Madhumeha kc023 hyd

A STUDY ON THE EFFECT OF UMA SAMBHU RAS WITH MADHU

GHRITADI YAPANA VASTI IN THE MANAGEMENT OF

PRAMEHA W.S.R. TO MADHUMEHA

DISSERTATION SUBMITTED IN THE PARTIAL FULFILLMENT FOR THE

DEGREE OF DOCTOR OF MEDICINE (Ayurveda) IN KAYACHIKITSA

BY

DR. T.SIRISHAB.A.M.S

GUIDEDr. V.VIJAYA BABU M.D. (AY)

READER,POST GRADUATE DEPT.OF KAYACHIKITSA

DR. B.R.K.R. GOVT. AYURVEDIC COLLEGE & HOSPITALHYDERABAD – 38

POST GRADUATE DEPARTMENT OF KAYACHIKITSADR. B.R.K.R. GOVT. AYURVEDIC COLLEGE & HOSPITAL

ERRAGADDA, HYDERABAD – 38, A.P., INDIA.

Dr. N.T.R. UNIVERSITY OF HEALTH SCIENCES, VIJAYAWADA.

2008

Ayurmitra

TAyComprehended

Dr. N.T.R. UNIVERSITY OF HEALTH SCIENCESVIJAYAWADA

POST GRADUATE UNIT

DEPARTMENT OF KAYACHIKITSA

Dr. B.R.K.R. GOVT. AYURVEDIC COLLEGE & HOSPITAL

HYDERABAD

CERTIFICATE

This is to certify that Dr. T.SIRISHA of M.D. (Ayu) Kayachikitsa has worked for the

thesis on the topic ‘A Study On The Effect Of Uma sambhu ras with Madhu ghritaadi

yapanavasti In The Management Of Prameha w.s.r. to Madhumeha’, as per

requirements of the order laid by the N.T.R. University of Health Sciences, for the purpose. The

hypothesis submitted by him in the first year MD (Ayu) is one and the same to that of the

dissertation submitted.

I am fully satisfied with his work and hereby forward the dissertation for the evaluation of

the adjudicators.

Date: Dr.PRAKASH CHANDERPlace: Hyderabad MD (Ayu)

Professor& HOD,Post graduate Dept. of KayachikitsaDr. B.R.K.R. Govt. Ayurvedic College,

Hyderabad.

Dr. N.T.R. UNIVERSITY OF HEALTH SCIENCESVIJAYAWADA

POST GRADUATE UNIT

DEPARTMENT OF KAYACHIKITSA

Dr. B.R.K.R. GOVT. AYURVEDIC COLLEGE & HOSPITAL

HYDERABAD

CERTIFICATE

This is to certify that the present dissertation embodies the outcome of original

observations made by Dr. T.SIRISHA on ‘A Study On The Effect Of Uma sambhu ras

and Madhu ghritaadi yapanavasti In The Management Of Prameha w.s.r. to

Madhumeha’, for the degree of ‘Doctor of Medicine’ (Ayurveda). This work has

been completed under my direct supervision after a series of a scientific discussion.

The scholar has put in commendable effort for designing and executing the

methods and plans for the study. The results achieved through this work are authentic and

reproducible. Hence, I recommend this dissertation to be submitted for adjudication.

Signature of Co guide Signature of Guide

Dr. S.RAMALINGESWAR Dr. V.VIJAYA BABUM.D. (AY) M.D. (AY)

LECTURER,TECHNICAL ASST, READER,Post Graduate Dept.of Kayachikitsa. Post Graduate Dept.of KayachikitsaDr.B.R.K.R.govt.ayurvedic college Dr.B.R.K.R.govt.ayurvedic collegeHyderabad Hyderabad

ACKNOWLEDGEMENTS

I owe an enormous debt to my parents and mother-in-law who have been a

constant psychological support and backup throughout the research work

I express my deep sense of gratitude to my guide DrV.Vijayababu, M.D.

(Ayu).Reader, department of Kayachikitsa, for his time to time help and critical

suggestions associated with expert guidance at the completion of this dissertation.

I am privileged to express my thanks to my co-guide Dr.S.Ramalingeswar

Rao MD(Ay), lecturer and technical assistant, PG. Unit, K.C. Department, who

grilled a lot to make out the qualitative work. His out standing advises,

Interpretations, correlative & Analytical Excellency rendered the out come of the

work very scientifically.

I am highly indebted to Dr.Prakash chander MD (Ay), Professor and H.O.D,

P.G.Unit, K.C. Department, for his valuable advice and overall guidance with his

Enormous knowledge and Experience.

I would like to extend special thanks to Dr.M.S.Rao, Principal, Dr. B.R.K.R.

Govt. Ay. College, Hyd., for his careful supervision in providing all necessary

facilities for this research work.

I am extending my sincere thanks to Dr. V.V.Ramasastry former guide Rtd.

Reader and Dr. K.V.Bhaswant rao MD (Ay), former co guide Rtd.Asst.Professor,

K.C. Department, B.R.K.R.Govt. Ay. College, Hyd for their guidance in selecting

the topic for dissertation and their initial support, encouragement and expertise in

shaping, collation and illustration regarding my work thus giving an inspirational

start to this challenging and exciting task.

It is a great pleasure to acknowledge my deep sense of gratitude to my

former guide Dr.M.L. Naidu MD(Ay), Reader,P.G.unit,Kayachikitsa department,

for his inspiring guidance, Consistent encouragement, Valuable suggestions, Keen

interest with which he guided and enabled me to initiate this work.

I pay my humble and deep sense of respect to Dr.K.Vasudeva rao, my

former guide, rtd.Reader, P.G. Unit, K.C. Dept, who have been a source of

constant inspiration and encouragement to me for the successful completion of

this work.

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

Rama Prasad, M.D. (Ayu), M.A.Ph.D., professor, department of Kayachikitsa,

D.G.M. College, Gadag and thank him for his encouragement and guidance.

I am very thankful to Dr. Rama Krishna MD (Ay), Annapurna Bioved for

his tremendous effort in manufacturing the drug.

I convey my special thanks to the staff of the college library and technicians

of Hospital lab, for their valuable cooperation.

I should pay my due regards to my beloved brother T.V.V.Phani Kumar

whose suggestions inspired me and helped me in computing my dissertation.

I convey my special thanks to Ch.Suresh for his inestimable and invaluable

work.

I express my heartful gratitude to my husband Y.V.Samba siva rao, for his

extended support, encouragement, concern & care.

I send my sincere thanks to all those who rendered a helping hand in

framing out my dissertation.

INDEX

S.No TITLE Pg. No

I INTRODUCTION 1

II HISTORICAL REVIEW 4

LITERARY REVIEW

1 The Concept of Agni 8

2 Modern 12

DISEASE REVIEW

1 Definitions & Derivations 28

2 Nidana 30

3 Samprapti 36

4 Purva Roopa 46

5 Roopa 49

6Bhedas (classification)

52

7 Vyavacchedaka Nidana 55

8 Sadhya-Asadhya 57

9 Upadrava 58

10 Arista Lakshanas 63

11 Chikitsa 64

12 Pathya-Apathya 67

III

DRUG REVIEW 71

IV METHODOLOGY

1 Aims & Objectives 86

2 Methodology 87

3 Observations 90

4 Results 117

5 Discussion 126

6 Conclusion 146

7 Summary 148

V BIBILIOGRAPHIC REFERENCES 150

VI APPENDIX171

1 Case Sheet2 Master Chart3 Hypothesis

LIST OF TABLES AND DIAGRAMS

S.No TITLE Pg.No

1 Relation between Dosha- Agnis – Dhatu 11

2 Pancreas-anatomy 14

3 Insulin structure 14

4 Insulin physiology 18

5 Citric acid cycle 24

6 Metabolic interrelation among major tissues 25

7 Homeostasis of Blood Glucose 26

8 Hormonal regulation of blood glucose 27

9 Nidana of prameha – vataja prameha – madhumeha 31

10 Postulated Mechanism in the pathogenesis of type I Diabetes Mellitus 43

11 Purva rupas of prameha 46

12 Differential diagnosis of Type –I & Type-II diabetes 56

13 Patya 67

14 Apatya 68

15 Main ingredients of Uma Sambhu ras 73

16 Bhavana dravyas of Uma Sambhu ras 76

17 Madhu Ghritadi Yapana vasti procedure 80

18 STATUS OF PATIENTS OF PRESENT STUDY 90

19 AGE WISE DISTRIBUTION OF PATIENTS 90

20 GENDER WISE DISTRIBUTION OF PATIENTS 92

21 RELIGION WISE DISTRIBUTION OF PATIENTS 94

22 DISTRIBUTION OF PATIENTS ACCORDING TO OCCUPATION 96

23 DISTRIBUTION OF PATIENTS ACCORDING TO FAMILY HISTORY 96

24 DISTRIBUTION OF PATIENTS ACCORDING TO SOCIO ECONOMIC STATUS 100

25 DISTRIBUTION OF PATIENTS ACCORDING TO SOCIO ECONOMIC STATUS 101

26 DISTRIBUTION OF PATIENTS ACCORDING TO STRESS FACTOR 103

27 DISTRIBUTION OF PATIENTS ACCORDING TO CHRONICITY 105

28 DISTRIBUTION OF PATIENTS ACCORDING TO BMI 106

29 DISTRIBUTION OF PATIENTS ACCORDING TO DRUG GROUP 107

30 DISTRIBUTION OF PATIENTS ACCORDING TO ADDICTIONS 107

31 DISTRIBUTION OF PATIENTS ACCORDING TO PRAKRITI & NIDANA 108

32 DISTRIBUTION OF PATIENTS ACCORDING TO AGE GROUP & NIDANA 110

33 DISTRIBUTION OF PATIENTS ACCORDING TO PURVA RUPA 111

34 DISTRIBUTION OF PATIENTS ACCORDING TO PURVA RUPA 112

35 DISTRIBUTION OF PATIENTS ACCORDING TO SUBJECTIVE PARAMETERS GI &G II

113

36 DISTRIBUTION OF PATIENTS ACCORDING TO FUS GI & G II 113

37 DISTRIBUTION OF PATIENTS ACCORDING TO PLUS GI & G II 114

38 DISTRIBUTION OF PATIENTS ACCORDING TO FBS G-II 114

39 DISTRIBUTION OF PATIENTS ACCORDING TO FBS GI 115

40 DISTRIBUTION OF PATIENTS ACCORDING TO PLBS GI 115

41 DISTRIBUTION OF PATIENTS ACCORDING TO PLBS GII 116

42 MEANS & PERCENTAGE DIFFERENCE OF ALL THE SELECTED VARIABLES IN

INDIVIDUAL SUBJECT OF GROUP- I117

43 MEANS & PERCENTAGE DIFFERENCE OF ALL THE SELECTED VARIABLES IN

INDIVIDUAL SUBJECT OF GROUP- II119

44 PERCENTAGE CHANGE IN FASTING BLOOD SUGAR GI 120

45 PERCENTAGE CHANGE IN POST LUNCH BLOOD SUGAR G I 121

46 PERCENTAGE CHANGE IN FASTING BLOOD SUGAR G II 122

47 PERCENTAGE CHANGE IN POST LUNCH BLOOD SUGAR G II 122

48 EFFECT OF THE TREATMENT OBJECTIVE PARAMETERS G I 123

49 EFFECT OF THE TREATMENT SUBJECTIVE PARAMETERS G I 123

50 EFFECT OF THE TREATMENT OBJECTIVE PARAMETERS G II 124

51 EFFECT OF THE TREATMENT SUBJECTIVE PARAMETERS G II 124

52 Comparison of objective parameters between selected subjects of G I & G II 124

A Study on the effect of Uma sambhu ras with Madhu ghritaadi yapana vasti in the management of pramehaw.s.r.to Madhumeha

1

INTRODUCTION

Ayurveda, the science of 5000 yrs standing, has ample description of syndrome

‘Madhumeha’, a type of prameha. The disease Madhumeha finds its clear mention in the

ancient books of ‘Ayurveda, i.e.; Charaka Samhita sutra sthana 17th chapter, charaka nidana

sthana 4th chapter, Astanga Hridya nidana 10th chapter Susruta nidana 6th chapter…

Broadly speaking, the term ‘prameha’ means passing of fairly large amounts of unclear

Urine. It covers a large aspect of symptoms as well as local diseases involving Genito

urinary system. However, the definition of “Madhumeha” – to pass “Madhu samam” (1)

Urine i.e. Sweet like honey, makes it much closes to glycosuria. Vagbhata has also quoted

that in Madhumeha, another essential feature i.e.; “Madhuryaccha tonoratah’ probably

hyperglycemia condition along with “Madhviva mehati” glycosuria for a disease to be

labeled as “Madhumeha” (2)

The Synonyms for madhumeha are ojomeha & kshoudra meha (3). Ojomeha represents

increased susceptibility of patients suffering form this disease to infective & non-infective

ailments because of reduced vitality (immunity) Kshoudra meha signifies honey like

sweetness of Urine.

“Thomas Willis (1621-1675 AD) had described such condition where the urine is

wonderfully sweet as if imbued with honey or sugar” in diabetes or pissing evil”. (4)

Diabetes mellitus is a clinical condition characterized by increased blood glucose levels

due to insufficient or in efficient (incompetent) insulin. In other words, insulin is either not

produced in sufficient quantity or in efficient in its action on the target tissues.

Consequently, the blood glucose level is elevated which spills over into urine in Diabetes

mellitus. (5)


2

PREVALENCE6:

Prevalence of diabetes mellitus is increasing globally. This un precedent increase is

evident from the report of W.H.O India, which shows, that India top the world with the

larges number of diabetic subjects., According to recent WHO estimates, the total number

of people with diabetes is projected to increase to 366 million by 2030 and in India, it is

projected to increase to 100 million, i.e.; rise by 250% by the year 2035.

- India has maximum increase during the last 5 years with 2.4% in rural population,

11.6 % urban population and 5.9 % prevalence in population being urbanized.

- A younger age of onset of diabetes is noted in Asian Indians.

- Important risk factors for high prevalence include high familial aggregation,

obesity, especially central one, Insulin resistance and life style changes due to rapid

urbanization.

- Sedentary life style, one of the contributing factors for diabetes increased the risk

for diabetes 3 fold

PURPOSE OF THE STUDY:

Diabetes mellitus is a metabolic disorder which had a wide range of etiological factors right

from endocrine to auto immune, but usually considered Metabolic influenced by various

systemic & environmental factors. Usually, the patient is not aware of disease in the initial

stages, but more often accidentally gets investigated for Urine / Blood sugars, as be

confirmed as Diabetic in the due course. For most patients, diabetes once diagnosed is for

life. The Perseverance & self-discipline needed to achieve control over a lifetime can tax

even the most robust of people to the limit.

Madhumeha / Ojomeha - represent the degenerative state of the body with increased

susceptibility to various infections & associated dhatu kshaya. So, the management should

include drug, which could repair the tissues very fast ie; Rasayanam and provide faster and

better control over the disease to prevent further damage.


3

Even though, the contemporary medical sciences are able to pacify the disease by various

medications. There is a need of effective and quick / fast acting therapeutic measure to

counter the under lying pathology in Ayurveda Uma sambhuras in this regard, acts as a

rasayana & sarva prameha hara & may correct both dhatukshaya & ultimately ojovikara. It

is expected to provide a faster control over the disease and show good hypoglycemic action

as it is potencified with various rasayana & meha hara herb & minerals.

Madhue Ghntadi yapana Vasti is also considered along with uma sambhuras, expecting to

have a synergiec effect, which too is rasayana mehahara, nirupadrava, to have better &

faster control over disease.

Uma sambhuras along with madhu ghntadi yapana vasti were considered as the theropy in

this study.


4

HISTORICAL REVIEW

The history and literature enable us to understand the ever-changing modalities of

life and its associated diseases. Ayurveda the science of life, replete the references

regarding various aspects of medicine and it considerably influenced the knowledge of

medicine of other nations of the world. The literary aspect plays on important role in

understanding the various aspects of disease Madumeha chronologically from prevedic/

Vedic period to till date.

Pre Vedic & Vedic period: (4000 BC to 1000 BC) (7)

Seeds of knowledge of medicine were sown in pre historic times, which can be

traced even today linked with medicine in modern India.

Rig-Veda: Ojas, the product of metabolism was compared with madhu(8)

Atharva Veda sounakiya: Term ‘Asrava’ was mentioned -generally of Polyuria or

discharge of fluid through urine (mutra) stool (mala), wound (vrana) etc (9)

Vishanaka was mentioned to treat Asrava, Specifically vata predominant type(10)

Atharvana Veda: A mantra (2-3-1-3) says the drug emerged from valmeeka is indicated in

treating Ati mootra(11)

Agni Purana(12) & Vishnu Purana (13) Ojas & bala were described as strength of senses,

body.

Garuda purana: Garuda, Tarksya or Vainateeya

Nidana of prameha was dealt in separate chapter role of psychic state in metabolism was

well-emphasized “SWASTHA CHITTE DHATAWAH SAMBHAVANTI 1:114:73(14).

Twenty types of prameha & the disease Madhumeha were first mentioned

The treatment of the disease along with upadravas was described (15)

YAGNAVALKA SMRITI: Prameha was mentioned under Badhyaruk i.e.; chronic &

painful diseases(16)

BRAHMA SAMHITA: Prameha was indicated by the words ‘Prasrava’ Asrava’

Momutrate (17)

Vinaya pitaka & Pacittiya: (6BC-2 AD) – Madhumeha was mentioned (18)

Milindi Panha: 2B.C. some of the organs like yakrit, kloma, pleeha etc were mentioned(19)


5

Kalyana Karaka (815- 877AD): Only authoritative text available on pranavaya tradition of

medicine by ugraditya charya mentioned prameha in maha mayas (Great diseases) (ch.11-

13)(20)

Koutilya Arthasastra:

In the chapter on Secret means (14.177.1) a number the of diseases – prameha,

Sosa… were mentioned(21) Method of producing disease on experimental bases the

smoke produced by burning of krkanda (a kind of partridge), krkatasa (lizard),

Grhagodhika (a small house lizard) andhahika (blind snake) together with chitrabheka (a

kind of variegated color) & madhu (celtis orientalis? or honey) causes diabetes (22)

Samhitas:

Charaka Samhita: (2B.C.)

o Samprapti of madhumeha was described in sutrasthana 17th chap. Showing the

involvement of pitta & kapha (23)

o Jata prameha / Beeja dosha . ch.chi (24)

o Nidana, pragnosis, were described in ch. Ni (25)

Susruta Samhita: 2 ADo Susruta described prameha in Nidana sthana 5th chap & chikitsa sthana 11th chap (26)

o Explained Prameha chikitsa in three different chapters Prameha chikitsa,

madhumeha chikitsa, & prameha pitaka chikitsa (27)

Astanga Hridayam: 6ADo Vagbhata described ‘Madhuryaccha tanoratah’ in madhumeha. (28)

Madhava nidana:

Described Prameha, Prameha pitaka, Madhumeha after chapter on Asmari (29)

Kasyapa samhita: (5-6BC)

Described Prameha in children (Juvenile diabetes) in sutra sthana vedanadyaya(30)

Sarangdhara samhita(31) Bhava Prakasa (32), Yogaratnakara (33)

o Has mentioned twenty pramehas & Madhumeha. (16AD)

Bheda Samhita: (1000 BC) (34)

Have incomplete descriptions of prameha in chikitsa sthana 7th chapter. Vataja, Pittaja,

kaphaja types were mentioned but the term ‘madhumeha’ was not mentioned.


6

Harita Samhita (10-12AD) (35)

Twenty types of pramehas were mentioned. Only 14 names & term ‘Madhu prameha’

was mentioned as one of the types of prameha.

Rasa ratna samucchaya: (36)

Prameha chikitsa chapter includes various popular Rasa preparations in prameha.

Basavarajeeyam: (37)

Quantitative urine analysis for prognosis of prameha was described.

After 17th century, no development in any form occurred in ayurveda & changed its face

with much modern advancements.

Modern Medicine:

o Hippocrates makes no mention of diabetes.

o The only convincing description in classical literature is that of Aretaeus ,the

cappodocian (2AD)

o The often quoted Papyrus ebers, merely refers to polyuria (38)

o The term ‘diabetes’ meaning a ‘siphon’ or ‘running through’ He also noted thirst

& emaciation as features of this fatal disease .(39)

o Galen (131-201 AD) - thought diabetes was the result of weakness of kidneys.

o Avicenna (980-1037 AD) – suggested the disturbance of liver function in

Diabetes.(40)

o The knowledge of Diabetes Persists in a cingalese treatise of 15th century, but no

mention of it appears in European writing until two centuries later. (41)

o Thomas Willis (1621-1675) author of The Diabetes or pissing evil was the first

person to notice sweetness of urine.

o Richard mead (1673-1754) was first in the modern times to consider diabetes a

disease of the liver.

o John Rollo (1809) - Diabetes was a disease of stomach affecting digestion &

assimilation.


7

o Claude Bernard (1813-78) - Discovered concept of glucose production into blood

from storage form glycogen by liver .Pancreatomy causes Diabetes (O.von mering

& J.Minkowski, Strasbourg – 1889 (42)

o Naunyn (1839 – 1925) believed that disease of the nervous system & of the

pancreas could produce Diabetes .(43)

o Laguesse (1893) – Suggested the possibility that islets secreted a substance into the

milieu interieuro Opie (1901) described abnormal appearance of islets in some cases of diabetes(44)

o Insulin N paulesco (Romania) extracted insulin (1921) sir Fredrick, Banting &

Charles Best together with JJR Macleod & biochemist James collip, shared Nobel

prize for extraction & organizing the manufacture & distribution of insulin.(45)

o French chemist cherrevl (1815) discovered that sugar in diabetic urine was

glucose.(46)


8

THE CONCEPT OF AGNI47

The Concept of biological agni has been described in ayurveda in two references

1. Agni 2. Pitta

The functions attributed to them are Dahana, pachana, tapana etc, similar to those of Agni.

Pitta- Agni:-

Broadly five types of pitta- pachaka, Ranjaka, sadhaka Alochaka, Brajaka & thirteen types

of Agni Jataragni, Bhutagnis-5, Dhatwagnis-7. have been described, which are quite

different in their identity.

I.Jataragni:- Is known by various names viz., pachakagni, Antaragni, kayagni,

Kostagni, oudareeyagni.

Seat of Jataragni: - It is located at the site of grahani or in between amasaya &

pakwasaya.

Functions:-

Digestion of all types of food- madhura, amla, lavana, katu, tikta, kashaya, taken in any

form asitam, lihyam, peetam, khaditam.

Sara kitta vibhajana- separation of digested food & undigested or waste part &

rendering them fit for absorption & excretion. In addition, it exercises control upon

the other agnis situated as different sites – i.e., Dhatwagnis – Pachakamsa.

II. Bhutagnis- Bhutagni paka

Five kinds of Bhutagnis, respective to each Bhuta have been conceived in Ayurveda,

viz., parthiva, Apya, Agneya, Vayavya & Nabhas.

These are expected to act on the give basic elemental constituents of food in order to

digest or modify them.

The product of the food formed by Jataragni paka under goes bhutagni paka, which

reforms the food materials into five distinct groups physically & chemically.

Each of the five bhutagnis selects the food materials of the qualities it digests and

metabolizes those substances to become homogenous to the mahabhutas of the shareera.

Ex: Parthivagni selects the food of prithiva tatwa by processing that food makes it

available to be assimilated in to the body.


9

These 5, representing each bhuta are meant for digestion & assimilation of objects having

panchabhoutic configuration.

The non congenial (vijateeya) food will be processed by Jataragni & bhutagnis

concurrently and converted into congenial substances resulting in the separation of Sara,

which will be absorbed immediately & kitta bhaga which traverses down & Eliminated.

Bhutagni paka takes place in adho amasaya & pakwasaya, can be comparable to auto

digestions where heterogeneous complex materials are broken down into their elemental

forms as proteins into amino acids before being synthesized as organic specific proteins

like albumins, globulins, fibrinogen etc.

Bhutagni paka is required to process & convert them further, making them suitable as pre

homologues of substances, which may be able to compose the seven Dhatus.

III DHWATWAGIS - Dhatwagni paka:

They are seven different agnis-named as rasagni, raktagni, mamsagni, medogni, asthyagni,

majjagni & sukragni.

The dhatwagni represent Jataragni in each dhatu to metabolize the end products of bhutagni

paka. Dhatwagnis mediate or catalyze further metabolic reactions leading into formation of

two products prasada & kitta.

Samana vata mediates & controls all the three types of agni vyapara. It motivates &

controls the digestion at every level.

Systemic control of Jataragni on other Agnis & pitas:

An interesting concept has been forwarded in Ayurveda that Jataragni has a systemic

influence on other agnis of the body.


10

Similarly pachakagni- a component of Jataragni is known to have influence on the

remaining types of pittas.

i.e.; in toto twelve types of remaining agnis along with four types of remaining pitta are

governed by Jataragni including pachaka pitta.

Action of the moities of Jataragni on Dhatus:

Pachakamsas / kayagneyamsas are the moities of Jataragni located in dhatus (vagbhata)

The function of these moities is to regulate the quality & quantity of the Dhatus. This

action of pachakamsas is the same as that of pachakagni; the only difference is of the level.

Broadly the function of Jataragni is to cause sanghatabheda of the food matter. By virtue

of disintegration, it renders the food suitable for absorption, similarly the pachakamsas act

upon the nutrients or on the tissues in their absence.

Bhutagni – Dhatus

The process of Bhutagni paka is not limited up to the kosta but it extends up to the Dhatu

level also.

Thus it seems that the range of Bhutagnipaka during Bhutagni vyapara remains in between

the Jataragni paka & the Dhatawagni paka viz, the entire agni vyapara operating upon the

food after it has been digested and till its utilization starts in dhatus.


11

Relation between Dosha- Agnis – Dhatus

Dosha prakopana Disturbances of Doshas(etiological factors)

Disorders of Jataragni productionof diseases

formation of Ama

BHUTAGNIDISTURBANCE

DHATWAGNIDISORDERS


12

MODERN

Diabetes mellitus, a complex metabolic disorder, occurs due to insufficient release

or inefficient action of an anabolic hormone Insulin.

An important feature of diabetes is that the body cells are slaved of glucose despite

its very high concentrates around i.e., scarcity is plenty (48)

For a comprehensive understanding of diabetes,

1. Anatomy of pancreas

2. Endocrine pancreas

3. The relevant hormone - insulin

4. Metabolic path ways

5. Carbohydrate metabolism

6. Homeostasis of blood glucose

are discussed in this chapter

1. Anatomy – Pancreas

Pancreas is a soft lobulated yellow pint gland lying transversely in the posterior abdominal

wall behind the stomach extending from the duodenum to the spleen. It is retroperitoneal

lying at the level of L1 & L2. It lies obliquely to the left and slightly upwards in the epigastrac

and hypo chondriac regions. (49) Normal adult pancreas weighs 50 – 75g (50) (60- 100gm)

length is about 12-15 cm. (51) (15 – 20 m long) 3cm broad, 2cm thick (52).It is divided into

four parts.

1) The head

2) Neck

3) Body

4) Tail

Head of Pancreas: It is lodged with in the curve of the duodenum. From the lower and left

part of the head there is a prolongation named the uncinate process which projects upwards

and to the left behind the superior mesenteric vessels.


13

Neck of Pancreas: It is about 2cm in length. It supports the pylorus with omental bursa

intervening.

Body of Pancreas: It has three surfaces. (1) Anterior (2) Posterior (3) Inferior

It lies to the left of the superior mesenteric vessels passing over the aorta & L2

vertebrae, posterior to omental bursa.

Tail of Pancreas: The tail is narrow and is contained with in the two layers of the lieno

renal ligament together with the splenic vessels.

The Pancreatic duct: (main duct of wirsung) begins in the tail of the pancreas and

gradually increases in size as it passes to the right. At the neck it comes in relation with the

bile duct & together passes obliquely into the wall of duodenum & unites to form hepato

pancreatic ampulla (a short dilated duct) before opening on the duodenal papillae.

Accessory pancreatic duct (duct of santorini), is frequently seen, running in front of main

pancreatic duct and communicate with it, at the neck of the pancreas. (53)

Arterial supply(54)

1. Mainly pancreatic branches of the splenic artery

2. Superior pancreatico duodenal artery

3. inferior pancreatico duodenal artery

4. also supplied by branches from both the coeliac & superior mesenteric arteries

Venous drainage1. Superior pancreatico duodenal vein

2. Portal vein, splenic vein

3. Superior mesenteric vein

4. Inferior pancreatico duodenal vein

Lymphatic drainage:

Lymphatics follow the arteries & drain into the pancreatic, splenic, coeliac &

superior mesenteric groups of lymph nodes.

Nerve supply:

Vagus (parasympathetic)

Splanchnic (Sympathetic nerves)

Supply the pancreas through the plexuses around its arteries. (55)


14

INSULIN STRUCTURE


15

Endocrine Pancreas:

The endocrine part consists of islets of langerhans. There are between 1-2 million islets in

a pancreas (56) each being 75 to 175 cm in diameter & is about 1gm weight in toto. (57)

The islets cell tissue is greatly concentrated in the tail(58) secreting several critically

important hormones directly into the blood stream. (59) The islets consists of a mass of

polyhedral endocrine cells, pervaded by a net work of fenestrated capillaries (Glodskin &

Davies 1968) and with a rich autonomic innervations (Gerick & Lorenz 1978) (60)

Types of Cells:

Each islet in the mammalian pancreas consists of several cell types that differ in

morphology, staining properties & functions (orci -1976, monger 1981, and orci 1982) (61)

1. A cells – Secreting glucagons (also designated as α/ α2 cells)

2. B cells – Secreting insulin ( βCell)

3. D Cells – Secreting Somatostatin (α1 cells)

4. F Cells – Secreting pancreatic polypeptide (pp cells)

The missing C & E cells are seen in some animal species but not established as unique cell

type.(61) The βcells, the predominant cell type, make up the large central mass of the islet

(70-80%).(62)

The A cells the second most common cell type, about 20% of the total; form a rim

around this central mass of the islets.

In the inferior portion of the head of the pancreas, islets contain very few A cell & many

more F cells. D cells are also found almost exclusively near the outer rim, in close

proximity to both A cells & the inner core of B cells (63) (Orci & Unger 1975) the islets

may consist of two functionally distinct regions, a homocellular medulla, containing mainly

B cells where insulin is secreted at a constant rate and a heterocellular complex of A,B &

D cells particularly rich in vascular & neural elements, where rapid changes in secretary

activity are made in response to various environmental s stimuli.

In this later region, somatostatin release by the D cells may inhibit the secretory

activity of adjacent A/B cells. (Orci 1976) (64) (65)


16

The neuro hormones of autonomic nervous system, acetyl choline augment insulin

& glucagon release, while nor adrenalin inhibits glucose induced somatostatin & pancreatic

polypeptide secretion (66).

Islet cell types communicate directly through ‘Gap junctions’ providing potential

for the second.(67)

Characteristics of α– βCells:

The different cell types are best characterized by the secretary granules which they

contain.

αCells: Their secretary granules are, round or ovoid, of high electron density & variable

in size. They contain immuno reactive glucagon.

βCells: Contain fewer & larger granules of less electron density than in αcells. Many of

the granules show as rhomboid crystals surrounded by a clear zone with in the limiting

membrane. These βcell granules contain insulin & Zinc.

The delta cells ‘δ’ cells: Contains granules of low electron density and secrete small

amounts of gastrin & somatostatin.(68)

Insulin:

Insulin, a polypeptide hormone produced by the βcells of islets of langerhans

of pancreas, has profound influence on the metabolism of carbohydrate, fat and protein.

It is considered as anabolic hormone, as it promotes the synthesis of glycogen, tricacyl

glycerols & proteins. (69)

Structure of insulin: (70)

Insulin is a poly peptide containing two chains of amino acids linked by disulfide

bridge. (71)Human insulin (mol.wt.5734) contains 51 amino acids, arranged in two

polypeptide chains. The chain A has 21 amino acids while B has 30 amino acids. Both are

held together by two inter chain disulfide bridges, connecting A7 to B7 & A20 to B19.

In addition there is an intra chain disulfide link in chain A between amino acids 6 & 11(72)

Synthesis & Secretion of Insulin: The βcells of the islets at first, synthesize a big chain

of amino acid chain portion, called “signal sequence” is removed & now what remains is

called proinsulin (73)


17

This pro insulin is packaged into secretary vesicles. Which contain mainly insulin,

small percentage of proinsulin & a high concentration of zinc, which is know to form tight

complexes with Insulin. (74)

In the proinsulin chain A & B are present & connected together by a 31 amino acid

chain called ‘C’ peptide. Finally the ‘C’ peptide is enzymically removed – insulin is

formed & stored. (75)

The proportion of ‘C’ peptide increases as proinsulin is converted to insulin &

plasma C peptide concentration is an index of plasma insulin concentration. (76)

Plasma Insulin level: (77)

Fasting – 10mm μu /ml.

After meals – 50-70 μu /ml.

