Sthoulya kc004 gdg

EVALUATION OF THE EFFICACY OF TRYUSHANADYA LOHAM IN STHOULYA (OBESITY) WITH SPECIAL REFERENCE TO

HYPERLIPIDAEMIA

By Shakuntala C. Garwad

As partial fulfillment of the Post-graduation degree

Ayurveda Vachaspati M.D. (Kayachikitsa)

Under Rajiv Gandhi University of Health sciences

Bangalore, Karnataka.

Guide

Dr. Vangipuram Varadacharyulu M. D. (Ayu)

Professor and Head of the department, Kayachikitsa.

Post graduation studies and research.

D.G.Melmalagi Ayurvedic Medical College

Gadag- 582103.

Ayurmitra

TAyComprehended

Department of Postgraduate Studies and Research Kayachikitsa.

POST GRADUATION AND RESEARCH CENTER,

KAYACHIKITSA.

D.G.M. Ayuyrvedic Medical College, Gadag.

Certificate

This is to certify that the thesis entitled “Evaluation

of the efficacy of Tryushanadya Loham in Sthoulya

(Obesity) with special reference to Hyperlipidaemia” is a

record of research work conducted by Dr. Shakuntala C.

Garwad under my close supervision and guidance.

The candidate has put in sincere effort after making

an intense study coupled with theoretical and clinical

observations.

This title has not found title of degree, associateship,

fellowship and similar other studies in this University.

I recommend the same for being submitted for

evaluation to the adjudicators.

Guide Place : Dr. Vangipuram Varadacharyulu

M. D. (Ayu)

Date : Professor and Head of the department Post graduation studies and research,

Kayachikitsa.

J.S.V.V.S. SAMSTHE’S

SHRI D.G. MELMALAGI AYURVEDIC MEDICAL COLLEGE,

POST GRADUATION AND RESEARCH CENTER, GADAG-582103.

Certificate

This is to certify that Dr. Shakuntala C. Garwad has

worked for her thesis on the topic entitled“Evaluation of

the efficacy of Tryushanadya Loham in Sthoulya

(Obesity) with special reference to Hyperlipidemia”

She has successfully done the work under the

guidance of Dr. Vangipuram Varadacharyulu M. D. (Ayu)

This particular study helps in treating the disease

Sthoulya with present scientific approaches.

I here with forward this thesis for the evaluation and

adjudication.

Dr. G.B. Patil.

Principal / C. M. O.

Contents

Page No. 1. Introduction 1-3

2. Literary review 4-33

a) Historical review 4 - 6

b) Nidana 7-11

c) Samprapti 12 -15

d) Poorva roopa 16-16

e) Roopa 17-23

f) Classification 24-25

g) Sadhyasadhyata 26-26

h) Upadrava 27-29

i) Chikitsa 30-33 3. Modern view 34-54

4. Drug review 55-74

5. Materials and methods 75-85

6. Observations and results 86-106

7. Master charts 107-115

8. Discussion 116-123

9. Conclusion 124-124

10. Summary 125-126

11. References and Bibliography 127-135

Case sheet

Appendix

List of abbreviations

Cha. – Charaka Samhita

Sus. – Sushruta Samhita

As. – Ashtanga Sangraha

Ah. – Ashtanga Hridya

Ma. Ni. – Madhava Nidana

Bh. P. – Bhavaprakasha

Sha. Sa. – Sharangadhara Samhita

Chak. – Chakrapani

Gang. – Gangadhara

Aru. – Arundatta

Dal. – Dalhana

Sa. – Shareera Sthana

Ni. – Nidana Sthana

Chi. – Chikitsa Sthana

Su. – Sutra Stahna

Ka. – Kalpa Sthana

List of graphs

Page No.

01.Graph showing the age incidence 86

02.Graph showing the sex distribution 87

03.Graph showing the religion distribution 88

04.Graph showing the occupation distribution 89

05.Graph showing the economical status 90

06.Graph showing the distribution food habit 91

07.Graph showing the incidence family history 92

08.Graph showing the chronicity of the disease 93

09.Graph showing the distribution personal history 94

10.Graph showing the adhyashana of the patients 95

11.Graph showing the Vyayama of the patients 96

12.Graph showing the diavaswapna of the patients 97

13.Graph showing the Vyavaya of the patients 98

14.Graph showing the distribution of the mental status 99

15.Graph showing the pattern of sleep 100

16.Graph showing the data related to results 101

Master charts

Page No.

01.Data related to demography 107

02.Data related to personal history 108

03.Data related to complaints 109

04.Data related to associated symptoms 110

05.Data related to upadrava 111-112

06.Data related to weight, height, and circumference 113

07.Data related to objective parameters 114-115

List of tables

Page No.

01.Table showing nidana of Sthoulya by different authors 7

02.Table showing laxanas of Sthoulya by different authors 17

03.Table showing ideal weights for men 21

04.Table showing ideal weights for women 22

05.Table showing optimal BM I value 23

06.Table showing of waist measurement 23

07.Table showing Upadrava of Sthoulya by different authors 27

08.Table showing type of physical activities 31

09.Table showing percentage of composition of dietary fats 36

10.Table showing cholesterol content of the different food 45

11.Table showing classification of hyperlipidaemia 51

12.Table showing total cholesterol pippetting scheme 79

13.Table showing HDL cholesterol pippetting scheme 79

14.Table showing triglycerides pippetting scheme 79

15.Table showing the NCEP CAD risk factors 85

Acknowledgement

At the onset my devotional Pranams to his Holiness Shri Jagadguru

Abhinava Shivananda Swamiji, Shivanada Matha, Gadag.

I take this glorious opportunity to acknowledge with the deep sense of

gratitude to my guide, Dr. V. Varadacharyulu, Professor, Head of the department,

Department of Postgraduate Studies and Research (Kayachikitsa), D.G.M.A.M.C.,

Gadag, for his valuable guidance and close supervision during entire phase of the

study.

With profound sense of gratitude I express my sincere thanks to Dr. G. B.

Patil, Principal, D. G. M. A. M. C, Gadag. For encouragement and facilities provided

during my postgraduate studies.

I am very much thankful to Late. Dr. C. M. Sarangamath who is the root

cause of my entry into this noble profession. I remain ever great full to him.

I wish to add my warmest thanks to my PG teaching faculty Dr. M. C. Patil,

Dr. K. Siva Rama Prasad, Dr. Shashidhara Doddamani, Dr. Kuber Sankh, Dr. R. V.

Shetter, Dr.Girish Danappagoudar for their valuable suggestions and timely help

which made me to complete this dissertation work successfully.

I am very much thankful to Dr.S A Patil, Dr.G S Hiremath, Dr.C S Hiremath

& Dr.S S Avvanni for their encouragement and moral support during the study.

I extend my gratefulness and sincere heartfelt gratitude to my colleagues Dr.

B. G. Swami, Dr. U. V. Purad, Dr. K S Paraddi, Dr. Shyju O. Dr. Shankaragouda

and Dr. Hanumantagouda, for their timely support during the course.

I am very much thankful to all UG staff and college librarian Shri. V. M.

Mundinmani and other library staff for their timely help and co-operation during the

study.

I am very much thankful to my parents Smt / Dr.C M Garwad, my Brother &

Sister who inspired me for higher study, rendered their valuable suggestions and

encouragement throughout the study.

I express my deepest gratitude to my husband Dr. M. C. Patil, without whose

help and encouragement the work would have not been completed. Also my

gratitudes are deserved for my beloved children Akshata, Arpita, Chinmaya and all

my family members who have inspired me to continue my PG study with their

constant moral support.

I thank Dr. R. S. Sarashetty for their valuable suggestions throughout the

study.

I wish to thank RMO, physicians and other hospital staff for their co-

operation and all the patients who agreed to under go the treatment with trial drug.

I wish to thank Giridhara North South Computer services Adarsha Nagar,

Gadag. In spite of their busy schedule they completed the dissertation work neatly

and in time.

I wish to thank all the persons who have helped me directly and indirectly

with apologies for my inability to identify them individually.

Shakuntala C. Garwad

Efficacy of Tryushanadya loham in Sthoulya

INTRODUCTION

Ayurveda is a comprehensive health system in gaining incontrovertible

acceptability worldwide. It has a very special approach towards diseases, the patient and

the science of medicine itself.

The entire system of treatment of Ayurveda revolves around Shadvidhopakramas,

much importance has been given to these principles in alleviating diseases and

maintaining the good health. All the measures which are explained in Ayurvedic classics

will benefit the person or diseased in acquiring the perfect health.

Thus a Comprehensive research and development within the frame of philosophy,

cosmology and psychology through the scientific methodology is needed. To achieve this

goal the integrated organization of various disciplines of sciences in the spirit of scientific

inquiry coupled with zest for the social service to the mankind would also essential.

Sthoulya is a Global problem and it is common among those who consume

excessive Kapha kara ahara-vihara etc. We find no satisfactory remedies for Sthoulya in

contemporary medical science.

Obesity patients usually do not approach a doctor in its initial stage, but they do

so in its later stage for the purpose of cosmetic value and many a time they won’t have

patience for long term therapy as complicated therapies like physical exercise and so on.

In Samhita period like Charaka,Sushruta,Vagbhata samhita we get references

regarding Sthoulya and also later works like Yogaratnakara,Bhavaprakasha And

Bhaishajya ratnavali.

Among the drugs used in the management of Obesity Amphetamine has a limited

scope because of its benefit for a short term goal and being contraindicated in coronary

Introduction 1


heart disease, hypertension etc. Secondly Fenfluramine has associated adverse effects like

nausea, diarrhoea, lethargy, breathlessness etc. Further an abrupt withdrawal gives rise to

depression.

The discovery of chemical tests for Cholesterol in the last century & finding this

substance in atheromatous lesions, suggests a causative atherogenic role for this sterol. In

addition, Cholesterol is a component of animal fat and it was not surprising that the

development of atherosclerosis should be linked with diet and consumption of animal

fats.

Sthoulya (obesity) is a chronic disease, prevalent in both developed and

developing countries affecting children as well as adults.

01. The major health consequences with obesity are NIDDM, raised cholesterol, and

hypertension. Coronary heart disease, gall bladder disease, psychosocial

disturbances and certain types of cancer. These diseases are definitely associated

with an increased risk of mortality.

02. Obesity is the mother of many degenerative diseases in adult life, where

hyperlipidaemia is common and responsible for cardiovascular and

cerebrovascular diseases. Prevention as control of this problem therefore, claims

priority attention.

03. Ayurveda opines that there is no specific treatment for Sthoulya, hence it has been

challenging medical problem from the Samhita period to this day.

Hence, the above subject was selected with an aim of understanding the

Subject in detail along with its management.

Introduction 2


Due to above reasons an attempt was made to suitable remedy for

Sthoulya mentioned in Charaka samhita and in all available Ayurvedic literatures. Thus,

Thryushanadya loham yoga was taken,which yoga is praised in by yogaratnakara as a

remedy for disease Sthoulya (Obesity).

To evaluate the effect of Thryushanadya loham in Sthoulya with special reference

to Hyperlipidaemia, clinical trial was conducted on 30 patients with pre & post test

design.

All the patients received Tryushanadya Loham yoga for 60 days and followed by

follow up for 30 days. The total duration of the treatment was 90 days

The lipid values and also sign and symptoms before and after the treatment were

compared. Totally five assessment were made to observe the effect in different stages.

To assess the effect of the treatment, variables were subjected for student’s ‘t’

test.

The result of the clinical study showed Tryushanadya Loham Shamana therapy

has a role in Sthoulya (Hyperlipidaemia).

Introduction 3


HISTORICAL REVIEW

Our ancient scripture Yajurveda quotes, “Oh God ! Give us a food which will keep us

away from diseases.” Charaka affirmed that in the beginning of Kritayuga people were

completely disease free and Ojovan like Devatas as they were getting foods which rich in

rasa, guna, veerya, and vipaka. As days passed some become rich and habituated to eat more,

which lead to increase in body weight. This increase in body weight lead the disease free

people of Kritayuga to the disease-full world. Thus, Medoroga is known since the times of

Kritayuga and is one of the causes for the disease to develop.

Two thousand five hundred years ago Hippocratus, noted that fat men “die suddenly”.

This suggests not only the disease but also he knew the severity of the increased mortality

rate due to obesity.

SAMHITA PERIOD

Charaka Samhita (Before 1000 BC)

Increase of disease may be high during that period, hence they able to study the

disease clinically and mention the specific line of treatment, and many single and

compounds. Outstanding being the knowledge of genetic role in the etiopathogenesis.

Sushruta Samhita (1000-1500 BC).

Increased incidences might have forced them to find the root cause. So Sushruta

clarify quotes Rasa is the cause for both obese and lean.

Astanga Hridaya (550 C A D)

Discussed Sthoulya in Dwividhopakramaneeya and included it under Langhana

therapy. Treatment aspect of Sthoulya is discussed but states, as there is no medicine for

Sthoulya.

Roopa 4


MEDIEVAL PERIOD

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

commentators. Hence most of the books of this period are collections of thoughts of previous

authors, commentaries of previous works.

Madhavakara (9 C AD)

Madhavakara renamed Sthoulya as Medoroga and compiled the disease from the

works of previous authors. But change of nomenclature indicates, instead of considering

anatomical change i.e. Shareera Sthulata he wanted to consider physiological changes in the

disease condition.

Chakrapani (11 C AD)

The commentator of Charaka Samhita gives a critical commentary over it but he has

not emphasized much about the disease in his own book Chakradatta.

Dalhana (12 C AD)

A commentator of Sushruta Samhita, clarify important queries by giving logical

answers.

Sharangadhara (13 C AD)

Even-though mentioned the disease in roganana prakarana, not considered in his

explanations.

Bhavamisra (16 C AD)

He specifies profuse sweating due to excess Medas creates a media for external germs

on the skin.

Yoga Ratnakara (17 C AD)

His views are almost similar to previous Acharyas,

Roopa 5


Few recent works done at different research centers are mentioned below.

Effect of Turmeric extract on Lipid profile BY Deshapande U.R. and group, at Tata

Memorial Hospital, Parel.

Development of Hypolipidaemic agents from plants and Traditional remedies By

Nityanand. S. at Central drug research Institute, Lacknow.

Hypolipidaemic effect of Fenugreek seeds, BY Sharma. R.D. at P.G. Department S.

N. Medical College, Agra.

Effect of Prunus amygdylus seeds on lipid profile, By Sunita Teotia at Centre for

Biomedical Engineering, IIT, Delhi.

Hypolipidaemic activity of Eleven different pectins, BY Valsa A. K. at Department of

Biochemistry, University of Kerala, Karivettam.

Hypocholesterolaemia action of three Guggulu preparations, By Nair R.B. RRI,

Trivendrum.

Hypocholesterolaemic effect of Terminalia arjuna tree bark, BY P. Gupta, at Dept. of

Pharmacology, SMS Medical College, Jaipur.

Terminalia arjuna : an Ayurvedic cardio tonic, regulates lipid metabolism in

hyperlipidaemic rates, by Kapoor N. K. at Div. Of Biochemestry, C.D.R.I. Lakhnow.

Effect of boiled Barley rice feeding in Hypocholesterolaemic and Normolipidaemic

subjects, By Tomia, M at National Institute of Health and Nutrition, Tokyo.

Preliminary screening of Hypocholesterolaemic activity in Solanum indicum, By

Badar, Y. at Pharmaceutical and fine Chemical Research Center, PCSIR Laboratory

Complex, Karachi.

Roopa 6


HETU

For a crystal clear picture of a diseased condition, it is necessary to be well versed

with the cardinal factors causing the medoroga (Obesity), which are five in number. They are

Hetu or Etiology, Purvarupa or Prodromal sings and symptom, Rupa or actual sign and

symptoms of the disease, Dosha samprapti the actual disease process or pathology occurring

in the body, and Upashaya, Positive response with treatment adopted for diagnosing a

disease.

Among them Hetu, which literally means the causative factor has its own place of

significance. It is a fact highlighted by the assertion of ancient seers that Nidana parivarjana,

removal of causative factors itself is treatment. A disease treated symptomatically tends to

recur, it the causative factors are allowed to persist. Hence knowledge of nidana is a must.

Comparative study of nidana according to different texts is given.

Table1: Nidanas of Sthoulya by different authors as fallows

Sl.N Nidanas Ch Su As BP MN Y.R

1 Shlesmala ahara - a - - a a

2 Guru, Madhura, Sheeta, Snigdha ahara a - a a - -

3 Adhika matra sevana a - - - - -

4 Adhyashana - a - - - -

5 Avyayama a a - a a a

6 Divashayana a a a a a a

7 Avyavya a - - - - -

8 Na chinta and shoka a - - - - -

9 Beeja swabhavaja a - - - - -

Aharaja hetu

Roopa 7


Shleshmala ahara, guru, madhura, and snigdha ahara, adhika matra sevana and

adhyashana all these come under aharaja nidana. Panchabhoutika level of their study revels.

Guru - Prithvi and Jala

Snigdha - Jala

Sheeta - Jala

Madhura - Prithvi and Jala

Meda - Prithvi and Jala

Kapha - Prithvi and Jala

There by as a rule, a similar quality increases the quantity, the increase kapha and

medas.

Ayurveda is not only very particular about quality but also about quantity and mode

of taking food. Annapana vidhi, Matrashriteya, Drava Dravyavijnaneeya etc chapters are

specifically meant for this. Quantities of the food and jataragni are interdependent. It means

food taken in a proper quantity only maintains Agni and this matra depends on Agni bala. So

adhika matra bhojana i.e. excess intake of food causes immediate aggravation of all the

tridoshas. This leads to disease manifestation in the body. Adhyashana is intake of the food

before the completion of digestion of previously consumed food. Dalhana has clearly told, in

the presence of deeptagni also adhyashna produces ama and leads to the formation of

madhura anna rasa, which in turn forms medovridhi.

The term Obesity is derived from the Latin word “obsus” which means having eaten.

Its very name suggests the root cause of obesity is over eating. Body needs 3000k cal/day to

meet basal needs, 500-2500 k k cal/day re required to meet the energy demands of daily

activities, if consumed more than this (i.e. dhika matra sevana) leads to obesity especially

Roopa 8


fats and carbohydrates having more caloric value 9.3 kcal/g and 4.1 kcal/g respectively

becomes the main cause for obesity.

Viharaja hetu

Avyayama, Avyavaya, Divashayana are categorised under Viharaj Nidana.

References from the classics revels Vyayama is a must for a person who takes more fatty

foods, since it reduced fat. Importance of Vyayama is exaggerated by saying “one who does

regular exercise need not think of guruta and laghuta of the foods.” Contrary to this lack of

exercise or Avyayama along with guru ahara definitely lead to madovriddhi. Vyavaya is also

a kind of physical work where in more calories is spent for one intercourse. If a person is not

indulging in vyavaya dhatu kshaya will not take place instead it gives dhatupusti which leads

to medovriddhi. It is strictly advised for an obese person not to sleep in the day and less sleep

even in the night. Because walking in the night causes rukshata and daytime sleep increases

snigdhata that causes kaphavriddhi and leads to Sthoulya.

Manasika hetu

Achinta and shoka can be included under this heading Ayurveda considers manasika

karana also as an important entity for disease manifestation. Here is Sthoulya also harsha

nityatwa and Achinta and shoka that are manasika karanas definitely influence the Sthoulya.

Mental disturbances cause vata vriddhi that indirectly causes dahtu kshaya where as prasanna

manas always increases kapha hence becomes hetu of the Sthoulya.

Beeja swabhava

Charaka samhita is the only text in Ayurveda that explains beeja swabhava as a

causative factor. Commenting over the word beeja swabhava Gangadhara and Chakrapani

have clearly told, “atisthula mata pitra sonitha sukra swabhavat which means the character of

Roopa 9


Sthoulya is inherited from obese parents. Study also revels there is 50% of chance for

children being obese when one of the parents is obese, this proportion rinsing to 75% with

both parents obese. Obesity runs in families. Further more, identical twins usually maintain

weight leaves within 2 pounds of each other through out life, it they live under similar

condition. Or within 5 pounds of each other if there condition of life differ markedly, this

might result from eating habits engendered during childhood but it is generally believed that

this close similarity between twins is genetically controlled.

Hormonal cause

Ayurveda is silent abut endogenous obesity Dr. Jeffrey’s Flier explains there is no

established endocrine cause for most cases of obesity. However endocrinologists frequently

are consulted because of concern that the patient may have cushing syndrome or

hypothyroidism. Endocrine syndromes that may be associated with obesity are3 cushing

syndrome, Hypothyroidism, insulinoma, Craniopharyngioma, Turner syndrome, Male

hypogonadism.

Influence of dietetics in Pregnancy

Disorders such as obesity, diabetes, cancer, heart disease etc are not only the result of

inheritance but also etiological factors. The new science of fetal programming suggests that

as pregnancy progresses, each month in the womb shapes our health for life. Under nutrition

during the fetus’s first trimester makes obesity more likely in adult hood, perhaps the appetite

control center in the brain programmed to over eat. One best evidence can be quoted here. In

world war II Nazis tried to starve the population of western Holland from September 1944

until the following may. Men who were fetuses during all or part of the period are studied. If

their mothers were starving during the first trimester from March to May 1945 but got

Roopa 10


adequate food later delivered heavier, longer and with larger head babies than in normal

period. As adults they were more likely to be obese. If their mothers went hungry only in the

final trimester (born in Nov 1944) they were lean.

It the food is scarce during the first trimester, the fetus develops a so-called thrifty

phenotype. Its metabolism is set so that every available calorie sticks and scarcity of food

may effect the appetite centers in the fetal brain, and sets as “eat whatever is around, you

never know when famine will hit”.

SAMPRAPTI

Roopa 11


The samprapti for the disease explains the method or process by which the vitiated

doshas reach the dooshyas and produce the anatomical and physiological changes in the

target organs leading to expression as a disease. Usually this process follow a regular pattern

according to samanya siddhantas of Ayurveda that is why “Samyak prapti or vyadhi is

known as samprapti” Exceptionally in diseases like medoroga it differs from regular

samprapti. Hence deep study and detai9led analysis over pathogenesis of Medoroga carries

importance. The samprapti of medoroga has been vividly described in almost all the

textbooks of Ayurveda. Views of all the authors goes on a similar line, accept Astanga

Sangrahakara, where he deviates a little.

Absence of physical activity, sleeping during day and kaphakara aharas induced

madhuryata to annarasa, which in turn increase the medas by its snigdha guna. This obstructs

the nutrients channels of the by its Snigdha guna. This obstructs the nutrients channels of the

remaining tissue depriving them of nutrition. So only fat accumulates in large quantities in

the body. Because of obstruction, Vayu in kosta begins to act fast, increases the digestive

activity rapidly, making voracious hunger an d craving for large quantity of food, just as the

forest fire destroy the forest, the Vata and Agni destroy the body resulting into hyper

metabolic activity.

This samprapti of medoroga is confusing due to the Medoagni mandyata and

formation of ama in presence of teekshnagni and where as successive dhatus are not

nourished even the medas is over nourished. Hence here “Rasat Raktam tato Masam” theory

fails. Thus clarification at the level of process of pathogenesis is required. At this junction

discussion abut agni, dhatu poshana and ama concerned to Medoroga is essential.

Jataragni

Roopa 12


In medoroga both the extremes of vitiated Agni can be seen at different levels.

Mandagni, in the manifestation of the disease and teekshagni, in aggravating the condition. In

the beginning none of the authors have specified about teekshagni, instead it is mentioned

after Medodhatu vriddhi.

All the nidanas specified for Medoroga like excessive intake of, Guru, Sheeta aharas

and not indulging in sufficient physical exercise are the supportive factors for the production

of Ama, which is formed due to hypo function of ushna. This ama or Madhura annarasa by

its snigdha guna increases medas there by like other diseases here also mandagni is the root

caused of the disease. After the accumulation of fat, teekshnagni play an important role.

Vayu obstructed by Medas in kosta increased Agni under kumbakar pawan nyaya, making

for voracious hunger and craving for large quantity of food. This Agni will be so strong and

harmful if proper food is not supplied to it, it destroys body as fire destroys the forest.

Dhatwagni

In Medoroga a ling between Jataragni and Medodhatwagni is broken and therefore

even when the function of Jataragni is good the functions of Medogni is not so. This is

because whatever the outcome of the Ahar i.e. either pakwa rasa or ama rasa, it has to be

supplied to all dhatus for their nourishment; in medoroga rasa is rich in snigdha guna, and is

similar to medas. There by it is supplied to Medodhatwagni, which increases the medodhatu.

Agni and Ahara are interdependent. Ahara is the fuel for agni and agni bala depends on the

material supplied to it for digestion. In medoroga excess quantity of ahara rasa is supplied to

Medodhatwagni, which causes agnimandya and forms ama at medodhatu level.

Dathu poshana in Medoroga

Roopa 13


Since ama represents the vitiated or deficiently formed ahara rasa of rasadhatu with

poor nutritional capacity, there is a disturbance in dhatu poshana. In Medoroga, medas is

increased abundantly. Hence there will be disparity between medas and other dhatus.

