snehapana samedarakta pk002-gdg

THE STUDY OF AROHANA SNEHAPANA AND ITS

EFFECT ON SAMEDARAKTA WITH SPECIAL

REFERENCE TO HYPERLIPIDAEMIA AND NORMAL

LIPID VALUES

By

Varsha S. Kulkarni.

Dissertation Submitted to the Rajiv Gandhi University of Health Sciences,

Karnataka, Bangalore.

In partial fulfillment of the requirements for the degree of

AYURVEDA VACHASPATHI M. D.

In

PANCHAKARMA

Under the guidance of

Dr. P. Shivaramudu, M.D. (Ayu)

And co-guidance of

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

DEPARTMENT OF PANCHAKARMA, POST GRADUATE STUDIES AND RESEARCH CENTER,

SHRI D. G. MELMALAGI AYURVEDIC MEDICAL COLLEGE, GADAG – 582103.

2005

Ayurmitra

TAyComprehended

Rajiv Gandhi University of Health Sciences, Karnataka, Bangalore.

DECLARATION BY THE CANDIDATE

hereby declare that this dissertation / thesis entitled “The Study

of Arohana Snehapana and its Effect on Samedarakta with

special reference to Hyperlipidaemia and Normal Lipid Values”

is a bonafide and genuine research work carried out by me under the

guidance of Dr. P. Shivaramudu M.D. (Ayu), Asst. Professor, Post graduate

department of Panchakarma and Co-guidance of Dr. Shashidhar H.

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

Panchakarma.

I

Date: Place: Gadag Varsha S. Kulkarni.

Ayurmitra

TAyComprehended

SHRI D. G. MELMALGI AYURVEDIC MEDICAL COLLEGE, GADAG.

POST GRADUATE DEPARTMENT OF PANCHAKARMA

CERTIFICATE BY THE CO- GUIDE

This is to certify that the dissertation entitled “The Study of

Arohana Snehapana and its Effect on Samedarakta with special

reference to Hyperlipidaemia and Normal Lipid Values” is a

bonafide research work done by Varsha S. Kulkarni in partial

fulfillment of the requirement for the degree of Ayurveda Vachaspathi.

M.D. (Panchakarma).

Date:

Place: Gadag Dr. Shashidhar. H. Doddamani, M.D. (Ayu). Assistant Professor,

Department of Panchakarma.

Post Graduate studies and research center

DGM Ayurvedic Medical College. Gadag

COPYRIGHT

Declaration by the candidate

hereby declare that the Rajiv Gandhi University of Health

Sciences, Karnataka shall have the rights to preserve, use and disseminate

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

research purpose.

I

Date:

Place: Gadag Varsha S. Kulkarni.

© Rajiv Gandhi University of health Sciences, Karnataka

Effect of Arohana Snehapana on Samedarakta

Acknowledgement This work is the result of the combined effort of a good number of people who include

researchers, academicians, friends, colleagues, and above all the patients who cooperated with us in all

aspects. Moreover it is because of Gods’ grace only the work could be completed as per to my

expectation.

My deep sense of gratification is due for my parents who are the architects of my career. The

culture, discipline and perseverance, which I could imbibe, is solely because of their painstaking,

upbringing and strong moral support.

I am deeply indebted and sincerely gratefulness to my Principal, Dr. G. B. Patil, D. G.

Melmalgi Ayurvedic Medical College, Gadag for their continues cooperation and timely encouragement

at various levels of my study.

I express my deep gratitude to my respected guide Dr. P. ShivaramuduMD.(AYU) for his

sympathetic, compassionate, extensive guidance, suggestion, encouragement and kindheartedness.

I am extremely happy to express my deepest sense of gratitude to my beloved and respected

HOD, Prof. G. Purushothamacharyulu,MD.(AYU) whose sympathetic, scholarly suggestions and ablest

guidance at every step have inspired me not only to accomplish this work but in all aspects.

Indeed, the affectionate guidance of my co-guide Dr. Shashidhar H. Doddamani,MD.(AYU) will

be cherished by me for long. His invincible and radical thinking were very valuable in achieving this

research work invoking scientific spirit throughout the course of the study.

I am grateful to Dr. Santosh N. Belavadi,MD(AYU) Lecturer, for his co-operation and advice in this

study.

I take this opportunity to thank HOD’s, of other departments Dr. Varadhacharyulu, Dr.

M. C. Patil, Dr. G. V. Mulgund. For their inspiration and valuable suggestions.

I am grateful to all the PG, teachers Dr. K. S. R. PrasadMD.(AYU), Dr. DilipkumarMD.(AYU), Dr. R. Y. ShettarMD.(AYU), Dr. Kuber SankMD.(AYU), Dr. G. N. DanappagoudarMD.(AYU), Dr. Jagadish MittiMD.(AYU), Dr. MulkiPatil, Dr. Yasmin, MD.(AYU), Dr. Shashidhar NidagundiMD.(AYU), and Dr. D. M. Patil MD.(AYU), for their valuable inputs and suggestions.

I extend my immense gratitude to Dr. R. K. Gacchinmath, Dr. G. S. Hiremath, Dr. S. A. Patil, Dr. B. G. Swami, Dr. Reddar, Dr. U. V. Purad and other teaching staff who helped during my study.

My sincere thanks are extended to Dr. Basavaraj SaraganachariMD.(AYU), and Dr. Muralidhar Pujar for their inspiration and valuable suggestions.

I would like to express my sincere thanks to Mr. V. M. Mundinamani, Librarian and Asst.

Librarian Mr. S. B. Sureban for providing valuable books in time throughout the study.

I am thankful to Mr. P. M. Nanadkumar, Statistician, who helped me in Statistical Analysis.

I seek privilege to extend my obligations to my seniors Dr.Srinivas Reddy, Dr. Hanumanth

Gowda, Dr. Shankar Gowda.

I can not move further before thanking to my intimate friend Dr. Ravikumar who has been stood

indefatigable with me in each and every circumstances and gave me in depth sense of friendship.

I am highly under the debt of my beloved friends Smt. Manjula, Dr. Naganur, Dr. Hosalli, Dr.

Seema. M.B., Dr. Pampanagowda, Dr. Manjula, Dr. Girish and Dr. Deepa, who have helped in all

the moments during my Post Graduate studies.

Acknowledgement - I


I take this moment to express my thanks to all my Post Graduate colleagues Dr. Subin, Dr.

Febin, Dr. Satheesh, Dr. Santosh, Dr. Joshi, Dr. Chetan, Dr. V.S. Hiremath, Dr. Santoji, Dr. Koteshwar,

Dr. Jaggal, Dr. Veena, Dr. Mangala, Dr. Shashikala, Dr. K. S. Hiremath, Dr. Paraddi and Junior

Colleagues Dr. Shaila, Dr. Hugar, Dr. Chandramouli, Dr. Jayaraj, Dr. Kendadmath, Dr. Lingareddi,

Dr. Vijay, Dr. Akki, Dr. Hakkandi, Dr. Ashwin, Dr. Umesh, Dr. Suvarna, Dr. Anitha, Dr. Jagadish, Dr.

Sharanu and Dr. Anand.

I am very much thankful to Smt. P. K. Belavadi, Mr. M. M. Joshi, Mr. Shankar, Mr.

Biradar, Mr. Kallanagoudar, Mr. Dasar and Smt. Sarangamath.

I am very much thankful to Raghu S. K. and Raju S. K., Net Nota Cyber Café, Gadag for their

timely help in typing and bringing out this computer print.

Last but not least, I thank to the patients who are pillars of my research work, Khona pathology

laboratory staff and Hospital staff and to all those names my memory fails to recollect.

Dr. Varsha S. Kulkarni.

Acknowledgement - II


ABSTRACT

yurveda uses two main modalities in the treatment of disease each with its

own distinct purpose. These modalities are Shodhana and Shamana chikista. The

Snehana is the one of the main preparatory procedure to be performed before

Shodhana Karma.

A

In the present study the Shodhananga Snehapana with Murchita Tila Taila was

given in certain specific quantity in the Arohana Krama till the appearance of

Samyak snigdha laxanas seen. Large quantities of Sneha is using for Snehapana, the

people in this era are afraid of this therapy, because it may increase fat specially

Cholesterol and Triglycerides which was the important causative factor for

Atherosclerosis, Heart attack etc., It becomes essential to clear the cloud from the

mind of people. Hence the present study has been undertaken to assess the effect of

Arohana Snehapana over the Samedarakta (Hyperlipidaemia & Normal Lipid Values).

The objectives of this study was to evaluate and to compare the effect of

Arohana Snehapana with Murchita Tilataila on Samedarakta with special reference to

Hyperlipidaemia and Normal Lipid Values.

In the present Clinical study, two groups were made. In one group, the 15

patients with primary Hyperlipidaemia (especially raised values of either Cholesterol

or Triglycerides) and who are fit for Snehana and Shodhana karma excluding

secondary Hyperlipidaemia were selected. In another group 15 voluntaries with

Normal Lipid Values who were desirous to under go Shodhana therapy for

maintenance of good health were selected.

Abstract - III


In both the groups after Ama Pachana, Snehapana was done in Arohana

krama till the Samyak snigdha laxanas are observed. Snahapana was given 30ml as

Hrisiyasi matra at morning around 6 to7am with ushnajala as anupana. Next day dose

was increased depending upon the previous days sneha digestion. Lipid profile values

are done on first day before Snehapna and after Samyak snigdha laxanas, with 12

hours fasting in the morning.

Tilataila is having special properties like Teekshna, Ushna, etc., by these it

enters sthoola and sukshma srotases and does chedana, kshapana of Medodhatu.

Both the groups showed Samyak Snigdha Laxanas without producing vyapat.

On the basis of the results of both the groups it was observed that there was a

decrease in the total Cholesterol, Triglycerides, LDL, VLDL & raise in HDL level

which shows the protective role of the Shodhanapoorva Arohana Snehapana therapy

in Samedarakta (Hyperlipidaemia & Normal Lipid Values).

Key words

Snehana, Shodana, Arohana Snehapana, Murchita Tilataila, Samyak Snigdha

Laxanas, Samedarakta, Meda, Hyperlipidaemia, Lipids, Lipid Profile.

Abstract - IV

CONTENTS

INTRODUCTION 1- 4

OBJECTIVES 5

REVIEW OF LITERATURE 6 - 92

HISTORICAL RIVIEW 6 - 8

SHODHANA POORVA AROHANA SNEHAPANA 8 - 32

NIRUKTI AND PARIBHASHA OF SNEHA 8 - 9

MAHA SNEHAS 11

CLASSIFICATION OF SNEHA AND SNEHANA 12 -18

SNEHANA YOGYAYOGYA 18 - 22

SNEHA PRAKARSHA KALA 22 - 23

SHODHANANGA SNEHANA VIDHI 23 - 32

KARMUKATA OF SHODHANANGA SNEHANA 33 - 38

MEDA 39 - 42

CONCEPT OF LIPIDS 43 - 68

SAMEDARAKTA AND HYPERLIPIDAEMIA 69 - 84

DRUG REVIEW 85 - 92

Methodology 93 - 99 Results 100 -126

Observations 100 -117 Results 118 -126

Contents - V

Discussions 127 -143

Conclusions 144 -145

Summary 146 -148

Bibliographic References 149 -164

Annexure

Contents - VI


ABBREVIATIONS

C.S. Charaka Samhita

S.S Sushruta Samhita

A.S. Astanga Sangraha

A.H. Astanga Hridaya

B.P. Bhava Prakasha

Sha.S Sharanghadhara Samhita

K.S Kashyapa Samhita

Ckd Cakradatta

M.N Madhavanidana

Y. R Yogaratnakar

Va.Se Vangasena

Su Sutrasthana

Sha Shareerasthana

Vi. Vimanasthana

Abbreviations- VII


LIST OF TABLES

Sl. No. Tables Pages 1 Showing the Sneha Guna, Bhoutika Sanghatana & Karmukata of

Sneha Dravys. 11

2 Showing Properties of Taila 12 3 Source of Sthavara Sneha according to Charaka 13 4 Sushruta’s Sthavara Sneha classification 13 5 Paka Bhedha of Sneha 13 6 Opinion about Sneha Matra 15 7 Sneha Matra according to Sushruta 16 8 Indications of Sneha Matra 16 9 Opinion of Vangasena regarding dosage of Arohana Snehapana 18 10 Shamana and Brumhana Snehana Yogya 19 11 Showing General Indications of Shehana According to Different

Acharyas. 19

12 Showing the Deserving Condition for Snehana 20 13 General Contraindications of Snehana. 22 14 Sneha Jiryamana and Jirna Lakshana114 27 15 Samyak Snigdha Lakshanas 28 16 Asnigdha Lakshanas 29 17 Ati Snigdha Lakshanas 29 18 Showing classification of fatty acids 52 19 Showing the characteristics of lipoproteins 53 20 Showing fat digestion 60 21 Showing the Nidana of Medovriddhi according to different Acharyas 69 22 Showing Roopa of Medoroga 72 23 Showing the Classification of Hyperlipidaemia 79 24 showing the Pharmacodynamics of Ingredients of Panchakola

choorna 86

25 Showing Pharmacodynamics of Drugs Used For Moorchana of Tilataila

88-89

26 Age wise Distribution of the Sample 100 27 Sex wise Distribution of the Sample 101 28 Religion wise Distribution of the Sample 101 29 Occupation wise Distribution of the Sample 102 30 Marital status wise Distribution of the Sample. 102 31 Socio Economical Status wise Distribution of the Sample 103 32 Type of Diet wise Distribution of the Sample 103 33 Diet Pattern wise Distribution of the Sample. 104 34 Nature and Character of food wise Distribution of the Sample 104 35 Nature of work wise distribution of the Sample 105 36 Sleep wise distribution of the Sample 105 37 Vyayama wise distribution of the Samples 105 38 Vyasana wise distribution of the Samples 106 39 Menstrual History of 14 female patients 106 40 Jataragnibala wise distribution of the Samples. 106

List of Tables - VIII


41 Koshta wise distribution of the Samples 107 42 Prakriti wise Distribution of the Sample 107 43 Sara wise Distribution of the Sample 107 44 Showing Samhanana of the Samples 108 45 Showing Pramana of the Samples 108 46 Showing Satmya of the Samples 108 47 Showing Satva of the Sample 109 48 Showing Abhyavaharana Shakti of the Sample 109 49 Showing Jarana Shakti of the Samples 109 50 Showing Vyayama Shakti of the Samples 110 51 Shows the matra of Arohana Snehapan with Murchita Tila Taila in

both groups. 111

52 Showing the mean on set of Jeeryamanya laxanas of both Groups 112 53 Showing time taken for Sneha Jeerna laxanas 113 54 Showing Summary of time taken for Sneha Jeerana (in minutes) 114 55 Showing Mean time taken for Samyak Snigadha laxanas of both

Groups A & B. 115

56 Showing Samyak Snigdha Laxanasa of each individual in both the groups

116

57 Showing the Total number of Samyak Snigdha Laxanas observed on last day of Snehapana in both the groups

117

58 Showing Serum Cholesterol levels in both groups before and after Arohana Snehapana.

118

59 Showing Serum Triglycerides levels in both groups before and after Arohana Snehapana.

119

60 Showing HDL levels in both groups before and after Arohana Snehapana

120

61 Showing LDL levels in both groups before and after Arohana Snehapana

121

62 Showing VLDL levels in both groups before and after Arohana Snehapana.

122

63 Showing the weight and BMI of Group A before and after Arohana Snehapana

123

64 Showing the weight and BMI of Group B before and after Arohana Snehapana

124

65 Showing the overall results of Serum Lipid Values 124 66 Showing statistical results of Group A samples 125 67 Showing statistical results of Group B samples 125 68 Showing comparative statistical results of Group A & Group B

samples 125

List of Tables - IX


LIST OF FIGURES

Sl. No. Figures Pages 1 Showing Bio Synthesis of Cholesterol 48 2 Showing Metabolism Summary 67

LIST OF FLOW CHARTS Sl. No. Flow Charts Pages

1 Showing Sthana and Swaroopa of Meda dhathu 40 2 Showing Samprapthi of Medo vriddhi 76

LIST OF GRAPHS

Sl. No. Graphs Pages 1 Showing Age of the Samples 100 2 Showing Sex of the Samples 101 3 Showing Religion of the Samples 101 4 Showing Occupation of the Samples 102 5 Showing Socio Economical Status of the Samples 103 6 Showing Type of Diet of the Samples 103 7 Shwoing Nature and Character of food of the Samples 104 8 Showing Sleep of the Samples 105

LIST OF PHOTOGRAPHS

Sl. No. Photographs Pages 1 Ingredients of Panchakola Choorna 87 2 Drugs Used for Murchana of Tilataila 90

List of Tables - X


he ancient Indian science of health, Ayurveda is now being increasingly

accepted by the world at large for its facilities and adoptability even to the modern

times.

T

It is not surprising that, the ancient science is accorded such importance in

countries where modern medicine itself has made immense advances. The only

reasonable explanation for this phenomenon is the fact that Ayurveda remains the

only system of medicine that possesses a natural form of treatment, one that

prescribes remedies in accordance with nature itself. It approaches a patient

holistically, taking in to account while treating person, not only the patient but also his

general condition.

Shodhana and Panchakarma are the two terms we can come across in the

Ayurvedic classics that have seen almost used synonymously. If we meticulously

explore the literature regarding these two terms, we may unveil the subtle differences

existed between both of them.

The term Shodhana has been used in broader perspective in Ayurvedic

classics. This envisages the wider meaning and implication of the Shodhana therapies.

Samshodhana is a term used for various eliminating procedures. Panchakarma

therapy which is known as Samshodhana therapy is designed to eliminate the vitiated

doshas. In order for these therapies to work the vitiated doshas must be brought to the

kostha. This is accomplished by two primary means i.e., Snehana and Swedana

therapies. Snehana is one such procedure, mentioned under Shadvidhopakrama.

Snehana can act as a Poorvakarma for Shodhana procedures, i.e., Shodhana sneha, as

Introduction - 1


a Pradhana karma in alleviating diseases ie., shamana snehana and as a paschat karma

in bringing compactness to the body i. e., Bruhmana sneha.

Almost all the Acharyas have given the prime importance to Snehana therapy

as a Poorva karma, Pradhanakarma and Paschat karma according to the need of the

person or disease. Acharya Sushruta beautifully delineates the importance of Sneha as

a “Human being is composed of Sneha, prana is predominantly contains Sneha.

Hence prana can be protected or preserved by Snehana”.

Even though various varieties of Snehas are available, only four of them are in

regular usage and known as uttama Snehas. They are Sarpi, Taila, Vasa and Majja.

In Taila vargs Tilataila is best.

By examining the Rogabala, Doshabala and Shareera bala, the proper Sneha

should be administered after the complete digestion of food which was taken in the

previous night and Snehas are given in certain specific quantity in the increasing order

for specific number of days or till Samyak Snigdha Laxanas get manifested. After

adopting the necessary regimen in Vishrama kala Shodhana i.e, either Vamana or

Virechana are performed.

In this most advanced modernised era, the humans are gifted with lot of

sophistication, luxuries but at the same time left with sedentary ways of life, stress

induced hectic, unhealthy schedules. Further indiscriminate dietary habits,

overeating, consuming high quantity and high caloric foods etc., propping into one’s

life are strongly influencing the homeostasis leading to the maximum number of

pathological conditions, one amongst them is Hyperlipidaemia.

Introduction - 2


On the theoretical grounds it has been tried to co-relate the Hyprlipidaemia

with many diseases described in Ayurveda i.e., Medoroga, Medhovriddhi,

Abhadhamedus, Sthaulya etc.,

These are getting manifested due to vitiation of Medadhatu. Hence the excess

amount of Meda in Rakta will be considered as Hyperlipidaemia and the normal

amount of Meda in Rakta is taken as normal Lipid.

The term coined for the word Lipidaemia is Samedarakta whether it is

physiological or pathological. Literally Samedarakta means Rakta associated with

Meda.

Hyperlipidaemia refers to an increased concentration of either Cholesterol or

Triglycerides or both lipids in the Plasma.

• The amount of Cholesterol in the blood can range from 3.6 to 7.8 mmol / ltr.

A level above 6 mmol / ltr is regarded as high and is a risk factor for arterial

disease.

• The high Cholesterol level can cause narrowing of the arteries, heart attacks

and Strokes. The risk of CHD also raises as blood Cholesterol level increases.

When other risk factors like HT, DM are present, CHD risk increases even

more.

• The first step in the treatment of Hyperlipidaemia is attention to diet. A single

dietary approach to all form of Hyperlipidaemia includes reduced in take of

calories and saturated fats, but Mustered oil, Tila oil, Fish fat can be taken in

desirable quantity. Weight reduction is essential for prevention of these above

risk factors.

Introduction - 3


In the present study Murchita Tilataila was taken in increasing order (Arohana

Snehapana). But people in this era are afraid of this Snehana therapy which is taken

in large quantities, may leads to increase of plasma lipids, especially Cholesterol and

Triglycerides which are the important risk factors for Atherosclerosis and CHD

further life threatening conditions.

But Tilataila is having special characters as “Krishanam Bhrimhanayalam

Sthoolanam Karshanaya Cha” means in Krisha people it acts as Bhrimhana and in

Sthoola person it does Karshana of Meda. By its teekshana Ushnadi gunas enters all

sukshma, sthoola srotases and does Chedana, Kshapana of Medodhatu.

Hence this study has been intended to assess the effect of Arohana Snehapana

on Samedarakta (Hyperlipidaemia and Normal Lipid Values).

Introduction - 4


Objectives - 5

To evaluate the effect of Arohana snehapana with Murchita Tilataila on

Samedarakta (Hyperlipidaemia and Normal Lipid Values).

To compare the effect of Arohana Snehapana in both Hyperlipidaemia and

Normal Lipid Values.


HISTORICAL REVIEW:

On Sneha karma:

It would be quite judicious to review the reference of Sneha which is available

from Vedic period to modern period.

Veda Kala

In Rigveda description of many herbal plants and qualities of Tilataila,

Sarshapa etc., are available1. Atharva Veda, gives plenty of references regarding the

use of Sneha therapeutically. We find the use of both animal product (ghee) and plant

products (oil) in the Materia Medica of Atharvanas. Among the plant products, oil of

Ingida and Tila taila are found embodied in the pharmacopoeia of Atharvanas.

Samhita Kala

In Charaka Samhita (800 BC), we find ample of references regarding the

therapeutically use of Sneha in various disorders. The author has devoted an entire

chapter in the Sutra Sthana on “Shadvidopakramas”2. Snehana as pradhana karma is

the most significant therapeutic procedure. Among them Charaka has extensively

dealt with the subject “Snehana” and its salient features separately in 13th chapter of

Sutra Sthana3 and about Shodhananga snehana in Charaka siddhisthana4. Here he has

described in detail the properties of Sneha dravyas, basic sources of Sneha dravya,

indication and contraindications of Snehana etc.

Acharya Sushruta (600 BC) has contributed separate chapter on “Sneha” in his

Chikitsasthana. Here he has classified Snehana on the basis of its Karmukata as

Shodhana, Shamana and Brumhana. Sushruta explained the preparation of “Sneha”

i.e., Ghrita and Taila5. Also we find good number of references regarding the use of

sneha in the Shodhana and Shamana or alleviation of different diseases. Sushruta,

Historical Review - 6


being a surgical man has also used “Sneha” in various surgical ailments. Detailed

explanation about Sneha, nishapatti of Taila, type of Snehas, sources of Snehas,

qualities of Tailas and their preparation have been mentioned in Sushruta sutrasthana.

Types of Tailas, qualities of Tailas, method of preparation of Aushadhisiddha

tailas and method of preparation of Hingutriguna taila have been mentioned in

Sutrasthana and Chikitsasthana of Astanga Hridaya6.

Kasyapa (600 BC), an eminent personality in Koumarabhritya has dealt in

detail regarding Snehana in 22nd chapter of his Sutrasthana. Also he has used

different ghrita and taila in managing various Balarogas7. Bhela, one of the six

celebrated disciples of Atreya has mentioned the use of different Sneha in treating

different disorders8. Qualities of each taila their specific indications have been

mentioned in 14th Chapter in Harita samhita9.

Sangraha Kala

Common qualities of each taila and shresthatha of Tila taila is mentioned in

Yogaratnakara 1st Chapter10. In Bhavaprakash Nigantu detail explanation of

paryayas, swaroopa utpattisthana guna of taila are available11.

During this period, authors like Chakrapani Datta12, Vangasena13 and

Sharangadhara14 have included Sneha, both ghrita and taila in the cure of various

disorders.

Adhunika Kala

Detailed explanation about oils, fats, classification of oils, properties and

sources of oil, expression of oils, have been mentioned in text of pharmacognocy15

Teiz’s text book of clinical Bio – Chemistry16.



On Meda and Vyadhi:

About Meda and Medoroga there is no any direct reference is available in

Veda but all most Samhitas of Ayurveda refereed these ailment with their different

aspects. All the Bhrahatrayees, Laghutrayees, Vangasena and Yogaratnakara have

explained about Meda and Medoroga as follows;

C. S. Sha. 7/6 - Meda pramana

C. S. Vi. 5/8, 16 - Medovaha sroto moola, Medovahasroto dusti karana

C. S. Vi. 8/106 - Medasara purusha laxana

C. S. Su. 13/5 - Taila sevana yogya

C. S. Su. 21/3-19 - Asta dosha of Sthoulya and Madhyama pramana of

purusha

C. S. Su. 28/15 - Abaddha medas

S. S. Su. 14/11 - Meda is forming from mamsa

S. S. Su. 15/ 6, 13 - Meda karya, Medovriddhi

S. S. Su. 24/13 - Medodhatudusti, Granthi, Osta prakopa, Madhumeha,

Sthoulya are manifesting due to dusti of Meda dhatu.

S. S. Sha. 9/12 - Moola of Meda

A. H. Su. 11/18,26 - Medovriddhi, Ashrayaashrayee Bhava of kapha and Meda

A. S. Su. 19/26 - Sthoulya is counted as disorder of Shleshma dosha seated

in Medadathu.

M. N. 34/1-9 - Medoroga nidana, samprapti laxanas.

Va. Se. 39/1-10 - Medorogadhikara Karana, Samprapti, laxana, Chikista.

Modern concept of Lipids, Lipid metabolism and Hyperlipidaemia available in

Guyton Medical physiology17, Ganonge Medical physiology18, API text book of

medicine19, Davidson text book of medicine and Basic pathology20.



Arohana Snehapana - 9

SHODHANA POORVA AROHANA SNEHAPANA

Snehana is the classical poorvakarma to be administered as a preparatory

measure before Shodhana therapy i.e., vamana, virechana etc, independently21.

Charaka has described Snehana as one among the Shadvidhopakrama and can be

adopted as treatment22.

Snehana is a therapy intended for alleviation of vitiated doshas as a part of

preparatory therapy for Shodhana & imparts strength, unctuousness to the body23.

NIRUKTI OF SNEHA

The word Sneha is Masculine in gender and is derived from ‘Snih’ Dhatu by

suffix ‘lyut’ Pratyaya. (Vachaspatya )24

The mool ‘Snih’ has two implications or meanings --‘Snih - Preetau’ to render

affection and ‘Snih – Snehane’ to render lubrication. Among these the later will be

more adopted in the present context.

The term Sneha implies that, a substance that brings oiliness or unctuousness.

Sneha literally means oiliness, unctuousness, fattiness, greasiness, lubricity, viscidity,

affection, love, kindness and tenderness. (Monier Williams 1889 & Apte 1970)25

PARIBHASH OF SNEHA:

‘Snehanam snehavishyand mardavakledakarakam’ 26

Charaka defines Snehana as, the procedure by which Snigdhata, Vishyandana,

Mardavata and Kledana are produced in the body .The measures adopted to bring

about Snigdhata in the body is known as Snehana.



• In Rajanighantu the word Sneha is used to describe the external application of

Sneha dravyas.27

• Charaka has explained the value of Sneha as “Snehoanilamhanti

mrudukarotideham, Malanam vinihantisangam” ie., Sneha helps in bringing

balance in vitiated vata, renders the body, softens and clears the accumulated

malas which have obstructed the srotamsi.28

Hence Shodhanaga abhyantara Snehapana indicates the administration of

Sneha dravyas before the Shodhana procedures ie., Vamana and Virechana.