Normal insulin release: The normal basal rate of insulin release from βcells is l iu h -1 &

the total daily release in man is about 50 iu out of a pancreatic store of 200-250 iu of

insulin – (78)

Factors that stimulate or inhibit insulin secretion (79)are summarized as follows.

Stimulated by Inhibited by

1 Glucose 1 Adrenalin

2 Amino acids 2 Nor Adrenalin

3 Glucagon 3 D. mannoheptulose

4 Sulphonyl ureas 4 2 Deoxyglucose

5 Gastrin 5 Diazoxide

6 Secretin 6 Vagotomy

7 Pancreozymin 7

8 Vagal Stimulation

Samotostatin (growth hormonerelease inhibiting hormone)

Further more the net impact of insulin will depend on the number of receptors available on

the level of substrate available & on the number of substrate determined autoregulatory

controls.(80)


18

Insulin Secretion in vivo is controlled by a finely integrated combination of metabolic,

hormonal & neural mechanisms (81)

Degradation of Insulin: In the plasma, insulin has a normal half life of 4-5 min. This

short half life permits rapid metabolic changes in accordance to alterations in the

circulating levels of insulin. A protease enzyme namely insulinase (mainly found in liver

& kidney) degrades insulin.(82)

Insulin Physiology: (83), (84)

INSULIN½ Quantity ½ quantity

VIA PORTALVEIN ENTERS SYSTEMIC CIRCULATION

LIVER BINDS to receptors on target cells(has intrinsic tyrosine kinase activity)

Degraded ACTIVATES Post receptor intracellularin liver signaling pathway molecules

Results inGLYCOGEN SynthesisGLUCOSE TransportPROTIEN SynthesisLIPOGENESIS

Metabolic effects of insulin in major metabolic tissues (85)

TISSUE Metabolic processCarbohydrate Metabolism

Increase1. Muscle, adipose tissue __ Glucose transport

Liver, adipose tissue __ Glucose phosphorylation

Liver, Muscle __ Glycogenesis


19

Liver, Muscle, adipose tissue __ Glycolysis

Decrease

Liver, Muscle __ Glycogenolysis

Liver __ Gluconeogeneis

Lipid metabolism

Increase

Liver __ Fatty acid synthesis

Liver, adipose tissue __ Triglyceride synthesis

Liver __ VLDL formation

Adipose tissue __ lipoprotein degradation

Decrease

Liver __ Lipolysis

Liver adipose tissue __ Fatty acid oxidation

Liver __ Ketogenesis

Muscle __ Lipoprotein degradation

Protein metabolism

Increase

Liver, Muscle etc __ Amino acid transport protein synthesis

Decrease

Liver Muscle __ Protein degradation

Liver __ Urea genesis

Electrolyte metabolism

Increase

Muscle & liver etc __ K+ entry ,phosphate entry, sodium output

Metabolic Pathways


20

Metabolism is a continuous process, with thousands of reactions simultaneously occurring

in the living cell. Biochemists present metabolism in the form of reactions & metabolic

path ways for better understanding.(86)

This metabolic process comprises of

(i) Dissimilation or Catabolism: The total breakdown process under

gone by food stuff down to the final end product- carbohydrates &

fats – the end products are Co2 & H2o, amino acids, end products

containing nitrogen (urea) also appear.

(ii) Assimilation or Anabolism: The opposite transformation i.e.;

building up of storage, structural and functional materials from

simple food stuffs or intermediates.

Catabolic processes liberate energy because the energy content of a complex food stuff is

greater than that of its simpler degradation product.

Anabolic process will only proceed if energy from else where is “pumped into them’

The form in which metabolic energy is made manifest and usable occurs in three phases; in

a specific pathway – metabolic pathway- defined by the sequence of intermediate chemical

structures through which the food stuff passes until the final waste products are reached

catalyzed by its own highly specific enzymes.

Phase-I: This corresponds to the processes of intestinal digestion and absorption and the

similar process in tissues when storage material is mobilized for dissimilation .Poly

saccharides are converted to simple hexose sugars, fats to glycerol & fatty acids , proteins

to amino acids. The hydrolytic reactions of phase-I themselves liberate relatively little

energy but they prepare food stuffs for metabolism proper.

Phase-II : The various products from phase-I are partially oxidized along converging path

ways ,such that the products are Co2 , H2o , nitrogenous discard materials & one of three

acids:

1. Acetic acid

2. αketo gluteric

3. Oxalo acetic acid


21

During this phase about 1/3rd of the available energy of complete dissimination is released.

Phase-III: Is the complete oxidation of the three acids remaining from phase-II

metabolism. For this, cells adopt a complicated metabolic cyclical pathway common to all

three acids. This is citric acid cycle (kreb’s cycle). These transformations result in the

acids being oxidized to Co2 & H2o with the release of remaining 2/3rd of the available

chemical energy. This is the final metabolic pathway common to the carbon structures of

all major food stuffs.(87)

Carbohydrate metabolism.(88)

The principal carbohydrates in the food are:

1. Poly Saccharides - Starch (cellulose & pectin cannot be digested by the enzymes

of the human gut)

2. Disaccharides - Sucrose (saccharose, cane /beet sugar lactose (milk), maltose.

3. Mono saccharides - Hexoses – glucose, fructose, Galoctose

Phase – I .(89) : GUT phase

1. Amylase (ptyalin) of salvia digests starch after the natural plant granules have been

burst (by cooking) starch erythro dextrin achroo-dextrin maltose(some extent)

2. Hcl of gastric juice may hydrolyse some sucrose.

3. Pancreatic amylase, rapidly converts all forms of starch & dextrin completely into

maltose.

4. Succus entericus contains three classes of enzymes invertase, maltose & lactose,

which convert disaccharides to mono sacharides as follows:

Sucrose Invertase Glucose + fructose

Maltose Maltase 2 Glucose

Lactose Lactase Glucose + Galactose


22

Digestion of these disaccharides probably occurs in the luminal part (brush border) of the

epithelial cells.

Absorption of sugars from the stomach and colon is normally negligible. The mono

saccharides are absorbed from jejunum & upper ileum in to the blood capillaries by simple

diffusion or by more complex transport.

Phase-II .(90) Intermediary metabolism of carbohydrates. The following reactions occur

in the body:

1. Glycogenesis - Synthesis of glycogen from glucose

2. Glycogenolysis - Conversion of glycogen to glucose, mainly in liver

3. Glycolysis - Oxidation of glucose or glycogen to pyruvate & lactate by

E.M.pathway.

4. Gluconeogenesis - Formation of glucose or glycogen from non carbohydrate

sources – lactate & glycerol.

1) Glycogenesis .(91) Occurs in most of the body tissues, particularly in liver & muscle.(Reaction) (Enzyme/ co enzyme)Phosphorylation Hexokinase/ Glucokinase

Phospho gluco mutase

(i) UDP Glucose Phosphorylase (ii)

GlycogenSynthetase

The final reaction (i) Concerned with glycogen synthesis is not reversible. Glycogen

synthesis is promoted by insulin.

Glucose 6 Phosphate

Glucose / Phosphate

Glycogen


23

2) Glycogenolysis(92) Occurs in liver not in muscle. The reaction (ii) & reversible

reaction of conversion of glucose, phosphate to glucose 6 phosphate .Free glucose from

Glucose 6 phosphate is released in to the blood only in liver but not in muscle, by specific

enzyme glucose 6 phosphatase.

3) Glycloysis (93) (Embden Meyerhof pathway). Glucose 6 Phosphate, whether formed by

break down of glycogen or phosphorylation of glucose, undergoes series of reactions in its

conversion to pyruvate. Pyruvic acid is the key substance in phase –II metabolism. It is a

metabolic stage reached by glycerol (from fact) and many amino acids (from protein) as

well as all carbohydrates its further transformations include those to

1. Lactic acid

2. Glucose

3. O.A.A (Oxaloacetic acid)

4. Acetyl co-A

The latter two substances react together in the phase-III common metabolic pathway for

final dissimilation

Phase III metabolism(94) (95) : Citric acid cycle.

The citric acid cycle provides various intermediates for the synthesis of many compounds

needed by the body.

Krebs cycle is both catabolic & anabolic in nature, hence amphibolic

TCA cycle is actively involved in

1. Gluconeogenesis

2. Transamination &

3. Deamination


24

(95) Citric acid cycle


25

(96)


26

Homeostasis of Blood Glucose (98)

Glucose is carbohydrate currency of the body. An adult human body contains about 18gm

free glucose, just sufficient to meet basal energy requirements of the body for 1hr.

The liver has about 100gm stored glycogen & is capable of producing about 125-150mg

glucose/min or 180-220gm /24 hr.

The fasting blood glucose level in at absorptive stele is 70-100 mg/d/

following the ingestion of a Carbohydrate meal, blood glucose may rise to 120-140 mg/dl.

Hyperglycemia refers to an increase in the blood glucose above the normal level – seen in

DM.

Hypoglycemia represents a decreased blood glucose concentration.

Glycosuria - is excretion of glucose in urine

OVER VIEW OF BLOOD GLUCOSE HOMEO STASIS(99)

Dietary carbohydrate(starch, sucrose, glucose)

Digestion & absorptionGlycolyses & TCA Glucose Co2; H2o

Glycogenolysisin muscle

Glucose Hormonalin liver regulation Glycogenesis in liver & kidney

Lactate

Gluconeogenesis Synthesis of other monoSaccharides & amino sugars

Amino acidsGlycerol, propionate

HMP shunt for Pentoses &NADPH4

Glycogenolysis Excreted intoin liver Urine (>180mg/d/ Synthesis of fat

blood glucose)Sources of blood Utilization of

Glucose Blood Glucose

BLOOD GLUCOSEFasting 70-100 mg/d/Post prondial 120-140mg/dl


27

Hormonal regulation of blood glucose(100)

Hypoglycemic effect Hyperglycemic effect

Insulin Glucagon

Glucose Uptake Gluconeogenesis

Glycolysis Glucogenolysis

Glycogenesis Epinephrine

HMP Shunt Glycogenolysis

Lipid synthesis Thyroxine

Gluconeogenesis Gluconeogenesis

Glycogenolysis Glucocorticoids

Gluconeogenesis

Glucose utilization

(extra hepatic)

Growth harmone & ACTH

Glucose Uptake

Glucose utilization


28

NIRUKTI AND PARIBHASHA

Madhumeha Nirukti :

Madhumeha is derived from two words

– madhu(101) ( vi) (stri) which means manyante viseshene jana; priya,

madhura rasa, derived from ‘man’ dhatu with ‘ud’ pratyay.

– Meha(102) (pu) which means to pass more urine or excessive urination

derived from ‘mih’ dhatu with ‘han’ pratyay

– Madhumeha means passing of excessive sweetened urine.

Paribhasha:

Madhumeha

is passing of Kashaya , madhura, and pandu varna Mutra (103).

is madhusamam mehana i.e.; passing urine resembling that of

honey(104).

Is madhviva mehana (glycosuria) & madhryaaccha tano ratah

(hyperglycemia)(105).


29

Derivation (106):

DIABETES MELLITUS derived from Greek words

Diabetes – a siphon, or running through

Mellitus – sweetness

i.e.; passing of excessive sweetened urine.

Definition(107):

Diabetes mellitus is a clinical condition characterized by increased blood glucose levels

due to insufficient or inefficient (incomplete) insulin.


30

NIDANA

Nidana panchaka – Nidana, Purvarupa, rupa, upasaya and samprapti, plays an important

role in understanding the disease – Diagnose Aetio pathogenesis and plan the treatment.

The Prime factor – Nidana – Cause of the disease:

Nidana/ cause of disease are also termed as ‘Hetu’, Karana. Nimitta, Ayatana. Each term

specifies the kind and cause. Classification of Nidana 108

1. Samanya Nidana

2. Visishta Nidana

Nidana of prameha – vataja prameha – madhumeha described in various classics is as

follows:


31

NIDANA: AS SAID IN CHARAKA(109) , BHAVAPRAKASA(110),YOGARATNAKARA ( 111)

GADANIGRAHA(112)VANGASENA(113), BASAVARAJEEYAM(114),

MADHAVANIDANAM(115)

PRAMEHA 109-113,115,118 VATAJA PRAMEHA(114) MADHUMEHA(115)

AHARA: DHADHI RUKSHA AMLAGRAMYA RASA LAGHU LAVANAOUDAKA RASA SITA GURUANUPA RASA KATU RASA SNIGDHA AHARA

PAYAMSI / GORASA TIKTA RASA NAVANNAMNAVANNAM KASHAYA RASA NAVAPANAM

NAVADHANYAMNAVAPANAM

GUDA VIKRITA

KAPHAKARA AHARAVIHARA : ASYASUKHAM ANASANA NIDRA

SWAPNA SUKHAM ABHIGHATA ASYASUKHAMKAPHAKARA VIHARA ATAPA AVYAYAMA

JAGARANAVISHAMA SARERANYSAM

UPASEVANA

MANASIKA: UDVEGAM CHINTASOKAM

PANCHAKARMA: VAMANAVIRECHANA

SAMSODANAMAKURVATAAM

ASTHAPANASIROVIRECHANA

ATIYOGA / SANDHARANASONITATISEKAM

In addition Susruta, vagbhata, Basavaraj & Hareeta have described – few more causes for

prameha


32

VAGBHATA (116) SUSRUTA (117) HAREETA(118)

AHARA:MADHURA MADHURA DRAVA MADYA PRASEVANA

AMLA ANNA PANAM USHNALAVANA RASA TEEKSHNA

MEDOVAHA DRAVYAS KATU VIBHOJANASEETA MEDYADRAVAANNAM AMBUPANA(13)

SNIGDHA SEETAGURU SNIGDHA

PICCHALASURAIKSHU

MUTRAVAHA DRAVYAS

VIHARA :EKASTANA RATI DIWA SWAPNAM SRAMA

VIDIVARJITA SAYANA AVYAYAMAM VYAVAYA

MEDO DHOOMA NISHEVANA(119)

MUTRAKAPHA VARDHAKA

VIHARAOTHERS:

ALASYA PRASAKTAM DHARMAVIRUDHAM

Effect of Nidana on sampraptighatakas of Prameha-Madhumeha

Madhura rasa: -

. Kapha Prakopam (120)

vahni sadakaram

medo mamsa vardhakam (121)

Amla, Lavana rasa:-

Vitiate Kapha dosha(122)

Causes kleda vardhanam(123) & results in

Sleshma dravatwam(124)

Snigdha, guru & Picchala, seetala ahara:-

Kapha prokopakaram(125)

Vahni sadakaram , ama karam


33

Increased consumption causes obstruction of medavaha srotas (sroto

abhishyandakaram)

Guda – Gudavikaras-

Kapha karam

Medo vardhakam(126)

Ksheera / Payamsi:-

Due to their snigdha , guru & seetala nature – they are Kapha Vardakas

Ikshurasa:-

Kapha prakopam(127)

Mutralam

Gramya – oudaka- Anupa rasa

Vitiates kapha

Guru, abhishyandi

Vahni sadakaram

Medo mamsa vardhakam

Navannam. Navadhanyam:-

Guru , Snigdham

Kapha vardhakam(128) (Bahu drava sleshma)

Kleda vardhakam & results in

Agnimandya , Ama rasadhatu

Srotavarodham

Navapanam:-

Sroto abhishyandakaram(129)

Dadhi:-

Kapha prakopa karam(130)

Abhishyandi: - causes obstruction to rasovaha siras.

Guru- takes longer time for digestion

Produces apakwa rasa dhatu Ama rasa

Ambu / Dravapanam:-

Causes Agnimandya


34

Mutra vaha / Vardhaka dravyas:-

Increases mutra / kleda in the body

Kaphakara ahara vihara:-

Causes kapha prakopam

Agni mandhyam

Medo, mamasa vardhakam

Asya Sukham:-

Kaphakaram

Eka sthanarati -Avyayama:

Apanavata prakopakaram.(131)

Swapna sukham-Diva swapnam:

Kaphavardhanam, vata prakopam

Agninasam

Srotavarodham(132)

Vidhi Varjita Sayana:-

Vitiate samana vata(133)

Medovardhaka Ahara Vihara:

Increases medodhatu

Alasya Prasaktam :

(Garbadyiah Jadyam )

Kapha Prakopam (134) (Tamoguna increases)

Srama :

Vata Vridhi

Dhatu Kshayam

Katu tikta kashaya rasa:-

Cause vata prakopa (135)

Laghu seeta bhojana:

Increases vata (136)

Panchakarma Atiyogam -Sonitati sekam:

Causes Vata prakopam


35

Agni Vaishamyam

Dhatu Kshayam

Anasana & Jagarana:

Vitiates Samana vata

Causes Agnivaishamyam

Chinta, udvega, soka:

Vitiate vata (Manovaha srotas)

Agnimandhya.


36

SAMPRAPTI

Samprapti of the disease explains the process by which the initiation of Vitiation of

doshas starts and circulates to reach the dushyas and settle in vyadhi sthana to produce the

disease. To understand the samprapti of a disease, the basic elements of samprapti i.e.

Samprapti ghatakas should be analyzed.

Dosha: - Prameha - Bahudrava sleshma

Madhumeha - Vata

Dushyam: - Prameha -Bahvabadha Medo, Mamsa, Sareera kleda, Sukra, Sonita,

Vasa,Majja,Lasika,Rasa,Ojus

Madhumeha – medo, mamsa, ojas.

Agni- Bhutagni along with Jataragni & dhatwagni (medo, mamsa)

Srotas: - Mutravaha srotas

Ojovaha (rasavaha)

Srotodusti: - Mutravaha- Ati Pravritti

Sthana: - Vyadhi Utpathi sthana – Ama pakwasaya

Vyadhi adhistana stana – Vasti sarva sareeram.

I SLESHMA:

Though prameha is, considered to be, due to vitiation of the tridoshas, the specific

morbid factor of the humor is Bahudrava sleshma i.e. excessive fluidity of kapha.

‘Sleshma ‘– derived from ‘slish alingane’ – slish- to embrace, to cohere or to keep

together(137)

Kapha is derived from “kena jalena phalateti kaphah” (138) – a product of water with AP &

Pridvi bhuta Predominance embodying the characters of snigdha, murtata & gurutwa

Seat of Kapha:

o Amasaya, medas & rasadhatu – are important to be considered ,as these are

vyadhi udbhava sthana & dushya in prameha.

o Other sthanas are uras, Shiras, Griva, Parvani, Kloma, and Jihwa.

o Amasaya is the special seat for kapha(139)

o All the seven dhatus, malas except sweda are the seats of kapha(140)


37

The important function of this humor is Ambu Karma, i.e. to maintain the optimum

qualities of all the fluids a vital process to maintain life(141)

This kleda karma / oudaka karma in the body is maintained by kledaka kapha &

Avalambaka kapha.

Kledaka kapha:

o Sthana of kledaka kapha is Amasaya, which is the seat for Agni also.

o Kledaka kapha aids in sukha jarana of ahara by oudaka guna & maintains pachaka

pitta in normalcy.

o It protects the other seats of sleshma by Snehana, poshana & udaka karma.

o Its vridhi causes increased kleda of annarasa, Gouravam in kosta & vahni sadam-

whcih are primary / important factors for madhumeha samprapti.

Avalambaka kapha:

o The seat for Avalambaka kapha is uras

o Along with Annarasa (kledaka kapha), it causes Avalambana of other

kaphasthanas.

o It is stated to support the trika by its own process, the hridaya together with the

annarasa & other kapha sthanas by virtue of its Ambu karma.

Ambu Karma indicated that this kapha is a fluid & it had contact with Anna rasa, which

circulates regularly in the body on one side & the cells of the organs like Hridaya or

trika(142)

Vata:

o Vyanavata & Apana vata are stated to be vitiated in prameha(143)

o Samana vata too had it’s role in the prameha samprapti.Important functions of

vata:

o Sarva sareera dhatu vyuhakara. I.e. Synthesis of the dhatus from the nutrients

present

in the rasadhatu / Ahara rasa into definite structures according to the plan of

requirement to the body.

o Also regulates the functions of dhatus.

Vyana Vata:


38

o Located in Hridaya & traverses through out the body very swiftly(144)

o One of it’s functions is the regulation of the circulation of rasa dhatu through out

the body , through which the ambukarma is being maintained by Avalambaka &

kledaka kapha i.e. it also regulates / maintains the optimum qualities of all fluids

(ambukarma) (145)

o Effect the out flow of sweat (imp function is kleda vidruti).(146)

Apana Vata(147):

o The Vata which has a specific tendency to move downwards is called Apana vata

o Important sites of location are vasti & Antram pakwasaya(148)

o The nutrients, which are the products of digestion, are simultaneously absorbed

from the intestine by presence of Apana Vata.

Samana Vata: (149)

o Located in the neighbor hood of the seat of agni (150)

o Courses through the Amasaya & Pakwasaya and the channels carrying dosha,

sweda & Ambu & regulates them(151)

o It had an overall control on agni – doshas Ambu vaha srotases important prameha

samprapti.

Dushyas:

‘Medo, Mamsa, Sareera kleda, Sukra, Sonita, Vasa, Majja, Lasika, Rasa, Ojas.”(152)

The important quality of these dushyas is “Bahvabadham”(153) Bahutwam- is aghanatwam

& Abadham is Asamhatam (non union) i.e.; non solid immiscible forms of these dushyas

.Of these 10 dushyas, medo, mamsa are more vitiated in all pramehas & ojas is main

dushya in madhumeha.(154)

Medo dhatu:

Medo dhatu vridhi leads to mainly obesity / medoroga (155) & features related to stoulya are

visible to some or other extent.

Mamsadhatu:

Mamsa dhatu vridhi results in sareera sthulata & gouravam.(156) Obesity has often

been linked to type 2 diabetes. It is found by Dr. Das & Dr.Rao. A.U. Vizag that Genes

involved in cell adhesion, insulin signaling and immune system pathways were down

regulated in obese people (157)


39

This statement supports the statement of our acharyas that the doshas. Sleshma (function is

cell coherence), Vata (important function is gati – gandhana) & dushya Ojas (bala / vyadhi

kshamatwa sakti) are vitiated in madhumeha & kapha kara ahara viharas – a causative

factor for obesity is considered as main etiological factor in madhumeha.

Ojas:

o ‘Ojasah – madhumeha”(158)

o Apara ojas / sleshmika ojas is vitiated in madhumeha it’s quantity is ½ anjali(159)

o Ojas , the sleshmika dravya – is the essence of all dhatus(160)

o Located in Hridaya & transported thro ojavaha srotas

o The entire body is permeated with ojas, due to it’s miscibility with rasadhatu which

circulates thro’ dhamanis for tarpana kriya.(161)

Agni: - All the three Jataragni, Bhutagni & dhatwagni are affected: Primarily Bhutagni

vitiation with subsequent involvement of dhatwagni & Jataragni: Occurs in madhumeha.

Srotas:

Mutra vaha Srotas:

o Mulam is Vasti & Vankshana (162) / Medram (163)

o Sroto Vikriti is Ati pravrithi- seen in prameha.

o Ojovaha, Dhatu vaha Srotases (excluding Asti) are vitiated in madhumeha.

Sthana:

o Vasti – vyadhi adhistana sthana – refers to entire mutra samsthan – KUB.(164) The

Primary function of Kidneys is Maintenance of the normal volume & compositon

of body fluids.

o Kidneys are the only source to expel out the metabolic waste form entire body(165).

Samprapti:

Samprapti of a disease can more conveniently be explained using shat kriya kalas,

which can be framed under three phases.

1. Doshic Phase – vitiation of doshas occurs in three stages – chaya, prakopa &

prasara.

2. Phase of Dosha dushya sammurcchana


40

3. Phase of vyadhi utpathi – vyaktavasta, when untreated in this phase goes to Bheda

Vasta.

I Doshic Phase:

During this phase, the vitiation of doshas will be initiated & progressed to other stages.

In Prameha, though considered tridoshajam, the predominant dosha is sleshma / kapha.

Characters of sleshma are Sandra & guru, in prameha, the sandrata of sleshma decreases

resulting in the ‘Bahu dravta’ to sleshma, the dosha visesha in prameha. If the sleshma is

Ghana / Sandra, it will not precipitate prameha.

Formation of Bahudrava Sleshma:-

In Kosta:-

Excessive intake of kapha prakopakara ahara, Guru Snigdha Ahara results in kapha

chayam initially & then prakopa. However, when this associated with subsequent intake of

more amla & lavana rasas results in the decreased sandrata / increased dravatwa quality to

sleshma. As the amla lavana rasas are kleda karam & Katu, tikta, kashaya rasas aid in

kleda soshanam, normally, these two maintain the equilibrium & thus maintains the normal

constitution of kapha.

This bahu drava sleshma, subsequently effects the Jataragni (kostagni – resulting in vahni

sadam & on long standing produces ama.

When this sleshma (bahu drava) further increase, it comes out of its sthana (kosta)

(prasaravasta) with the aid of samana vata, enters the sweda, dosha and ambu vaha srotas.

This sleshma- along with vyana vata circulates through out the body thus increasing the

dravatwam or kledam in all the kapha sthanas & kleda sthanas (swedam, mutra, sareera

kledam).

Phase-II: Dosha dushya sammurcchana: - Includes two stages:-

(i) Vitiation of dushyas

(ii) Dosha dushya sammurcchana.

Vitiation of dushya:

The main quality of the dushyas i.e. “Bahvabadhata” is already described. The vitiation of

dushyas starts simultaneously with doshas but for better understanding described separately

here.

o Ati snigdha & guru ahara are medo vridhi karam. &


41

o Jataragni sadam too affects the medo & mamsa dhatwagni resulting in ‘Ama’ at

medo & mamsa dhatus.

o Kleda Vridhi / circulating kleda too results in the bahu / aghanatwa or liquidity to

dhatus and and abadham- immiscible nature makes them circulate in the body along

with kleda.

In this phase of dosha dushya Sammurcchana, there will be only the Purva rupas of

Prameha noted, which are mostly the Sama medo, mamsa lakshanas along with sama rasa

lakshanas.

i.e.chikkana dehe, Guru picchala gatra,

dourgandhyam & Jatilee bhava kesa etc.

Avila mutra – is also mentioned as purvarupa which indicates the presence of mala

in mutra ie; these circulating kleda with immisible dushyas – initially gets expelled out

along with urine as Excretion of kleda is the main feature of mutra.

Phase - III: Vyadhi utpathi:-

These circulating doshas & dhatus, along with sareera kleda, reach the vasti – the

only organ to expel out excess kleda thro’ mutra, & causes kaphaja, Pittaja or vataja

pramehas depending on the doshic predominance.

In madhumeha, because of ruksha guna, vata prakopa occurs, which by virtue of its

naturality increases kashaya rasa, which interferes with the madhura tatwa in ojas, brings it

to vasti & Expels out along with urine resulting in madviva mehanam / Ojo meha. As ojas

circulates all over body, thus madhura tatva too is present all over the body resulting in

madhuryaccha tanorata (madhura rasa & kashaya rasa – are pridvi bhuta predominant

dravyas madhura associated with AP & kashaya with vayu which may result in mutual

interference during bhulagni paka / dhatwagni paka)

If untreated in this stage or not managed properly, the disease progresses to bheda vasta,

which is presented with pidaka & upadravas.


42

AETIO PATHOGENESIS

Based on etiology Diabetes mellitus is classified into type-I (Insulin dependent) & type 2

(non- insulin dependent)(166)

Etiology of type-II Diabetes:

1. Genetic factors

2. Environmental factors

3. Immunological factors.

1. Genetic factors:

(1) The Presence of genes that encode the antigens present on all nucleated

surfaces (HLA-A, HLA-B,HLA-C, Class-I) or some cells only (HLA-D,HLA

DR, Class-II) on the short arm of chromosome-6 – increase the relative risk of

developing type-I diabetes (167)

(2) Over 95% Patients with IDDM express HLA DR3, HLA DR4, antigen or

both.(168)

2. Environmental Factors:

Non-HLA linked second diabetogenic gene induces primary auto immunity, where

immune response occurs against normal unaltered βCells causing initial insulitis(169)

The main factors identified as having potential for precipitating IDDM are viruses,

chemical toxins & stress.

Viruses: Coxsackie B4(170)

Chemical toxins: Alloxon, streptozotocin: Smoked meat, fish, cow’s milk protein (in

infants)(171)

(3)Immunological factors:

Auto immunity & immunopathologic mechanism clearly play a role in type-I

Diabetes by causing βcell loss.(172)


43

Postulated Mechanism in the pathogenesis of type I Diabetes Mellitus (173)

CLASS-II CLASS ID ABC

βcell damage insulitis

Altered βcell ACTIVATION OF ALTERED βcellAUTO IMMUNITY TO (Induction of class II

βcell antigen)

Immuneβcell damage

INSULIN

DIABETES MELLITUS

Aetiopathogenesis of type – II Diabetes:-

Type 2 DM is a heterogenous disorder with a more Complex Etiology. A number

of factors, excluding HLA association & autoimmune phenomena are implicated as under.

1. Genetic factors

2. Constitutional factors / Environmental

3. Insulin resistance – obesity

4. impaired insulin secretion

5. Increased hepatic glucose synthesis (174)

HLA-D LINKEDSUSCEPTIBILITY GENES

ENVIRONMENTALAGENT? VIRUS

OTHERSUSCEPTIBILITY

GENES


44

1. Genetic Factors:

The heterogeneity of Type-2 Diabetes has made it impossible to identify precisely

the genetic background to this disease.(175)

A rare single gene defect in production of glucokinase, a key enzyme in the early

stages of metabolism of glucose, accounts 15% of cases of (MODY) (176)

2. Environmental Factors:

(i) Obesity: - Strongest risk factors in the development of type-II Diabetes.(177)

o GTT deteriorates as weight increase

o In spite of higher insulin levels than lean subject as a result f insulin resistance,

there may still be insufficient insulin to restore blood glucose to normal leading

to diabetes.(178)

o Weight gain as a result of gluttony leads ultimately to exhaustion of the islets &

thereby Diabetes.(179)

(ii) Exercise:

o Exercise, or more strictly lack of exercise, has been considered as on

Environmental factor in precipitating NIDDM.

o Change in life style from traditional to more sedentary

o Disease related inactivity, can be considered here.(180)

(ii) Stress:

o Stressful events – injury or ill ness may unmask diabetes by way of catabolic

hormone response & forced immobilization(181)

o In Emergency situation like stress, extreme exercise & trauma, the nervous

system stimulates adrenal medulla to release Epinephrine which suppresses

insulin release.(182)

(iii) Early nutrition:

Early life nutrition, inutero nutritional factors that determine fetal & infant growth

influence the size & vascularity of the adult pancreas combined with later life

obesity – lead to Glucose intolerance (183)


45

Predisposing & Risk factors of Prameha(184)

Predisposing Factors:

1. Snana dweshi

2. Karma vidveshi

Risk Factors:

The personalities (prone to) madhumeha / Prameha are:

1. Atisthula

2. Mandotsahi

3. Atisnigdha

4. Mahasana

Risk Factors of Types-2 diabetes (185)

1. Obesity

2. Physical inactivity

3. Western diet

4. Urbanization

5. Family history.


46

PURVA RUPA

The prodromal symptoms of the disease, produced during the process of sthana samsraya,

are known as purva rupas. They may be analyzed under Doshaja, amaja or vyadhi nimitta

visesha purvarupas. Purva rupas of prameha incorporating the versions of various texts are

as follows: -

Charaka186

Susruta187

A.H.188M.N.

189

KAPHAJA Asyamadhuryam - + +

-Chikkana gatra(Angeshusneha) - +

Alasyam - - -- Picchala gatra - -- - Angasaidhilya -- Mutra Suklatwam - -

PITTAJAPipasa + - Trit

Panipada daha + + +Paridaha - - -

VATAJAAngasuptata - - -

AMAJA SAMAKAPHA

- Durgandha swasa - -Gurugatratwam Ghanangata

SAMARASA- Sadam - -

Sama Medo-asthi- Nakhabheda + -

- - Kesa vridhi

Sama MedaBahir maladikyam Jihwa Mala -

Talu Mala -(DantadeenamMaladyatwam)

Danta Mala - +Gala Mala - +

Talusosha - + NetramalaKanta sosha - - -Mukha sosha - Galasosha -

Hridayanetra


47

Charaka186

Susruta187

A.H.188M.N.