Charaka accepts atimedovriddhi but not mentioned any cause for it. Sushruta tried to clarify

it and he tells remaining dahtus are not nourished because of Margavarodhata. Astanga

sangrahakara further gives the explanation as, the remaining portion of rasa dhatu being very

little in quantity is not enough to nourish the raktadi dhatus and also quotes one samanya

siddhanta as “that which has undergone increase first will only undergo increase further and

tells like vayudi fat also follow it, there by only Medo vriddhi is seen compared to other

dhatus. Dalhana divides dhatus as Poorvadhatu and Uttaradhatu and explains

undernourishment of uttaradhatu is due to Avruta marga and because of vishista aharavashat,

Adrastavashat and Medasavruta margata, over sending Rakta and mamsa directly Medas is

increased. Hence poorvadhatu undernourishment is justified and present context.

The specific nutrients of one dhatu are not channeled to any other dhatu. The portion

of Ahara rasa meant to provide nourishment to a particular dhatu does not come in contact

with other dhatus. According to khalekapota nyaya, as there resting places attract pigeons,

the sthayi dhatus attract their requisite nutrients from the Ahararasa through their specific

dhatuvaha srotases and nourish themselves. Hence when Madhura annarasa rich in

snigdhaguna moves through channels, nourish only medas and as ahararasa is having less

quantity of requisite nutrients of otherdhatus they are not properly nourished.

Ama

Roopa 14


As both jataragni and dhatwagni are impaired in medoroga, production of jataragni or

dhatwagnijanya ama is common. All the authors have used the word madhura annarasa.

Vagbhata specially tells kapha mishrita annarasa acts as ama. Madhukosha commentary says

if annavaha srotas is coated with madhura annarasa that turns all the food into madhura.

Sushruta tells, at the time of production of Pitta in annavaha srotas (ama vipaka), if food is

consumed it turns into vidhahi. As dalhana tells adhyashana sheelata is the cause for

production of ama in presence of teevragni, there by it can be said during the time of

production of kapha in annavaha srotas (madhura vipaka), food is again consumed because of

adhyashanasheela that leads to the production of madhura annarasa or kaphamishrita

annarasa. This avipakwa Rasa is known as ama.

Now it is more appropriate to say, because of jataragnijanya ama dhatwagni is

impaired and dhatwagnijanya ama is formed. Proper conversion of poshakadhatu to poshya

dhatus dose not takes place due to medoagni mandyata and more dusta medas is formed. This

medodhatu being produced due to dhatwagni mandya is knows as samadhatu. Thereby

medoroga is included under sama medodhatu janya vikaras.

POORVA ROOPA

Roopa 15


The poorvaroopa of Medoroga are not specifically mentioned by any of the authors.

The roopas mentioned for medoroga are

- Increase in Medodhatu

- Pendulum movements of buttocks, abdomen and breast

- Lack of enthusiasm in physical activities

- Disproportion growth of the body.

However the general principle about poorvaroopa states that, “roopa of the vyadhi

when found in Avyakta or alpa avastha is considered as poorvaroopa. So, medovriddhi

before to the pendulum movement of Spik, Sthana, Udara can be considered as Poorvarupa.

Before the manifestation of the disease, Agni is depraved and once the medas start

accumulating, it turns into teekshagni. Similarly as kapha vriddhi is observed, lakshanas told

in kriyakalavastas of kapha are seen.

ROOPA

Roopa 16


Roopa is the prominent diagnostic parameter of a disease. At this stage, Dosha

Dooshya Samuchhaya is completed & the onset of the diseases takes place, which gives the

symptomology of the disease. These sign & symptoms may change from time to time

according to the progress of the diseases. Certain symptoms may newly appear while some

may disappear. We cannot find all the symptoms in every patient at once unless the diseases

becomes grave.

Table2: Laxanas of Sthoulya by different authors as fallows.

Sl.No. Laxana Ch Su AS MN BP YR

01. Chala Spik Udara & Stana * - * * - *

02. Kshudra Shwasa - * - * * *

03. Ayasa - - * - - -

04. Alpa Bala * - * - * -

05. Ati Kshudha * * * * * *

06. Ati Pipasa * * * * * *

07. Ati Nidra - * * * * *

08. Ati Swada - * * * * -

09. Dourgandhya * * * * * *

10. Moha - - - * * *

11. Kratana - * - - * *

12. Utsaha Hani * - * * - -

13. Javoparodha * - - - - *

14. Jadya - - * - - -

15. Soukumaratva - - - * - -

16. Krachhra Vyavayatva * - - * * *

17. Gadgadatwa - * * - - -

18. Alpa Ayu * - * * - *

It is very interesting to study how these lakshanas are manifested.

Roopa 17


1. Chala Spik, Udara, Sthana

Through the medas is spread throughout the body, its seats of accumulation are

Udara, Spik, and sthana. Thus increased medas accumulates more at these places and leads to

pendulum movement of them.

2. Kshudra Swasa

Excessive fat accumulation in the abdomen interferes with the mechanism of

respiration. Respiration act depends on the movement of the diaphragm. Because of

accumulated fat, diaphragm fails to move up and down o the expected extent, hence pressure

created during contraction phase will not be sufficient to expel out air from the lungs. This

excess carbondioxide present in the blood stimulate the respiratory center, which leads to

kshudra swasa.

3. Alphabala, Ayasa and Sukumarata

The main function of medas is giving dridata and bala to the body. In Sthoulya we

find abundant medas but controversy to it we get symptoms like alphabala, ayasa,

sukumarata. Chakarapani has commented over the word medodosha as dustamedas.

Dustamedas cannot be expected to do its normal function i.e. dridatwa to the body and at the

same time poorva dhatus and uttardhatus of meda are undernourished. So all the sapta dhatu

dourbalya takes place which from the above said conditions.

4. Atikshuda and Pipasa

The increased fat obstructs the channels of vata. Vata then begins to act within

Amashya, increases the digestive activity, making for voracious hunger and thirst, which are

appetitive mechanisms.

5. Kricchra Vyavaya

Roopa 18


Sthoulya rogi faces difficulty in intercourse because of two reasons. Foremost is

undernourished shukra dhatu and on the other hand is the alpa bala or inability to perform

any act. Proper quantity of shukra raised the feeling of enjoyment (arousal) contrary in

shukrakshaya condition. After prolonged intercourse in shukra kshaya condition, instead

of secretion of shukra, sarakta veerya is being secreted. This is definitely a difficult

intercourse or kricchra vyavaya. Whole of this act needs utsaha, bala or ability, which is

absent in medorogi. So it is a common symptom we find in Sthoulya rogi which disturb

his mental state as well as sexual life.

6. Alpa Ayu.

Life is very important factor and body is like a driver for chariot. Ayurveda is

meant for maintenance and fulfilling the desire of long living. So leaving aside all other

things body is to be protected. Since body is produced and maintained by food person should

take wholesome foods. Those who cultivate the habit of taking whole some food will not

gives rise the victims premature death, loss of strength and enthusiasm. Where as medorogi

become a self-victim for his reduced longevity by adopting unwholesome food habits. Excess

increase of medas causes the dhatu kshaya of all other dhatus and is associated with an

increased incidence of cardiovascular, gall bladder diseases, diabetes, and other conditions,

which are fatal important sings of increased mortality rate.

7. Ati Nidra

In obese patents excess sleep is commonly observed. Kapha, because of its increased

quantity, which is not undergoing regularity, obstructs the srotas. This srotorodha causes

heaviness of the body, from heaviness follows laziness, which in turn causes excess sleep and

lethargic ness in the body.

Roopa 19


8. Sweda and Dourgandha

All classics consider atisweda and dourgandha as lakshanas of Sthoulya and further

gives explanations 1.By the presence of fat, at the origin of the channels of sweat increase in

secretary activity and 2. Association of kapha makes profound increase of sweat.

Contrary to this Charaka use the word swedabhadha and Chakrapani commenting over it as,

“production of sweda is the function of meda where as in Sthoulya due to shleshma samsarga

this produced seat is obstructed”. Gangadhara have also clearly commented swedabhadha

means “sweda is not excreted” So Charaka accepts the excess production of seat but he is

differing from others by saying as it is not excreted out properly. Meda is having amaghanda

by nature, in the presence of dusta medas in Sthoulya gives raise still worse odour. Excess

production of sweat, which is the mala of meda, gives daurgandha in the body.

9. Gadgadhatwa

Gadgadhatwa means the “Avyakta vachanam” according Dalhana. Which means

stammering or unclear pronouncetion of word or even hoarseness of the voice, which is the

more appropriate word to be considered.

10. Krathana.

Excess kapha obstructs pranavaha srotas resulting in krathana. In Ayurveda, even

though all the above said lakshanas are explained for Sthoulya, a diagnostic key for

considering a person as obese is given specifically. The person can be said as obese when he

has lack of enthusiasm in physical activities, disproportional to the growth of his body,

intense increase in mamsa and meda, and has movement of the buttocks, abdomen and

breast.

Roopa 20


Parallel to this some more keynotes are available from modern concepts. A number of

different criteria have been suggested to identity the obese person. Important among them are

mentioned here.

1. Standard height and weight relation

The most influential application of this approach has been through the use of life

insurance data that assesses mortality as a function of body weight per height, adjusted for

frame size, with obesity defined on purely statistical grounds as a weight that is above the

average weight for given height. The charts are given below:

Table No. 3: Ideal weights for men

Height (ft) Small frame (kg) Medium frame (kg) Large frame (kg) 5.2 50.8-54.4 53.8-58.5 57.2-64.0

5.3 52.2-55.8 54.9-60.3 58.5-67.1

5.4 53.5-57.2 53.2-61.7 59.9-67.1

5.5 54.9-58.5 57.6-63.0 61.2-68.9

5.6 56.2-60.3 59.0-64.9 62.6-70.8

5.7 58.1-62.1 `60.8-66.7 64.4-73.0

5.8 59.9-64.0 62.6-68.9 66.7-75.3

5.9 61.7-65.8 64.4-70.8 68.5-77.1

5.10 63.5-68.0 66.2-72.6 70.3-78.9

5.11 65.3-69.9 68.0-74.8 72.1-81.2

6.0 67.1-71.7 69.9-77.1 74.4-83.5

6.1 68.9-73.5 71.7-79.4 76.2-85.7

6.2 70.8-75.7 73.5-81.6 78.5-88.0

6.3 72.6-77.6 75.7-83.5 80.7-90.3

6.4 74.4-79.4 78.1-86.2 82.7-92.5

Table No. 4: Ideal weights for women

Height (ft) Small frame (kg) Medium frame (kg) Large frame (kg)

Roopa 21


4.10 41.7-44.5 43.5-48.5 47.2-54.0

4.11 42.6-45.8 44.5-49.9 48.1-55.3

5.0 43.5-47.2 45.8-51.3 49.4-56.7

5.1 44.9-48.5 47.2-52.6 50.8-58.1

5.2 46.3-49.9 48.5-54.9 52.2-59.4

5.3 47.6-51.3 49.9-55.3 53.5-60.8

5.4 49.0-52.6 51.3-57.2 56.7-64.0

5.5 50.3-54.0 52.6-59.0 56.7-64.0

5.6 51.7-55.8 54.4-61.2 59.5-66.2

5.7 53.3-59.4 58.1-64.9 62.1-69.9

5.8 55.3-59.4 58.1-64.9 62.1-69.9

5.9 57.2-61.2 59.9-66.7 64.0-71.7

5.10 59.0-63.5 61.7-68.5 65.8-73.9

5.11 60.8-65.3 63.5-70.3 67.6-76.2

6.0 62.6-67.1 65.3-72.1 69.4-78.5

2. Body mass index

A second approach for defining the obese state is body mass index (BMI). It can be

calculated by using the formula

BMI = Weight in Kg

Height in (meter)2

Table No. 5: Optimal BMI values are given below

Roopa 22


Height (cms)

Body weight in Kilogram

90 85 80 75 70 65 60 55 50 45

135 49.4 46.6 43.9 41.2 38.4 35.7 32.9 30.2 27.4 24.7

140 42.8 43.4 40.8 38.3 35.7 33.2 39.6 28.1 25.5 23.0

145 42.8 40.4 38.0 35.7 33.3 30.9 28.5 26.2 23.6 21.4

150 40.4 37,8 35.6 33.3 31.1 28.9 26.7 24.4 22.2 20.0

155 37.5 35.4 33.3 31.2 29.1 27.1 25.0 22.9 20.2 18.7

160 35.2 33.2 31.3 29.3 27.3 25.4 23.4 21.5 19.5 17.6

165 33.1 31.2 29.4 27.5 25.7 23.9 22.0 20.2 18.4 16.5

170 31.1 29.4 27.7 26.0 24.2 22.5 20.8 19.0 17.3 15.6

175 29.4 27.8 26.1 24.5 22.9 21.2 19.6 18.0 16.3 14.7

180 27.8 26.2 24.7 23.1 21.6 20.1 18.5 17.0 15.4 13.9

185 26.3 24.8 23.4 21.9 20.5 19.0 17.5 16.1 14.6 13.1

With BMI 25 to 30 are defined as over weight and of those in excess of 30 are

defined as obesity.

3. Waist- to- hip ratio

Recent evidence suggests that central obesity as judged by the waist to hip ratio is

evident as many of the most important complications of obesity, including insulin resistance

diabetes, hypertension and hyperlipidaemia are linked to the amount of intra abdominal fat,

rather than to lower body fat (i.e. buttocks and leg) or subcutaneous abdominal fat. A waist-

to – hip ratio for men is 0.9 while that for women if > 0.85 is ideal.

Table 6: Waist measurement in cms Hip 50 55 60 65 70 75 80 85 90 95 100 105 110 115 120 125 130

Roopa 23


Cms

50 1.00 1.10 1.20 1.30 1.40 1.50 1.60 1.70 1.80 1.90 2.00 2.10 2.20 2.30 2.40 2.50 2.60

55 0.91 1.00 1.09 1.18 1.27 1.36 1.45 1.55 1.64 1.73 1.82 1.91 2.00 2.09 2.18 2.27 2.36

60 0.83 0.92 1.00 1.08 1.17 1.25 1.33 1.42 1.50 1.58 1.67 1.75 1.83 1.92 2.00 2.06 2.17

65 0.77 0.85 0.92 1.00 1.06 1.15 1.23 1.31 1.38 1.46 1.54 1.62 1.69 1.77 1.85 1.92 2.00

70 0.71 0.79 0.86 0.93 1.00 1.04 1.14 1.21 1.29 1.36 1.84 1.50 1.57 1.67 1.78 1.70 1.86

75 0.67 0.73 0.80 0.87 0.93 1.00 1.02 1.13 1.20 1.28 1.41 1.40 1.47 1.61 1.60 1.67 1.73

80 0.63 0.69 0.75 0.81 0.88 0.94 1.00 1.06 1.13 1.19 1.25 1.31 1.38 1.44 1.50 1.56 1.63

85 0.59 0.65 0.71 0.76 0.82 0.88 0.94 1.00 1.06 1.12 1.18 1.24 1.29 1.35 1.41 1.47 1.53

90 0.56 0.61 0.68 0.72 0.78 0.83 0.89 0.94 1.00 1.06 1.11 1.18 1.22 1.28 1.33 1.39 1.44

95 0.51 0.56 0.63 0.68 0.74 0.79 0.84 0.89 0.95 1.00 1.05 1.11 1.16 1.21 1.26 1.32 1.37

100 0.50 0.55 0.60 0.65 0.70 0.75 0.80 0.85 0.90 95 1.00 1.05 1.10 1.15 1.20 1.25 1.30

105 0.48 0.52 0.57 0.62 0.68 0.71 0.76 0.81 0.86 0.90 0.95 1.00 1.05 1.10 1.14 1.19 1.24

110 0.45 0.50 0.55 0.59 0.64 0.68 0.73 0.77 0.82 0.86 0.91 0.95 1.00 1.05 1.09 1.14 1.18

115 0.43 0.48 0.52 0.57 0.61 0.65 0.70 0.74 0.78 0.83 0.87 0.91 0.96 1.00 1.04 1.09 1.13

120 0.47 0.46 0.50 0.54 0.58 0.63 0.68 0.71 0.76 0.79 0.83 0.88 0.88 0.98 1.00 1.04 1.08

125 0.40 0.44 0.48 0.52 0.56 0.60 0.64 0.68 0.72 0.76 0.80 0.84 0.85 0.92 0.96 1.00 1.04

130 0.38 0.42 0.46 0.50 0.54 0.58 0.62 0.65 0.69 0.73 0.77 0.81 0.81 0.86 0.92 0.96 1.00

135 0.37 0.41 0.44 0.48 0.52 0.56 0.59 0.63 0.67 0.70 0.74 0.78 0.79 0.85 0.88 0.93 0.96

140 0.36 0.39 0.43 0.46 0.50 0.54 0.57 0.61 0.64 0.68 0.71 0.75 0.76 0.82 0.86 0.84 0.91

145 0.34 0.38 0.41 0.43 0.48 0.52 0.55 0.59 0.62 0.66 0.69 0.73 0.75 0.78 0.81 0.83 0.88

150 0.33 0.37 0.40 0.41 0.46 0.50 0.54 0.57 0.60 0.64 0.67 0.70 0.74 0.77 0.80 0.81 0.84

CLASSIFICATION OF MEDOROGA

Supporting references from the classics are not available to discuss the types of

medoroga. Astodareeya Adhyaya of Charaka, Rogagnana Prakarana of Sharangadhara

specially deal with types of disease. Charaka have not mentioned Modoroga in his

Astodareeya chapter where as Sharangadhara clearly said Medoroga is of only one type.

Though the description of Medoroga/Sthoulya is mentioned in most of the classical

texts like Charaka samhita, Sushruta Samhitas, Astanga Sangraha, Bhavaprakasha, Madhava

nidana, Yoga Ratnakara, Chakradatta etc., but none of the author have classified Medoroga.

Roopa 24


Vitiation of doshas may take place at the level of samprapti but ultimately meda dhatu is the

only one that has to be increased, to consider the condition as Medoroga. This may be the

reason for not making any types in it. Hence it can be said that according to Ayurveda

medoroga is of only one type.

But for the convenience of study it can be classified as following.

Type 1

1. Aharajanya - Cosnuming Snighdadi Ahara, Adhyashana, Atimatra sevan etc,

2. Viharajanya - Diwaswapna etc,

3. Manasika Janya – harsha nityatwa etc.

4. Beeja swabhava – heredity.

Type 2

1. Sahaja - Beejaswabhava

2. Janmottaraj – Ahara, Vihara and Manasikakarana janya

Type 3

1. Sandhya medoroga – navotpanna, Alpalakshanayukta

2. Asadhya Medoroga – Puratna Upadravayukta

Beejaswabhavaja etc.

In modern text we find classification of obesity as

Type I

1) Exogenous – this is more common and due to excessive caloric intake.

Here uniform distribution of fat with little execs under chin and

abdomen is seen

Roopa 25


2) Endogenous- here endocrine factors are at fault and obesity occur in

spite of small caloric intake.

Type II

Depending on the distribution of fat this classification is made.

1. Generalised type – uniform distribution of fat.

2. Centr4al or trunk – at trunk and neck

3. Superior or buffalo – at face, neck, arms and upper part of trunk

4. Inferior at lower trunk and legs

5. Girdle – at hips, buttocks, abdomen

6. Breeches or trochentric- only buttocks

7. Lipomatous- localized deposits of fat over body.

Type III

1. Hypertrophic obesity – increase in amount of fat per fat cell.

2. Hyper plastic obesity – increase in number of fat cells.

SADHYASADHYATA

Before starting the treatment of any disease it is essential to know whether that

particular state of the disease is curable or incurable. Almost all the texts consider Sthoulya

as kasta sadhya when compared with treatment of krishatwa. But Vagbhata goes to an extent

of saying there is not treatment for Sthoulya; neither Brimhana therapy nor Langhana therapy

are sufficient to control excessive fat accumulation and to decrease agni and Vata. Indu

commenting over it states, brimhana therapy given to a obese person will decrease agni and

Roopa 26


Vata but not the medas, where as Langhana therapy will decrease medas but increases agni

and Vata. So treatment is very difficult.

Modern texts say successful treatment of obesity means sustained attainment of

normal body weight and composition without producing unacceptable treatment induced

morbidity, is rarely achievable in clinical practice.

Medoroga can be considered as kasta sadhya, if it is navotpanna, having less

intensity, and without complications.

UPADRAVA

Complications appearing after the manifestation of the Prime disease and which are

difficult to treat are termed as upadravas. Agni sand vata, in their aggravated state cause

many of upadravas in Medoroga.

Table No. 7 : Upadravas of Sthoulya by different authors Sl.No. Upadravas Ch Su

A S B P M N Y R

1 Vata pitta Vikara a - - - a -

Roopa 27


2 Prameha Pidika - a a - - -

3 Jwara - a a a - a

4 Bhagandara - a a a - a

5 Vidradhi - a a - - -

6 Vatavikara - a - - - -

7 Udar roga - - a - - -

8 Prameha - - a a - a

9 Urustambha - - a - - -

10 Kushta - - - a - -

11 Visarpa - - - a - a

12 Atisara - - - a - a

13 Arsha - - - a - a

14 Shleepada - - - a - a

15 Apachi - - - a - a

16 Kamala - - - a - a

17 Jantavo Anavaha - - - a - -

Key : a = Present - = Absent

It is clearly mentioned, increased medas cause profuse sweating and bad odour of the

skin, which creates a media for production and survival of germs (anu jantus). There by

many of of the skin diseases like kusta, visarpa etc are seen as upadravas and atisweda

mentioned as poorvarupa for kusta. Impairment of Medovaha srotas in medoroga may lead to

the disease Prameha and prameha pidika.

Roopa 28


Ama condition present in Sthoulya may lead to urustamba, atisara, jwara etc. the

etiological factors viz Avyavya, Avyayama, diwaswapna are similar to both Medoroga and

Arsha. These factors are increased more because of inactive nature of obese person, which

probably leads to arsha. Obstruction of swedavaha and ambuvaha srotas leads to udara, as

excess medas obstruct the srotases, this condition may arise as upadrava in obese person.

Vata get aggravated because ofobstruction and give rise many of the vata vyadhis as

upadravas.

Modern concept

Obesity has psychological, behavioral and medical consequences; the nature and

severity of which are influenced by the degree of obesity. The common pathological

consequences of obesity are discussed here.

Non-insulin dependent diabetes -

Obesity is major risk factors for NIDDM and as many as 80% of patents with

NIDDM are obese.

Cardiovascular Disease –

Epidemiological studies reveal that obesity is associated with an increased mortality

and morbidity from cardiovascular disease. Increased mass of tissues result in increased

cardiac work. Blood volume, stroke volume and cardiac out put are all increased. Obesity is

also associated with an atherogenic lipid profile.

Pulmonary disease -

The increased metabolic rate in obese subjects increases oxygen consumption and

CO2 production, and these changes result in increased minute ventilation. In subject’s with

marked obesity, compliance of the chest wall is reduced, the breathing is increased and the

Roopa 29


respiratory reserve volume and vital capacity are reduced, a resultant mismatch between

ventilation and perfusion may result in hypoxemia. Severe obesity may cause

hypoventilation, defined by the development of CO2 retention.

Gall stones –

Obesity is associated with enhanced billiary secretion of cholesterol. This results in

super saturation of bile and a higher incidence of gallstones.

Endocrine consequences –

Many changes injunction of Thyroid, Gonadal, Adrenal and Pituitary functions can be

seen in patients with established obesity.

CHIKITSA

Ahara

Even-though the disease is Santarpanajanya; langhana is contraindicated 1 as it

increases the vata that is the prime cause for the Medoroga. There by if the food is not

supplied timely aggravates agni & creates many disturbances in the body. Keeping this in

the mind, dietetics has to be planned in such a way that ahara should be guru for agni but at

Roopa 30


the same the time it should cause Apatrapana. Many of the Aharadravyas are advised on this

line, which are mentioned in Pathyapathya. Many of the experimental studies have been done

on the fasting & the inference is that during the period of fasting, the blood pressure goes

down, ketosis & hyperureceamia occurs. Thus it is advised to undertake prolonged fasting

programme under medical supervision. So instead of advising for langhana it is better to

follow the classical treatment which explains to Agni, which does not cause Santarpana. It

almost sounds similar to more quantity but less calorie diet.

Diet for obese person should be planned that the body weight get about 50 – 60 gm.

of protein per day, which is necessary for maintaining nitrogen balance in the body, 100 gm

of carbohydrate, 40 – 50 gm. of fat. This proportion of protein, carbohydrate & fat has to be

maintained which otherwise disturbs the metabolism. The total calories allowed to an

individual will depend upon the present weight, activity levels of the patient.

Vihara

Vyayama, Vyavaya, Anidra, Chinta, Shoka, Shrama, Gamana are the vihara roopa

treatment mentioned in the classics. Lacks of the factors are mentioned as for Stholya.

Hence, we can say this is one of the nidana parimarjana line of the treatment. Regular

exercise is recommended as an important component of all obese management regimens.

Exercise help a person to spend energy & reduce his weight; & increases the basal

metabolic rate of the body which in turn burns away the excess fat & benefits in lipid

abnormalities. An exercise improves the muscle tone & remove wrinkles & flabbiness of the

skin. Simple walking or exercise, when energy worth 3500 calories is spent, the weight is

reduced by 1 pound. Table below show energy spend in different types of the physical

activity.