SYNONYMS

The synonyms mentioned for Snehana are Sneha, Snigdhata, Mrtkshana,

Mrksha, Abhyanga and Abhyanjana.27

GUNAS OF SNEHA DRAVYAS: 29,30,31

Gunas in the drugs are responsible for the different functions of drug. The

Properties of Sneha Dravya’s are like Sukshma, Sara, Snigdha, Drava, Picchila,

Guru, Shita, Manda and Mrdu, which are having opposite properties of Rukshana

Dravyas. Though drug having these qualities but always it may not produce Snigdhata

in the body. There are few exceptions to this general rule like Yava, though it

possesses Guru, Sheeta, Sara gunas produces Rukshata. Rajamasha inspite of having

guru guna produces rukshata. Tila Taila even though it is Tikshna and Ushna it acts

like Snehana. That may be the reason why Acharyas have used the term Prayo, while

explaining Sneha Dravya properties.



Table No. 1: Showing the Sneha Guna, Bhoutika Sanghatana & Karmukata of Sneha

Dravys32.

Dominent Mahabhutha Guna Prathvi Ap Teja Vayu Akasha Karmukata

Picchila ++++ Lepana, Jivana, Samghata, Sandhana, Balya, Gouravata

Sukshma ++ ++ +++ Sroto Vishodhana, Vivarana, Soushiryakara

Sara ++ + Anulomana, Vyaptisheela, Preranasheela

Snigdha + ++++ Snehana, Mardavata, Kledana Bandhana, Vishyandana,

Drava ++++ Prakledana, Vilodhana, Prasari.

Guru ++++ ++ Brumhana, Malavriddhikara, Tarpana, Angaglani, Balakara,

Shita +++ ++ Sthambhaka, Hladana

Manda ++ + Shamana

Mrdu ++ +++ Shaithilya of Avayava, Mardavata.

By seeing above table it can be justified that Sneha Dravyas are of apyamahabhuta

predominant.

MAHA SNEHAS OR PRAVARA SNEHA:33,34,35

Among all the Sneha Dravyas, Ghrita, Taila, Vasa and Majja are the most

important Snehas because of their excellence in Snehana qualities.

Sneha Action of on Doshas :36

1. On Vata Shleshma- Taila – Vatashleshmaghnatama

Majja - Vatashleshmaghna

Vasa - Vatashleshmaghnatara

2. On Pitta Dosha- Vasa - Pittaghna

Majja - Pittaghnatara

Ghrita - Pittaghnatama



PROPERTIES OF TAILAS: 37, 38

Table No. 2: Showing Properties of Taila

Rasa Anurasa Virya Vipaka Guna

Madhura Tikta,Kashaya Ushna Madhura. Tikshna,Guru,Snigdha,Vikasi,Sara

Karma 39

VataKaphahara, Pittakara, Balakara, Varnakara, Mardava Kara, Tvachya,

Krimighna, Garbhashaya Shodhaka, Bhagna Sandhanakara , Subsides Shula in Yoni,

Shira and Karna.

Seasonal indication : Pravrt, Shita Kala

Suitable condition for Taila Snehana:40,41

Vata Prakrti, Pravriddha Shleshma Medaska, Chala Sthula Gala Udara, Taila

Satmya, Vatavyadhi, Krimikoshta, Nadivrna, Bhagna, Krura Koshta, those desires of

Bala, Tanutva, Laghuta, Drdhata and Sthiragatrata.

CLASSIFICATION OF SNEHA

I. BASED ON YONI (SOURCE)42,43

There are two sources of Dravys viz., Sthavara and Jangama

Based On Yoni (Source)

Sthavara Jangama

A) Sthavara Sneha (Vegitable Origin)

Sthavara Sneha is extracted from plant source. Phala, Sara, Mula, Tvak, Patra

& Pushpa are the main sources of Sthavara Sneha. Charaka has told eighteen

Ashayas of Sthavara snehas.



Table No. 3 Source of Sthavara Sneha according to Charaka44

Tila Sarshapa Eranda Bibhitaki Priyala Abhishuka Bilva Moolaka Chitra Atasi Madhuka Kusumbha

Akshodha Abhaya Karanja Shigru Nikothaka Haritaki

Sushruta has classified Sthavara Sneha according to their action.

Table No. 4 Sushruta’s Sthavara Sneha classification45

Action Virechanopayogi Pittasamsrusta Vayu Upayogi Vamanopayogi Krshnikarana Upayogi Shiro Virechanopayogi Pandukarana Upayogi Dushta Vranopayogi Dadru, Kushta, Kitibha Upayogi Maha Vyadhi Upayogi Ashmari Upayogi Mutra Sangopayogi Prameha Upayogi

B) Jangama Sneha (Animal Origin)

Jangama Sneha is derived from animal sources. Ex: Kshira, Dadhi, Ghrita,

Mamsa, Vasa, Majja etc

II. PAKA BHEDA

Opinion of different authors regarding varieties of Sneha Paka and its

indications

Table No. 5 Paka Bhedha of Sneha 46,47,48

Snehana Caraka Sushruta Sharangdhara

Abhyanga Khara Madhyama Madhyama

Pana Madhyama Mrdu Madhyama

Nasya Mrdu Madhyama Mrdu

Basti Madhyama Khara Madhyama

Karnapurana - Khara Madhyama



III. SAMYOGA BHEDA:49

Samyoga Bheda

Yamaka Sneha Trivrut Sneha Maha Sneha (Taila + vasa) (Taila+ Vasa + Majja) (Sarpi +Taila +Vasa+ Majja)

IV. UPAYOGA BHEDA:50,51 52

Based on the route of administration, Snehana is classified as –

Upayoga Bheda

Abhyantara Snehana Bahya Snehana (Pana, Basti, Nasya, Bhojana) (Abhyanga, Lepa, Udvartana, etc.,)

V. PRAYOGA BHEDA 53,54

Based on the method of administration Snehana is of 2 types viz,

Prayoga Bheda

Accha Peya Vicharana Snehana.

VI. ACCORDING TO VISHISTHA SAGNA 55,56,57

Vishistha sagna

Sadyo Snehana Pancha Prasrta Peya Achapeya

(Sneha without mixing with any other Dravya)

(Sneha with various preparations like Vilepi and Yavagu etc.)



VII. MATRA BHEDA:58,59

The following dosage schedule is advocated in the classics based on the time

required for digestion of sneha taken.

(i) Hrasva Matra - The dose of Sneha that is digested within 6 hours.

(ii) Madhyama Matra - The dose of Sneha that is digested within 12 hours.

(iii) Uttama Matra - The dose of Sneha that is digested within 24 hours

Vagbhata has mentioned about Hrasiyasi Matra the quantity of Sneha, which

digests within three hours, is known as Hrasiyasi Matra. This is used when the Koshta

of the person has not been properly diagnosed60.

Fixing the Dosage of Sneha in numerical value is not possible with the reason

that, dose will vary from person to person based on Dosha, Kostha and Agni level.

Hence dosage of the Sneha is explained based on the time required for the digestion

of Sneha viz,

(i) Hrasiyasi Matra

(ii) Hrasva Matra

(iii) Madhyama Matra

(iv) Uttama Matra

Table No. 6 Opinion about Sneha Matra60, 61, 62

Author Hrasiyasi Matra Hrasva Matra Madhyama

Matra Uttama Matra

Hemadri 1 Pala, 2 Pala, 4 Pala, 6 Pala - - -

Sharangdhara Cakradatta - 2 Tola 3 Tola 4 Tola



Table No. 7 Sneha Matra according to Sushruta63

Dose Time

required for digestion

Action Indication

Sadharana Matra (1/4th day) 3 Hrs. Agnidipti Alpa Dosha Atur

Bruhmana Matra (1/2 day) 6 Hrs. Brumhana, Vrushya Madya Dosha Atur

Prabhala Dosha Matra (3/4th day) 9 Hrs. - Bahu Dosha Atur

Shrestha Matra (Full day) 12 Hrs. - Glani, Murcha, Mada

Uttama Matra (Day & Night) 24 Hrs. -

Kushta, Visha, Unmada, Graha,

Apasmara

Table No. 8 Indications of Sneha Matra64, 65

Criteria for selection of Dose Person Disease Action

Uttama Matra

• Prabhuta Sneha nitya • Kshut–Pipasa Saha • Uttama – Agnibala Sharira Bala Manasa Bala

Gulma Sarpa-damshtra Visarpa Unmatta Mutrakrcchra GadhaVarcha

• Shighravikara Shamana • Doshanukarshini • Pervades through all

marga • Balya • Rejuvenates-body,

sense organs and mind

Madhyama Matra

Madhyama – Sharira bala Manasa bala Agnibala Mrudu Koshta

Arushka Sphota Pidaka Kandu Pama Kushta Vatarakta

• No much complication • Does not effect strength

much • Brings Snehana

comfortably • Used as Shodhanartha

Snehana Hrasva Matra

• Vriddha • Bala • Sukumara/Sukhocita • Mandagni • Durbala/Avara bala • Person not able to

withstand hunger.

Chronic condition of disease like-

Jvara Atisara Kasa

• Brumhaniya • Snehaniya • Vrushya • Balya • Long lasting benefits • Does not cause Complications



Hrasiyasi Matra is a trail dose, which is administered on the first day of

Snehapana.

One of the actions of Uttama Matra Snehapana is explained as Vikara

Shamana and that of Hrasva Matra as Brumhana Cakrapani mentions that Uttama

Matra should be used for Shamana and not for Shodhana Purva Snehana. So doubt

may arise regarding usage of Uttama and Hrasva Matra as Shodhana Purva

Snehapana Dosage.

VIII. KARMUKATA BHEDA:

Based on the action of Sneha, Snehana are of 3 types viz.

(i) Shamana Snehana

(ii) Brumhana Snehana

(iii) Shodhana Snehana

(i) Shamana Snehana:

Shamana Snehana is a procedure of administration of Madhyama Matra of

Accha Sneha during Annakala when one feels hungry without taking the meal.66,67

Hemadri defines Shamana Snehana is one which normalizes the aggravated doshas

without expelling them and disturbing the normal doshas68.

(ii) Brumhana Snehana:

The snehana used for Brumhana is called as ‘Bhrumhana Snehana’. The

administration of Sneha along with Mamsa Rasa, Madya, Kshira etc., are known as

Brumhana Snehana69. Before food if Brumhana Snehana is given will cures

Adhobhaga rogas, in the middle of food cures Madhyamabhaga rogas, after food

cures Urdhwabhaga rogas and strengthens the body70. The dose of Sneha should be

Alpa or even less than quantity of Hrasiyasi Matra71.



(iii) Shodhana Snehana:

The Uttama Matra of Accha Sneha is administered in morning hours when

preceeding evening food has been digested but individual have shown less hunger is

called as Shodhana Snehana. 66,67,72

Shodhana snehana is carried out through Matranusara or Arohana or

Pravicharana. Matranusara and Pravicharana snehapana were already explained.

Arohana Snehapana:

The word Arohana means rising or ascending Arohana Snehapana can be

defined as an oral administration of Sneha in the periodical increasing dosage.

Vangasena clearly described the method of Arohana Snehapana.

Table No. 9 Opinion of Vangasena regarding dosage of Arohana Snehapana73

DAY Matra (Dosage) 1 2 3 4 5 6 7 Uttama 6 pala 7 pala 8 pala 9 pala 10 pala 11 pala 12 pala Madhyama 6Karsha 7Karsha 8Karsha 9Karsha 10Karsha 11Karsha 12Karsha Hrasva 3Karsha 3½Karsha 4Karsha 4½Karsha 5 Karsha 5½Karsha 6 Karsha

Through all the opinions mentioned regarding the Arohana Krama Snehapana

is advised to achieve Snigdha Lakshana with in 7 days. But the method of Arohana

Krama Snehapana is left to the physican.

SNEHANA YOGYA

In the classics we find the indications of Snehana therapy in general. However

it is to the intelligence of the physician to decide the type of Snehana and implicate

the same appropriately in each of the different conditions.



Table No. 10 Shamana and Brumhana Snehana Yogya: 74,75

Abala Vata Vikari Vyayama – Madya – Stree nitya Bala Chintaka Vriddha Daruna pratibodha MadhyasevitaTimira Krsha Abhishyanda Mandagni Ruksha Mrudukostha with alpa dosha

Shodhana Snehana Yogya:

Shodhananga Snehapana is one of the essential Purvakarma for Shodhana.

Hence in almost all the Shodhana Arha conditions Shodhananga Snehapana is

advised.

Table No. 11 Showing General Indications of Shehana According to Different

Acharyas.76, 77, 78, 79, 80

Snehya C.S A. S A.H S.S K.S I As a Poorva Karma i) Swedya + + + + - ii) Samsodhya + + + + - II Different Stage of Life i) Vruddha - + + + - ii) Bala - + + + - III In Different Conditions i) Rooksha + + + + - ii) Krusha - + + + - iii) Abala - + + - - IV In Different Viharas i) Vyayama nitya + + + + + ii) Madhya nitya + + + + + iii) Stree nitya + + + + + iv) Chintaka + + + + + v) Srama - - - - + VI In Different Diseases i) Vatavikara + + + + - ii) Kshinasra - + + + - iii) Ksheena retasa - + + + - iv) Abhishyanda - + + + - v) Timira - + + + - vi) Daruna practibodha - - - + -



Table No. 12 Showing the Deserving Condition for Snehana 81,82,83,84

Ghrita Taila Vasa Majja

Vataprakruti Pravruddha shleshma Asthiroga Deepthagni Pittaprakruti Pravruddha medhas Sandhiroga Kleshasaha

Vatarogi Sthoola Siraroga Snehasevi Pittarogi Vatharoga Snayuroga Vatarogi

Chaksukama Vathaprakriti Marmaroga Krurakosta Kshataksheena Balarthina Kostangaroga

Vruddha Tanuthwarthina Vasasathmya Bala Laghuvarthina Avruthavata

Abala Dhardhyarthina Ayuprakasha kama Sthiaryarthina

Balarthina For snigdhatwak Swararthina For Slashnatwak Pustikama Krimikosta

Soukumaryarthina Krurakoshta Agnideepti Nadeevrana

ojus Smruti Medha

Bhuddhi Indriyabala

Daha Shastraghata

Visha

SNEHA ANARHA:

Acharyas have told different contra indications of Snehana karma in general.

By going through (Table No. 14) a few condition of the Shodhana Snehana Anarha

are analyzed as follows:

• Rukshana Arha-As mentioned by Charaka - Rukshana Anarha persons are

generally Abhishyandhya, Bahudosha, Rogas manifested in Marmastana,

Urhusthambha. If Snehana administered in such condition, it will further

aggravates the condition85,86.

• Dattabasti, Virikta- Soon after Basti and Virechana, Agni will become Manda.

Hence Snehapana is contraindicated.



• Agni Vikruti- Tikshnagni and Mandagni are considered in Agnivikriti 87

i) Tikshnagni – If Sneha is administered in this condition, then Agnibala

further enhances and leads to many complications such as Trishna etc.

ii) Mandagni – If Sneha administered in Mandagni it will leads to Sneha

Ajirna or Ama.

• Mada and Murcha- Even though Shodhananga Snehapana is indicted in Mada

and Murcha, it is included under Snehana Anarhata with the intention to

specify that during attack of Mada, Murcha Snehapana is contraindicated.

• Kshirapa- In Kshirapa Avastha the body of the child will be having Snigdha

Guna. Hence Snehapana is not indicated.

• Garardita- If Snehapana administered in Garardita, then Sneha by virtue of

Vyavayi and Sara property further potentiate and facilitate the spreading of the

poison all over the body. Hence Snehapana is contraindicated in Garardita.

• Durdina-

Durdina means the day of cloudy atmosphere. In this atmosphere the

chances of aggravation of Kapha and Mandagni is high. So Snehana is

contraindicated.

• Ama Pradosha- As Ama and Sneha are having homologues property, if

Snehapana administered in Ama condition, then condition will be aggravated.

• Akala- Shodhana Snehana will not give desired benefit if it is administered

untimely.



Table No. 13 General Contraindications of Snehana 88,89,90,91,92

Asnehya C.S. S.S. A.H. K.S. Sh.S.Rukshanam Samshodhanadrute + Utsanna Kapha medasa + Kapha Prakopa,Dagdha + Abhishyanna anana guda + Nitya Mandagni + + Shleshma Pittopahata antaragni + Tikshnagni + Durbala + + + + Pratanta (Klamayukta) + Shranta + Shramanvita, Akala Prasuta + Garbhini + + Prasuta + Apaprasuta, Urustambha,Udara + Kshirapa, Ativruddha, Jadya, Glani + Madatura, Murcha, Trishna + + Talu Shoshi + Sneha Glani + Garardita + Amajahara + Anna Dvesha + + Arochaka + + Ajirna + + Chardi + + + + + Atisara + Vit Prakopa + Taruna Jvara + + + Sthula + + Gala roga + + Datta Vireka + + Datta Basti + + + + Datta Nasya + + + Akala, Durdina + +

SNEHANA PRAKARSHA KALA: 93,94,95,96

Prakarsha kala is the time taken for snehana procedure. Shodhananga

Snehapana is a process of administering Sneha to achieve the desired Doshotkleshana

within a specific number of days.The minimum and maximum number of days for



Shodhananga Snehapana is 3 to 7 respectively. i.e. if the person with Mrdu Koshta for

3 days, in Madhyama Koshta for 4 to 5 or 6 days and Krura Koshta for 7 days

Bhoja is of the opinion that a person having Kaphaja, Pittaja and Vataja

Prakrti needs 3, 5 and 7 days of Snehapana respectively.

Vagbhata emphasizes that Shodhananga Snehapana should be continued till

one develops the manifestation of Snigdha Lakshana irrespective of any time limit.

On seeing different opinion regarding prakarsha kala, it can be concluded that,

irrespective of Prakrti or Koshta, the duration of administration of Shodhananga

Snehapana should be till the appearance of Samyak Snigdha Lakshana. But maximum

duration is with in 7 days.

Sneha Prakarsha Kala –why 7 days? 97,98,99

Shodhananga Snehapana creates Doshotkleshana in the body. If

Shodhananga Snehapana continued after 7 days, then Sneha becomes Satmya and fail

to produce Doshotkleshana. Here Satmya refers to the meaning that individual get

accustomed to Sneha just as food article. If the dose of administered Sneha is less,

then it will fail to produce the desired effect in 7 days. In such cases higher dose of

Sneha should be given after some interval.

SHODHANANGA SNEHAPANA VIDHI:

The administration of Shodhananga Snehapana is followed in three

different stages such as Purvakarma, Pradhana karma and Paschat karma.

I. Purvakarma

II. Pradhana karma and

III. Paschat karma.



I. PURVAKARMA:

It includes-(i) Atura Pariksha, (ii) Atura Siddhata, (iii) Sambhara Sangraha

i. Atura Pariksha 100

Dasha Vidha Pariksha, Prakruti, Vikruti, Sara, etc in the Atura is to be

examined. Specific importance is given for deciding Agnibala and nature of Koshta.

Depending upon Atura Pariksha we can easily assess

a. Snehana yogya and Ayogya.

b. Understanding Snehapana Prakarsha Kala.

c. Selection of appropriate Sneha Dravyas and Shodhananga Snehana method.

d. Matra nirnaya and Anupana.

ii. Atura Siddhata

Individual Aturas should be prepared physically and mentally through

following procedures -

(a) Deepana – Pachana (b) Diet regimen (c) Manasopachara

a] Deepana – Pachana

People having mandagni & Amavastha condition. So it is essential to take

Deepana & Pachana before undergoing Snehana therapy.

• Deepana –Is the drug which effectively enhances the state of agni. It increases

appetite remarkably & increases the better absorption of drug.101 Deepaniya Gana

drugs,102 Guduchyadi Gana drugs103 can be used for Dipana effect. Deepana –

Pachana are used as conventional therapeutic regimens before undergoing snehana

therapy & should be given till the Nirama Avastha is seen.

• Pachana – The drug or action which has the capacity of digesting Ama but doesn’t

increases the agni of an individual is known as Pachana Dravyas like

Nagakeshara,103 Pippalyadi Gana, Musthadi gana,104 Dashamooladi gana etc as

Amapachana dravyas.



b] Diet regimen 105,106,107

For shodhananga snehana Indicated diet ;

• Drava – Liquid

• Ushna – Warm

• Anabhishyandi – not having ‘Abhishyandi’ property

• Na Atisnigdha – Not too much Snigdha

• Pramanayukta – Regulated quantity

c] Manasopacara

In Shodhananga Snehapana, a large quantity of Sneha is administered.

Because of non-palatability, discomfortness felt during Sneha Jirna Kala, individual

might show avertion to drink Sneha. So prior to Snehapana, complete procedure of

Snehapana and Shodhana should be explained to the individual and he should be

encouraged to drink Sneha. This may give confidence to the patient.

iii. Sambhara Sangraha

One should keep ready the required medicaments and first aids and essential

materials to treat the Vyapat or arises if any .108

II. PRADHANA KARMA

Pradhana karma includes following steps viz,

1. Administration of Sneha and Anupana

2. Observation of

a) Sneha Jiryamana Lakshanas and Sneha Jirna Lakshanas

b) Snigdha, Ati Snigdha and Asnigdha Lakshanas



1. Administration of Sneha 109

In the early morning when the Sun rises Athura is advised to take medicated

Taila or Gritha. The sneha should administered after complete digestion of food

which was taken on previous night. After performing auspicious rituals, appropriate

quantity of selected Sneha should be given to drink.

Anupana : 110,111,112

Anupana should be given along with the Snehadravya. It helps in breakdown,

softening, digesting, proper assimilation and instant diffusion of the Sneha taken. It

also helps in refreshing the patient & will give pleasure, energy to the patient.

For Chaturvidha snehas the Anupana used are :

Ushna jala – For Grith, Yusha – For Taila , Manda – For Vasa and Majja,

Shitala Jala – For Bhallataka and Tuvaraka Taila

For all the Snehas Ushnajala is used as Anupana, except Tuvaraka and

Bhallataka Taila.The dosage of the Anupana may be decided on the basis of normal

digestion capacity or according to the pharmaceutical process involved.

2. (a) Observation of Sneha Jiryamana and Jirna Lakshana

The administered Sneha undergoes various digestive phases, which produces

some symptoms called as ‘Sneha Jiryamana Lakshanas’. These Lakshanas will be

subsided after Sneha Jirna and does not need any sort of therapeutic intervention.

During first phase of avastha paka. Production of kapha takes place, which is

having similar qualities to sneha. Thus production of kapha will be more which causes

lalasrava. Due to large amount of sneha the quantity of secretions of Jataragni

increases and Jataragni is having Agneya quality which may cause Trishna, Bhrama,

Murcha, Daha etc.,



The onset of symptoms like Kshut, Trshna, etc. indicates the completion of

Sneha digestion (Sneha Jirna). In doubtable cases regarding digestion or indigestion

of Sneha one should take hot water, which brings Shuddha Udgara, Laghuta, and

desire for food. If sneha does not digest after administration of warm water and takes

more time than required. It should be eliminated by vamana further cold water

sprinkling and applying of chandna paste on scalp and cold water bath should be

employed.113

Table No. 14 Sneha Jiryamana and Jirna Lakshana114

Jiryamana Lakshana Jirna Lakshana Shiroruja Shirorujadi Jiryamana Lakshana Prashamana Bhrama Vatanulomana Nishtiva(Lalasrava) Kshudha pravrtti Murcha Trishna pravrtti Sada Udgarashudhi Arati Laghuta Klama Trishna Daha

2. (b) Observation of Snigdha–Asnigdha–Ati Snigdha Lakshanas 115, 116, 117, 118, 119, 120, 121

All acharyas have mentioned about important laxanas of samyak snigdha,

asnigdha and atisnigdhata, which serves the purpose of further administration of

swedana and shodhana therapies.

Evaluation of Snehapana based on parameters like –

i) Samyak Snigdha Lakshanas

ii) Asnigdha Lakshanas

iii) Ati Snigdha Lakshanas



i) Samyak Snigdha Lakshanas

Attainment of Samyak Snigdha Lakshana is an important action of

Shodhananga Snehapana. After observing these laxanas snehapana will be stopped.

Table No. 15 Samyak Snigdha Lakshanas

Lakshanas C.S. S.S. A.H. K.S. Sh.S Ckd Va Se

Vatanulomana + + + + + Deeptagni + + + + + + + Snigdha Varcha + + + + + Asamhata Varcha + + + + + + Purisha Mrduta - - - + - - - Adhastat Sneha Darshana - + - - - - - Gatra Mardavata + + + - + - + Gatra Snigdhata + - + - + - + Tvak Snigdhata - + - - - - - Anga Laghava - + + - + - - Klama - - - - - + - Glani - + + - + - - Snehodvega - - + - + - - Vimalendriyata - - - + - - - Medha - - - + - - - Pusthi - - - + - - - Dhrti - - - + - - - Kale Sharira Vrtti - - - + - - - Teja Vrddhi - + + - + + -

ii] Asnigdha

Asnigdha Lakshanas may be present prior to Snehana therapy, if Snehana

therapy is not done properly then these Lakshana persist at the end also. By observing

these Lakshana Physician should rectify and adjust matra or snehana and carry out

Snehana properly. If snehana is not done properly the following symptoms are

observed.



Table No. 16 Asnigdha Lakshanas Lakshanas C.S. S.S K.S. Va Se A.H.

Grathita Purisha + + + + - Ruksha Purisha + + - - - Shushka Purisha - - + - - Vayu Pratilomana + + + + - Agnimandhya + - + + + Avipaka / Krcchrat Annnam Vipachyate - + - - + Anila Purita Udara - - - - + Gatra Rukshata + - + - + Gatra Kharata + - + + - Urovidahata, Dourbalya - + - - + Dourvarnyata - + - - + Adhrti - - + - -

iii] Ati Snigdha Lakshanas

Shodhananga Snehapana is to be continued till the appearance of Samyak

Snigdha Lakshana, but if Snehapana is continued even after that then it may lead to

increase of Apyamsa in the body and Atisnigdha Lakshana may manifest.

Table No. 17 Ati Snigdha Lakshanas Lakshanas C.S. S.S A.H K.S Sh.S Ckd Va Se Panduta + - - + + + + Gaurava + - - + - - - Jadya + - - + - - + Apakva Purisha + - - + - - + Purisha ati pravrutti - + + - + - - Guda Srava - - - - - + - Ghrana Srava - - - - - + - Mukha Srava - + - - + + - Pravahika - + + - + - - Utklesha + - + + - - + Aruci + - + + - - + Bhakta Dvesha - + - - + - - Adhmana - - - + - - - Tandra + - - + + - + Moha - - + - - - - Angadaha - - + - - - + Gudadaha + + +



III. PASCHAT KARMA:

Paschat Karma is categorized as –

• Paschat Karma on the days of Snehapana

• Paschat Karma after attainment of Samyak Snigdha Lakshanas

On the days of Snehapana: During Snehapana individual is advised to

follow instructions like-122

(i) Guru Pravarana - covering body with thick cloth.

(ii) Nivata Shayana Sthitaha - residing in a room devoid of breeze.

(iii) Jaranantam Pratiksheta-awaiting digestion of Sneha.

(iv) Drinking little quantity of Ushna Jalapana or any other specified

Anupana if feels thirsty.

(v) When Sneha is digested taking hot water bath, and consuming Yavagu

etc. food

(vi) During snehana the diet should be mrudu which affects in stimulation

of digestive power & lightness of abdomen.

Paschat Karma after attaining Samyak Snigdha Lakshanas:123,124,125,126

After Samyak Snigdha Lakshanas, Shodhananga Snehapana is stopped and

they are advised for further process like Sarvanga Abhyanga, Svedana and Shodhana.

Pathya

(a) Ushna Jalapana - Ushna Jala is having Dipana, Pachana and

Vatanulomana properties, hence helps in Snehapachana process.