189

JihwaSravanopadeham

Sareera VisragandhaMutra visragandha - - -

Kapha+Sama medoNidra -

Tandra +Jatilakesa +

Vyadhi NimittajaVisesha P.R

Mutra pipeelika - + -sareera pipeelika - + -

Avila mutrata - + -- Madhura Mutrata Sayyasana swapna- sukhabhishangi -

Seeta Prasaktam / Priyatwam were specially mentioned by vagbhata & Basavaraj(190)

Mutra sangham was mentioned as purvarupa in Gadanigraha

Bhava prakasa (191), Yogaratnakara (192), Vangasena(193) & Gadanigraha(194) mentioned

same as madhavakara.

o Asya Madhuryam & Lavanasyata are due to kapha vridhi

o Angeshu sneha: Is because of increased snigdhata & dravata due to pitta vridhi.

o Dehe chikkanata: i.e. Excessive oiliness is due to kapha vridhi.

o Picchala gatra:- Increased viscosity / stickiness is due to kapha prakapam

o Alasyam: Lethargy is due to kapha vridhi.

o Anga saidhilya: - / Sandhi sladhana – looseness of body / Joints occurs due to kapha

prakopa & vitiated ojas.

o Pipasa: Excessive thirst

o Panipada daha: / Pani pada tala daha – Burning sensation of plams & soles

o Paridaha: Generalized all over burning are due to pitta vridhi at kosta. Extremities

sarvangaja.

o Anga suptata & Kara pada suptata: Anaesthesia / Parasthesia is due to increased

vata dosha

o Guru gatram: Increased weight


48

oro Ghanangata:- Solidification are because of kapha vridhi & also sama rasa

o Durgandha swasa:- Because of sama kapha

o Sadam: - Inertia – Anga sadam (debility) is due to pravridha vata & Gatra sadam is

ojo vikriti janyam.

o Kesa Nakhati vridhi & Nakha bheda: Occurs as sama rasa enters medo & asthi

dathu / asthi dhatwagni is affected.

o Danatadeenam Maladyatwam: (Jihwa, talu, Danta, Gala Netra mala) &

o Bahirmaladhikyata is mainly due to the primary dushya medo dhatu, where sama

medodhatu resulted from dhatwagnimadhya.

Also causes Talu, mukha, Gala, Kanta sosha.

o Sareera & Mutra Visragandha: - is due to sama medodhatu & increased kleda /

fluidity in the body.

o Tandra / Nidra : are due to kapha vridhi & samamedo dhatu which are the primary

o Jatileebhava kesa: Dosha & dushya in prameha (Vyadhi, visesha niyatamena)

Mutra Pipeelika

Sareera Pipeelika

Madhura mutrata is due to increased madhurata of mutra & entire body

Avila Murtata


49

RUPA

The knowledge of Rupa- clinical manifestation of the disease aids in accurate diagnosis of

the disease & plan the treatment.

Rupas can be discussed under following headings:

1. Prameha rupas

2. madhumeha rupas

I Prameha rupas:

The pratyatma niyata lakshana / cardinal symptom of prameha are:

1. Prabhoota mutrata

2. Avila mutrata (195) (196)

1. Prabhoota Mutra: Bahudrava sleshma affecting the dushyas (medo mamsa etc)

results in kleda vridhi (increased fluidity). This Excess kleda being excreted

through mutra (kleda vahanan) results in probhoota mutrata.

2. Avila Mutrata: - Avilam is sa-malam(197) is because of the presence of various

dushyas in the mutra.

Samanya lakshanas(198)

1. Sosha

2. Karsya

3. Tapam

4. Bahu Mutrata

5. Aswasthyam Sarvagatreshu

6. Trishna(199)

Gamanath Sthanam

Sthanath Asanam

Asanath Sayanam

Sayanath Swapnamichati(200)

indicates the grades of malaise.


50

Lakshanas of Sahaja & Apathya nimittaja prameha :(201)

1. Sahaja:

Krusa

Ruksha

Alpasi

Pipasa

Brisam parisarana seela.

2. Apathya nimittaja :

Stula

Bahvasi

Snigdha

Sayyasana swapna seela

Madhumeha Rupa:

Madhumeha, ojomeha 202, kshoudra meha (203) though considered synonymous, their rupas

were discussed separately in various classics.

Kshoudra meha:

1. Kashaya madhura mutram 204

2. Ruksham – is because of vata prakopam.

3. Kshoudra rasa varna mutram (205)

4. Pandu varna mutram(206)

Ojomeha:

1. Ojasanvitam – Contains ojas (207)

Madhumeha:

The cardinal symptoms of madhumeha are:

1. Madhura / madviva mehanam – sweetness of urine madhu samam mehanam

2. Madhuryaaccha tanoratah - Excessive sweetness of entire body.

may correspond with Glycosuria & Hyper glycaemia


51

Clinical features of diabetes:

A careful clinical history of the severity of symptoms is the best guide for assessing

appropriate treatment .Thirst ,polyuria, weight loss, fatigue, pruritis vulvae are the most

frequently reported symptoms(208).

1. Thirst: It is the most prominent symptom of diabetes, which may reasonably be

attributed to loss of water from osmotic diuresis (209)

2. Polyuria: Especially nocturia is a major symptom(210). The ability of the renal, tubules

to reabsorb glucose is exceeded when the blood glucose rises and the glucose, of necessity,

takes rises and the glucose, of necessity, takes with it an excess of water in the urine(211)

3. Weight loss: Loss of weight in the diabetic may be attributed to the mobilization of fat

stores & break down of protein.

Wasting seems to be more common than weight loss(212)

4. Fatigue & tiredness: Fatigue & tiredness are common symptoms of untreated

diabetes.(213) Insufficient utilization of glucose or electrolyte losses explain the muscular

weakness, which is the basis of fatigue.(214)

5. Cramps in the legs are also common(215)

6. Pruritis vulvae – It is a presenting symptom in diabetic woman & balanitis in man. It is

a result of presence of glycosuria (216)

7. Skin may loose elasticity & become dry with a yellowish tint on hands & face (rarely

seen) (217)

Other Symptoms:

o Abnormalities of taste: A sweet taste in the mouth is an uncommon symptom of

untreated diabetes, more often a sensation of stickiness with no precise taste is

described.

o Impotence , Amenorrhea, infections of skin / wounds may be the first indication

of the presence of diabetes.(218)

The symptoms of diabetes are so well known that it is surprising that the diagnosis is so

often overlooked.


52

CLASSIFICATION OF DISEASE

Prameha, a tridoshaja vikara, is of innumerable types which are caused by one or

two doshas. Tridoshaja pramehas are twenty. Described under three groups :(219)

1. Vataja prameha – 4

2. Pittaja prameha - 6

3. Kaphaja prameha- 10

Madhumeha is one of the four Vataja pramehas(220).

Classification of madhumeha – prameha:

I According to etiology: (221)

(i) Sahajam

(ii) Apathya nimithaja

II According to Clinical presentation (222)

(i) Sthula pramehi

(ii) Krisa Pramehi

III According to predominance of dosha (223) (224)

(i) Kaphaja madhumeha / Santarpanaja

(ii) Vataja Madhumeha / Dhatukshayaja or Apatarpanaja

IV According to pathogenesis – madhumeha is again of two types (225)

(i) Dhatu Kshayajam

(ii) Margavarodhajam

V According to prognosis:

Vataja pramehas are Asadhya. this may be

(i) Yapya

(ii) Pratyakheya.


53

CLASSIFICATION OF D.M.:

Two main methods of classification of diabetes mellitus have appeared in the past few

years.

The first refers to type-I & type-II diabetes, with a debatable sub categorization of type-I

into Type Ia & Ib.

The second refers to IDDM (Insulin dependent) & NIDDM (Non- Insulin dependent) &

others (226) (227)

(1) Type I diabetes (IDDM) / Juvenile onset diabetes.

(i) Types I a

(ii) Type I b.

(2) Type II diabetes (NIDDM)

(i) Non- obese Type II diabetes

(ii) Obese type-II Diabetes

Also know as MODY – Maturity onset diabetes of the young.

(3) Types III diabetes: - Malnutrition related diabetes & tropical diabetes are

included.

J type (Jamaica), K type (Kerala), Z type (Zudema) are included in tropical

diabetes.

(4) Other types:

(i) Secondary diabetes:

(a) Pancreatic diseases - Chronic Pancreatitis / Pancreatic classification

(b) Hormonal - Acromegaly

- Corticosteroid excess (exolendogenous)

- Thyrotoxicosis

- Glucagonomas.

(c) Drug induced - Diuretics

- Catecholaminergic agents (Ex: salbutemol)


54

(d) Insulin receptor abnormalities

(e) Genetic Syndromes

(f) IGT (impaired Glucose tolerance)

(g) Gestational diabetes

(f) Pre diabetes / Potential abnormality of glucose tolerance (Pot.AGT)


55

VYAVACCHEDIKA NIDANA

- Prameha is characterized by bahumutrata probhoota mutrata & avila mutrata.(227)

- Madhumeha is specifically a prameha with madhviva mehana & Madhuryaccha

tanoratah (228) i.e. presence of Madhuratwa in urine & entire body.

- Atyardha madhura & seta – urine, is found in Ikshumeha & Seeta meha (229) – a

variety of Kaphaja prameha. Here specific features of madhumeha / Ojo meha

described above are absent.


56

Differential diagnosis of Type –I & Type-II diabetes(231)(232)

Type – I Type- II

Clinical - Onset - < 20 yrs Onset >30 yrsWeight - Normal Weight - ObeseDecreased blood – Insulin Normal/ Increased blood InsulinIslet Cell antibodies (+) No Islet Cell antibodiesKetoacidosis Common Ketoacidosis - Rare

Genetics: 50% concordance in twins 90 – 100% Concordance in twinsHLA –D linked No HLA – D Association

Pathogenesis: Autoimmunity Insulin ResistanceImmunopathologic mechanismsServe insulin deficiency Relative insulin deficiency

Islet Cells: Insulinitis + earlier No InsulinitisMarked atrophy & fibrosis focal atrophy & amyloidβCells depletion seen only mild βcell depletion


57

SADHYA SADHYATA

- Madhumeha, being a vataja prameha, is considered yapya / asadhya.(233)

- Madhumeha is considered Yapya: (234)

- When Vata is associated with other doshas (in madhumeha)

- Apathya nimittaja madhumeha.

- Asadhya Madhumeha:

- Beeja doshaja Madhumeha (235)

- Upadrava yukta, Atiprasruta pidaka peeditam (236)

- Prameha, - being one of the maha gadas., is considered asadhya when associated

with following symptomatology.(237)

Atisara

Murcha

Hikka

Swasa

Prana, mamsa kshaya

Sosha

Trishna

Chardi &

Jwara


58

UPADRAVAS

Upadravas are produced after the manifestation of pradhana vyadhi & it is

dependent of on it. It is dependent on it madhumeha on longstanding with out proper

treatment results in upadravas, which further makes the management difficult.

I Prameha upadravas: (238) Are commonly seen in all the 20 pramehas.

(1-10)

1. Trishna

2. Atisara

3. Jwara

4. Daha

5. Dourbalya

6. Arochaka

7. Avipaka

8. Putimamsapidaka

9. Alaji

10. Vidradhi

(11-16)(239)

11. Angamarda

12. Kasa

13. Brama

14. Tama

15. Sula

16. Kandu

II Vataja Prameha Upadravas: (240-247) commonly seen in all four vataja pramehas and

madhumeha.

1. Hridgraha

2. Kampa

3. Sula

4. Sosha


59

5. Kasa

6. Swasa

7. Udavarta

8. Lolata

9. Munnidrata

10. Kantagraha

11. Aloulyam

12. Stamba

13. Badhapureeshatwam

Pramehapidakas are also considered as upadravas of prameha 7 (248) 10 (249) types of

Pidakas are explained.

(1-7)

1. Saravika

2. Kacchapika

3. jalini

4. Sarshapika

5. Alaji

6. Vinata

7. Vidradhi

(8-10)

8. Putrini

9. Masurika

10. Vidarika


60

COMPLICATIONS

Control of hyperglycemic is the best approach to prevent chronic tissue damage. Along

term tissue damage results from the metabolic disturbances and uncontrolled diabetes (250),

the extent of tissue damage depends upon the interaction of the hyper glycemia with other

factors (both environmental & Inherited)

Diabetic complications can be categorized according to reason as (251)

(1) Micro Angiopathic lesions

(a) Retinopathy

(b) Nephropathy

(c) Neuropathy

(2) Macro Angiopathic lesions

(a) Atherosclerosis

I Micro Angiopathy/Micro Vascular

(a) Retinopathy:

o Micro aneurysms, which appear around macula as one or two single dots close to

main vein is the characteristic and early diagnostic manifestation of diabetes (252)

o Micro aneurysms, hemorrhages along with hard exudates around macula is termed

as maculopathy(253)

Other disorders of eye are. (254)

1. Transitory changes in refraction

2. Weak ness of accommodation

3. Diabetic cataract, glaucoma

4. IRIS depigmentation


61

(b) Nephropathy: (255)

o Generalized renal hypertrophy is noted in IDDM

o Micro albuminuria occurs at on early stage of diabetes followed by

protenuria the first clinical manifestation of nephropathy.

o HTN, oedema, raised serum creatinine & Urinary proteins are seen as

Nephropathy progresses to Renal failure; seen mainly in elderly with poor

glycaemic control

Other renal disorders:

1. Pyelonephritis

2. Pneumaturia (due to chronic UTI)

(c) Neuropathy:

o Peripheral nerves are more prone to damage in diabetes. Diffuses sensory &

Autonomic poly neuropathy occurs, probably of metabolic & ischemic in origin (256)

o Diffuse sensory lesions:- Paresthesiae, Numbness sensation of coldness, painful

syndromes are symmetrically distributed in OM.(257)

o Autonomic neuropathy- includes Gustatory sweating erectile dysfunction,

Neurogenic bladder, postural hypotension, watery diarrhoea with fatal incontinence(258)

II Macro vascular complications:

o Atherosclerotic lesions of large & medium sized arteries, characterized by focal

thickening of intima in Diabetes.

o Diabetes, hyperlipidaemia, obesity are the risk factors for atherosclerosis.

Clinical manifestation are mainly seen in

1. Coronary arteries (259) resulting in increased risk of myocardial infarction &

coronary thrombosis.

2. Neck & cerebral vessels (260) results in cerebro vascular accidents.


62

(2) Diabetic foot (261): Different types of diabetic tissue damage interact & summate in the

fact resulting in simple painless traumatic abrasions to more serious dry or wet gangrene.

Other special problems associated with D.M (262)

1. UTI in females

2. Tuberculosis

3. Cholecystitis

4. Influenza

5. Furunculous

6. Mucocutaneous candidiasis.


63

ARISTA LAKSHANAS

Arista is sign indicating certain death these arista lakshanas of disease are bad

prognostic science and are considered fatal to the patient. Some of the arista lakshanas of

prameha rogi are

1. Aristas related to purvarupa stage(263)

If flies swarm round the body, even though has taken bath; the patient dies though he is in

purvarupa stage of disease.

2. Trit, daha, pidaka, mamsa kodha & atisara, if present in case of prameha the patient

shows bad prognosis / dies(264)

3. Arista Swapnas of prameha rogi:

(a) When drinks various snehas (Unctuous) dravyas in the company of

chandala. (265)

(b) When just drinks various sneha dravyas in swapna(266)

(c) If the pramehi & atisari drinks water in his dreams, it heralds death. (267)

4. In prameha rogi, if bala mamsa Kshayam is observed he should be left out / discarded

by the doctor. (268)


64

CHIKITSA

Treatment of a disease in Ayurveda starts with nidana parivarjana(269). This has to be

initiated first before administering any medicine or adopting any line of treatment.

The chikitsa karma / line of treatment varies with etiology

- Jata pramehi chikitsa

- Apathya nimithaja pramehi Chikitsa

And

- Santarpana Janya pramehi Chikitsa

- Apatarpana Janya pramehi Chikitsa

And rogi bala

Stula - Balwan

Krisa - Durbala

(1) Jata Prameha Chikitsa:(270)

- Yavannam / Prameha hara kashaya sidha yavagu,

- Madweekam

- Angara sulyavadamsa mamsa

- Chitraka mula kashyam with honey

(2) Apathya nimithaja prameha Chikitsa: (271)

- Vyayama was given rare importance in this rogi

- Vyayama and yudha kreeda with Radha, Gaja, Turaga, Padhati

Sevana.

- Follow the life style of ‘munis’, walk for sata yojana daily along with

strict dietary restrictions.


65

(3) Santarpana Janya pramehas(272)

- Yava, Sulyani mamsa are adviced along with Aristas, Kashayas &

lehas.

- Virukshana Chikitsa should be adopted here (273)

- Pragaada Vyayama, udvartana, Jalavasekam & Snana are indicated.(274)

- Sugandha lepas are advised.

(4) Apatarpana Janya prameha (275)

- Triphala kashaya nisi sthita yava with madhu

- Saktu & apoopas, which are bhavita with pramehahara kashayas, are to

be taken with guda …. for santarpanam.

(5) Stula - Krusa:

- Brimhanam (276) is indicated for krusa – durbala patient along with

Samsamana kriya and Sodhana is advised in dosha baladhikya

condition.

- Sodhana: Snigdha Sodhana dravyas are used.

- Apakarshana & Langhana are indicated in sthula prameha rogi.

Line of treatment according to doshic predominance.

- Kapha Pramehi(277)

- Samsodhana

- Ullekhana / Vamana

- Langhana


66

- Pitta Pramehi:

- Virechana (Teekshana)

- Santarpana

- Samsamana

- Vata Pramehi(278)

- Kashaya sidha snehas (taila – VK, Grita- VP are indicated.

In asadhya pramehas Kashayas are indicated for yapyam.(279)

Rasayana: .(280)

Shilajit rasayana and makshika sevana are indicated in Asadhya prameha.

Treatment for prameha pidakas :(281)

- Apakwa pidakas - Sopha Chikitsa is adopted

- Pakwa Pidakas - Vrana Chikitsa, Vrana ropana tailas are used.

PATHYAPATHYA


67

Patya

Sl.No.Puraana

Bh.P(282) Chakradatta(283) Gadanigraha(284) Yogaratnakaram(285) Suchi (286)

1 Syamaka + + + +

2 Kodrava + + + + +

3 Udhalaka + + + + +

4 Godhuma + + + + +

5 Chanaka + + + + +

6 Adyaki + + + + +

7 Kulutha + + + + +

8 Tikta Saka + + + + +

9 Jangala Mamsa + + + + +

10 Harini + + +

11 Andaja + +

12 Mudga + + + +

13 Sali + + + +

14 Sastika + + + +

15 Yavannam + + +

16 Srama +

17 Madhu +

18 Patola +

19 Saindhava +

20 Maricham +

21 Kashaya rasa +

22 Oil Ingudi +

Sarshapa +

Atasi +

Apatya


68

Sl.No. Bh.Prakasa(287)

Chakradatta(

288)Gadanigrah

a(289)

Yogaratnakaram

(290)

Su chi(291)

1 Souveeraka + + + + +

2 Sura + + + + +

3 Takram +

4 Tailam + + + + +

5 Ksheeram + + + + +

6 Gritam + + + + +

7 Gudam + + + + +

8 Amla + + + + +

9 Ikshurasa + + + + +

10 Pistanna + + + + +

11 Anupamamsa + + + + +

12 Suktam + + + + +

13 Sadasanam +

14 Diva nidra +

15 Navannam +

16 Dadhi + +

17 Dhumapanam +

18 Swedam +

19 Sonitamokshana +

TREATMENT


69

The management of diabetes does not revolve around glycaemic control alone. In addition,

various aspects like BMI / obesity. HTN, cholesterol, triglycerides etc should be checked

either by diet modifications, Exercise or drugs.(292)

I. DIET:

o Active dietary management is required through out the disease as it plays

important role reducing Insulin resistance (293)

o Important aspects of dietary advice: (294)

o Correct calorie intake: to support necessary activates and & normal growth

& bring patient weight to correct valve.

o Content of meal: Ideal diet comprises of 60% calories by carbohydrates

30% from fats with daily intake of 50-60 gm protein / day.

o Timing of meal: Slowly taken, frequent small means are more

advantageous in avoiding sudden peaks of glucose.

II Exercise:

o The role of exercise in the treatment of diabetes is uncertain, but, is the major factor

influencing the diabetic control.(295)

o Any particular activity has very different energy demands in different people, & so

each diabetic must work out the right balance between extra food intake & extra

energy output (296)

o Insulin sensitivity increases by regular physical training through “up regulation” of

insulin receptors. This can obviously benefit glucose tolerance substantially even

with out any weight loss, but training must be sustained.(297)

III Education: (298)

It is self evident that diabetics who know little or nothing about their disease are unlikely to

maintain good day today control.

o A good knowledge of dietary needs & good compositions with respect to calories &

Carbohydrates, proteins & fat content is important for all diabetics.

o Other general principles include the knowledge of the effect of exercise, alcohol &

of the need of self-monitoring glucose levels.


70

IV Drug (299)

When diet & exercise fail to achieve glycaemic control, medication is needed.

1. Oral hypo glycaemic agents

2. Insulin

I Oral hypo glycaemic agents: are categorized as

(1) Insulin sensitizers

Ex: Biguinides- metformin, pioglitazone

(2) Insulin Secretagogues- Stimulates cells of pancreas

Ex: Sulphonyl ureas- Glibenclamide, chlorpropamide,

Tolbutamide

(3) Retartants of glucose absorption from the gastro intestinal

lumen.

Ex: Guar gum

Alpha glucosidase inhibitors

However, all the above require residual insulin Secretary Capacity in patients to be

effective.

II. Insulin: When oral drugs fail to achieve normoglycaemic levels, then insulin is

suggested. Depending on duration of action, Insulin is categorized:

1. Short acting

2. Long Acting

3. Intermediate

Are selected accordingly.

All the above treatments help achieve glycaemic control in type-II diabetes but insulin is

the only source for type-I diabetes.


71

DRUG REVIEW

CRETERIA FOR SELECTION OF DRUG

Madhumeha is a gambhira vyadhi involving the deep-seated dhatus – mamsa, medo, majja,

all drava dhatus & ojas. Though the clinical manifestation of disease includes - madhviva

mehana & madhuryaccha tonoratah the pathogenesis, when evaluated shows the deep-

rooted nature of the disease. Madhumeha is a vatakapha disorder, with depleted dhatus &

ojas.

The main aim of the treatment is samprapti vighatana and, nourishes the dhatus &

ojas as the disease is yapyam, to maintain positive health of the individual.

So, in selecting the treatment modality for madhumeha, a combination of a drug –

umasambhuras & yapana vasti are considered.

Uma Sambhu ras:

The drug ‘uma sambhu ras’ selected for the present study is a herbomineral

preparation in tablet form. The drug has its reference in Rasa ratna samucchaya, prameha

chikitsa.

The drug mentioned, had a Sarva prameha hara property along with sosha hara

effect, when taken for a short period of 3 -7 days. Thus, reference of vast therapeutic

effects in short duration of medication shows the fast acting nature of the drug. In view of

the following points, the drug was considered for the present study:

When the drug, its ingredients & their actions are observed, they clearly support the

fast acting & prameha hara nature of the drug.

The key ingredients, Rasa sindooram, Abhraka bhasma, Tutha bhasma- are prameha

hara & Rasayana, thus.

In addition, Rasa sindooram is a potent therapeutic agent having wide range of

therapeutic efficacy. The vegetable drug combined with it decides its target point of action.

Abhraka bhasma – is a proven drug helps in monitoring blood glucose homeostasis.

Further, the 7 Putas of these ingredients with subsequent bhavana with Jambeera ras

and 27 bhavanas with 13 bhavana dravyas having Rasayana, Deepana, Prameha hara

qualities the quick & fast acting nature of the drug & it’s selection in present clinical study.


72

MADHU GHRITADI YAPANA VASTI

The vasti formulation ‘madhu ghritadi yapana vasti’ selected for the present study is

a type of yapana vasti mentioned in charaka sidhi sthana 12th chapter

The vasti combination mentioned, had prameha hara property & it is balyam,

rasayanam, & nirupadravam, an ideal requirement for consideration.

Since Vasti is best, in treating Vata, madhumeha being a vata predominant

prameha, it is selected along with drug, aiming to have a synergic effect & thus help in

gaining quick control over the disease.

Vasti stimulate the ANS, and as the islets are inervated by in myelenated fibers

from both parasympathetic (Vagal) and Sympathetic nerves whose endings are in close

contact with αand βcells & it can readily influence their secretary activities.


73

Ingredients

Rasa sindooram Abhraka bhasma

Tutha bhasma Uma shambu ras tablets

Uma shambu ras(during process) Varitaratwa of Tutha bhasma


74

Uma Sambhu ras :(300)

The main ingredients of the drug are

1. Rasa Sindooram – 1 part2. Abhraka bhasma – 1 part3. Tutha bhasma –1 part

Bhavana dravyas:

1. Jambeera - 7 bhavanas2. Beejahwa - 1 bhavana3. Aksha - 1 bhavana4. Yuga - 1 bhavana5. Kakubha - 2 bhavanas6. Yastimadhu - 3 bhavanas7. Sita / Durva - 3 bhavanas8. Ketaka - 3 bhavanas9. Jeera - 3 bhavanas10. Rambha - 3 bhavanas11. Kharjurika - 3 bhavanas12. Jatidala - 3 bhavanas13. Mushkaka. (NA) - 3 bhavana

Dose: 1 Valla (375 mg)Anupana: Vasa swarasam.

Method of Preparation:-

The three ingredients were taken, and bhavana with Jambeera ras was done for

3days & then was subjected to puta; again the process was continued for 7 times.

The resultant fine bhasma was subjected to bhavana with the drugs mentioned in the

list in sequence for mentioned number of times & made into 125 mg tablets.

In view of the practical difficulty in taking Vasa swarasa as anupana, the same was

used for bhavana, in order, not to miss its therapeutic effect, before making into a pill.

RASA SINDOORAM :(301)

Pharmaco therapeutic properties:

Rasa - Madhura, tikta


75

Guna - Guru, Snigdha

Veerya - Seeta

Vipaka - Madhura

Karma - Rasayana

Doshaprabhava - Tridosha Samakam

Vyadhi Prabhava - Prameha, pandu, puranajwara, apasmara haram.

Abhraka Bhasma:302


Rasa - Kashaya, Madhura

Guna - Snigdha

Veerya - Seeta

Vipaka - Madhura

Karma - Rasayana, Deepana, pachana, Balyam, Brimhanam,

Yogavahi

Doshaprabhava - Tridosha haram

Vyadhi Prabhava - Prameha haram, Jeernajwara Grahani

Tutha bhasma:303


Rasa - Katu, Kashaya, Madhura

Guna - Laghu, Ushna

Veerya - Ushna

Vipaka - Katu

Karma - Rasayanam, balyam, lekhana, bhedana

chakshushyam

Doshaprabhava - Kapha pittaharam, Tridosha Samakam

Vyadhi Prabhava - Prameha, medo haram (param) Kandu,

Twakvikara


76

Bhavana dravyas

Arjuna yastimadhu sita

Ketaka jeeraka kadali

Kharjurika jati vasa

jambeera vibhitaka Rudraksha

A Study on the effect of Uma sambhu ras with Madhu ghritaadi yapana vasti in the management of prameha w.s.r.to Madhumeha

77

304,305

Sl.No

Dravya nama &Latin name & F

Rasa Guna Veerya VipakaDoshagnaProperty

Karma

1 Jambeera Citrus medicavar.acida Rutaceae Amla Katu Laghu

Teekshna Ushna Amla Vata kapha haram deepana,Pachana, Chakshushyam

2 Beejahwa Citrus medicaLinn Rutaceae

AmlaMadhura

LaghuSnigdha Ushna Amla Vata Sleshmahara Hridya, Deepana, Grahi

3Aksha (Vibhitaka)Terminalia belliricacombretaceae

Kashaya RukshaLaghu Ushna Madhura Kapha pittaharam

Bhedana, Chakshushyam, Kesya,Madakari. Rasa, rakta, mamsa medodhatugata dosha haram.

4 Yuga

5 Kakubha Terminaliaarjuna combreteceae Kashaya Ruksha

LaghuSita

Ushna(R.N) Katu Kapha pittaharam Hridya,Udardhaprasamana,Vranasodhana rasayanam

6 Yasti Glycyrrhiza glabraFabaceae Madhura Guru Snigdha Sita Madhura Tridosha hara

Varnya,kantyajeevaneeya,medhya,Rasayana,Vrishya,chakshushya

7 Sita Cynodon dactylonPoaceae

KashayaMadhura Laghu Sita Madhura kapha pittaharam

Samakam Varnya, prajasthapana

8

KETAKA Pandanustectorius solona Ex.Parkinson,Pandonaceae.

Tikta MadhuraKatu

LaghuSnigdha Ushna Katu Pitta Kapha haram Chakshushyam, Varnyam, Balyam,

Rasayanam

9 Jeera, Cuminumcyminum Apiaceae Katu Laghu

Ruksha Ushna Katu Kapha VataSamakam

Deepana, Pachana, Grahi, balyam,chakshushyam, Garbhasayasudhikara, visha hara, vrishya

10RambhaMusaparadisicamusaceae

Madhura Guru Snigdha Sita Madhura Pitta VataSamakam Vrishyam, Brimhanam

11 Kharjurika Phoenixsylvestris Arecaceae Madhura Snigdha Guru Sita Madhura Vata Pitta Samana Hridaya,Balyam,Brimhanam,Vrishyam

12Jatidala Jasminiumgrandifolium Linn.Oleaceae

MadhuraLaghu

Snigdhamrudu

Ushna Katu Tridosha hara Vrana Sodhana, ropona

13Vasa Adhatoda VasicaJusticia adhatodaAcanthaceae

Tikta Kashaya Laghu ruksha Sita Katu Kapha pittaharam Swaryam, Hridyam

A Study on the effect of Uma sambhu ras with Madhu ghritaadi yapana vasti in the management of prameha w.s.r.to Madhumeha

78

S.NO Name/Botanical name Part used Chemical constituents Action Indications

1 Jambeera citrus medicavar.acida Phalam Phosphoric & malic acid citrates

of potassium, mucilage & ashesRefrigerant, antiscobuticantiseptic

Dyspepsia, bilious fevers inflammatoryaffections

2 Beejahwa citrus medica linn Phalam Phosphoric & malic acid citratesof potassium, mucilage & ashes

Expellent of poisons,Aromatic, stomachic,antiscorbutic, refrigerantastringent, digestive

Scorbutic affections, internal hemorrhagesrheumatic, dyspeptic diabetic complaints

3 Aksha Terminalia bellerica Phalam Gallotonic acid, resins Astringent, tonic,expectorant, laxative

Cough, dyspepsia, dyspnoea,rheumatism, 01.thalmia

4 Yuga Phalam - - -

5 Kakubha Terminalia arjuna Twak

Glucotonic acid, Glucosidalbody, ash contain sodium, pureCa Co3 ,traces of alkalinechlorides

Astringent, cardiacstimulant, tonic, Lithotriptic

Harmorrhages,diarihoea, dysentery Heartdiseases, Spermatorrhoea fracturescontusions

6 Yasti Glycyrrhiza glabra Mulam

Glycyrrhizin, aspergin,starch,acid resin, gum, mucilage,phosphoric, sulphuric, & malicacids, Ca mg salts

Tonic, demulcent,diuretic, gentle laxativeexpectorant, emenagogue

Sore throat, cold, catarrhs, cough, biliousfevers, influenza, leucorrhoea & otheruterine complaints.

7 Sita (Cynodon, dactylon) Panchangam -Demulcent, astringent,diuretic, haemostaticlaxative

Urinary irritation dropsy, internalhemorrhages, vescical calculi, catarrh

8 Ketaka, Pandanusodaratissimus Pushpa, mula Essentials oils Bitter Purgative, aromatic,

stimulant, antispasmodicSterility, threatened abortion, Headache,rheumatism, epilepsy

9 Jeera cuminum cyminum BeejaFatty oil, resin ,mucilage ,gum,protein compounds, malates, anessential oil (thymene)

Carminative, aromaticstomachic, stimulantAstringent.

Chr.diarrhoea, dyspepsia Urinarycomplaints, hiccough

10 Rumbha musa paradisicaM.sapientum kutze

Kandam,Pushpam,Phalam - -

Sprue, diarrhoea, dysentery, dropsy,scanty micturition, gastritis, flatulence,Ext. hemorrhages, eye diseases.

11 Kharjurika phoenixsylvestris Phalam, patram Valuable salts, Iron, tannin,

extractive matter, mucilage, lime

Expectorant, tonic,demulcent, laxative,diuretic

gen.debility, bronchial & Genito urinaryinfection opthalmia, corneal opacity

12 Jati dala Jasminiumgrandifolium

Patram, Mulam,pushpam

Resin, salicylic acid, alkaloidJasminine

Astringent Insanity, hysteria, amenorrhea, bronchial,Obstruction, eye complaints,

13 VASA Adhatoda vasica Patram,Pushpam,Mula

Essential oil, fat resin, bitter non-volatile alkaloid- Vasicine,Organic acid, sugar gum

Expectorent,diuretic, antispasmodic

Cough, Asthma, bronchitis, pertussis, TBof lung.

14 Mushkaka Not Available Not Available Not Available Not Available


79

Madhu Ghritadi Yapana vasti :(306)

Ingredients:

Madhu - 1 Prasruta (80ml)

Gritha - 1 Prasruta (80ml)

Ushnodaka - 2 Prasruta (160ml)

Satapushpa - ½ Pala (20gm)

Saindhavalavana - ½ Karsha (5gm)

Karma: Deepana, Rasayanam, Brimhanam, Bala varnakara, Nirupadravam,

Vrushyatamao

Vyadhi Prabhava: Krimi, Kusta, Udara, Gulma, Arsas, Bradna, Pleeha disorders,

Prameha.