Roopa 31


Table No. 8 : Type of Physical Activity

Sl.No. Type of Physical Activity Energy spent per minute

01. Sitting, Standing, Reading, Writing 1.5

02. Driving Car, Tailoring 2.0

03. Household chores 2.2

04. Gardening 5.0

05. Walking 5 km/hr. speed 3.0

06. Fast walking speed 9 km/hr. speed 9.0

07. Light exercie of yoga 4.0

08. Cycling (Depending upon speed) 3.5 – 8.0

09. Table tennis 5.5

10. Games like Kho-Kho, etc. 8.0

11. Lawn tennis 6.0

12. Dancing 5.0

13. Swimming 3 km / h. speed 9.0

14. Skipping 7.0

15. Running (Depending upon speed) 10 – 25

16. Heavy exercise 8.0

Aushadhi: This can be discussed under two headings

1) Shodhana

2) Shamana

Shodhana

Under the shodhana we can consider Rookshna Udwarthana, Snana, Lekhana Basti,

& Shodhana.The general term shodhana is used by Vagbhata which indicates all the

panchakarmas. But when we see the Dosha & contraindications of Panchakarma it reveals –

Snehana – As a general rule Snehana should not be administered in

medoroga. But tila taila prayoga is indicated in Medoroga. It may be

Roopa 32


because of its Sukshma & Vyavayi through which it opens the

Medoavritha Srotas & Ushna guna of it reduces the kapha.

Swedana – Swedana for obeses patient is contraindicated but if

essential mrudu sweda is adviced

Vamana – Not ondicated in Shoulya where as in conditions like

Amadosha & Kapholbana vamana can be adviced with Yastimadhu.

Virechana – Not indicated but with special precautions can be used.

Basti – Lekhana Basti is indicated.

Nasya & Raktamokshna – Clear- cutindication is not available.

Shamana

Eventhough Meda, Vata & Kapha Nashana is said as Chikitsasutra , the drug

planned should have Deepana & Pachana property to enhance Agni & Amapapaka. As

obstruction of srotasa is main factore in medoroga, the drugs must have Rookshna &

Chedana property to produce srotovishodhana. Along with these Ati teekshna, ushna,

rooksha, guna dravyas are adviced as they are opposite to manda, snigdha & sheeta gunas of

kapha & meda. These by they subside Meda & Kapha.

Five types of fat reducing drugs are used in modern sciences.

Anti appetite

Drugs reducing the level of sugar in the

Metabolic stimulants

Laxative drugs

Roopa 33


Diuretics

And surgical treatment is also advised in the treatment of obesity as lipo suction.

Roopa 34


The disease obesity considered under the metabolic disorder. Metabolism refers all

chemical processes in living beings producing energy and growth. The changes which occur

in the digested food stuffs time of ingestion till the elimination in the form of excretion, the

sum of total chemical changes which takes place within the body is to be considered as

metabolism which yields energy and enriches growth. As obesity is deposition of fat in the

body, it is justified to be under the heading of metabolic disorders.

Origin of the body fat is from fats, carbohydrates and proteins in the food. The

carbohydrates and proteins consumed in excess are converted into fats through the citric acid

cycle. Hence study of metabolism of carbohydrate, protein and lipid are essential in this

regard.

Carbohydrates

Carbohydrate metabolism takes place under three headings- Supply, Storage & utility.

Supply is regulated through the diet temporary storage in liver and utility by the cell & tissue

& muscles. Absorption of glucose takes place mainly into the capillaries of the small

intestine. These capillaries take the contains into the portal circulation to the liver.

The liver cells take the glucose from the blood and convert into the glycogen which

stored in the liver cells. The sugar stored in the liver as a glycogen is converted as a glucose

whenever needed it is released into the blood stream which will be taken up by the muscles

and the other tissues. The maximum storage of the glycogen in the body is about 400 gms.

Protien

Proteins are hydrolised into the amino acids after digestion and absorbed by the villi

and through the portal circulation enter the liver. The tissues select some of these substances

and in each organ either synthesized into new tissues or used to maintain and repair tissues.

Amino acids not used in synthesis are broken down or diminished in the liver. In demisation,

the amino groups are removed from amino acids molecules. The non-nitrogenous portion of

the amino acid molecules is oxidized to liberate energy or is synthesised in to glycogen or

fat. Therefore this portion of the amino acid molecule may be regarded as a source of energy.

Lipids 34


LIPIDS

Lipids may be defined as compounds, which are relatively insoluble in water, but

freely soluble in organic solvents like benzene, ether, chloroform, etc. Lipids constituted a

heterogeneous group of compounds of biochemical importance.

They are found in the membranes, which maintain the integrity of cells & allows the

compartmentalization of cytoplasm in to specific organelles. Lipids function as a major form

of stored nutrients (TGs), as a precursor for adrenal & gonadal steroids & bile acids

(cholesterol) & as an extra cellular & intra cellular messenger (prostaglandins). Lipoproteins

provide a vehicle for transporting the complex lipids in the blood as water – soluble

complexes & deliver lipids to cells through out the body.

Classification of Lipids

Lipids are classified into simple lipids, compound lipids, derived lipids &

miscellaneous one.

A. Simple Lipids : Esters of fatty acids with various alcohols

i) Neutral fats

ii) Waxes

B. Compound Lipids

Esters of fatty acids containing groups other than & in addition to an alcohol & fatty

acids.

i) Phospolipids

ii) Glycolipids

iii) Sulpholipids

iv) Aminolipids

v) Lipoproteins

C. Derived Lipids

Derived lipids obtained by hydrolysis of those given in those group A & B

which still possesses the general characteristics of lipids.

i) Fatty acids

ii) Monoglyceriods

iii) Alcohols

Lipids 35


D. Miscellaneous

i) Aliphatic hydrocarbons including iso-octa-decome

ii) Carotenoids

iii) Squalence

iv) Vit. E & K.

Fatty Acids

Fatty acids may be defined as an organic acid that occurs in a neutral TG & are

monocarboxylic acid ranging in chain length from 6-24 carbon atoms. In human body free

fatty acids are formed only during metabolism due to hydrolysis of fat.

Fatty acids

A. Depending upon no. Of Carbon atoms

i) Even Chain i.e., having 2-4-6 carbon atoms

ii) Odd chain i.e., having 3-5-7 carbon atoms

B. Depending length

i) Short chain 2-6 carbon atoms

ii) Medium chain 8-14

iii) Long chain 16 & above (24)

C. Nature of hydrocarbon chain

i) Saturated fatty acids

ii) Unsaturated fatty acids

a) Mono unsaturated

b) Polyunsaturated

iii) Branched chain FA

iv) Hydroxy FA

v) Cyclin FA

The lipids in the body physiologically exist in two forms –

a) Element constant or structural lipids.

b) Element variable – stored lipids.

Elements constant is a part of the essential structure of the cells. The organelles are

composed of macromolecules of lipids & protein, the lipid is mainly phospholipid. The

Lipids 36


amount in the body between 0.5 to 1 kg & is independent of the state of nutrition. Cholesterol

is another lipid present in cell membranes; it has also an important role in the blood.

Element variable lipid, which is stored in the body, is in excess. The amount

fluctuates & it is composed mainly of TG also called as neutral fats. Thus fat is chiefly

composed of glyceriods of various fatty acids & usually contains 75 % of oleic acid, 20 %

palmitic acid 5 % stearic acid. Traces of lacithic & cholesterol as well as little amount of

PUFA are also present. The deposition of fat takes place adipose tissue.

Dietary Fat

Ghee & Ginger oil is two major dietary fats in India & is pure fats with no protein

components. In a diet with both plant & animal foods the absorption of fats are 90% while

the carbohydrate & proteins are 90% while the carbohydrate & proteins are 90%.

The dietary fat, despite being a source of energy, vitamins & EFAs improves the

palatability of food & helps to reduce the bulk of food is starchy ones absorbs a lot of water

during cooking. A comprehensive review of the effects of cooking on proteins, carbohydrates

& fats by Lans (1970’s) indicating that this subject is of little importance, but one which the

food technologies should be informed, the percentage of composition of these two dietary

fats are like this.

Table9: Percentage of composition of dietary fats

C4- C11 C14 C16 C18 Oleic Linolenic Arachidonic

Butterfat 11 08 26 11 33 38 0.4

Sesame oil ---- ---- 08 04 45 41 ----

The dietary need for fat

The exact human requirement of fat is unknown. But a desirable range is with at least

15 gms of vegetable fats totally accounting, not more than 30 % of daily caloric requirement

as recommended by ICMR Nutritional expert’s group.

The Institute of health, USA has also recommended intake of cholesterol less than

300mg/day & increase in the poly-saturated fatty acids contents but more than 10%.

The daily requirements of fats are normally by other nutrients. But there are many

experiments conducted in past years proving that the level of blood lipids is also determined

Lipids 37


in part by the nature of dietary carbohydrates (90%) each. In healthy individuals intestine can

absorb up to 300gms of fats. Normally fats never form more than 10% of the dietary intake.

With the fat intake more than 100mg/day or less, the presence of more than 7 gms of fat in

the feces constitute an evidence for fat absorption, (if found) at least for 5 consecutive days.

Grain or less in tissue mass is determined by net balance between calories intake &

caloric expenditure. Half of the normal diet intake is spend for basal process. Active person

spends 40 % in physical activity, athletes – 50 %. In non-obese non-sedentary subjects 10%

of indigestion calories are related as heat associated with absorption of food for dietary

thermo genesis.

So on estimating caloric requirements, physical activity, body size, composition, age,

ex, physiological state, climate & environment are to be taken into consideration.

A typical South Indian diet will be based on plain rice having 504 gm/2 servings at a

rate of 118k cal/100 gms. The average intake of dietary fats, milk products, and meat,

fishless in the whole India is 17 gms, 69 gms respectively.

PLASMA LIPOPROTEINS

The plasma lipoproteins are the molecular complexes of lipids & specific proteins called

Adipoproteins. Theses dynamic particles are in constant state of synthesis, degradation &

removal removal from the plasma. The lipoprotein particles includes –

Chylomicrons (CM)

Very Low Density Lipoprotein (VLDL)

Low Density Lipoprotein (LDL)

High Density Lipoprotein (HDL)

Lipoprotein functions both to keep lipids soluble as they transport them in plasma &

to provide an efficient mechanism for delivering their lipids contents of the tissues. In

humans, the delivery system is less perfect than in other animal, as a result, humans

experience a gradual deposition of lipids especially Cholesterol in tissues. This is a

potentially life threatening occurrence when the lipid deposition contributes to plaque

formation causing narrowing of blood vessels – known as Atherosclerosis.

Lipids 38


Composition of plasma lipoprotein The principle lipids carried by the lipoprotein particles are triglycerols & Cholesterol

(free or esterified), obtained either from diet or de-novo synthesis.

Lipoproteins are composed of a neutral lipocore surrounded by a shell of

apolipoproteins, phospolipids & non esterified Cholesterol all oriented so that their polar

portions are exposed on the surface of the lipoproteins, thus making soluble in aqueous

solutions.

I. Size & Density of Lipoprotein Particles

The chylomicrons are the lipoprotein particles lowest in density & largest in size

contain the most lipids & smallest percentage of protein. VLDLs & LDLs are successive

more dense, having a higher content of protein & lower content of lipid. HDL particles are

the most dense of the plasma lipoproteins.

II. Apolipoproteins

The apolipoproteins associated with lipoprotein particles have a number of diverse

functions including serving as structural components of the particles, providing recognition

sites for cell-surface receptors & serving as activators or co-enzymes for enzymes involved

in lipoprotein metabolism. Apoproteins are derived by structural & functions into classes A

to H with the most classes having subclasses.

Chylomicrons

These are the major exogenous lipoprotein synthesized in the intestinal mucosal cells

from the products off lipid digestion. Hey are large complexes rich in the Triglyceriodes. The

particles enter the lactates in the intestinal villi & are transported via the thoracic duct to the

blood stream. In the lymph & blood, the chylomicron particles acquiring apoprotein C & E

from HDL. As they pass through peripheral capillary beds of hydrolysed by adipose tissue &

skeletal muscle, their triglycerides are hydrolysed by apoprotein CII activated lipoprotein

lipase, an enzyme bound to the endothelial surface, releasing fatty acids & glycerols.

The results cholesterol rich chylomicron remnant with its apoprotein B & E is

recognized by specify receptors on the hepatic parenchymal cells & is rapidly cleared from

the plasma. Glycerol enters the liver to be converted to glucose or used for synthesis of

Triglycerides.

Lipids 39


Thus chylomicrons are the transport from the transport from of dietary triglycerides to

be delivered to adipose tissue for storage & muscle for storage & muscle for its energy needs.

Hence chylomicrons paricles are not considered to be atherogenic. The atherrogenic potential

of chylomicron remnants is a matter of dispute.

VLDL

These lipoprotein are the major carries of endogenous Triglycerides. They are

synthesized in the liver from glycerol & fatty acids & incorporated into VLDL along with

hepatic cholesterol, Apo B, C, E. Apoprotein B100 & E are required structural components

for this secondary process. In the fasting state, majority of plasma Triglyceriods are carried in

this particles.

The VLDL is secreted into blood stream grains more apoC from HDL. When they

reach the peripheral tissue, they are acted upon by the lipoprotein lipase liberating fatty acids

that are taken up by the muscle. The VLDL remnant is now designed as IDL (Intermediate

Density Lipoprotein) & contains TG. Cholessterol, apo-B & E. Part of the IDL is taken up by

the Liver. A major fraction of IDL further loses Triglycerides & gets converted into LDL.

Normally VLDL is probably not atherogenic. The smaller & more cholesterol rich

VLDL remains appear to have atherogenic potential. Persons with the genetic disorder

familial dysbeta lipoprroteinaemia have accelerated atherosclerosis. Although elevation of

plasma triglyceriodes are common in patients with CHD, they are not uniformely predictors

for CHD risk.

LDL

The LDL molecules are cholesterol rich lipoprotein molecules containing only Apo-B

(B-100). Most of the plasma cholesterol is incorporated into LDL particles. Being small in

size they can infiltrate through arterial walls & have a longer life than others. LDL receptors

recognize the apo-B & apo-E & can there fore take up LDL or IDL. Once the LDL particles

binds to the cells, they are internalized & cholesterol is related into the cells. Most of the

cholesterol metabolized into in to steroid hormones.

There is a cellular feed back regulating mechanism which inhibits intra cellular

synthesis of cholesterol when extraneous cholesterol is taken up from LDL. When the

cellular cholesterol pool is increased, further uptake is also preventing by decreasing the

synthesis of the LDL or cholesterol & removes & removes cholesterol through bile.

Lipids 40


The cholesterol which is thus excreted into the intestine is partly reabsorbed (30-

60%). The rest is excreted as fecal sterols, caprostanol & cholesterol after bacterial action.

the liver also controls body cholesterol pool by converting to bile acids.

Excess intracellular cholesterol can lead to 3 metabolic events.

a) Inhibition of HMG –CoA reductase, the rate limiting step in cholesterol synthesis.

b) Activation of enzyme Acylcoenzyme A cholesterol acyl Transferase (ACAT) which

estrifies cholesterol for storage.

c) Inhibition of production of additional LDL receptors, there by reducing cellular

uptake of plasma cholesterol.

Individuals with homozygous or heterozygous familial hypercholesterolemia can have

absent diseased or defective receptors. Undiscovered abnormalities or numbers LDL

receptors & Apo-B maay be causal in the majority of patients with CHD.

When the LDL levels in the plasma becomes become excessive they are removed by the

macrophages of reticulo endothelial system in the scarvenger pathway. Macrophages seated

in the arterial wall eventually become over loaded with cholesterol ester & the converted into

the foams cells that characterized early atherosclerosis. Because the majority of plasma

cholesterol (60-75%) is carried in the LDL particles, elevation of the total usually reflects

increased LDL levels. The anatomical degree of coronary atherosclerosis has been directly

linked to the concentration off LDL.

HDL

The HDL mainly plays an important role in the transport of cholesterol from

peripheral tissue to liver. The only excretory route of cholesterol from the body is bile. HDL

is synthesized mainly in the hepatic cells & intestinal cells & is seen as complexes of Apo A

& Apo E with phospholipids. The cholesterol derived from peripheral tissue & other

lipoproteins are esterified in HDL because it has a LCAT activity. After esterification, the

esterification, the ester from of cholesterol maay be transferred to other lipoprotein &

transported to liver. A small portion of esterified cholesterol is stored in the case of HDL also

acts as a carrier of Apo-C to be derived to the Triglyceride rich lipopprotein like VLDL &

chylomicrons. HDL is protective, but low HDL concentration < 30mg/dl is a potent risk for

CHD. HDL appears to expert a protective influence by removing cholesterol from tissues.

Total body cholesterol is inversely related to HDL levels.

Lipids 41


Important functions of lipoproteins

Chylomicrons transported mainly TG & smaller amounts of plasma lipoproteins,

cholesterol esters & fat soluble vitamin from intestine to liver & adipose tissue.

The lipids carried by chylomicrons principally dietary lipids.

VLDL transported mainly “Endogenous TG” synthesized in hepatic cells from

liver to extra hepatic tissue including adipose tissue for storage. High

carbohydrate intake, high ratio of insulin/glucogen, high plasma free acids &

alcohol intake increase the hepatic synthesis of both TG & VLDL so that

enhanced amount of fatty acid reaching the liver is speedily mobilized in VLDL

to adipose issue.

LDL rich cholesterol esters transports cholesterol & its estrs from hepatic cells to

extra hepatic tissues.

LDL also regulates cholesterol synthesis in extra hepatic tissue, as regulates

cholesterol delivered by LDL to cells inhibits HMG-CoA reductase, the rate

limiting enzyme for cholesterol synthesis.

HDL transports cholesterol & its esters from peripheral tissue to liver for its

catabolism.

Apo-D of HDL3 functions as the cholesterol ester transfer protein.

Albumin FFA complexes transport mainly FFA, released by adipose tissue

lipolysis & small amounts of lysophospholipids from extra hepatic tissues to the

liver.

Certain apoprotein can act as activators/inhibitors of specific enzymes.

CHOLESTEROL AND LIPOPROTEIN METABOLISM Exogenous Pathway

Exogenous lipid transport being with intestinal incorporation of dietary triglycerides

& cholesterol into large lipoprotein particles called chylomicrons (diameter, 80-500 nm.),

which are secreted into the lymph & subsequently enter the blood stream. When

chylomicrons reach the capillaries of adipose tissue & muscle, they are digested by an

enzyme lipoprotein lipase, which is bound to the surface of the endothelial cells. Lipoprotein

lipase hydrolyses the triglycerides in the core of the chylomicrons, & the liberated fatty acids

Lipids 42


cross the endothelium & enter the underlying adipocytes or muscles cells, they are then either

esterified again to form triglycerids for storage or oxidized to provides energy.

After most of the triglycrides have been removed in this fashion, the chylomicron

dissociates from the capillary endothelium & enters the circulation again. Its size has been

reduced & its contents of triglycerides diminished, but its cholesterol esters remain intact.

The particle is now designated as a chylomicron remnant (diameter 30-50 nm.).

When the remnant reaches the liver it is cleared from the circulation by a receptor

that recognizes two of its protein components, apoproteins E & B-48. The receptor bound

remnant is taken into the hepatic cell by a process termed receptor mediated endocytosis.

Within the cell the remnant is digested in lysosomes, & the cholesterol esters are cleaved to

generate free cholesterol. The free cholesterol has several fats; it can be used for membrane

synthesis, it can be stored esters, it can be excreted into the bile acids, or it can be used to

form endogenous lipoprotein that are secreted into the plasma.

Endogenous pathway –

Endogenous lipid transport begins when the liver secretes triglycerides & cholesterol

into the plasma in very-low-density lipoproteins (VLDL: diameter, 30-80 nm.). The major

stimulus for such secretion is a high-calorie intake especially a high-carbohydrate intake),

while induces the liver to assemble Triglycerides for export & storage in adipose tissue. The

Triglycerides of VLDL are cleaved in capillaries by the same lipoprotein lipase that digest

lipoprotein lipase that digests chylomicrons.

Digestion produces a VLDL remnant that is designated as intermediate-density

lipoprotein (IDL: diameter, 25-35nm.). After release from the endothelium, the IDL particles

have two metabolic fates. Some of the particles are cleared rapidly by the liver, again by

receptol-mediated endocytosis. The receptor that acts on the IDL particle is called Low

density Lipoprotein (LDL) receptor. It binds lipopretein that contains apoproteins that

contain apoprotein E or B – 100 & it therefore interacts with both IDL & LDL particles.

About half of the IDL particles are not cleared rapidly by the liver. Rather they

remain in the circulation, where most of the remaining Triglyceriods are removed, & the

density of the particle increase further, until it becomes LDL (diameter 18-28 nm.). LDL

circulates for a relatively long time in man (half-life of about 1.5 days ).

Lipids 43


The particles are eventually degraded by binding to LDL receptors in liver &certain

extra hepatic tissues. Circulating LDL constitutes the major reservoir of cholesterol in human

plasma, accounting for 60-70% of the total. When liver or extrahepatic tissues require

cholesterol for the synthesis of new membranes, steroids hormones or bile acids, they

synthesize LDL receptors & obtain cholesterol by receptor mediated endocytosis of LDL.

Conversely, when tissues no longer require cholesterol for cell metabolic purposes, they

decrease the synthesis of LDL receptors.

As cells of the body die & as cell membranes undergo turnover, free cholesterol is

continually released into the plasma. This cholesterol is immediately absorbed into high

density lipoproteins (HDL : diameter, 5-12 nm.) & in this location it is esterified with a long-

chain fatty acid by an enzyme in plasma, lecithin: cholesterol acyltransferase (LCAT). The

newly formed cholesterol esters are rapidly transferred from HDL to VLDL or IDL particles

by a cholesterol from transfer protein in plasma. The HDL promotes the removal of

cholesterol to as cholesterol transport. This transport is facilitates by the synthesis &

secretion of apoprotein E by peripheral tissues.

In addition to degradation by specification receptors, lipoproteins are also disposed of

by specific pathways, some of which operate in macrophages & other seavenger cells. When

the plasma concentration of a lipoprotein rises, the rate of its degradation by such pathway

increases. This contributes to arterial walls (producing atheromas) & macrophages of tendons

& skin (producing xanthomas).

Recent evidences has implicated oxidized LDL as a major source of cholesterol in

macrophages within atheromas. Macrophages & endothelial cells possess few LDL receptors,

but they do produces a “scavenger receptor” that recognizes LDL only after it’s lysine

reduces have been chemically modified. When LDL is oxidation productes of fatty acids.

This modifies particles taken up rapidly by macrophages through the scavenger receptor,

such oxidation is likely to occur locally when LDL penetrates into arterial walls, & this event

may be responsible for much of the deposition of cholesterol in the atherosclerotic plaques.

Triglycerides Triglycerides are the form in which fats are chiefly occurs both in foodstuff & in the

fat depots of most animals. They are valuable sources of energy storage & transport & are

Lipids 44


carried lined to apoproteins yielding VLDL (Prebeta), LDL (beta), HDL (alpja) molecules

while excess are stored in adipose tissue.

There are the esters of the trihydric alcohol glyceroids with fatty acids.The naturally

occurring fats & oils are mixtures of triglyceriodes. If all the hydroxyl group of esterified to

same fatty acid, simple triacyl is formed.

Eg. Tripalmitin, Triolein.

If all hydroxyl groups are esterifed, then mixed Triacyl glyceriods is formed which are

more common in nature.

Phospholipids

After the triglycerides the next largest lipid component of the body are phospolipids.

They are synthesized in the body from lipid phosphate & nitrogen & are important in

regulation of cell permeability. The principle phospolipids in man is lecithin (a – diester of

glycerol) cephalin, 2 fatty acids & phosporyl choline. Sphyngomyelin, contain sphigosine

instead of glycerol. The phospote nitrogenous salts are water-soluble making it beneficial in

lipid transport.

The Sterol

This comprises the most important & widely distributed class of biological

substances, all of which have the same basic ring structure. Cholesterol is the most important

among all these & is present in all foods of animal’s origin.

In a 70 kg. Individual, about 6000 gms. of fats almost 90% pure form, is stored

subcutaneous, intra muscular, perinephric, omental & mesenteric tissues. Nearly 300 gms. In

brain & nervous tissue 75 gms in liver & blood pool, altogether 10 kg individual. Each gram

of TG can supply twice the amount of energy compared to the protein & carbohydrates per

gram.

The weight of adipose tissue in normal individual is 10-15% body weight. In these

individual it can go up to 30% of body weight.

In post-absorptive state, the blood plasma contains about 550 ml. Of lipids. Elevated

levels of the profile is important since they cause two life-threatening diseases atheroscerosis

& pancreatities.

Lipids 45


CHOLESTEROL

The name of cholesterol is derived from Greek word meaning “solid bile”, cholesterol

is the most important sterol in human body. Its molecular formula is C27H45OH. It possess

“Cyclopentanoper hydro Phenathrene nucleus” cholesterol is a white waxy solid found

associated with fats but chemically different from fats. It is insoluble in water, sparing

soluble in alcohol. It is not saponifiable & its melting point is 147 0C to 150 oC.