(b) Bramhacharya - Helps in Snehana process.

(c) Kphashaya - As day sleep and Ratri Jagarana aggravates Kapha and Vata

Dosha respectively, only night sleep is advised.



Apathya

a) Vyayama - Exercise

b) Uccha Vacana - Loud speech

c) Vega Samrodha - Suppression of Urges

d) Shoka, Krodha - Anger, anxiety.

e) Hima, Atapa - Mist, Sunlight.

f) Pravata - Open breeze

g) Atyasana-Sitting at a place for long time.

h) Neecha/Uccha Upadhana - Usage of too low or too high pillows.

Pathya- Apathya is to be followed sincerely for equal number of days during

the course of Snehana therapy and after therapy also.

POST SNEHANA THERAPIES 127, 128, 129, 130, 131, 132

The period between completion of Shodhananga Snehapana to the day of

Virechana or Vamana is known as Vishrama Dina. During this period the individual

will be subjected for Sarvanga Abhyanga, Svedana and provided with appropriate

diet.

SNEHA VYAPAT 133, 134, 135

Sneha vyapat is produced either by faultly administration of sneha by vaidya

without considering matra, kala, rutu, anupana etc. or by the patient when he doesnot

follows the rules during snehana karma.

(i) Ashu Utpanna Vyapat: These types of disorders may have acute onset and

may needs immediate manegement

(1) Ajirna (2) Aruci (3) Amapradosha (4) Shula

(5) Jvara (6) Anaha (7) Trshna (8) Sthambha

(9) Utklesha (10) Tandra (11) Samjna Nasha.



(ii) Chira Utpanna Vyapat: These disorders may manifest in due course of time.

(1) Kandu (2) Kushta (3) Grahani (4) Pandu (5) Arsha

(6) Shotha (7) Udara (8) Staimitya (9) Vakgraha.

These complications should be treated for long time as explained in various

classical text.

Sneha Vyapat Chikitsa:136, 137, 138

Classics has metioned to treat Sneha Vyapat’s through different therapies like-

1 Upavasa/Trshna :Beneficial in alpa Dosha Avastha and enhances Agni Bala.

2. Ullekhana :In Utklishta Dosha Avastha SadyoVamana is beneficial and is

also advised in conditions like Sneha Ajirna, Utklesha,

Snehajanya Trshna.

3. Svedana :In conditions such as Sthambha, Svedana is beneficial.

4. Rukshana :Rukshana therapy is highly beneficial in Sneha Atiyogajanya

Vyapat. Rukshana Dravya can be administered in the form of

Pana, Anna and Bheshaja.

Sneha Ajirna Janya Trshna Chikitsa:139, 140, 141

If Sneha Ajirna produces severe thirst, the patient’s head and face should be

splashed with cold water. If this does not relieve the thirst, the Pitta dominant patient

should be given Ruksha Anna and Shita Jala and then made to vomit. In case of

persons who have predominance of Kapha and Vata or all the Doshas increased in

equal proportion, Vamana is induced after giving Ushna Jala.


KARMUKATA OF SNEHANA AS A PURVAKARMA OF SHODHANA

When Doshas are present in their vitiated condition, which have left the

Shakha (periphery) and have occupied Koshta (central place) as well as their Linatva

(latency) has withered away and their Uthkesha Avastha (Patency) has been acquired.

Thus, Panchakarmas are indicated when vitiated Doshas have become Utkleshita and

when they have accumulated in Kostha and are not scattered in remote srotases.

1. Importance of Shodhananga Sneha

To substantiate the importance of Shodhananga Snehana many references are

available in the classics.

• Snehana is required to be administered first, then Swedana; finally followed

by Shodhana.142

• Acharya Sushruta has described the importance of Snehana as “Snehasaro

Ayam Purusha: Pranascha Sneha Bhuyistha: Sneha Sadhyascha Bhavati.” 143

Sneha is the saravasthu of the human body believed to be present in all parts

of the body, which has been considered to be in prana. Agni, Soma, Vayu,

Satva, Raja, Tama, Panchendriya and Bhootatma all these are called Prana.

By going through this version we can understand that Snehana brings softness

in the Srotas by that Doshas will come back to Koshta from Shakha and when

Shodhana is administered vitiated Doshas are expelled out without causing

discomfortness to the individual.

As the dirt of the cloth is washed with water after deterging (with alkali etc.),

the impurity of the body is eliminated by Shodhana measures after deterging

(Utklesha) with Snehana and Svedana. This version is of extreme importance

for explaining the mode of Action of Snehana and Svedana as Purvakarmas to

Karmukata of Snehana - 33


Shodhana in bringing Doshotkleshana. Among these two Purvakarmas

Snehana by virtue of its Vishyandana, properties aids in bringing Lina and

Anutklishta Doshas to Utklishta Avastha. 144

When the inner portion of the vessel is smeared with ghee and then it is filled

with water, water can be removed completely without living a single drop in

it. In the same way after administering Sneha as a preoperative measure to

Shodhana procedure the excited doshas are eliminated completely.

As a cloth absorbs certain amount of water but oozes out the water in excess.

Similarly the Snehana therapy used just in proportion with the digestive power

gets digested, it oleates only when it is administered in excess.

Acharya Caraka has mentioned about the ways to bring vitiated Doshas form Shakha

to Koshta by means of-145

⇒ Vrddhi -increasing

⇒ Vishyandana - Dissolving / by increasing fluidity of Doshas

⇒ Paka- results in detachment of the Dosha from the place of lodgment.

⇒ Srotomukha Vishodhanat – Clearing the orifice of Srotas.

⇒ Vata Nigrahat – By controlling Vata Dosha .

Here Sneha acts in every aspect of the above processes to bring Doshas to

Koshta and bring Utkleshana of the Doshas. In this connection, Vagbhata while

narrating the different therapies that precedes the Shodhana renders Snehana in equal

position to other therapies.

2. Actions of Snehana:

Actions of Snehana can be attributed to properties present in the Sneha

Dravyas. In this regard it is very much necessary to discuss the actions of these

properties with respect to Shodhana Snehana.146



• Drava :

It imparts some sort of moisture to the Srotas that removes impediment of

doshas. Helps in diffusion of Sneha over the body. Helps in Dosha Vilayana process.

Acts like a dissolving media to the Doshas by Alodhana Sandhan Karaka property.

• Sukhshma :

By virtue of Sukshma property of Sneha easily enters into the minute channels

of body. Sukshma is having Sroto Vishodhana property, thus aiding in bringing the

Doshas back to Koshta. It was defined by some as the capabilities of dilatation of

channels, which augment the movement of Sneha Dravyas freely even through the

minute channels.

• Sara

Sara is having ‘Vyaptishilatva’ i.e., spreading nature, thus helps in spreading

of Sneha all over the body. Prerana and Vatanulomana action of Sara Guna helps in

movement of Doshas back to Koshta.

• Snigdha

Snigdha brings softness of Srotas and by this there is a better conveyance of

Dosha, Dhatu and Mala.

• Picchila

Shleshmala property is important to bring Dosha Utklesha. Helps Sneha to

come in contact with Doshas for longer duration. It is termed as Sandra &

Cikkanattva by Arunadatta. The properties attributed to this are Jivana, which would

be shown on Raktadi Dhatus, Balya by imparting strength, Sanghata by the

compactness of morbid elements.



• Guru

It can be defined as the quality by virtue of which the body dimensions will be

increased.

• Shita

It keeps intactness of the body, by virtue of this quality it creates satiety and

prevents the occurrence of Murcha, Sveda and Daha.

• Mrdu

Brings Srotomardavata. By generating softness, laxity, loosens the Dosha

Sanghata.

Though Guru, Shita and Manda are mentioned as properties of Sneha, but

these have more of Shamana or Brumhana value than aiding in Shodhana Snehana

action.

In Siddhisthana, while dealing with the Snehana Karya, Charaka very vividly

explains as-147

♦ Sneho Anilam Hanti

♦ Mrdu Karoti Deham

♦ Malanam Vinihanti Sangam.

Cakrapani clarifies that these are functions of Shodhana Snehana; on the basis

of above version actions of Shodhananga Snehana may be analysed as follows-148

♦ Sneho Anilam Hanti

Vata Nigraha is one of the criteria mentioned by Charaka to bring

Doshas back to Koshta. As Sneha is having exactly opposite Guna to Vata

Dosha, Sneha attains the proper Gati of Vata and helps to bring the

Shakhagata Dosha into Koshta. Vatashamana effect of Snehana can be known

by observing Vatanulomana action.



♦ Mrdu Karoti Deham

Sneha by virtue of its Snigdha, Mrdu qualities brings softness in Dosha

Sanghata, Srotas and Deha, which are very important to bring Doshas to

Koshta in Utkleshana stage. This Mrdukarana effect of Sneha can be

confirmed by observing Gatra Mardavata.

♦ Malanam Vinihanti Sangam

Mala Sanga generally occurs due to Rukshata, Sneha overcomes this Rukshata

by its Snigdha and Vishyanda properties and the Sanga get relieved.

3. Karmukata of Shodhana Poorva Snehapana

The reason behind its action as a Purvakarma to various Sodhana procedures

they are highly esteemed the following actions can be clearly observed.

o It acts as a solvent.

o It increases the Apyamsha of the body.

o It brings the lodged morbid and unexcreted waste products to gastro

intestinal tract.

o Action as a solvent.

According to Sushruta the disease is produced due to the sthana samshraya of

vitiated Doshas through srotases during their circulation in the body.149 Sneha

administered inside the body reaches the Srotamsi and acts as solvent to remove

obstruction by dissolving those morbid factors in it, resulting in the removal of Sroto

vibhandha which is one of the important steps in the Samprapti Vighatana.

This view can be emerged by the study related to the permeability of Dravyas

into the innermost recess of the body. It can be recognized that Kalas surround the

Dhatus and Srotamsi are semi permeable. 150



Chakrapani favors this by that every Dhatu will have specific srotases

pertaining to them and by the srotases concerned with a particular Dhatu, other

Dhatus will not be nourished.151

Thus Sneha acts as a solvent both for lodged morbid factors and as well as

unexcreted tissue waste products.

o Increases the Apyamsa of the body

The nature of Sneha has the predominance of Apa Mahabhuta152. So by this

property of Sneha liquefied Malas brought from the tissues, the levels of fatty acids

etc., and increases in the blood, resulting in the high plasma volume. To keep up the

equilibrium of the normal plasma level, the extra amount of liquid from it are reached

in the Kostha for excretion. Later on when Shodhana Karma are administered this

increased amount of body fluid are evacuated by which the vitiated Doshas and

unexcreted Malas also expelled out resulting in the cure of the ailment.

o It brings the lodged morbid and unexcreted waste products to gastro

intestinal tract

The main purpose of Purvakarma is to promote elimination of the accumulated

malas from Sakhas, by bringing them to Kostha which are afterwards expelled from

the body by Shodhana Karma. In this connection Acharya Sushruta expound his

views that due to Snehana and Svedana, the morbid humor of the disease being

instigated, become liquefied and brought to Kostha for easy elimination by the

Sodhana or radical therapies.153



MEDA:

The topic of the study is Samedarakta (i.e Hyperlipidaemia and Normal lipid

values). Hence important aspects of Meda are discussed here.

Basic concept of Meda :

Meda is an important dhatu among Saptadhatu. Being a dushya dominant

disorder, Meda plays a major role in pathogenesis of Medoroga.

Nirukti :

Literally, the word Meda is derived from root “Jhimida Snehana”. Which

stands for Sneha, Fat, Oil etc. (Vachaspathya). It means the substance which has

snigdhatva property is called Medas.

In Sabdakalpadruma, it is mentioned that Meda is the fourth dhatu which

performs the Dharana-support the body, mind and life. “Medhyate anen iti medah” 154

Formation of Meda dhatu : 155

According to Charaka, the Rakta dhatu is combined with Teja, Apa and is

made solid by the agni so that it gets converted into Mamsa, that again being digested

by its own agni, “Medodhatvagni” and stirred up by the agni and getting combined

with Apa and unctuous substances and finally gets converted into the Medodhatu.

Pramana of Meda dhatu :156

The total quantity of Meda is two Anjali and the Vasa (Muscle’s fat) is three

Anjali. Thus, total Meda content of body is enumerated as 5 Anjali and total

measurable body elements are counted as 56.5 Anjali, from this proportion, it is

evident that total Meda content of body is 11 to 12% approximately. Modern

physiology also mentioned the same amount of fat i.e 12%. This quantity may vary

from person to person and exact measurement of body humeral is not possible due to

unpredictable and ever changing nature of body.

Meda - 39


Flow chart No. 1 Showing Sthana and Swarupa of Meda dhatu157

Medadhatu

Poshaka (Mobile in nature)

Poshya (Immobile in nature)

Which is circulated in whole body along with Gatiyukta Rasa-Rakta dhatu for nourishing the Poshya

Meda dhatu

Which is stored in Medodharakala in its sites. i.e. Udara, Sphika, Stana, Gala, etc. and Vasa (Mamsagata

sneha)

It can be correlated with cholesterol and lipids, which are present in

circulating blood.

It can be correlated with adipose tissues / fat.

Body Mass Index : 158

It is one of the diagnostic criteria for measuring the Medovriddhi.

The B.M.I. is the actual body weight divided by the height squared (kg/m2).

This index provides a satisfactory measure of obesity in people who are not

hypertrophied athletes. The classification of obesity as per B. M. I.

Under weight - <18.5 kg/m2

Normal weight - 18.5 - 24.9 kg/m2

Over weight - 25 - 29.9 kg/m2

Obesity (Class-I) - 30 - 34.9 kg/m2

Obesity (Class-II) - 35 - 39.9 kg/m2

Morbid Obesity (Class-III) - > 40 kg/m2

BMI = Weight in Kgs

Height in Meter2

Meda - 40


Functions of Meda Dhatu :

According to Sushruta, Sneha, Sweda, Drudhatva and Asthipushti are the

functions of Medadhatu. Again Netra and Gatrasnigdhata are the additional functions

of Meda mentioned by Astang Sangraha. Snehana is the main function of Meda dhatu

and with Sneha property it helps to keep luster of skin, hair, eye, etc. Snigdha gatrata

symptom of Medoroga may arise through increased Snehana function of Meda.159, 160

Another function of Meda is nourishment of Asthi Dhatu and Upadhatu Snayu

and Sandhi. Snayu provides support to the Asthi and Sandhi helps in joint formation.

Another function of Meda is creation of Sweda and Sweda is mentioned as mala of

Meda. One more function of Meda is Drudhatva, which is possible through help of

Snayu.161

Ashryashrayeebhava of Meda :162

Dhatu, which is the shelter for any doshas of its allied nature depicts the

concept of Ashryashrayeebhava. Similar allied properties of homogenous Dhatu or

Dosha may serve as a cause to the nutrition or vitiation of Dosha or Dhatu and it is in

this context Meda can be considered as a location of the sthanika Kapha, since Meda

plays a major role in nutrition or vitiation of Kapha and vice versa.

Medovaha Srotasa :

The internal transport system of the body is represented as Srotamsi. It has

been given a place of fundamental importance in Ayurevda both in health and disease

condition. Dhatus are nourished through their respective srotases and one srotas

cannot provide nourishment to another dhatu. The Meda Dhatu gets nutrition from the

preceding dhatu i.e. Mamsa (Poshaka) through its own srotas called Medovaha Srotas.

As per Dr. C. Dwarkanath, the channels through which nutrition to the adipose tissue

is transported are to be termed as the Medovaha Srotas.

Meda - 41


Moola of Medovaha Srotas :

Each and every srotas has two parts or endings one is from which the srotas is

originated i.e. the moola and another is through which nutritive material travel to their

respective places in the body. According to Charaka and Sushruta, Mool may be

enumerated as fallows:

Charaka - Vrikka and Vapavahana,163 Sushruta - Vrikka and Kati164

The Acharyas have considered unanimously Vrikka as one of the moola of

Medovaha Srotas but Vapavahana and Kati are mentioned as second moola

separately. Sushruta have given more anatomical preference than the physiological

point of view by considering Kati as “Moola” of the Medovaha Srotas while

Charaka’s consideration was a physiological one.

Vrikka :

Vrikka, one of the Kosthanga formed by the Sara of Rakta and Meda dhatu.

Sharangadhara says that Vrikka nourish the Meda dhatu inside the stomach area of the

abdominal cavity, while Charaka has considered as “Moola” so these structures must

be directly related with fat metabolism. But, there is no such exact evidence in

Modern science as well as Ayurevdic Science. If we take into the consideration of two

structures situated above the two kidneys i.e. Supra-renal glands as Vrikka that fulfils

the all aspects of fat metabolism.

Vapavahana :

Vapavahan is also a Kosthanga and second root of Medovaha Srotas Dr.

Ghanekar has considered it as omentum, where the maximum Meda is stored.

Kati :

Acharya Sushruta has clearly pointed out the exact site of the Kati but

normally the Kati is the place where the fat accumulates.

Meda - 42


BASIC CONCEPT OF FAT / LIPID : 165,166,167

Lipids constitute a heterogeneous group of compounds of biochemical

importance. Lipids may be defined as compounds which are relatively insoluble in

water, but freely soluble in organic solvents like benzene, ether, chloroform etc. They

are found in the membranes, which maintain the integrity of cells and allow the

compartmentalization of cytoplasm in to specific organelles. Lipids functions as a

major farm of stored nutrients (TGs), as a precursor for adrenal and gonadal steroids

and bile acids (cholesterol) and as a extra cellular and intra cellular messengers

(prostaglandins). Lipoproteins provide a vehicle for transporting the complex lipids

in the blood as a water - soluble complexes and deliver lipids to cells through out the

body.

CLASSIFICATION OF LIPIDS:

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

miscellaneous one.

1. Simple lipids: Esters of fatty acids with alcohols.

(a) Neutral fats : Triglyceride, Esters of various fatty acids with glycerol.

(b) Waxes : Cholesterol and its esters.

2. Compound lipids : Esters of fatty acids with alcohols and containing other

groups.

(a) Phospholipids : Esters containing phosphoric acid and a nitrogenous

base i.e. lecithin, cephalin.

(b) Glycolipids : Esters containing a carbohydrate and a nitrogenous base

i.e. cerebrosides.

(c) Sulpholipids : Esters containing sulphuric acid.

(d) Lipoproteins : Lipids attached with proteins.

Concept of Lipids - 43


3. Derived lipids : Derivatives obtained by the hydrolysis of 1 and 2 mol. and

which still possess the physical characteristics of lipids which are divided as :

(a) Fatty acids : Saturated and unsaturated

(b) Sterols

(c) Fat soluble vitamins

4. Miscellaneous : a) Aliphatic hydrocarbons include iso-octa-decome

b) Carotenoids c) Squalene d) Vit E and K

The lipids in the body physiologically form two components:

A. Elements constant or structural lipids:

The value of this lipid remains constant even under extreme starvation.

Cytoplasm and cell membrane of all organs are composed of element constant, so that

their fat content does not diminish in starvation. Chiefly element constant is

composed of phospholipids & is independent of the state of nutrition. Cholesterol is

another lipid present in cell membranes, it has also an important role in fat transport in

the blood.

B. Elements variable:

It is stored in the body in excess. It is composed mainly of neutral fat. It

present mostly in the depot fat or adipose tissue in free form and represents stored

energy. It has been observed that depot fat is not static but in a continuous state of

change is due to its continuous synthesis and breakdown in the body. Thus fat is

chiefly composed of glyecrides of various fatty acids and usually contains 75% of

oleic acid, 20% palmitic acid and 5% stearic acid.

A third type of fat, brown fat, which has a high metabolic rate has been

observed in infants but not in adults.



Depot fats:

Fat in the body is present in two form i.e. Blood fat and Depot fat. About 12%

of the total body weight of a man consists of fat. The major part of it remains stored in

the so-called fat depots. Which is known as Depot fats.

Distribution of Fat in Body tissue :

(i) Subcutaneous tissue - 50% (ii) Peripheral tissue - 15%

(iii) Mesentry - 20% (iv)Omentum - 10%

(v) Intramuscular connective tissue - 05%

Composition of Depot fats :

Depot fat is chiefly composed of mixed triglycerides. Trace of lecithin and

cholesterol, as well as a little amount of polyunsaturated fatty acids.

PLASMA LIPIDS:

Although the lipids are present in both body cells and plasma of blood, but the

composition of lipids in plasma and cells widely vary. Since the composition of

plasma lipids accurately reflects the actual state of lipid metabolism, so the

composition of plasma lipids is generally studied.

The composition of blood lipids is not a static because of process of addition

and removal of lipids from blood:

Addition of lipids Removal of lipids (i) Absorption from intestine (i) Deposition of fat in the depot (ii) Synthesis of fat and its (ii) Oxidation of fat in the tissue

Mobilization (iii) Utilization for formation of tissue structures components.

Main plasma lipids are –

I. Cholesterol and its esters II. Triglycerides

III. Phospholipids IV. Non-esterified fatty acids



(I) Cholesterol :168

The Cholesterol is a waxy, fat-like compound that belongs to a class of

molecules called steroids. Cholesterol is made primarily in liver (about 1,000

milligrams a day), but also by cells lining the small intestine and by individual cells in

the body. Cholesterol might feel like a soft, melted candle and is essential for:

Cholesterol is an important component of biomembranes cholesterol, is

present in plasma either as free form or esterified. Bile has high concentration of

cholesterol and so bile serves as the major excretory route for cholesterol.

Occurrence

It is widely present in the body tissues, cholesterol is found largest amounts in

normal human adults.

Brain & Nervous Tissue - 2%

In the Liver - 0.3%

Skin - 0.3%

Intestinal mucosa - 0.2%

Certain endocrine glands Viz - adrenal cortex contains -10% or more Corupus

leutiem is also rich in cholesterol. Cholesterol is present in blood and bile usually a

major constituent of Gall Stones.

Sources

Exogenous - Dietary cholesterol approximately 0.3gm/day. Diet rich in

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

Cholesterol content of different food items

Food Item Cholesterol mg/100gm.

Food Item Cholesterol mg/100gm.

Hens egg-whole 500 Brain 2000 Egg Yolk 1330 Butter 280 Liver 300-600 Ghee 310 Meat and Fish 40-200 Milk 10 Milk Powder 90 Milk P (Skimmed) <1



Endogenous

Synthesized in the body from Acetyl CoA, approximately 1g/day.

Forms of Cholesterol

Cholesterol occurs both in free form and in ester form. The various fatty

acids, which form cholesterol esters are

Linoleic Acid 50% Oleic Acid 18% Palmitic Acid 11% Arachidonic acid 50% Other Fatty Acids 16%

Biosynthesis of Cholesterol

Essentially all tissue forms cholesterol. Liver is the major site of

cholesterol biosynthesis and also other tissues which are active in this aspect are -

adrenal cortex, gonads, skin, intestine. Low order of synthesis occurs in adipose

tissue, muscle, aorta and nervous tissues. Brain of the new born 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% and in the

intestines approximately 15%, of the amount produced each day. Cholesterol

synthesis occurs in the cytoplasm and microsomes from the two-carbon acetate group

of acetyl-CoA. The process has five major steps,

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

2. HMG-CoA is converted to mevolonate

3. Mevalonate is converted to the isoprene based molecule, isopentenyl

pyrophosphate (IPP), with the concomitant loss of CO2.

4. IPP is converted to squalene

5. Squalene is converted to cholesterol.



Figure No. 1 Showing the Biosynthesis of Cholesterol

1. The acetyl-CoA utilized for cholesterol biosynthesis is derived from an oxidation

reaction (eg. fatty acids or pyruvate) in the mitochondria and is transported to the

cytoplasm by the same process as that described for fatty acid synthesis. Acetyl-

CoA can also be derived from cytoplasmic oxidation of ethanol by acetyl-CoA

Synthetase. All the reduction reaction of cholesterol biosynthesis use NADPH as

a cofactor. The isoprenoid intermediates of cholesterol biosynthesis can be

diverted to other synthesis reaction, such as those for dolichol (used in the

synthesis of N-linked glycoproteins coenzyme Q (of the oxidative

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

intermediates are used in the lipid modification of some proteins.

2. Acetyl-CoA units are converted to mevalonate by a series of reactions that begins

with the formation of HMG-CoA. Unlike the HMG-CoA formed during ketone

body synthesis in the mitochondria, this form is 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, forming acetoacetyl-CoA. Acetoacetyl-CoA and a third mole of

acetyl-CoA are converted to HMG-CoA by the action of HMG-CoA synthase.

HMG-CoA is converted to mevalonate by HMG-CoA reductase (this enzyme is

bound to the endoplasmic retuculum). HMG-CoA reductase absolutely requires

NADPH as a cofactor and two moles of NADPH are consumed during the

conversion of HMG-CoA to mevolanate.

3. The reaction catalyzed by HMG-CoA reductase is the rate limiting step of

cholesterol biosynthsis, and this enzyme is subject to complex regulatory controls.

4. Mevalonate is then activated by three successive phosphorylations, yielding 5-

pyrophosphomevalonate. In addition to activating mevalonae, the

phosphorylations maintian its solubility, since otherwise it is insoluble in water.

After phosphorylation, an ATP-dependent decarboxylation yields isopentenyl

pyrophosphate, IPP, an activated isoprenoid molecule.

5. Isopentenyl pyrophosphateis in equilibrium with its isomer, dimethylallyl

pyrophosphate, DMPP. One molecule of IPP condenses with one molecule of

DMPP 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 tightly associated with the endoplasmic reticlulum.

Squalene undergoes a two step cyclization to yield lanosterol. The first reaction is

catalyzed by squalene mnoxygenase. This enzyme uses NADPH as a cofactor to

introduce molecular oxygen as an epoxide at the 2,3 position of squalene. Through a

series of 19 additional reactions, lanosterol is converted to cholesterol.



Factors 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

increases cholesterol level. Substitution in the diet of saturated fatty acids by

poly unsaturated fatty acids has beneficial effect and lowers the cholesterol

levels.

• Dietary Cholesterol - Increased feeding of cholesterol in diet decreases

endogenous synthesis and reduces cholesterol level.

• Dietary Carbohydrates - Increased consumption of carbohydrates increases

cholesterol levels. Consumption excessive amount of sucrose and fructose

cause increase in plasma lipids particularly Triglycerides and Cholesterol.

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

observed.

• Calorie Intake - Intake of excess calories increases cholesterol level

• Blood Groups - Cholesterol level found to be slightly higher in the persons

belonging to blood group ‘A & ‘AB’.

• 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

• Vit-B-Complex - Nicotinic acid in large doses has cholesterol lowering effect.

Pyridoxine deficiency produces increase in cholesterol level.

• Mineral - In vitro acetate to cholesterol conversion in tissue cell culture

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

and manganese salts. Conversion of mevalonate to cholesterol is inhibited by

vanadyl So4.



• Physical Exercise - Hard physical exercise brought about lowering in serum

cholesterol level and increased level of HDL Cholesterol.

• Dietary Fibres - Increased fibres in the diet caused an increased exerction of

choolesterol and bile acids in feces.

Functions of Cholesterol:

Structural component of cell membrane.

Acts as precursors in biosynthesis of bile acids.Control cell permeability.

Protects the red cells from being easily haemolysed.

Prevent toxins from entering into the cells.

It is also needed for synthesis of Vitamin-D to form cell membrane.

It helps in the synthesis of steroid hormones of sex glands in adernal cortex

and synthesis of vitamins.

Cholesterol helps in the synthesis of mylein sheath of nerves and acts as

insulator for nerve impulses.

In human being 60-70% cholesterol is transported by LDL, 20-30% by HDL

and 5-10% by VLDL.

(II) Triglyceride:

Triglycerides are esters of three fatty acids and glycerol. They are divided into

two types according to fatty acid contents.

1. Simple - in which all three fatty acids are same.

2. Mixed - in which all three fatty acids are different.

They are transported primarily as chylomicrones and VLDL but in minor

amounts as LDL and HDL also. They are main form of lipid storage in men.



(III) Phospholipid :

It is compound type of lipid, containing phosphoric acid with nitrogen base

and constitutes 20% LDL and 30% HDL. The phospholipids and cholesterol always

remain together, which are not stored in adipose tissue, but present in all other tissues.