Pharmaco therapeutic properties: (of Ingredients)

Madhu:

Rasa - Madhura, Kashaya

Guna - Ruksha, Sita, Laghu, Sukshma

Virya - Sita

Karma - Deepana, Lekhana, Srotosodhana, Yogavahi, Hridya.

Dosha Prabhava - Tridoshagnam, Vata pitta haram.

Vyadhi Prabhava - Kusta, Kasa, prameha, Klama.

Ghrita:

Rasa - Madhura

Guna - Snigdha, guru, Yogavahi

Veerya - Sita

Vipaka - Madhura

Karma:

Medhya, Ojo vardhaka, vayasthapana, Rasayana, Deepana, Chakshushyam.


80

Yapana vasti

Apparatus for Vasti Ingredients

Apparatus and Ingredients Step 1

Step 2 Step 3


81

Yapana vasti

Step 4 Step 5

Step 6 Step 7

Step 8 Residual amount


82

Dosha Prabhava: Vata, pitta, Kapha haram.

Ushnodakam: (307)

Karma - Deepana

Dosha prabhava - Kapha vata haram

Vyadhi prabhava - Swasa, Kasa, Jwara.

Sata pushpa:

Rasa - Katu tikta

Guna - Laghu, Teekshna

Veerya - Ushna

Vipaka - Katu

Karma - Agni deepana

Dosha prabhava - Vata kapha haram

Saindhava lavanam:

Rasa - Lavana, Madhura

Guna - Laghu, Snigdha, Sita, Sukshma

Veerya - Anushna, Sita

Vipaka - Madhura

Karma - Deepana pachana, Vrushyam, Netryam

Dosha prabhava - Tridosha haram.

Chemical Composition:

Sodium Chloride - 65 – 85 %

Calcium Sulphate - 0.55%

Calcium Chloride - 0.53%

Magnesium Chloride - 0.43%

Sodium bicarbonate - 0.74%

Insoluble Matter - 30 - 34%


83

Method of administration of Vasti:

The administration of Vasti is divided into three phases.

1. Purvakarma

2. Pradhana karma

3. Paschat karma

I. Purvakarma:- ( Pre operative procedures)

1. Examination of the patient.

2. Preparation of Vasti dravya

3. Preparation of the patient

1. Examination of the Patient:

Though, Yapana Vasti is indicated for all the persons, it is important to note

that the Patient is having deeptagni, Snigdha Sareera & Mrudu Kosta.

On the days of yapana vasti, the patient was instructed to take

normal diet (laghu ahara). So that he is neither too hungry nor too full. No Other

Purvakarmas ( Snehana / Swedana) are required for Yapanavasti.

2.Preparation of Vasti Dravyas:-

The Preparation of Vasti dravya was done by adding, chronologically

Saindhava Lavanam (1/2 Karsha (5 gm), madhu (1 Prasruta – 80ml),

Goghrita(1Prasruta – 80ml) Sata Pushpa (1/2 Pala - 20 gm), Ushnodakam (2

Prasruta 160ml). Initially Saindhava lavan was taken in a clean khalwa yantra & to

it, madhu is added & triturated properly until the crackling sound disappears & to it,

Gogrita is added slowly while continuing the trituration until a homogenous

mixture is formed. To it Satapushpa is added & finally ushnodaka is added &

triturated properly. Then it is filtered & filled in vasti yantra & used for

administration.

Precaution:

Ushnodaka taken should be luke warm. To have homogenous mixture,

if too hot water is added to Vasti dravyas, the ghee gets separated from mixture &

Settles at periphery / rim of kalva.


84

Pradhana Karma:

The patient was asked to lie down on the Vasti table in the left lateral

position with it leg flexed at knee & hip joints & left leg straight left arm, flexed &

used as pillow below his head. After anointing the Vasti netra, air was removed

from the vasti yantra & the netra was slowly but steadily introduced into the anus of

the patient along the direction of the vertebral column. The patient was advised to

take deep breath while the procedure is being continued.

Paschat Karma:

The patient was asked to lie in supine position, & allowed to take rest Vasti

pratyagamana & pranidana kala were noted. Patient was observed for any

complications during Vasti schedule.

The patient was advised to avoid during the Vasti Schedule.(308)

1. Vyayama

2. Maidhuna

3. Madyam

4. Madhu

5. Sisirambhu

6. Sambhojana / Adhika bhojana

7. Radhakshobha / Excessive traveling

8. Diwaswapna

Upadravas / Complications of Ati Sevana of yapanavasti (309)

1. Sopha

2. Agni nasa

3. Pandu

4. Sula

5. Arsas

6. Parikartika

A Study on the effect of Uma sambhu ras with Madhu ghritaadi yapana vasti in the management ofprameha w.s.r.to Madhumeha

85

7. Jwara

8. Atisara

Treatment of upadravas:(310)

Deepanam, ksheera, madya / Arista Sevana.


86

OBJECTIVES

- To determine the efficacy of Uma sambhu ras in madhumeha

- To determine the efficacy of Uma sambhu ras and madhu Ghritadi yapana vasti in

madhumeha

- To compare the efficacy of Uma sambhu ras to group given Uma sambhu ras and

madhu Ghritadi yapana Vasti.


87

METHODOLOGY

TYPE OF STUDY AND STUDY DESIGN:

The present study is a Randomized clinical Trail (RCT) & open trial, selected to

minimize the bias.

SAMPLING:

- The sampling technique selected in selecting Group - Group & I – II subject is

randomized Sampling technique.

- For comparative study, as only a small number of patients are available for trial,

paired randomization is applied.

- Balancing of the combination of the factors affecting the prognosis can be

obtained by matching each patient in the Group – I with similar patient in Group

II, i.e. by the method of pairing.

- Here, age, Gender, occupation, S.E.Status stress & BMI were considered & a

maximum balancing is tried to obtain.

I DETAILS OF STUDY SUBJECTS (CASES) AND CONTROLS:

- 40 Patients were selected randomly into two groups (Group –I & Group – II) from

the OPD & IPD of Dr.B.R.K.R Government Ayurvedic Research hospital,

Erragadda and 29 patients were placed in Group patients were placed in Group I

and 11 patients in Group-II

- No Control group was selected.

II DURATION OF STUDY:

The duration was planned for 30 days to have a complete or detailed analysis.


88

III MODE OF ADMINISTRATION:

The drug was administered at a dose of 125 mg with plain water after meals, three

times a day i.e. after breakfast, after lunch and after dinner, with minimum of 6

hours gap between each.

DETAILS OF MATERIALS (APPARATUS / LABTESTS) &

EXPERIMENTAL DESIGN:

MATERIALS:

SUBJECTIVE PARAMETERS:-

The following clinically presented Symptoms, found common in all subjects were

Selected as subjective parameters and considered as criteria for assessment of

results

1. Excessive thirst

2. Voracious appetite

3. Cramps in legs

4. Weakness or fatigue

5. Pruritis

6. Nocturnal Enuresis

Gradation was not given to the parameters, but only present or absent were

considered.

OBJECTIVE PARAMETERS:

- Fasting Urine sugar level

- Post lunch Urine sugar levels

- Fasting Blood Sugar levels


89

- Post lunch Blood sugar levels

Were considered for the assessment of effect of treatments in G-I & G-II

EXPERIMENTAL DESIGNING:

Factorial design was applied, as the effects of drug singly as well as in

combination are to be determined, and looking for the possibility of interaction of the two

treatments, such as synergism.

PROCEDURE OF DATA COLLECTION:

Values of a single selected variable (Subjective parameters) in all subjects and

values of all variables in each subject were recorded in 2 periods VIZ B.T (Before

treatment) at (after treatment). The values of FUS, PLUS, FBS, PLBS were recorded BT,

I wk & AT for all the subjects of G-I & G-II

STATISTICAL METHODS EMPLYOD:

For determining the efficacy of drug in G-I & drug & Vasti in G-II paired‘t’ test was

applied.

- P Value was analyzed.

- ‘t’ Value was analyzed for at the 0.1% to 5% levels of significance.

(b) To test the significance difference between G-I & G-II, Un paired‘t’ test – testing

the difference between the means is applied.

- ‘t’ value was analyzed for at 0.1% to 5% levels of significance.


90

OBSERVATIONS

Status of patients: 48

Patients were selected for the present study, out of which 37 were registered in-group I

i.e., uma sambhu ras group and 11 were registered in-group II i.e., uma sambhu ras &

madhu ghritaadi yapana vasti group. 8 patients in group I & 0 patients in group II

dropped out during treatment. Hence, a total of 29 patients in group I & 11 patients in

group II completed the study.

TABLE NO-2AGE WISE DISTRIBUTION OF PATIENTS

AGE GROUP GROUP 1 GROUP 2 TOTAL PERCENTAGE20-29 0 1 1 330-39 7 4 11 2840-49 11 3 14 3450-59 8 2 10 2560-69 3 1 4 10

TOTAL 29 11 40 100

TABLE NO-1STATUS OF PATIENTS OF PRESENT STUDY

GROUP TOTAL REGISTERED DROP OUTS COMPLETED

GROUP 1 37 8 29

GROUP 2 11 0 11

TOTAL 48 8 40

02468

1012

20-29 30-39 40-49 50-59 60-69AGE

DISTRIBUTION OF PATIENTS ACCORDING TO AGE

GROUP 1GROUP 2


91

AGE WISE DISTRIBUTION OF PATIENTS GROUP 1

0, 0%7, 24%

11, 38%

8, 28%

3, 10%

20-29

30-39

40-49

50-59

60-69

Out of 40 Subjects selected for the study 1 subject (5%) belong to the age group of 20 –

29 yrs, 11 subjects (28%) belong to the age group of 30 – 39 yrs, 14 subjects (34%)

AGE WISE DISTRIBUTION OF PATIENTS GROUP 2

1, 9%

4, 37%

3, 27%

2, 18%

1, 9%

20-29

30-39

40-49

50-59

60-69

AGE WISE DISTRIBUTION OF PATIENTS G I &G II

1, 3%

11, 28%

14, 34%

10, 25%

4, 10%

20-29

30-39

40-49

50-59

60-69


92

belong to the age group of 40 – 49 yrs. 10 subjects (25%) belong to the age group of 50 –

59 yrs,4 subjects (10%) belong to the age group of 60 – 69 yrs.

In Group – I, Out of 29 subjects, 0 subjects (0%) belong to the age group of 20 – 29 yrs,

7 subjects (24%) belong to the age group of 30 – 39 yrs, 11 subjects (38%) belong to the

age group of 40 – 49 yrs. 8 subjects (28%) belong to the age group of 50 – 59 yrs.

3 subjects (10%) belong to the age group of 60 – 69 yrs.

In Group – II , Out of 11 subjects 1 subject (9%) belong to the age group of 20 – 29 yrs,

4 subjects (37%) belong to the age group of 30 – 39 yrs, 3 subjects (27%) belong to the

age group of 40 – 49 yrs. 2 subjects (18%) belong to the age group of 50 – 59 yrs,

1 subject (9%) belongs to the age group of 60 – 69 yrs.

TABLE NO-3GENDER WISE DISTRIBUTION OF PATIENTS

GENDER GROUP 1 GROUP 2 TOTAL PERCENTAGEMALE 15 4 19 48

FEMALE 14 7 21 52TOTAL 29 11 40 100

1514

4

7

0

5

10

15

GROUP 1 GROUP 2

GENDER WISE DISTRIBUTION OF PATIENTS G I & G II

MALE

FEMALE


93

Data Table No.

Out of 40 Subjects selected for the study, 19 subjects (48%) are males and 21 subjects

(52%) are females.

GENDER WISE DISTRIBUTION OF PATIENTS GROUP 2

4, 36%

7, 64%

MALE

FEMALE

GENDER WISE DISTRIBUTION OF PATIENTS GROUP 1

15, 52%

14, 48%

MALEFEMALE

GENDER WISE DISTRIBUTION OF PATIENTS G I & G II

19, 48%

21, 52%

MALEFEMALE


94

In Group I, Out of 29 Subjects, 15 subjects (52%) are males and 14 subjects (48%) are

females.

In Group II, Out of 11 subjects, 4 subjects (36%) are males and 7 subjects (64%) are

females.

TABLE NO-4RELIGION WISE DISTRIBUTION OF PATIENTS

RELIGION GROUP 1 GROUP 2 TOTAL PERCENTAGEHINDU 21 10 31 72

MUSLIM 8 1 9 28CHRISTIAN 0 0 0 0

TOTAL 29 11 40 100

21

108

1 0 00

5

10

15

20

25

HINDU MUSLIM CHRISTIAN

RELIGION WISE DISTRIBUTION OF PATIENTS G I & G II

GROUP 1

GROUP 2


31, 77%

9, 23%0, 0%

HINDU

MUSLIM

CHRISTIAN


95

RELIGION WISE DISTRIBUTION OF PATIENTS GROUP II

1, 9% 0, 0%

10, 91%

HINDU

MUSLIM

CHRISTIAN

Out of 40 Subjects selected for the study, 31 subjects (77%) are Hindus and 9 subjects

(23%) are Muslims, 0 subjects (0%) are Christians.

In Group I, Out of 29 Subjects, 21 subjects (72%) are Hindus and 8 subjects (28%) are

Muslims, 0 subjects (0%) are Christians.

In Group II, Out of 11 subjects, 10 subjects(90%) are Hindus and 1 subject (23%) are

Muslims, 0 subjects (0%) are Christians.

RELIGION WISE DISTRIBUTION OF PATIENTS GROUP 1

21, 72%

8, 28%0, 0%

CHRISTIAN

MUSLIMHINDU


96

TABLE NO-5DISTRIBUTION OF PATIENTS ACCORDING TO OCCUPATION

OCCUPATION G-I % G-II % TOTAL %RTD.CLERK 1 3.45 0 0 1 2.50ADVOCATE 1 3.45 0 0 1 2.50ARTIST 1 3.45 0 0 1 2.50DOCTOR 1 3.45 0 0 1 2.50ATTENDER 2 6.90 0 0 2 5.00BUSINESS 4 13.79 1 9.09 5 12.50LABOURER 2 6.90 1 9.09 3 7.50HOUSE-WIFE 11 37.93 6 54.55 17 42.50MASON 1 3.45 1 9.09 2 5.00RTD.SUPERITENDENT 2 6.90 0 0.00 2 5.00SALES ENGINEER 1 3.45 1 9.09 2 5.00STUDENT 1 3.45 0 0.00 1 2.50TAILOR 1 3.45 1 9.09 2 5.00TOTAL 29 11 40

TABLE NO 6DISTRIBUTION OF PATIENTS ACCORDING TO FAMILY HISTORY

FAMILY HISTORY G-I % G-II % TOTAL %MOTHER/ FATHER 10 34.48 5 45.5 15 37.50SIBBLINGS 7 24.14 3 27.3 10 25.00NO HISTORY 12 41.38 3 27.3 15 37.50TOTAL 29 100 11 100 40 100.00

10

5

7

3

12

3

0

2

4

6

8

10

12

MOTHER/ FATHER SIBBLINGS NO HISTORY

DISTRIBUTION OF PATIENTS ACCORDING TO FAMILY HISTORY GI&GII

G-I

G-II


97

DISTRIBUTION OF PATIENTS ACCORDING TO FAMILY HISTORY G-I

7, 24%

10, 34%12, 42%

MOTHER/FATHER

SIBBLINGS

NO HISTORY

DISTRIBUTION OF PATIENTS ACCORDING TO FAMILY HISTORY G-II

3, 27%

5, 46%

3, 27%

MOTHER/FATHER

SIBBLINGS

NO HISTORY

DISTRIBUTION OF PATIENTS ACCORDING TO FAMILY HISTORY G I &G-II

10, 25%

15, 37%15, 38%

MOTHER/FATHER

SIBBLINGS

NO HISTORY


98

Out of 40 subjects selected for the study, 25 subjects (58%) possess Diabetes family

history ,15 (38%) in parents ,10 (25%)in sibblings and 15 subjects (38%) did not possess

any family history.

In Group I, Out of 29 subjects selected for the study, 17 subjects (66%) possess Diabetes

family history ,10 (25%) in parents , 7(24%)in sibblings and 12 subjects (42%) did not

possess any family history.

In Group II, Out of 11 subjects selected for the study, 8 subjects (73%) possess Diabetes

family history ,5 (46%) in parents 3 (27%)in sibblings and 3 subjects (27%) did not

possess any family history.

TABLE NODISTRIBUTION OF PATIENTS ACCORDING TO PRAKRITI

PRAKRITI G-I % G-II % TOTAL %VP 3 10.34 1 9.09 4 10.00PK 6 20.69 2 18.2 8 20.00VK 20 68.97 8 72.7 28 70.00TOTAL 29 100 11 100 40 100.00

31

6

2

20

8

0

5

10

15

20

VP PK VK

DISTRIBUTION OF PATIENTS ACCORDING TO PRAKRITI GI & GII

G-I

G-II


99

DISTRIBUTION OF PATIENTS ACCORDING TO PRAKRITI GI & G-II

4, 10%

8, 20%

28, 70%

VP

PK

VK

DISTRIBUTION OF PATIENTS ACCORDING TO PRAKRITI G-I

3, 10%

6, 21%

20, 69%

VP

PK

VK

DISTRIBUTION OF PATIENTS ACCORDING TO PRAKRITI G-II

1, 9%

2, 18%

8, 73%

VP

PK

VK

Out of 40 subjects considered for the study, 4 subjects (10%) were of Vata – Pitta

Prakriti, 8 subjects (20%) were of Pitta – Kapha Prakriti, 28 subjects (70%) were of Vata

– Kapha Prakriti.


100

In Group I, Out of 29 subjects considered for the study, 3 subjects (10.34%) were of Vata

– Pitta Prakriti, 6 subjects (20.69%) were of Pitta – Kapha Prakriti, 20 subjects (68.97%)

were of Vata – Kapha Prakriti.

In Group II, Out of 11 subjects considered for the study, 1 subject (9.09%) was of Vata –

Pitta Prakriti, 2 subjects (18.2%) were of Pitta – Kapha Prakriti, 8 subjects (72.7%) were

of Vata – Kapha Prakriti.

TABLE NO 7DISTRIBUTION OF PATIENTS ACCORDING TO SOCIO ECONOMIC STATUS

SES G-I % G-II % TOTAL %POOR 13 44.83 9 81.8 22 55.00MIDDLE 12 41.38 1 9.09 13 32.50UPPER MIDDLE 4 13.79 1 9.09 5 12.50HIGH 0 0 0 0 0 0.00TOTAL 29 100 11 100 40 100.00

13

9

12

1

4

10 0

0

2

4

6

8

10

12

14

PO O R MIDDLE UPPER MIDDLE HIGH

DISTRIBUTION OF PATIENTS ACCORDING TO SOCIO ECONOMIC STATUS GI& G II

G-IG-II


101

DISTRIBUTION OF PATIENTS ACCORDING TO SOCIO ECONOMICSTATUS G I & G II

22, 54%13, 33%

0, 0%5, 13%

POORMIDDLEU

HIGHUPPERMIDDLE

Out of 40 subjects considered for the study, 22 subjects (55%) belong to low income

group and 13 subjects (32.5%) belong to middle income group, 5 subjects (12.5%) belong

to upper middle-income group and 0 subjects (0%) belong to high-income group.

In Group I, Out of 29 subjects considered for the study, 13 subjects (44.53%) belong to

low income group and 12 subjects (41.38%) belong to middle income group, 4 subjects

(13.79%) belong to upper middle-income group and 0 subjects (0%) belong to high-

income group.

In Group II, Out of 11 subjects considered for the study, 9 subjects (81.2%) belong to low

income group and 1 subject (9.09%) belong to middle income group, 1 subject (9.09%)

belong to upper middle income group and 0 subjects (0%) belong to high income group..

Graph No.4

TABLE NO 8DISTRIBUTION OF PATIENTS ACCORDING TO DIET

DIET G-I % G-II % TOTAL %Veg 8 27.58621 3 27.27273 11 27.50

Mixed 21 72.41379 8 72.72727 29 72.50TOTAL 29 100 11 100 40 100.00


102

8

3

21

8

0

5

10

15

20

25

Veg Mixed

DISTRIBUTION OF PATIENTS ACCORDING TO DIET G I & G II

G-IG-II

DISTRIBUTION OF PATIENTS ACCORDING TO DIET GI &G-II

11, 28%

29, 72%

MIXED

VEG

DISTRIBUTION OF PATIENTS ACCORDING TO DIET G-I

8, 28%

21, 72%

MIXED

VEG


103

DISTRIBUTION OF PATIENTS ACCORDING TO DIET G-II

3, 27%

8, 73%

MIXED

VEG

Out of 40 subjects considered for the study, 29 subjects (72.5%) belong to mixed diet

group and 11 subjects (27.5%) belong to vegetarian diet group.

In Group I, Out of 29 subjects considered for the study, 21 subjects (72.41%) belong to

mixed diet group and subjects (27.59%) belong to vegetarian diet group.

In Group II, Out of 11 subjects considered for the study, 8 subjects (72.73%) belong to

mixed diet group and 3 subjects (27.27%) belong to vegetarian diet group.

TABLE NO 9DISTRIBUTION OF PATIENTS ACCORDING TO STRESS FACTOR

STRESS G-I % G-II % TOTAL %NO 6 20.69 3 27.3 9 22.50MILD 7 24.14 0 0 7 17.50MODERATE 8 27.59 6 54.5 14 35.00SEVERE 8 27.59 2 18.2 10 25.00TOTAL 29 100 11 100 40 100.00


104

6

3

7

0

8

6

8

2

0

2

4

6

8

NO MILD MODERATE SEVERE

DISTRIBUTION OF PATIENTS ACCORDING TO STRESS GI& GII

G-IG-II

DISTRIBUTION OF PATIENTS ACCORDING TO STRESS GI & G-II

9, 23%

7, 18%

14, 34%

10, 25%NO

MILDMODERATE

SEVERE

DISTRIBUTION OF PATIENTS ACCORDING TO STRESS G-I

6, 21%

7, 24%

8, 27%

8, 28%NO

MILDMODERATE

SEVERE


105

DISTRIBUTION OF PATIENTS ACCORDING TO STRESS G-II

3, 27%

0, 0%

6, 55%

2, 18%

NO

MILDMODERATE

SEVERE

TABLE NO 10DISTRIBUTION OF PATIENTS ACCORDING TO CHRONICITY

CHRONICITY (yrs) G-I % G-II % TOTAL %< 1 year 18 62.07 6 54.5 24 60.00

1-5 5 17.24 4 36.4 9 22.506-10 3 10.34 1 9.09 4 10.00

11-15 0 0 0 0 0 0.0016-20 1 3.448 0 0 1 2.50>25 2 6.897 0 0 2 5.00

TOTAL 29 100 11 100 40 100

Out of 40 subjects considered for the study, 24 subjects (60.00%) have the chronicity of

less than 1 yr. 9 subjects (22.50%) have the chronicity of 1 – 5 yrs, 4 subjects (10%) have

chronicity of 6 – 10 yrs and 0 subjects (0.00%) have the chronicity of 11 – 15 yrs. 1

subject (2.50%) have the chronicity of 15 – 20 yrs , 2 subjects (5.00%) have the

chronicity of > 25 yrs

In Group I, Out of 29 subjects considered for the study, 18 subjects (62.07%) have the

chronicity of less than 1 yr. 5 subjects (17.24%) have the chronicity of 1 – 5 yrs, 3

subjects (10.34%) have chronicity of 6 – 10 yrs and 0 subjects (0.00%) have the

chronicity of 11 – 15 yrs. 1 subject (3.45%) have the chronicity of 15 – 20 yrs , 2 subjects

(6.89%) have the chronicity of > 25 yrs


106

In Group II, Out of 11 subjects considered for the study, 6 subjects (59.5%) have the

chronicity of less than 1 yr. 4 subjects (36.40%) have the chronicity of 1 – 5 yrs, 1

subjects (9.09%) have chronicity of 6 – 10 yrs and 0 subjects (0.00%) have the chronicity

of 11 – 15 yrs. 0 subject (0.00%) have the chronicity of 15 – 20 yrs, 0 subjects (0.00%)

have the chronicity of > 25 yrs.

TABLE NO 11DISTRIBUTION OF PATIENTS ACCORDING TO BMI

BMI G-I % G-II % TOTAL %≤25 19 65.52 9 81.8 28 70.00≤30 4 13.79 1 9.09 5 12.50≤32 3 10.34 1 9.09 4 10.00>32 3 10.34 0 0 3 7.50TOTAL 29 100 11 100 40 100

19

9

41

31

3

00

5

10

15

20

≤25 ≤30 ≤32 >32

DISTRIBUTION OF PATIENTS ACCORDING TO BMI GI & GII

G-I

G-II

DISTRIBUTION OF PATIENTS ACCORDING TO BMI GI & GII

28, 69%

5, 13%

4, 10%

3, 8%

≤25

≤30

≤32

>32


107

Out of 40 subjects considered for the study, 28 subjects (70.00%) had the BMI of less

than or equal to 25, 5 subjects (12.50%) had the BMI of less than or equal to 30, 4

subjects (10.00%) had the BMI of less than or equal to 32, 3 subjects (7.50%) had the

BMI of more than 32.

In Group A, Out of 29 subjects considered for the study, 19 subjects (65.52%) had the

BMI of less than or equal to 25 , 4 subjects (13.79%) had the BMI of less than or equal

to 30, 3 subjects (10.34%) had the BMI of less than or equal to 32, 3 subjects (10.34%)

had the BMI of more than 32.

In Group II, Out of 11 subjects considered for the study, 9 subjects (81.80%) had the

BMI of less than or equal to 25 , 1 subject (9.09%) had the BMI of less than or equal to

30, 1 subject (9.09%) had the BMI of less than or equal to 32, 0 subjects (0.00%) had the

BMI of more than 32.

TABLE NO 12DISTRIBUTION OF PATIENTS ACCORDING TO DRUG GROUP

DRUG GROUP G-I % G-II % TOTAL %With out any oral medication 16 55.17 6 54.5 22 55.00With oral uncontrolled 3 10.34 1 9.09 4 10.00With oral discontinued 6 20.69 3 27.3 9 22.50Oral+insulin controlled 1 3.448 1 9.09 2 5.00Oral+insulin uncontrolled 3 10.34 0 0 3 7.50

TOTAL 29 100 11 100 40 100

All the patients in Group I & Group II were categorized depending on the drug they were

using and their disease status before starting the trail drug.

TABLE NO 13DISTRIBUTION OF PATIENTS ACCORDING TO ADDICTIONS

ADDICTIONS G-I % G-II % TOTAL %SMOKING 1 3.448 0 0 1 2.50TOBACCO(CHEWING) 2 6.897 1 9.09 3 7.50ALCOHOL 8 27.59 4 36.4 12 30.00PAN 3 10.34 1 9.09 4 10.00NO ADDICTION 15 48.28 5 45.5 20 50TOTAL 29 100 11 100 40 100


108

Out of 40 subjects considered for the study, 20 subjects (50.00%) had no addictions, 4

subjects (10.00%) had addiction of pan, 12 subjects (30.00%) had addiction of alcohol, 3

subjects (7.50%) had addiction of smoking, 1 subject (3.00%) had addiction of chewing

tobacco

In Group I, Out of 29 subjects considered for the study, 15 subjects (48.28%) had no

addictions ,1 subject (3.45%) had addiction of chewing tobacco , 2 subjects (6.90%) had

addiction of smoking , 8 subjects (27.59%) had addiction of alcohol , 3 subjects

(10.34%) had addiction of pan.

In Group II, Out of 11 subjects considered for the study, 20 subjects (50.00%) had no

addictions, 4 subjects (10.00%) had addiction of pan, 12 subjects (30.00%) had addiction

of alcohol, 3 subjects (7.50%) had addiction of smoking

, 1 subject (3.00%) had addiction of chewing tobacco

DISTRIBUTION OF PATIENTS ACCORDING TO ADDICTIONS GI &GII

1, 3% 3, 8%

12, 30%

4, 10%20, 49%

SMOKING

TOBACCO (CHEWING)ALCOHALPANNO ADDICTION


109

Table no.14

DISTRIBUTION OF PATIENTS ACCORDING TO PRAKRITI & NIDANA

PRAKRITI

AHARAVP % PK % VK % TOTAL %

MADHURA 0 0.00 2 5.00 6 15.00 8.00 20.00

AMLA 3 7.50 2 5.00 11 27.50 16.00 40.00

LAVANA 2 5.00 4 10.00 5 12.50 11.00 27.50

KATU 2 5.00 5 12.50 16 40.00 23.00 57.50

TIKTA 0 0.00 0 0.00 0 0.00 0.00 0.00

KASHAYA 0 0.00 0 0.00 0 0.00 0.00 0.00

SNIGDHA 3 7.50 4 10.00 18 45.00 25.00 62.50

GURU 1 2.50 1 2.50 10 25.00 12.00 30.00

PICCHALA 2 5.00 1 2.50 2 5.00 5.00 12.50

SEETA 2 5.00 8 20.00 17 42.50 27.00 67.50

LAGHU 0 0.00 0 0.00 1 2.50 1.00 2.50

GRAMYA 3 7.50 1 2.50 9 22.50 13.00 32.50

OUDAKA 1 2.50 1 2.50 12 30.00 14.00 35.00

ANUPA 0 0.00 0 0.00 4 10.00 4.00 10.00

IKSHU 0 0.00 2 5.00 1 2.50 3.00 7.50

GUDA 1 2.50 0 0.00 3 7.50 4.00 10.00

PAYAS 2 5.00 2 5.00 4 10.00 8.00 20.00

DADHI 2 5.00 5 12.50 16 40.00 23.00 57.50

VIHARA

EKASTHANARATI 3 7.50 6 15.00 15 37.50 24.00 60.00

VIDHIVARJITASAYANA 3 7.50 7 17.50 23 57.50 33.00 82.50

DIVASWAPNA 3 7.50 5 12.50 20 50.00 28.00 70.00

VEGASANDHARANA 1 2.50 7 17.50 22 55.00 30.00 75.00

VYAYAMA 1 2.50 0 0.00 7 17.50 8.00 20.00

MANASIKA

UDVEGA 3 7.50 7 17.50 26 65.00 36.00 90.00

SOKA 3 7.50 7 17.50 23 57.50 33.00 82.50


110

Table no.15

DISTRIBUTION OF PATIENTS ACCORDING TO AGE GROUP & NIDANA

AGE

AHARA20-29 30-39 40-49 50-59 60-69 TOTAL %

MADHURA 0 2 2 3 1 8 20.00

AMLA 1 2 5 6 2 16 40.00

LAVANA 1 2 5 2 1 11 27.50

KATU 1 7 8 6 1 23 57.50

TIKTA 0 0 0 0 0 0 0.00

KASHAYA 0 0 0 0 0 0 0.00

SNIGDHA 1 7 8 5 4 25 62.50

GURU 1 2 4 4 1 12 30.00

PICCHALA 1 3 1 0 0 5 12.50

SEETA 1 10 8 6 2 27 67.50

LAGHU 0 0 1 0 0 1 2.50

GRAMYA 1 2 4 4 3 14 35.00

OUDAKA 0 0 2 1 1 4 10.00

ANUPA 0 3 4 5 1 13 32.50

IKSHU 0 2 1 0 0 3 7.50

GUDA 0 0 1 2 1 4 10.00

PAYAS 0 1 4 3 0 8 20.00

DADHI 0 8 7 5 3 23 57.50

VIHARA

EKASTHANARATI 1 8 8 5 2 24 60.00

VIDHIVARJITASAYANA 1 11 10 8 3 33 82.50

DIVASWAPNA 1 8 8 8 3 28 70.00

VEGASANDHARANA 0 10 10 6 4 30 75.00

VYAYAMA 0 3 1 2 2 8 20.00

MANASIKA

UDVEGA 1 10 14 8 3 36 90.00

SOKA 1 9 12 8 3 33 82.50


111

Table no 16

DISTRIBUTION OF PATIENTS ACCORDING TO PURVA RUPA

PURVA RUPA VP % PK % VK % TOTAL %

Madhurasyata 2 5.00 3 7.50 5 12.50 10 25.0

Lavanasyata 0 0.00 0 0.00 0 0.00 0 0.0

Tiktasyata 2 5.00 0 0.00 2 5.00 4 10.0

Swasa 3 7.50 2 5.00 13 32.50 18 45.0

Nidra 2 5.00 3 7.50 16 40.00 21 52.5

Tandra 2 5.00 5 12.50 21 52.50 28 70.0

Alasya 3 7.50 7 17.50 17 42.50 27 67.5

Gurugatra 3 7.50 4 10.00 13 32.50 20 50.0

Dantadimala 0 0.00 4 10.00 3 7.50 7 17.5

Durgandhaswasa 0 0.00 0 0.00 4 10.00 4 10.0

Sayyabhishanga 2 5.00 5 12.50 22 55.00 29 72.5

Swapnabhishanga 2 5.00 6 15.00 20 50.00 28 70.0

Kantasosha 4 10.00 3 7.50 14 35.00 21 52.5

Mukhasosha 3 7.50 4 10.00 16 40.00 23 57.5

Pipasa 4 10.00 6 15.00 17 42.50 27 67.5

Seeta Priyatwam 3 7.50 3 7.50 10 25.00 16 40.0

Angeshusweda 4 10.00 5 12.50 10 25.00 19 47.5

Panipadadaha 3 7.50 3 7.50 10 25.00 16 40.0

Mutra Visragandha 1 2.50 1 2.50 0 0.00 2 5.0

Sareera Visragandha 0 0.00 0 0.00 0 0.00 0 0.0

Anga Saidhilyam 1 2.50 0 0.00 7 17.50 8 20.0

Angasuptata 3 7.50 2 5.00 13 32.50 18 45.0


112

Table no 17

DISTRIBUTION OF PATIENTS ACCORDING TO PURVA RUPA

(2) (14) (11) (10) (2) (40)