Cholesterol is an important component of bio membranes Cholesterol is present in

plasma either as free or esterified. Bile has high concentration of Cholesterol & so bile serves

as the major excretory route for Cholesterol.

Occurrence

It is widely present in the body tissues, Cholesterol is found largest amount in normal

human adults.

Brain & Nervous Tissue – 2 % In the Liver – 0.3 % Skin – 0.3 % Intestinal mucosa – 0.2 % Certain endocrinal glands Viz-adrenal cortex contains – 10 % or more. Corpus leutiem is also rich in Cholesterol. Cholesterol is present in the blood & bile

usually a major constituent of gallstones.

Sources

Endogenous – Dietary Cholesterol approximately 0.3gm / day. Diet rich in

Cholesterol are butter. Cream, milk, egg yolk, meat, etc.

Table 10 : Cholesterol content of different food items Food Item Cholesterol content mg/100gm.Hens egg-whole 500 Egg yolk 1330 Liver 300-600 Brain 2000 Butter 280 Ghee 310 Meat & fish 40-200 Milk 10 Milk powder (whole) 90 Milk powder (Skimmed) <1

Lipids 46


Endogenous

Synthesized occurs both in free form & in ester form. In ester from it is esterified

with fatty acids at – OH group at C3 position, this ester form of Cholesterol is also known as

“bound” forms. The various fatty acids, which form Cholesterol esters, are –

Linoleic Acid – 50 %

Oleic Acid – 18 %

Palmitic Acid – 11 %

Arachiodonic Acid – 50 %

Other fatty acids – 16 %

Free Cholesterol is equally distributed in between plasma & red blood cells, but later

do not contain esters. In brain & nervous tissue – free form predominates where as in adrenal

cortex it occurs mainly as esterified form.

BIOSYNTHESIS OF CHOLESTEROL

Essentially all tissues from Cholesterol. Liver is the major site of Cholesterol

biosysthesis & also other tissues which are active in this aspect are – adrenal cortex, gonads,

skin, and intestine. Low order of synthesis occurs in adipose tissue, muscle, aorta & nervous

tissues. Brain of the newborn baby can synthesize the Cholesterol while adult brain cannot

synthesize the Cholesterol.

Slightly less than half of the Cholesterol in the body derived from biosynthesis de

novo, Biosynthesis in the liver accounts for approximately 10 % & in the intestines

approximately 15 %, of the amount produced each day. Cholesterol synthesis occurs in the

cytoplasm & microsomes from the two-carbon acetate group of acetyl-CoA. The process has

five major steps,

01. Acetyl-CoAs are converted to 3-methyglutaryl-CoA (HMG-CoA).

02. HMG-CoA is converted to mevolonate.

03. Mevalonate is converted to the isoprene-based molecule, isopentyl pyrophosphate

(IPP), with concomitant loss of CO 2.

04. IPP is converted to seualene.

05. Squalene is converted to Cholesterol.

The acetyl-CoA utilized for Cholesterol biosynthesis is derived from an oxidation

reaction (eg. Fatty acids or pyruvate) in the mitochondria & is transported to the cytoplasm

Lipids 47


by the same process as that described for fatty acid synthesis. Atyl- CoA can also be derived

from cytoplasmic oxidation of the ethanol by acetyl-CoA Synthesis. All isoprenoids

intermediates of Cholesterol biosynthesis can be derived to other synthesis reaction, such as

those for dolichol (used in the synthesis of N-linked glycoproteins coenzyme Q (of the

oxidative phosphoryation) path way of the side chain of the heme a. Additionally, these

intermediates are used in the lipid modification of the someprotein. Acetyl-CoA units are converted to mevalonate by a series of reactions that being with

the formation of HMG-CoA. Unlike the HMG-CoA formed during ketone body synthesis in

the mitochondria, this form in synthesized in the cytoplasm. However, the pathway and the

necessary enzymes are the same as those in the mitochondria. Two moles of acetyl-CoA are

condensed in a reversal of the thiolase reaction, froming acetoacetyl-CoA. Acetoacetyl-CoA

& a third mole of acetyl-CoA are converted to HMG-CoA by the action of HMG-CoA

synthase. HMG-CoA is converted to menavalonate by HMG-CoA reductase absolutately

requies NADPH as a cofactore & two moles of NADPH are consumed during the conversion

of HMG-CoA to mevalanate.

The rreaction catalyzed by HMG-CoA reductase is the limiting step of cholesterol

biosynthesis, & this enzyme is subjected to complex regulatory controls.

Mevalonate is then activated by three successive phosporylations, yielding 5-

pyrophosphomevalonate. In addition to activating mevalonate, the phosphorylations maintain

its solubility, since otherwise it is it is soluble in water. After phosphorylation, an ATP-

dependant decarboxylation yields isopentetyl pyrophosphate is in equilibrium with its

isomer, dimethyl pyrophosphate, DMPP. Once molecule of IPP, condensed with one

molecule of DAMPP to generate geranyl pyrphosphate, GPP. GPP further condenses with

another IPP molecule to yield farnesyl pyrophosphate, FPP.

Finally, the NADPH-requiring enzyme, squalene synthase catalyzes the head-to-tail

condensation of two molecules of FPP, yielding squalene (squalene synthase also ttightly

associated with the endoplasmic reticulum. Squalene undergoes a two step cyclization with

the to yield lanosterol. The first reaction is catalyzed by squalene monoxygenase. This

enzyme uses NADPH as a cofactore to introduce molecular oxygen as an epoxide at the 2,3

position of sualene. Through a series of 19 additional reactions, lanostrol is converted to

cholesterol.

Lipids 48


Regulation of cholesterol biosynthesis

HMG-CoA reductase is an intrinsic membrane protein of the Endoplasmic reticulum:

the enzymes activity site extends into to cytosol. HMG-CoA reductase is the rate-limiting

enzyme in cholesterol synthesis & is subjected to different kinds of metabolic control.

01. Feed back Inhibition

Cholesterol is a feedback inhibitor of HMG-CoA reductase, thus decreasing further

cholesterol synthesis.

02. Hormonal Regualtion

HMG-CoA reductase activity is controlled hormonally through a complx cascade of

enzyme activations & inhibitions similar to regulation of glycogen synthesis. The net effect is

that glucgon favours farmation of inactive form of HMG-CoA reductase & hence decreases

rate control synthesis.

Insulin – favors the formation of the active (unphosphorylated) form of the HMG-CoA

reductase & results in increase blood cholesterol.

Thyroid Hormone – Stimulating HMG-CoA reductase activity, lack of thyroid hormone

decrese the cholesterol. Where as excess of thyroid hormone decreases the cholesterol. This

is because of increased metabolism of all lipids substances under the influence of thyroxin.

Sex Hormone – Female sex hormones, estrogen decreases the blood cholesterol while

male sex hormones, androgens increases the blood cholesterol. Sex effects are very important

because, the higher incidence of heart attacks in earlier age.

III. Sterol – Mediated Regulation of Transcription The

synthesis of cholesterol is also regulated by the amount of cholesterol taken up by the cells

during lipoprotein metabolism. Chylomicrons remnant internalized by liver cells & LDL

internalized by the cells off liver & peripheral tissues, provides cholesterol which causes a

decrease in transcription of the HMG-CoA reductase gene, leading to decrease in do-novo

cholesterol synthesis.

IV . Fasting / Starvation

This also inhibits the enzyme & activity HMG-CoA lyase to from Ketone bodies.

V. Inhibition by drugs

Lovastatin & mevostain are reversible competitive inhibitators of HMG-CoA

reductase.

Lipids 49


Factros that influence cholesterol level in the blood

Dietary Fats – Increased intake of fats in the diet increases the level of

cholesterol by increased synthesis. Greater amount of saturated fatty acids by

polyunsaturated fatty acids has beneficial effects & lowers levels.

Dietary Cholesterol – Increased feeding of Cholesterol in diet decreases

endogenous synthesis & reduces Cholesterol level.

Dietary Carbohydrates – Increased consumption of carbohydrates increases

Cholesterol levels. Consumption excessive amount of sucrose & fructose

cause increase in plasma lipids particularly Triglyceriods & Cholesterol.

When ratio between starch: Sucrose is 1: 4, an increase in plasma Cholesterol

is observed.

Heredity – Heredity factors play greatest role in determining individual blood

Cholesterol concentrations. Persons, who are prone to become obese, have a

high level of plasma Cholesterol.

Blood Group – Cholesterol level found to be slightly higher in the persons

belonging to blood group “A” & “AB”.

Calorie Groups – Intake of excess calories increases Cholesterol level.

Vit.-B-Complex – Nicotinic acid in large doses has Cholesterol lowering

effect. Pyridoxine deficiency produces increases in Cholesterol level.

Mineral – In vitro acetate to Cholesterol conversion in tissue cell culture

depressed by addition of vanadium & iron salts & increased by chromium &

manganese salts. Conversion of mevalonate to Cholesterol is inhibited by

vanadyl SO 4.

Dietary Fibers – Increased fibers in the diet caused an increased excretion of

Cholesterol & bile acids in faeces.

Physical Exercise – Hard physical exercise brought about lowering in serum

Cholesterol level& increased level of HDL Cholesterol.

Cholesterol Functions –

Cholesterol is essential component of cells membrane.

It controls cells permeability & thus equilibrium of ions & substrates.

It helps in the formation of the bile salts & cholic acid.

Lipids 50


It helps in the synthesis of steroid hormones of sex glands in adrenal cortex &

synthesis of vitamins.

Largest part of fat is transported as Cholesterol ester.

Mobility of cells surface, receptors & membrane bound enzymes activity thus

transmission of transmembrane signals.

Cholesterol helps in the synthesis of the mylein sheath of nerves & acts as insulator

for nerve impulses.

Change in brain membrane Cholesterol: Phospolipid, this ratio is associated with

ageing & diseases.

Problems of high fat intake

The major complications of higher dietary contents of fats are obesity, increased

cholesterol & triglycerides levels in serum. Atherosclerosis, pancreaitits & increased risk to

coronary artery disease.

Obesity is defined as body weight higher than normal by 20%, 30%, & 40% as mild,

moderate & severe respectively. Further assessment includes estimation of total body fats.

Skin fold measurements & BMI more than 25 are taken as obese.

Important contributory factor for atherosclerosis are high caloric intake, high

saturated fat & cholesterol intake, increased level of cholesterol in the blood, sedentary life

style stress & strain in albino rats on high fat diet, through the wait gain was loss, serum

cholesterol & TG were higher than the normal diet.

The increased concentration of TG has shown an increased risk of ischemic heart

disease (IHD). Naturally occurring animal, fish & vegetable fatty acids are largely 16-18

carbons in length. But the medium chain TG are more useful clinically because they are

absorbed through the portal vein, not through splanchenic lymphatics, they are cleared from

circulation more rapidly than long chain TG & their & fatty acids can be oxidize by carotene

independent mechanism in mitochondria.

Both quantity of dietary PUFA are significant for health. The body contains four

classes of PUFA designed according to location of double bonds & among these precursor of

PUFA 18 +W+ & 6 + W + are obtained from vegetable origin of fats.

Animals fed on a fat diet develop a generalized syndrome consisting growth failure,

dermatitis, fatty liver, neurologic & visual abnormalities. Most of these are corrected by 106-

Lipids 51


precursor linolenic acid, but neurologic & visual changes reflects depletion of +W+ 3 class &

require linolenic acid for correction. It is now recommended that the human diet should

contain about 4 % of calories as linolenic acid 1% as linolenic acid.

HYPERLIPIDEMIA & HYPER LIPOPROTEINEMIA

Hyperlipidemia refers to an increased concentration of either cholesterol or

Triglyceriods or both this lipids in the plasma. The elevation of lipids concentration in the

plasma is often the manifestation of disorders in the synthesis, absorption or degradation of

plasma lipids & lipoproteins.

Classification

The most widely employed classification system is that Fredrickson / WHO

classification according to phenotypic manifestation of increase lipoprotein fractions. This

system takes as axiomatic the view of that a plasma lipids are transported in complex macro

molecules, the lipoproteins are free from, raised lipids levels are consequences

Hyperlipoprotenemia.

Table No. 11: Showing the classification of Hyperlipidaemia.

Lipoprotein Major elevation Lipids Example

Pattern In plasma LP

Type I Chylomicrons TGs LPL deficiency

Type II a LDL Cholesterol Familial

Hypercholesterolemia

Type II b VLDL+LDL TG +

cholesterol

Familial combined

Hyperlipidemia

Type III Remnants

(B-VLDL)

TG +

cholesterol

Ttype III

Hyperlipoprotenemia

Type IV VLDL TG Familial

Hyperglyceridemia

Type V Chylomicron +

VLDL

TG +

cholesterol

APO C II deficiency

Several different genetic disease can cause these patterns. Conversely some genetic

disease can occur as a secondary consequences of another metabolic disease. Etiologically

Lipids 52


Hyperlipoprotenemias have been classified into primary & secondary. Primary is the direct

result in the synthesis or degradation of lipoprotein particles, in secondary the elevated

plasma lipoprotein level occurs as a part of constallation of abnormalities caused by insulin

deficiencies or thyroid hormone deficiency.

The primary hyper lipoprotenemias have been further derived into

Single gene disorders.

Multi factorial disorders.

Single gene disorders are transmitted by simple dominant or recessive mechanism. Multi

factorial disorders – here there is complex – inheritance pattern which multiple varieties

genes, each having a subtle, interact with environmental factors to produce varying degree of

hyper lipoprotenemias in membranes of a family.

Eg. Polygenic hypercholesterolemia

Spordiac hyperglyceridemia

Familial hyper α lipoprotenemia

Increased level of cholesterol are seen in

Familial hypercholesterolemia

Familial defective apo B-100

Polygenic hypercholesterolemia.

Where as increased cholesterol & Triglyceride levels are seen in

Familial combined hyperlipidemia

Type III hyper Lipoprotenemia

Hypercholesterolemia (type I HLP )

Familial hypercholesterolemia is a rare disease caused by deficiency of lipoprotein

lipase. It is inherited as autosomal recessive trait. Majority of the cases develop symptoms by

the age 10 years, mainly recurrent abdominal pain often due to pancreatities, Eruptive

Xanthomata may be evident in early childhood & heptosplenomegaly in later year.

There is no evidence of accelerated vascular diseases or glucose in tolerance. Serum

triglyceriods levels are high (1000 – 5000 mg / dl). Plasma cholesterol absorptive stage is

grossly turbid & creamy layer separate out at the tip on storage overnight. Both the

abnormalities are mitigated by a fat free diet for 3 – 5 days. Deficiency of LPL is evident

Lipids 53


markedly reduced post heparin lipolytic activity. Treatment consists of a low diet not more

than 15 % of the total calories of i.e. 25 – 35 gms / days.

Secondary hypercholesterolmia occure in uncontrolled diabetes & in dysproteinemia

in multiple myeloma & macroglobenemia. High dose of coticosteriods may induce lipamia.

II. Familial Hyper Cholesterol (Type IIa – HLP )

(Hyper β Lipoproteinmia )

The primary individuals type of this disorder is characterized by raised LDL.

Triglyceries & VLDL are within normal limits. It is inherited as an dominant trait.

Hetrozygous individuals typically have plasma cholesterol that are two to three fold above

average & homozygous individuals have cholesterol concentration that are elevated three to

six folds. Xanthomata & premature vascular disease are major manifestation of the familial

disorder. In the homozygotes important symptoms occurs early in the childhood & are florid

by 20th year. Xanthomatas deposits over Achilles & plantar tendons are characteristics. CHD

& calcific arotic stenosis are evident by puberty.

Hetrerozygous have 10 times incidences of CHD than the control of population up to

50 years of age. Tuberous xanthomata over elbow & tibial tubrosity, Xanthoamasma &

premature corneal arcus are common but latter two are of lesser diagnostic importance.

Diabetes mellitus, Obstructive Jaundice, Cushing’s syndrome & Dusglobunamias.

III. Familial Combined Hyperlipidemia (Type – Hb – HLP) Although familial combined hyper lipedemia is a common disorder neither its genetic

pathogenesis is clear. Familial hypercholesterolemia are more common either of these alone.

Inheritance pattern is same as Type IIa. Depending on age, diet & obesity one of the lipids

may rise higher than the other, thus giving the impression of transmission between Type II

Type IV & Type V HLP.

Xanthomata are usually absnt but xanthelesma may be present as in acrus normal.

There is an increased risk of accelerated. Atherosclerosis & Vascular disease. Diabetes is the

common metabolic disorder that leads to Type IIb HPL. Low plasma HDL, obesity, insulin

resistance & hyperuricemia are often present.

Broad β hyperlipoproteinemia (Type III HLP)

This is a rare familial disorder with raised levels of lipoprotein (IDL), which migrates

over the range of beta & prebeta on electrophoresis but float in the range of VDRL in

Lipids 54


ultracentrifuge. IDL is the cholesterol rich remnant of VDRL formed in course of its

conversion to LDL & hence synonym LDL. Plantar Xanthomata as yellow plaque on the

elbows, knees & buttocks appear around 20 years age or later. Some of the atherosclerotic

vascular disease is usually present by middle age. Glucose intolerance & obesity occur

sooner or later. Diabetes Melletes & hyper thyrodism are the commonest causes of secondary

Type – III HLP.

Hyper Pre β Lipoproteinemia (Type IV HLP )

This disorder is characterized by isolated increase in TG rich VLDL in plasma.

Unlike Type Ia, hyperttriglyceredemia is endogenous & not dependant on dietary fat intake.

There is increase in the synthesis & release of VLDL from the Liver as well as autosomal

dominant expression of the trait appears to depends on certain promoting factors such as

glucose intolerance, hyperinsulinaemia, hypothyroidmia, hypothyroid state or excess of

alcohol consumption. Rise in TGs may be moderate (150 – 200) until some of the above lead

to rise in VLDL production particularly in response to excess intake of carbohydrate.

This disorder is not apparent until puberty. Premature coronary disease occurs, but

the contribution of VLDL percentage is difficult to assess in view of high incidence of

diabetes, obesity & hyperuricemia among these patients. Pancreatities may develop during

the period of exacerbation.

Mixed Hypertriglyceridemia (Type V – HLP)

This is a rare disorder manifests as combination of abnormalities of type I & type IV

HLP. Lipaemia is due to excess production of endogenous VLDL & defective removal of

exogenous chylomicrons may be because of LPL deficiency. This disease is may be familial

or spordiac. In the familial 50 % of the adult relatives of the patients have

Hyperglyceridemia. There is often genetic overlap between type IV & HLP.

The disorder manifest in adult life with Hepatosplenomegaly, recurrent abdominal

pain & Xanthomatous eruptions. Obesity, glucose intolerance & premature vascular disease

are common concomitants. Secondary Type V HPL is observed in uncontrolled Diabetes,

Hypothyroidism Nephrotic syndrome & gout.

Lipids 55


Drug review 55

TRYUSHANADYA LOHAM

The medicament Tryushanadya loham under taken for the study. Its ingredients and

method of preparation is explained as below.(Yoga ratnakara uttarardha medoroga nidana pp 99).

Ingredients : Drugs Quantity

Shunti 1 Part

Maricha 1 Part

Pippali 1 Part

Haritaki 1 Part

Amalaki 1 Part

Bibhitaki 1 Part

Chavya 1 Part

Chitraka 1 Part

Bida Lavana 1 Part

Oudbhida Lavana 1 Part

Bakuchi 1 Part

Saindhava Lavana 1 Part

Souvarchala Lavana 1 Part

Loha Bhasma 1 Part

Preparation:

All the above ingredients are collected from the reliable sources and

powdered separately into fine powder. Equal quantity of fine powder of each drug are mixed

well and stored in an airtight bottle. This medicine has been served in the form of powder to

the patients.

SHUNTI (Zinziber officinale)

Gana : Truptighna, Arshoghna, Deepaniya, Shoolaprashaman, Trushnanigrahan (C.);

pippalyadi trikatu (S.); panchakola, Shadushan (Bh.)

Kula : Haridra kula.


Drug review 56

Family : Scitaminaceae.

Latin name : Zinziber officinale

English name : Fresh ginger/Dry ginger. When skin of the fresh ginger rhizome is peeled

off and then dried it is called as dry ginger.

Sanskrit names : Shunti, Vishva, Nagar, Vishvabheshaj, Visvoushadha, Katugranthi,

Katubhadra, Katushan, Sauparna.

Botanical description : Plants grow up to 1 to 15 mtr. high. Leaves are 13-30 cms. long,

broad and tapering at the top. Stalk of the flower is 5 to 8 cms long, stamens are dark violet

coloured.

Varieties : According to habitat and processing, there are many varieties. Dry ginger is

smoky in colour. White coloured ginger (ardrangager kaiyadev) is found in south India,

which is used in practice, peeled rhizome boiled in milk and dried is called ‘Dudhiyasuntha’

Chemical composition : 1/5% yellow volatile oil, gingerol, gingerin (pungent resin),

carbohydrates, oil and resin is found just under the skin. Gingerol does not evaporates with

oil

Habitat : Hot and damp climate like Madras, Kerala (Kochin), Bengal, and Punjab.

Properties :

Guna : Laghu, Snigdha (fresh ginner is ruksha, tikshana and guru)

Rasa : Katu Veerya : Ushna : Vipaka : Madhur.

Karma : It is useful in kaphavata diseases.

External uses :

Anti inflammatory and analgesic properties, it is used as local application in swollen

joints and rheumatoid arthritis. It helps to reduce cold and stiffness.

Internal uses :


Drug review 57

Digestive system : Ginger is an excellent appetizer, digestive, antiflatulent,

anthihaemorrhoidal and antipasmodic. It helps in alleviating vatakapha and pitta. Ginger is

used in anorexia, nausea, vomiting, loss of appetite, indigestion, flatulence, abdominal pain,

jaundice and piles.

Circulatory system : It purifies blood and as it stimulates heart and circulatory system it is

useful in cardiac debility, cardiac pain, elephantiasis, oedema, arthritis and urticaria.

Respiratory system : It is kaphaghna and antiasthamatic. Tenacious sputum of pharyngitis is

relieved by chewing ginger.

Reproductive system : Ginger acts an aphrodisiac and sex stimulant.

Temperature : In fever with chills, ginger containing formulations are useful. In typhoid

fever and innumerable conditions ginger juice is used as adjuvant.

Useful parts : Rhizomes.

Dosage : Ginger juice 2-4 ml. ; Powder. 0.75 to 1.5 gms.

Formulations : Ardrakhanda, Panchasama churna, Samasharkara churna, Saubhaghyashunti

paka, Yoshadi ghrut. Many drugs are triturated in ginger juice for formulations.

MARICHA (Piper nigrum)

Gana : Deepaniya, Shulaprashamana. Krumighna, Shirovirechana ( C) ; Pippalyadi,

Tryushan (S).

Kula : Pippali kula

Family : Piperaceae

Latin name : Piper = derived from Sanskrit word pippali also from Greek word peperi, ;

nigra = black, slightly tinged with gray.

English name: Black pepper.


Drug review 58

Sanskrit name : Maricha, Palita, Shyma (used in the Westen countries instead of chillies),

Vrittaphala, Shakanga, Katuka, Krishna, Krimihara.

White Pepper : Sitamaricha, Shavala.

Botanical description : It is a parasite which grows mostly on coconut and getelnut plants.

The roots grow out of the nodes by which it creeps on the host. Leaves resemble betel leaves,

12.7 cms. and have airborne pollination Fruit round, grows in long clusters when tender it is

green in colour, turns red on ripening and black on drying.

Habitat : Malaya, Singapore, Bihar, Assam, Kerala and Konkan.

Phytochemistry : The thin pungent skin of the fruit contains piperine, a volatile compound

5.9%, piperidine 5%, an aromatic oil 1-2%and 7% fatty acids. The fruit pulp has a bitter resin

called chavicin, starch, oil, gum, fats 1%, protein 7% and alkaloids 4%.

Properties :

Guna : Laghu, Tikshna ; Rasa: Katu Veerya : Ushna

The green (fresh) fruit has madhur vipak but not ushna veerya

Dosha : Vatakaphashamaka.

Internal use :

Central Nervous System - Stimulant & tonic for nerves. Useful in nerve weakness.

Digestive System –Appetiser& stimulates the digestive juices. It is vermifuge. Used in

indigestion, liver dysfunction, etc.

Circulatory System – It is stimulates circulatory system. The blockage in small capillaries is

gradually removed on giving a very fine power of black pepper with water.

Respiratory System – There is no better substance than pepper to reverse sluggishness of

pranvaha srotas & reduces mucus secretions.


Drug review 59

Urinary System –Pepper corrects urinary disorders by reducing the viscosity of phlegum. It

increases the flow of the urine by stimulating the blood vessels in the kidney.

Reproductive System – It has a stimulating action on this system. It is useful in

dysmenorrhoea, amenorrhoea & impotency.

Skin –Useful in reducing the pruritis & skin disorders.

Parts Used : Leaf, Fruit (for external use)

Dose : 0.25 to 0.50 gms.

Formulations: Marichyadi Gutika, Marichyadi Leha, Marichyadi Churna, Shwasakuthara

Rasa, Trikatu churna.

Adulteration : Seeds of evening primerose are mixed.