Phospholipids are an important constituent of Lipoproteins in the blood & are

essential for the formation & function of most of these; in their absence serious

abnormalities of transport of cholesterol & other lipids can occur.

(IV) Fatty acid :

These are basic units of fats & are grouped as saturated & unsaturated fatty

acids. Fatty acids 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. They are very small fraction in plasma protein.

Table No. 18 showing classification of fatty acids

FATTY ACIDS Depending upon no. of

Carbon atoms Depending length Nature of Hydrocarbon

chain i) Even Chain ie., having 2-4.6 carbon atoms

i) Short chain 2-6 carbon atoms

i) Saturated fatty acids

ii) Odd chain ie., having 3-5.7 Carbona atoms

ii) Medium chain 8-14

ii) Unsaturated

iii) Long chain 16 & above (24)

a) Mono unsaturated

b) Poly unsaturated iii) Branched chain FA iv) Hydroxy FA v) Cyclin FA.

(V) The Sterols

Sterols are not true fats. These are derivatives of phenanthrene & have the

parent nucleus with 17 carbon atoms consisting in 3 hexagon & 1 pentagon rings.

When the natural



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

subcutaneous, intra muscular, perinepheric, omental and mesentric tissues. Nearly

300gms in brain and nervous tissue 75gm in liver and blood pool, altogether 10kgs in

70kg individual. Each gram of TG can supply twice the amout of energy compared to

the protein and carbohydrates per gram.

In post absorptive state, the blood plasma contain about 550mg of lipids.

Elevated levels of the profile is important since they can caues two life threatening

disease atherosclerosis and pancreatities.

PLASMA LIPOPROTEINS:

They are formed almost entirely in liver and transport cholesterol and

triglyceride in the blood steram. Which are classified in four types :

(a) Chylomicrons

(b) VLDL

(c) LDL

(d) HDL

Table No. 19 showing the characteristics of lipoproteins

Composition Chylomicrons VLDL LDL HDL Protein % 1-2 7-10 18-22 45-55 Lipid % 99 93 80 50 Major lipid Triglyceride Triglyceride Cholesterol Cholesterol

phospholipids Diameter(nm) 80-500 30-100 21.5 7.5-10.5 Origin Intestine Liver and

intestine End product of VLDL

Liver and Intestine

Function Transport Exogenous Triglycerides

Transport Endogenous Triglycerides

Transport of cholesterol and phospholipids to peripheral cells

Proposed to transport cholesterol from peripheral cells to liver



a. Chylomicrons

These are the major exogenous lipoproteins synthesized in the intestinal

mucosal cells form the products of lipid digestion. They are large complexes rich in

Triglycerides. The particles enters the lacteals in the intestinal villi and are

transported via the thoracic duct to the blood stream. In the lymph and blood, the

chylomicron particles acquire apoprotein C and E from HDL. As they pass through

peripheral capillery beds of adipose tissue and skeletal muscles, their Triglycerides

are hydrolysed by apoprotein CII activated lipoprotein lipase, an enzyme bound to the

endothelial surface, releasing fatty acids and glycerols. The resultant cholesterol rich

chylomicron remnant with its apoprotein B48 and E is recognised by specific

receptors on the hepatic parenchymal cells and is rapidly cleared from plasma.

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

Triglycerides.

Thus chylomicrons are the transport form of dietary Triglycerides to be

delivered to adipose tissue for storage and muscles for its energy needs. Hence

chylomicron particles are not considered to be atherogenic. The atherogenic potential

of chylomicron remnants is a matter of dispute.

b. VLDL

These lipoproteins are the major carriers of endogenous Triglycerides. They

are synthesized in the liver from glycerol and fatty acids and incorporated into VLDL

along with hepatic cholesterol, ApoB, C, E. Apoprotein B100 and E are required

structural components for this secretary process. In the fasting state, majority of

plasma Triglycerides are carried in this particles.



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

they reach the peripheral tissues, they are acted upon by the Lipoprotein lipase

liberating fatty acids that are taken up by the adipose tissue and muscle. The VLDL

remnant is now designated as IDL (Intermediate Density Lipoprotein) and contains

TG. Cholesterol, apo-B & E. Part of the IDL is taken up by the Liver. A major

fraction of IDL further loses Triglycerides and gets converted into LDL.

Normal VLDL is probably not atherogenic. The smaller and more cholesterol

rich VLDL remnants appear to have atherogenic potential. Persons with the genetic

disorder Familial dysbeta lipoproteinaemia have accelerated atherogenesis. Although

elevation of plasma Triglycerides are common in patients wth CHD, they are not

uniformely independent predictors for CHD risk.

c. 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 and have a longer half life

than others. LDL receptors are present on all cells but most abundant in hepatic cells.

The receptors recognise the apo-B and apo-E and can therefore take up LDL or IDL.

Once the LDL particles binds to the cell, they are internalised and chlesterol is

released into the cell. Most of the Cholesterol metabolised into steroid hormones.

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

syntheis 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 LDL receptors. The liver therefore has a major role in controlling the

plasma level of the LDL or cholesterol. most of the LDL receptors are present in the



liver, the liver synthesis cholesterol and removes cholesterol from lipoprotein

remnants. It is also the only organ that can excrete cholesterol through bile. The

cholesterol which is thus excreted into the intestine is partly reabsorbed (30-60%).

The rest is excreted as fecal sterols, caprostanol and cholestenol after bacterial action.

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

Excess intracellular cholesterol can lead to 3 metabolic events.

♦ Inhibition of HMG - CoA reductase, the rate limitig step in cholesterol

synthesis.

♦ Activation of enzyme Acylcoenzyme A Cholesterol acyl Transferase (ACAT)

which esterfies cholesterol for storage.

♦ Inhibition of production of additional LDL receptors, thereby 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 and Apo-B may be casual in the majority of patients with

CHD.

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

macrophages of retculoendothelial system in the scavenger pathway. Macrophages

seated in the arterial wall eventually become over loaded with cholesterol esters and

are converted into the foam cells that characterise early atherosclerosis. Because the

majority of plasma cholesterol (60-75%) is carried int he LDL particles, elevation of

the total cholesterol usually reflect increased LDL levels. The anatomic degree of

coronary atheroselerosis has been directly linked to the concentration of LDL.



d. HDL

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

peripheral tissues to liver. The only excretory route of cholesterol from the body is

bile. HDL is synthesized mainly in the hepatic cells and intestinal cells and are seen

as complexes of Apo A and Apo E with phospholipids. The cholesterol derived from

peripheral tissues and other lipoprotein are esterified in HDL because it has a LCAT

activity. After esterification, the ester form of cholesterol may be transferred to other

lipoprotein and transported to liver. A small portion of esterified cholesterol is stored

in the case of HDL and this cholesterol rich HDL may be taken up by the liver. When

cholesterol esters are internalised, the discoid HDL molecules becomes spherical,

HDL also acts as a carrier of Apo-C to be delivered to the Triglyceride rich

lipoprotein like VLDL and Chylomicrons. HDL is protective, but low HDL

concentration <30mg/dl is a potent risk for CHD.

HDL appears to exert a protective influence by removing cholesterol from

tissues. Total body cholesterol is inversly related to HDL levels.

Important Functions of Lipoproteins

Chylomicrons transport mainly TG and smaller amounts of plasma

lipoproteins, cholesterol esters and fat soluble vitamins from intestine to liver

and adipose tissue. The lipids carried by chylomicrons principally dietary

lipids.

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

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

carbohydrate intake, high ratio of insulin / glucogen, high plasma free fatty

acids and alcohol intake increases the hepatic synthesis of both TG and VLDL



so that enhanced amount of fatty acid reaching the liver is speedily mobilized

in VLDL to adipose tissue.

LDL rich cholesterol esters transports cholesterol and its esters from hepatic

cells to extrahepatic tissues.

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

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

limiting enzyme for cholesterol synthesis.

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

catabolism (scavanging action).

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

Albumin - FFA complexes transport maily FFA, released by adipose tissue

lipolysis and small amouts of Lyso-phospholipids from extra hepatic tissues to

the liver.

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



DIGESTION AND ABSORPTION OF SNEHADRAVYA (FATS):

Bile plays an important role in fat digestion & absorption, not because of any

enzymes in the bile that cause fat digestion, but the bile acids of bile do two things.

♦ They helps to emulsify the large fat particles of the food in to many minute

particles that can be attacked by lipase enzyme secreted in pancreatic juice.

♦ They aid in absorption of the digested fat end products through the intestinal

mucosal membrane

The digestion of fats and other lipids process special problem because of (a)

the insolubility of fats in water and (b) because Lipolytic Enzymes, like other

enzymes are soluble in the aqueous medium. This problem is solved in the gut by

emulsification of fats, particularly by bile salts, present in the bile and plasma

lipoproteins. The breaking of large fat particles or oil globules into smaller fine

particles by emulsification increases the surface exposed to interaction with Lipase

and thus, the rate of digestion is proportionally increases.

The whole process of digestion of dietary lipids and its subsequent absorption

may arbitrarily divided into three phases.

1) Preparatory Phase - Which includes the digestion of lipids in the intestine.

The large lipid particles are broken down into smaller particles with the help of

Lipolytic enzymes. This is called emulsification of fat.

2) Transport Phase - Which includes the transport of digested fats across the

membrane of intestinal villous layer into intestinal epithelial cells.

3) Transportation Phase- Which includes the events of action that takes place

inside intestinal epithelial cells and its passage through lacteals to lymph or in portal

blood.



Fat Digestion169

Table No. 20 showing fat digestion

Organs Digestive juice Enzyme and Action Mouth Saliva No action Stomach Gastric juice No action Small intestine Bile Bile salts emulsify fats Small intestine Pancreatic juice Lipase converts fats into fatty

acids and glycerol Small intestine In microvilli Lipase completes the digestion of

fats to fatty acids and glycerol

1. Preparatory Phase

Digestion in Mouth & Stomach - No fat digestion takes place in the mouth. Recently

a lipase has been detected called Lingual lipase which is secreted by the dorsal surface

of the tongue.

Lingual Lipase - pH range of activity 2.0 to 7.5. Its activity is continued in the

stomach also where pH value is low. Due to retention of food bolus for 2-3 hours,

about 30% of dietary TG may be digested. Lingual lipase is more specifically active

on TG having shorter FA chains and is found to be more specific for ester linkage at 3

position rather than position 1.

Gastric Lipase - There is a evidence of presence of small amounts of gastric lipase in

gastric secretion. The overall digestion of fats, brought about by Gastric Lipase is

negligible because where gastric lipase activity is more effective at alkaline pH

(average pH 7.8). Gastric lipase activity requires presence of Ca++. Activity of

gastric lipase is seen when intestinal contents are regurgitated in to gastric lumen.

Role of fats in the Stomach - Fats do play an important role in the stomach in that they

delay the rate of emptying of stomach, presumably by way of the hormone

enterogastrome, which inhibits gastric mobility and retards the discharge of bolus of

food from the stomach. Thus fats have a high “Satiety Value”.



Digestion in Small Intestine - The major site of fat digestion is the small intestine.

This is due to presence of powerful lipase (steapsin) in the pancreatic juice and

presence of bile salts, which acts as an effective emulsifying agent for fats. Pancreatic

juice and bile enter the upper small intestine, the duodenum, by way of the panereatic

and bile ducts respectively. Secretion of pancreatic juice is stimulated by i) passage

of an acid gastric contents (acidic chyme) in to the duodenum, and ii) by secretion of

the GI harmones. Secretion and CCK-PZ.

Secretion increases the secretion of electrolytes and fluid components of

pancreatic juice, whereas pancreozymin of CCK-PZ, stimulates the secretion of

paneratic enzymes.

Cholecystokinin of CCK-PZ in turn causes contraction of gall bladder and

discharge the bile into the doudenum. Discharge of bile is also stimulated by

secretion and bile salt themselves. Hepatocrinin released by the intestinal mucosa

stimulates more bile formation whch is relatively poor in the bile salt content.

The above sequences of events prepares the small intestine for the digestion of

fats. Pancreatic juice has been shown to contain number of lipolytic enzymes.

Pancreatic lipase, Phospho lipase A2 (Lecithinase) and Cholesterol esterase.

The pancreatic lipase is the most important which hydrolyses TG containing

short chain FA as well as long chain FA. Other two are required for phospholipids

and cholesterol respectively.

Emulsification of Fat by Bile Acids

The first step in fat digestion is to break the fat globules into small sizes so

that water soluble digestive enzymes can act on the globule surfaces. This process is

called as Emulsification of fat. It is achieved by the influence of bile, which does not

contain any digestive enzymes. But bile contains large quantity of bile salts, mainly



in the form of ionized salts, which are extremely important for emulsification of fat.

The carboxyl and other polar parts of bile salts molecule are highly soluble in water.

Where as most of sterol portion of the bile salt dissolves in the surface layer of the fat

globule but with the polar portion of the salt projecting outward and soluble in

surrounding fluids, this effect greatly decreases the surface tension of the fat. And

this property of the bile acids is multiplied even several more times by the small

amounts of Lecithin that are also in bile.

Each time the diameter of the fat globules are decreased by a factor, as a result

of agitation in small intestine the total surface area of fat increases two times. Since

the average size of the emulsified fat particles in the intestine is only 1 micron, this

represents as increase of as much as 1000 fold in the total surface area of fats caused

by the emulsification process.

Digestion of Fats by Pancreatic Lipase

The lipases are water soluble compounds and can attack the fat globules only

on their surfaces. Important enzyme pancreatic lipase and Enteric lipase causes

hydrolysis of fat. Most of TGs of the diet are split into FFA and 2 mono glycerides.

The cholesterol in the diet is in the form of cholesterol esters, which are

combination of free cholesterol and one molecule of fatty acids. Phospholipids also

contain molecules of fatty acid. Both are hydrolysed by lipases in the pancreatic

secretion which frees the fatty acids.

2 Transport Phase

The hydrolysis of TG is a highly reversible process, therefore accumulation of

monoglycerides and free fatty acids in the vicinity of digesting fats vary quickly

blocks further digestion. Fortunately, Bile salts play an important role in removing



monoglycides and FFA from the vicinity of the digesting fat globules almost as

rapidly as these and products of digestion are formed.

Bile Salt Micelle

Bile salts have the propensity to form micelles, which are small spherical

globules about 25 A0 in diameter composed of 20-40 molecules of bile salts. The

products of digestion namely monoglycerides, long chain fatty acids, cholesterol,

phospholipids and lysophospho lipids are all incorporated into molecular aggregates

to form mixed micelle. Because of highly charged exterior and diameter is 2.5

nanometer, they are soluble in chyme. In this form monoglycerides and fatty acids

are transported to the surfaces of brush border microvilli, even penetrating into the

recesses among the moving and agitating microvilli.

On coming into contact with these surfaces both monoglycerides and fatty

acids with traces of cholesterol and phospholipids immediately diffuse through the

epithelial membrane, because they are equally soluble in this membrane as in the

micellae. This leaves behind the bile acid micelles still in the chyme. The micelles

then diffuse back through chyme. And absorb still more monoglycerides and fatty

acids and similarly transport these to epithelial cells. Thus bile acids perform a

“ferrying” function, which is highly important for the fat absorption. In the presence

of abundance of bile acids, approximately 97% of the fat is absorbed, in the absence

of bile acids only 50% is normally absorbed.

3. Transportation Phase

After entering the eithelial cells, the fatty acids and monoglycerides are taken

up by the smooth endoplasmic reticulum, here they are mainly recombine to form new

Triglycerides. However, a few of monoglycerides are further digested into glycerol

and fatty acids by an epethelial cell lipase. Then fatty acids are reconstituted by



smooth endoplasmic reticulum in to Triglycerides. Most of the glycerol that is utilized

for this purpose is synthesized de novo from alpha-glycerophosphate, this synthesis

requiring both energy from ATP and a complex of enzymes to catalyze the reactions.

Once formed, the Triglycerides aggregate within the ER into globules along

with absorbed cholesterol & phospholipids. This provides an electerical charged

surface that makes these globules miscible with the fluids of the cells. In addition

small amounts of β lipoprotein, also synthesized by ER, coat part of the surface of

each globule. In this form the globule diffuses to the side of epithelial cells and is

excreted by the process of cellular exocytosis in the space between the cells, from

there it passes into lymph in the central lacteal of the villus. These globules are then

called Chylomicrons.

From the sides of the epithelial cells the chylomicrons wend their way into the

central lacteals of the villi and from here are propelled, along with the lymph, by the

lymphatic pump upward through the thoracic duct to be emptied into the great vein of

the neck. Between 80-90% of all fat absorbed from the gut is absorbed in this manner

and is transported to the blood by way of thoracic lymph in the form of chylomicrons.

Small quantities of short chain fatty acids, such as those of butter fat are absorbed

directly into the portal blood rather than being converted into Triglycerides and

absorbed into the lymphatics.

FAT METABOLISM IN AYURVEDA:

According to Ayurveda, Kapha is seated in Rasa, Mamsa, Majja and Sukra-

dhatu. Kapha and Meda are having similar properties. On the basis of

Ashrayashrayeebhava vitiation of Kapha also lead to vitiation of above dushyas. In

this way, vitiation of Kapha also leads to vitiation of Meda dhatu. Except Asthi dhatu

all the dhatus contain Snigdha guna.



Hence, Hyperlipidaemia is the disease of Medodhatvagni vikriti. If Agni will

be good and potent, through passing from the level of Rasagni, Raktagni and

Mamsagni the Medodhatuvriddhi will occur and if Agni will be poor, it will create

Dhatvagnimandya. So, Rasagata, Raktagata, Mamsagata and Medogata Snehamsa

will be increased due to their own Dhatvagnimandya respectively.

The circulating triglycerides, cholesterol and lipids should be treated as Rasa

Raktagata Sneha. only the fat deposited in adipocytes should be accepted as

Medadhatu.

CHOLESTEROL AND LIPOPROTEIN METABOLISM, 170, 171

Exogenous Pathway

Exgenous lipid transport begins with intestinal incorporation of dietary

triglycerides and cholesterol into large lipoprotein particles called chylomicrons

(diameter, 80-500nm) which are secreted into the lymph and subsequently enter the

blood stream. When chylomicrons reach the capillaries of adipose tissue and muscle,

they are digested by an enzyme lipoprotein lipase, that is bound to the surface of the

endothelial cells. Lipoprotein lipase hydrolyzes the triglycerides in the core of the

chylomicrons, and the liberated fatty acids cross the endothelium and enter the

underlying adipocytes or muscle cells, they are then either esterfied again to form

triglycerides for storage or oxidized to provide energy.

After most of the triglycerides have been removed in this fashion, the

chylomicron dissociates from the capillary endothelium and enters the circualtion

again. Its size has been reduced and its content of triglycerides diminished, but its

cholesterol esters remain intact. The particle is now designated as a chylomicron

remnant (diameter 30-50nm). When the remnant reaches the liver it is cleared from

the circulation by a receptor that recognizes two of its protein components,



apoproteins E and 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, and 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 by the liver cell as cholesterol esters, it can be excreted into

the bile either as cholesterol or after conversion to bile acids, or it can be used to form

endogenous lipoproteins that are secreted into plasma.

Endogenous Pathway

Endogenous lipid transport begins when the liver secretes triglycerides and

cholesterol into the plasma in very-low-density lipoproteins (VLDL: diameter, 30-

80nm.). the major stimulus for such secretion is a high-calorie intake (especially a

high - carbohydrate intake),which induces the liver to assemble Triglycerides for

export and storage in adipose tissue. The Triglycerides of VLDL are cleaved in

capillaries by the same 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 lipoproteins that contain

apoprotein E or B-100 and it therefore interacts with both IDL and 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 Triglycerides are

removed, and the density of the particle increases further, until it becomes LDL

(diameter 18 - 28 nm). LDL circulates for a relatively long time in man (half-life of

about 1.5days). The particles are eventually degraded by binding to LDL receptors in



liver and certain extrahepatic 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, steroid

hormones or bile acids, they synthesize LDL receptors and 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.

Figure No. 2 Showing the Metabolism summary



Reverse Cholesterol transport

As cells of the body die and as cell membranes undergo turnover, free

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

absorbed into high-density lipoproteins (HDL; diameter, 5-12nm.) and in this location

it is esterified with a long - chain fatty acid by an enzyme in plasma, lecithin;

cholesterol acyltransferase (LCAT). The newly formed cholesteryl esters are rapidly

transferred from HDL to VLDL or IDL particles by a cholesterol from transfer protein

in plasma. The HDL promote the removal of cholesterol from the peripheral cells and

facilitates its delivery back to the liver is referred to as reverse cholesterol transport.

This transport is facilitates by the synthesis and secretion of apoprotein E by

peripheral tissues.

In addition to degradation by specific receptors, lipoproteins are also disposed

of by less specific pathways, some of which operate in macrophages and other

scavenger cells. When the plasma concentration of a lipoprotein rises, the rate of its

degradation by such pathways increases. This contributes to deposition of cholesterol

in macrophages of arterial walls (producing atheromas) and macrophages of tendons

and skin (producing xanthomas).



SAMEDARAKTA AND HYPERLIPIDAEMIA

The topic of the study is Samedarakta (i.e Hyperlipidaemia and Normal lipid

values). Here the term Samedarakta is coined for Lipidaemia. The lipids present in the

plasma in the abnormal or pathological condition like Hyperlipidaemia. So here in

this study medovriddhi laxanas have been taken for the study with respect to

Hyperlipidaemia.

Medovriddhi, Medoroga, and Sthoulya are synonyms. Here Medovriddhi was

main pathological phenomena of the disease. Hence it is necessary to explain about,

Nidana, Laxshanas, Samprapthi of Medovriddhi. These are explained as fallows.

Nidana

The law of nature say that without cause, affect is not possible. As per the

sequence of pathogenesis of disease given by Madhavakara and Vagbhat Nidana is

the first and foremost step for the manifestation of the disease and it gives the

particular knowledge about the pathogenesis of disease.

Table No. 21 showing the Nidana of Medovriddhi according to different

Acharyas. 172, 173, 174, 175,176

Nidana C.S. S.S M. N. B. P. Y. R. Ati sampoorana + - - - - Adhyashana - + - - - Kaphakarak ahara sevana - + + - + Guru,Seeta,Snigdha ahara sevana + - - - - Madhura rasa pradhana ahara + - - + - Adhika snehayukta ahara sevana + - - + - Avyayama + + + + + Divaswapna + + + + + Avyavaya + - - - - Harsha nityatwa + - - - - Achitana + - - - - Beeja swabhava + - - - -

Medovriddhi and Hyperlipidaemia - 69


• Adhyashana, Atimatra ahara and Atiamporana:

Improper consumption of food interns of quality, quantity and not abiding the

rules of intake of food Produces Ama and ultimately leads to the formation of adhura

annarasa, which intern forms Medovriddhi.

• Kaphakarak ahara sevana

Kaphakara ahara means Atiguru, Snigdha, Sheeta etc., guna pradhana ahara.

These gunas predispose aggravation of Kapha, ultimately Medadhatu Upachaya will

occurs. Meda is seat of shelshma. So Shelshmavardaka ahara can cause production

of excessive fat in the body by Ashrayashrayi bhava and samanyavriddhikarana

siddhanta. An excess of calories leads to eventually a large accumulation of fat.

• Madhura rasa pradhana ahara

Madhura rasa is Apa and prithvi mahabhoota predominant leading to vriddhi

of samanagunas ie., Kapha and Meda. By this Medovriddhi will occur. Biochemically

madhura rasa dravyas comes in the category of carbohydrates more and less fat.

Carbohydrates when metabolized get converted into fat for the purpose of deposition

and storage leading to Medovriddhi.

• Avyayama

A person, who will not does physical exercise, lives luxuriously with

sedentary life style will always tend to accumulate Kapha dosha and then Meda dhatu

in the body. This leads to Medovriddhi in the long course of time. Along with

madhura, sheeta, snigdhadi ahara, if person not does exercise will leads to

Medovriddhi.



• Divaswapna

Day sleep is the major santarpaka hetu hence this will lead to kaphavriddhi.

During sleep the BMR will be minimal and the energy for the body is also minimal

and probably there are greater chances of accumulation of energy, especially in the

form of adipose tissue in the body, in turn increasing the bulk.

• Avyavaya: It is also a kind of physical work. If person not indulging in vyavaya leads to

dhatu pusthi and also Shukra is seat for Kapha. Hence due to samana guna vriddhi,

leads to Medovriddhi.

• Beeja swabhava: Chakrapani clearly told that “ati sthula mata pitra souitha sukra swabhavat”

means the character of Medhovriddhi is inherited from obese parents.

• Harsha nityatwa and Achintana:

Psychological factors play an important role in the manifestation of

Medoroga. Achientana can be divided as the complete relaxed psychological mode of

the person or tranquility of mind which always helps in the nourishment of body

and may leads to Medoroga and secondly can be considered as a depression state of

the mind,in that time person does not want to think and tend to eat more as a

compensatory mechanism and become obese.



RUPA :

The symptomatology of Medoroga is asserted by Acharyas in broad manner,

to understand them, need to elaborate as follow.

Table No. 22 showing Roopa of Medoroga177, 178, 179, 180,181

Roopa C.S. S.S A.H M. N. B. P.Chala Spik, Sthana, Udara + - + + - Ayurhasa + - + + - Javoparodha + - - - - Krichravyavayata + + + + + Dourbalya + - + + - Dourghandhyata + + + + + Swedadhikyata + + + + + Atikshudha + + + + + Atipipasa + + + + + Atinidra - + - + + Krathana - + - + + Gadgadhatwa - + - + + Soukumarata - - - + -

• Spik, sthana udara vriddhi

Madhuratara ama annarasa produced will be responsible for Medo Dhatwagni

mandyata leading to Medovriddhi in the body. The seat of meda is Udara, Spik,

Sthana hence increased meda accumulates more at these places and leads to Udara,

Spik, Sthana Vriddhi.

• Dourgandhyav and Atiswedha

Sweda is the mala of Medodhatu. When Medodhatu is excessively formed

and deposited in the body. The mala of Medodhatu i.e., sweda is also excessively

formed leading to swedadhikyata. As dustha meda is Amagandhi in nature. Hence it

gives bad odour and also due to excessive sweat produces dourgandhya in the body.



• Kshudra swasa and Krathana

An increased amount of fat in the chest wall and abdomen has an effect on the

mechanical properties of the chest to diaphragm and leads to an alteration of

respiratory excretion during inspiration and expiration.

• Ayushohrasa :

The other dhatus do not grows to the extent that of the fat grows in Medashi

persons hence it shortens the life span.

• Javoparodha (lethoergy) :

The deficient co-ordination, shaitilyata, Gurutwata of Meda may causes

Medaroga with slowed down movement.

• Snigdhangata :

As the Medodathu and Kaphadoshas are having Sadharmya guna. Samana

gunas when combined will increases further in there gunas. Hence due to snigdhadi

gunas it gets Snigdhangata.

• Kasa:

Kapha dosha and Medodhatu are present in Ashrayashrayi bhava. So the

vitiated Meda will vitiates Kapha. This will in turn causes cough reflex.

• Krichravyavayata :

The deficient semen production and avarana of Meda to channels of Shukra

leads to poor sexual performance or difficulty in sexual act.

• Dourbalya (General debility) Weakness is the consequence of disturbed equilibrium of dhatus.



• Atikshadha and Atipipasa :

Due to Meda avarana leads to Vata vriddhi in kostha. This vitiated Vata

stimulates Jatharagni excessively, this leads to Agni sandhukshana. By this person

feels Atikshudha and Atipipasa.

• Atinidra :

It persons sleeps in day time. This will increases the Kapha due to this

accumulation of Meda will takes place and leads to Medovriddhi.