PURVA RUPA 20-30 30-40 40-50 50-60 60-70 Total %

Madhurasyata 0 7 0 3 0 10 25.0

Lavanasyata 0 0 0 0 0 0 0.0

Tiktasyata 0 1 1 0 0 2 5.0

Swasa 2 4 5 5 2 18 45.0

Nidra 2 7 5 7 0 21 52.5

Tandra 2 9 8 7 2 28 70.0

Alasya 1 12 7 6 1 27 67.5

Gurugatra 2 7 5 5 1 20 50.0

Dantadimala 0 5 1 1 0 7 17.5

Durgandhaswasa 0 1 0 2 1 4 10.0

Sayyabhishanga 1 10 8 9 1 29 72.5

Swapnabhishanga 2 10 8 7 1 28 70.0

Kantasosha 2 7 6 6 2 23 57.5

Mukhasosha 2 9 9 6 2 28 70.0

Pipasa 2 11 10 8 2 33 82.5

Seeta Priyatwam 2 6 5 6 0 19 47.5

Angeshusweda 2 8 8 5 0 23 57.5

Panipadadaha 2 6 7 3 1 19 47.5

Mutra Visragandha 0 2 1 1 0 4 10.0

Sareera Visragandha 0 0 0 0 0 0 0.0

Anga Saidhilyam 1 1 2 3 1 8 20.0

Angasuptata 1 7 9 7 1 25 62.5


113

Table no 18DISTRIBUTION OF PATIENTS ACCORDING TO SUBJECTIVE PARAMETERS GI & G II

G I GII GI+GIIS.NO

SUBJECTIVEPARAMETERS

BT AT BT AT BT AT1 EXCESSIVE THIRST 16 4 6 1 22 52 VORACIOUS APPETITE 6 2 1 0 7 23 CRAMPS IN LEGS 13 3 8 1 21 44 FATIGUE 21 3 8 1 29 45 EXCESSIVE SWEATING 14 5 6 0 20 56 PRURITIS 7 1 0 0 7 17 FROZEN SHOULDER 1 0 0 0 1 08 NOCTURNAL ENURESIS 7 3 5 2 12 5

Table no 19DISTRIBUTION OF PATIENTS ACCORDING TO FUS GI & G II

FUS GI GII GI+GIIBT AT BT AT BT AT

0 12 16 3 1 15 170.5 4 4 1 4 5 81 7 4 2 2 9 6

1.5 1 0 1 0 2 0TOTAL 24 24 7 7 31 31

0

5

10

15

20

O <.5 <1 <1.5

GI BT

GI AT

GII BT

GII AT

0

5

10

15

20

25

GI BT 16 6 13 21 14 7 1 7

GI AT 4 2 3 3 5 1 0 3

GII BT 6 1 8 8 6 0 0 5

GII AT 1 0 1 1 0 0 0 2

1 2 3 4 5 6 7 8


114

Table no 20DISTRIBUTION OF PATIENTS ACCORDING TO PLUS GI & G II

PLUS GI GII GI+GIIBT AT BT AT BT AT

0 5 10 2 2 7 120.5 3 5 0 1 3 61 6 3 0 1 6 4

1.5 5 4 4 3 9 72 3 0 1 0 4 0

TOTAL 22 22 7 7 29 29

0

24

68

1012

0 < .5 <1 <1.5 <2

GI BT

GI AT

GII BT

GII AT

TABLE NO 21DISTRIBUTION OF PATIENTS ACCORDING TO FBS G-II

FBS BT 1STWEEK AT80-100 1 1 1

100-120 0 0 2120-140 1 1 1140-160 2 1 3160-180 1 3 0180-200 3 3 3200-220 1 1 0

>220 2 0 1

00.5

11.5

22.5

33.5

80-100 100-120 120-140 140-160 160-180 180-200 200-220 >220

BT1STWEEKAT


115

TABLE NO 22DISTRIBUTION OF PATIENTS ACCORDING TO FBS GI

FBS BT 1STWEEK AT80-100 2 5 7

100-120 5 5 7120-140 7 4 4140-160 3 4 2160-180 2 2 2180-200 3 3 4200-220 2 1 1

>220 4 1 1

01234

5678

80-100 100-120 120-140 140-160 160-180 180-200 200-220 >220

BT1STWEEKAT

TABLE NO 23DISTRIBUTION OF PATIENTS ACCORDING TO PLBS GI

PLBS BT 1STWEEK AT100-130 0 0 0130-160 2 5 7160-190 3 3 6190-220 8 4 5220-250 2 4 3250-280 4 3 3280-310 6 5 3310-340 3 3 2340-370 0 0 0

>370 1 0 0

0

2

4

6

8

10

100-130 130-160 160-190 190-220 220-250 250-280 280-310 310-340 340-370 >370

BT1STWEEKAT


116

TABLE NO 24DISTRIBUTION OF PATIENTS ACCORDING TO PLBS GII

PLBS BT 1STWEEK AT100-130 0 0 0130-160 0 0 2160-190 1 1 0190-220 1 3 2220-250 2 1 2250-280 2 3 3280-310 1 0 0310-340 3 1 1340-370 0 1 1

>370 1 0 0

0

0.5

1

1.5

2

2.5

3

3.5

100-130 130-160 160-190 190-220 220-250 250-280 280-310 310-340 340-370 >370

BT1STWEEKAT


117

NAME ET VA CL WK ES PR NE MEAN M.DIFF %DIFF

BT 1 0 0 1 0 0 1 0.431 V.S.SASTRY

AT 0 0 0 0 0 0 0 0.00

0.43 100

BT 1 0 0 0 0 1 1 0.432 S.Padmavati

AT 0 0 0 0 0 0 1 0.14

0.29 67.44

BT 1 0 0 1 1 0 0 0.433 Nazeersultana

AT 0 0 0 1 1 0 1 0.43

0 0

BT 0 0 0 0 0 1 0 0.144 I.V.Reddy

AT 0 0 0 0 0 0 0 0.00

0.14 100

BT 1 1 0 1 1 1 0 0.715 G.Venkatesh

AT 1 1 0 0 0 0 0 0.29

0.42 59.15

BT 1 0 0 1 1 0 0 0.436 K.Ammaji

AT 0 0 0 0 0 0 0 0.00

0.43 100

BT 1 1 1 1 1 1 0 0.867 SurayyaBegum

AT 1 1 0 1 1 0 0 0.57

0.29 33.72

BT 1 0 1 1 1 0 0 0.578 Y.V.S.Rao

AT 0 0 1 0 0 0 0 0.14

0.43 75.44

BT 1 0 1 1 0 0 1 0.579 ST.Nirmala

AT 0 0 1 0 0 0 0 0.14

0.43 75.44

BT 1 0 0 1 1 0 0 0.4310 Md.Begum

AT 0 0 0 0 0 0 0 0.00

0.43 100

BT 0 0 1 1 0 1 0 0.4311 JaffriBegum

AT 0 0 0 0 0 0 0 0.00

0.43 100

BT 1 0 1 1 0 0 0 0.4312 Jayaprakash

AT 1 0 0 0 0 0 0 0.14

0.29 67.44

BT 0 0 0 1 0 0 0 0.1413 P.Umapaty

AT 0 0 0 0 0 0 0 0.00

0.14 100

BT 0 1 0 0 1 1 1 0.5714 V.Nirmala

AT 0 0 0 0 0 0 0 0.00

0.57 100

BT 1 0 0 1 0 0 0 0.2915 P.Indira

AT 1 0 0 0 0 0 0 0.14

0.15 51.72

BT 1 0 0 0 1 0 1 0.4316 T.Srinivasulu

AT 0 0 0 0 0 0 1 0.14

0.29 67.44

BT 0 1 1 1 1 0 0 0.5717 C.Nagender

AT 0 0 0 0 1 0 0 0.14

0.43 75.44

BT 1 0 0 1 0 0 1 0.4318 Noorjahan

AT 0 0 0 1 0 0 0 0.14

0.29 67.44

RESULTSTable no. 25 MEANS & PERCENTAGE DIFFERENCE OF ALL THE

SELECTED VARIABLES IN INDIVIDUAL SUBJECT OF GROUP- I


118

NAME ET VA CL WK ES PR NE MEAN M,DIFF %DIFF

BT 0 1 1 1 1 0 0 0.5719 K N Rao

AT 0 0 1 0 1 0 0 0.29

0.28 49.13

BT 0 0 0 1 0 1 0 0.2920 Umadevi

AT 0 0 0 0 0 1 0 0.14

0.15 51.72

BT 0 0 1 1 0 0 0 0.2921 R Seshagirirao

AT 0 0 0 0 0 0 0 0.00

0.29 100

BT 0 0 0 1 0 0 0 0.1422 Md.Yasin

AT 0 0 0 0 0 0 0 0.00

0.14 100

BT 0 0 0 0 1 0 0 0.1423 M G Rao

AT 0 0 0 0 0 0 0 0.00

0.14 100

BT 0 0 0 0 0 0 0 0.0024 YasmeenAtiya

AT 0 0 0 0 0 0 0 0.00

0 0

BT 1 1 1 1 1 0 0 0.7125 AneezBegem

AT 0 0 0 0 1 0 0 0.14

0.57 80.28

BT 1 0 0 1 1 0 0 0.4326 B Ganesh

AT 0 0 0 0 0 0 0 0.00

0.43 100

BT 0 0 1 1 0 0 0 0.2927 Amruthamma

AT 0 0 0 0 0 0 0 0.00

0.29 100

BT 1 0 1 1 1 0 0 0.5728 Laxminarayana

AT 0 0 0 0 1 0 0 0.14

0.43 75.44

BT 0 0 1 0 0 0 1 0.2929 N.Srinivasrao

AT 0 0 0 0 0 0 0 0.00

0.29 100

NOTE: ET = Excessive ThirstVA = Voracious AppetiteCL = Cramps in LegsWK = FatigueES = Excessive SweatingPR = PruritisNE = Nocturnal EnuresisMEAN = Mean of all subjective parametersM,DIFF = Difference between means of subjective parameters BT & AT% DIFF = % of Difference between means of subjective parameters BT & ATBT = Before Treatment.AT = After Treatment


119

Table no.26MEANS & PERCENTAGE DIFFERENCE OF ALL THE SELECTED VARIABLES IN

INDIVIDUAL SUBJECT OF GROUP- II

S.No NAME ET VA CL WK ES PR NE MEAN M,DIFF % DIFF

BT 1 0 1 1 1 0 1 0.711 Lalitha

AT 1 0 0 0 0 0 1 0.29

0.42 59.15

BT 1 0 1 1 1 0 0 0.572 Y.V.S.Rao

AT 0 0 1 0 0 0 0 0.14

0.43 75.44

BT 1 0 0 1 0 0 1 0.433 ST.Nirmala

AT 0 0 0 0 0 0 0 0.00

0.43 100

BT 1 0 1 1 1 0 1 0.714 Jyoti

AT 0 0 0 0 0 0 0 0.00

0.71 100

BT 0 0 1 0 1 0 0 0.295 Farzanabegum

AT 0 0 0 0 0 0 0 0.00

0.29 100

BT 1 1 1 1 0 0 1 0.716 T.Anasuya

AT 0 0 0 0 0 0 0 0.00

0.71 100

BT 0 0 1 1 1 0 1 0.577 Kousalya

AT 0 0 0 0 0 0 1 0.14

0.43 75.44

BT 0 0 1 0 0 0 0 0.148 Chandrasekhar

AT 0 0 0 0 0 0 0 0.00

0.14 100

BT 1 0 1 1 1 0 0 0.579 P.V.Lakshmi

AT 0 0 0 0 0 0 0 0.00

0.57 100

BT 0 0 0 1 0 0 0 0.1410 Raju

AT 0 0 0 1 0 0 0 0.14

0 0

BT 0 0 0 0 0 0 0 0.0011 R.Venkatrao

AT 0 0 0 0 0 0 0 0.00

0 0

NOTE: ET = Excessive ThirstVA = Voracious AppetiteCL = Cramps in LegsWK = FatigueES = Excessive SweatingPR = PruritisNE = Nocturnal EnuresisMEAN = Mean of all subjective parametersM.DIFF = Difference between means of subjective parameters BT & AT% DIFF = % of Difference between means of subjective parameters BT & ATBT = Before Treatment.AT = After Treatment


120

MEANS & PERCENTAGE DIFFERENCE OF ALL THE SELECTED VARIABLES IN

INDIVIDUAL SUBJECT OF GROUP- I

Table no.27PERCENTAGE CHANGE IN FASTING BLOOD SUGAR

BT1stweek

BT-1Week

% DIFF1st WK A T

BT-4Week

% DIFF 4th

WKGROUP-IV.S.SASTRY 145 100 45 31.03 90 55 37.93S.Padmavati 195 150 45 23.08 135 60 30.77Nazeersultana 201 191 10 4.98 190 11 5.47I.V.Reddy 120 105 15 12.50 105 15 12.50G.Venkatesh 160 120 40 25.00 100 60 37.50K.Ammaji 235 136 99 42.13 220 15 6.38SurayyaBegum 125 132 -7 -5.60Y.V.S.Rao 209 172 37 17.70 160 49 23.44ST.Nirmala 155 150 5 3.23 100 55 35.48Md.Begum 140 200 -200JaffriBegum 105 115 -10 -9.52Jayaprakash 85 99 -14 -16.47P.Umapaty 127 154 -27 -21.26 200 -73 -57.48V.Nirmala 161 201 -40 -24.84 173 -12 -7.45P.Indira 180 190 -10 -5.56 100 80 44.44T.Srinivasulu 230 180 50 21.74 165 65 28.26C.Nagender 110 140 -30 -27.27 160 -50 -45.45Noorjahan 127 95 32 25.20 110 17 13.39K N Rao 100 110 -10 -10.00 100 0 0.00Umadevi 126 99 27 21.43 110 16 12.70R Seshagirirao 182 150 32 17.58 140 42 23.08Md.Yasin 128 120 8 6.25YasmeenAtiya 137 135 2 1.46 90 47 34.31AneezBegem 190 195 -5 -2.63 240 -50 -26.32B Ganesh 240 255 -15 -6.25 200 40 16.67Amruthamma 135 100 35 25.93 108 27 20.00Laxminarayana 120 80 40 33.33 90 30 25.00N.Srinivasrao 120 118 2 1.67 120 0 0.00

BT = Reading of Fasting Blood Sugar Before Treatment.AT = Reading of Fasting Blood Sugar After Treatment1st Week = Reading of Fasting Blood Sugar after 1st week% Diff 1st WK = Difference of Reading of Fasting Blood Sugar after 1st WeekBT 4 WK = Reading of Fasting Blood Sugar after 4th week% Diff 4th WK = Difference of Reading of Fasting Blood Sugar Before

Treatment & 4th wee


121

Table no.28PERCENTAGE CHANGE IN POST LUNCH BLOOD SUGAR

BT1stweek

BT-1WK % DIFF AT

BT-4WK % DIFF

GROUP-IV.S.SASTRY 296 205 91 30.74 175 121 40.88S.Padmavati 290 310 -20 -6.90 205 85 29.31Nazeersultana 312 264 48 15.38 255 57 18.27I.V.Reddy 200 155 45 22.50 150 50 25.00G.Venkatesh 265 205 60 22.64 190 75 28.30K.Ammaji 285 203 82 28.77 335 -50 -17.54SurayyaBegum 215 254 -39 -18.14Y.V.S.Rao 284 334 -50 -17.61 234 50 17.61ST.Nirmala 260 302 -42 -16.15 175 85 32.69Md.Begum 295 275 20 6.78 285 10 3.39JaffriBegum 180 170 10 5.56Jayaprakash 139 155 -16 -11.51 160 -21 -15.11P.Umapaty 212 290 -78 -36.79 330 -118 -55.66V.Nirmala 247 258 -11 -4.45 220 27 10.93P.Indira 290 240 50 17.24 205 85 29.31T.Srinivasulu 330 290 40 12.12 240 90 27.27C.Nagender 200 340 -140 -70.00 290 -90 -45.00Noorjahan 210 190 20 9.52 230 -20 -9.52K N Rao 146 152 -6 -4.11 142 4 2.74Umadevi 215 242 -27 -12.56 184 31 14.42R Seshagirirao 256 200 56 21.88 190 66 25.78Md.Yasin 200 175 25 12.50 150 50 25.00M G Rao 315 240 75 23.81 208 107 33.97YasmeenAtiya 184 161 23 12.50 140 44 23.91AneezBegem 270 285 -15 -5.56 300 -30 -11.11B Ganesh 380 320 60 15.79 270 110 28.95Amruthamma 183 160 23 12.57 150 33 18.03Laxminarayana 250 140 110 44.00 160 90 36.00N.Srinivasrao 215 245 -30 -13.95 210 5 2.33

BT = Reading of Post Lunch Blood Sugar Before Treatment.AT = Reading of Post Lunch Blood Sugar After Treatment1st Week = Reading of Post Lunch Blood Sugar after 1st week% Diff 1st WK = Difference of Reading of Post Lunch Blood Sugar after 1st WeekBT 4 WK = Reading of Post Lunch Blood Sugar after 4th week% Diff 4th WK = Difference of Reading of Post Lunch Blood Sugar Before

Treatment & 4th week


122

MEANS & PERCENTAGE DIFFERENCE OF ALL THE SELECTED VARIABLES IN

INDIVIDUAL SUBJECT OF GROUP- II

Table no.29PERCENTAGE CHANGE IN FASTING BLOOD SUGAR

GROUP-II BT1stweek

BT-1WK % DIFF AT

BT-4WK % DIFF

Lalitha 225 190 35 15.56 200 25 11.11Y.V.S.Rao 139 126 13 9.35 118 21 15.11ST.Nirmala 100 100 0 0.00Jyoti 200 156 44 22.00 236 -36 -18.00Farzanabegum 218 180 38 17.43 155 63 28.90T.Anasuya 190 170 20 10.53 130 60 31.58Kousalya 200 205 -5 -2.50 190 10 5.00Chandrasekhar 247 170 77 31.17 150 97 39.27P.V.Lakshmi 155 100 55 35.48 105 50 32.26Raju 150 194 -44 -29.33 195 -45 -30.00R.Venkatrao 180 200 -20 -11.11 160 20 11.11

Table no.30PERCENTAGE CHANGE IN POST LUNCH BLOOD SUGAR

GROUP-II BT1stweek

BT-1WK

% DIFF1st WK AT

BT-4WK

% DIFF4th WK

Lalitha 330 345 -15 -4.55 340 -10 -3.03Y.V.S.Rao 225 213 12 5.33 206 19 8.44ST.Nirmala 175 150 25 14.29Jyoti 380 212 168 44.21 368 12 3.16Farzanabegum 335 265 70 20.90 225 110 32.84T.Anasuya 320 250 70 21.88 270 50 15.63Kousalya 255 315 -60 -23.53 270 -15 -5.88Chandrasekhar 300 220 80 26.67 200 100 33.33P.V.Lakshmi 274 170 104 37.96 156 118 43.07Raju 242 256 -14 -5.79 280 -38 -15.70R.Venkatrao 210 280 -70 -33.33 240 -30 -14.29

BT = Reading of Post Lunch Blood Sugar Before Treatment.AT = Reading of Post Lunch Blood Sugar After Treatment1st Week = Reading of Post Lunch Blood Sugar after 1st week% Diff 1st WK = Difference of Reading of Post Lunch Blood Sugar after 1st WeekBT 4 WK = Reading of Post Lunch Blood Sugar after 4th week% Diff 4th WK = Difference of Reading of Post Lunch Blood Sugar Before

Treatment & 4th week


123

B) EFFECT OF THE TREATMENT

OBJECTIVE PARAMETERS

Table no.31GROUP I Mean

StandardDeviation

Standard Error

N BT AT

MeanDiff

BT AT

SDDifference BT AT

t df p Result

FUS 26 4.29 4.08 0.21 19.73 19.66 0.45 3.87 3.84 2.39 25 0.025 S

PLUS 24 5.08 4.65 0.44 20.44 20.32 0.66 4.17 4.15 3.23 23 0.004 SFBS IWk 26 158.89 140.19 18.69 46.96 42.63 37.13 9.21 8.36 2.57 25 0.017 SFBS4 Wk 26 157.29 136.18 21.11 44.97 42.72 39.82 8.50 8.07 2.81 27 0.009 SPLBSI Wk 28 243.93 229.86 14.07 63.25 65.79 54.79 11.95 12.43 1.36 27 0.185 NsPLBS4 Wk 28 240.83 210.23 30.60 62.32 59.51 59.15 11.38 10.86 2.83 29 0.008 S

SUBJECTIVE PARAMETERSTable no.32

GROUP I MeanStandardDeviation

Standarderror

N BT AT

Mean

Difference

BT AT

SDDifference

BT AT

t df p Result

Excessive thrust 29 0.59 0.14 0.45 0.57 0.35 0.57 0.10 0.07 4.22 28 0.000 SVoraciousAppetite 29 0.21 0.07 0.14 0.41 0.26 0.65 0.08 0.05 2.12 28 0.043

S

Cramps in Legs 29 0.45 0.10 0.34 0.51 0.31 0.48 0.09 0.06 3.84 28 0.001 S

Fatigue 29 0.72 0.10 0.62 0.46 0.31 0.49 0.08 0.06 6.77 28 0.000 S

ExcessiveSweating 29 0.48 0.17 0.31 0.51 0.38 0.47 0.09 0.07 3.55 28 0.001

S

Frozen Shoulder DATA NOT SUFFICIENT

Pruritis 29 0.24 0.03 0.21 0.44 0.19 0.41 0.08 0.03 2.70 28 0.012 S

Fungal Infection DATA NOT SUFFICIENTNocturnalEnuresis 29 0.24 0.10 0.14 0.44 0.31 0.44 0.08 0.06 1.68 28 0.103

NS


124

OBJECTIVE PARAMETERSTable no.33

GROUPI I Mean

StandardDeviation Standard error

N BT AT

MeanDifference

BT AT

SDDifference

BT AT

t df pResult

FUS 8 13.13 13.00 0.13 35.51 35.16 0.64 0.23 10.66 0.55 7 0.60 Ns

PLUS 8 13.63 13.25 0.38 35.31 35.06 0.58 0.30 0.26 1.82 7 0.11 Ns

FBS 1Wk 11 182.27 162.82 19.45 42.72 38.16 35.11 11.05 10.66 1.84 10 0.10 Ns

FBS 4Wk 11 175.42 153.25 22.17 47.15 44.69 40.98 12.94 13.10 1.87 10 0.09 NsPLBS 1Wk 11 270.18 238.73 31.45 76.51 67.55 73.09 17.34 16.48 1.43 10 0.18 NSPLBS 4Wk 11 262.25 233.75 28.50 77.95 78.07 54.42 18.70 20.79 1.81 10 0.10 Ns

SUBJECTIVE PARAMETERSTable no.34

GROUP I I MeanStandardDeviation Standard error

N BT AT

MeanDifference BT AT

SDDifference BT AT

t df p Result

Excessive thrust 11 0.55 0.09 0.45 0.52 0.30 0.52 0.16 0.09 2.89 10 0.02 SVoraciousAppetite 11 0.09 0.00 0.09 0.30 0.00 0.30 0.09 0.00 1.00

100.34 Ns

Cramps in Legs 11 0.73 0.09 0.64 0.47 0.30 0.50 0.14 0.09 4.18 10 0.00 SFatigue 11 0.73 0.09 0.64 0.47 0.30 0.50 0.14 0.09 4.18 10 0.00 SExcessiveSweating DATA NOT SUFFICIENT

Frozen Shoulder DATA NOT SUFFICIENT

Pruritis DATA NOT SUFFICIENT

Fungal Infection DATA NOT SUFFICIENTNocturnalEnuresis 11 0.45 0.18 0.27 0.52 0.40 0.47 0.16 0.12 1.94 10 0.08 Ns

Comparison of objective parameters between selected subjects of G I & G IITable no.35

Mean Standard DeviationN BT AT BT AT

t df p Result

FBS I Wk 11 30.17 30.50 41.93 34.01 0.00 10.00 0.99 NsFBS 4Wk 12 15.33 44.43 46.31 32.91 0.00 11.00 0.21 NsPLBSIWk 12 2.14 44.33 71.02 63.66 0.00 11.00 0.29 NsPLBS4Wk 13 14.00 56.00 75.21 55.46 0.00 12.00 0.26 Ns


125

NOTE:FUS = Reading of Fasting Urine SugarPLUS = Reading of Post Lunch Urine SugarFBS 1 Wk = Reading of Fasting Urine Sugar after 1st weekFBS 4 WK = Reading of Fasting Urine Sugar after 4th weekPLBS 1 Wk = Reading of Post Lunch Urine Sugar after 1st weekPLBS 4 Wk = Reading of Post Lunch Urine Sugar after 4th weekN = Number of PatientsMean – BT = Mean Reading Before TreatmentMean - AT = Mean Reading After TreatmentMean Diff = Mean differenceStandard Deviation-BT = Standard Deviation before treatmentStandard Deviation- AT = Standard Deviation after treatmentSD Difference = Difference of Standard Deviation before and after treatmentStandard Error – BT = Standard Error before treatmentStandard Error – AT = Standard Error after treatmentt = Student t-test valuedf = degrees of freedomp = Probability of occurrenceResult = ResultsS = SignificantNS = Not significant


126

D I S C U S S I O N

Discussion of the facts, which have emerged from the study, can be done

under following headings; for interpretation of implication of results:

1) Discussion on demographic data

2) Discussion on disease aspect

3) Statistical discussion of parameters

4) Limitations of interpretation & Study.

5) Validating Test Hypothesis

1) Discussion on demographic data:

In the present study, 40 subjects were considered for the research, with 29

subjects in Group- I and 11 subjects in Group – II.

Incidence of the DM:

According to:

Age: 34% of the subjects were in Group 40 – 49 years age group, with 28%

in 30 – 39 years age group showing its prevalence more in the middle age group

(30 – 50).

Gender: Had slightly more incidence in female; with 48% Male and 52%

female, showing male & female had equal incidence of DM.

Religion: More in Hindus 72%, Muslims 28% may be due to increased

dominance of Hindus in this geographical area.

Occupation: The disease was predominant in all occupations with 42.5% in

Housewives and 12.5% in Business people

Socio economic conditions: 55% in poor and 32.5% in middle class &

12.5% in upper middle class. This high incidence in poor & middle class indicate

their varied food habits and their habit of incompatible diet & irregular dietary

habits.


127

Diet: 72.5% have mixed diet, 27.5% are vegetarians

Prakriti: 70% had VK prakriti 20% PK and 10% VP) which is an important

physical factor playing vital role in the Pathogenesis of Madhumeha

vyadhi.

Genetic predisposition: The factor of family history of genetic predisposition

was noted 62.5% with 25% with diabetic history in siblings and 37.5% in

Father or Mother; 37.5% had no family history. This high incidence of

37.5% of no familial history implies other environmental factors are acting

as the predisposing causes for diabetes.

Chronicity of disease: 60% of the subjects had less than one year chronicity and

22.5% 1- 5 years chronicity.

Stress: Stress was observed in 77.5% with 25% under severe Stress condition,

35% moderate, 17.5% mild stress, and only 22.5% subjects had no stress.

DM. In situations like stress, the nervous system stimulates adrenal

medulla to release Epinephrine, which suppresses insulin release. This

implies stress is having a major role in precipitating DM.

BMI: Most of the subjects 69% had BMI ≤30, 10% had BMI ≤32 and only 8%

>32, implies, normal BMI

(2) Discussion on disease aspect

NIDANA

Ahara

57.5% showed high incidence of dadhi as Nidana in madhumeha.

62.5% showed high incidence of Snigdha ahara as Nidana in madhumeha

67.5% showed high incidence of seetala ahara as Nidana in madhumeha

57.5% showed high incidence of katu rasa as Nidana in madhumeha

Vihara:

82.5% shows vidhi varjita sayana, shows the increased globalization is

altered shifts and work effects the people and may be a predisposing factor

to MM.

70% - Diwaswapna


128

60% - Ekasthana rati/ sedentary life styles have worse effects on causing

disease.

75% Vegasandharana, i.e. suppressing natural urges, cry, sorrow, grief,

etc., increases stress and predispose diabetes.

Manasika: 90% subjects present with udvega i.e. physical exertion due to mental

stress and 82.5% shows soka i.e., grief, which had effect on the

insulin secretion.

Purva rupas:

82.5% showed pipasa

70% mukhasosha

57.5% Kantasosha

70% showed swapnabhishanga

72.5% showed sayyabhishanga

70% tandra

52.5% nidra

67.5% alasya

shows states of fatigue / weakness

62.5% Angasupata

57.5% Angeshu sweda

47.5% Panipada daha is because of increased snigdhata & dravata due to

pitta vridhi.

47.5% Seeta priyatwam those are due to increased vata dosha

10% Mutra visragandha is due to sama medodhatu & increased kleda /

fluidity in the body.

10% Durgandha swasa is because of sama kapha

17.5% Dantaadi mala

50% Gurugatrata is because of kapha vridhi & sama rasa

20% Angasaidhilya which occurs due to kapha prakopa & vitiated ojas.

25% Madhurasyata because of kapha vridhi


129

RISK FACTORS: Physical inactivity: (60%),Family History: (62.5%) are

observed in most of the subjects.

(3) Statistical discussion of parameters

Analysis of results

The % difference of the result in the individual subjects in Group I , 2

subjects showed a marginal (0-25%) relief of the symptoms, 2 subjects Mild (25-

50%) relief of the symptoms , 6 subjects Moderate (50-75%) relief of the

symptoms, 5 subjects marked relief (75% & above) and 11 subjects complete

relief (100%).

The % difference of the result in the individual subjects in Group II , 1

subject showed a marginal (0-25%) relief of the symptoms, 0 subjects Mild (25-

50%) relief of the symptoms , 1 subject Moderate (50-75%) relief of the

symptoms, 2 subjects marked relief (75% & above) and 6 subjects complete

relief (100%).

The % difference of the FBS in 1st week in the individual subjects in Group

I, 11 subjects showed a marginal (0-25%) change in FBS levels, 5 subjects Mild

(25-50%) change in FBS, 0 subjects Moderate (50-75%) change in FBS levels, 0

subjects marked change in FBS levels (75% & above) and 0 subjects complete

change in FBS levels (100%) 8 subjects showed no change/raise in FBS levels

The % difference of the FBS in 4th week in the individual subjects in Group

I, 13 subjects showed a marginal (0-25%) change in FBS levels, 7 subjects Mild



change in FBS levels (100%) 6 subjects showed no change/raise in FBS levels.

The % difference of the PLBS in 1st week in the individual subjects in

Group I, 13 subjects showed a marginal (0-25%) change in PLBS levels, subjects

Mild (25-50%) change in PLBS, 0 subjects Moderate (50-75%) change in PLBS

levels, 0 subjects marked change in PLBS levels (75% & above) and 0 subjects


130

complete change in PLBS levels (100%) 11 subjects showed no change/raise in

PLBS levels

The % difference of the PLBS in 4 th week in the individual subjects in

Group I, 11 subjects showed a marginal (0-25%) change in PLBS levels, 5

subjects Mild (25-50%) change in PLBS, 0 subjects Moderate (50-75%) change in

PLBS levels, 0 subjects marked change in PLBS levels (75% & above) and 0

subjects complete change in PLBS levels (100%) 8 subjects showed no change

/raise in PLBS levels.

The % difference of the FBS in 1st week in the individual subjects in Group

II, 5 subjects showed a marginal (0-25%) change in FBS levels, 2 subjects Mild



change in FBS levels (100%) 3 subjects showed no change/raise in FBS levels

The % difference of the FBS in 4th week in the individual subjects in Group

II, 5 subjects showed a marginal (0-25%) change in FBS levels, subjects Mild



change in FBS levels (100%) 2 subjects showed no change/raise in FBS levels.

The % difference of the PLBS in 1st week in the individual subjects in

Group II, 3 subjects showed a marginal (0-25%) change in PLBS levels, 3



subjects complete change in PLBS levels (100%) 4 subjects showed no

change/raise in PLBS levels

The % difference of the PLBS in 4 th week in the individual subjects in

Group II, 4 subjects showed a marginal (0-25%) change in PLBS levels, 4



subjects complete change in PLBS levels (100%) 3 subjects showed no change

/raise in PLBS levels.


131

An important observation among the subjects during treatment (DT) i.e.,

after 30 days showed some undesirable results with completely nil significance in

few and aggravated FBS /PLBS levels in some others. This was attributed to the

untimely intake of the drug or altered dosage of the drug consumed by that

particular subjects

The total study confer that

Group I & Group II have shown remarkable response in treating the

symptoms except Nocturnal enuresis in G I& both nocturnal enuresis & voracious

appetite in G II.