PIPPALI (Piper longum)

Gana:Kasahara, Hikkanigarahan, Shirovirechan, Truptighna, Vamaka, Deepaneeya,

Shoolaprashamana (C) , pippalyadi, Oordhavabhagahara, Shirovirechana. (S)

Kula : Pippali Kula.

Family : Piperaceae

Latin name : piper (according to meaning of pepper), Krishna (Greek), or pippal (derived

from Sanskrit names); longum = long.

English name : long pepper.

Sanskrit names : Pippali, Magadhi, Krishna, Vaidehi, Chapala, Kana, Ushna, Upkoolya,

Krukara Katubija, Korangee.

Botanical description : It is a creeper which spreads on the ground or climbs up nearby trees

for support. Leaves 5 to 6 cms long, resemble betel leaves and has 5 veins. They are bitter to


Drug review 60

taste. Flowers unisexual. Fruits long, reddish on ripening and turn black when dried. It

flowers during rainy season and gives fruits during autumn.

Habitat : P. longum is grown chiefly in the following places – Bengal, Bihar, Assam,

Travancore, Nepal, Bhutan, Terai region of the Himalayas, Islands of Phillipines, Malaysia,

Singapore.it is cultivated in Bangladesh.

Chemical composition : Resin, volatile oil, starch gum, fatty oil, inorganic matter and resin

piperin 1-2%.

Properties :

Guna : Laghu, Snigdha, Tikshna ; Rasa : Katu; Vipaka : Madhura ; Veerya :

Anushnasheeta.

When the fruits of pippali are wet and dry, they are guru, sweet and sheeta veerya.

Karma :

Dosha : Katu- kaphashamaka, snighda- vatashamaka, when fresh it is sheeta and thus is

vatakaphavardhaka and pittashamaka. Disorders related to kapha and vata are the main uses

of shushka (dry) pippali.

External uses : It increases blood flow when applied locally. Therefore it is used in swelling

accompanied with pain.

Internal uses :

Nervous system : P. longum is a brain tonic and alleviates vata.

Digestive system : P. longum is appetizer, truptighna carminative, analgesic and mild

laxative. It helps in reducing hepatomegaly and splenomegly. It acts as a vermicide

Circulatory system : It is used to treat anemia and various blood disorders. Long pepper in

increasing dose is a boon for chronic fever, typhoid, agnimandya and spleenomegaly.


Drug review 61

Respiratory system : Long pepper is an excellent medicine for cough caused due to kapha

dosha asthama and hiccoughs.

Urinary system : In diabetes mellitus it reduces ama stage of kapha, meda and mutra (urine),

It reduces seminal debility and acts as a rejuvenator.

Skin : Long pepper nourishes rasa and rakta dhatu and is useful in skin disorders.

Useful parts : fruit.

Dose : Powder – 5-10 gms; can be used in any dose for rasayana therapy.

Formulations : Gudapippali, Vardhamanapippali, Chavasthipippali.

HARITAKI ( Terminalia chebula)

Gana : Triphala , Amalakyadi , Parushaka, Trivrutta, Prajasthapana, Jwaraghna, Kushtaghna,

Kasaghna, Arshoghna.

Kula : Haritaki kula

Family : Combertaceae

Latin Names : Terminlia = proceeding from the extremity at the end; chebula = distorted

from of the world Kabul.

English Name : Myrobalanas; chebulic myrobalan.

Sanskrit Names : Haritaki, Haimavati, Shiva, Pathya, Rohini, Shreyasi, Chedanika, Pachani.

Botanical Description : A big tree, 25 to 30 mts. Its wood is hard & bulky. Leaves are 10 –

30 cm in length has 6 to 8 pairs of veins. The flowers have short stalk, white or yellow in

colour & have a string & have a strong smell. Each fruit contains one seed, an oval shaped

pulp is obtained.

Habitat : Haritaki is found almost everywhere in India. This tree grows at places up to a

height of about 2000 mts. from the sea level.


Drug review 62

Properties : Guna : Laghu, Rooksha. Rasa : Five rasas (lavana rasa is absent but kashaya

rasa is predominant.) Vipaka : Madhura. Veerya : Ushna. Prabhava : Tridoshahara.

Dosha : Haritaki is particularly vatashamaka. It is helpful in many tridoshajanya diseases,

particularly useful as a rasayana in vatavyhadhi.

Part Used : Fruit (Various preparations of the ripen fruits)

Dose : 3 to 6 gms for the Shodhana (purgation) ; 1 gm for use as rasayana. Bala-haritaki is

given in a dose of 1 to 3 gms

Formulations : Abhayadi Modaka, Abhayarishta, Pathyadi Vati, Pathyadi Kadha,

Vyaghraharitaki Leha, Agastyaharitaki Leha, Gandharvahastadi Choorna.

AMALAKI (Emblica officinalis)

Gana: Vayahsthapan, Virechanopaga (C), Triphala, Parushakadi (S.)

Kula : Eranda kula (Euphoribiaceae).

Family : Euphorbiaceae (Spurge); Euphortous physicin to king Juba of Mauretania.

Latin name: Emblica officinalis.

English name : Emblic Myrobalan

Botanical Description : Middle sized tree 8 to 10 mtrs. High. Bark whitish, thin. Its wood is

strong and red. Leaves having the appearance of tamarind leaves but more thin and small.

Long petioles. Flowers stalk is long. Flowers are small and yellow, flowering in autumn.

Fruits round and greenish yellow.

Habitat : All over India.

Properties :

Guna : laghu, ruksha, sheeta ; Rasa : pancharasa (except salt taste); Vipaka: madhura;

Veerya : sheeta (atisheeta).


Drug review 63

Karma :

Dosha : Tridoshahara.

External uses : Refrigerant, hair tonic, complexion enhancer.

Internal uses : Strengthens nervous system, bone marrow and sense organs.

Digestive system : It improves taste and appetite, curative, antacid, biliousness. Small dose

causes constipation while large dose is laxative.

Circulatory system : Cardiac tonic and haemostatic

Respiratory system : Reduces cough.

Reproductive system : Aphrodisiac and helps in conception.

Urinary system : Useful in diabetes though it is a diuretic.

Skin : Useful in skin diseases.

Temperature : Antipyretic, refrigerant.

Doshas : It is used in diseases induced by tridosha, mainly pitta.

Internal uses :

Nervous system : Strenghthens bone marrow, incipient blindness and any weakness of sense

organs.

Digestive system : It acts in loss of taste, loss of appetite, constipation, liver disorders, acid

peptic diseases, ascities and piles through its properties of digestion, laxative and rasayana.

Respiratory system : Used in diseases like cough, asthma tuberculosis etc. Being a

rejuvenating agent.

Reproductive system : It is useful in spermatorrhoea, menorrhagia, uterine debility.

Urinary system : Fresh amla juice is used in dysuria and pittaja prameha. Bark and leaves are

also useful.


Drug review 64

Skin : In skin diseases and erysipelas, it is given internally for longer period.

Temperature : Useful in chronic fever, thirst, burning sensation etc.

Part uses : Fruit, leaf juice, seeds.

Dosages : fruit juice –1 2 ml.; powder – 3-6 gms; being a dietary product, large dose is

harmless.

Formulations : Chavyavanprasha, Bramharasayana, Dhatriloha, Amrutprasha, Amalaki

rasayana.

BIBHEETAKA (Terminalia bellerica)

Guna : Jwarahara, Virechanopaga ( C ) ; Tripahla, Mustadi (S).

Family : Combretaceae

Latin name : Terminalia bellerica

Sanskrit names : Bibheetaka, karshaphala, Aksha, Kalidrum, Bhootawasa, Kalivruksha,

Romaharsha, kalinda

Botanical Description : The tree grows up to a height of 16 to 32 mts. The bark is brownish

in colour. The wood of the trunk is hard. The leaves resemble those of banyan tree and are 9

to 16 cms. in length. The leaves may be long or circular. At the base of the leaves, where the

lamina ends. There are two small nodules. Flowers are very small and yellow. There are five

small and five large stamens. Fruits are round in shape, brownish and hairy. Each fruit

contains one seed. The tree bears flowers in the summer and fruits in the winter. The fruits

ripen in the spring. The seed pulp is sweet to taste but it produces milk intoxication

Habitat : It is predominantly found in India, Burma and hilly areas

Properties :

Guna : ruksha, laghu; Rasa : kashaya ; Vipaka : madhura; Veerya : ushna

Karma:

Dosha : It is tridoshanashaka, but mainly kaphanashaka


Drug review 65

External uses : Antinflammatory, analgesic, haemostatic and gives black colour to the skin

and hair. Oil is a hair tonic.

Internal uses :

Nervous system : The pulp is intoxicant and analgesic

Digestive system: it is deepana, laxative and anthelmintic. Half ripened fruits are purgative

and ripened fruit are astringent. It is anti emetic and reduces excessive thirst.

Circulatory system: It is used as a blood coagulant due to its astringent property.

Respiratory system: It helps in asthma and cough by reducing the inflammation of the

bronchi.

Reproductive system : The pulp is an aphrodisiac.

Temperature : Febrifuge.

Indication :

Dosha : Tridoshaghna but is more useful in diseases caused by kapha.

External uses : An application of the fruit or oil extracted from the fruit pulp is useful in

painful inflammatory conditions. The oil is used in skin diseases, leucorrhoea and in

premature graying of hair.

Internal uses :

Nervous system: The pulp is used in vata disorders and insomnia.

Digestive system : Useful in indigestion, flatulence, emesis, haemorrhoids, helmenthiasis.

Half ripe fruit relieves constipation whereas dried fruit is useful in diarrhoea and dysentery.

Circulatory system : Useful in internal bleeding. More useful in haemoptysis.

Respiratory system : Cold, cough, asthama and hoarseness of voice are relieved by keeping

the rind of the fruit in the mouth.


Drug review 66

Reproductive system : By consuming the pulp of one seed everyday, impotency is eliminated

and libido is improved.

Parts used : Fruit.

Dosha : Powder -0.75 to 1.5 gms

Formulations : Bibhetaka taila, Triphala churna, Phalatrikadi kwatha, Lavangadi vati,

Baibheetaki sura.

CHAVYA ( Piper chaba)

Nirukti : Chavyate iti charva adena I

The one, which is suitable for chewing, is known as chavya

Latin name:Piper chaba

Kula: Pippali kula

Morphology: A climbing glabrous pepper rather fleshy.

Leaves -Oblong, ovate or lanceolate, acuminate. Base is round, cordata. Nerves at base. 2

pairs from midrib 12.5 cm to 18 cm long and 6.3-7cm wide

Petioles - 6 to 13 mm long

Fruits - Are ovoid with a nipple like point and peltate, bract beneath.

Stem - Spikes jointed as the ring finger Bark covering them

Bark - Brittle, smooth, slightly rugous and of a dirty brown color. It is easily

removable.

Wood - Arranged in numerous wedges color the same as that of barks.

Taste is slightly pungent and acrid and has smell somewhat aromatic.

PROPERTIES

According to different Authors

Guna Rasa Veerya Vipaka

Dhanvantari Nighantu

-- Katu Ushna --

Kaiyadeva Nighantu Laghu Tikshna Rooksha

Katu -- Katu

Vanoushadhi Laghu Katu Ushna Katu


Drug review 67

Nidarshika Bhavaprakasha Nighantu

Laghu, Rooksha Katu Ushna --

Indian material medica

Laghu Katu Ushna --

Ayurveda Charya Laghu Katu Ushna Katu Brahat dravya gunadarsha

Laghu Katu Ushna Katu

Properties- Acrid, pungent, aromatic, stimulant. Some are narcotic at others astringent

and febrifuge. There are due to presence of all volatile oil and resin.

System wise action and uses

Dosha - Vatahara and kaphahara

Uses - Vatavyadis and Kaphavyadis

Digestive - Deepaka, Pachaka, Rechana, Krimighna malabhedaka,

Shoola hara Vatanulomana yakrituttejaka, Triptighna

Arshohghna

Uses - Aruchi, Agnimandya, Ajeerna, Anaha, Arsha Anaemia,

Grahani Gulma and krimirogas and Diarrhoea

Respiratory - Kasaghna, Swasghna

Uses - Kasa, Swasa, Pratishyaya

Vishista yoga

Panchakola Phanta, Pranada Gudika, Kankayana Modaka, Chavyadi grutha, Chavyadi

kwatha

Dosage

1. Choorna1-2 gms

2. ½ gm to 1 ½ gm or 4 Ratti to 1 ½ Masha

3. Decoction 1-10 in dose of 2-10 drachms

Useful part

Root

Stem

Fruit


Drug review 68

CHITRAKA (Plumbago zeylanica)

Gana : Deepaniya, Truptighna, Shoolaprashamana, Bhedaniya, Arshoghna, Lekhaniya,

Katukaskanda ( c ) ; Pipalaydi, Mustadi, Amalakyadi, Mushkakadi, Varunadi, Aragwadadi

(S). Panchakola, Shadushna (Bhavaprakash).

Kula : Chitraka kula

Latin name : Plumbum = lead. Plumbago – that cures lead palsy; zeylanic = of Ceylon.

English name : Leadwart.

Sanskrit names : Chitraka, Agni, Shardula, Chitrapali, Krushnanudahana, Jyoti, Palaka,

Anala.

Botanical Description : Long living herb, 1 to 2.5 mtrs. High. Stem thin, round, nodular and

delicate having vertical stariations onit. Leaves oval shaped resembling bilva leaves, 10cm.

long and 4 cm. broad. Stalk of flowers 10 to 20 cm, long, having many branches. Fruits-

legumes, oval shaped with cover. It is sticky to touch. Seeds - each fruit has one oval seed.

Roots are finger like thick, like shatavari.

Habitat : White chitraka at Bengal, Uttar Pradesh, South Iindia, Srilanka . Red chitraka at

Hills, Sikkim, Kuchabihar.

Chemical composition : Plumbagin, 91% Active principle does not dissolve in cold water. In

boiling water or alcohol it dissolves easily. So cold water should not be used for

formulations.

Properties :

Guna : tikshna, laghu, ruksha; Vipaka :Katu Rasa : katu, tikta; veerya : ushna (excessive).

Dosha : Useful in various disorders induced by kapha and vata.


Drug review 69

Internal uses :

Central nervous system : It acts as an appetiser, digestive, but astringent and anthelmintic.

Circulatory system : It is effective in chronic rhinitis and cough

Reproductive system : It causes uterine contraction, cures menstrual disorders.

Skin : Diaphoretic, useful in skin disorders

Temperature : Febrifuge. It is used in chronic fever (kapha) and malaria. It improves liver

function, digestion and helps in spleenomegaly.

Parts used : Root bark (use fresh).

Dosage : 0.5 to1 gm. high dose causes burning and intoxication. (to be used cautionly).

BAKUCHI (Psoralea corylifolia)

Kula : Shimbikula

Family : Leguminosae.

English name : Purple fleabane.

Sanskrit names : somareka, shashanklekah, somaraji, Chandralekha, Bakuchi, Somavalli,

Botanical Description : Seasonal plant 0.5 to 1.5 mt. in height. Trunk straight and branches

are strong and elastic. Leaves 2.5 to 8cm long round or heart shaped, border is undulate.

Flowers yellow, blue 1-30 flowers in branches appear on a long stalk. Fruits blackish in

bundles. Seeds black, small tender and give a peculia r scent on rubbing in fingers or hand.

Habitat : India and Srilanka. Predominantly found in Assam and Uttar Pradesh.

Chemical composition : In contains a volatile yellow oil 20.15%, stable oil, resin, alkaloids

(7.5%), albumin, sugar, manganese and vermonine.

Properties :

Guna : laghu, ruksha Rasa : katu, tikta; Vipaka: katu ; Veerya : ushana

Dosha : Since it has ushna veerya, it acts as kaphavata shamaka and hence used in disorders

of kaphavata.

External uses : It is used locally in leucoderma, wounds and alopecia.

Internal uses :

Nervous system : Since it is nervine tonic, it is useful in vata disorders.

Digestive system : It acts as deepana, pachana, anulomana, anthelmintic and liver stimulant.

Circulatory system : Since it stimulates the heart and the circulatory system, it is used in

cardiac failure and oedema produced by it.


Drug review 70

Respiratory system : Used in cough and asthama

Urinary system : Useful in diabetes.

Reproductive system : Since it is a stimulant and an aphrodisiac, it is used in impotency.

Skin : Diaphoretic and kustaghna. I

Temperature : Febrifuge, used in chronic fever.

Parts used : Seeds, oil.

Dose : Powder 1 to 3 gms. For worms 4 to 6 gms.

Purification : The seeds of Bakuchi are purified by keeping them in cow’s urine or juice of

ardraka for seven days.

VIDALAVANA

Rasaratna samucchaya by Rasendra chudamani included this under Sadarana rasa. In

Ayurveda Prakash they included in this under kshara where as it is included under lavana

varga by rasendrasara sangraha.

Synonyms

1. Vidalavana

2. Chullika lavana

3. Navasara

4. Navyasara

5. Nasara

6. Nrusadara

7. Narasadara

8. Kittakshara

9. Gaja

10. Gomala

English : Solammoniak

Latin : Arnomonil chloridum, NH4CLI

Types : Two types

Yogambari - Best variety

Chullika


Drug review 71

Swaroopa :

Shweta, Nirgandha, Crystal form

Properties

Guna - Laghu, Sukshma, Teekshna

Rasa - Lavana

Vipaka - Madhura

Veerya - Ushna

Doshagnata - Pittashamaka

Actions :Lekhana,Nadibalya,Deepaka,Pachaka,Anulomaka,Kaphanissaraka,Artavajanaka.

OUDBIDA LAVANA (NA2CO3)

Synonyms : Oudbida lavana

Parnsha lavana

Kacha lavana

English : Sodium carbonate

Chemical composition

Sodium carbonate

Soda sulphate

Magnesium sulphate

Properties:

Guna - Guru, Snigdha

Rasa - Tikta, Katu, Kshara

Vipaka - madhura

Veerya - Sheeta

Doshagnata - Vatashamaka

Actions - Deepaka Pachaka Mutrala


Drug review 72

SAINDHAVA LAVANA

Sanskrit :Saindhava Lavana

English :Rock salt

Hindi :Sendhalon

Kannada :Saindhava Lavana

Source - Found in nature in extensive beds mostly associated with clay and calcium

sulphate. To obtain it, holes are dug into these rocks which son become filled up with salt

water; the water is evaporated and the salt is left ready for use.

Characters- It is found in small white crystalline grains or transparent cubes. It is

brownish white externally and white internally. It has a pure saline taste and bums with a

yellow flame.

Action –In small doses it is highly carminative, stomachic and digestive. It promotes

the appetite and assists digestion and assimilation. In large doses (4 to 8 drachms) it is

emetic. Rock salt possesses stronger purgative properties than cream of tarter; but like this it

is not a satisfactory cathartic given alone. Combined with other purgatives it is equal, if not

superior to it.

Uses – It is given in dyspepsia and other abdominal disorders. To rouse digestion

weakened by diarrhoea, rock salt and yavakshara (alkali potassium carbons impure) are

given, in convalescence.

RUCHAKA LAVANA (Souvarchala lavana)

Sanskrit : Souvarchala lavana

English : Black salt

Kannada : Turaimannu


Drug review 73

Synonyms: Ruchaka, Souvarchala, Ruchyaka, Hridyagandhaka

Nirukti : Su- Sushtu, varchala deeptim.

Al- Prapthi, sarvata alati, anena iti souvarchala

Means vahni uttejaka i.e. Agnivardhaka

Swaroopa: It is in the form of dark coloured crystal. This salt is aromatic and agreeable.

Souvarchala lavna is one among the five lavana (Lavana panchaka)

Preparation: Ruchaka lavana is made artificially by dissolving common salt in a solution of

sajimti (crude soda) and evaporating it.

Constituents: This salt contains chloride of sodium; sulphate of sodas, caustic soda but does

not contains carbonate of salt.

Medicinal properties

Rasa :Lavana

Guna :Laghu, sukshma

Veerya :Ushna

Vipaka :Katu

Karma :Deepana, Pachana, Vatanulomana

Dosaghnata :Vibandhara, hridya

Therapeutic use:

1. Useful in stomachic, indigestion

2. Used as purgative

3. Beneficial in shula, abdominal tumours, intestinal worms and dysentery.

LOHA (FERUM, IRON)

Synonyms : Louha

Aya


Drug review 74

Ayasa

Loha is available in the form of

1. Haematite (2Fe2O3)

2. Magnetite (Fe3O4)

3. Limonite (2Fe2O3, 3 H2o)

4. Iron pyrite (FeS2)

5. Siderite

6. Feco3

Types:

1. Kanta loha

2. Teekshna loha

3. Munda loha and Cast Iron,Wrought, Iron steel

Properties:

Guna - Guru, Ruksha

Rasa - Kashaya, Tikta, Madhura

Vipaka - Sheeta

Doshagnata - Tridoshashamaka

Action -Krimighna

Nadibalya

Deepaka grahi

Anulomaka

Kaphaghna.


MATERIALS

Materials for literary Study Research

Literary Research is done from

Classical Ayurvedic texts

Modern Texts

Updated from journals

Materials taken for Clinical Study

Tryushanadya loham composed of

Shunti

Maricha

Pippali

Haritaki

Amalaki

Bibhitaki

Chavya

Chitraka

Bida Lavana

Oudbhida Lavana

Bakuchi

Saindhava Lavana

Souvarchala Lavana

Loha Bhasma

METHOD

Scientific method of research is a combination of observations, reasoning &

experimentation. For gaining knowledge in research, one proposes the problem, constructs

suitable experimental model, makes the honest observation & arrives at logical conclusions

Material & Methods 75


The clinical therapeutic trails are of importance due to the fact that Ayurvedic therapeutic

measures & procedures have remained in practice since long on 6th methodology prevalent in

ancient times. It is high time that the rationality of ayurvedic therapeutic approach is

explained on the scientific measures & attempts made to level. Some new therapeutic

combinations, the clinical trial which is carefully & ethically designed by taking the serum

lipid profile & other parameters before & after study achieve the above objects at present

study “Evaluation of the efficacy of Tryushanadya loham in Sthoulya with special reference

to hyperlipidaemia”

Research approach

In the present study the objects is to determine therapeutic effect of “Tryushanadya

loham” which is a combination of – Shunti, Maricha, Haritaki, Amalaki, Bibhitaki, Chavya,

Chitraka, Bida Lavana, Oudbhida Lavana, Bakuchi, Saindhava Lavana, Souvarchala Lavana,

Loha Bhasma in Sthoulya. Efficacy can be determined by finding out the difference between

the base line data & assessment data.

Research design

Before starting the study base line data were collected then the Trushanadya loham

was administered for 60 days then the assessment data were collected.

Availability

Most of the cases were reported in medical camp held at Shri. D.G.Melmalagi

Ayurvedic Medical College, Gadag.

Some cases were reported at O.P.D. of P.G. research center Kayachikitsa Department

Shri. D.G.Melmalagi Ayurvedic Medical College, Gadag.



Selection Criteria

Thirty cases of Sthoulya patients are selected as per the inclusive criteria & were

treated as out patients. Patients who are attending the Kayachikitsa O.P.D.were selected for

the present study. Strictly on the basis of detailed case sheet.

Inclusive Criteria

The patients with clinical symptoms of Sthoulya will be selected for the clinical

study. Both male & female cases will be selected in the age group between 30 – 65 years.

Primary hyperlipidaemia cases will be included.

Exclusive criteria

The patients with severe form of the hyperlipidaemia will be excluded.

Secondary hyperlipidaemia cases will be excluded.

Sthoulya with severe form of Diabetes mellitus & Hypertension will be excluded.

Duration of study

Duration of study was 60 days for the day of initiation of Trushanadya loham.

Posology

1 Masha T.D.S. or 2.250 gms. /day in dividing doses.

Anupana

Madhu & Ghruta in unequal ratio.

Collection of the data

The data were collected according to the case sheet & are conveniently segregated

under the following headings –

1. Demographic Data -

It includes age, sex, religion, income, occupation, diet, family history and chronicity.



2. Data related to the habit & habitat of the patient

It includes food, exercise, sleep pattern, habits, mental conditions, pulse, blood

pressure, temperature, respiration & height.

3. Data related to disease (subjective parameters)

It includes chief complaints, associated complaints & upadravas.

4. Data related to disease (objective parameters)

It includes weight, circumference of udara, spik, stana, lipid profile & random blood

sugar.

Assessment

Considering the difference seen in the assessment data from the base line data

concerned to each of the parameters did the assessment. The efficacy of the treatment was

assessed under three headings – Relieved palliative (moderate response), & not responded.

Objective assessment is done statistically. Allotting 2, 1, 0 points for good response,

moderate & poor response respectively the subjective assessment is done. The percentage of

total is taken as criteria for assessment.

Estimation of the serum lipids

Blood sampling method

The blood was taken from the patient randomly according to the advice of

pathologist. The venous blood was collected in sterilized test tube that was not heparinized &

allowed to settle in vertical position for one hour. Then centrifuged at 3000 rpm for 30 min.

& the serum separated. Modified Allain’s method Cholesterol kit & GPO-PAP method

triglyceride kit is used for lipid profile.



