 times/night B) Pipasadhikya: Grade O - Normal Grade 1 - Slightly Increased Grade 2 - Severely Increased C) Kshudadhikya: Grade O - Normal Grade 1 - Increased, but can tolerate Grade 2 - Increased, but cant tolerate without consuming food D) Karapada daha: Grade O - Absent Grade 1 - Slightly present Grade 2 - Present E) Ati Sweda: Grade O - Absent Grade 1 - Present

Documents

Virechana madhumeha pk006-gdg