The objective parameters have also shown difference in its results among

Group I & Group II subjects

Group I have shown remarkable response when compared (Group II), in

controlling the fasting & post lunch urine sugars and maintaining the fasting &

post lunch blood sugars.

The drug Uma sambhu ras alone appears to have worked more in combating

the symptoms of Diabetes mellitus & in controlling the fasting & post lunch urine

sugars and maintaining the fasting & post lunch blood sugars than when

associated with Madhu ghritaadi yapana vasti.

Overall, the significant role of the Uma sambhu ras can be attributed to its

Hypo glycaemic action

In the present research the Hypo glycaemic effect was ascertained for a period

of 30 days yielding improved objective parameters FUS ,PLUS,FBS,PLBS.

Though the levels of FUS ,PLUS,FBS,PLBS have not reached completely to

normal in some cases , there is a clear reduction in the elevated levels, after

treatment in G I& G II

(4) Limitations of interpretations & Study

The study scope to assess the Hypo glycaemic property of the drug and

synergic effect of Madhu ghritaadi yapana vasti.definitely needs much more


132

duration and large sample to analyze the complete variations of objective

parameters taken for the study as there is a significant effect on subjective

parameters with in a period of 30 days.

The facility of assessing Glycosylated Hb levels & C peptide levels

periodically is not available so assessment of treatment & raise in Insulin levels

could not be done

Lab test like serum Cholesterol & Triglycerides are not available and so

they are excluded from the study

Future scope for the further study: Same study can be repeated by

taking a large number of samples and longer duration with Glycosylated Hb levels

& C peptide levels interpretation.

(5) Validating Test Hypothesis: Hypothesis is usually considered as a

principal instrument in research. The hypothesis may not be proved absolutely,

but in practice, it is accepted if it has withstood a critical testing.

TESTING HYPOTHESIS IN GROUP-I:

a) Subjective parameters:

1) Excessive thirst:

H0 -There is no effect of uma sambhu ras on excessive thirst in DM.

Ha - There is a significant effect of uma sambhu ras excessive thirst in DM.

p = 0.000

t = 4.22

df = 28

Referring to table values of t at 28 degrees freedom experimental t value (4.22) is

much higher than the highest obtainable value of t at 0.1% level of

significance ( 3.67). Hence H0 is rejected, as the result obtainable by

chance is much less than 0.001(i.e. 1 in 1000).

2) Voracious Appetite:


133

H0 -There is no effect of uma sambhu ras on Voracious Appetite in DM.

Ha - There is a significant effect of uma sambhu ras on Voracious Appetite in

DM.

p = 0.043

t = 2.12

df = 28


much higher than the highest obtainable value of t at 5% level of



3) Cramps in legs:

H0 -There is no effect of uma sambhu ras on Cramps in legs in DM.

Ha - There is a significant effect of uma sambhu ras on Cramps in legs in DM.

p = 0.001

t = 3.84

df = 28


much higher than the highest obtainable value of t at 0.1% level of



4) Fatigue:

H0 -There is no effect of uma sambhu ras on Fatigue in DM.

Ha - There is a significant effect of uma sambhu ras on Fatigue in DM.

p = 0.000

t = 6.77

df = 28

Referring to table values of t at 28 degrees freedom experimental t value (6.77)

is much higher than the highest obtainable value of t at 0.1% level of


134



5) Excessive Sweating:

H0 -There is no effect of uma sambhu ras on Excessive Sweating in DM.

Ha - There is a significant effect of uma sambhu ras on Excessive Sweating in

DM.

p = 0.001

t = 3.55

df = 28


is much higher than the highest obtainable value of t at 1% level of



6) Pruritis:

H0 -There is no effect of uma sambhu ras on Pruritis in DM.

Ha - There is a significant effect of uma sambhu ras on Pruritis in DM.

p = 0.012

t = 2.7

df = 28





7) Frozen Shoulder: Data not sufficient for evaluation

8) Fungal Infection: Data not sufficient for evaluation

9) Nocturnal enuresis:

H0 -There is no effect of uma sambhu ras on Nocturnal enuresis in DM.


135

Ha - There is a significant effect of uma sambhu ras on Nocturnal enuresis in DM.

p = 0.103

t = 1.68

df = 28


is lesser than the highest obtainable value of t at 5% level of significance (

2.05). Hence, H0 is accepted, as the result obtainable by chance is more

than 0.05(i.e. 5 in 100).

b) Objective parameters:

1) Fasting Urine Sugar:

H0 -There is no effect of uma sambhu ras on Fasting Urine Sugar in DM.

Ha - There is a significant effect of uma sambhu ras Fasting Urine Sugar in DM.

p = 0.025

t = 2.39

df = 25





2) Post-lunch Urine Sugar:

H0 -There is no effect of uma sambhu ras on Post-lunch Urine Sugar in DM.

Ha - There is a significant effect of uma sambhu ras on Post-lunch Urine Sugar

in DM.

p = 0.004

t = 3.23

df = 23




136



3) Fasting Blood Sugar (1st Week):

H0 - There is no effect of uma sambhu ras on Fasting Blood Sugar (1st

Week): in DM.

Ha - There is a significant effect of uma sambhu ras on Fasting Blood

Sugar (1st Week): in DM.

p = 0.017

t = 2.57

df = 25





4) Fasting Blood Sugar (4th Week):

H0 - There is no effect of uma sambhu ras on Fasting Blood Sugar (4th

Week) in DM.

Ha - There is a significant effect of uma sambhu ras on Fasting Blood

Sugar (4th Week) in DM.

p = 0.009

t = 2.81

df = 27






137

5) Post Lunch Blood Sugar (1st Week):

H0 - There is no effect of uma sambhu ras on Post Lunch Blood Sugar (1st

Week) in DM.

Ha - There is a significant effect of uma sambhu ras on Post Lunch Blood

Sugar (1st Week) in DM.

p = 0.185

t = 1.36

df = 27


is much lower than the highest obtainable value of t at 5% level of

significance ( 2.05). Hence H0 is accepted, as the result obtainable by

chance is much more than 0.05(i.e. 5 in 100).

6) Post Lunch Blood Sugar (4th Week):

H0 - There is no effect of uma sambhu ras on Post Lunch Blood Sugar (4th

Week) in DM.

Ha - There is a significant effect of uma sambhu ras on Post Lunch Blood

Sugar Week (4th) in DM.

p = 0.008

t = 2.83

df = 29






138

TESTING HYPOTHESIS IN GROUP-II:

a)Subjective parameters:

1) Excessive thirst:

H0 - There is no effect of uma sambhu ras with Madhughritadi yapanavasti

on excessive thirst in DM.

Ha - There is a significant effect of uma sambhu ras with Madhughritadi

yapanavasti excessive thirst in DM.

p = 0.02

t = 2.89

df = 10





2) Voracious Appetite:


on Voracious Appetite in DM.


yapanavasti on Voracious Appetite in DM.

p = 0.34

t = 1.00

df = 10


much lesser than the highest obtainable value of t at 5% level of


chance is much higher than 0.05(i.e. 5 in 100).

3) Cramps in legs:


on Cramps in legs in DM.


139


yapanavasti on Cramps in legs in DM.

p = 0.00

t = 4.18

df = 10





4) Fatigue:

H0 - There is no effect of uma sambhu ras with Madhughritadi yapanavasti on

Fatigue in DM.


yapanavasti on Fatigue in DM.

p = 0.000

t = 4.18

df = 10


is much higher than the highest obtainable value of t at 0.1% level of



5) Excessive Sweating: Data not sufficient for evaluation.

6) Pruritis: Data not sufficient for evaluation.

7) Frozen Shoulder: Data not sufficient for evaluation

8) Fungal Infection: Data not sufficient for evaluation.

9) Nocturnal enuresis:


Nocturnal enuresis in DM.


140


yapanavasti on Nocturnal enuresis in DM.

p = 0.08

t = 1.94

df = 10


is lesser than the highest obtainable value of t at 5% level of significance

(2.23). Hence, H0 is rejected, as the result obtainable by chance is more

than 0.05(i.e. 5 in 100).

b) Objective parameters:

1) Fasting Urine Sugar:


Fasting Urine Sugar in DM.


yapanavasti Fasting Urine Sugar in DM.

p = 0.60

t = 0.55

df = 7


much lower than the highest obtainable value of t at 5% level of



2) Post-lunch Urine Sugar:


Post-lunch Urine Sugar in DM.


yapanavasti on Post-lunch Urine Sugar in DM.

p = 0.11

t = 1.82

df = 7


141







Fasting Blood Sugar (1st Week): in DM.


yapanavasti on Fasting Blood Sugar (1st Week): in DM.

p = 0.10

t = 1.84

df = 10







Fasting Blood Sugar (4 th Week) in DM.


yapanavasti on Fasting Blood Sugar (4th Week) in DM.

p = 0.09

t = 1.87

df = 10


is much lesser than the highest obtainable value of t at 5% level of


142





Post Lunch Blood Sugar (1st Week) in DM.


yapanavasti on Post Lunch Blood Sugar (1st Week) in DM.

p = 0.18

t = 1.43

df = 10







Post Lunch Blood Sugar (4th Week) in DM.


yapanavasti on Post Lunch Blood Sugar (4th Week) in DM.

p = 0.10

t = 1.81

df = 10






143

3) TO TEST THE SIGNIFICANCE OF DIFFERENCE BETWEEN THE

SELECTED SUBJECTS OF GROUP-I AND GROUP-II.

1) Objective parameters:


H0 - There is no real difference between the effect of uma sambhu ras (Group-

I) and the effect of uma sambhu ras with Madhughritadi yapanavasti (Group-II)

on Fasting Blood Sugar (1st Week): in DM.

Ha - There is a significant difference between the effect of uma sambhu ras

(Group-I) and effect of uma sambhu ras with Madhughritadi yapanavasti (Group-

II) on Fasting Blood Sugar (1st Week): in DM.

p = 0.99

t = 0*

df = 10

Referring to table values of t at 10 degrees freedom experimental t value (0) is


significance ( 2.23). Hence H0 is accepted, as the difference obtainable by





on Fasting Blood Sugar (4th Week) in DM.

Ha - There is a significant difference between the effect of uma sambhu

ras (Group-I) and effect of uma sambhu ras with Madhughritadi

yapanavasti(Group-II) on Fasting Blood Sugar (4 th Week) in DM.

p = 0.21

t = 0*

df = 11


144


much lesser than the highest obtainable value of t at 5% level of


chance is much more than 0.05( i.e. 5 in 100).




on Post Lunch Blood Sugar (1st Week) in DM.


ras (Group-I) and effect of uma sambhu ras with Madhughritadi yapanavasti

(Group-II) on Post Lunch Blood Sugar (1st Week) in DM.

p = 0.29

t = 0*

df = 11








on Post Lunch Blood Sugar (4th Week) in DM.


ras (Group-I) and effect of uma sambhu ras with Madhughritadi

yapanavasti(Group-II) on Post Lunch Blood Sugar (4th Week) in DM.


145

p = 0.26

t = 0*

df = 12





(*NOTE: Since the experimental t value in the above case is negative, the t

value has been taken as ‘0’.)


146

C O N C L U S I O N

1. Madhumeha is a Vata kapha disorder, characterized by Madhusamam mehana

(Glycosuria) and Madhuryaccha tanorath (Hyper Glycaemia).

2. The Doshic entities in Madhumeha are vyana vata, samana vata and apana vata

and Bahudrava sleshma includes kledaka kapha.

3. It is a metabolic disorder involving all the three agnis – Jataragni, Bhutagni and

Dhatwagni.

4. Sarva dhatus kshayam and ojas vikara are mainly observed in Madhumeha with

circulating medo mamsa dhatus which, when enter vasti precipitate madhumeha.

5. The prevalence of Diabetes Mellitus is more in people aged 30 – 50 years i.e.

middle age.

6. The incidence is equal in both Male & Female indicating equal risk in both

genders.

7. Role of religion socio economic status and occupation could not be explored in

the incidence of Madhumeha, however,

8. Madhumeha is more prevalent in persons with Vata kapha prakriti as Madhumeha

is Vata kapha disorder.

9. Equally prevalent in people with or without familial intervention / known history.

10. More prevalent in people having mixed diet than having Vegetarian diet (3:1)

11. BMI could find no inreference as subjects with BMI ≤25 are more prevalence

with Diabetes Mellitus.

12. Stress was found to have more impact on precipitating Diabetes Mellitus as 3 in 4

had stress as one of the factors. Regarding Nidana – Katu, amla are seen in most

of patients than the madhura rasa.

13. Dadhi was observed being the more common nidana in many patients.

14. Guru, Snigdha ahara, seetala are equally noted.

15. Sedentary life styles and altered life styles, Ekastana rati, vidhivarjita sayana and

diwa swapna are observed in most of the cases.


147

16. Psychological factors like udvega and soka were observed in 80% to 90%

subjects, in age group 30-50 confirming the role of psychological factors in

precipitating Madhumeha / Diabetes Mellitus in middle age more predominant.

17. Sayyabhishanga, swapana bhishanga, nidra and tandra were commonly observed

purva rupa in more than 50% cases (30 – 40 years age group) showing the

lethargic state of Diabetes Mellitus patients.

18. Mukha sosha, Kanta sosha and pipasa are also equally observed in age group 30-

60 years.

19. Panipada daha and anga suptata were observed in age group 30 – 50 years.

20. Samprapti of Madhumeha is a complex mechanism, which confirms the present

knowledge of pathogenesis of Diabetes Mellitus.

21. Lakshanas are due to circulating ama doshas (medo mamsa), along with ama rasa

and kapha.

22. Chikitsa mentioned in classic gave equal importance to role of diet, exercise and

medicine in treating Madhumeha.


148

SUMMARY

The Present Study entitled ‘a study on the effect of Uma Sambhu ras with

Madhughritadi yapanavasti in management of prameha was to Madhumeha,

comprises of an introductory part followed by historical literary and drug review,

methodology observation results discussion, conclusion and summary.

Diabetes Mellitus vis-à-vis madhumeha is a global problem, increasing

with urbanization and changing life styles.

Madhumeha is a disorder causing Glycosuria and hyperglycemia, if not

treated in time, can cause many micro/macro vascular complications.

Stress, diet, sedentary lifestyles are playing a major role in precipitating

Diabetes Mellitus.

The present study intended to focus on disease evaluation i.e. madhumeha

and diabetes Mellitus and management with uma sambu ras internally and

madhugrutadi yapanvasti. Vagbhata mentioned Umasambhuras in Rasa ratna

samucchaya in prameha chikista and madhugrutadi yapanvasti by Charaka in

Sidhistana 12th Chapter.

The aim of the study was to evaluate the hypo glycaemic effect of Uma

sambu ras and synergic effect of madhugrutadi yapanavasi when given with

umasambhuras. Two groups were selected to evaluate the treatment plan.

The evaluation was done for objective parameters after 1st and 4th week

and subjective parameters after 4th week. There was a significant relief in subject

parameters in both groups except for nocturnal enuresis.

The symptoms Cramps in legs and fatigue significantly improved in both

the Groups.

The data was insufficient to evaluate frozen shoulder, fungal infection,

excessive sweating.

The objective parameters Fasting Urine Sugar, Post Lunch Urine Sugar,

when evaluated after 4 th week showed significant results in Group-I and no

significant results in Group-II.


149

The objective parameters Fasting Blood Sugar showed significant

improvement after 1st and 4th week in Group-I and no significant results in Group-

II.

The objective parameters Post Lunch Blood Sugar showed significant

improvement after 4th week and no significant results after 1st week in Group-I.

The objective parameters Post Lunch Blood Sugar showed no significant

improvement after 1st and 4th week in Group-II.

When the results of selected subjects of Group-I and Group-II are

compared, no significant difference was observed in Fasting Blood Sugar and

Post Lunch Blood Sugar levels after 1st and 4th week.

It is therefore evident that umasambhu ras is a potent fast acting hypo

glycaemic drug with no adverse affects observed.

Madhugrutadi yapanvasti, showed significant results in improving

subjective parameters and hence it is felt that long-term evaluation of the

objective parameters may give significant results.


150

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112. Indradev Tripati,Shodala,Gadanigraham, 1st edition,1969, Chowkhambha

Sanskrit samstan, Varanasi, pp 658

113. K.Krishna Das Sresti, Vangasena, 1st edition,1976,Sri Venkateswara press,

Mumbai,

pp 486

114. P.Suryanarayana ,Basavaraj’s Basavarajeeyam,9chapter, 1st

ed, 1998,A.B.S.

publication,Rajamundry ,pp 427,428


33,publication no158 Chowkhambha prakashan, 1998,pp 235

116. Aridev gupta edited Vagbhata, Astanga Hridaya Nidana 10/1,2,3 publication

no 150,, chowkhambha Sanskrit sansthan, varanasi, pp 253

117. Susruta, Susruta Samhita Nidana 6/2,Vavilla rama swamy sastrulu

&sons,Chennai 1953 , p. 55,

118. Ravi Datta Shastri ed, Hareeta, Hareeta Samhita, Truteeya sthan , 28 chapter

1st

ed, 1984, Prachya Prakashan, Vranasi, pp 385


ed, 1998,A.B.S.

publication,Rajamundry ,pp 427,428

120 Agnivesa, Charaka Samhita sutra sthana 27/5. Vavilla rama swamy sastrulu

&sons,Chennai 1937 p. 652,


&sons,Chennai 1937 pp. 605





124 Agnivesa, Charaka Samhita sutra sthana 23/65,66. Vavilla rama swamy

sastrulu &sons,Chennai 1937 pp. 607,608




&sons,Chennai 1937 pp. 725,


158



128 K.C.Chunekar,Bhavamisra’s Bhava prakasa Nighantu,1st edition,1979,

publication no 28, chowkhambha Sanskrit sansthan, varanasi, pp 253



130 Aridev gupta edited Vagbhata, Astanga Hridaya sutra sthana 5/29-

32,publication no 150,, chowkhambha Sanskrit sansthan, varanasi, pp44

131 Aridev gupta edited Vagbhata, Astanga Hridaya Nidana 16/27,28, publication



&sons,Chennai 1937 pp478,

133 Aridev gupta edited Vagbhata, Astanga Hridaya Nidana 16/25,26publication


134 Sri. Taranatha Tarkavachaspathi,Vachaspatyam,vol 1,work no 94,1962,

chowkhambha Sanskrit sansthan, varanasi,



136. Agnivesa, Charaka Samhita sutra sthana 1/66. Vavilla rama swamy sastrulu


137.V.V.SubhramanyaSastry, TridoshaTheory,supplement to Ayurveda

seminar,1977,Arya vaidyasala Kottakkal,pp.107

138 ibid pp.108

139. ibid pp.109

140 ibid pp.111

141. ibid pp.125

142 ibid pp.127,128

143 . Chakrapani datta, Ayurveda Deepika 1st edition 1949..Choukhambha Sanskrit

Series,Varanasi, pp 213

144 V.V.SubhramanyaSastry, TridoshaTheory,supplement to Ayurveda

seminar,1977,Arya vaidyasala Kottakkal,pp.41,42


159

145 ibid pp.42

146 ibid pp.41,42

147. ibid pp.49

148. ibid pp.53

149. ibid pp.46

150. ibid pp.47

151. ibid pp.47

152. Agnivesa, Charaka Samhita nidana sthana 4/8. Vavilla rama swamy sastrulu

&sons,Chennai 1937 p. 65

153. Chakrapani datta, Ayurveda Deepika 1st edition 1949..Choukhambha Sanskrit


154. Agnivesa, Charaka Samhita nidana sthana 4/36-40. Vavilla rama swamy

sastrulu &sons,Chennai 1937 p. 75

155. S.Suresh Babu, Kaya chikitsa, 1st edition,2001, Chaukhambha

orientalia,varanasi,pp162

156. ibid. pp.162

157. Vizag links Obesity to Diabetes,Deccan Chronicle dt. December 22,2007,pg 1

158. Chakrapani data,Ayurveda Deepika ,1st edition 1949,Choukhambha Sanskrit

Series,Varanasi,pp 445

159.V.V.SubhramanyaSastry, TridoshaTheory,supplement to Ayurveda

seminar,1977,Arya vaidyasala Kottakkal,pp.122

160. ibid pp.123

161. ibid pp.124

162. Agnivesa, Charaka Samhita vimana sthana 5/12. Vavilla rama swamy sastrulu


163. Susruta, Susruta Samhita sareera sthana, chapter 9 1st

ed, 1989,A.B.S.


164. Parishadyam Sabdhartha sareeram, 2nd edition, 1979,Sree Bhaidhyanath

Ayurveda Bhavan , publication,nagpur,pp101


160

165. Best & Taylor,Physiological basis of medical practice ,11 th edition,1981,

Williams & Wilkins ,London.,pp 438

166. A.C.Ritchie,Boyd’s Text book of Pathology, 9th edition,1990,Lea &

Febiger,London,pp.1213

167. Malcolm Nattrass,Malin’s Clinical Diabetes,2nd edition,1996,Champman&Hall


Britian,pp6


Febiger,London,pp.1213

169 Cotran Kumar Collins ed, Robbin’s Pathologic basis of disease, 4th

ed, 1989,

Saunders the Curtis center, Philadelphia, p998

170 Malcolm Nattrass,Malin’s Clinical Diabetes,2nd edition,1996,Champman&Hall


Britian,pp11

171 ibid,pp.12

172 Cotran Kumar Collins ed, Robbin’s Pathologic basis of disease, 4th

ed, 1989,


173 ibid,pp.997

174 Harsh Mohan’s Pathology quick review,2nd ed,2006 reprint ,jaypee

brothers,medical pub, new delhi, India ,pp. 162

175. Peter J. Watkins, et.al Diabetes and Its Management,6th edition,2003,Blackwell


176. ibid,pp.44



Britian,pp16





Britian,pp17


161

180. ibid,pp.17

181 ibid,pp.18

182 Satyanarayana,Biochemistry,chapter 36,3rd edition2006,Books & allied

pvt.ltd,kolkata



Britian,pp18

184. Agnivesa, Charaka Samhita nidana sthana 4/52,53. Vavilla rama swamy sastrulu




186. Agnivesa, Charaka Samhita nidana 4/49.Vavilla rama swamy sastrulu


187. Susruta, Susruta Samhita Nidana 6/4,Vavilla rama swamy sastrulu &sons,Chennai

1953 , p. 55




33/1,publication no158 Chowkhambha prakashan, 1998,pp 1


ed, 1998,A.B.S.



khanda chapter 24, 1938, Panditaraya publication, ,pp636,637

192. . Lakshmipathi Sastri, Yogaratnakara, Prameha Nidana, Chowkhambha Sanskrit

samstan, Varanasi, 1973, pp 76


Mumbai,

pp 486

194. Indradev Tripati,Shodala,Gadanigraham, 1st edition,1969, Chowkhambha Sanskrit

samstan, Varanasi, pp 658


162





197. Susruta, Susruta Samhita Nidana 6, Dalhana , p.290

198. V.Sharma,Vagbhata Rasa Ratna Samucchaya, Uttara khanda , Prameha Chikitsa

1st

ed, 1963, IMPCOPS publication,Chennai,pp 127


ed, 1998,A.B.S.


200. Susruta, Susruta Samhita Nidana 6/4,Vavilla rama swamy sastrulu

&sons,Chennai 1953 , p. 55

201. Susruta, Susruta Samhita chikitsa 11,Vavilla rama swamy sastrulu


202. Chakrapani datta Ayurveda Deepika1st edition 1949,Choukhambha Sanskrit


203. Susruta, Susruta Samhita Nidana 6, Dalhana , p.292


khanda chapter 24, 1938, Panditaraya publication, ,pp638

Lakshmipathi Sastri, Yogaratnakara, Prameha Nidana, Chowkhambha Sanskrit


Indradev Tripati,Shodala,Gadanigraham, 1st edition,1969, Chowkhambha


Sudarshansastry, Madhava Nidana IIvol, Vijayarakshita- madhukosha,


205. Agnivesa, Charaka Samhita nidana sthana 4/37-40. Vavilla rama swamy


206. Agnivesa, Charaka Samhita nidana sthana 4/46 Vavilla rama swamy sastrulu


207. Agnivesa, Charaka Samhita chikitsa sthana 6/11. Vavilla rama swamy sastrulu



163





Britian,pp67

210 Peter J. Watkins, et.al Diabetes and Its Management,6th edition,2003,Blackwell




Britian,pp67

212 Malcolm Nattrass,Malin’s Clinical Diabetes,2nd edition,1996,Champman&Hall


Britian,pp68





Britian,pp69

215. E.C.Warner,Savill’s Clinical Medicine,14th edition,1st Indian edition

reprint,1988,CBS Publishers,Newdelhi,pp587

216. Peter J. Watkins, et.al Diabetes and Its Management,6 th edition,2003,Blackwell


217. E.C.Warner,Savill’s Clinical Medicine,14th edition,1st Indian edition

reprint,1988,CBS Publishers,Newdelhi,pp587



Britian,pp69,70

219. P.V. Sharma, Agnivesa, Charaka Samhita vol 2,6th edition,

2001,Chaukhambha orientalia; Varanasi:, pp295




164



Susruta, Susruta Samhita chikitsa 11/3,Vavilla rama swamy sastrulu


222. Agnivesa, Charaka Samhita chikitsa sthana 6/14. Vavilla rama swamy


223. P.V. Sharma, Agnivesa, Charaka Samhita critical notes, 6th edition,


224. Agnivesa, Charaka Samhita chikitsa sthana 6/52. Vavilla rama swamy


Aridev gupta edited Vagbhata, Astanga Hridaya Nidana 10/40 publication no


225. Agnivesa, Charaka Samhita sutra sthana 17/77-80. Vavilla rama swamy

sastrulu &sons,Chennai 1937 p. 399,



press.pp9.51-9.58


Febiger,London,pp.1212-1217





230. Agnivesa, Charaka Samhita nidana sthana 4/14,19. Vavilla rama swamy

sastrulu &sons,Chennai 1937 p. 70,71


Oxford Medical Publications, pp508

232. Cotran Kumar Collins ed, Robbin’s Pathologic basis of disease, 4th

ed, 1989,





165

Susruta, Susruta Samhita Nidana 6/27,Vavilla rama swamy sastrulu


234. P.V. Sharma, Agnivesa, Charaka Samhita critical notes, 6th edition,




236. Susruta, Susruta Samhita sutra 33/7,Vavilla rama swamy sastrulu


Susruta, Susruta Samhita nidana 6/24,Vavilla rama swamy sastrulu


237. Susruta, Susruta Samhita sutra 33/3,4,5,Vavilla rama swamy sastrulu




239. .S.Venkata Subhramanya sastry,& Rajarajeshwar Sharma,Bhela Samhita,

Chikitsa 7/3, 1977 CCRIM Pub 31,pp 279

240. Susruta, Susruta Samhita nidana 6/13,Vavilla rama swamy sastrulu




242. Sudarshansastry, Madhava Nidana IIvol, Vijayarakshita- madhukosha, 33/1,15

,publication no158 Chowkhambha prakashan, 1998,pp 1-14



244. Lakshmipathi Sastri, Yogaratnakara, Prameha Nidana, Chowkhambha Sanskrit



ed, 1998,A.B.S.





166


Mumbai, pp 488

248. Agnivesa, Charaka Samhita nidana sthana 17/81,82. Vavilla rama swamy

sastrulu &sons,Chennai 1937 pp.400.

249. Susruta, Susruta Samhita nidana 6/14,Vavilla rama swamy sastrulu

&sons,Chennai 1953 , pp. 61

Aridev gupta edited Vagbhata, Astanga Hridaya Nidana 10/25,26 publication




press.pp9.64,9.65

251. ibid.pp.9.79



Britian,pp269

253. ibid.pp270

254. ibid.pp276-278

255. ibid.pp281-283



257. ibid.pp.155

258. ibid.pp.157

259. MalcolmNattrass,Malin’sClinicalDiabetes,2nd edition,1996,Champman&Hall

Medical publications,Cambridge university press.Cambridge ,Great

Britian,pp329,333

260. ibid.pp.337



press.pp9.89

262. ibid.pp.9.91


167

263. Agnivesa, Charaka Samhita indriya sthana 5/16,17. Vavilla rama swamy


264. Ravi Datta Shastri ed, Hareeta, Hareeta Samhita, Truteeya sthan , 28 chapter

1st

ed, 1984, Prachya Prakashan, Vranasi, pp 205

265. Agnivesa, Charaka Samhita indriya sthana 9/8,9. Vavilla rama swamy sastrulu




267. Susruta, Susruta Samhita sutra 29/68,Vavilla rama swamy sastrulu

&sons,Chennai 1953 , pp

268. Agnivesa, Charaka Samhita indriya sthana 9/8,9. Vavilla rama swamy sastrulu


269. Agnivesa, Charaka Samhita vimana sthana 7/. Vavilla rama swamy sastrulu

&sons,Chennai 1937

270. Susruta, Susruta Samhita chikitsa 11/33,Vavilla rama swamy sastrulu

&sons,Chennai 1953 , pp188,189


&sons,Chennai 1953 , pp188,189


&sons,Chennai 1937 p. 326,327


&sons,Chennai 1937 p.327



275. Agnivesa, Charaka Samhita chikitsa sthana 6/22-24. Vavilla rama swamy




Susruta, Susruta Samhita chikitsa 11/4,Vavilla rama swamy sastrulu

&sons,Chennai 1953 , pp181


168

277. Agnivesa, Charaka Samhita chikitsa sthana 6/25 Vavilla rama swamy sastrulu


278. Agnivesa, Charaka Samhita chikitsa sthana 6/33,34 Vavilla rama swamy



&sons,Chennai 1953 , pp181

280. Susruta, Susruta Samhita chikitsa 12,Vavilla rama swamy sastrulu

&sons,Chennai 1953


&sons,Chennai 1953 , pp194.

282 Mukkamala venkata sastry translated, Bhava misra,Bhavaprakasha madhyama


283. Jagadeswar Prasad Tripati,Chakrapani datta, Chakra datta,35/6, 3rd

edition,1961 Chowkhambha Sanskrit samstan, Varanasi, pp292





286. Susruta, Susruta Samhita chikitsa 11/15Vavilla rama swamy sastrulu


287 Mukkamala venkata sastry translated, Bhava misra,Bhavaprakasha madhyama


288.Jagadeswar Prasad Tripati,Chakrapani datta, Chakra datta,35/6, 3rd

edition,1961 Chowkhambha Sanskrit samstan, Varanasi, pp297





291. Susruta, Susruta Samhita chikitsa 11/15Vavilla rama swamy sastrulu



169



press.pp9.65

293. ibid. 9.65

294. ibid. 9.67,68

295. ibid. 9.76

296. ibid. 9.66

297. ibid. 9.76

298. ibid. 9.76

299. Peter J. Watkins, et.al Diabetes and Its Management,6 th edition,2003,Blackwell


300. V.Sharma,Vagbhata Rasa Ratna Samucchaya, Uttara khanda , Prameha

Chikitsa 1st

edition, 1963, IMPCOPS publication,Chennai,pp 127

301. Siddhinandan misra,Ayurvedeeya rasasastra, publication no.32, 1st

edition,1981 Chowkhambha orientalia, Varanasi, , pp367

302. ibid.

303. ibid.

304. K.C.Chunekar,Bhavamisra’s Bhava prakasa Nighantu,1st edition,1979,

publication no 28, chowkhambha Sanskrit sansthan, varanasi

305. Nadkarni.K.M., Indian materia medica, Vol.I & II, 3rd Edition,1982 Popular

book Depot, Bombay.