SAMPRAPTI GHATAKAS :

i. Tridosha : Kapha dominant, Vyanavayu, Samanavayu, Pachaka pitta

ii. Dushya : Rasa, Meda.

iii. Agni : Jataragni, Medodhatvagni

iv. Srotas : Rasavaha, Medavaha.

v. Srotodusti prakara : Sanga

vi. Agni : Jatharagni & medodhatwagnimandyajanya

vii. Udbhavasthana : Amashaya

viii. Sancharasthana : Rasayani

ix. Adhisthana : : Medodhara kala, Vapavaham

x. Vyaktasthana Specially Udara, Spika, Sthana

xi. Roga swabhawa : Chirakari

Dosha

Kapha : As Medoroga is considered as Kaphaja Nanathamaja Vyadhi. Due to

excessive intake of Guru, Snigdha, Madhura, Sheeta ahara and Viharas like

Divaswapna, Achintana etc., leads vitiation of kapha. Hence kapha is predominately

present as a Dosha.



Pitta

Due to Margavarodha by Medovriddhi, Sandukshana of Jataragni will takes

place. Hence person has excessive Jataragni.This is due to vitiation of Pitta.

Vata

Margavarodha causes inactiveness of Vyanavayu which in turns responsible

for the improper circulation and distribution of nutrients to the Dathus.

Due to Sanga in the Medovahasrotasa the nutrients cannot be carried out by

Vyanavayu to their respective Dhatus. Vitiated Samanavayu makes agni

sandhukshana and improper distribution of fat in the body.

Dushya

In this disease excessive production of abnormal Medadhatu is present. Here

Rasa, Meda, Mamsa, Majja, Shukra are Dushyas, as kapha is seated in all these dhatus

on the basis of ashryaashryibhava.

Srotas

Avyayama, Divaswapna, excessive intake of madhur dravyas are vitiating

factors for Medovaha srotodusthi as mentioned in Charaka samhita.

Agni

Tikshnagni is predominant feature due to vitiation of vata. In tikshnagni

condition if person consumes adhyashana, which leads to disturbance in agni and

subsequently formation of Ama may takes place, this leads to improper formation of

Dhatus.



Flow chart No. 2 SAMPRAPTHI

Due to Nidana

Vitiation of Kaphadi doshas

Spreads all over the body very quickly

Mixes with Medodhatu first because of Ashrayashrayi bhava and vitiates it

Vikruta poshaka Meda circulates all over the

body along with gatiyukta rasa, rakta

dhatu

Excessive accumulation of vikruta poshya meda

Vata dusthi in Kostha leading to Sandhukshana of Jataragni

Increase of Meda in Rasa (plasma) ie.,

Medovriddhi (raised level of lipids or fats in

the Plasma)

Rapid digestion of food and does crave for food

Medovriddhi does margavarodha for other dhatus

Accumulates in Spik, Sthana, Udara (Accumulation of depot fat)

Medoroga



CHIKITSA: 182

Shodhana karma is indicated in following condition of Medoroga as explained

by Vagbhata.

Snehana should not be administered in Medoroga but Tilataila is indicated.

(C.S.Su.13/5). Essential Mrudu swedana is indicated.

Those who are very obese, strong and having predominance of Pitta and

Kapha, those suffering from Amadosha, Jwara, Chardhi, Atisara Hrudaya rogas,

Vibhandha, Gaurava, Hrullasa conditions, Shodhana karma is adopted.

Those who are madhyama sthoulya, previously Deepana and Pachana drugs

are given then Shodhana karma is adopted.

Those who are Heena sthoola, Kshudita, Pipasita, those who are troubled by

increased doshas, madhyama and alpa bala persons by exposing them to breeze

sunlight and exercise should be administered but not the Shodhana.



HYPERLIPIDAEMIA

Lipoprotein disorder or dyslipidaemias are among the most common

metabolic diseases seen in clinical practice. They are important because they may

lead to number of sequel including CHD dermatological manifestations (xanthelasma

and xanthomata), pancereatitis and (more rarely) neurological and ocular anomalies.

Hyperlipidaemia is the excessive accumulation of lipid (especially plasma

lipids) in the body leading to acute or chronic condition.

Hyperlipidaemia refers to an increased concentration of either cholesterol or

Triglycerides or both lipids in the plasma. The elevation of lipid concentration in the

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

degradation of plasma lipids and lipoproteins.

ETIOLOGY

It includes both primary and secondary causes as follows:

1. Smoking >10 cigarettes, bidi / day.

2. Diabetes mellitus

3. Hypertension

4. Family history of premature CHD.

5. Excess Alcohol intake

6. chronic renal failure

7. drugs e.g., thiazides

8. beta adrenoceptor antagonists hypothyroidism

9. Nephritic syndrome



CLINICAL FEATURES

Hyperlipidaemia should be suspected from;

1. Xanthomas (cholesterol deposit in skin histicocytes located in buttocks,

pressure points, knees and elbows etc.,)

2. Xanthelasmas (cholesterol deposits in eyelids)

3. Premature arcus in cornea

4. Premature atherosclerosis

5. Attacks of pancreatitis

6. White and pale appearance of retinal vessels (lipemia retinalis).

CLASSIFICATION

A. Fredrickson Classification

Considering the raised levels of Triglyceride, cholesterol or both and the

Lipoprotein molecule which is excess in the circulation, hyperlipoproteinaemias have

been classified by Fredrickson into five major groups.

Table No. 23 Showing the Classification of Hyperlipidaemia

Lipoprotein Major elevation Lipid 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 Type III

Hyperlipoprotenemia Type IV VLDL TG Familial

Hypertriglyceridemia Type V Chylomicron

+ VLDL TG + Cholesterol APO C II deficiency



I. Type I Hyperlipoprotenaemia (Hyper Chylomicronaemia)

This autosomal recessive abnormality manifests itself in childhood as an

intolerance of dietary fat and failure to thrive. It presents clinically as a widespread

cutaneous popular rash, often accompanied by abdominal pain which may progress to

full blown pancreatitis. Plasma triglyceride values often exceed 50 mmol/1, reflecting

the increased amount of chylomicrons in the blood stream. In molecular terms, the

disease results from faulty operation of the plasma enzyme lipoprotein lipase, either

as a result of mutation in the lipase gene itself or because of a sequence defect in its

essential apoliporotein cofactor, apo CII, which normally circulates in association

with triglyceride – rich lipoproteins.

Secondary hyperchylomicronemia may occur in uncontrolled diabetes and in

dysprotenemia in multiple myeloma and macroglobenemia. High doses of cortico

steroids may induce lipaemia.

II. (a) Type II a Hyperlipoprotenaemia (Familial Hyper Cholesteremia )

This is the commonest type of primary disorder of cholesterol metabolism

where plasma LDL levels may rise up to 4 to 5 folds in heterozygotes and 6 to 8 folds

in homozygotes as a result of LDL receptor defect.

Plasma triglyceride levels and HDL cholesterol levels are normal or reduced.

As would be expected with a decreased number of LDL receptors, the fractional

clearance of LDL apo B is decreased. LDL production is increased because more

VLDL and more IDL are secreted by the liver and more LDL particles are converted

to LDL rather than taken up by the hepatic LDL receptors.

Besides premature Atherosclerosis and CAD, which manifest as early as the

fourth decade of life, xanthomas over the Achilles and other tendons as well as over



bony prominences (knuckle legs, elbow, knee, etc) on the dorsal aspect of the

extremities holds the clinical diagnosis of FHC. Theses xanthomas are soft to firm,

nodular structures incorporating macrophage laden with cholesterol. Similarly, these

cells can get deposited at many other sites like the soft tissue of the eyelid

(xanthelasma) within the cornea (arcus corneae) buttocks, inter digital webs of hands,

etc.,

The homozygous form of FH occurs in one out of 1 million individuals and is

associated with plasma cholesterol levels > 13 mmol/L (>500 mg/dL), large

xanthelesmas, and prominent tendon and planar xanthomas. These individuals have

an aggressive, premature CHD that can be manifested in childhood.

II. (b)Type II b Hyperlipoprotenaemia (Familial Combined Hyperlipidaemia)

FCHL is inherited as an autosomal dominant disorder, and the initial case

discovered within a family may have combined Hyperlipidemia isolated

hypertriglyceridemia, or isolated elevated levels of LDL cholesterol.

Interestingly there is no Hyperlipidaemia in childhood nor do xanthomas

develop, but young adults suffering from FCHL may manifest with mild

hypercholesteremia, triglyceridaemia or both. The diagnosis is often prompted when

an individual has mixed Hyperlipidaemia with changing patterns of lipids in the

blood. The prevalence of impaired glucose tolerance / diabetes mellitus,

hyperuricaemia and obesity is more frequent in these subjects. Almost half of the first

degree relatives manifest with lipid abnormalities at some point of time. The lipid

abnormality could be types lla, IV or IIb.



III. Type III Hyperlipoprotenaemia (Broad β Hyperlipoprotenemia)

Transmitted as a single gene defect, this leads to partial catabolism of VLDL

with consequent accumulation of remnants in plasma; this leads to rise in both

cholesterol and Triglycerides. This disorder is also know as “Familial

dysbetalipoproteinaemia”. The genetic defect is in the gene that encodes the structure

of Apo E. Coexistent diabetes mellitus, Hypothyrodism and obesity are seen in many

patients with this lipid disorder. Patients present with xanthoma distributed as streaks

on the palmar creases and inter digital space, as also tuberous swellings over the

dorsal aspect of the body. Glucose intolerance and obesity occur sooner or later.

Diabetes Mellitus and Hyperthyroidism are the commonest causes of secondary Type

- III HLP.

IV. Type IV Hyperlipoprotenaemia (Hyper Pre β Lipoprotenemia)

This disorder is characterized by isolated increase in TG rich VLDL in

plasma. Unlike Type I a, Hypertriglyceredemia is endogenous and not dependent on

dietary fat intake. There is increase in the synthesis and release of VLDL from the

Liver as well as inadequacy of catabolism in the peripheral tissues. Although

inherited as autosomal dominant expression of the trait appears to depend on certain

promoting factors such as glucose intolerance, Hyperinsulinaemia, 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 is difficult to assess in view of

high incidence of diabetes, obesity and hyperuricemia among these patients.

Pancreatitis may develop during the period of exacerbation.



V. Mixed Hypertriglyceridemia (Type V - HLP)

This is a rare disorder manifests as combination of abnormalities of Type I and

Type IV HLP. Lipaemia is due to excess production of endogenous VLDL and

defective removal of exogenous chylomicrons may be because of LPL deficiency.

This disease is may be familial or sporadic. In the familial 50% of the adult relatives

of the patients have Hypertriglyceridemia. There is often genetic overlap between

Type IV and V HLP. The disorder manifest in adult life with Hepatospleenomegaly,

recurrent abdominal pain and Xanthomatous eruptions. Obesity, glucose intolerance

and premature vascular disease are common concomitants. Secondary Type V HLP is

observed in uncontrolled Diabetes, Hypothyroidism, Nephrotic syndrome and Gout.

B. CLASSIFICATION ACCORDING TO PRACTICAL POINT OF VIEW

From a practical point of view it is now more usual to divide the

Hyperlipideamia according to the pattern of abnormality on blood testing, namely

hyperceholesterolaemia, hypertiglyceridaemia or mixed hyperlipidaemia.

Hyperceholesterolaemia

Elevated levels of fasting plasma total cholesterol in the presence of normal

levels of triglycerides are almost always associated with increased concentrations of

plasma LDL cholesterol (type IIa) since LDL carries about 65 to 77 percent of total

plasma cholesterol. The rare patient with markedly elevated HDL cholesterol may

also have increased plasma total cholesterol levels. Elevations of LDL cholesterol

can result from single gene defects, polygenic disorders, and secondary effects of

other disease states.



Hypertriglyceridaemia

The diagnosis of Hypertriglyceridaemia is made by determining levels of

plasma lipids after an overnight fast. Because of the less certain association of

Triglycerides with CHD, plasma concentration greater than the 90th or 95th percentile

for age and sex have been used to define Hypertriglyceridaemia. Isolated elevations

of plasma triglycerides can be due to increased levels of VLDL and Chylomicrons

(type IV) or combination of VLDL and Chylomicrons (type V). Rarely only

Chylomicron levels are elevated (type I). Plasma is usually clean when Triglyceride

levels are < 4.5 mmol /L (<400 mg/dL) and becomes cloudy when levels are higher

and VLDL (and / or Chylomicron) particles become large enough to diffuse light.

When Chylomicrons are cold for several hours. Tendon xanthomas and xanthelasma

do not appear but small orange – red papules, can appear on the trunk and extremities

when triglyceride levels are > 11 mmol/L (>1000 mg/dL) (i.e., when

Chylomicronemia is present).



Drug Review - 85

DRUG REVIEW:

The Present study has been carried out to evaluate the effect of Arohana

Snehapana in Samedarakta with special reference to Hyperlipidaemia and normal

lipid values. Murchita Tilataila is the cheapest medicated Tilataila available; hence

this was selected as a Snehana Dravya.

The following drugs were used in this study:

1. Panchakola Churna (For Amapachana)

2. Murchita Tilataila (For Arohana Snehapana and Abhyanga)

I. Panchakola Churna :188

The ingredients of Panchakola Churna are

Pippali,

Pippali Mula,

Chavya,

Chitraka and

Shunti.

II. Murchita Tilataila:189

Drugs for murchana of Tila taila are

Manjistha - 1/16th part

Haritaki - 1/64th part

Vibhitaki - 1/64th part

Amalaki - 1/64th part

Mustha - 1/64th part

Haridra - 1/64th part

Lodra - 1/64th part

Vatankura - 1/64th part

Hrivera - 1/64th part

Nalika - 1/64th part

Ketakipushpa - 1/64th part

Tila taila - 1 part

Jala - 4 part

Table No. 24 showing the Pharmacodynamics of Ingredients of Panchakola choorna : 190, 191, 192, 193

Drug Family Name Latin Name Paryaya nama Rasa Guna Virya Vipaka Dhoshagnatha Karma Useful part

Pippali Piperaceae Piper longum Magadi, Vaidehi, Kana, Krishna

Katu Laghu, Snigdha, Tikshna

Anushna sheeta

Madhura Vatakaphahara Deepana, Vatanulomana

Phala, Moola

Pippali moola

Piperaceae Piper longum Magadi,Vaidehi, Kana, Krishna

Katu Laghu, Ruksha

Ushna Katu Kaphavatahara Deepana, Pachana, Anaha prashamana

Moola

Chavya Piperaceae Piper retrofractum Chavika Katu Laghu, Ruksha

Ushna Katu Kaphavatahara Deepana, Pachana Shoolaprashaman

Twak, Moola

Chitraka Plumbaginaeceae Plumbagozyelenica Agni, Jyoti, Shardula

Katu Laghu, Ruksha, Sheeta

Ushna Katu Kapha vata Shamaka

Deepana, Pachana, Pittasaraka, Grahi

Moola Twak

Nagara Zingiberaceae Zingiber officinalis Shunti, Mahoushadha

Katu Laghu, Ruksha

Ushna Madhura Kapha vata Shamaka

Trptighna, Rochana, Deepana, Pachana

Kanda

Drugs Chemical composition

Pippali Essential oil, caryophyllene, piperine, piplartine, piperlongumine, piperlognuminine, pipernonaline, pipercide, sesamin, β-sitsterol.

Pippali moola Essential oil, piperine, piplartine, piperlongumine, piperlognuminine, pipernonaline, pipercide, sesamin, β-sitsterol.

Chavya Piperine, sitosteral, piplatine. New amides – retrofractamide A, B, C & D isolated from aerial parts.

Chitraka Chitranone plumbagin, 3-chloroplumbagin, drosesone, elliphinone, isozeylinone, isozeylan – one, maritone, plumbagic acid, β- silosterol

Nagara Zingiberol, Zingerone, gingerols, paradol, gingerenone A, ginger glyeolipids A, B & C, gingerdiol, gingerone B & C etc.,

86

Table No. 25 Showing Pharmacodynamics of Drugs Used For Moorchana of Tilataila.194, 195, 196, 197, 198, 199, 200, 201, 202, 203, 204

Drug Family Name Latin Name Paryaya nama Rasa Guna Virya Vipaka Dhoshagnatha Karma Useful

part Manjistha Rubiaceae Rubia

Cordifolia Yojanavalli, Rakthangi, Vastrabhushana

Madhura Kashaya

Guru Ushna Madhura Kaphanashaka Rakth prasadaka Kanda

Haritaki Combretaceae Terminalia chebula

Abhaya, Pachani, Shiva

Lavana Varjita Kashayapradhana Pancha Rasa

Laghu Ruksha

Ushna Madhura Tridoshahara Deepana, Pachana, Anulomana, Rechana

Phala

Vibhitaki Combretaceae Terminalia bellirica

Karshaphala, Aksha, Kalidruma

Kashaya Laghu Ruksha

Ushna Madhura Tridoshanara, Especially Kaphahara

Deepana, Anulomana

Phala

Amalaki Euphorbiaceae Emblica Officinalis

Shriphala, Gayatri

Lavana Varjita Amlapradhana Pancha Rasa

Guru Ruksha, Sheeta

Sheeta Madhura Tridoshahara Deepana, Pachana, Anulomana, Rasayana

Phala

Mustha Cyperaceae Cyperus rotundus

Varida, Mustaka

Tikta, Katu Kashaya

Sheeta Sheeta Katu Kaphapitta Shamaka

Deepana, Pachana, Grahi, Mutrala

Kanda

Hardira Zingiberaceae Curcuma longa

Kanchani, Nisha, Krimighna

Titka, katu Ruksha, Laghu

Ushna Katu Tridoshahara Ruchya, Anulomana, Pitta Rechaka.

Kanda

Lodra Symplocaceae Symplocos recemosa

Sthulavalkala Kashaya Laghu, Ruksha

Sheeta Amla Kaphapitta shamaka

Shothahara, Kustagni, Raktastambana, Vrunaropana, Stambana

Twak

Vatankura Moraceae Ficus bangalensis

Nyagrodha, Bahupada

Kashaya Guru Ruksha,

Sheeta Katu Kaphapitta shamaka

Shothahara, Raktashodhaka, Vrunaropana, Chakshushya

Twak, kshira, patra, phala

Ketakipushpa Pandanaceae Pandanus odorotissimus

Suchipushpa Tikta, Madhura, katu

Lagu Snigdha

Ushna Katu Kaphapitta shamaka

Varnya, Vedanastapaka, Vrunaropana, Keshya , Dourgandhyahara

Pushpa, Mula

88

Hrivera* (Rasna)

Compositae Pluchea lanceolata

Sugandha, Gandhanakuli, Nakuli, Ishwarimoola

Tikta Guru Ushana Katu Kaphapitta shamaka

Shotahara, Vedanashaymak, Raktashodhaka, Rasayana

Patra

Nalika** (Tamala patra)

Lauraceae Cinnamomnm tamala

Naluka, Tamala patra, Teja patra

Katu Tikta madhura

Laghu, Ruksha, Teekshana

Ushana Katu Kaphapitta shamaka

Lekhana, Raktashodhaka, Sleshmahara

Twak, Taila, patra

Drugs Chemical composition Manjistha Anthraquinones manjistin, purpuroxanthin, rubiatriol, rubi coumaric acid, rubifolic acid, rubiadin, rubimallin, purprin, Haritaki Chebulinic acid, tannic acid, terchebin, vit C, behenic, lindeic, oleic, palmitic and stearic acids, chebulin. Vibhitaki Fructose, galactose, glucose, mannitol, edible oil, gallic acid, chebulagic acid, ellagic acid. Amalaki Ellagic acid, oleanolic, aldehyde, tannin vit C, phyllemblin, linolic acid, acetic acid, ellagic acid, phyllemblic acid and salts. Mustha Cyperenone, Cyperen, Cypertundone, cyperol, cyperolone, isocyperol, mustakone, rotundone, sugenol, β- sitosterol. Hardira Curcumene, curcumenone, curcone, curdione, cineole, curzorenone, eugenol, comphene, camphor, curcumins. Lodra Symposide, loturine, loturidie, colloturine Vatankura Leucoanthocyanin, tiglic acid, β - sisterol – a – d - glucoside Hrivera Kwarsitin, isoramnitin, pluchin. Nalika Cinnamaldehyde, Eugenol, Yuginal, fixed oil. Ketakipushpa Sughandita taila. Note : Hrivera* The Synonyms of Rasna mentioned in Nigantus are Hrivera, Nakuli, Gandhanakuli, Ishwarimoola, Note : Nalika** Indian Taj = Cinnamomum Tamala (Lauraceae) is known is Bengal as Naluka its leaves are known as Teja patra or Tamala Patra. Brihatrayi have mentioned as only Nalika. 205

89


Drug Review - 91

TILA: 206, 207

Family : Pedaliaceae

Latin Name : Seasamum indicum

Charaka : Svedopaga,

English : Sesamum seeds

Hindi : Til

Kannada : Yellu

Habitat :

This is small bush bearing white or light pink coloured flowers is indigenous

to India and extensively cultivated in the warmer region.

Varieties :

Three varieties of seasmum seeds are found: black, white and red or brown.

The black variety is the most common and yields the best quality of oil and is best

suited for medicinal purposes. But white variety is richer in oil.

Constituents :

Seeds contain fixed oil 50 to 60 percentage (White varieties 48%, black and

red varieties about 46%)

Analysis:

Moisture Oil Black Til 2.0 to 5.2 % 44.6 to 56.9 % Red Til - 45.7 to 55.5 % White Til 2.0 to 4.4 % 44.9 to 58.2 %

Oil contains 70% of liquid fat of the glycerides of oleic and linolic acids and 13

to14% of solid gats, stearin, palmitin and myristin, and crystalline substance and a

phenol compound seasamol.


Drug Review - 92

Method of preparation :

Seasame seeds contains about 50% of fixed oil. They are cleaned in

necessary, washed sundried and expressed to yield oil at room temperature.

Subsequently the temperature and pressure are raised. The oil is purified by refining

method and used.

Identification :

Badouin’s test : Shake 2ml of sesame oil with 1m of 1% of solution of sucrose

in hydrochloric acid . A pink or red colour is produced due to seasamol.

Description

Colour : Pale yellowish liquid.

Odour : Slight characteristic

Taste : Bland

Solubility : It is slightly soluble in alcholo.

Pharmacological properties

Rasa : Madhura, Anurasa : Kashaya, tikta

Vipaka : Mashura

Virya : Ushna

Guna : Guru snigdha

Doshaghnata : Vata Kapha shamaka

Karma : Agneya, Bhrimanakaraka, Indriyamanaatmatrupti,

Twaka prasadana, mamsasthirata, varna

balakarak, amadosha pachaka, kriminashaka.

Uses : Seeds are laxative, emollient and demulcent,

diuretic, nourishing, lactagogue and

emmenagogue.

Useful part : Seeds.


MATERIALS:

The materials taken for the clinical study were

1. Panchakola Choorna (Ama pachana)

2. Murchita Tila taila (Arohana snehapana and abhyanga)

1. Panchakola Choorna:

The ingredients of Panchakola Choorna were Pippali, Pippalimoola, Chavya,

Chitraka and Nagar. All are taken in equal quantity and powdered well. Filtered

through cloth and made into fine powder. Panchakola Choorna was prepared in

Department of Rasashastra D.G.M.A.M.C, Gadag.

2. Murchita Tilataila :

Tila taila was purchased from the local market and taila moorchana was done

in Department of Rasa Shastra D.G.M.A.M.C, Gadag.

Drugs for murchana of Tila taila are

Manjistha - 1/16th part Haritaki - 1/64th part

Haridra - 1/64th part Vatankura - 1/64th part

Hrivera (Rasna)- 1/64th part Nalika - 1/64th part (Tamala patra)

Ketakipushpa - 1/64th part Lodra - 1/64th part

Vibhitaki - 1/64th part Amalaki - 1/64th part

Mustha - 1/64th part Tilataila - 1 part

Jala - 4 part

Collections of drugs:

All the raw drugs were purchased from the local market Gadag.

Methodology - 93


Method of preparation :

Tilataila is heated over mandagni till the foam and sound is subsided

(phenashamana) then vessel is taken out from the fire. Above mentioned drugs are

made into coarse powder form, then made into kalka form by adding little amount of

water, then this kalka and mentioned quantity of water is added to Tilataila and heated

for making paka tillo attaining the Taila siddha laxanas. Then vessel is taken out from

the fire and Taila is filtered. Such Murchita Tilataila is not possess any durgandha

and it is having its own specific colour and odor.

METHODS: CLINICAL STUDY:

1. Sources of data:

The healthy voluntaries who were desirous to undergoing Shodhana therapy

for maintaining good health and patients of either sex suffering from Hyperlipidaemia

(i.e., raised Serum Cholesterol or Serum Triglycerides or both) were selected from the

OPD & IPD of D.G.M.A.M.C Hospital, Gadag.

The voluntaries and patients were selected on the basis of pre-selection

interview proforma specially designed for the purpose.

2. Selection of Individuals

Out of 36 individuals, 30 individuals of Samedarakta (15 patients of

Hyperlipidaemia and 15 voluntaries of Normal lipid value) with confirmed diagnosis

were selected.

The selection of healthy voluntaries was done as follows

i. Presently not suffering from any disorders. i.e. Healthy persons.

ii. Routine Blood and Urine investigations showing normal limits.

iii. A clinically performed physical and mental examination reveals no

significant findings.

Methodology - 94


Desirable Criteria:

Feeling appetite in proper time, Proper digestion at proper time, Proper

evacuation of nature urges, Feeling lightness of body, Feeling alert and interested in

duties/ activities, Getting sound sleep regularly and feeling satisfaction of sleep.

Selection of Hyperlipidaemic cases were done as follows

Patients with raised Serum Cholesterol or Serum Triglycerides or both were

selected for the clinical study.

Investigations:

• Lipid profile was done as mandatory test before and after the treatment in

local diagnostic Laboratory, Gadag.

• Like Hb%, TC, DC, ESR, RBS as routine tests were done from D.G.M.A.M.C

Laboratory, Gadag.

3. Inclusion criteria:

The patients suffering from only Primary Hyperlipidaemia and who are fit for

Snehana karma and Pradhana karma were selected in Group A.

The voluntaries with Normal Lipid Values who were desirous to undergo

Shodhana therapy were selected in Group B.

Only those in whom Samyak snigdha laxanas appeared within Snehapana Kala

were included.

Persons between the age group of 20 to 60 years of both sexes were selected.

4. Exclusion criteria:

Secondary Hyperlipidaemia patients were not included eg. Hypothyroidism,

Diabetes mellitus etc.

Persons unfit for Snehana karma and Shodhanakarma were excluded.

Severe form of other systemic disorders.

Methodology - 95


5. Grouping:

Total number of cases selected for the present study were 30. The cases were

divided into 2 Groups, Group A and Group B each consisting of 15 individuals

Group A- 15 patients of Hyperlipidaemia.

Group B- 15 voluntaries of Normal Lipid Values (Healthy persons)

Study design: Prospective clinical study

Sample size: 30 samples

Study durations: 15 days and fallow up 15 days.

Intervention:

All the individuals were administered with Panchakola churna 3-6 gms as

Ama pachana ½ hour before food with hot water till appearance of nirama lakshanas

or 3 -7 days.

• In the both groups, individuals were given test dose (30 ml) of Murchita

Tilataila at around 6.00 to 7.00 am. The second day onwards Murchita

Tilataila was administered in Arohana Krama (increasing dosage). The

increase (Arohana) per day was decided on the basis of Jiryamana, Jirna

lakshana etc. Thus the increase was not fixed and the dose schedule was

variable from person to person. After attainment of Samyak Snigdha

lakshanas individuals were subjected to Shodhana karma.

Procedure of Snehapana:

• Individuals were instructed to take Drava, Ushna, Anabhishyandi,

Pramanayukta Bhojana at night on the day before Snehapana.

• Early morning on the day of Snehapana after going through routine urges,

Jirna ahara lakshana (but Akshudhita Avastha) was assessed. Then at 6.00 to

Methodology - 96


7.00 a.m. individuals with a fresh mind, enthusiasm, courage, by preying God,

the dose of Murchita Tilataila was administered. Hot water was given as an

Anupana followed by Tilataila intake.

• Individuals were instructed to follow Pathyapathya as explained in Snehapana

vidhi chapter.

• Individuals were instructed not to take any type of food until he/she feels

hungry.

• During those days individuals were given light diet like Peya, Rice and

Rasam.