Table 12: For total cholesterol pipetting scheme

Blank Standard Test

Working enzyme reagent (ml.) 1.0 1.0 1.0

Distilled water (ml.) 0.01 - -

Cholesterol Standard (ml.) - 0.01 -

Sample (ml.) - - 0.01

Table 13: For HDL cholesterol pipetting scheme

Blank Standard Test



HDL cholesterol Standerd (ml.) - 0.01 -

Supernatant from step 1 (ml.) - - 0.01

Table 14: For Triglyceride pipetting scheme

Blank Standard Test



Cholesterol Standard (ml.) - 0.01 -

Sample (ml.) - - 0.01

Mixed well & allowed at room temperature for 10 min. measured the absorbance of

test & standard against Blank on a photocolorimeter with green filter. This procedure is

followed separately for total cholesterol, HDL & Triglycerides & reading is recoded.

Calculations

1. Total cholesterol in mg % = A of (T) /A of (S) X 200.

2. HDL Cholesterol in mg % = A of (TH) /A of (S) X 50.

3. Triglycerides in mg % = A of (T) /A of (S) X 200.



4. VLDL Cholesterol = Triglyceride / 5.

5. HDL Ratio = HDL / Total Cholesterol – HDL

6. For Random Blood Sugar, it is done using Glucometer.

Screw guage

In medical field there are two capillaries used to measure SFT. They are Harpenden

skin fold calipers & long skin fold calipers.

But in present – clinical study the physics instrument screw gauge is used to measure

the SFT for the first time in the medical field. Therefore advantages & disadvantages are

discussed,

Advantages

1. Screw – gauge is cheaper than both the calipers & easily available.

2. Methodology is very simple.

Disadvantages

The reading taken by the screw – gauge are not as accurate as that of the calipers. But

this accuracy can also be maintained the same pressure at the screw – gauge.

Exercise – cycle

The variable taken for the study was assessed by counting the respiration rate. Every

time the patient both were asked to climb the cycle & the adjustable knob rotated to “10”

rotations & patients were asked to rotate the paddle for 70 to 75 rotations per minute for “2”

minutes immediately respiration rate was counted & this was done before starting the

treatment. After completion of treatment, keen observation was made & time of the

appearance of droplets of sweat over forehead were noted. Further allowed to paddle to their



maximum ability, that time was recoded as exhaustion time & follow – up of the patient done

belonging to the both groups.

Moderate calorie diet (MCD)

Diet is the most important factor in the clinical study of obesity patients. As food is

the prominent – item in the physical development of the human beings. There are different

opinions regarding the prescription of calorie food per day.

As per reports & research papers it had been confirmed that MCD is the best kind of

diet prescription, through there are different in connection with duration. But the better one is

the 20-week course. Therefore the Sthoulya patients for the clinical study were given MCD

90days, followed by one month of follow-up.

Diet was designed with following points

The diet should consists of relatively large volumes of low energy complex

carbohydrates that would require more than average time in digestion with the intent to

displace more energetically dense items. This is nothing but “Guru cha apatarpanam” , it is

adopted their in the principles of measurements.

Daily diet intake records were asked to be maintained by the patients throughout the

period of the treatment & follow-up. These records were studied on their clinical visits after

every 15 days & were educated about the advantages & disadvantages.

In the clinical study the MCD that is 1200 k. calorie per day was very satisfactory as

there were no complaints.

Physical activity intervention (PAI)

A report by the US surgeon on PIA & the significant health benefits which are

associated with regular PAI they include –



1. Decreased risk of Cardio vascular disorder mortality.

2. Prevention or delayed development Hypertension.

3. Reduced blood pressure in those with Hypertension

4. Decreased risk of the colon cancer.

5. Decreased risk of developing NIDDM.

6. Relief from symptoms of depression & anxiety.

When PAI is alone used in the treatment of obesity. Weight loss in moderate &

average around 2 – 3 kg. However, evidence dose exist that PAI alone can produced much

larger reduction in weight when it is of sufficient frequency, intensity & duration.

There appears to be a relationship between level of exercise & degree of weight loss.

One study, which compared dieting, verses PAI on weight loss & lipoproteins. In one year or

randomized control trial found that both intervention group lost significant weight compared

to controls. Dieters lost an average of 7.2 kg after 12 months compared to exercise that lost

an average of 4 kg.

Potential mechanism linking exercise with weight maintenance include.

1. Enhanced resting metabolic rate.

2. Preservation of lean tissue during weight loss.

3. Increased total daily energy expenditure.

A combination of diet & exercise generally produce greater weight loss that of diet alone.

How much PAI is required?

The US surgeon report on PAI & health recommended that activity leading to an

increase in daily approximately 1,000 k. cal. /week is associated with substantial health

benefits & that the activity does not need to be vigorous to achieve benefits.

Although these recommendations were not specially designed for these people they

have been included in the US department of health & human services dietary guidelines for

weight maintenance. The American college of sports medicine has recommended that the



weight loss programmes of PAI that promote a daily calorie expenditure of 300 k. cal. or

more.

In Ayurveda, it is suggested that Vyayama is good pathya for Sthoulya patients. Here

it is better to discuss about what vyayama means, how much & how long a Sthoulya patient

should do. The Bruhatrayees were not particular in this context about the maximum range of

Vyayama gradually but Vagabhata said that, one’s vyayama should be up to one’s ardha

shakti pramana.

Thus we find the utility of vyayama in Sthoulya chikitsa, Charaka has mentioned that

Chankramana (walking for 6 km. /day allows loss of 300 k. cal. (The American College of

Sports & Medicine, 1995.) Taking all the above points into consideration, patients were

prescribed daily morning walk of 6 kms.

Body mass index (BMI)

Obesity is a common health problem, which is recognized as a disease in its own right

but also a major risk factor for a number of other diseases including cardiovascular disease,

NIDDM, Hypertension. Normally measured through the use of BMI, obesity has been

classified as a BMI above 30.

Ayurvedic reference of BMI

Even though there is no exact reference of BMI in ayurveda there is a similar kind of

the features of the Swastha Purusha described that mamsa must be “Sama Mamsa Pramana”.

BMI naturally influence the calculation of skeleton & muscle mass. Which is nothing but

BMI.



Skin fold thickness

The measures of SFT has been proposed as a useful technique for evaluating body fat,

but there are several major problems with it.

1. Selection of an appropriate site.

2. Obtaining & using an appropriate instrument.

3. Defining accurately the area to be measured.

4. Having sufficient practice to reproducible & reliable results.

The body has scores of suitable sites for taking SFT measurement. But over the years,

scientist have identified about six sites as being most respective of over all body fat. These

are triceps, biceps, subscapular, suprapatellur, suprailiac & abdomen.

George A. Bray et al have published an article in the “American Journal Of clinical

nutrition MAY 1978 on – USE OF ANTHROPOMENTRIC MEASURES TO ASSESS

WEIGHT LOSS ” in which it is described that skin fold thickness measurements have

frequently been proposed as criteria for assessing obesity & particular triceps muscle can be

measured using special spring loaded caliper. Obesity is indicated by reading 20mm. in men

& above 28mm. in females.

Ayurvedic references of SFT

Even though there is no exact reference in ayurveda of SFT , there is similar kind of

theory for the consistence of skin & muscles. Charakacharya in explaining the features of

Swastha Purusha described that mamsa peshi must be sama samhanana (equally consistant.)

Measurements

Since the publication of Jean – Vague (1940) it slowly accepted that different body

morphology or types of fat distribution are independent related to the death risks associated



with obesity. Starting with Jean – Vague’s Brachio femoral adopio muscularation as an index

of fat distribution.

In the present clinical study the measurements were taken from the sites such as

chest, abdomen, hip, & left arm. Because in Ayurveda it is said that meda deposits more in

spik, stana, & udara. The chest is measured covering both the nipples & abdomen at

umbilicus at the expiration time; stana is rather difficult & inconvenient.

Ayurvedic refernces of measures

There is no references of measuring the Sthoulya rogi but there is reference for

measuring the organs of Swastha purusha.

Table 15: Showing the NCEP CAD Risk Factors

Low risk Boarder line High risk

Cholesterol <200mg/dl 200-239mg/dl >240mg/dl

Triglyceriods <165-200mg/dl 200-400mg/dl 400-100mg/dl

LDL <130mg/dl 130-159mg/dl > 160mg/dl

HDL > 60mg/dl <35mg/dl



Distribution of the patients by age –

Age No. of the Patients Percentage Responded Percentage

31 – 40 12 40% 10 83.33%

41 – 50 9 30% 7 77.77%

51 – 60 6 20% 4 66.66%

61 –65 3 10% 1 33.33%

Largest incidence is found in the III decade. This shows middle aged people are more

prone to get this. May be because of their less physical activities & younger age dietary

habits.

1210

97

64

31

02468

1012

31 – 40 41 – 50 51 – 60 61 –65

No. of the Patients Responded

Observation & Results 86


Distribution of the patients by sex –

Sex No. Of the patients Percentage Responded Percentage

Male 12 40% 9 75%

Female 18 60% 13 72.22%

The data shows among 30 patients 12 (40 %) are male & 18 (60%) this indicates the

incidence of Sthoulya is more in female & they responded less compare to male.

12

9

18

13

02468

101214161820

No. Of the patients Responded

Male Female



Distribution of the patients by religions –

R eligion No. of the Patients Percentage Responded Percentage

Hindu 14 46.66% 11 78.57%

Muslim 9 30.00% 6 66.66%

Christian 3 10.00% 2 66.66%

Others 4 13.33% 3 75.00%

Among 30 patients 14 (46.66 % ) belongs to Hindu, 9 (30 % ) belongs to Muslim, 3

(10 % ) belongs to Christian & 4 (33.33 % ) belongs to other religion.

14

119

6

32

43

02468

101214

Hindu Muslim Christian Others

No. of the Patients Responded



Distribution of the patient by occupation –

Occupation No. of

patients

Percentage Responded Percentage

Sedentary 24 80 % 18 75 %

Active 6 20 % 4 66.66 %

Labour 0 0 % 0 0 %

Among 30 patients 24 (80 %) belongs to sedentary occupation group, 6 (20 % )

belongs to active occupation group. No incidence observed from labour group.

24

18

64

0 00

5

10

15

20

25

Sedentary Active Labor

No. of patients Responded



Distribution of patient by Economical Status –

Income No. Of Patient ePercentage Responded Percentag

Under 1lakh 0 0% 0 0 %

1-2lakh 7 23% 6 85.70 %

2-3lakh 11 37% 8 72.72 %

3lakh above 12 40% 8 66.66 %

Among 30 patients no belongs to under 1lakh group, 7 (23 %) belongs 1 –2lakh

income group, 11 (37 %) belongs to 2 – 3lakh income group. 12 (40 %) belong to 3lakh

above income group. It shows that the incidence of the disease more in the higher economical

class.

0

7

1112

0

68 8

02468

101214

Under 1lakh 1-2lakh 2-3lakh 3lakh above

No. Of Patient Responded



Distribution of patients by diet –

D iet No. of the patients Percentage Responded Percentage

Veg 9 30 % 7 77.77 %

Mixed 21 70 % 15 71.42 %

Among 30 patients 9 (30 % ) belongs to vegeterian group, 21 (70 % ) belongs to

mixed group. In vegetarian group 7 (77.77 %) responded well compare to mixed group 15

(71.42 %)

97

21

15

0

5

10

15

20

25

Veg Mixed

No. of thepatientsResponded



Distribution of patients by family history –

F amily History No. of Patients Percentage Responded Percentage

Paternal 13 43.33% 10 76.92%

Maternal 10 33.33% 7 70.00%

Nil 7 23.33% 5 71.42%

Among 30 patients 13 (43.33 %) belongs to paternal family history group,

10 (33.33 % ) belongs to maternal family history group & 7 (23.33 %) belongs to nil family

history group.

13

10

7

10

7

5

0

2

4

6

8

10

12

14

No. of Patients Responded

Paternal Maternal Nil



Distribution of patients by chronicity –

C hronicity No. of Patients Percentage Responded Percentage

1 year 6 20.00% 5 83.33%

2 year 6 20.00% 5 83.33%

3 year & above 18 60.00% 12 66.66%

Among 30 patients 6 (20.00 % ) belongs to 1 year chronicity group, 6 (20.00 % )

belongs to 2 year chronicity group & 18 (60.00 % ) belongs to 3 & more than 3 year

chronicity group.

6 6

18

5 5

12

0

2

4

6

8

10

12

14

16

18

No. of Patients Responded

1 year 2 year 3 year & above



Data related to personal history –

01. Ahara

Ahara No. Of Patients Percentage

Guru 25 83%

Snigdha 26 86%

Sheeta 28 93%

Madhura 28 93%

No. Of Patients

25

26

28 28

23.524

24.525

25.526

26.527

27.528

28.5

Guru Snigdha Sheeta Madhura

No. Of Patients





02. Adhyashana

T ime Arrival No. of patients Percentage

30 min. 03 10%

1 hr. 09 30%

1.5 hr. 11 36.66%

2 hr. 04 13.33%

3 hr. 03 10%

Above tables (i.e. T. No. 01. & 02.) reveal that more than 83 % of the patients are

habituated to guru sheeta snigdha & madhura ahara. 90 % of the patients have habituated for

adhyashana.

No. of patients

3

911

43

02468

1012

30 min. 1 hr. 1.5 hr. 2 hr. 3 hr.

No. of patients

Observation & Results

95


03.Vyayama

Vyayama No. Of Patients Percentage

Present 07 23.33%

Absent 23 76.66

Above table reveals that more than 77 % of the patients are belonging to Vyayama

category.

7

23

0

5

10

15

20

25

Present Absent

No. Of Patients


96


04.Divashayana

Divashayana (Day Sleep) No. Of Patients Percentage

No Day Sleep 05 16.66%

Less than 1 hr. 09 30.00%

1 hr. 12 40.00%

2 hr. 02 6.66%

More than 2 hr. 02 6.66%

Above table reveals that more than 25 (82 %) of the patients are habituated to

sleeping in the day. It is one of the causative factors for Sthoulya.

5

9

12

2 2

0

2

4

6

8

10

12

NoDay

Sleep

Lessthan 1

hr.

1 hr. 2 hr. Morethan 2

hr.

No. Of Patients


97


05.Vyavaya

Vyavaya No. Of Patients Percentage

Active 12 40%

Passive 18 60%

Above table reveals that 12 (40%) are active, 18 (60%) are passive in Vyavaya.

No. Of Patients

12

18

Active Passive


98


06.Manasika

Manasika No. Of Patients Percentage

Harsha 20 66.66%

Chinta 7 23.33%

Shoka 03 10%

Above table reveals that 20 (66.66 %) of the patients are leading happy life, &

remaining 10 (33.33%) of the patients are suffering from chinta & shoka.

20

7

3

02468

101214161820

Harsha Chinta Shoka

No. Of Patients


99


07.Nidra

Nidra No. Of Patients Percentage

Sound 25 83.33%

Disturbed 5 16.66%

Above table reveals that more than 25 (83.33 %) of the patients are having sound

sleep & 05 (16.66 %) of the patients are having disturbed sleep.

25

5

0

5

10

15

20

25

Sound Disturbed

No. Of Patients


100


Data related to results –

Results No. of patients Percentage

Relieved 18 60.00 %

Palliative 9 30.00 %

Not responded 3 10.00 %

Among 30 patients 18 (60.00 %) of the patients relieved, 9 (30.00 % ) of the patients

palliative & 3 (10.00 % ) of the patients not responded.

No. of patients

189

3

Relieved Palliative Not responded


101


Data Related to Diseases –

Subjective

Complaints No. Of Patients Percentage Relived or

Reduced

Percentage

Spik Chalatwa 18 60.00% 14 77.77%

Spik guruta 26 86.66% 22 84.62%

Spik vriddhi 26 86.66% 22 84.62%

Udara lambana 24 80.00% 20 83.33%

Udara chalatva 18 60.00% 12 66.66%

Stana vriddhi 24 80.00% 20 83.33%

Stana chalatwa 16 53.33% 14 87.5%

Shareera gouravata 28 93.33% 26 92.85%

Alasya 26 86.66% 22 84.62%

Kshudra swasa 16 47.77% 14 87.5%

Kriya Asamarthata 22 23.33% 20 90.90%

Vyavaya Asamarthata 12 40.00% 10 83.33%

Snigdhata 20 66.6% 16 80.00%

Aruchi 12 40.00% 08 66.66%

Talushosha 26 86.66% 22 84.61%

Sthula shopha 10 33.33% 06 60.00%

Above table reveals that most of all the patients got relief from the symptoms.


102


Associated Complaints

Associated

Complaints

No. Of Patients

Percentage Relived or

Reduced

Percentage

Adhika Trishna 26 86.66% 20 76.92%

Adhika Kshudha 27 90.00% 21 77.77%

Adhika Sweda 18 60.00% 14 77.77%

Adhika Nidra 26 86.66% 20 76.92%

Alpa Bala 18 60.00% 12 66.66%

Shareera Durgandha 12 40.00% 08 66.66%

Krathan 20 66.66% 14 70.00%

Adhika trishna, nidra, adhika kshudha, are found in maximum patients & these

symptoms are reduced in all patients.


103


Upadrava

Upadrava No. Of Patients Percentage

Relived or

Reduced

Percentage

Jwara 02 06.66% 02 100.00%

Atisara 05 16.66% 05 100.00%

Kamala 01 3.33% 01 100.00%

Prameha 08 26.66% 06 75.00%

Arsha 10 33.33% 05 50.00%

Kushta 00 00.00% 00 00.00%

Bhagandara 00 00.00% 00 00.00%

Visarpa 01 3.33% 01 100.00%

Shleepada 00 00.00% 00 00.00%

Apachi 00 00.00% 00 00.00%

Vatavyadhi 12 40.00% 10 83.33%

High incidence of upadrava is Vatavyadhi found in 12 (40.00 %) of the patients.

Patients suffering from upadravas like Jwara, atisara kamala, visarpa, are got complete relief.

Patients suffering from arsha are got 50.00% of the relief.


104


Showing the statistical analysis of mean weight loss before & after the treatment at different intervals.

Assessment Xt + SD Difference between mean

PSE t P Remarks

15th day 2.23+1.49 1.56 0.46 3.39 < 0.001 HS

30th day 3.13+1.61 2.00 0.50 4.00 < 0.001 HS

45th day 4.03+1.45 2.40 0.55 4.36 < 0.001 HS

60th day 4.63+1.47 2.93 0.50 5.86 <0.001 HS

Follow-up 4.63+1.47 2.93 0.50 5.86 < 0.001 HS

The following assessment done after interval of 15 days showed the fall in ‘P’ value

< 0.001, which is significant, and interval of 30th, 45th, 60th and follow up day showed the fall

in ‘P’ value < 0.001 which is highly significant.

Showing the statistical analysis of mean lipid profile before and after the treatment.

Assessment (X) SD+ SE+ PSE t P Remarks

Total

cholesterol

3.54 13.31 13.77 3.77 6.37 <0.001 HS

HDL 6.67 4.01 4.15 1.25 2.88 <0.001 HS

LDL 24.87 14.96 15.48 4.19 4.6 <0.001 HS

VLDL 3.13 4.62 4.78 1.52 0.04 <0.001 HS

Triglycerides 6.93 7.70 7.97 2.41 0.39 <0.001 HS

The statistical assessment done after treatment total cholesterol and LDL showed fall

in P value < 0.001 which is highly significant, HDL showed fall in < 0.001 which is

significant and VLDL and triglycerides showed in P value is not significant.


105


Showing the statistical analysis of mean systolic before, after and F. U.

Assessment (X) SD + SE PSE t P R

Post test 3.7333 2.4074 2.4919 0.8742 2.44 < 0.001 HS

FU 3.7333 2.2.8158 2.9147 0.9042 2.6543 < 0.001 HS

Showing the statistical analysis of mean diastolic before, after and F. U.

Assessment (X) SD + SE PSE t P R

Post test 1.4667 1.8571 1.9923 0.5833 2.1303 < 0.001 HS

FU 1.4667 1.8571 1.9923 0.5833 2.1303 < 0.001 HS

The statistical assessment of systolic, diastolic pressure after treatment and follow up

showed the fall in P value < 0.001 which is highly significant.


106


Thirty patients are selected for the clinical study & the data collected as follows –

Master Chart No. 1 Sl.No. O.P.D.No. Age Sex R O ES Diet FH CH Result

01. 550 31 F M A 3 M P 1 Relieved

02. 556 33 F H A 3 V P 1 Relieved

03. 2388 35 M H A 3 M P 1 Relieved

04. 2452 35 F C S 3 M M 1 Relieved

05. 2357 35 M O S 4 M P 2 Relieved

06. 2359 37 F H S 4 V P 2 Relieved

07. 2365 38 F H S 4 V M 1 Relieved

08. 2367 38 M H S 4 M M 1 Relieved

09. 2467 39 F H S 2 V P 2 Palliative

10 2470 39 F M A 2 M M 2 Palliative

11. 2480 40 F M S 4 M P 2 Palliative

12. 2019 40 M M S 4 M P 2 Palliative

13. 2021 41 F M S 4 M P 3 Not Responded

14. 2750 42 F H A 4 V M 3 Relieved

15. 2751 43 M H S 3 M N 3 Not Responded

16. 2755 43 M M S 3 M N 3 Palliative

17. 2195 43 M M S 3 M M 3 Palliative

18. 2198 44 M O S 2 M P 3 Palliative

19. 2130 45 F M S 2 M N 3 Relieved

20. 2149 46 F H A 3 V N 3 Relieved

21. 2111 48 F O S 2 M N 3 Relieved

22. 2211 52 M M S 4 M P 3 Relieved

23. 2312 53 F H S 3 V P 3 Relieved

24. 2492 55 M O S 3 M M 3 Palliative

25. 2788 57 F C S 4 M M 3 Palliative

26. 2730 58 F C S 3 M M 3 Relieved

27. 555 58 F H S 3 V N 3 Relieved

28. 662 61 F H S 2 V N 3 Relieved

29. 2473 63 M H S 2 M P 3 Relieved

30. 2310 63 M H S 4 M M 3 Not Responded

A = Age in years.S = Sex (M- Male , F- Female.)R = Religion (H- Hindu, M – Muslim, C – Christen, O – others.)O = Occupation (S – Secondary, A – Active, L – Labor.) ES = Economical Status. (1 : 0-1Lakhs, 2 :1-2Lakhs, 3 : 2-3Lakhs & above.) Diet = ( V – Vegetarian, N- Non vegetarian.) FH = Family History (P – Paternal, M – Maternal, Nil.)CH = Chronicity (1 – Since 1 year, 2 – Since 2 year, 3 – Since 3 & more than 3 year.)

Master charts 107


Data Related To Personal History

Master Chart No. 2

Ahara Sl. No. 1 2 3 4

Adhyashan Vyayama DivaShayana

Vyavaya Manasika Nidra

01. + + + + 3 + 1 1 1 1 02. + + + - 2 - 4 1 3 1 03. + + + + 3 - 2 2 3 1 04. + + + + 4 + 2 2 3 1 05. + + + + 2 - 2 2 3 1 06. + - + + 3 - 1 1 3 1 07. - + + + 3 - 2 0 1 2 08. + + - + 1 - 4 0 3 1 09. + + + + 2 - 3 2 3 1 10. + + + + 2 - 3 0 3 1 11. + + - + 3 + 0 1 3 1 12. + + + + 4 - 2 0 3 1 13. + + + - 3 - 1 2 3 1 14. + + - + 2 - 1 0 3 1 15. + + + + 3 - 2 2 3 1 16. + + + + 2 + 1 1 3 1 17. + + + + 3 - 2 2 1 1 18. - + + + 2 - 2 1 3 1 19. + + + - 2 - 3 0 3 1 20. - + = + 2 - 2 0 1 1 21. + + - + 3 - 0 2 2 2 22. - + + + 2 - 1 2 3 1 23. + + + - 3 - 2 2 3 1 24. + + + + 4 - 4 0 3 1 25. + + + + 4 - 3 0 1 1 26. + + + + 2 - 4 0 2 1 27. + + + + 3 - 3 2 3 1 28. + + + + 1 - 4 0 3 1 29. + - + + 4 - 2 2 1 1 30. + + - + 3 + 1 1 3 1 Ahara – ( 1 – Guru, 2 – Snigdha, 3 – Sheeta, 4 – Madhura.)

Adhyashana – ( 1 – 15 min., 2 – 30 min., 3 – 1 hr., 4 – 2 hrs. )

Vyayama – ( + - Yes., - - No. ) Diva Swapna – ( 1 : less than 1 hour, 2 : 1 hour, 3 : 2

hours, 4 : more than 2 hour.0 Vyavaya – ( 1: active, 2 : passive.)Manasika – ( 1 : Chinta,

2 : Shoka, 3 : Harsh nityatwa.) Nidra – ( 1: Sound, 2 : Disturbed.).