306. Agnivesa, Charaka Samhita siddhi sthana 12/51 Vavilla rama swamy sastrulu


307. Lakshmipathi Sastri, Yogaratnakara, Prameha Nidana, 5 sloka, Chowkhambha







170


171

s.no

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1 1 1 2763 V.S.SASTRY 42 M Advocate Hindu 2 2 1 1 3 1.58 72 28.84 422 1 1 2948 S.Padmavati 42 F Student Hindu 2 3 1 1 3 1.62 86 32.77 423 1 3 5541 Nazeersultana 55 F Housewife Muslim 1 1 0 2 1 1.58 60 24.03 534 1 1 6427 I.V.Reddy 52 M Business Hindu 2 0 0 1 2 1.61 85 32.79 515 1 1 7779 G.Venkatesh 44 M Business Hindu 2 1 1 1 2 1.86 75 21.68 446 1 3 24200 K.Ammaji 38 F Housewife Hindu 1 3 1 3 1 1.51 57 25.00 307 1 2 9623 SurayyaBegum 42 F Factoryworker Muslim 1 2 2 1 3 1.58 50 20.03 42

8 1 1 2097 Y.V.S.Rao 33 M SalesEngineer Hindu 2 2 1 2 2 1.55 74 30.80 30

9 1 1 5499 ST.Nirmala 38 F Housewife Hindu 1 2 0 1 2 1.45 38 18.31 3810 1 3 3189 Md.Begum 40 F Housewife Muslim 1 3 2 1 2 1.51 50 21.93 4011 1 1 12379 JaffriBegum 38 F Housewife Muslim 2 3 2 1 3 1.51 69 30.26 3812 1 5 5456 Jayaprakash 56 M Asst.proffesor Hindu 3 1 0 6 1 1.69 64 22.41 2913 1 3 14564 P.Umapaty 35 M Business Hindu 2 2 0 3 3 1.73 81 27.06 2914 1 1 13608 V.Nirmala 57 F Housewife Hindu 3 3 1 1 3 1.58 61 24.44 5715 1 1 389 P.Indira 35 F Housewife Hindu 1 2 1 1 3 1.56 40 16.44 3516 1 5 16033 T.Srinivasulu 40 M Artist Hindu 3 3 2 1 3 1.69 62 21.71 4017 1 3 12736 C.Nagender 40 M Mason Hindu 1 2 0 2 2 1.65 67 24.61 35

18 1 1 14886 Noorjahan 49 F Housewife Muslim 1 0 1 1 3 1.57 75 30.43 49

19 1 4 15861 K N Rao 48 M Business Hindu 3 3 0 5 3 1.7 65 22.49 3020 1 3 14244 Umadevi 44 F Tailor Hindu 1 1 1 2 3 1.59 63 24.92 4121 1 5 19938 R Seshagirirao 63 M Rtd.Supdt Hindu 1 0 2 6 3 1.81 76 23.20 3622 1 1 21522 Md.Yasin 58 M Rtd.Attender Muslim 1 1 0 1 3 1.58 62 24.84 5823 1 1 19836 M G Rao 64 M Rtd.Supdt Hindu 2 1 0 3 3 1.71 68 23.26 5824 1 1 21704 YasmeenAtiya 30 F Housewife Muslim 2 0 1 1 3 1.58 67 26.84 3025 1 2 22915 AneezBegem 57 F Housewife Muslim 2 0 2 2 3 1.58 90 36.05 5326 1 1 21735 B Ganesh 46 M Attender Hindu 1 1 0 1 3 1.66 65 23.59 4627 1 1 23172 Amruthamma 55 F Housewife Hindu 2 3 2 1 3 1.48 53 24.20 55

28 1 1 24875 Laxminarayana 60 m Labourer Hindu 1 0 0 1 3 1.58 65 26.04 60

29 2 3 11465 Lalitha 52 F Labourer Hindu 1 3 2 2 3 1.53 50 21.36 5030 2 1 2097 Y.V.S.Rao 33 M SalesEngineer Hindu 2 2 1 2 2 1.55 74 30.80 3031 2 1 5499 ST.Nirmala 38 F Housewife Hindu 1 2 0 1 2 1.45 38 18.31 3832 2 1 1861 Jyoti 27 F Housewife Hindu 1 3 0 1 1 1.56 52 21.37 2733 2 1 15425 Farzanabegum 40 F Housewife Muslim 1 2 2 2 3 1.49 55 24.77 3834 2 1 17052 T.Anasuya 38 F Housewife Hindu 1 2 1 1 3 1.42 55 27.28 3835 2 3 15504 Kousalya 48 F Housewife Hindu 1 0 2 2 3 1.52 57 24.67 4536 2 2 21570 Chandrasekhar 39 M Business Hindu 3 2 2 3 3 1.74 71 23.45 3337 2 4 22319 P.V.Lakshmi 43 F Housewife Hindu 1 2 0 1 3 1.64 61 22.68 43

38 2 3 23192 Raju 50 M Mason Hindu 1 0 1 1 3 1.65 62 22.77 49

39 2 1 21404 R.Venkatrao 60 M Tailor Hindu 1 0 2 1 3 1.58 58 23.23 6040 1 2 22753 N.Srinivasrao 58 M Rtd. Clerk Hindu 2 2 0 1 3 1.55 58 24.14 58

MASTER CHART

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1 0 0 0 0 1 1 1 0 0 0 1 1 0 0 1 0 0 1 0 0 0 1 1 0 0 0 0 0 1 0 0 0 0 0 0 0 0 02 0 0 0 0 0 0 1 0 1 0 1 1 0 1 1 0 1 0 1 0 0 1 1 0 0 0 0 0 0 0 0 0 1 0 1 0 0 03 1 0 0 0 1 1 1 0 0 0 1 0 1 1 1 0 1 1 0 0 0 1 1 0 0 0 0 0 1 1 1 1 0 0 0 0 0 04 0 0 0 0 1 0 0 0 0 0 1 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 0 0 05 0 0 0 0 0 1 1 1 0 0 0 0 1 1 1 1 1 0 0 0 0 1 1 1 1 1 0 0 1 0 1 0 0 0 1 0 0 06 1 0 0 1 0 0 1 1 0 0 0 0 1 1 1 1 1 1 0 0 0 1 2 0 0 0 1 0 1 0 1 0 0 0 0 0 0 07 0 0 0 0 0 1 0 0 0 0 1 1 1 1 1 1 1 1 0 0 0 1 1 1 1 1 1 1 1 1 1 1 0 0 1 0 0 08 0 0 0 0 0 1 1 1 1 0 1 1 0 0 1 1 1 0 0 0 0 0 1 0 0 0 1 1 1 0 1 0 0 0 0 0 0 09 1 0 0 1 1 1 1 0 1 0 0 1 1 1 1 0 0 1 0 0 0 0 1 0 0 0 0 0 1 0 0 0 0 0 0 0 0 0

10 1 0 0 0 0 0 1 0 0 0 1 1 0 1 1 0 1 1 0 0 0 1 1 0 0 0 1 0 1 0 1 0 0 0 0 0 0 011 1 0 0 1 1 1 1 1 1 1 1 0 0 0 0 0 0 1 0 0 0 1 0 0 0 0 1 0 1 0 0 0 0 0 1 0 0 012 0 0 0 1 0 0 0 1 0 0 1 1 1 0 1 1 1 0 1 0 1 1 1 1 0 0 0 0 1 0 0 0 0 0 0 0 0 013 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 0 0 0 0 1 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 014 0 0 0 0 1 1 0 0 0 1 1 1 0 1 1 1 0 0 0 0 0 1 0 0 1 0 0 0 1 0 1 0 0 0 1 0 0 015 0 0 1 0 1 1 1 0 0 0 1 1 0 1 1 0 0 0 0 0 0 0 1 1 0 0 0 0 0 0 0 0 0 0 0 0 0 016 0 0 0 0 1 1 1 1 0 0 1 1 1 1 1 1 1 0 1 0 0 1 1 0 0 0 1 0 1 0 1 0 0 0 0 0 0 017 0 0 0 0 0 0 1 1 0 0 1 1 0 0 0 0 1 0 1 0 0 0 0 0 0 0 0 0 1 1 1 1 0 0 0 0 0 018 0 0 0 1 1 1 0 0 0 0 1 1 1 1 1 1 1 1 0 0 0 1 1 0 1 0 1 1 1 0 0 0 0 0 0 0 0 019 0 0 1 0 0 0 1 0 0 0 1 1 1 1 1 0 1 1 0 0 0 1 0 0 0 0 0 0 1 0 1 1 0 0 0 0 0 020 0 0 0 1 0 1 1 1 0 0 1 1 0 1 0 0 0 1 0 0 0 1 0 0 1 0 1 0 1 0 0 0 0 0 1 1 0 021 0 0 0 1 0 1 0 1 0 1 0 0 1 1 1 0 0 1 0 0 0 1 0 0 0 0 0 0 1 0 0 0 0 0 0 0 0 022 0 0 0 0 1 1 1 1 0 0 1 1 1 1 1 1 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 023 0 0 0 1 0 1 1 0 0 0 1 1 1 1 1 0 0 0 0 0 1 0 0 0 0 0 0 0 0 0 1 0 0 0 0 0 0 024 0 0 0 1 1 1 0 1 0 0 1 1 1 1 1 1 1 1 0 0 1 1 0 0 0 0 1 0 0 0 0 0 0 0 0 0 0 025 0 0 0 1 0 1 1 1 0 0 1 1 1 0 1 1 1 1 0 0 0 1 1 0 0 0 0 0 1 0 1 1 0 0 0 0 0 026 0 0 0 1 0 0 0 1 0 0 0 0 1 1 1 0 1 1 0 0 0 0 1 0 1 0 1 0 1 0 1 0 0 0 0 0 0 027 0 0 0 1 1 1 1 0 0 0 1 1 0 1 1 0 0 0 0 0 0 0 0 0 0 0 1 0 1 0 0 0 0 0 0 0 0 028 1 0 0 1 1 1 1 0 0 0 0 0 1 1 1 1 1 0 0 0 1 1 1 0 0 0 1 0 1 0 1 0 0 0 0 0 0 029 0 0 0 1 1 1 0 0 0 1 1 0 0 1 0 0 1 0 0 0 1 1 0 0 0 0 0 1 0 0 0 0 0 0 0 0 0 030 0 0 0 0 0 1 0 1 0 1 1 0 1 1 0 1 0 1 0 0 1 1 0 0 0 0 0 0 0 0 0 1 0 1 0 0 0 031 0 0 0 1 1 1 0 0 0 1 0 1 1 1 0 1 1 0 0 0 1 1 0 0 0 0 0 1 1 1 1 0 0 0 0 0 0 032 0 0 0 1 0 0 0 0 0 1 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 0 0 0 033 0 0 0 0 1 1 1 0 0 0 0 1 1 1 1 1 0 0 0 0 1 1 1 1 1 0 0 1 0 1 0 0 0 1 0 0 0 034 0 0 1 0 0 1 1 0 0 0 0 1 1 1 1 1 1 0 0 0 1 2 0 0 0 1 0 1 0 1 0 0 0 0 0 0 0 035 0 0 0 0 1 0 0 0 0 1 1 1 1 1 1 1 1 0 0 0 1 1 1 1 1 1 1 1 1 1 1 0 0 1 0 0 0 036 0 0 0 0 1 1 1 1 0 1 1 0 0 1 1 1 0 0 0 0 0 1 0 0 0 1 1 1 0 1 0 0 0 0 0 0 0 037 0 0 1 1 1 1 0 1 0 0 1 1 1 1 0 0 1 0 0 0 0 1 0 0 0 0 0 1 0 0 0 0 0 0 0 0 0 038 0 0 0 0 0 1 0 0 0 1 1 0 1 1 0 1 1 0 0 0 1 1 0 0 0 1 0 1 0 1 0 0 0 0 0 0 0 039 0 0 1 1 1 1 1 1 1 1 0 0 0 0 0 0 1 0 0 0 1 0 0 0 0 1 0 1 0 0 0 0 0 1 0 0 0 040 0 0 1 0 0 0 1 0 0 1 1 1 0 1 1 1 0 1 0 1 1 1 1 0 0 0 0 1 0 0 0 0 0 0 0 0 0 0

OBJECTIVE PARAMETERSSl

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NE FUS PLUS FBS PLBS1 1 0 0 0 1.5 0 145 100 90 296 205 1752 1 1 1 0 1 0.5 195 150 135 290 310 2053 0 1 1 1 2 1.5 201 191 190 312 264 2554 0 0 0 0 1 0.5 120 105 105 200 155 1505 0 0 0 0 0.5 0.5 160 120 100 265 205 1906 0 0 1 1 1 1 235 136 220 285 203 3357 0 0 1.5 0 2 0.5 125 132 215 2548 0 0 209 172 160 284 334 2349 1 0 0 0.5 0 0 155 150 100 260 302 175

10 0 0 140 200 295 275 28511 0 0 0.5 0 0.5 0 105 115 180 17012 0 0 85 99 139 155 16013 0 0 0 0 1 1.5 127 154 200 212 290 33014 1 0 0.5 0 2 0 161 201 173 247 258 22015 0 0 1 0.5 180 190 100 290 240 20516 1 1 1 0.5 1.5 1 230 180 165 330 290 24017 0 0 1 1 1.5 1.5 110 140 160 200 340 29018 1 0 0 0 127 95 110 210 190 23019 0 0 0 0 0 0 100 110 100 146 152 14220 0 0 0 0 0.5 0.5 126 99 110 215 242 18421 0 0 0 0 1 0 182 150 140 256 200 19022 0 0 128 120 200 175 15023 0 0 0.5 0 1.5 0 240 120 140 315 240 20824 0 0 0 0 0 0 137 135 90 184 161 14025 0 0 0.5 1 1 1.5 190 195 240 270 285 30026 0 0 1 0.5 1.5 1 240 255 200 380 320 27027 0 0 0 0 0 0 135 100 108 183 160 15028 0 0 0 0 0 0 120 80 90 250 140 16029 1 1 1 0.5 1.5 1.5 225 190 200 330 345 34030 0 0 139 126 118 225 213 20631 1 0 0 0.5 0 0 100 100 175 15032 1 0 1.5 1 2 0.5 200 156 236 380 212 36833 0 0 1 0.5 1.5 1 218 180 155 335 265 22534 1 0 190 170 130 320 250 27035 1 1 0.5 0.5 1.5 1.5 200 205 190 255 315 27036 0 0 247 170 150 300 220 20037 0 0 155 100 105 274 170 15638 0 0 0 1 1.5 1.5 150 194 195 242 256 28039 0 0 0 0 0 0 180 200 160 210 280 24040 1 0 0 0 1.5 0 145 100 90 296 205 175

SES: SOCIO ECONOMIC STATUS

1-POOR, 2-MIDDLE, 3-UPPER MIDDLE, 4-HIGH

FAMILY HISTORY: 0-NO HISTORY, 1-FATHER/MOTHER, 3-SIBLINGS

STRESS AT WORK: 0- NO, 1-MILD, 2-MODERATE, 3-SEVERE

CHRONICITY: 1. <1YEAR, 2. 1-5YEARS,, 3. 6-10YEARS, 4. 11-15 YEARS, 5. 16-20 YEARS, 6.21

& ABOVE.

DRUG GROUP: 1. WITHOUT ANY MEDICINES,2.WITH ORAL,3. WITH ORAL BUT

DISCONTINUED,4. ORAL+INSULIN-CONTROLLED, 5. ORAL+INSULIN-UNCONTROLLED

PRAKRITI: 1. VATAPITTA,2.PITTAKAPHA,3. VATAKAPHA

Et: excessive thirst

Va: voracious appetite

Cl: cramps in legs

Wk: weakness

Es: excessive sweating

Fs: frozen shoulder

Pr: pruritis

Fi: fungal infection

NE: Nocturnal enuresis

FUS: fasting urine sugar

PLUS: post lunch urine sugar

FBS: fasting blood sugar

PLBS: post lunch blood sugar

A STUDY ON THE EFFECT OF UMA SAMBHU RASA STUDY ON THE EFFECT OF UMA SAMBHU RASWITH MADHU GHRITADI YAPANA VASTI IN THEWITH MADHU GHRITADI YAPANA VASTI IN THE

MANAGEMENT OFMANAGEMENT OFPRAMEHA W.S.R. TO MADHUMEHAPRAMEHA W.S.R. TO MADHUMEHA

DR. T.SIRISHADR. T.SIRISHA

GUIDEGUIDEDr. V.VIJAYA BABU M.D. (AY)Dr. V.VIJAYA BABU M.D. (AY)

READER,READER,POST GRADUATE DEPT.OF KAYACHIKITSAPOST GRADUATE DEPT.OF KAYACHIKITSA

DR. B.R.K.R. GOVT. AYURVEDIC COLLEGEDR. B.R.K.R. GOVT. AYURVEDIC COLLEGE& HOSPITAL& HOSPITALHYDERABADHYDERABAD –– 3838

INTRODUCTIONINTRODUCTION

Ayurveda, the science of 5000 yrs standing, has ample descriptioAyurveda, the science of 5000 yrs standing, has ample description ofn ofsyndromesyndrome ‘‘MadhumehaMadhumeha’’, a type of prameha., a type of prameha.

The termThe term ‘‘pramehaprameha’’ means passing of fairly large amounts of unclearmeans passing of fairly large amounts of unclearUrine. It covers a large aspect of symptoms as well as local diUrine. It covers a large aspect of symptoms as well as local diseasesseasesinvolving Genito urinary system.involving Genito urinary system.

the definition ofthe definition of ““MadhumehaMadhumeha”” –– to passto pass ““MadhuMadhu samamsamam”” Urine i.e. SweetUrine i.e. Sweetlike honey, makes it much closer to glycosuria.like honey, makes it much closer to glycosuria.

VagbhataVagbhata has also quoted another essential featurehas also quoted another essential feature ““MadhuryacchaMadhuryacchatonoratahtonoratah’’ probably hyperglycemia condition along withprobably hyperglycemia condition along with ““MadhvivaMadhvivamehatimehati”” glycosuria for a disease to be labeled asglycosuria for a disease to be labeled as ““MadhumehaMadhumeha””

““Thomas Willis (1621Thomas Willis (1621--1675 AD) had described such condition where the1675 AD) had described such condition where theurine is wonderfully sweet as if imbued with honey or sugarurine is wonderfully sweet as if imbued with honey or sugar”” in diabetes orin diabetes orpissing evilpissing evil””..

Diabetes mellitus is a clinical condition characterized by increDiabetes mellitus is a clinical condition characterized by increased bloodased bloodglucose levels, hyperglycemia due to insufficient or in efficienglucose levels, hyperglycemia due to insufficient or in efficientt(incompetent) insulin.(incompetent) insulin. ConsequentlyConsequently it spills over into urine resulting init spills over into urine resulting inglycosuriaglycosuria

PURPOSE OF THE STUDY:PURPOSE OF THE STUDY: MadhumehaMadhumeha -- represent the degenerative state of the body with increasedrepresent the degenerative state of the body with increased

susceptibility to various infections & associatedsusceptibility to various infections & associated dhatudhatu kshayakshaya..

There is a need of effective and quick / fast acting therapeuticThere is a need of effective and quick / fast acting therapeutic measure tomeasure tocounter the under lying pathology in Ayurvedacounter the under lying pathology in Ayurveda

Uma sambhu ras in this regard, acts as aUma sambhu ras in this regard, acts as a rasayanarasayana && sarvasarva prameha hara &prameha hara &may correct bothmay correct both dhatukshayadhatukshaya & ultimately& ultimately ojovikaraojovikara..

It is expected to provide a faster control over the disease andIt is expected to provide a faster control over the disease and show goodshow goodhypoglycemic action as it ishypoglycemic action as it is potencifiedpotencified with variouswith various rasayanarasayana & meha hara& meha haraherb & minerals.herb & minerals.

MadhuMadhu GhritadiGhritadi yapanayapana Vasti is also considered along with uma sambhuVasti is also considered along with uma sambhuras, expecting to have a synergic effect, which too isras, expecting to have a synergic effect, which too is rasayanarasayana mehaharamehahara,,nirupadravanirupadrava, to have better & faster control over disease, to have better & faster control over disease

THE CONCEPT OF AGNITHE CONCEPT OF AGNI

Broadly five types ofBroadly five types of pittapitta & thirteen types of& thirteen types of AgniAgni have been described,have been described,which are quite different in their identity.which are quite different in their identity.

..JataragniJataragni::--it renders the food suitable for absorptionit renders the food suitable for absorptionSaraSara kittakitta vibhajanavibhajana-- sanghatabhedasanghatabheda of the food matterof the food matter

BhutagnisBhutagnis-- BhutagniBhutagni pakapaka reforms the food materials physically &reforms the food materials physically &chemically to become homogenous to thechemically to become homogenous to the mahabhutasmahabhutas of theof the shareerashareera

The process ofThe process of BhutagniBhutagni pakapaka is not limited up to theis not limited up to the kostakosta. But remains in. But remains inbetween thebetween the JataragniJataragni pakapaka & the& the DhatawagniDhatawagni pakapaka vizviz, the entire, the entire agniagnivyaparavyapara operating upon the food after it has been digested to till itsoperating upon the food after it has been digested to till itsutilization starts in dhatus.utilization starts in dhatus.

DHWATWAGISDHWATWAGIS -- DhatwagniDhatwagni pakapaka::DhatwagnisDhatwagnis mediate or catalyze further metabolic reactions leading intomediate or catalyze further metabolic reactions leading into

formation of two productsformation of two products prasadaprasada && kittakitta..An interesting concept has been forwarded in Ayurveda thatAn interesting concept has been forwarded in Ayurveda that JataragniJataragni has ahas a

systemic influence on othersystemic influence on other agnisagnis of the body.of the body.SamanaSamana vata mediates & controls all the three types ofvata mediates & controls all the three types of agniagni vyaparavyapara. It. It

motivates & controls the digestion at every level.motivates & controls the digestion at every level.

Physiology: InsulinPhysiology: Insulin

INSULININSULIN½½ QuantityQuantity ½½ quantityquantity

VIA PORTALVEIN ENTERS SYSTEMIC CIRCULATIONVIA PORTALVEIN ENTERS SYSTEMIC CIRCULATION

LIVER BINDS to receptLIVER BINDS to receptors on target cellsors on target cells(has intrinsic tyrosine(has intrinsic tyrosine kinasekinase activity)activity)

Degraded ACTIVATES Post receDegraded ACTIVATES Post receptor intracellularptor intracellularin liver signaling pathwain liver signaling pathway moleculesy molecules

Results inResults inGLYCOGEN SynthesisGLYCOGEN Synthesis

GLUCOSE TransportGLUCOSE TransportPROTIEN SynthesisPROTIEN Synthesis

LIPOGENESISLIPOGENESIS

NIDANANIDANA

SAMSODANAMSAMSODANAMAKURVATAAMAKURVATAAM

VAMANAVIRECHANAVAMANAVIRECHANAASTHAPANASIROVIRASTHAPANASIROVIRECHANAATIYOGA /ECHANAATIYOGA /SANDHARANASANDHARANASONITATISEKAMSONITATISEKAM

PANCHAKARMAPANCHAKARMA

CHINTACHINTAUDVEGAMUDVEGAMSOKAMSOKAM

MANASIKA:MANASIKA:

NIDRANIDRAASYASUKHAMASYASUKHAMAVYAYAMAAVYAYAMA

ANASANAANASANAABHIGHATAABHIGHATAATAPAATAPAJAGARANAVISHAMAJAGARANAVISHAMASARERANYSAMSARERANYSAMUPASEVANAUPASEVANA

KAPHAKARAKAPHAKARAAHARAAHARAASYASUKHAMASYASUKHAMSWAPNA SUKHAMSWAPNA SUKHAMKAPHAKARAKAPHAKARAVIHARAVIHARA

VIHARA :VIHARA :

AMLAAMLALAVANALAVANAGURUGURUSNIGDHA AHARASNIGDHA AHARANAVANNAMNAVAPANAVANNAMNAVAPANAMNAM

RUKSHARUKSHALAGHULAGHUSITASITAKATURASAKATURASATIKTARASATIKTARASAKASHAYA RASAKASHAYA RASA

DHADHIDHADHIGRAMYA RASAGRAMYA RASAOUDAKA RASAOUDAKA RASAANUPA RASAANUPA RASAPAYAMSI / GORASAPAYAMSI / GORASANAVANNAMNAVANNAMNAVADHANYAMNAVADHANYAMNAVAPANAMNAVAPANAMGUDA VIKRITAGUDA VIKRITA

AHARA:AHARA:

MADHUMEHAMADHUMEHAVATAJA PRAMEHAVATAJA PRAMEHAPRAMEHAPRAMEHA

NIDANANIDANAcontcont……dd

Kaphaja pramehaKaphaja prameha nidananidana AharaAhara::

atiati pramanapramana,, atiati velamvelam sevanasevanahayanakahayanaka,, chinakachinaka,, uddalakauddalaka ---------- yavayavanaishadanaishada,, itkataitkata,, mukundakamukundakasougandakasougandaka,, navanava ,,mahamaha ---------- vrihivrihi

harenuharenu ,, mashamasha supamsupam---------- sarpishmataamsarpishmataamGRAMYA,OUDAKA,ANUPA MAMSAGRAMYA,OUDAKA,ANUPA MAMSA

PAYASA, KRISARA, VILEPI, PISTAANNA, KSHEERA,DADHI, DRAVA, MADHURPAYASA, KRISARA, VILEPI, PISTAANNA, KSHEERA,DADHI, DRAVA, MADHURAA

VIharaVIhara::MRUJA,VYAYAMAMRUJA,VYAYAMA ----------VARJANAVARJANASWAPNA,SAYANA,ASANASWAPNA,SAYANA,ASANA------------PRASANGAHPRASANGAH

NIDANANIDANAcontcont……dd

DHARMAVIRUDHADHARMAVIRUDHAMM

ALASYAALASYAPRASAKTAMPRASAKTAM

OTHER:OTHER:

SRAMASRAMAVYAVAYAVYAVAYADHOOMADHOOMANISHEVANANISHEVANA

DIWA SWAPNAMDIWA SWAPNAMAVYAYAMAMAVYAYAMAM

EKASTANA RATIEKASTANA RATIVIDIVARJITA SAYANAVIDIVARJITA SAYANAMEDO,MUTRA,KAPHAMEDO,MUTRA,KAPHAVARDHAKA VIHARAVARDHAKA VIHARA

VIHARA :VIHARA :

MADYAMADYAPRASEVANAPRASEVANAUSHNAUSHNATEEKSHNATEEKSHNAKATU VIBHOJANAKATU VIBHOJANAAMBUPANAAMBUPANA

MADHURA DRAVAMADHURA DRAVAANNAPANAMANNAPANAMMEDYADRAVAMEDYADRAVAANNAMPANAMANNAMPANAMSEETASEETASNIGDHASNIGDHA

MADHURA, AMLAMADHURA, AMLALAVANARASALAVANARASAMEDOMEDO VARDHAKAVARDHAKA DRAVYASDRAVYASSEETA,SNIGDHA,GURUSEETA,SNIGDHA,GURUPICCHALAPICCHALASURA,IKSHU,MUTRASURA,IKSHU,MUTRAVARDHAKAVARDHAKA DRAVYASDRAVYAS

AHARA:AHARA:

))HAREETAHAREETASUSRUTASUSRUTAVAGBHATAVAGBHATA

PURVA RUPAPURVA RUPA

KaphaKapha ::AsyamadhuryamAsyamadhuryam,, AlasyamAlasyam,, ChikkanagatraChikkanagatra((AngeshusnehaAngeshusneha) ,) ,PicchalaPicchala gatra,Mutragatra,MutraSuklatwamSuklatwam,, AngasaidhilyaAngasaidhilya

PittaPitta ::Pipasa,PanipadaPipasa,Panipada daha,Paridaha,Trit,swedadaha,Paridaha,Trit,sweda VataVata ::AngasuptataAngasuptata AmajaAmaja --Sama Kapha:Sama Kapha: Durgandhaswasa,Gurugatratwam,GhanangataDurgandhaswasa,Gurugatratwam,Ghanangata Sama rasaSama rasa : Sadam: Sadam Sama MedoSama Medo--asthiasthi :: Nakhabheda,KesaNakhabheda,Kesa vridhivridhi SamaSama MedaMeda :: BahirBahir maladikyammaladikyam,,

((DantadeenamMaladyatwamDantadeenamMaladyatwam ))NetramalaTalu,KantaNetramalaTalu,Kanta ,,Mukha,GalasoshaMukha,Galasosha,,SareeraSareera MutraMutra visragandhavisragandha

Kapha+SamaKapha+Sama medomedo :: NidraNidra TandraTandra JatilakesaJatilakesa VyadhiVyadhi NimittajaNimittaja ViseshaVisesha :Mutra:Mutra pipeelikapipeelika,, sareerasareera pipeelikapipeelika,,

AvilaAvila mutrata,Madhuramutrata,Madhura MutrataMutrata,,SayyasanaSayyasana swapnaswapna ,,sukhabhishangisukhabhishangi

RUPARUPA

I PramehaI Prameha rupasrupas:: PrabhootaPrabhoota mutratamutrata AvilaAvila mutratamutrataMadhumeha,Madhumeha, ojomehaojomeha ,, kshoudrakshoudra meha though considered synonymous, theirmeha though considered synonymous, theirrupasrupas were discussed separately in various classics.were discussed separately in various classics.

Kshoudra meha:Kshoudra meha: Kashaya madhuraKashaya madhura mutrammutram RukshamRuksham –– is because of vatais because of vata prakopamprakopam.. Kshoudra rasaKshoudra rasa varnavarna mutrammutram PanduPandu varnavarna mutrammutramOjomeha:Ojomeha: OjasanvitamOjasanvitam –– Contains ojasContains ojasMadhumeha:Madhumeha: cardinal symptoms are:cardinal symptoms are: Madhura /Madhura / madvivamadviva mehanammehanam –– sweetness of urinesweetness of urine madhumadhu samamsamam mehanammehanam MadhuryaacchaMadhuryaaccha tanoratahtanoratah -- Excessive sweetness of entire body.Excessive sweetness of entire body.Clinical features of diabetesClinical features of diabetes:: Thirst ,polyuria, weight loss, fatigue, pruritis vulvae are theThirst ,polyuria, weight loss, fatigue, pruritis vulvae are the most frequentlymost frequently

reported symptomsreported symptomsOther SymptomsOther Symptoms:: Abnormalities of tasteAbnormalities of taste: a sensation of stickiness with no precise taste: a sensation of stickiness with no precise taste Impotence , Amenorrhea, infections of skin / woundsImpotence , Amenorrhea, infections of skin / wounds may be the firstmay be the first

indication of the presence of diabetesindication of the presence of diabetes

SAMPRAPTISAMPRAPTISampraptiSamprapti ghatakasghatakas.. DoshaDosha:: -- PramehaPrameha -- Bahudrava sleshmaBahudrava sleshma

MadhumehaMadhumeha-- VataVata DushyamDushyam:: -- PramehaPrameha --BahvabadhaBahvabadha Medo, Mamsa,Medo, Mamsa, SareeraSareera kleda,kleda, SukraSukra,,

SonitaSonita,, Vasa,Majja,Lasika,Rasa,OjusVasa,Majja,Lasika,Rasa,OjusMadhumehaMadhumeha –– medo, mamsa, ojas.medo, mamsa, ojas.

AgniAgni-- BhutagniBhutagni along withalong with JataragniJataragni && dhatwagnidhatwagni (medo, mamsa)(medo, mamsa) SrotasSrotas:: -- MutravahaMutravaha srotassrotas

OjovahaOjovaha ((rasavaharasavaha)) SrotodustiSrotodusti:: -- MutravahaMutravaha-- AtiAti PravrittiPravritti SthanaSthana:: -- VyadhiVyadhi UtpathiUtpathi sthanasthana –– AmaAma pakwasayapakwasaya

VyadhiVyadhi adhistanaadhistana stanastana –– VastiVasti sarvasarva sareeramsareeram.. Obesity has often been linked to type 2 diabetes. It is found bObesity has often been linked to type 2 diabetes. It is found byy Dr.Dr. DasDas &&

Dr.RaoDr.Rao. A.U.. A.U. VizagVizag that Genes involved in cell adhesion, insulin signalingthat Genes involved in cell adhesion, insulin signalingand immune system pathways were down regulated in obese peopleand immune system pathways were down regulated in obese people

This statement supports the statement of ourThis statement supports the statement of our acharyasacharyas that the doshas.that the doshas.Sleshma (function is cell coherence), Vata (important function iSleshma (function is cell coherence), Vata (important function is gatis gati ––gandhana) &gandhana) & dushyadushya Ojas (Ojas (balabala // vyadhivyadhi kshamatwakshamatwa saktisakti) are vitiated in) are vitiated inmadhumehamadhumeha

kaphakapha karakara aharaahara viharasviharas –– a causative factor for obesity is considered asa causative factor for obesity is considered asmain etiological factor in madhumehamain etiological factor in madhumeha

Samprapti:Samprapti: DoshicDoshic PhasePhase Phase ofPhase of DoshaDosha dushyadushya sammurcchanasammurcchana Phase ofPhase of vyadhivyadhi utpathiutpathi II DoshicDoshic Phase:Phase:

TridoshajamTridoshajam,, the predominantthe predominant doshadosha is sleshma / kaphais sleshma / kapha.. Excessive intake of kaphaExcessive intake of kapha prakopakaraprakopakara aharaahara, Guru Snigdha, Guru Snigdha AharaAhara

kaphakapha chayamchayam initially & theninitially & then prakopaprakopa amlaamla && lavanalavana rasasrasas decreasedecrease sandratasandrata / increase/ increase dravatwadravatwa

quality to sleshma.quality to sleshma.sleshma is Ghana / Sandra, it will not presleshma is Ghana / Sandra, it will not precipitate prameha.cipitate prameha.

bahubahu dravadrava sleshma, subsequently effects thesleshma, subsequently effects the JataragniJataragniresulting inresulting in vahnivahni sadamsadam & on long standing produces& on long standing produces amaama..

sleshma (sleshma (bahubahu dravadrava) further increase, come out of its) further increase, come out of itssthanasthana ((kostakosta) () (prasaravastaprasaravasta) with the aid of) with the aid of samanasamana vata,vata,enters theenters the swedasweda,, doshadosha andand ambuambu vahavaha srotassrotas

sleshmasleshma-- along withalong with vyanavyana vata circulates through out thevata circulates through out thebody thus increasing thebody thus increasing the dravatwamdravatwam oror kledamkledam in all thein all thekaphakapha sthanassthanas & kleda& kleda sthanassthanas ((swedamswedam,, mutramutra,, sareerasareerakledamkledam

Samprapti:Samprapti:ContCont……dd

PhasePhase--II:II: DoshaDosha dushyadushya sammurcchana:sammurcchana: --AtiAti snigdhasnigdha & guru& guru aharaahara --------medo vridhimedo vridhi karamkaram.. JataragniJataragnisadamsadam resulting inresulting in ‘‘AmaAma’’ at medo & mamsa dhatus.at medo & mamsa dhatus.Kleda Vridhi / circulating kleda too results in theKleda Vridhi / circulating kleda too results in the bahubahu //aghanatwaaghanatwa or liquidity to dhatusor liquidity to dhatusabadhamabadham-- immiscible nature makes them circulate inimmiscible nature makes them circulate inthe body along with kleda.the body along with kleda.