• The duration of Jiryamana Lakshana as well as the time required for

appearance of Jirna Lakshana was assessed.

The individuals were observed for Samyak Snigdha Lakshana daily. After

getting Samyak Snigdha Lakshanas, Snehapana was stopped and then individuals

were subjected for Shodhana Karma.

6. Parameters for Assessment of Treatment:

The individuals of both the groups were assessed for Samyak Snigdha laxanas

on the basis of Subjective Parameters and assessed for results on the basis of

Objective parameters.

Samyak Snigdha Lakshanas :

The following subjective criteria were considered for assessment of Samyak

Snigdha Lakshanas.

• Vatanulomana - Assessed by normal expulsion of flatus, feces

and Urine.

• Diptagni - Based on the time and Dose of Sneha.

Methodology - 97


• Asamhata Varcha - Based on the loose consistency of the faeces.

• Snigdha Varcha - Confirmed by Greasy / Sticky stool, floating of

fatty stool over water. Sense of oiliness over the

fingers on washing after defecation (Enquired

from the Volunteers)

• Twak Snigdhata - Assessed by comparing the touch, luster and

texture of skin before, during and after Snehana.

• Glani - It was assessed by presence of exhaustion /

fatigue / debility or weakness

• Anga Laghava - By enquiring with the Volunteers.

• Snehodvega - Confirmed by presence of aversion

towards Snehapana

OVER ALL ASSESSMENT OF RESULTS:

Results of Arohana snehapana with Murchita Tilataila, who had Samyak

snigdha laxanas, assessed mainly on the bases of changes in the Serum lipid values as

mentioned below.

Increased Abnormality :

o Any one or more Serum Lipid values i.e. i) Serum Cholesterol, Serum

Triglycerides, LDL, and VLDL values should increase ( No values

should decrease apart from normal limits ) and /or ii) HDL value

should decrease (Its values should not increase apart from normal

limits).

o Some values may be within normal limits.

Methodology - 98


Decreased Abnormality :

o Any one or more Serum Lipid values i.e. i) Serum Cholesterol, Serum

Triglycerides, LDL, and VLDL values should decrease ( No values

should increase apart from normal limits ) and/or ii) HDL value should

increase (Its values should not decrease apart from normal limits).

o Some values may be within normal limits.

Normal Limits:

All the Serum Lipid values should present within the normal limits

irrespective of increase or decrease in the Lipid values.

Variable :

All the persons who do not come under above three criteria were fall under

this criteria.

7. Statistical Analysis

For better understanding the effect of Shodhana Poorva Arohana Sehapana on

Lipid profile, 2 groups were made.

Group A consists of Hyperlipidaemic patients, Group B consists healthy

individuals. Both the groups received same medication i.e., Ama pachana done with

Panchakola choorna 6 grams and Snehapana with Murchita Tilataila and then

necessary Shodhana procedures were done according to the need.

Statistical analysis was done for serum lipid profile before and after

Snehapana procedure. Analysis was done by calculating Mean, Standard deviation

(SD), Standard error (SE) and‘t’ value and ‘p’ value.

Methodology - 99


OBSERVATIONS:

In the present Observational study 30 individuals were registered to evaluate

the efficacy of Shodhananga Arohana Snehapana on Samedarakta (Hyperlipidaemia

and normal lipid values). The prevalence of age, sex, socioeconomic status, Vyayama

Shakti etc. was observed. The details of which are as follows-

Table No. 26 Age wise Distribution of the Sample

Age Group Group A % Group B % 20–30 Years 0 0 7 46.62 30- 40 Years 8 53.28 2 13.32 40–50 Years 5 33.30 3 19.98

50 – 60 Years 2 13.32 3 19.98

Age: Group A (Hyperlipidaemia) : Among 15 patients, 8(53.28%) patients in

group 30 – 40 Years, 5 (33.30%) in group 40- 50 Years, 2 (13.32%) in group 50- 60

Years age group. GroupB (Narmolipidaemic) : Among 15 healthy persons,

7(46.62%) persons in group 20-30 Years, 2(13.32%) persons in group 30 – 40 years, 3

(19.98%) persons in group 40- 50 Years and 3(19.98%) persons in group 50- 60

Years age group.

0

46.62%

53.28%

13.32%

33.3%

19.98%

13.32%

19.98%

0

10

20

30

40

50

60

20–30 30- 40 40–50 50 – 60

Group AGroup B

Graph 1 :

Results - 100


Results - 101

67%

33%

Group B

40%

60%

MaleFemale

86.58%

13.32%

0

86.58%

6.66% 6.66%

0102030405060708090

Group A Group B

HinduMuslimChristian

Table No. 27 Sex wise Distribution of the Sample

Gender Group A % Group B %

Male 10 66.60 6 39.96 Female 5 33.30 9 59.94

Sex : GroupA (Hyperlipidaemia) : Out of 15 patients 10 (66.60%) were male and 5

(33.30%) were female patients. GroupB (Narmolipidaemic) : Out of 15 persons

9(59.94%) were female and 6 (39.96%) were male patients.

Graph 2 : Group A

Table No. 28 Religion wise Distribution of the Sample

Religion Group A % Group B % Total % Hindu 13 86.58 13 86.58 26 86.66

Muslim 2 13.32 01 6.66 03 10.00 Christian 0 0 01 6.66 1 3.33

Religion : GroupA (Hyperlipidaemia) : Out of 15 patients 13 (86.58%) were from

Hindu and 2(13.32%) patients were from Muslim. GroupB (Narmolipidaemic) : Out

of 15 persons 13 (86.54%) were from Hindu, 1(6.66%) was from Muslim and 1

(6.66%) was from Christian religion.

Graph 3:


Table No. 29 Occupation wise Distribution of the Sample

Occupation Group A % Group B % Total %

Labour 02 13.32 7 46.62 9 30.00

Student 0 0 4 26.64 4 13.33 Executive 04 26.64 2 13.32 6 20.00 Sedentary 09 59.94 2 13.32 11 36.66

Occupation: GroupA (Hyperlipidaemia) : Out of 15 patients 9 (59.94%) were

Sedentary 4(26.64%) patients were Executive and 2(13.32%) were labour. GroupB

(Narmolipidaemic): Out of 15 persons 7 (46.62%) were Labour, 4(26.64%) were

student, 2(13.32%) were Executive and 2 (13.32%) were Sedentary.

13.32%46.62%

026.64%

26.64%13.32%

59.94%13.32%

0 10 20 30 40 50 60

Labour

Student

Executive

Sedentary

Group BGroup A

Graph 4:

Table No. 30 Marital status wise Distribution of the Sample.

Marital status Group A % Group B % Total %

Married 15 100 11 73.26 26 86.66

Un married 00 0 04 26.64 04 13.3

Marital Status : GroupA (Hyperlipidaemia) : Out of 15 patients 15 (100%) were

Married GroupB (Narmolipidaemic): Out of 15 persons 11 (73.26%) were Married

and 4(26.64%) were unmarried.

Results - 102


Results - 103

13.32%

73.26%

13.32%6.66%

79.92%

13.32%

0

10

20

30

40

50

60

70

80

Group A Group B

Poor ClassMiddle classHigher class

Group B

60%

40%VegetarianMixed

Group A

33%

67%

Table No. 31 Socio Economical Status wise Distribution of the Sample

Socio Economical Status Group A % Group B % Total %

Poor Class 02 13.32 01 6.66 03 10 Middle class 11 73.26 12 79.92 23 76.66 Higher class 02 13.32 02 13.32 04 13.33

Socio Economical Status : GroupA (Hyperlipidaemia) : Out of 15 patients, 11

(73.26%) were belongs to Middle Class, 2(13.32%) were belongs to Poor Class and

2(13.32%) were belongs to Higher class. GroupB (Narmolipidaemic): Out of 15

persons 12 (79.92%) were belongs to Middle Class, 2(13.32%) were belongs to

Higher Class and 1(6.66%) was belong to Poor class.

Graph 5:

Table No. 32 Type of Diet wise Distribution of the Sample

Type of Diet Group A % Group B % Total %

Vegetarian 05 33.30 09 59.94 14 46.66

Mixed 10 66.60 06 39.96 16 53.33

Type of diet: GroupA (Hyperlipidaemia) : Out of 15 patients 10 (66.60%)

were Mixed Diet & 5(33.30%) were Vegetarian. GroupB (Narmolipidaemic): Out of

15 persons 9(59.94%) were Vegetarian and 6(39.96%) were Mixed Diet.

Group 6 :


Table No. 33 Diet Pattern wise Distribution of the Sample.

Diet Pattern Group A % Group B % Total % Samashana 11 73.26 11 73.26 22 73.33 Adhyashana 3 19.99 02 13.32 05 16.66

Vishamashana 1 6.66 02 13.32 03 10

Diet Pattern: Group A (Hyperlipidaemia) : Out of 15 patients, 11 (73.26%) had

Samashana Diet, 3(19.99%) had Adhyashana Diet & 1(6.66%) had Vishamashana

Diet. Group B (Narmolipidaemic): Out of 15 persons, 11(73.26%) had Samashana

Diet, 02(13.32%) had Adhyashana Diet and 02(13.32%) had Vishamashana Diet.

Table No. 34 Nature and Character of food wise Distribution of the Sample.

Nature of food Group A % Group B % Total %

Sammishra 08 53.28 11 73.26 19 63.33 Snigdha Pradhana 07 46.62 02 13.32 9 30 Ruksha Pradhana 0 0 02 13.32 2 6.66

Nature and Character of food: Group A (Hyperlipidaemia) : Out of 15 patients

08(53.28%) were taking Sammishra ahara, 7(46.62%) were taking Snigdha Pradhana

ahara. Group B (Narmolipidaemic): Out of 15 persons 11(73.26%) were taking

Sammishra ahara, 02(13.32%) were taking Snigdha Pradhana ahara and 02(13.32%)

were taking Ruksha Pradhana ahara.

53.28%46.62%

0

73.26%

13.32%13.32%

0

10

20

30

40

50

60

70

80

Group A Group B

SammishraSnigdha PradhanaRuksha Pradhana

Graph 7 :

Results - 104


Table No. 35 Nature of work wise distribution of the Sample.

Nature of work Group A % Group B % Total % Day 13 86.58 14 93.24 27 90.00

Night 02 13.32 1 6.66 3 10.00

Nature of work : GroupA (Hyperlipidaemia) : Out of 15 patients 13(86.58%)

were day workers & 2(13.32%) were night workers. GroupB (Narmolipidaemic): Out

of 15 persons 14(93.24%) were day workers and 1(6.66%) was night worker.

Table No. 36 Sleep wise distribution of the Sample.

Sleep Group A % Group B % Total % Sound 13 86.58 14 93.24 27 90

Disturbed 2 13.32 1 6.66 3 10

86.58%

13.32%

93.24%

6.66%

0

1020304050607080

90100

Group A Group B

SoundDisturbed

Sleep : GroupA (Hyperlipidaemia) : Out of 15 patients, 13(86.58%) had

sound sleep and 2(13.32%) had disturbed sleep. GroupB (Narmolipidaemic): Out of

15 persons, 14(93.24%) had sound sleep and 1(6.66%) had disturbed sleep.

Graph 8 :

Table No. 37 Vyayama wise distribution of the Samples.

Vyayama Group A % Group B % Total % Yes 5 33.30 12 79.92 17 56.66 No 10 66.60 3 19.98 13 43.33

Vyayama : GroupA (Hyperlipidaemia) : Out of 15 patients, 10(66.60%) were

doing vyayama & 5(33.30%). GroupB (Narmolipidaemic): Out of 15 persons,

12(79.92%) were doing vyayama and 3(19.98%) were not doing vyayama.

Results - 105


Table No. 38 Vyasana wise distribution of the Samples.

Vyasana Group A % Group B % Total % Alcohol 3 19.98 2 13.32 5 16.66 Smoking 4 26.64 0 0 4 13.33

Tobacco chewing 2 13.32 4 26.64 6 20 No habit 6 39.96 9 59.94 15 50

Vyasana : GroupA (Hyperlipidaemia) : Out of 15 patients, 6(39.96%) had no

habit, 4(26.64%) were smokers, 3(19.98 %) were Alcoholic & 2(13.32%) were

tobacco chewers. GroupB (Narmolipidaemic): Out of 15 persons, 9(59.94%) had no

habit, 4(26.64%) were tobacco chewers and 2(13.32%) were Alcoholic.

Table No. 39 Menstrual History of 14 female patients

Menstrual History Group A % Group B % Total %

Regular 2 13.32 8 53.28 10 33.33 Scanty 1 6.66 0 0 1 3.33 Heavy bleeding 0 0 0 0 0 0 Menopause 2 13.32 1 6.66 3 10

Menstrual History : Observation of menstrual history of 14 female showed

that maximum females i.e. 10(33.33%) were having regular mentstrual history,

3(10%) were having menopause and 1(3.33%) had scanty menstruation.

Table No. 40 Jataragnibala wise distribution of the Samples.

Jataragnibala Group A % Group B % Total % Pravara 3 19.98 1 6.66 4 13.33

Madhyama 12 79.92 14 93.24 26 86.66 Avara 0 0 0 0 0 0

Jataragnibala : GroupA (Hyperlipidaemia) : Out of 15 patients, 12(79.92%) had

Madhyama jataragni, 3(19.98%) had pravara jataragni. GroupB (Narmolipidaemic):

Out of 15 persons, 14(93.24%) had Madhyama jataragni, 1(6.66%) had pravara

jataragni.

Results - 106


Table No. 41 Koshta wise distribution of the Samples.

Kostha Group A % Group B % Total % Krura 2 13.32 3 19.98 5 16.66

Madhyama 11 73.26 11 73.26 22 73.33 Mrudu 2 13.32 1 6.66 3 10

Vyasana : GroupA (Hyperlipidaemia) : Out of 15 patients, 11(73.26%) had

Madhyama kostha, 2(13.32%) had krura kostha and 2(13.32%) had mrudu kostha.

GroupB (Narmolipidaemic): Out of 15 persons, 11(73.26%) had Madhyama kostha,

3(19.98%) had krura kostha and 1(6.66%) had mrudu kostha.

Table No. 42 Prakriti wise Distribution of the Sample

Prakrti Group A % Group B % Total % Kapha Vataja 3 19.98 2 13.32 5 16.66 Kapha Pittaja 11 73.26 10 66.60 21 70 Pitta Vataja 1 6.66 3 19.98 4 13.33

Prakrti: GroupA (Hyperlipidaemia) : Out of 15 patients, 11(73.26%) were had

Kaphapittaja prakriti,3(19.98%) were Kapha vataja prakriti and 1(6.66%) was Pitta

vataja prakriti. Group B: Out of 15persons, 10(66.60%) were had Kaphapittaja

prakriti, 3(19.98%) were Pitta vataja prakriti. and 2(13.32%) were Kapha vataja

prakriti .

Table No. 43 Sara wise Distribution of the Sample

Sara Group A % Group B % Total % Pravara 3 19.98 4 26.64 7 23.33

Madhyama 11 73.26 11 73.26 22 73.33 Avara 1 6.66 0 0 1 3.33

Sara: GroupA (Hyperlipidaemia) : Out of 15 patients, 11(73.26%) were Madhyama

sara,3(19.98%) were Pravara sara and 1(6.66%) was Avara sara. Group B: Out of

15persons, 11(73.26%) were Madhyama sara, 4(26.64%) were Pravara sara.

Results - 107


Table No. 44 Showing Samhanana of the Samples

Samhanana Group A % Group B % Total % Pravara 3 19.98 2 13.32 5 16.66

Madhyama 11 73.26 12 79.92 23 76.66 Avara 1 6.66 1 6.66 2 6.66

Samhanana :. GroupA (Hyperlipidaemia): Out of 15 patients, 11(73.26%) were had

Madhyama samhanana, 3(19.98%) were had Pravara samhanana and 1(6.66%) had

Avara Samhanana. Group B: Out of 15 persons, 12(79.92%) were had Madhyama

samhanana, 3(13.32%) were had Pravara samhanana and 1(6.66%) had Avara

Samhanana.

Table No. 45 Showing Pramana of the Samples

Pramana Group A % Group B % Total % Pravara 2 13.32 5 33.30 7 23.33

Madhyama 12 79.92 10 66.60 22 73.33 Avara 1 6.66 0 0 1 3.33

Pramana :. GroupA (Hyperlipidaemia): Out of 15 patients, 12(79.92%) were had

Madhyama pramana, 2(13.32%) were had Pravara pramana and 1(6.66%) had Avara

pramana. Group B: Out of 15 persons, 10(66.66%) were had Madhyama pramana,

5(33.30%) were had Pravara pramana.

Table No. 46 Showing Satmya of the Samples

Satmya Group A % Group B % Total % Pravara 3 19.98 5 33.30 8 26.66

Madhyama 11 73.26 9 59.94 20 66.66 Avara 1 6.66 1 6.66 2 6.66

Satmya:. GroupA (Hyperlipidaemia): Out of 15 patients, 11(73.26%) were had

Madhyama Satmya, 3(19.98%) were had Pravara Satmya and 1(6.66%) had Avara

Satmya. Group B: Out of 15 persons, 9(59.94%) were had Madhyama Satmya,

5(33.30%) were had Pravara Satmya and 1(6.66%) had Avara Satmya.

Results - 108


Table No. 47 Showing Satva of the Sample

Satva Group A % Group B % Total %

Pravara 4 26.64 7 46.62 11 36.66 Madhyama 11 73.26 8 53.28 19 63.33

Avara 0 0 0 0 0 0

Satva: GroupA (Hyperlipidaemia): Out of 15 patients, 11(73.26%) were had

Madhyama Satva, 4(26.64%) were had Pravara Satva. Group B: Out of 15 persons,

8(53.28%) were had Madhyama Satva, 7(46.62%) were had Pravara Satva.

Table No. 48 Showing Abhyavaharana Shakti of the Sample

Abhyavaharana Shakti Group A % Group B % Total %

Pravara 2 13.32 4 26.64 6 20 Madhyama 12 79.92 11 73.26 23 76.66

Avara 1 6.66 0 0 1 3.33

Abhyavaharana Shakti: GroupA (Hyperlipidaemia): Out of 15 patients,

12(79.92%) were had Madhyama Abhyavaharana Shakti, 2(13.32%) were had

Pravara Abhyavaharana Shakti And 1(6.66%) had Avara Abhyavaharana Shakti.

Group B: Out of 15 persons, 11(73.26%) were had Madhyama Abhyavaharana Shakti,

4(26.64%) were had Pravara Abhyavaharana Shakti.

Table No. 49 Showing Jarana Shakti of the Samples

Jarana Shakti Group A % Group B % Total % Pravara 5 33.30 2 13.32 7 23.33

Madhyama 10 66.60 13 86.58 23 76.66 Avara 0 0 0 0 0 0

Jarana Shakti: GroupA (Hyperlipidaemia): Out of 15 patients, 10(66.60%) were

had Madhyama Jarana Shakti, 5(33.30%) were had Pravara Jarana Shakti. Group B:

Out of 15 persons, 13(86.58%) were had Madhyama Jarana Shakti, 2(13.32%) were

had Pravara Jarana Shakti.

Results - 109


Table No. 50 Showing Vyayama Shakti of the Samples

Vyayama Shakti Group A % Group B % Total %

Pravara 1 6.66 4 26.64 5 16.66 Madhyama 12 79.92 11 73.26 23 76.66

Avara 2 13.32 0 0 2 6.66

Vyayama Shakti: GroupA (Hyperlipidaemia): Out of 15 patients, 12(79.92%) were

had Madhyama Vyayama Shakti, 2(13.32%) were had Avara Vyayama Shakti and

1(6.66%) had Pravara Vyayama Shakti. Group B: Out of 15 persons, 11(73.26%)

were had Madhyama Vyayama Shakti, 4(26.64%) were had Pravara Vyayama Shakti.

OBSERVATION OF SNEHAPANA LAXANAS :

The present study has been undertaken to see the effect of Arohana Snehapan

in Samedarakta (Hyperlipidaemia & Normal lipid values). Matra of Sneha taken,

time taken for digestion, on set of Jeeryamana Laxanas. Samyak snigdha laxanas

were recorded in both groups. Out of 30 samples all showed following Snehapana

laxanas.

PANA KALEEN LAXANAS :

Hrullasa – Out of 14 Females, 10 Females showed this laxanas and Out

of 16 Males, 5 males showed this laxana.

Udgara - 21 persons of the sample showed Udgara.

However the laxana chardhi was not observed by any persons.

Results - 110


MATRA OF MOORCHITA TILA TAILA ADMINISTERED:

Table No. 51 The matra of Arohana Snehapan with Murchita Tila Taila in both groups.

Group A Group B Sl. No. 1st day 2nd day 3rd day 4th day 5th day 1st day 2nd day 3rd day 4th day 5th day 1 30 65 100 135 X 30 65 100 135 X 2 30 55 80 X X 30 60 90 X X 3 30 65 100 135 X 30 65 100 135 X 4 30 60 90 120 X 30 55 80 X X 5 30 60 90 X X 30 70 110 150 190 6 30 60 90 120 X 30 55 80 X X 7 30 65 100 135 170 30 65 100 X X 8 30 55 80 105 X 30 55 80 105 X 9 30 60 90 120 X 30 55 80 X X

10 30 55 80 X X 30 65 100 135 X 11 30 60 90 X X 30 55 80 105 X 12 30 60 90 X X 30 55 80 105 X 13 30 60 90 120 X 30 60 90 X X 14 30 60 90 120 X 30 65 100 X X 15 30 60 90 X X 30 60 90 X X

Men dose in ml.

30 60 90 123 170 30 56 84 124 190

Moorchita Tila Taila was given in the dose of 30 ml on the first day to all the

30 individuals which was considered as Hrisiyasi Matra. On the basis of digestion of

this Snehamatra second day dose was decided.

Group A (Hyperlipidaemia):In this group second day dose was minimum 55 ml.

and maximum dose was 65 ml. with mean value of 60 ml. The third day dose was

minimum 80 ml & maximum 100 ml. with mean value of 90 ml. Fourth day dose was

minimum 105 ml & maximum 135 ml. with mean value of 123 ml. Fifth day dose was

170 ml.

Group B (Normolipidaemic):In this group second day dose was minimum 55 ml.

and maximum dose was 70 ml. with mean value of 56 ml. The third day dose was

minimum 80 ml & maximum 110 ml. with mean value of 84 ml. Fourth day dose was

minimum 105 ml & maximum 135 ml. with mean value of 124 ml. Fifth day dose was

190 ml.

Results - 111


JEERYAMANYA LAXANAS

The table No. 52 The mean on set of Jeeryamanya laxanas of both Groups

1st day mean onset time in

minutes

2nd day mean onset time in

minutes

3rd day mean onset time in

minutes

4th day mean onset time in

minutes

5th day mean onset time in

minutes Jeeryamanya

laxanas A B A B A B A B A B

Shiroruk 90 105 200 190 270 230 360 340 420 400 Bhrama - - - - - 320 - 350 - - Nistiva 80 100 130 110 180 165 200 190 300 230 Sada - - - 180 360 300 400 360 330 420

Klama - - - - 450 400 480 510 480 410

Group A (Hyperlipidaemia) : On the first day after snehapana the mean on set time

of Shiroruk & Nistiva were 90 and 80 minutes respectively. On the second day the

mean on set time of Shiroruk, Nistiva were 200, 130, minutes respectively. On the

third day the mean on set time of Shiroruk, Nistiva, Sada and Klama were 270, 180,

360, 240 minutes respectively. On the fourth day the mean on set time of Shiroruk,

Nistiva, Sada and Klama were 360, 200, 400, 480, minutes respectively. On the fifth

day the mean on set time of Shiroruk, Nisteeva, Sada and Klama were 420, 300, 330,

480 minutes respectively. Bhrama was not occurred in Group A. Klama was not

occurred on 1st and 2nd day.

Group B (Normolipidaemic): On the first day after snehapana the mean on set time

of Shiroruk & Nistiva were 105 and 110 minutes respectively. On the second day

the mean on set time of Shiroruk, Nistiva & Sada were 190, 110, 180 minutes

respectively. On the third day the mean on set time of Shiroruk, Bhrama, Nistiva,

Sada and Klama were 230, 320, 165, 300, 400, minutes respectively. On the fourth

day the mean on set time of Shiroruk, Bhrama, Nistiva, Sada and Klama were 340,

350, 190, 360, 510, minutes respectively. On the fifth day the mean on set time of

Shiroruk, Nisteeva, Sada and Klama were 400, 230, 420, 410 minutes respectively.

Results - 112


TIME TAKEN FOR SNEHA JEERNA LAXANAS:

Table No. 53 showing time ( in minutes ) taken for Sneha Jeerna laxanas Group A Group B Sl.

No. 1st day

2nd

day 3rd day

4th day

5th day

1st day

2nd

day 3rd day

4th day

5th day

1 185 360 480 720 X 180 390 660 900 X 2 240 510 720 X X 210 420 660 X X 3 165 360 540 660 X 180 450 540 780 X 4 195 360 480 720 X 240 480 690 X X 5 215 480 780 X X 155 390 480 690 810 6 210 450 600 750 X 230 420 600 X X 7 180 380 540 780 900 180 390 600 X X 8 240 300 480 660 X 240 375 480 750 X 9 190 420 660 780 X 270 360 660 X X 10 230 390 660 X X 180 360 600 790 X 11 205 460 720 X X 270 450 600 810 X 12 210 450 630 X X 240 330 480 770 X 13 200 420 720 840 X 210 360 660 X X 14 195 410 690 960 X 180 420 720 X X 15 205 410 600 X X 210 450 660 X X

Group A (Hyperlipidaemia) : On the first day the minimum time taken for digestion

was 165 and maximum was 240 minutes respectively. On the Second day the

minimum time taken for digestion was 300 and maximum was 510 minutes

respectively. On the third day the minimum time taken for digestion was 480 and

maximum was 780 minutes respectively. On the fourth day the minimum time taken

for digestion was 660 and maximum was 960 minutes respectively. Fifth day time

taken for digestion was 900 minutes.

Group B (Normolipidaemic): On the first day the minimum time taken for digestion

was 155 and maximum was 270 minutes respectively. On the Second day the

minimum time taken for digestion was 330 and maximum was 480 minutes

respectively. On the third day the minimum time taken for digestion was 480 and

maximum was 720 minutes respectively. On the fourth day the minimum time taken

for digestion was 690 and maximum was 900 minutes respectively. Fifth day time

taken for digestion was 810 minutes.

Results - 113


Table No. 54 showing Summary of time taken for Sneha Jeerana (in minutes)

Percentage of Individual Group A & B

1st day 2nd day 3rd day 4th day 5th day Duration (in minutes)

A B A B A B A B A B 0 – 180 13.32 39.96 - - - - - - - -

180 – 360 86.58 59.94 26.64 26.64 - - - - - - 360 – 540 - - 73.26 73.26 33.30 26.64 - - - - 540 – 720 - - - - 59.94 73.26 19.99 6.66 - - 720 – 900 - - - - 6.66 - 39.96 39.96 6.66 6.66 A = Group A (Hyperlipidaemia), B = Group B (Normolipidaemic)

Group A : Out of 15 Hyperlipidaemic patients, on the first day 2(13.32%) patients

within 180 minutes and 13(86.58%) patients were had Snehajeerna Laxanas between

180 – 360 minutes. On the second day 4(26.64%) patients within 180 - 360 minutes

and 11(73.26%) patients were had Snehajeerna Laxanas between 360 - 540 minutes.

On the third day 5(33.30%) patients within 360 – 540 minutes, 9(59.94%) patients

between 540 – 720 minutes and 1(6.66%) patient had Snehajeerna Laxanas between

720 - 900 minutes. On the fourth day 3(19.99%) patients within 540 - 720 minutes,

and 6(39.96%) patient had Snehajeerna Laxanas between 720 - 900 minutes. On Fifth

day 1(6.66%) patient had Snehajeerna Laxanas between 720 - 900 minutes.

Group B : Out of 15 Nomolipidaemic persons, on the first day 6(39.96%) persons

within 180 minutes and 9(59.94%) persons were had Snehajeerna Laxanas between

180 – 360 minutes. On the second day 4(26.64%) persons within 180 - 360 minutes

and 11(73.26%) persons were had Snehajeerna Laxanas between 360 - 540 minutes.