Master charts 108

Data related to complaints – Master Chart No. 3

Complaints Sl. No. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16

B A B A B A B A B A B A B A B A B A B A B A B A B A B A B A B A01. - - - - - - + * + * + * - - + - + - + - - - + - + * - - + - - -

02. - - + - + * + * - - - - - - + - + - - - - - - - + * - - + - - -

03. + * + - + * + * + * + * + * + - + - + - + - + - + * + - - - - -

04. + * + - + * + * + * + * - - + - - - + - - - - - + + - - + - + *

05. + * + - + * + * + * + * + * + * + - + - + * + - + * + - + - + *

06. - - - - + - + * + * - - - - + - + - + - + - + - + * - - - - - -

07. + * + - + * + * + * + * + * + - - - - - + * - - + * + - + - - -08. + * + - + * + * + * + * - - + - + - + - + - - - + * - - + - - -

09. + * + - + * + * + * + * + * + - + - + - + - + * - - - - + - + *

10. + * + - + * + * - - + * + * + - - - - - + - - - + * - - + - - -

11. - - + - + * + * - - + * - - + - - - - - - - - - + * - - + - + +

12. + * + - + * + * + * + * + * + - + - + - + - - - + - + - + - - -

13. + - + - + - + * + * + - + * - - + - - - + - - - + - + - - - + -

14. + * + - + * + * + * + * + * + - + - - - + - - - + + - - + - + *15. - - + - + * + * - - + * - - + - + - - - + - + - + * - - + - - -

16. - - - - - - + * + * + * - - + - + - - - + - + - - - - - + - + +

17. - - + - + - + * + * + * - - + - + - - - + - + - - - - - + - - -

18. + * + - + - + * + * + * + * + - + - + - + - + - + * + - + - - -

19. - - + - + - + * - - + * + * + - + - - - - - - - + * - - + - - -

20. - - + - + - + - - - + * + * + - + - - - + - - - + - + - - - - -21. + * + - + - + * + * + * + * + - + - - - + - + - - - - - + - - -

22. - - + - + - + * + * + * + * + - + - + - + - - - + * - - + - - -

23. + * + - + - + * - - + * - - + - + - - - + - + - - - - - + - - -

24. + * + - + - + * + * + * + * + - + - + * + - - - + * + - + - + *

25. - - + - + - + * - - + * - - + - + - + - - - - - + * - - + - - -

26. + * + - + - + * - - + * + * + - + - - - + - + - - - + - + - - -

27. - - - - + - + * + - + * - - + - + - - - + - + - - - + - + - - -28. + * + - + * + * - - + * + * + - + - - - - - - - + * + - + - - -

29. - - + - + * + * - - + * - - + - + - + - - - - - + - - - + - - -

30. + * + - + * + * + * + * - - + - - - - - - - - - - - - - + - - -

1 – Spik Chalatwa, 2 – Spik Guruta, 3 – Spik Vriddhi, 4 – Udara lambana, 5 - Udara Chalatwa, 6 – Stana Vruddhi, 7 – Stana Chalatva, 8 – Shareera Gouravata, 9 – Alasya, 10 – Kriya Asamrthatata, 12 – Vyavaya, Asamrthatha, 13 – Snigdhangata, 14 – Aruchi, 15 – Talushosha, 16 – Shopha. Symptoms - ( + : Present, - : Absent, * : Reduced.).

Master charts 109


Data related to associated symptoms – Master Chart No. 4

Associated Symptoms 1 2 3 4 5 6 7

SL. NO.

B A B A B A B A B A B A B A 01. + - + * + * + - - - + - + + 02. + - + * + * + - - - + + - - 03. - - + * + * + - - - - - + + 04. + - + * + + + - + - + - + + 05. + - + * + + + - + - + + + + 06. - - - - + * - - + - + - + + 07. + - - - + * - - + - - - + + 08. + - + * - - + - + - - - + + 09. + - + * + * + - + - - - + + 10. + - + * + + + - + - - - - - 11. + - + * - - + - - - - - + + 12. + - + * + + + - + - + - + + 13. + - + + - - + - + - - - + + 14. + - + * + + + - + - - - + + 15. + - + * - - + - + - + + + + 16. + - + * + + + - + - - - + + 17. + - + * - - + - + - - - + + 18. + - + * + + + - + - + - + + 19. + - + * + + + - - - - - - - 20. - - + * + * + - - - + + - - 21. + - + * - - - - + - - - - - 22. + - - - - - + - + - - - - - 23. + - + * - - + - + - - - + + 24. + - + * + + + - + - - - + + 25. + - + * + + + - - - + + + + 26. + - + + - - + - - - - - - - 27. + - + * + + + - + - + + + + 28. + - + * - - + - - - - - - - 29. + - + + + * + - - - + - - - 30. + - + * - - - - - - - - + +

1 – Adhika Trishna, 2 – Adhika Kshudha, 3 – Adhika Sweda, 4 – Adhika Nidra,

5 – Alpa Bala, 6 – Shareera Dourgandhya, 7 – Krathana.

Master charts 110


Data related to upadrava –

Master Chart No. 5

Upadrava

1 2 3 4 5 6 7 8 9 10 11

Sl.

No.

B A B A B A B A B A B A B A B A B A B A B A

01. - - + - - - + * + + - - - - - - - - - - + -

02. - - - - - - + * + + + + - - + - - - - - - -

03. - - - - - - - - - - - - - - - - - - - - + *

04. - - - - - - - - + + - - - - - - - - - - + -

05. - - + - + - + - + + + - - - - - - - - - + -

06. - - - - - - + * + + + + - - - - - - - - + -

07. - - + - - - - - + * - - - - - - - - - - - -

08. - - - - - - - - + - - - - - - - - - - - + -

09. + - + - - - - - + + - - - - - - - - - - + *

10. - - - - - - - - + + + + - - + - - - - - + -

11. - - - - - - + * + * - - - - - - - - - - - -

12. + - - - - - - - + - + - - - - - - - - - - -

13. - - - - - - - - - - - - - - - - - - - - + -

14. - - - - + - - - + - + + - - - - - - - - - -

15. - - + - - - - - + * - - - - - - - - - - + *

16. - - - - - - - - + + - - - - - - - - - - - -

17. - - - - - - - - + + - - - - - - - - - - + -

Page No. 111

Master charts 110


Master Chart No. 5. contd….

Upadrava

1 2 3 4 5 6 7 8 9 10 11

Sl.

No.

A B A B A B A B A B A B A B A B A B A B A B

18. - - - - - - - - + + - - - - - - - - - - - -

19. - - - - - - - - - - - - - - - - - - - - - -

20. - - - - - - - - + + - - - - - - - - - - + -

21. - - - - - - - - + + - - - - - - - - - - + *

22. - - - - - - - - - - - - - - - - - - - - - -

23. - - + - + - - - + + - - - - - - - - - - + *

24. - - - - - - + + + + - - - - - - - - - - + -

25. - - - - - - - - - - - - - - - - - - - - + -

26. - - - - - - - - + + + + - - - - - - - - - -

27. - - - - - - + + + + - - - - - - - - - - + -

28. - - + - + - - - + + - - - - - - - - - - - -

29. - - - - - - - - + + - - - - - - - - - - + -

30. - - - - - - - - + + - - - - - - - - - - + *

1 – Jwara, 2 - Atisara, 3 – Kamala, 4 – Prameha, 6 – Kushta, 7 – Bhagandara, 8 –

Visarpa, 9 – Slepada, 10 – Aruchi, 11 – Vatavyadhi, B – Before treatment, A – After

treatment. Symptom – ( + : Present, - : Abesent, * : Reduced. )

Page No. 112.

Master charts 110


Data related to height, weight and circumference - Master Chart No. 6

Weight (In Kg.) Circumference of (in cms.) Sl.

No.

Height

(in ft.) SW B A Dif UB UA Dif SpB SpA Dif StB StA Dif

Result

01. 5.1 58 104 099 05 125 122 03 140 134 06 119 117 02 Relieved

02. 5.1 45 65 60 05 88 85 03 106 97 09 109 107 02 Relieved

03. 5.1 48 84 80 04 114 110 04 118 111 07 103 100 03 Relieved

04. 5.2 46 67 65 02 107 105 02 122 120 02 101 101 00 Relieved

05. 5.2 46 84 80 04 123 121 02 135 127 08 116 111 05 Relieved

06. 5.4 51 88 85 03 107 102 05 120 115 05 109 104 05 Relieved

07. 5.4 52 91 84 07 117 115 02 121 119 02 113 111 02 Relieved

08. 5.4 52 89 87 02 99 97 02 95 94 01 88 88

00 NotResponded

09. 5.1 50 86 80 04 109 106 03 115 110 05 92 86 06 Relieved

10. 5.2 47 83 80 03 117 114 03 116 114 02 92 90 02 Palliative

11. 5.2 49 82 79 03 118 114 04 116 114 02 88 85 03 Relieved

12. 5.3 50 68 64 04 97 95 02 121 119 02 99 98 01 Palliative

13. 5.3 50 67 63 04 108 104 04 120 116 04 100 95 05 Relieved

14. 5.2 61 85 81 04 93 90 03 87 79 08 86 82 04 Relieved

15. 5.5 58 89 86 03 98 96 02 94 89 05 87 84 03 Relieved

16. 5.5 52 66 63 03 97 95 02 121 119 03 99 97 02 Palliative

17. 5.4 52 91 87 04 102 99 03 98 96 02 90 87 03 Palliative

18. 5.1 48 56 52 04 88 84 04 95 91 04 91 88 03 Relieved

19. 5.4 43 80 78 02 118 117 01 120 117 03 114 112 02 Palliative

20. 4.11 51 86 82 04 107 102 05 118 115 03 112 109 03 Relieved

21. 5.5 54 76 75 01 104 103 01 120 120 00 108 107

01 NotResponded

22. 5.7 64 125 122 03 123 122 01 121 120 01 108 106 02 Palliative

23. 5.6 59 106 102 04 122 118 04 119 114 05 115 113 02 Relieved

24. 5.5 54 76 75 01 104 103 01 120 120 00 108 107

01 NotResponded

25. 5.8 61 85 80 05 93 89 04 87 80 07 86 81 05 Relieved

26. 5.9 64 125 123 02 123 120 03 120 118 02 118 116 02 Palliative

27. 5.0 51 86 83 03 107 102 05 118 116 02 108 107 01 Palliative

28. 5.1 48 84 80 04 114 110 04 118 111 07 103 100 03 Relieved

29. 4.10 48 56 55 01 88 87 01 95 92 03 91 89 02 Palliative

30. 5.8 61 85 80 05 93 89 04 87 80 07 86 81 05 Relieved

SW – Pre calculated Standard weight, UB – Udara before treatment, SpB – Udara After Treatment, SpB – Spik before treatment, SpA – Spik After treatment, StB – Stana Before treatment, Dif. – Difference, B – Before treatment, A – After treatment, R - Result.

Page No. 11

Master charts 110


Master chart No. 7 Serum Cholesterol

Triglyceriods HDL Cholesterol

LDL Cholesterol

VLDL Cholesterol

Random BS

Sl. No.

B A

Dif

B A

Dif

B A

Dif

B A

Dif

B A

Dif

B A

Dif RT

01. 216 180 36 224 118 06 32 37 05 122 107 15 45 42 03 108 102 06 R

02. 250 226 24 212 195 17 47 45 02 146 121 25 38 28 10 150 139 11 R

03. 204 218 06 294 172 12 45 48 -4 137 116 21 37 33 04 130 110 20 R

04. 260 230 30 186 175 11 48 44 04 170 153 17 37 39 08 135 123 12 R

05. 240 226 14 197 186 11 50 55 -5 119 103 16 39 37 02 121 108 13 R

06. 212 184 18 142 130 12 44 40 04 139 125 14 28 26 02 156 146 10 R

07. 230 199 31 74 79 -5 43 41 02 173 164 09 29 26 03 118 110 08 R

08. 230 220 10 131 116 15 36 38 -2 170 166 04 26 24 02 132 129 03 NR

09. 204 218 06 294 172 12 45 48 -4 137 116 21 37 33 04 130 110 20 R

10. 225 210 15 92 86 06 35 38 -3 186 166 20 33 13 03 150 148 02 P

11. 213 192 21 104 91 13 37 39 -2 181 163 18 24 21 03 135 120 15 R

Sl. No.

Serum Cholesterol

Dif Triglyceriods Dif HDLCholesterol

Dif LDLCholesterol

Dif VLDLCholesterol

Dif Random

BS

Dif RT

Master charts 110


B A B A B A B A B A B A

12. 219 205 14 138 126 12 41 40 01 192 187 05 32 31 01 187 162 25 P

13. 245 220 25 158 151 07 48 52 -4 169 156 13 30 25 05 134 120 14 R

14. 212 184 18 142 130 12 44 40 04 139 125 14 28 26 02 156 146 10 R

15. 190 160 30 172 157 15 33 35 -3 114 105 09 35 33 02 185 160 25 R

16. 248 225 23 189 176 13 49 46 03 132 104 28 49 47 02 152 140 12 P

17. 255 220 35 162 152 10 41 44 -3 133 111 22 72 26 16 132 121 11 P18. 213 192 21 104 92 12 39 37 02 178 163 15 24 20 04 135 116 19 R19. 212 182 30 102 87 15 36 39 -3 150 139 11 25 20 05 124 104 20 P20. 230 199 31 74 79 -5 43 41 02 173 164 09 29 26 03 118 110 08 R21. 233 197 36 131 116 15 39 36 03 168 164 04 26 24 02 141 139 02 NR22. 208 201 07 134 122 12 39 38 01 181 163 18 24 21 03 135 116 19 P

23. 220 201 19 184 172 12 44 47 -3 137 116 21 37 33 04 132 111 21 R

24. 237 221 16 243 220 23 48 43 05 146 135 11 43 42 02 118 116 02 NR

25. 234 221 13 157 139 18 48 44 04 155 151 04 32 30 02 132 128 04 R

26. 212 182 30 102 87 15 36 39 -3 150 139 11 25 20 05 124 104 20 P

27. 248 225 23 189 176 13 49 46 03 132 104 28 49 47 02 152 140 12 P

28. 212 184 18 142 130 12 44 40 04 139 125 14 28 26 02 156 146 10 R

29. 219 205 14 138 126 12 41 40 01 192 187 05 32 31 01 187 162 25 P

30. 213 192 21 104 92 12 39 37 02 178 163 15 24 20 04 135 116 19 RPage No. 114-115

Master charts 110


Discussion on materials and methods

After considering the Ayurvedic view regarding the Sthoulya Tryushanadya Loham

was selected for the present study.

Criteria for the selection of the Tryushanadya Loham

It is mentioned that Tryushanadya Loham is very effective Yoga in Sthoulya.

There is no satisfactory research on the clinical efficacy of Tryushanadya Loham.

Tryushanadya Loham is safe Yoga.

Its ingredients are easily available in the market.

Method of preparation is very simple.

It is very easy palatable and no diet restriction.

Probable mode of action of Tryushanadya Loham

Pharmacodynamics in Ayurveda mainly based on the fundamental doctrines of

Panchamahabhoota and Tridosha, which govern the Physiochemical and Biological

phenomena respectively.

On assessing the ingredients of Tryushanadya Loham including Madhu and Ghrita

(an unequal quantity) for anupana. Drugs are having Kapha-vata shamaka property and also

anulomana, srortovishodhaka, deepana and pachana etc.

As explained earlier Sthoulya is the Kapha-vatajanya Vyadhi, Samprapti will be

pacified by the above mentioned yoga. Drugs containing Laghu guna, Ushna veerya, Katu

vipaka, Katu rasa will act on Kapha-vata Dosha.

Dose

The dosage of the Tryushanadya Loham is clearly mentioned 1 masha T.D.S. or

2.250 gms/day in divided dosage.

Discussion 116


Anupana

Madhu and Ghrita (in unequal ratio) was given based on the classics.

Method of sampling

The patients were incidentally selected exclusively conducted medical camp, O.P.D and

I.P.D. at P.G. Research Center Kayachikitsa Department Shri D.G.M.Ayurvedic Medical

College, Gadag. Method of sampling was incidental because of the availability of the cases in

O.P.D. and free medical camp.

Selection of the patients

The patients of both sexes were selected for the clinical study strictly on the basis of

detail case sheet.

Inclusive and Exclusive criteria

Only mild and moderate obesity patients were selected for the clinical study, which

we can treat and excluded morbid obesity, severe and secondary hyperlipidaemia, severe

diabetes mellitus and hypertension cases because of lack of emergency treatment.

Laboratory investigation

The selected patients were subjected to laboratory investigation to rule out the

secondary hyperlipidaemia and other systemic disorders to confirm positively belong to the

obesity.

Diagnosis

Diagnosis made on the basis of clinical symptoms of Sthoulya mentioned in the

classics and on the basis of laboratory investigation primary hyperlipidaemia cases were

diagnosed.

Discussion 117


Observation

Drop outs

For the clinical trail 38 patients were taken up, out of these 08 patients discontinued

the treatment during the various stages of the study. The cause of the discontinuity in the

patients remained obscure. So clinical study was completed in 30 patients.

Availability

Most of the cases were reported in medical camp. Some cases were reported at O.P.D

and I.P.D. at P.G. Research Center Kayachikitsa Department Shri D.G.M. Ayurvedic

Medical College, Gadag.

Education

There were maximum number of patients with higher level of education and followed

by higher secondary and primary education. None of them were illiterate. It dose not mean

that illiterates are not suppose to get obesity. Education is directly linked with job involving

lot of sedentary work, the same factor is mentioned in the contemporary sciences.

Occupation

80% of the patients were sedentary jobholders. Here obesity is due to nature of

sedentary work, which can be justified.

Sex

It is evident that females are more prone to obesity. In this present study also

incidence is more in female. The reason behind this, could be the because of less physical

activities.

Discussion 118


Age

It is well known fact that majority of the cases develop obesity in the middle aged

people. In this present study maximum number of patients found in the third decade. Hence it

holds good as for as this study is concern.

Family history

Maximum patients had family history in present study; most researchers would agree

that there is a majority of hereditary contribution in producing obesity. Hence it holds good

as far as this study is concern.

Religion

Majority of the patients were Hindus. It dose not mean that Hindus are more prone to

this disease, this may be due to method of sampling, patients were selected incidentally.

Socioeconomic status

It is clear that more number of patients were from upper class compare to middle and

lower class. Usually upper class people have high calorie diet. This may be the reason for

finding the more people from upper class. Lower class people were less compare to upper

and middle class people because they do hard work or physical work will be more.

Symptoms

Majority of cases were symptomatic and asymptomatic patients were less compare to

symptomatic. Majority of the cases had Shareera Gouravata, Alasya, Kriya asamarthata,

Talushosha followed by Adhika trishna, Adhika kshudha, Adhiak sweda, Shareera

douragandha and Adhika nidra.

In early stage most of the obesity patients are asymptomatic, but in current study most

of them are symptomatic may be due to chronicity of the disease.

Discussion 119


Chronicity

In this clinical study, chronicity showed that 60% patients had chronicity more than

three year varying from one year to ten years and patients has history of previous treatment

and 80 % of the patients were treated cases. 20% cases were fresh. This study suggests that

obesity is a chronic disease.

Habit

In current study it was observed that majority of the patients had habits of day sleep,

less physical activity and adhyashana. Here in this study also same holds good.

Food habit

In this study it was observed that most of them had mixed food habit. Studies have

reported that there is a clear association between high calorie diet and obesity. This also

observed in this clinical work.

Assessment of the Ayurvedic features

An attempt was made to assess the involvement of Dosha, Deha Prakriti, Mana

Prakriti, Agni, Satwa, Vyayama Shakti and Koshta, etc.

Involvement of Dosha

Deha Prakriti

On the basis of symptoms mentioned in Shoulya, it is observed that involvement of

both Kapha and Vata is present. In present clinical study most of the patients had Kapha vata

and Vata kapha Prakriti. So the present study supports the classical symptoms.

Manasika Prakriti

The study revealed that a majority of patients had Harsha, followed by Chinta and

Shoka. It suggests that interlink between the Kapha Prakriti and Satwa Prakriti.

Discussion 120


Agni

The assessment of agni was made on the abhyavarana shakti and jarana Shakti which

revealed that majority of the patients were mandgni and samagni. So by this clinical study

evidences of Vishamagni in Sthoulya can be justified and which supports the classical texts.

Vyayama

Assessment of Vyayama Shakti was made on the basis of the nature of the work.

Maximum patients belonging to avara vyayama shakti. It suggests that hard workers not

suppose to get Sthoulya.

Nidana

Ahara

In this clinical study more consumption of Guru, Madhura, Sheeta, Snigdha nidanas

were observed. Most of them are Kapha vardhaka. So it can be establish that intake of high

calorie food causes obesity.

General observations

During the intervention various observations were made on every step of the

treatment. When the patient visited time that is considered as base line measurement and then

was asked to discontinue the previous medicines if patient was on treatment. In earlier stage

of treatment all patients had showed good appetite, Shareera laghavata. Some patient’s

complained Uraha daha in such cases dose of anupana (ghee and honey in unequal quantity)

was increased.

All the patients received standard dose of Tryushanadya Loham during the period of

treatment. Agni deepti, Vatanulomana, Shareera laghavata, Nidra, was improved. Just after

the treatment final data’s were collected then patients were kept under observation for 30

days.

Discussion 121


Results

The results of the clinical study showed Tryushanadya Loham Shamana therapy has a

role in Sthoulya (Hyperlipidaemia).

A1-A2 (15th –30th day)- Assessment showed symptomatically insignificant.

A2-A3 (30th –45th day)- Showed signs and symptoms are significantly reduced.

A3-A4 (45th –60th day)- Third assessment showed symptomatically significant.

A1-A5 (15th –60th day)- Last assessment made on the basis of signs and symptoms showed

highly significant and statically significant i.e. P value is less than 0.001.

Total assessment

The statistical analysis of the effect of Tryushanadya loham after treatment revealed

that it was significant, but the observations revealed that Tryushanadya loham was very

useful in mild and moderate Obesity cases.

Discussion 122


RECOMMENDATION FOR FUTURE STUDY

The following recommendations are made on the basis of observations and

conclusions for the further studies as well as to overcome the limitations.

01. Same study can be repeated by taking a large number of samples.

02. The efficacy of Tryushanadya loham has to be estimated in double blind

randomized controlled study.

03. The effect of the Tryushanadya loham can be studied in longer duration of the

even in severe hyperlipidaemic cases.

LIMITATION OF STUDY

01. Sample size is small to generalize the result.

02. Drug being a compound formation is difficult to draw its mode of action.

03. Samples were selected incidentally.

Discussion 123


CONCLUSION

Based on the literature and observations made in the clinical study, the following

conclusion can be drawn.

Hyperlipidaemia is common condition, which represents Sthoulya disease in

Ayurveda.

Sthoulya (Obesity) can be treated on the basis of the Dosha-dushya vivechana.

Tryushanadya Loham was found equally effective in mild and moderate

hypertension.

It is more effective in fresh cases compared to treated cases.

Tryushanadya Loham was found to be more effective in patients a history of smaller

duration (chronicity) when compared to cases a history of large duration (chronicity).

Conclusion 124


SUMMARY

The disease Sthoulya is a global problem and more common in civilized man.

Sthoulya (Obesity) is said to be mother of many dangerous diseases. Now a day Sthoulya has

becoming initiating and influencing factor for life threatening diseases like hypertension,

diabetes mellitus, coronary heart disease (CAD), myocardial infraction (MI).

Hyperlipidaemia is a common clinical condition, which is most common in obese person and

cause for many dangerous cardiovascular disease. For hyperlipidemia there is no satisfactory

remedy in contemporary medical science. But in Ayurveda many recipes have vividly

explained for Sthoulya (Obesity) which are very effective in controlling condition

hyperlipidaemia. Today the world is eagerly looking for effective, safe, cost effective remedy

for hyperlipidaemia such being the case Ayurvedic modalities play an important role. So

keeping in mind Tryushanadya Loham yoga taken for clinical trial to evaluate the effect of

Tryushanadya Loham in Sthoulya with special reference to hyperlipidaemia (on lipid values).

The Tryushanadya Loham yoga was selected for the clinical study as its efficacy is

praised by Yogaratnakara in Uttarardha as a best modohara yoga and easy availability of its

ingredients and easy preparation.

The epidemology, etiology, pathogenesis clinical features, diagnosis, complications

and treatment of the Hypertlipidaemia and Sthoulya were reviewed.

On the basis of Ayurvedic principle and with modern principles, physiology of fat

metabolism, nidana panchakas, upadrawa, upashaya, anupashaya, sadhya, asadhya and

chikitsa were explained.

Summary 125


The single blind observational study was carried out on thirty patients. 30 cases of

both sexes between the age group of 30 – 65 years with a diagnosis based on ICD – 10

criteria and Sthoulya signs and symptoms mentioned in Ayurvedic texts.

All the patients received Tryushanadya Loham yoga for 60 days and followed by

follow up for 30 days. The total duration of the treatment was 90 days.

It was observed that hyperlipidaemia usually appears in between third and sixth

decade of life. The people belonging to urban area, upper class, non-vegetarians, long

exposure to stress and strain are susceptible for this disease.

The disease is more prevalent in people with Kapha – Vata Prakriti, involvement of

Kapha appears as a prominent feature.

The lipid values and also sign and symptoms before and after the treatment were

compared. Totally five assessment were made to observe the effect in different stages.

To assess the effect of the treatment, variables were subjected for student’s ‘t’ test.

The result of the clinical study showed Tryushanadya Loham Shamana therapy has a

role in Sthoulya (Hyperlipidaemia).

A1-A2(15th –30th day)- Assessment showed symptomatically insignificant.

A2-A3(30th –45th day)- Showed signs and symptoms are significantly reduced.

A3-A4 (45th –60th day)- Third assessment showed symptomatically significant.