In this phaseIn this phase PurvaPurva rupasrupas of Prameha noted, which areof Prameha noted, which aremostly the Sama medo, mamsamostly the Sama medo, mamsa lakshanaslakshanas along with samaalong with samarasarasa lakshanaslakshanas..i.e.chikkanai.e.chikkana dehedehe, Guru, Guru picchalapicchala gatra,dourgandhyamgatra,dourgandhyam && JatileeJatileebhavabhava kesakesa etc.etc.AvilaAvila mutramutra –– is also mentioned asis also mentioned as purvarupapurvarupa which indicates thewhich indicates thepresence ofpresence of malamala inin mutramutra ieie;; these circulating kleda withthese circulating kleda withimmisibleimmisible dushyasdushyas –– initially gets expelled out along withinitially gets expelled out along withurineurine

PhasePhase -- IIIIII:: VyadhiVyadhi utpathiutpathi::-- These circulating doshas & dhatus, along withThese circulating doshas & dhatus, along with sareerasareera kleda, reachkleda, reach

the vastithe vasti –– the only organ to expel out excess kleda throthe only organ to expel out excess kleda thro’’ mutramutra, &, &causescauses kaphajakaphaja,, PittajaPittaja or vatajaor vataja pramehaspramehas depending on thedepending on thedoshicdoshic predominancepredominance

Samprapti:Samprapti:ContCont……dd In madhumeha,In madhumeha,

ruksharuksha gunaguna, vata, vata prakopaprakopa occurs,occurs, by virtue of itsby virtue of its naturalitynaturality increasesincreases kashayakashaya rasarasa interferes with the madhurainterferes with the madhura tatwatatwa in ojasin ojas brings it to vasti & Expels out along with urine resulting inbrings it to vasti & Expels out along with urine resulting in

madvivamadviva mehanammehanam // OjoOjo meha.meha. AsAs ojas circulates all over bodyojas circulates all over body, thus, thus madhuramadhura tatvatatva too istoo is

present all over the body resulting in madhuryacchapresent all over the body resulting in madhuryacchatanoratatanorata (madhura rasa &(madhura rasa & kashayakashaya rasarasa –– areare pridvipridvi bhutabhutapredominant dravyas madhura associated with AP &predominant dravyas madhura associated with AP & kashayakashaya withwithvayuvayu which may result in mutual interference duringwhich may result in mutual interference during bhulagnibhulagni pakapaka //dhatwagnidhatwagni pakapaka))

If untreated in this stage or not managed properly, the diseaseIf untreated in this stage or not managed properly, the disease progresses toprogresses tobhedabheda vastavasta, which is presented with, which is presented with pidakapidaka & upadravas& upadravas..

UPADRAVAS complicationsUPADRAVAS complications

Micro AngiopathicMicro Angiopathiclesionslesions RetinopathyRetinopathy NephropathyNephropathy NeuropathyNeuropathy

Macro AngiopathicMacro Angiopathiclesionslesions AtherosclerosisAtherosclerosis

OTHERSOTHERS UTI in femalesUTI in females TuberculosisTuberculosis CholecystitisCholecystitis InfluenzaInfluenza FurunculousFurunculous MucocutaneousMucocutaneous

candidiasiscandidiasis..

TrishnaTrishna AtisaraAtisara JwaraJwara DahaDaha DourbalyaDourbalya ArochakaArochaka AvipakaAvipaka PutimamsapPutimamsap

idakaidaka AlajiAlaji VidradhiVidradhi AngamardaAngamarda KasaKasa BramaBrama TamaTama SulaSula KanduKandu

PramehapidakasPramehapidakas SaravikaSaravika KacchapikaKacchapika jalinijalini SarshapikaSarshapika AlajiAlaji VinataVinata VidradhiVidradhi PutriniPutrini MasurikaMasurika VidarikaVidarika

Predisposing & Risk factors of PramehaPredisposing & Risk factors of Prameha

Predisposing FactorsPredisposing Factors::The personalities (prone to) madhumeha / Prameha are:The personalities (prone to) madhumeha / Prameha are: GridnumGridnum abhyahareshuabhyahareshu SnanaSnana dweshidweshi KarmaKarma vidveshividveshi

Risk FactorsRisk Factors:: AtisthulaAtisthula MandotsahiMandotsahi AtisnigdhaAtisnigdha MahasanaMahasana

Risk Factors of TypesRisk Factors of Types--2 diabetes2 diabetes ObesityObesity Physical inactivityPhysical inactivity Western dietWestern diet UrbanizationUrbanization Family history.Family history.

CHIKITSACHIKITSA

Treatment of a disease in Ayurveda starts withTreatment of a disease in Ayurveda starts with nidananidana parivarjanaparivarjanaThe chikitsaThe chikitsa kramakrama / line of treatment varies with/ line of treatment varies with

etiologyetiology

JataJata pramehipramehi chikitsachikitsa ApathyaApathya nimithajanimithaja pramehipramehi ChikitsaChikitsa

SantarpanaSantarpana JanyaJanya pramehipramehi ChikitsaChikitsa ApatarpanaApatarpana JanyaJanya pramehipramehi ChikitsaChikitsa

AndAnd rogirogi balabala

StulaStula -- BalwanBalwan KrisaKrisa -- DurbalaDurbala

CHIKITSACHIKITSAThe management of diabetesThe management of diabetes

Diet modifications,Diet modifications,ExerciseExerciseDrugsDrugs

When diet & exercise fail to achieve glycaemic control, medicatiWhen diet & exercise fail to achieve glycaemic control, medication is neededon is needed(Oral hypo glycaemic agents /Insulin)(Oral hypo glycaemic agents /Insulin)

II Oral hypo glycaemic agentsOral hypo glycaemic agents:: are categorized asare categorized asInsulin sensitizers Ex:Insulin sensitizers Ex: BiguinidesBiguinides-- metforminmetformin,, pioglitazonepioglitazoneInsulinInsulin SecretagoguesSecretagogues-- StimulatesStimulates cells of pancreas Ex:cells of pancreas Ex: SulphonylSulphonyl

ureasureas-- GlibenclamideGlibenclamide,, chlorpropamidechlorpropamide,, TolbutamideTolbutamideRetartantsRetartants of glucose absorption from the gastro intestinal lumen Ex:of glucose absorption from the gastro intestinal lumen Ex:

Guar gum ,AlphaGuar gum ,Alpha glucosidaseglucosidase inhibitorsinhibitorsHowever, all the above require residual insulin Secretary CapaciHowever, all the above require residual insulin Secretary Capacity in patientsty in patients

to be effective.to be effective.InsulinInsulin:: When oral drugs fail to achieveWhen oral drugs fail to achieve normoglycaemicnormoglycaemic levels, then insulinlevels, then insulin

is suggested. Depending on duration of action, Insulin is categis suggested. Depending on duration of action, Insulin is categorized:orized:Short actingShort actingLong ActingLong ActingIntermediateIntermediate Are selected accordingly.Are selected accordingly.

DRUG REVIEWDRUG REVIEW Uma Sambhu rasUma Sambhu ras : The main ingredients of the drug are: The main ingredients of the drug are

Rasa SindooramRasa Sindooram –– 1 part1 partAbhraka bhasmaAbhraka bhasma –– 1 part1 partTutha bhasmaTutha bhasma ––1 part1 partBhavana dravyas:Bhavana dravyas:1. Jambeera1. Jambeera -- 7 bhavanas7 bhavanas 8. Ketaka8. Ketaka -- 3 bhavanas3 bhavanas2. Beejahwa2. Beejahwa -- 1 bhavana1 bhavana 9. Jeera9. Jeera -- 3 bhavanas3 bhavanas3. Aksha3. Aksha -- 1 bhavana 11 bhavana 10. Rambha0. Rambha-- 3 bhavanas3 bhavanas4. Yuga4. Yuga -- 1 bhavana1 bhavana 11. Kharjurika11. Kharjurika-- 3 bhavanas3 bhavanas5. Kakubha5. Kakubha -- 2 bhavanas2 bhavanas 12.12. JatidalaJatidala -- 3 bhavanas3 bhavanas6. Yastimadhu6. Yastimadhu -- 3 bhavanas3 bhavanas 13.13. Mushkaka.NAMushkaka.NA-- 3 bhavanas3 bhavanas7. Sita / Durva7. Sita / Durva -- 3 bhavanas3 bhavanasDose :Dose : 1 Valla (375 mg) Anupana :1 Valla (375 mg) Anupana : VasaVasa swarasamswarasam..

In view of the practical difficulty in taking VasaIn view of the practical difficulty in taking Vasa swarasaswarasa asas anupanaanupana, the same was, the same wasused for bhavana, in order, not to miss its therapeutic effect,used for bhavana, in order, not to miss its therapeutic effect, before making into abefore making into apill.pill.

The key ingredients, Rasa sindooram, Abhraka bhasma, Tutha bhasmThe key ingredients, Rasa sindooram, Abhraka bhasma, Tutha bhasmaa-- areareprameha hara & Rasayana, thus.prameha hara & Rasayana, thus.

In addition, Rasa sindooram is a potent therapeutic agent havingIn addition, Rasa sindooram is a potent therapeutic agent having wide range ofwide range oftherapeutic efficacy. The vegetable drug combined with it decidtherapeutic efficacy. The vegetable drug combined with it decides its target pointes its target pointof action.of action.

Abhraka bhasmaAbhraka bhasma –– is a proven drug helps in monitoring blood glucose homeostasis.is a proven drug helps in monitoring blood glucose homeostasis. Further, theFurther, the 7 Putas7 Putas of these ingredients with subsequent bhavana with Jambeeraof these ingredients with subsequent bhavana with Jambeera

ras andras and 27 bhavanas27 bhavanas with 13 bhavana dravyas having Rasayana, Deepana,with 13 bhavana dravyas having Rasayana, Deepana,Prameha hara qualities ,increases the quick & fast acting naturePrameha hara qualities ,increases the quick & fast acting nature of the drug &henceof the drug &henceit is selected for present clinical study.it is selected for present clinical study.

DRUG REVIEWDRUG REVIEWcontcont……dd

MadhuMadhu GhritadiGhritadi YapanaYapana vasti :vasti :Ingredients:Ingredients:

MadhuMadhu -- 11 PrasrutaPrasruta (80ml)(80ml)GrithaGritha -- 11 PrasrutaPrasruta (80ml)(80ml)UshnodakaUshnodaka -- 22 PrasrutaPrasruta (160ml)(160ml)SatapushpaSatapushpa -- ½½ PalaPala (20gm)(20gm)SaindhavalavanaSaindhavalavana -- ½½ KarshaKarsha (5gm)(5gm)

Karma:Karma: Deepana, Rasayanam, Brimhanam,Deepana, Rasayanam, Brimhanam, BalaBala varnakaravarnakara,,Nirupadravam,Nirupadravam, VrushyatamaoVrushyatamao

Vyadhi Prabhava:Vyadhi Prabhava: KrimiKrimi,, KustaKusta,, UdaraUdara,, GulmaGulma,, ArsasArsas,, BradnaBradna,, PleehaPleehadisorders,disorders, PramehaPrameha..

Since Vasti is best, in treating Vata, madhumeha being a vata prSince Vasti is best, in treating Vata, madhumeha being a vata predominantedominantprameha, it is selected along with drug, aiming to have a synergprameha, it is selected along with drug, aiming to have a synergic effect &ic effect &thus help in gaining quick control over the disease.thus help in gaining quick control over the disease.

Vasti stimulate the ANS, and as the islets areVasti stimulate the ANS, and as the islets are inervatedinervated by inby inmyelenatedmyelenated fibers from both parasympathetic (fibers from both parasympathetic (VagalVagal) and Sympathetic) and Sympatheticnerves whose endings are in close contact withnerves whose endings are in close contact with ααandand ββcells & it can readilycells & it can readilyinfluence their secretary activities.influence their secretary activities.

OBJECTIVESOBJECTIVES

To determine the efficacy of Uma sambhu ras inTo determine the efficacy of Uma sambhu ras inmadhumehamadhumeha

To determine the efficacy of Uma sambhu ras andTo determine the efficacy of Uma sambhu ras andmadhumadhu GhritadiGhritadi yapanayapana vasti in madhumehavasti in madhumeha

To compare the efficacy of Uma sambhu ras to groupTo compare the efficacy of Uma sambhu ras to groupgiven Uma sambhu ras andgiven Uma sambhu ras and madhumadhu GhritadiGhritadi yapanayapanaVasti.Vasti.

METHODOLOGYMETHODOLOGYTYPE OF STUDY AND STUDY DESIGNTYPE OF STUDY AND STUDY DESIGN::

RandomizedRandomized openopen trial, selected to minimize the bias.trial, selected to minimize the bias.SAMPLINGSAMPLING:: randomized Sampling techniquerandomized Sampling technique..ForFor comparative studycomparative study,, paired randomizationpaired randomization is applied.is applied.II DETAILS OF STUDY SUBJECTS (CASES) AND CONTROLSDETAILS OF STUDY SUBJECTS (CASES) AND CONTROLS::40 Patients were selected randomly into two groups (Group40 Patients were selected randomly into two groups (Group ––I & GroupI & Group ––

II) from the OPD & IPD ofII) from the OPD & IPD of Dr.B.R.K.RDr.B.R.K.R GovernmentGovernment AyurvedicAyurvedic ResearchResearchhospital,hospital, ErragaddaErragadda and 29 patients were placed in Group I and 11and 29 patients were placed in Group I and 11patients in Grouppatients in Group--IIII

No Control group was selected.No Control group was selected.DURATION OF STUDY:DURATION OF STUDY: 30 days.30 days.IIIIII MODE OF ADMINISTRATIONMODE OF ADMINISTRATION:: 125 mg with plain water after meals, three125 mg with plain water after meals, three

times a day with minimum of 6 hours gap between each.times a day with minimum of 6 hours gap between each.Inclusion & exclusion criteria :Inclusion & exclusion criteria : Inclusion:Inclusion:..TypeType II diabetesII diabetes (NIDDM)(NIDDM) (26(26--65) (Non65) (Non-- obese / Obese typeobese / Obese type--IIII

Diabetes)Diabetes) Exclusion:Exclusion: Type I diabetesType I diabetes (IDDM) / Juvenile onset diabetes(<25yrs)(IDDM) / Juvenile onset diabetes(<25yrs)

Secondary diabetes:Secondary diabetes:(a) Pancreatic diseases (b) Hormonal (c) Drug in(a) Pancreatic diseases (b) Hormonal (c) Drug induced (d) Insulinduced (d) Insulin

receptor abnormalities (e) Genetic Syndromes (f) IGT (impairedreceptor abnormalities (e) Genetic Syndromes (f) IGT (impairedGlucose tolerance) (g) Gestational diabetes (f) Pre diabetesGlucose tolerance) (g) Gestational diabetes (f) Pre diabetes

METHODOLOGYMETHODOLOGYContCont……dd

Diabetes with complicationsDiabetes with complications-- diabetic foot/neuropathy/nephropathy) ordiabetic foot/neuropathy/nephropathy) orassociated with other diseasesassociated with other diseases——HTN /cardiac problems.HTN /cardiac problems.

DETAILS OF MATERIALS (APPARATUS / LABTESTS) & EXPERIMENTALDETAILS OF MATERIALS (APPARATUS / LABTESTS) & EXPERIMENTALDESIGN:DESIGN:

MATERIALS:MATERIALS:SUBJECTIVE PARAMETERS:SUBJECTIVE PARAMETERS:--considered as criteria for assessment of resultsconsidered as criteria for assessment of results Excessive thirstExcessive thirst Voracious appetiteVoracious appetite Cramps in legsCramps in legs Weakness or fatigueWeakness or fatigue PruritisPruritis Nocturnal EnuresisNocturnal EnuresisGradation was not given to the parameters, but only present or aGradation was not given to the parameters, but only present or absent were considered.bsent were considered.OBJECTIVE PARAMETERS:OBJECTIVE PARAMETERS: Fasting Urine sugar levelFasting Urine sugar level Post lunch Urine sugar levelsPost lunch Urine sugar levels Fasting Blood Sugar levelsFasting Blood Sugar levels Post lunch Blood sugar levelsPost lunch Blood sugar levelsWere considered for the assessment of effect of treatments in GWere considered for the assessment of effect of treatments in G--I & GI & G--IIII

METHODOLOGYMETHODOLOGYContCont……ddEXPERIMENTAL DESIGNING:EXPERIMENTAL DESIGNING: Factorial design was applied, as the effects of drug singly as wFactorial design was applied, as the effects of drug singly as well asell as

in combination are to be determined, and looking for the possibiin combination are to be determined, and looking for the possibility oflity ofinteraction of the two treatments, such as synergism.interaction of the two treatments, such as synergism.

PROCEDURE OF DATA COLLECTION:PROCEDURE OF DATA COLLECTION: Subjective parameters were recorded in 2 periods VIZ B.T (BeforeSubjective parameters were recorded in 2 periods VIZ B.T (Before

treatment)treatment) AT(afterAT(after treatment). The values of FUS, PLUS, FBS, PLBStreatment). The values of FUS, PLUS, FBS, PLBSwere recorded BT, I wk & AT for all the subjects of Gwere recorded BT, I wk & AT for all the subjects of G--I & GI & G--IIII

STATISTICAL METHODS EMPLOYED:STATISTICAL METHODS EMPLOYED: For determining the efficacy of drug in GFor determining the efficacy of drug in G--I & drug & Vasti in GI & drug & Vasti in G--IIII

pairedpaired‘‘tt’’ test was applied.test was applied. P Value was analyzed.P Value was analyzed. ‘‘tt’’ Value was analyzed for at the 0.1% to 5% levels of significanceValue was analyzed for at the 0.1% to 5% levels of significance.. To test the significance difference between GTo test the significance difference between G--I & GI & G--II, UnII, Un pairedpaired‘‘tt’’ testtest ––

testing the difference between the means is applied.testing the difference between the means is applied. ‘‘tt’’ value was analyzed for at 1% & 5% levels of significance.value was analyzed for at 1% & 5% levels of significance.

OBSERVATIONS & RESULTSOBSERVATIONS & RESULTS STATUS OF PATIENTS OF PRESENT STUDYSTATUS OF PATIENTS OF PRESENT STUDY

4040884848TOTALTOTAL

1111001111GROUP 2GROUP 2

2929883737GROUP 1GROUP 1

COMPLETEDCOMPLETEDDROP OUTSDROP OUTSTOTALTOTALREGISTEREDREGISTERED

GROUPGROUP

100401129TOTAL

1041360-69

25102850-59

341431140-49

28114730-39

311020-29

PERCENTAGETOTALGROUP 2GROUP 1AGE GROUP

AGE WISE DISTRIBUTION OF PATIENTS

OBSERVATIONS & RESULTSOBSERVATIONS & RESULTScontcont……dd

100401129TOTAL

5221714FEMALE

4819415MALE

PERCENTAGETOTALGROUP 2GROUP 1GENDER

GENDER WISE DISTRIBUTION OF PATIENTS


31, 77%

9, 23%0, 0%

HINDU

MUSLIM

CHRISTIAN


100.00401001110029TOTAL

37.501527.3341.3812NO HISTORY

25.001027.3324.147SIBBLINGS

37.501545.5534.4810MOTHER/ FATHER

%TOTAL%G-II%G-IFAMILY HISTORY

DISTRIBUTION OF PATIENTS ACCORDING TO FAMILY HISTORY

100.00401001110029TOTAL

70.002872.7868.9720VK

20.00818.2220.696PK

10.0049.09110.343VP

%TOTAL%G-II%G-IPRAKRITI

DISTRIBUTION OF PATIENTS ACCORDING TO PRAKRITI


DISTRIBUTION OF PATIENTS ACCORDING TO SOCIO ECONOMICSTATUS G I & G II

22, 54%13, 33%

0, 0%5, 13%

POORMIDDLEU

HIGHUPPERMIDDLE

8

3

21

8

0

5

10

15

20

25

Veg Mixed

DISTRIBUTION OF PATIENTS ACCORDING TO DIET G I & G II

G-IG-II


100.00401001110029TOTAL

25.001018.2227.598SEVERE

35.001454.5627.598MODERATE

17.5070024.147MILD

22.50927.3320.696NO

%TOTAL%G-II%G-ISTRESS

DISTRIBUTION OF PATIENTS ACCORDING TO STRESS FACTOR

100401001110029TOTAL

7.5030010.343>32

10.0049.09110.343≤32

12.5059.09113.794≤30

70.002881.8965.5219≤25

%TOTAL%G-II%G-IBMI

DISTRIBUTION OF PATIENTS ACCORDING TO BMI


100401001110029TOTAL

5.002006.8972>25

2.501003.448116-20

0.000000011-15

10.0049.09110.3436-10

22.50936.4417.2451-5

60.002454.5662.0718< 1 year

%TOTAL%G-II%G-ICHRONICITY (yrs)

DISTRIBUTION OF PATIENTS ACCORDING TO CHRONICITY


100401001110029TOTAL

7.5030010.343Oral+insulin uncontrolled

5.0029.0913.4481Oral+insulin controlled

22.50927.3320.696With oral discontinued

10.0049.09110.343With oral uncontrolled

55.002254.5655.1716With out any oral med

%TOTAL%G-II%G-IDRUG GROUP

DISTRIBUTION OF PATIENTS ACCORDING TO DRUG GROUP

100401001110029TOTAL

502045.5548.2815NO ADDICTION

10.0049.09110.343PAN

30.001236.4427.598ALCOHOL

7.5039.0916.8972TOBACCO(CHEWING)

2.501003.4481SMOKING

%TOTAL%G-II%G-IADDICTIONS

DISTRIBUTION OF PATIENTS ACCORDING TO ADDICTIONS

OBSERVATIONS & RESULTSOBSERVATIONS & RESULTS

NsNs0.080.081.941.9425NSNS0.1030.1031.681.68

37NOCTURNALENURESIS7

00SS0.0120.0122.702.7017PRURITIS6

SS0.010.013.133.1306SS0.0010.0013.553.55514

EXCESSIVESWEATING5

SS0.000.004.184.1818SS0.0000.0006.776.77321FATIGUE4

SS0.000.004.184.1818SS0.0010.0013.843.84313CRAMPS INLEGS3

01SS0.0430.0432.122.1226

VORACIOUSAPPETITE2

SS0.020.022.892.8916SS0.0000.0004.224.22416

EXCESSIVETHIRST1

ResResultult

ppttATBTResResultult

ppttATBT

GIIG I

SUBJECTIVEPARAMETERS

S.NO

% difference of relief g 1% difference of relief g 1 g2g2Marginal(0Marginal(0--25%) 225%) 2 11Mild (25Mild (25--50%) 250%) 2 00Moderate (50Moderate (50--75%) 775%) 7 11Marked (75% & above) 5Marked (75% & above) 5 22Complete (100%). 13Complete (100%). 13 66


3131772424TOTAL

0201011.5

6922471

8541440.5

17151316120

ATBTATBTATBT

GI+GIIGIIGIFUS

0

5

10

15

20

O <.5 <1 <1.5

GI BT

GI AT

GII BT

GII AT

GROUPGROUP tt pp ResultResultII 2.392.39 0.0250.025 SSIIII 0.550.55 0.600.60 NsNs


2929772222TOTAL

0401032

7934451.5

4610361

6310530.5

127221050

ATBTATBTATBT

GI+GIIGIIGIPLUS

02468

1012

0 < .5 <1 <1.5 <2

GI BT

GI AT

GII BT

GII AT

GROUPGROUP tt pp ResultResultII 3.233.23 0.0040.004 SSIIII 1.821.82 0.110.11 NsNs


114>220

112200-220

433180-200

222160-180

243140-160

447120-140

755100-120

75280-100

AT1STWEEKBTFBS

DISTRIBUTION OF PATIENTS ACCORDING TO FBS GI

% difference of F.B.S.% difference of F.B.S. 1STWEEK AT

Marginal (0Marginal (0--25%) 1125%) 11 1313Mild(25Mild(25--50%)50%) 55 77No change/raisedNo change/raised 88 66

t p Resultt p Result1STWEEK 2.57 0.017 S2.57 0.017 SAT 2.81 0.009 S2.81 0.009 S


102>220

011200-220

333180-200

031160-180

312140-160

111120-140

200100-120

11180-100

AT1STWEEKBTFBS

DISTRIBUTION OF PATIENTS ACCORDING TO FBS G-II

% difference of% difference of FBS 1STWEEK ATMarginal (0Marginal (0--25%) 525%) 5 55Mild (25Mild (25--50%)50%) 22 44No change/raisedNo change/raised 33 22

t p Resultt p Result1STWEEK 1.84 0.101.84 0.10 NsNsAT 1.871.87 0.090.09 NsNs


001>370

000340-370

233310-340

356280-310

334250-280

342220-250

548190-220

633160-190

752130-160

000100-130

AT1STWEEKBTPLBS

DISTRIBUTION OF PATIENTS ACCORDING TO PLBS GI

% difference of PLBS% difference of PLBS 1STWEEK ATMarginal (0Marginal (0--25%) 1325%) 13 1111Mild (25Mild (25--50%)50%) 33 55No change/raisedNo change/raised 1111 88

t p Resultt p Result1STWEEK 2.81 0.0092.81 0.009 SSAT 2.83 0.0082.83 0.008 SS


001>370

110340-370

113310-340

001280-310

332250-280

212220-250

231190-220

011160-190

200130-160

000100-130

AT1STWEEKBTPLBS

DISTRIBUTION OF PATIENTS ACCORDING TO PLBS GII

% difference of PLBS% difference of PLBS 1STWEEK ATMarginal(0Marginal(0--25%) 325%) 3 44Mild(25Mild(25--50%)50%) 33 44No change/raisedNo change/raised 44 33

t p Resultt p Result1STWEEK 1.43 0.181.43 0.18 NSNSAT 1.81 0.101.81 0.10 NsNs


Comparison of objective parameters between selected subjectsComparison of objective parameters between selected subjectsof G I & G IIof G I & G II

t*t* pp ResultResultFBS I WkFBS I Wk 0.000.00 0.990.99 NsNsFBS 4 WkFBS 4 Wk 0.000.00 0.210.21 NsNsPLBSI WkPLBSI Wk 0.000.00 0.290.29 NsNsPLBS4 WkPLBS4 Wk 0.000.00 0.260.26 NsNs

* t is negative so taken as o* t is negative so taken as o

D I S C U S S I O ND I S C U S S I O NDiscussion on demographic dataDiscussion on demographic dataStatistical discussion of parametersStatistical discussion of parametersValidating Test HypothesisValidating Test HypothesisLimitations of interpretation & StudyLimitations of interpretation & Study needs much more duration and large sample to analyze theneeds much more duration and large sample to analyze the

complete variations of objective parameters taken for the studycomplete variations of objective parameters taken for the study The facility of assessingThe facility of assessing GlycosylatedGlycosylated HbHb levels & Clevels & C

peptide levels periodically is not available so assessment ofpeptide levels periodically is not available so assessment oftreatment & raise in Insulin levels could not be donetreatment & raise in Insulin levels could not be done

Lab test like serum Cholesterol & Triglycerides are notLab test like serum Cholesterol & Triglycerides are notavailable and so they are excluded from the studyavailable and so they are excluded from the studyFuture scope for the further study:Future scope for the further study:Same study can be repeated by taking a large number ofSame study can be repeated by taking a large number ofsamples and longer duration withsamples and longer duration with GlycosylatedGlycosylated HbHb levels & Clevels & Cpeptide levels interpretation.peptide levels interpretation.

CONCLUSIONCONCLUSION

Madhumeha / Diabetes Mellitus incidenceMadhumeha / Diabetes Mellitus incidenceage group 30age group 30 –– 50 years i.e. middle age.50 years i.e. middle age.equal in both Male & Femaleequal in both Male & FemaleVata kaphaVata kapha prakritiprakriti..with or without familial interventionwith or without familial interventionmixed diet than having Vegetarian diet (3:1)mixed diet than having Vegetarian diet (3:1)

BMI could find no interference as subjects with BMIBMI could find no interference as subjects with BMI ≤≤25 are more with25 are more withDiabetes Mellitus.Diabetes Mellitus.

Stress was found to have more impact on precipitating Diabetes MStress was found to have more impact on precipitating Diabetes Mellitusellitusas 3 in 4 had stress as one of the factors.as 3 in 4 had stress as one of the factors.

Regarding NidanaRegarding Nidana ––Katu,Katu, amlaamla more than the madhura rasamore than the madhura rasaDadhi,GuruDadhi,Guru, Snigdha,, Snigdha, seetalaseetala aharaaharaSedentary life styles and altered life stylesSedentary life styles and altered life stylesEkastanaEkastana ratirati,, vidhivarjitavidhivarjita sayanasayana andand diwadiwa swapnaswapna

CONCLUSIONCONCLUSIONCONTCONT……DD

Psychological factors likePsychological factors like udvegaudvega andand sokasoka were observed inwere observed in80% to 90% subjects, in age group 3080% to 90% subjects, in age group 30--50 confirming the role50 confirming the roleof psychological factors in precipitating Madhumeha /of psychological factors in precipitating Madhumeha /Diabetes Mellitus in middle ageDiabetes Mellitus in middle age

commonly observedcommonly observed purvapurva rupasrupas >50% cases>50% casesSayyabhishangaSayyabhishangaswapanaswapana bhishangabhishanganidranidra andand tandratandra (30(30 –– 40 years age group)40 years age group)

showing the lethargic state of Diabetes Mellitus patients.showing the lethargic state of Diabetes Mellitus patients.MukhaMukha soshasoshaKantaKanta soshasoshapipasapipasa age group 30age group 30--60 years.60 years.PanipadaPanipada dahadahaangaanga suptatasuptata age group 30age group 30 –– 50 years.50 years.

SUMMARYSUMMARY The aim of the study was to evaluate the hypo glycaemic effect oThe aim of the study was to evaluate the hypo glycaemic effect of Umaf Uma

sambusambu ras and synergic effect ofras and synergic effect of madhugrutadimadhugrutadi yapanavasiyapanavasi when givenwhen givenwith umasambhuras.with umasambhuras.

The evaluation was done for objective parameters after 1st andThe evaluation was done for objective parameters after 1st and 4th week4th weekand subjective parameters after 4th week.and subjective parameters after 4th week.

subject parameterssubject parameters significant relief in both groups except forsignificant relief in both groups except fornocturnal enuresis.nocturnal enuresis.

Cramps in legsCramps in legsfatiguefatigue significant relief in both the Grsignificant relief in both the Groups.oups.

frozen shoulderfrozen shoulderfungal infectionfungal infectionexcessive sweatingexcessive sweating data was insufficientdata was insufficient

objective parametersobjective parameters 4th week4th weekGroupGroup--I significant resultsI significant resultsGroupGroup--II. no significant resultsII. no significant results

Fasting Blood Sugar after 1st and 4th weekFasting Blood Sugar after 1st and 4th weekGroupGroup--I significant improvementI significant improvementGroupGroup--II no significant resultsII no significant results

Post Lunch Blood Sugar GroupPost Lunch Blood Sugar Group--I.I.4th week4th week significant improvementsignificant improvement1st week1st week no significant resultsno significant results

SUMMARYSUMMARYcontcont……dd

Post Lunch Blood Sugar GroupPost Lunch Blood Sugar Group--II.II.4th week4th week no significant resultsno significant results1st week1st week no significant resultsno significant results

When the results of selected subjects of GroupWhen the results of selected subjects of Group--I and GroupI and Group--II areII arecompared, after 1st and 4th weekcompared, after 1st and 4th weekFasting Blood SugarFasting Blood SugarPost Lunch Blood Sugar levels. no significant differePost Lunch Blood Sugar levels. no significant differencence

It is evident thatIt is evident that umasambhuumasambhu ras is a potent fast acting hypo glycaemic drug with no adverseras is a potent fast acting hypo glycaemic drug with no adverse

affects observed.affects observed. MadhugrutadiMadhugrutadi yapanvastiyapanvasti, showed significant results in improving, showed significant results in improving

subjective parameters and hence it is felt that longsubjective parameters and hence it is felt that long--term evaluation of theterm evaluation of theobjective parameters may give significant results.objective parameters may give significant results.

My commitment increases my level of energy. My energy increases my level of action. Myaction increases my level of success. My success increases my level of commitment.

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