On the third day 4(26.64%) persons within 360 – 540 minutes and 11(73.26%)

persons between 540 – 720 minutes. On the fourth day 1(6.66%) person within 540 -

720 minutes and 6(39.96%) persons had Snehajeerna Laxanas between 720 - 900

minutes. On Fifth day 1(6.66%) person had Snehajeerna Laxanas between 720 - 900

minutes.

Results - 114


Table No. 55 Mean time (in minutes) taken for Samyak Snigadha laxanas of both Groups A & B.

1st day mean time

2nd day mean time

3rd day mean time

4th day mean time

5th day mean time Samyak Snigadha

laxanas A B A B A B A B A B

Vatanulomana 230 220 430 400 600 630 780 760 920 830 Agnideepti 230 250 450 410 640 615 800 785 955 890 Purisha snigdhata - - - - 755 1075 1130 1080 960 900 Asamhat varchas - - - - 600 960 1000 980 840 800 Twak snigdata - - - - 600 540 720 660 - 660 Anga laghavatha - - - - 740 700 780 800 1000 900 Snehodwega - - - - 660 540 700 660 - 720 Glani - - - - 650 645 820 800 965 895 A = Group A (Hyperlipidaemia), B = Group B (Normolipidaemic)

Group A : Out of 15 Hyperlipidaemic patients, On the First day the mean time taken

for Vatanulomana and Agnideepti was 230, 230 minutes respectively. On the Second

day the mean time taken for Vatanulomana, Agnideepti was 430, 450 minutes

respectively. On the Third day the mean time taken for Vatanulomana, Agnideepti,

Purisha Snigdhata, Asamhat Varchas, Twak Snigdata, Agna laghavatha, Snehodwega

and Glani were 600, 640, 755, 600, 600, 740, 660 and 650 respectively. On the Fouth

day the mean time taken for Vatanulomana, Agnideepti, Purisha Snigdhata, Asamhat

Varchas, Twak Snigdata, Agna laghavatha, Snehodwega and Glani were 780, 800,

1130, 1000, 720, 780, 700 and 820 respectively. On the Fifth day the mean time taken

for Vatanulomana, Agnideepti, Purisha Snigdhata, Asamhat Varchas, Agna

laghavatha, and Glani were 920, 955, 960, 840, 1000 and 965 respectively.

Group B : Out of 15 Normolipidaemic persons, On the First day the mean time taken

for Vatanulomana and Agnideepti was 220, 250 minutes respectively. On the Second

day the mean time taken for Vatanulomana, Agnideepti was 400, 410 minutes

respectively. On the Third day the mean time taken for Vatanulomana, Agnideepti,

Purisha Snigdhata, Asamhat Varchas, Twak Snigdata, Agna laghavatha, Snehodwega

and Glani were 630, 615, 1075, 960, 540, 700, 540 and 645 respectively. On the

Fouth day the mean time taken for Vatanulomana, Agnideepti, Purisha Snigdhata,

Asamhat Varchas, Twak Snigdata, Agna laghavatha, Snehodwega and Glani were

Results - 115


760, 785, 1080, 980, 660, 800, 660 and 800 respectively. On the Fifth day the mean

time taken for Vatanulomana, Agnideepti, Purisha Snigdhata, Asamhat Varchas,

Twak Snigdata, Agna laghavatha, Snehodwega and Glani were 830, 890, 900, 800,

660, 900, 720 and 895 respectively.

Table No. 56 showing Samyak Snigdha Laxanasa of each individual in both the groups

Group A 1st day 2nd day 3rd day 4th day 5th day

Sl.

No. SSL No. % SSL No. % SSL No. % SSL No. % SSL No. %

1 1 11 1,2 22 1,2,7 33 1,2,3,4,5,6,7,8 88 - - 2 1 11 1,2 22 1,2,3,5,8 55 - - - - 3 - - 1,2 22 1,2,7 33 1,2,3,4,5,7,8 77 - - 4 - - 1,2 22 1,2,7 33 1,2,3,4,5,6,7 77 - - 5 1 11 1,2,7 33 1,2,3,4,7,8 66 - - - - 6 - - 1,2 22 1,2,3,4,7,8 66 - - - - 7 1 11 1,2,7 33 1,2,7 33 1,2,6,7 44 1,2,3,4,5,

6,7,8,9 100

8 - - 1,2 22 1,2,6,7 44 1,2,3,4,5,6,7,8,9 100 - - 9 - - 1,2,4 33 1,2,4,7,9 55 1,2,3,4,5 88 - -

10 1 11 1,2,4,7 44 1,2,3,4,7,8,9 77 - - - - 11 - - 1,2,7 33 1,2,3,4,6,7,8, 77 - - - - 12 1 11 1,2,7 33 1,2,3,4,6,7,8,9 88 - - - - 13 1 11 1,7 22 1,2,4,7 44 1,2,3,4,5,7,8,9 88 - - 14 - - 1,2 22 1,2,7 33 1,2,3,4,6,7,8 77 - - 15 - - 1,2,7 33 1,2,3,4,7,8,9 77 - - - -

Group B Sl.

No. 1st day 2nd day 3rd day 4th day 5th day SSL No. % SSL No. % SSL No. % SSL No. % SSL No. %

1 1 11 1,2 22 1,2 22 1,2,3,4,6,7,8 77 - - 2 - - 1,2,7 33 1,2,3,4,5,7 66 - - - - 3 1 11 1,2,4 33 1,2,4,7 44 1,2,3,4,6,7,8,9 88 - - 4 1 11 1,2,7 33 1,2,3,4,5,6,7,8,9 100 - - - - 5 - - 1,2,7 33 1,2,7 33 1,2,7,9 44 1,2,3,4,5,

6,7,8,9 100

6 1,7 22 1,2,4,7 44 1,2,3,4,5,6,7,8 88 - - - - 7 - - 1,2,7 33 1,2,3,7,8,9 66 - - - - 8 - - 2,7 22 1,2,7 33 1,2,3,4,7,8 66 - - 9 1 11 1,2 22 1,2,3,4,5,6,7,8 88 - - - -

10 - - 1,2 22 1,2,4,7 44 1,2,3,4,5,6,7 77 - - 11 7 11 1,2,7 33 1,2,7 33 1,2,3,4,5,6,7,8,9 100 - - 12 - - 1,2 22 1,2,7 33 1,2,3,4,5,6,7,8 88 - - 13 1 11 1,2 22 1,2,3,5,6,8 66 - - - - 14 1 11 1,2 22 1,2,3,4,5,7,8 77 - - - - 15 - - 1,2,7 33 1,2,3,4,5,6,7,8,9 100 - - - -

SSL No. - Samyak Snigda Laxanas Number Number 1 - Vatanulomana Number 2 - Agnideepti Number 3 - Purisha Snigdhata Number 4 - Asamhat Varchas Number 5 - Twak Snigdata Number 6 - Mrudugatrata Number 7 - Agna laghavatha Number 8 - Snehodwega Number 9 - Glani

Results - 116


Group A (Hyperlipidaemic) : 2(13.32%) patients got 100%, 5(33.30%) patients got

88%, 5(33.30%) patients got 77%, 2(13.32%) patients got 66% and 1(6.66%) patient

got 55% Samyak Snigdha Laxanas. On the Third day 6(39.96%) patients, on fourth

day 8(53.28%) patients and on the fifth day 1(6.66%) patient got Samyak Snigdha

Laxanas.

Group B (Narmolipidaemic) : 4(26.64%) persons got 100%, 4(26.64%) persons got

88%, 2(13.32%) persons got 77% and 5(33.30%%) persons got 66% Samyak Snigdha

Laxanas. On the Third day 7(46.62%) persons, on fourth day 7(46.62%) persons and

on the fifth day 1(6.66%) person got Samyak Snigdha Laxanas

Table No. 57 Showing the Total number of Samyak Snigdha Laxanas observed

on last day of Snehapana in both the groups

Total Number Percentage (%)Sl. No. Samyak Snigdha Laxanas A B A B

1 Vatanulomana 15 15 100 100 2 Agnideepti 15 15 100 100 3 Purisha snigdhata 15 15 100 100 4 Asamhat varchas 14 13 93.24 86.58 5 Twak snigdata 08 12 53.28 79.92 6 Anga laghavatha 15 13 100 86.58 7 Snehodwega 14 13 93.24 86.58 8 Klama 07 11 46.62 73.26 9 Glani 07 06 46.62 39.96

A = Group A (Hyperlipidaemia), B = Group B (Normolipidaemic)

Group A: Vatanulomana, Agnideepti, Purisha snigdhata, Anga laghavatha were

found in all the 15 patients. Asamhat varchas, Snehodwega found in 14 patients,

Twak snigdata in 8 patients, Klama, Glani were found in 7 patients.

Group B: Vatanulomana, Agnideepti, Purisha snigdhata, were found in all the 15

persons. Asamhat varchas, Snehodwega, Anga laghavatha found in 13 persons,

Twak snigdata in 12 persons, Klama in 11 persons, Glani was found in 6 persons.

Results - 117


RESULTS:

Table No. 58 showing Serum Cholesterol levels in both groups before and after

Arohana Snehapana. (Normal Value 130 to 200 mg /dl)

Group A Group B

BT AT BT AT Sl. No. O. P. D.

NO. mg / dl Changes Observed

O. P. D. NO. mg / dl

Changes Observed

1 3979 193 189 ↓ 04 4193 189 182 ↓ 07 2 3978 185 184 ↓ 01 4275 187 168 ↓ 19 3 4019 201 184 ↓ 17 4271 172 175 ↑ 03 4 4039 197 185 ↓ 12 4289 168 165 ↓ 03 5 4188 257 266 ↑ 09 4301 185 175 ↓ 10 6 4347 198 198 00 4652 165 165 ↓ 00 7 4581 194 190 ↓ 04 4658 184 175 ↓ 09 8 4596 213 201 ↓ 12 228 176 172 ↓ 04 9 673 172 170 ↓ 02 614 174 172 ↓ 02 10 793 179 171 ↓ 08 621 200 187 ↓ 13 11 1433 193 190 ↓ 03 1100 178 178 ↓ 00 12 1475 194 188 ↓ 06 1101 172 182 ↑ 10 13 1501 204 202 ↓ 02 1102 177 172 ↓ 05 14 1546 192 190 ↓ 02 1107 198 196 ↓ 02 15 1590 196 194 ↓ 02 1951 179 175 ↓ 04

BT-Before treatment. A.T – After treatment.

Group A (Hyperlipidaemia) Out of 15 Hyperlipidaemic patients, 11 (73.26%)

patients lied in the range below the normal range of Serum Cholesterol (200 mg / dl),

2 (13.32%) patients were in the range of 201 – 210 mg/dl, 1 (6.66%) patient was in

the range of 211 – 220 mg/dl and 1(6.66%) patient was in the range 250 – 270 mg/dl

before treatement.

12 (79.92%) patients were lied in the range below the normal range of Serum

Cholesterol (200 mg / dl), 2(13.32%) patients were in the range of 201 – 220 mg/dl

and 1(6.66%) patient was in the range of 250 – 270 mg/dl after treatment.

Group B (Narmolipidaemic) All the healthy person had Cholesterol level within

200 mg/dl had Before and After Treatment.

Results - 118


Table No. 59 showing Serum Triglycerides levels in both groups before and after

Arohana Snehapana. (Normal Value 25 to 200 mg /dl)

Group A Group B BT AT BT AT

Sl. No. O. P. D.



Changes Observed

1 3979 233 214 ↓ 19 4193 171 170 ↓ 01 2 3978 210 170 ↓ 40 4275 135 135 ↓ 00 3 4019 273 222 ↓ 51 4271 125 130 ↑ 05 4 4039 203 197 ↓ 06 4289 130 125 ↓ 05 5 4188 202 173 ↓ 28 4301 140 150 ↓ 10 6 4347 276 229 ↓ 47 4652 150 150 00 7 4581 270 210 ↓ 60 4658 160 150 ↓ 10 8 4596 290 227 ↓ 63 228 165 166 ↑ 01 9 673 229 200 ↓ 29 614 170 165 ↓ 05 10 793 221 198 ↓ 23 621 145 140 ↓ 05 11 1433 213 207 ↓ 06 1100 125 110 ↓ 15 12 1475 232 206 ↓ 26 1101 125 120 ↓ 05 13 1501 222 220 ↓ 02 1102 125 130 ↑ 05 14 1546 224 212 ↓ 12 1107 193 190 ↓ 03 15 1590 230 211 ↓ 19 1951 163 163 00


Group A (Hyperlipidaemia) : 4 (26.64%), 7 (46.62%), 3 (19.98%) and 1(6.66%)

patients were in the range of 200 – 220 mg / dl, 220 – 240 mg / dl, 260-280 mg / dl

and 280 – 300 mg / dl before treatment respectively.

5 (33.30%), 7 (46.62%) and 3 (19.98%) patients were in the range of below

the normal, 200 – 220 mg / dl, 220 – 240 mg / dl, after treatment respectively.

Group B (Normolipidaemia) : All the healthy person had Triglycerides level within

200 mg/dl before and after treatment .

Results - 119


Table No. 60 showing HDL levels in both groups before and after Arohana

Snehapana. (Normal Value 30 to 70 mg /dl)


Sl. No. O. P. D.



Changes Observed

1 3979 46 47 ↑ 01 4193 48 48 00 2 3978 46 47 ↑ 01 4275 40 42 ↑ 02 3 4019 43 44 ↑ 01 4271 43 43 00 4 4039 46 48 ↑ 02 4289 41 42 ↑ 01 5 4188 48 50 ↑ 02 4301 42 47 ↑ 05 6 4347 44 48 ↑ 04 4652 40 43 ↑ 03 7 4581 45 46 ↑ 01 4658 42 43 ↑ 01 8 4596 52 54 ↑ 02 228 48 46 ↓ 02 9 673 40 44 ↑ 04 614 49 48 ↓ 01 10 793 48 51 ↑ 03 621 45 45 00 11 1433 46 47 ↑ 01 1100 40 43 ↑ 03 12 1475 47 48 ↑ 01 1101 40 42 ↑ 02 13 1501 44 46 ↑ 02 1102 40 42 ↑ 02 14 1546 48 49 ↑ 01 1107 48 49 ↑ 01 15 1590 49 51 ↑ 02 1951 48 50 ↑ 02


Group A (Hyperlipidaemia) : 12(79.92%) and 3(19.98%) patients were in the

range of 40-50 mg / dl and 50-60 mg / dl after treatment respectively.

Group B (Normolipidaemia) : 5(33.30%) and 10(66.60%) persons were in the range

of 30 - 40 mg / dl and 40-50 mg / dl before treatment respectively. All the 15 (100%)

persons were in the range of 40-50 mg/dl after treatment.

Results - 120


Table No. 61 showing LDL levels in both groups before and after Arohana Snehapana.

(Normal Value 70 to 210 mg /dl)


Sl. No. O. P. D.

NO. mg / dl

Changes Observed


Changes Observed

1 3979 101 99 ↓ 02 4193 107 110 ↑ 03 2 3978 104 78 ↓ 26 4275 116 99 ↓ 17 3 4019 104 96 ↓ 08 4271 104 109 ↑ 05 4 4039 110 98 ↓ 12 4289 101 100 ↓ 01 5 4188 141 140 ↓ 01 4301 115 98 ↓ 17 6 4347 96 100 ↑ 04 4652 95 94 ↓ 01 7 4581 95 104 ↑ 09 4658 110 102 ↓ 08 8 4596 146 143 ↓ 03 228 95 94 ↓ 01 9 673 104 98 ↓ 06 614 91 91 00 10 793 87 87 00 621 126 114 ↓ 12 11 1433 104 102 ↓ 02 1100 113 113 00 12 1475 101 88 ↓ 13 1101 124 116 ↓ 08 13 1501 116 112 ↓ 04 1102 117 104 ↓ 13 14 1546 102 99 ↓ 03 1107 112 109 ↓ 03 15 1590 98 95 ↓ 03 1951 98 95 ↓ 03


Group A (Hyperlipidaemia): 1(6.66%), 11(73.26%), 1(6.66%) and 2(13.32%)

patients were in the range of 70 - 90 mg / dl, 90 - 110 mg / dl,110 - 130 mg/dl and

130 – 150 mg/dl before treatment respectively. 3(19.98%), 9(59.94%), 1(6.66%) and

2(13.32%) patients were in the range of 70 - 90 mg / dl, 90 - 110 mg / dl,110 - 130

mg/dl and 130 – 150 mg/dl after treatment respectively.

Group B (Normolipidaemia): 8(53.28%) and 7(46.62%) persons were in the range

of 90 - 110 mg / dl and 110 - 130 mg/dl before treatment respectively.12(79.92%)

and 3(19.98%) persons were in the range of 90 - 110 mg / dl and 110 – 130 mg/dl

after treatment respectively.

Results - 121


Table No. 62 showing VLDL levels in both groups before and after Arohana

Snehapana. (Normal Value 20 to 40 mg /dl)


Sl. No. O. P. D.

NO. mg / dl

Changes Observed


Changes Observed

1 3979 46 43 ↓ 03 4193 34 34 00 2 3978 48 34 ↓ 14 4275 27 27 00 3 4019 54 44 ↓ 10 4271 25 26 ↑ 01 4 4039 41 39 ↓ 02 4289 26 25 ↓ 01 5 4188 40.4 34.6 ↓ 5.8 4301 28 30 ↑ 02 6 4347 55 45 ↓ 10 4652 30 30 00 7 4581 54 42 ↓ 12 4658 32 30 ↓ 02 8 4596 49 46 ↓ 03 228 33 33 00 9 673 36 30 ↓ 06 614 34 33 ↓ 01 10 793 44 38 ↓ 06 621 29 28 ↓ 01 11 1433 43 41 ↓ 02 1100 25 22 ↓ 03 12 1475 46 41 ↓ 05 1101 25 24 ↓ 01 13 1501 44 44 00 1102 25 26 ↑ 01 14 1546 44 42 ↓ 02 1107 38 38 00 15 1590 42 39 ↓ 03 1951 33 33 00


Group A (Hyperlipidaemia) : 1(6.66%), 11(73.26%) and 3(19.98%) patients were

in the range of 30 – 40 mg / dl, 40 – 50 mg / dl and 50 - 60 mg / dl before treatment

respectively. 1 (6.66%), 5 (33.30%) and 9 (59.94%) patients were in the range of

20-30mg/dl, 30 – 40 mg / dl and 40 – 50 mg / dl after treatment respectively.

Group B (Normolipidaemia): 9(59.94%) and 6(39.96%) persons were in the range

of 20-30mg/dl and 30 – 40 mg / dl before treatment respectively. 10(66.60%) and

5(33.30%) persons were in the range of 20-30 mg / dl and 30 – 40 mg / dl after

treatment respectively.

Results - 122


Table No. 63.The weight and BMI of Group A before and after Arohana

Snehapana.

GROUP A (HYPERLIPIDAEMIA) Wt. in Kg BMI

Sl No. O. P. D. NO. BT AT Changes

Observed BT AT Changes Observed

1 3979 90 89 ↓ 01 29.12 28.8 ↓ 0.32 2 3978 72 70 ↓ 02 25.53 24.82 ↓ 0.71 3 4019 87 85 ↓ 02 26.85 26.23 ↓ 0.62 4 4039 80 79 ↓ 01 29.09 28.72 ↓ 0.37 5 4188 90 88 ↓ 02 28.06 27.78 ↓ 0.28 6 4347 93 91 ↓ 02 28.09 27.49 ↓ 0.6 7 4581 79 77 ↓ 02 27.33 213.32 ↓ 0.67 8 4596 78 76 ↓ 02 25.4 24.8 ↓ 0.6 9 673 75 72 ↓ 03 25 24.08 ↓ 0.92 10 793 73 71.5 ↓ 1.5 23.62 23.13 ↓ 0.49 11 1433 72 71 ↓ 01 26.86 26.49 ↓ 0.37 12 1475 68 66.5 ↓ 1.5 25.95 25.38 ↓ 0.57 13 1501 70 69 ↓ 01 24.56 24.21 ↓ 0.35 14 1546 69 69 00 25.34 25.34 00 15 1590 77 75 ↓ 02 25.75 25.08 ↓ 0.67

In the group A (Hyperlipidaemia) : 03 kg weight was reduced in 1(6.66%) patient,

2 kg weight was reduced in 7(46.62%) patients, 1.5 kg weight was reduced in

2(13.32%) patients, 1 kg weight was reduced in 4(26.64%) patients and no reduction

of weight was observed in 1(6.66%) patient after Arohana Snehapana. In all

15(100%) patients BMI was slightly reduced.

In the group B (Narmolipidaemia) : 2 kg weight was reduced in 4(26.64%) persons,

1.5 kg weight was reduced in 2(13.32%) persons, 1 kg weight was reduced in

7(46.62%) persons and no reduction of weight was observed in 2(13.32%) persons

after Arohana Snehapana. BMI was reduced in 13(86.58%) persons and no

reduction in BMI for 2 (13.32%) persons.

Results - 123


Results - 124

Group A -

66%

27%

7%Group B 0%

0%

100%

0%

Increased abnormality

Decreased abnormality

Normal limit

Variable

Table No. 64 The weight and BMI of Group B before and after Arohana Snehapana.

GROUP B (NARMOLIPIDAEMIA) Wt. in Kg BMI

Sl No. O. P. D. NO BT AT Changes

Observed BT AT Changes Observed

1 4193 62 60 ↓ 02 24.52 23.37 ↓ 1.15 2 4275 72 70 ↓ 02 25.8 25.1 ↓ 0.7 3 4271 66 64 ↓ 02 23.95 23.23 ↓ 0.72 4 4289 75 74 ↓ 01 25.95 25.60 ↓ 0.35 5 4301 81 80.5 ↓ 1.5 25.02 25.00 ↓ 0.02 6 4652 60 59 ↓ 01 24.03 23.63 ↓ 0.4 7 4658 59 59 00 23.63 23.63 0 8 228 80 78.5 ↓ 1.5 24.96 24.80 ↓ 0.16 9 614 60 58 ↓ 02 24.03 23.00 ↓ 1.03 10 621 66 65 ↓ 01 22.88 22.49 ↓ 0.39 11 1100 55 54 ↓ 01 23.8 23.37 ↓ 0.43 12 1101 60 60 00 21.77 21.77 0 13 1102 55 54 ↓ 01 23.8 23.37 ↓ 0.43 14 1107 69 68 ↓ 01 25.86 25.48 ↓ 0.38 15 1951 70 69 ↓ 01 24.82 24.46 ↓ 0.36

Table No. 65 Showing the overall results of Serum Lipid Values

Group A Group B Results No. of

Patients Percentage No. of Patients Percentage

Increased abnormality 0 0 0 0 Decreased abnormality 10 66.60 0 0 Normal limit 4 26.64 15 100 Variable 1 6.66 0 0

Group A (Hyperlipidaemia): Out of 15 patients, 10(66.60%) patients had decreased

abnormality, 1(6.66%) had variable in the values and 4(26.64%) patients had all the

lipid values within the normal range.

Group B (Normolipidaemic): In all the 15 persons, even after Samyak Snigdha

Laxanas the changes in the Serum Lipid values were within the Normal limits only.


STATISTICAL RESULTS OF OBJECTIVE PARAMETERS:

Table No. 66 showing statistical results of Group A samples

Parameters Mean S. D. S. E. t– value p-value Remarks

Sr. Cholestrol 5.6 4.968 1.282 4.368 <0.001 H. S. Sr. T. G. 28.73 19.579 5.055 5.683 <0.001 H. S. HDL 1.866 1.06 0.273 6.835 <0.001 H. S. LDL 6.4 6.674 1.723 3.714 <0.001 H. S. VLDL 5.586 4.153 1.072 5.21 <0.001 H. S.

Table No. 67 showing statistical results of Group B samples

Parameters Mean S. D. S. E. t– value p-value Remarks

Sr. Cholestrol 6.066 5.284 1.364 4.447 <0.001 H. S. Sr. T. G. 4.666 4.303 1.111 4.199 <0.001 H. S. HDL 1.666 1.345 0.347 4.801 <0.001 H. S. LDL 6.133 6.034 1.557 3.938 <0.001 H. S. VLDL 0.866 0.915 0.236 3.669 <0.001 H. S.

Table No. 68 showing comparative statistical results of Group A & Group B samples

Parameters Group Mean S. D. S. E. P. S. E. t-value p-value Remarks

A 193.46 22.04 5.691Sr. Cholestrol B 175.93 8.258 2.132 6.077 2.884 <0.02 H. S.

A 206.4 17.17 4.433Sr. T. G. B 146.26 21.861 5.644 7.176 8.38 <0.001 H. S.

A 48.0 2.699 0.696HDL B 44.86 2.875 0.742 1.017 3.087 <0.01 H. S.

A 102.6 17.646 4.556LDL B 103.2 8.16 2.107 5.019 0.119 <0.05 N. S.

A 40.173 4.493 1.16 VLDL B 29.26 4.382 1.131 1.62 6.736 <0.001 H. S.

Results - 125


When we compare except the parameter LDL the other parameters shows

highly significant (By paired t-test as p is less than 0.05). In group A the parameter

HDL has uniform effect on patients with least variations. The mean effect of

parameters Sr. Triglycerides is more and the Sr. Cholesterol has more variation in

Group A.

In group B the parameter Sr. Cholesterol shows stable effect of patients with

high mean effect. The parameter HDL has minimum variation and with more

variation in parameter weight in group B after the treatment.

Individually in Group A : All the parameters shows highly significant effect.

Assume that Tilataila is not responsible for changes in readings of observation before

and after of the Treatment. For this we use unpaired t – test. The parameter weight is

more significant in group A with least variance and the mean net effect and variation

is more in Sr. Triglycerides. The parameter HDL. Sr. Triglycerides shows more

effect in Group A than Group B, where as the Sr. Cholesterol is little more effect of

parameter LDL and variation in Sr. Cholesterol is more in group B. The parameter

VLDL is having less variation in group B (comparable II & III).

Results - 126


Discussion - 127

REVIEW OF LITERATURE:

Shodhana means Bio-purification. The therapy which eliminates the vitiated

doshas from the body is known as Shodhana.

Shodhana therapies while eliminates the vitiated doshas from the body,

enhances the agni, eradicatess the diseases and restores the normal health. Therefore

one should take proper Shodhana therapies in time. Shodhana enhances strength of

Buddhi, indriyas, stability to dhatus, enhancement of agni and delays the ageing

process.

In the treatment regimen the Shodhana therapies are the main procedures or

Pradhana Karma. They are preceded by certain preparative procedures known as

Purvakarmas. This Purvakarma includes Ama pachana, Snehana and Swedana.

Among these, Snehana therapy is intended for alleviation of vitiated doshas

hence called as Shodhananga snehana. Snehana elicited by Snehana, Vishyandana,

Mardavata, Kledana properties. These properties are the tools for producing Samyak

snigdha laxanas.

Meda means Sneha that is lipid in the body. The sthana and swaroopa of

meda is in two forms that is poshya and poshaka swaroopa. Poshaka meda is mobile

in nature and poshya meda immobile in nature.

Poshaka meda circulates in the whole body along with gatiyuakta rasa, rakta

dhatu for nourishing the poshya meda dhatu. According to modern science it can be

correlated with lipids which are present in the circulating blood. Poshya meda dhatu

is stored in Medodhara kala i.e., Udara, Spik, Sthana and Gala etc. According to

modern science it can be correlated with adipose tissue or fat present beneath the skin.

If any abnormality is present, Poshaka meda will leads to meda dushti which in turn


Discussion - 128

leads to Medovriddhi in rasaraktadi dhatus i.e raised level of serum cholesterol and

serum triglycerides in the plasma of the blood.

In the present study the term Samedarakta is coined for Lipidaemia i.e., the

lipids present in the plasma of blood whether physiological or pathological. Here the

literal meaning of word Samedarakta has been taken as Sa=with, meda = fat, rakth =

blood i.e., the fat or lipid present in the blood in the normal condition or abnormal

condition is taken as Samedarakta.