A1-A5(15th –60th day)- Last assessment made on the basis of signs and symptoms showed

highly significant and statically significant i.e. P value is less than 0.001.

Summary 126


LIST OF REFERENCES

Introduction :

1) Charaka Sutrasthana 27 / 345,346,347 (Chakrapani commentary)

2) Ashtanga Hridaya Sutrasthana 7 /51.

3) Shabdha stoma maha ndhi, Vachaspathyam

4) Review of Medical Physiology – W. Ganong pp 294

5) Dictionary English to Sanskrit By MM Williams pp64.

6) Your guide to health Clifford. R. Anderson. pp 67.

Disease review :

1) Ayurveda Ka Vaigyanika Itihasa pp 18,19,21,23,25,26,27,29,30.

2) Madhava Nidana 1/19

3) Charaka Sutrasthana 21/3

4) Sushruta Sutrasthana 15/32

5) Astanga Sangraha Sutrasthana 24/18

6) Bhava Prakasha Madhyamakhanda 39/1


8) Yoga Ratnakara Medoroga nidana /1

9) Astanga Sangraha Sutrasthana 11

10) Astanga Sangraha Sutrashtana 6

11) Astanga Hridaya Sutrasthana 8/2


13) Charaka Vimanasthana 2/7

14) Dalhana on Sushruta. Sutrasthana 15/32




18) Gangadara on Charaka sutrasthana 21/3

19) Madhava Nidana 21/5,6


21) Charaka Vimanasthana 2/7

22) Caraka Vimanasthana 15/42

References & Bibliography 127



24) Essentials of Basic Ayurveda concepts By V.V.S. Shastri. pp 92

25) Astanga Hridaya sutrashtana 13/25

26) madhava Nidana 31/1


28) Madhu kosha on Madhava nidana 34



31) Ashtanga Sangraha Sutrasthana 24/22


33) Astanga Hridaya sutrasthana 8/2

34) Charaka sutrasthana 21/4

35) Astanga sangraha sutrasthana 24/24

36) Chakrapani on charaka sutrasthana 21/4

37) Astanga Sangraha Sutrasthana 23,24

38) Chakrapani On Cahraakaa Sutrasthana 28/4

39) Sushruta Sutra Sthana 15/32


41) Ashtanga Samgraha Sutra Sthana 24/18

42) Madhukosha Vhyakhya On Madhava Nidana 34/1-7


44) Bhavaprakasha Madhyama Kahanda 1/16

45) Chakrapani On Charaka Sutra Sthana 21/3,4


47) Sushruta Samhita Sutrasthana 24/13


49) Ashtanga Samgraha Sutrasthana 24/26



52) Charaka SutraSthana 21/4




54) Ashtanga Samgraha Sutrathana 24/19,20


56) Bhavaprakasha Madhyamakahanda 39

57) Yoga Ratnakara Medoraga Nidana/1,2 & 8

58) Nidana Chikitsa Hastamalaka pp.197

59) Ashtanga Samgraha Sutrathana 19/20

60) Bhavaprakasha Poorvakhanda 3/149

61) Chakrapani On Charaka Sutra Sthana 21/4







68) Chakrapani On Charaka Sutra Sthana 21/3

69) Gangadhara On Charaka Sutra Sthana 21/3

70) Charaka Sutra Sthana 21/4

71) Dalhana On Sushruta Sutrasthana 15/32



74) Indu on Ashtanga Samgraha Sutrathana 24/45

75) Yoga Ratnakara Medoroga Chikitsa/17

76) Charaka Sutra Sthana 21/7



79) Bhavaprakasha Madhyamakahanda 39/10

80) Charaka Siddisthana 2/8,11


82) Bhaishyajya Ratnavali 39/1









89) Ashtanga Hridaya Sutrasthana 33/18


91) Sushruta Chikitsa 30/9

92) Madhva Nidana 34/8

93) Allied Ayurvedic Medical Research Abstracts (AAMRA)

94) Research in Ayurveda BY Dr. M.S. Baghel.

95) Text Book of Medicine by R.J. Vakil pp 287

96) Review of Medical Physology by W.F. Ganong pp 249

97) Text book of physiology by Gyton pp 367

98) The News week Sept 27 1999 34/1,2

100) Joslin’s Diabetes mellitus pp.352,355,358

101) Runcie, J & Itilditch, T.E. (1974) – B.M.J., ii , 250

102) From fat to fit pp 61,72

DRUG REVIEW

1) Dravya Guna Vignan : P.V.Sharma

2) Dravya Guna Vignan :Y.T.Acharya

3) Bhava prakash Nighantu

4) Nighantu Adarsha :Bapalalji Vaidya.

5) Unani Dravya Gunadarsha

6) Indian Medicinal plants: Kirtikar and Basu

7) Some controversial Drugs in Indian Medicine

8) Brahat Dravya Gunadarsha

9) Madanapala Nighantu

10) Vanoushadhi Nidarshaka

11) Madhav dravya Guna

12) Fruits & Vegetables In India

13) Indian material Medica



14) Materia Medica of India and Therapeutics

15) Dhanwanatri Nighantu

16) Raja Nighantu

17) Kaiyadeva Nighantu

18) Vanoushadhi Chandrodaya

19) The Treaties On Indian Medicinal Plants

20) Encyclopedia Of Plants: Plampona Roger.

21) Pharmacopoeia India

22) Charaka Samhita

23) Sushruta Samhita

24) Ashtanga Sangraha Sutrasthana

25) Shodhala Samhita

26) Ayurveda Dravyaguna Vignana :S.K.Vyasa.

27) Herbal & General History Of Plant: Jhon Gerarde.

28) Sandigdha Vanoushadhi Anka : V.N.Dwivedi.

29) Male Herbal: James Green.

30) Genetic Complex Of Ayurvedic Plants :C.R.Karnik.

31) Pharmacology of Ayurvedic Medicinal Plants :C.R.Karnik.

32) Pharmacopocial Standard Of Herbal Plants :C.R.Karnik.

33) Clinical Application Of Ayurvedic Remedies & List Of Ayurvedic

Preparation.

34) Compendium Of Indian Medicinal Plants :Malahotra & Rastogi.

35) Pharmocognosy: Purohita Gokkale & Kokate.

36) Material For Data Base Of Medicinal Plants :C.Rameshwara Rao.

37) Ayurvedic Encyclopedia :Sadashiva Ram Tirth.

38) Medicinal Plants Abstracts (CSIR Newdelhi) Vol. – 24 Vol.– 17

39) Ayurvedic Healing for healing :Atreya.

40) Ayurvedic Remedies: Lighter Miller.

41) Ayurvedic Secretes Of Healing :Maya Tiwari.



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SPECIAL CASE SHEET FOR “STHOULYA”

DEPARTMENT OF KAYACHIKITSA

POSTGRADUATE STUDIES AND REASEARCH, (KAYACHIKITSA)

SHRI D.G.M.AYURVEDIC MEDICAL COLLEGE GADAG.

“Evaluation of the efficacy of Tryushanadya Louham in Sthoulya (Obesity)

with special reference to Hyperlipidaemia”

PROFORMA OF SHOULYA Guide : Dr. V.Vardacharyulu ; Research Scholar : Dr. Shakuntala C. Garwad.

PART I : History Taking & clinical Examination. PART II : Interpretation PART III : Observation & Assessment PART I : Examination

Name : Serial No. :

Age : Years. O.P.D.No./I.P.D. :

Sex : M / F. D.C.T. :

Marital Status : M / U / W / D D.C.T. :

Religion : H / M/ Ch / Oth.

Education : UE / P / M / HS / Gr / PG.

Occupation : D / E / O / B / Ag / H. W / L / Rtd / Oth.

Socio – Economic Status : P / M / UM / R / VR.

Place : Urban / Rural.

Address : --------------------------------------------------------------------------- --------------------------------------------------------------------------- --------------------------------------------------------------------------- Results - Complete Remission

Subsidence Minor Subsidence

Discontinued

Consent :

I --------------------------------------------- Son / Daughter / Wife of ---------------------

Exercise my free will in the said study. I have been informed to my satisfaction by the

attending the purpose of the clinical evaluation & nature of drug treatment. I was also

aware of my right to quit at any time during the schedule.

Signature of the Patient

(A) HISTORY 01. a) Pradhana Vedana : Spik / Stana / Udara lambana. Kala

Others.

b) Anubandhi Vedana :

Atipipasa / Atikshudha / Dourgandhya / Swedabadha / Kasa /

Kshudra Shwasa / Krantana / Atinidra / Kruchra Vyavaya / Moha /

Shrama / Sandhishoola / Others.

02. Adhyathana Vyadhi Vrithantha.

03. Purva Kalina Vrithantha

04. Any Investigation done in past

05. Chikitsa Vrithantha :

Name of the drug Duration Purpose

06. Kula Vrithantha ; Similar to IIII / any other illness ;

07. Atura Chyarya.

I Ahara

A = Pramana – Alp / Sama / Atipramana.

B = Dominent rasa in diet – M/ A / L / Kt / T / Ks.

C = Snigdha / Sheeta / Ushna / Guru.

Mootra

Jivha

Akruti

02. Dashvidha Pareeksha a) Prakruti – Shareerika - V / P / K / VP / PK / KV / Sama. Manasika – S / R / T / SR / ST / TR / Sama. b) Vikruti - c) Saratha – Pravara / Madhyama / Avara . d) Pramana – Pravara / Madhyama / Avara . e) Satma – Pravara / Madhyama / Avara . f) Satvata – Pravara / Madhyama / Avara . g) Ahara Shakti – Abhyavarana Shakti - Pravara / Madhyama / Avara. Jarana shakti – Sama / Manda / Teekshna / Vishama. h) Vyayama Shakti - Pravara / Madhyama / Avara . i) Vaya – Bala / Madhyama / Vruddha.

03. Systemic Examination a) Respiratory System

b) Cardiovascular System

c) Gastrointestinal System

d) Nervous System

e) Sthoulya Pareeksha.

Weight Height BMI

Fat Distribution ( )

Vaksha Pradesha Vruddhi ( )

Spik Pradesha Vruddhi ( )

Xanthomata ( )

Udara Pradesha Vruddhi ( )

Corneal Arcus ( )

Xanthomata ( )

Deitic Habitat – Samnasana / Vishamasana / Adhyasana.

Type of food – Veg / Non- veg.

Particular food article –

II . Vihara

a. Nature of work : Manual / Secondary / Labour / Vishamasana /Adhyasana.

b. Vishrama : Proper / Less Exercise.

c. Vyayama : No / Less / Proper / Irregular.

d. Nidra : Excessive / Normal / Irregular / Day Sleep / Total Hours.

e. Harshanitya / Achinta .

III . Vyasana

Smoking Cigarate ……………………… / Day for …………………………. / Years.

Beedi ……………………… / Day for ……………………… / Years.

Quit Smoking ……………………… m / yr / back.

Tobacco Chewing / Betal nut Chewing

Alcohol – Yes / No.

Frequently / Occasional / Social / Regular.

……………………… m / Daily / Weekly for ……………………… years.

IV . If the patient is female

Age of menarche

Issue

Operation

Abortion

Menopausal age

B . Examination

01. Samanya Pareeksha

Nadi

Mala

Drak

Rakta Chapa

04. Investigations

Blood 01. Lipid Profile : 02. Hb

Total Se. Chole : TC

L.D.L. : DC-P E

H.D.L. : L M

Triglycerides : B

V.L.D.L. ESR

03. Urine – Alb Sugar Micro

Part – II Interpretation

A) Hetu

B) Poorvaroopa

C) Roopa

D) Upashaya / Anupashaya

E) Samprapti

F) Dosha

G) Dooshya

H) Agni

I) Ama

J) Udbhavasthana

K) Srotas

L) Rogamarga

M) Sanchayasthana

N) Dustiprakra

O) Adhishtana

P) Vyaktasthana

Q) Rogamarga

R) Desha – Janana Nivasa Vyadhi

S) Rogibala - Pravara / Madhyama / Avara .

T) Rogabala - Pravara / Madhyama / Avara .

U) Vyadhi vinischyaya

V) Arishta laxana

W) Sadhyasadhyata

Part III . Observation and Assessment

Intervention

Pososlogy : 01 . Mahsa T. D. S. or 2,225 gms / days in dividing doses.

Anupana : Madhu & ghruta ( in unequal ratio )

Diet : The patient will be suggested diet they used to have daily but with low fat diet.

Observation During Treatment

Days Date Weight Oservation

15th

30th

45th

60th

Assessment Date Sl.

No.

Name Before

Treatment

After

Treatment

01. Total Serum Cholesterol Values : Gr : Values : Gr :

02. L.D.L.

03. H.D.L.

04. Triglycerides

05. V.L.D.L.

06. Weight

07. Hb

08. T.C.

DC :

P

E

L

M

09.

B

10. ESR

Date:

Signature Of the Candidate Signature Of the H.O.D.

Caloric values of the uncooked & cooked food articles according to N I N (National Institute of Nutrition) Hyderabad.

Caloric value of uncooked foods Food water calories Protein(gms) Fat Carbohydrate Fiber(gms) Ca(mg) Fe(mg) Vit A

i.u

B1(mg) B2(mg) Niacin(mg) Vit

C(mg)

Almond 5 657 20 59 12 1.7 230 4.5 -- 0.3 0.6 4.5 --

Amla 81 55 0.5 0.10 14 3.4 50 1.2 -- -- -- -- 600

Animal fat 1 891 -- 99 -- -- -- -- -- -- -- -- --

Apple 84 61 0.3 0.4 14 1 4 1 20 0.02 0.04 0.2 5

Apricot 90 36 1 -- 8 0.4 15 1 2000 0.03 0.05 0.5 5

Bajra millet 13 361 11.6 0.5 67.5 1.2 42 5 -- 0.33 .25 2.3 --

Banana 70 116 1 0.3 27 0.3 7 0.5 100 0.1 0.08 0.8 7

Barley 13 336 22.5 1.3 62.6 3.9 2.5 8 -- 0.47 0.20 5.4 --

Bathua leaves 90 30 3.7 0.4 2.9 0.8 150 4.2 -- 0.01 0.14 0.6 35

Beetroot 87 45 1.8 -- 10 07 15 1 -- 0.02 0.03 3 5

Black pepper 13 347 0.12 7 59 4.9 130 10 -- 0.04 0.2 1 --

Brown

khandasari

1 389 0.2 -- 97 -- 30 2 -- 0.2 0.1 0.3 --

Butter 16 745 0.5 82.5 -- -- 15 0.2 3000 -- -- -- --

Butter oil pure 8 828 -- 92 -- -- --- -- 2000 -- -- -- --

Cane juice 81 73 .3 -- 18 -- 6 2 -- 0.02 0.02 0.1 10

Cardamom

dried

20 228 10 2 43 20 113 5 -- -- -- -- --

Carrot 90 33 1 -- 7 0.8 40 07 3000 0.05 0.05 0.5 0.6

Cashew nut 5 590 20 45 26 1.3 50 5 -- 0.6 0.2 2.1 --

Cauli flower 90 33 3 0.2 5 1 30 1 20 0.1 0.1 0.7 --

Cumin seed 12 356 19 15 36 12 1080 31 300 -- -- 2.6 --

Cinnamon 12 229 12 7.8 28 35 440 17 -- 0.1 0.4 2.4 --

Clove 23 293 5 9 48 10 740 5 -- 0.1 0.2 2 --

Coconut

kernel

20 375 4 35 11 4 10 2 -- 0.05 0.02 0.6 --

Cucumber 96 12 0.6 -- 2 0.5 15 0.3 -- 0.04 0.02 0.2 10

Custard apple 75 93 1 -- 22 1 25 0.5 -- 0.1 0.08 0.8 30

Dried dates 20 3030 2 -- 74 2.4 70 2 50 0.07 0.05 2 --

Dried pea 10 337 25 1 57 4.5 70 5 100 0.8 0.2 2.50 --

Egg plant 93 22 1 -- 4 1 10 1 -- 0.05 0.03 0.8 5

Fresh beans,

peas

70 104 7 -- 19 2.5 40 15 500 0.3 0.15 1.5 25

Fresh

mushroom

91 13 2.5 0.3 -- 1 20 1 -- 0.12 0.5 5.8 3

Garlic 63 139 6 -- 29 0.8 13 1.3 -- 0.25 0.08 0.4 10

Gourd 92 28 0.7 -- 6 0.3 20 0.6 -- 0.04 0.03 0.6 15

Gram. whole 10 338 22 0.5 61 5.3 280 8 40 0.4 0.15 2.5 --

Mung been 12 324 22 1 57 4.7 100 8 40 0.45 0.2 2 --

Grape 80 76 1 -- 18 0.5 20 0.3 50 0.04 0.02 0.3 5

Green pepper 90 37 2 0.5 6 1 20 -- 1130-

800

0.03 0.03 0.3 150

Food water calories Protein(gms) Fat Carbohydrate Fiber(gms) Ca(mg) Fe(mg) Vit A i.u

B1(mg) B2(mg) Niacin(mg) Vit C (mg)

Green spring

onion

90 36 1.8 0.5 6 1 40 3 500 0.05 0.1 0.5 50

Ground nut 6 579 27 45 17 3 50 2.5 -- 0.9 0.15 17 --

Guava 80 58 1 0.4 13 5.5 15 1 200 0.05 0.04 1 200

Honey 23 286 4 -- 76 -- 5 0.4 -- -- 0.05 0.2 --

Jam 29 260 0.4 - 69 0.6 12 0.3 -- -- -- -- 10

Lemon 85 55 1.1 0.9 11.1 1.7 70 2.3 -- -- -- 39

Lettuce 94 19 1.4 -- 3 0.5 35 2.4 2000 1 0.1 0.4 15

Lichi 82 71 0.9 0.5 16 0.3 5 0.5 -- 0.04 0.04 0.3 50

Maash 12 323 24.1 1 54.5 3.8 77 5.9 60 0.51 0.2 1.3 --

Lubia bean 11 329 24 1 56 4.5 150 9 40 0.4 0.2 2 --

Maize, whole 12 363 10 4.5 71 2 12 2.5 -- 0.35 0.13 2 --

Mango 83 63 0.5 -- 15 0.8 10 0.5 600 0.03 0.04 0.3 30

Mustard

leaves

85 34 4 0.6 3.2 0.8 155 16.3 -- 0.03 - -- 33

Melon seeds 6 581 25 45 19 2 50 8 -- 0.2 0.15 1.5 --

Methi leaves 85 49 4.4 0.9 6 1.1 395 16.5 -- 0.04 0.31 0.8 52

Musk melon 93 26 0.5 -- 6 0.4 10 0.4 500 0.03 0.03 0.5 30

Orange malta 86 53 0.8 -- 13 0.3 30 0.5 30 0.08 0.03 0.2 45

Papaya 89 39 0.8 -- 9 0.7 20 0.5 1000 0.03 0.03 0.2 50

Peach 85 56 0.8 -- 13 0.5 8 0.5 300 0.02 0.03 0.3 10

Pear 84 59 0.3 - 15 0.9 7 0.4 -- 0.02 0.02 0.2 4

Pineapple 85 57 0.4 -- 14 0.5 20 0.5 100 0.08 0.03 0.1 30

Pistachio 6 626 20 54 15 2 140 14 100 7 0.5 1.5 --

Plum 88 45 0.7 -- 11 0.4 10 0.4 30 0.02 0.03 0.3 5

Pomegranate 80 77 1 -- 18 0.2 3 0.7 -- 0.02 0.02 0.2 8

Potato 80 75 2 -- 17 0.4 10 0.7 -- 0.1 0.03 1.5 15

Pumpkin

seeds

4 610 30 50 10 2 40 10 30 0.2

0.2 2 --

Radish 94 18 1 -- 4 0.7 30 1 -- 0.03 0.03 0.3 25

Red kidney

bean

12 346 22.9 1.3 60.6 4.5 260 5.8 60 -- -- -- --

Rice, lightly

milled

12 354 8 1.5 77 0.5 10 2 -- 0.25 0.05 2 --

Sorghum 12 353 10 2.5 73 1.5 20 4 -- 0.4 0.1 3 --

Soya bean 8 382 35 18 20 4.5 200 7.11 -- 1.1 0.3 2 --

Spinach 85 48 5 0.7 5 1.5 250 10.9 3000 0.1 0.3 1.5 100

Sugar white -- 400 -- -- 100 -- -- -- -- -- -- -- --

Sweet lemon 84.6 55 1.5 1.0 10.9 1.3 90 0.3 26 0.04 -- 0.2 63

Sweet potato 70 114 1.5 0.3 26 1 25 1 100 0.1 0.04 0.7 30

Tamarind 20 304 2 -- 74 2 50 3 50 0.4 0.15 1.5 10

Tomato 94 20 1 -- 4 0.6 5 0.4 250 0.06 0.04 0.7 25

Wal nut 3 697 15 65 13 2.1 80 2 -- 0.4 0.1 0.7 --

Wheat flour 13 341 10 1 75 -- 16 1.5 -- 0.08 0.05 0.8 --

Wheat

sprouted

73 397 29.2 7.4 53.3 1.4 40 6 -- 1.4 0.54 2.9 --

Wheat whole 13 344 11.5 2 70 2 30 3.5 -- 0.4 0.1 5 --

Yam 13 104 2 0.2 24 0.5 10 1.2 20 0.1 0.03 0.4 10

(Amounts given per 100gms of edible portion) Caloric value of cooked foods

Sl

no

Food item App.Qty

gms

Calorie Sl

no

Food item App.Qty

gms

Calorie

1 Chapati(millet) 45 108 31 Onion bhajji (6) 60 197

2 Chapati(jawar) 45 106 32 Potato chips 20 108

3 Chapati(wheat) 20 40 33 Pattis 60 201

4 Poori (wheat) 16 68 34 Potato wada 45 118

5 Khakhara (wheat) 20 40 35 Dahi wada 45 83

6 Paratha (wheat) 55 304 36 Kachori (1) 45 190

7 Bread (2 slices) 45 120 37 Cutlets (1) 60 126

8 Wheat biscuits 2 20 64 38 Potato pauva (1 plate) 60 123

9 Kichri/ Rice 140 238 39 Sago khichri (1 plate) 45 182

10 Dal (1 small bowel) 200 105 40 Samosa (1) 30 103

11 Jam (1 spoon) 20 58 41 Chakari (1) 30 170

12 Jelly (1 spoon) 20 52 42 Mesur (1 piece) 56 345

13 Squash (Orange/ Lemon)

1 glass 69 43 Boondi ladu (1) 35 150

14 Squash (mango) 1 gl ass 72 44 Carrot halva 85 333

15 Butter (1 spoon) 5 36 45 Dudhi halva 85 300

16 Cream (1 spoon) 15 50 46 Glucose (1 spoon) 75 218

17 Ghee (1 spoon) 5 45 47 Honey (1 spoon) 21 66

18 Ground nut (1 spoon) ) 15 56 15 126 48 Jaggery (1 spoon

19 Paneer (1 spoon) 30 112 49 Sugar (1 spoon) 6 25

20 Ice cream 10 (1 cup) 150 196 50 Egg gravy 0 181

21 Horlicks/Bournvita 75 110 51 Omlet (1) 40 77

22 90 218 52 Frued fish 100 245 Cake (1 piece) without icing

23 Cake (1 piece) with icing 160 302 53 Fried meat 140 340

24 Pie 105 377 54 Soup (chicken/ mutton) 200 35

25 Pudding (1/2 cup) 68 185 55 Tea (1 cup) 150 60

26 Idli (1 piece) 260 65 56 Coffee (1 cup) 150 75

27 Upama (1 plate) 100 397 57 Lime juice (1glass) 200 75

28 Sada dosa (one) 100 216 58 Aerated drinks 200 80

29 Masala dosa 60 210 59 Beer ( glass) 200 100

30 Potato bhajji (4 ) 60 240 60 Alcohol (1 peg) 45 110

Ideal diet plan supplies about 1,000 calories per day is given below :

1) on juice.

2) Morning breakfast – any one or two items from the list given below

Early morning – A glass of hot water with lem

a) ¾ cup of milk without adding sugar or one cup of tea or coffee with

bottle milk. In tea or coffee saccharin, & not sugar, may be used.

b) An orange or a Mosambi or any other fruit (except banana) of an

ordinary size.

c) An orange slice of bread or one small cucumbers. Those who are

heavily over weight should avoid them.

d) One egg.

e) 2 to 3 small tomatoes or cucumbers.

3) Mid – Day Meal

a) Take a cup of vegetable soup or any other soup before starting the

meal or one glassful of water.

b) Before other courses are taken, take green – salad containing 4 to 85

tomatoes or 2 to 3 medium size cucumbers. Chew them well. These

can be taken in a larger quantity also.

c) One cup small bowl-full of a low calorie cooked vegetable from the

list given below; green leaf bhaji, carrots, cucucmber, unripe

tomatoes, brinjals, cabbage, radish, white gourd, French beans, etc.

d) One or two small chapaties or bred slices.

e) One small cupful of moong or any other soup made from a common

pulses or cereals.

f) Some meat or fish.

4) Afternoon / early evening – as per the morning breakfast, if patient feel

restless

5) Dinner – Same as the mid – day meal. But a small cupful rice or khichadi can

be taken instead of bread or chapati.

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