The dangerous pathological state may develop due to the morbidity of

Medodathu as Medovyapath. This Medovyapath is an abnormality of dathuparinama.

In case of emergency of insufficient supply of nutrients to the body, the adipose tissue

is disintegrated to provide the requisite fuel leading to dhatuja medovyapat. This

condition is common in severe Obesity, Diabetes mellitus, Nephritic syndrome etc

Kapha and Meda are interlinked as Ashrayashrayibhavas. Hence vitiation of

Kapha leads to vitiation of Meda, this is because of samanadharamvriddhi. Vitiated

Kapha leads to many vikaras known as kaphaja nanatmaja vyadhis which are 20 in

numbers. Among them Dhamani pratichaya is one, it means thickening of the arteries

which is due to vitiation of Kapha.

After scanning the both Ayurvedic and modern literatures, we get many

conditions like Samedarakta, Meda, Medavriddhi, Medovyapat, Abadha medasa,

Sthoulya, Medoroga, Dhamani pratichaya and some conditions like Hyperlipidaemia,

Atherosclerosis and Obesity etc., In the above said all the conditions, fat or lipids are

invariably present. In Hyperlipidaemia, circulating lipids like LDL, TG, Cholesterol,

VLDL etc. are increased and which can be compared with Poshakameda dhatu that

conditions may be considered as Samedarakta.


Discussion - 129

MATERIALS AND METHODS :

The materials selected for the clinical study were

i. Panchakolachoorna (as Amapachana)

ii. Murchita Tilataila (for Arohana Snehapana)

i. Panchakola Choorna

Importance of Ama pachana before snehana therapy : Amapachana is the

therapeutic regimen which is the treatment for further therapies like Snehapana on

which the success of entire treatment will depend. Amapachana treatment prior to

Snehapana, facilitates Snehapana to achieve better therapeutic results. Persons having

normal state of agni are also being given Amapanchana to prevent the complications

that may raise from Snehapana. This makes the need of Amapachana before

undergoing Snehana therapy.

In the present study, Panchakola choorna was selected as Amapachana drug

which checks the formation of Ama by increasing the Agni and digest the Ama. It is

indicated in Kapha vata disorders also.

ii. Snehapana with Murchita Tilataila:

Tilataila : Tilataila is best Snehadravya among sthavara sneha as explained by

Charaka. Taila is used widely for internal and external conditions. Taila is most

easily available fixed oil of herbal origin used extensively in the form of food and

medicines.

Acharya charaka mentioned that Tilataila is best amongst the taila vargas.

Taila alleviates vata but, at the same time does not aggravate kapha. From therapeutic

point of view the quality of taila is “Na Anyaha Snehastatha Kwachitsamskaram


Discussion - 130

nuvartate” ie., when taila treated with other dugs it takes the property of that drugs

after samskara.

Vagbhata explains the importance of Tilataila as “Krishanam Bhrimhanayalam

Sthoolanam Karshanaya Cha”. It does Bhrimahana Karya for Krisha persons and

does Karshana for sthoola persons.

In Krusha persons, Srotosankochana is present (i.e., constriction of channels).

Taila when administered, by its Tikshna Vyavayadi gunas enters the

Sukshmatisukshma Srotases and accomplishes Shodhana karya. By Shrotoshuddhi,

shareera pusthi will occur. Hence in this manner it does “Tasmath Krishanam

Bhrimhanayalam mittupanam”.

In Sthoola persons, by its sukshma, teekshnoshna gunas it enters

Sukshmasrotases does kshapana karya for meda. Due to kshapana of meda, the

person becomes krisha.

Importance of murchana of tila taila:

Crude oils contains Amadosha i.e, some enzyme lipase and racine (toxic

proteins), by morchana process Amadosha are removed and also durgandhata &

ugrata are removed. After doing Moorchana Samskara Sneha gets good smell and

colour. Apart from theses Sneha will gets the qualities of the drugs used for

Murchana. While by Sneha paka and Murchana the veerya of the Sneha is enhanced.

Before going to prepare any Aushadha siddha yogas, Taila Murchana is

required. Murchana means to enhance, to spread over. By this process amadosha is

removed. Usually Tailas are ushna veerya in nature. When treated with drugs like

Amalaki, Haritaki, etc., in the qualities of tailas changes takes place. i.e., Taila attains

Sheeta veerya. If Gritha & Tailas are treated with Rooksha, Ushna, Sheeta Dravyas,

snehatwa property will not be lost.


Discussion - 131

The drugs used for Murchana of Tilataila are Haritaki, Vibitaki, Amalaki,

Haridra, Mustha, Vatankura, Hrivera (Rasna), Ketaki pushpa, Manjistha, Lodra. With

their lekhaneeya property and also removes the Amadosh of Taila.

Beneficial effect of Moorchana sanskara reduces the degree of Saturation but

enhances the degree of Unsaturation. It indicates the essential role of unsaturated

fatty acids in reducing Serum Cholesterol, Serum Triglycerides and LDL levels which

are other wise risk factor for the development of Atherosclerosis, Hyper tension,

Coronary heart diseases etc. (Sneha Murchana B. S. Hiremath)

CLINICAL STUDY:

Selection of individuals: The individuals were incidentally selected from exclusively

conducted medical camp and OPD and IPD of D.G.M.A.M.C, Gadag. Method of

selection was incidental because samples cannot be randomized in short time and

medical camp was conducted to get number of cases.

The individuals of both sex who were fit for Snehana karma and Shodhana

karma in age group of 20- 60 years were selected.

Criteria for making two groups

For better understanding the effect of Shodhananga Arohana Snehapana on

Serum lipid levels, the subject made into two groups as follows.

Group – A : Shodhanapoorva Arohana Snehapana in Hyperlipidaemic patients was

debated and hence in Group A the patient suffering from Hyperlipidaemia were

selected. i.e. patients who were suffering from Primary Hyperilipidemia and whose

Serum lipids were in high levels excluding secondary Hyperilipidemia.


Discussion - 132

Group B : Healthy persons were selected in Group B. Healthy persons with their

lipid values under normal limits and who are intended to under go Shodhana karma

(virechana or vamana) for maintaining good health were selected.

Hence two groups were considered to study the effect of Shodhanapoorva

Arohana Snehapana on serum lipid levels of Hyperlipidaemia patients and healthy

persons.

Inclusive criteria:

Group A : The patients of either sex between the age group of 20-60 years. Patients

suffering from Primary Hyperlipidaemia whose Serum Cholesterol or Serum

Triglycerides level were found to be higher than the normal and who were fit for

Shodhana and Snehana therapies were considered.

Group B : The healthy persons of either sex between the age group of 20-60 years

with Normal Lipid Values and who were fit for Shodhana and Snehana therapies were

considered.

Exclusive Criteria:

Group A: The patients who were unfit for Shodhana procedure were excluded. The

patients secondary Hyperilipidemia were excluded because of the improper

metabolism of the lipids, which can alters the serum lipid levels.

Group B: The persons who were unfit for Shodhana procedure were excluded.

Intervention:

• All the individuals were administered with Panchakola churna as Ama

Pachana ½ hour before food with hot water till appearance of nirama

lakshanas. Amapachana was given for minimum of 3 days and maximum of 5


Discussion - 133

days. Some persons got burning sensation in the Chest after taking

Panchakola choorna. Hence dose was reduced according to the need.

• In this study shodhananga Arohana Snehapana was administered to 30

individuals in which 15 patients of Hyperlipidaemia and 15 healthy persons

were selected for the study.

First day Murchita Tilataila was given in the dose 30 ml to all the 30

individuals, which was considered as Hrasiyasi matra. On the basis of digestion of

the sneha on previous day, the next day dosage was decided. Though the Hrisiyasi

matra was equal to all the persons, Sneha Jeerna Laxanas were appeared in different

times. Because Prakruti, Kostha, Age group, Agnibala and Dosha are different in all

persons. Hence the digestion of Sneha had not appeared at same duration in all

persons.

Group A (Hyperlipidaemia) : On the first day the minimum time taken for

digestion was 165 and maximum was 240 minutes respectively. In this group second

day dose was minimum 55 ml. and maximum dose was 65 ml. with mean value of 60

ml. The third day dose was minimum 80 ml & maximum 100 ml. with mean value of

90 ml. Fourth day dose was minimum 105 ml & maximum 135 ml. with mean value

of 123 ml. Fifth day dose was 170 ml.

Group B (Normolipidaemic): On the first day the minimum time taken for digestion

was 155 and maximum was 270 minutes respectively. Second day dose was minimum

55 ml. and maximum dose was 70 ml. with mean value of 56 ml. The third day dose

was minimum 80 ml & maximum 110 ml. with mean value of 84 ml. Fourth day dose

was minimum 105 ml & maximum 135 ml. with mean value of 124 ml. Fifth day dose

was 190 ml.


Discussion - 134

This suggest that the Samyak Snigdha Laxanas had not manifested at the same

time. This may be because of Taratama Bhava of Kostha, Agni, Prakruti among

persons. This clearly suggests that snehapana increased the agnibala on each day,

though there was individual variation. Hence it can be said that agnibala is an

important factor in deciding the dosage of sneha along with other factors. In classics

also the snehapana kala was told as 3-7 days.

Blood samples were collected on day 1st before Snehapana in the morning

hours and after Samyaksnigdha laxanas appeared i.e., after completion of snehapana

with 12 hours fasting in the morning. After this, necessary shodhana karmas was

performed followed by vishrama kala.

Study duration:

In the present study duration was 15 days and fallow up for 15days.The study

duration was fixed upon the following points.

1. Time taken for Amapachana (i.e., till niramavastha seen)

2. Time taken for Arohana Snehapana

In the fallow up, 3 days for vishramakala ,1 day for shodhana karma and

Samsarjana karma for remaining days.

Laboratory Investigation:

The selected patients were subjected to laboratory investigation to role out the

secondary Hyperilipidemia and other systemic disorders and to confirm positively

whether they belong to Hyperilipidemic and Normolipidaemic groups.

Drop outs:

Out of 36 patients 4 patients were discontinued during Snehapana because of

aversion for drinking Sneha, 2 patients were discontinued due to inconvenience for

taking treatment and follow up.


Discussion - 135

OBSERVATIONS:

In the present study 30 cases of Samedarakta (15 Hyperlipidaemic & 15

Normal Lipidaemic) were selected for trial and categorized into 2 groups of 15 each.

Age :

Group A (Hyperlipidaemic): 13 (86.58%) patients were in between 30-50 years which

substantiate incidence of Hyperlipidaemia over the age of 30 years.

Group B (Narmolipidaemic): Most of the persons i.e. 7 (46.62%) healthy persons

belonged to the age group of 20-30 years (23.33%).

But it cannot be concluded by this fact by our study because of age restricted

selection criteria and limitations for number of subjects.

Sex :

Group A (Hyperlipidaemic): Among the 15 patients, 10 (66.60%) patients were male

which substantiate risk of Hyperlipidaemia occurrence in males.

Group B (Narmolipidaemic) : Among15 healthy persons,9 were female which shows

health consciousness in females.

Religions:

Maximum 86.58% persons each in the both Groups were Hindu, this may be

the representation of the total community distribution in Gadag and Surrounding areas

from where most of the persons come.

Occupation :

Group A (Hyperlipidaemic): Maximum 59.94% patients were sedentary, there energy

expenditure is less than calories consumed which may leads to become

Hyperlipidaemia.

Group B (Narmolipidaemic): Maximum 46.62% persons were Labour.


Discussion - 136

Marital Status:

It was observed that as for as marital status is concerned, there was no relation

for martial status has been found concerned to the Hyperlipidaemia and normal lipid

values.

Socio – Economic status:

This study shows that most of the persons in both groups belongs to middle

class. As most of the persons comes to this college hospital belongs to middle class.

Diet :

Group A (Hyperlipidaemic): Maximum 10 (66.60%) patients had mixed diet. This

shows clear association for high calories diet in Hyperlipidaemia.

Group B (Narmolipidaemic): Most of the persons i.e. 9(59.94%) were vegetarian.

Sleep :

Group A (Hyperlipidaemic): Maximum numbers of patients reported to have sound

sleep (86.58%). On this basis we cannot draw any conclusion relating to sleep and

hyperlipidaemia.

Group B (Narmolipidaemic) : 86.58% persons are having sound sleep.

Vyasana :

Group A (Hyperlipidaemic): It was observed that 39.96% patients were not having

any habits. But 26.64% persons were addicted for smoking, 19.98% persons were

addicted for alcohol and 13.32% were addicted for tobacco chewing. In allied science

also smoking and alcohol are considered as risk factors. So in this study it was


Discussion - 137

observed. Hence this shows the incidence of smoking and Alcohol as causative

factors for Hyperlipidaemia.

Group B (Narmolipidaemic) : 59.96% persons were not having any habits.

Koshta :

Group A (Hyperlipidaemic): Maximum 73.26% patients had Madhyama Kostha. In

normal condition, Madhyama Kostha found due to Kapha dominancy.

Group B (Normolipidaemic): Maximum 73.26% persons had Madhyama Kostha. In

normal condition, Madhyama Kostha found due to Kapha dominancy.

Prakriti :

Group A (Hyperlipidaemic): Maximum 73.26% patients were kapha pittaja, 19.98%

were Kaphvataja. In this group most of the patients were having kapha dominant

prakriti which is the most incidental factor for the disease Hyperlipidaemia.

Group B (Normolipidaemic): Maximum 66.60% persons were kapha pittaja.

Agni :

Assessment of agni was made on the abhyavarana shakti and Jaraha shekti

which relieved that majority of the person were Madhyama agni in both groups.

Majority of the persons were of Madhyama sara, Madhyama samhanana,

Madhyama pramana, Madhyama satmya, Madhyama satwa, Madhyama Abhyavarana

Shakti, Madhyama Jaranashakti, and Madhyama Jaranashakti in both the groups.


Discussion - 138

SNEHAPANA LAXANAS:

PANAKALEENA LAXANAS:

Hrullasa : Out of 14 females,16.66% in group A and 30% in group B showed this

laxana and out 16 male patients 20% showed this laxana because of higher dose of

sneha and may be they are more sensitive by their nature.

Udgara : This laxana was observed in 21(70%) of the samples and it was observed till

jeerna of sneha.

JEERYAMANA LAXANAS:

Among these laxanas except Murcha, Daha and Arati, all other laxanas were

observed in the individuals.

Shiroruja was found in 25 individuals the mean time of onset of shiroruja was

middle stage of the digestion of the sneha. Other laxanas Brama in 6 (20%) samples

Lalasrava in 23 (76.66%), Trishna 15 (50%) and Klama in 18 (60%) samples were

found. These may be due to higher intake of sneha.

SNEHA JEERNA LAXANAS

The individuals showed most of the Jeerna laxanas indicating the digestion of

administered sneha.

Jeerymana laxanas prashamana - in 30 (100%)

Shareera laghuta - in 28 (93.33%)

Kshudha pravritti - in 27 (90%)

Trishna pravritti - in 14 (46.66%)

Udgara shuddi - in 26 (86.66%)


Discussion - 139

SAMYAK SNIGDHA LAXANAS

Dosha Utkleshana is brought only by Shodhananga snehapana. It can be

assessed by observing samyak snigdha laxanas.

Vatanulamana : It was observed in 30 individuals (Both Groups) in all the

days of Snehapana. Sneha by virtue of its Snigdha, Sara properties normalizes

or brings balance in vitiated vata. By this Vatanulomana will occurs.

Deeptagni : In all the 30 persons(Both Groups) deeptagni was observed in all

the days. This is due to increased secretion of bile from cholesterol

destruction, as bile is an essential for the digestion of Sneha.

Asamhat varchas and snigdha varchas : These were observed in 27(90%)

persons and 30(100%) respectively of Group A and Group B . These laxanas

may be due to drava, sara, snigdha and mrudu guna of Sneha. Pureesh

becomes drava and snigdha and person may passes Asamhat and snigdha

varchas. This will indicates for stopping the continuation of Sneha pana which

is consider as one of the prime Samyak snigdha laxana.

Twak snigdhata : It was found in 8(53.28%) and 12(79.92%) persons in Group

A and Group B respectively. It occurs due to Sneha taken because each and

every cell of the body will be saturated with Sneha that is all the dhatus get

saturated gradually one by one and produces mruduta in skin.

Gatra laghvata : It was observed in 15(100%) and 13(86.58%) persons in

Group A and Group B. Snehapana removes obstruction in the gati of vata

which makes vatanulomana. Due to this person passes asamhat varchas.

Hence person may feels Gatra laghavata.

Snehodwega : It was observed in 14(93.24% ) and 13(86.58%) in Group A

and Group B. Due to large quantity of Sneha in the body will reaches optimum


Discussion - 140

level i.e., body is fully staturated with excess dose of sneha. Hence individual

will showing dislike towards Snehapana. This is also one of the symptom of

Samyak snigdha laxanas.

Glani : it was found in 7(46.66%) and 6 (39.96%) in Group A and Group B,

it may due to restriction of diet regimen and due to properties of Sneha.

Person may feel exhausted or Glani on the last day of Snehapana.

All these are different parameters to assess proper Snigdhata of the body.


Discussion - 141

RESULTS:

In both groups serum lipid profile was carried out and also weight and BMI

were taken before and after Shodhanaga Arohana Snehapana.

Total Serum cholesterol

Group A (Hyperlipidaemia): The statistical analysis was done at P value < 0.001

which shows highly significant effect on Serum Cholesterol level. 14(46.66%)

patients showed a significant reduction in cholesterol levels while only 1 (6.66%)

patient showed raised cholesterol.

Group B (Narmolipidaemic): The statistical analysis was done at P value < 0.001

which shows highly significant effect on Serum Cholesterol level. 13(86.58%)

persons showed a significant reduction in cholesterol levels while only 2 (13.32%)

persons showed raised cholesterol within normal limit only.

Serum Triglycerides

Group A (Hyperlipidaemia): The statistical analysis was done at P value < 0.001.

All patients showed highly significant results. i.e., marked reduction in the serum

Triglycerides levels.

Group B (Narmolipidaemic): The statistical analysis was done at P value < 0.001.

10 (66.60%) persons showed slight reduction in Triglyceride level, 3(19.98%) persons

showed increase in the Triglyceride within normal limit only and for two persons

there is no reduction in Triglyceride level.


Discussion - 142

HDL

Group A (Hyperlipidaemia): The statistical analysis was done at P value < 0.001. All

patients showed highly significant values i.e., HDL level increased in all 15 (100%)

patients. This indicates the safety of Shodhanaga Arohana Snehapana with Murchita

Tilataila.


10(66.60%) persons showed raise in the HDL, 3(19.98%) persons showed no

reduction and 2(13.32%) persons showed slight reduction, indicating the protective

action of Shodhanaga Arohana Snehapana.

LDL

Group A (Hyperlipidaemia): The statistical analysis was done at P value < 0.001. It

showed significant result. 12(79.92%) patients showed slight reduction in LDL

levels, 2(13.32%) patients showed slight increase and 1(6.66%) patient showed no

change. This decrease may be due to Murchana samsakar of Sneha.


11 (73.26%) persons showed slight reduction, 2(13.32%) persons showed no

reduction and 1(6.66%) person showed slight increase in the LDL level.

VLDL

Group A (Hyperlipidaemia): The statistical analysis was done at P value < 0.001.

Almost all 14(93.24%) patients showed marked reduction in VLDL levels, 1(6.66%)

patients showed no change in the value this shows the significance of Snehapana.

Group B (Narmolipidaemic): The statistical analysis was done at P value <0.001.

6(39.96%) persons showed slight reduction and 6(39.96%) persons showed no

reduction and 3(19.98%) persons showed slight increase in the VLDL level within

normal limits only.


Discussion - 143

Weight and BMI

Group A (Hyperlipidaemia): In this group 14(93.24%) patients showed 3 to 1 kg

reduction in Weight and BMI. It may be due to Chedhana, Karshana property of

Tilataila Snehapana.

Group B (Narmolipidaemic): 13 (86.58%) persons showed slight reduction in Weight

and BMI and 2(13.32%) persons showed no reduction in Weight and BMI.

On overall results:

The results shows that Snehapana with Murchita Tilataila was highly effective

in decreasing the abnormality of Serum Lipid Values at the same time it showed a

specific quality i.e, not increase (apart from normal limits) in the values of Serum

lipids of healthy persons even after undergoing Arohana Snehapana.


LIMITATIONS:

Samples were selected incidentally.

Sample size is small to generalize the results

Serum lipid values were taken before and after Snehapana but not after the

Shodhanakarma.

RECOMMENDATION FOR FURTHER STUDY :

Further specific studies like Poorvakarma with Shodhana karma to know the

effect on serum lipid values (Hyperlipidaemia and Normal Lipid Values) can

be taken up. So that better understanding of Shodhanang snehapana on Serum

lipid values is possible.

Along with Moorchita Tilataila, other classical Sneha yogas can be studied

comparatively.

Effect of Bhrumhana Snehana and Shamana Snehana on serum lipid profile is

to be estimated.

Present study pattern can be continued in the form of prospective clinical

study with increased sample size.

Conclusion - 144


CONCLUSION:

Shodhananga Arohana Snehapana plays a major role as a Poorva Karma to

Shodhana (Vamana Or Virechana) procedures.

Shodhananga Arohana Snehapana with Murchita Tilataila has a role in

Samedarakta by reducing the Serum Triglyceride and Serum Cholesterol and

in controlling the primary Hyperlipidaemia.

Literal meaning of word Samedarakta has been taken as Sa=with, meda = fat,

rakth = blood i.e., Rakta associated with Meda. The fat or lipid present in the

blood in the normal condition or abnormal condition is taken as Samedarakta.

Almost samples showed decrease in the total Cholesterol, LDL in both

groups. This shows significance of Shodhananga Arohana Snehapana.

Serum Triglyceride and VLDL values shows highly significant reduction in

Hyperlipidaemic group compared to Normolipidaemic group.

All Hyperlipidaemic samples showed rise in the HDL level and in

Normolipidaemic group most (67%) samples showed raise in HDL level

which indicates the protective role of the Shodhananga Arohana Snehapana.

After Arohana Snehapana in healthy persons the Serum Lipid Values were

within normal limits which shows the specificity of Murchita Tilataila.

Murchita Tilataila showed its effect in reducing weight & BMI through its

properties.

Conclusion - 145


hT e present work entitled as “The study of Arohana (Shodhanaga) Snehapana

and its effects on Samedarakta with special reference to Hyperlipidaemia and Normal

Lipid Values”. is designed into 5 main parts namely Review of Literature, Clinical Study,

Discussion, Summary and Conclusion.

The first part mainly deals with the Introduction, Objectives of the study, Nirukti,

Paribhasha of Sneha, Sneha Gunas, Panchabhautikata, General Classification, methods of

Shodhananga Snehana, indications of Snehana, procedure of Snehapana, Sneha

karmukata etc.

Regarding disease review about the term Samedarakta and about Meda Utpatti,

Swarupa Medovaha srotas, functions of meda dhatu, pramana, Ashrayashrayee bhava of

Meda, moola of Medovaha srotas and also about literary review of Medovriddhi along

with Nidana, Roopa and Samprapti, Medhodhatu srotodusti are dealt and also modern

review of the correlation Hyperlipidaemia was dealt.

The drug selected for this study was Murchita Tilataila and details of its

ingredients used for Murchana have been mentioned with their properties. The

pharmacodynamics of Ama pachana drugs i.e. about Panchakola Choorna have been

dealt.

In the second part, Clinical study deals with Methodology, Criteria for selection

of Individuals, the details of grouping, Criteria for assessment, Observations presented in

tabular form along with graphs. Later the results obtained in two groups were shown

with statistical analysis.

The observations pertaining to the literary and clinical study are discussed to draw

the logical conclusions in the second part of the dissertation.

Summary - 146


The brief summary of the results are as follows :

Among 30 individuals 15 patients were Hyperlipidaemic and 15 Volunteers were

Normo Lipidaemic. For all 30 patients Murchita Tilataila was given as Snehapana.

Group A (Hyperlipidaemic) : Maximum individuals were belonged to the age group of

30-50 years (53.30%), maximum (66.60%) persons were males, Hindu (86.58%),

Sedentary occupation (59.94%), Married (100%), Middle Class (73.26%),

Non – vegetarian (66.60%), Shamishra diet (53.28%), (86.58%) day workers, (66.60%)

were not doing exercise and also maximum persons were of Madhyama Jataragni

(79.92%), Madhyama Kostha (73.26%), Kaphapitta prakruti (73.26%), Madhyama Sara

(73.26%), Madhyam Samhanana (73.26%), Madhyama pramana (79.92%), Madhyama

Satmya (73.26%), Madhyama Satva (73.26%), Madhyama abhyavarana Shakti (79.92%),

Madhyama Jaranashakti (66.60%) & Vyayama Shakti (79.92%).

Group B (Narmolipidaemic) : Maximum individuals were belonged to the age group of

20-30 years (46.62%), maximum (59.94%) persons were females, Hindu (86.58%),

Labour occupation (46.62%), Married (73.26%), Middle Class (79.92%),Vegetarian

(59.94%), Shamishra diet (73.26%), (93.24%) day workers, (79.920%) were doing

exercise and also maximum persons were of Madhyama Jataragni (93.24%), Madhyama

Kostha (73.26%), Kaphapitta prakruti (66.60%), Madhyama Sara (73.26%), Madhyam

Samhanana (79.92%), Madhyama pramana (66.60%), Madhyama Satmya (59.94%),

Madhyama Satva (53.28%), Madhyama abhyavarana Shakti (73.26%), Madhyama

Jaranashakti (86.58%) & Vyayama Shakti (73.26%).

Summary - 147


Except Murcha, Arati and Daha, remaining Jeeryamana laxashanas were

observed in both Groups. All the 30 persons were showed Samyak Snigdha Laxashanas.

♦ Effect on Group A(Hyperlipidaemic) : All parameters Serum Triglycerides,

Serum Cholesterol, LDL and VLDL showed highly significant results. All

patients showed increase in HDL value.

♦ Effect on Group B (Narmolipidaemic) : All parameters showed highly

significant and most of the persons showed rise in the HDL level.

♦ Comparison :

The parameter HDL, Serum Triglycerides and VLDL showed more effective in

Group A than Group B, where as the Serum Cholesterol was little more effective than

parameter LDL in Group A and variation in Serum Cholesterol was more in group B. The

parameter VLDL was had less variation in group B.

On the basis of results finally this study concluded that Arohana Snehapana with

Murchita Tilataila showed safety and protective action in both Hyperlipidaemia patients

as well as healthy persons. Suggesting the fact that Chikista advised in Ayurveda is more

comprehensive, rational and can be adopted in the modern times also without any

untoward effects.

Summary - 148


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183. Vagbhata, Astanga Hridaya, Chikitshasthana, Chapter 11, Shloka 12-14. Edited by Kaviraj Atridev Gupta, 10th edn. Varanasi : Choukambha Sanskrit Sansthan ; 1992. p. 395.

184. Henry N, Ginsburg, Ira J. Goldburg, Harrison’s Principles of International Medicine, volume II. Chapter 341. Disorders of Intermediary Metabolism. 14th edn. New York. : Mc Graw Hill Companies 1998. p. 2138-2144.

185. API text book of medicine, Disorders of Lipid Metabolism. Edited by G. S. Sainani, 6th edn. Mumbai: Association of Physicians of India ; 1999. p. 191 -195.

186. Davidson’s Principles and Practice of Medicine. Nutrition, Metabolism and environmental diseases. Chapter10. Edited by CRW Edwards. 19th edn. London : Churchil Livngstone Publications ; 2002 p. 308-311.

187. The Antiseptic Journal, Amara k Uxa, Pranesh Nigam. Hyperlipidaemia-recent advances in management. November 2000 Vol 97.No 11.P.410.

188. West / Todd / Manson / Van Bruggen, Text book of Biochemistry, pp.991

189. Sharangadhara, Sharangadhara Samhita, Madyama Khanda, Chapter 6, Shloka 13-14, Edited by Dr. Smt. Shailaja Srivatsava, 3rd edn. Varanasi : Choukambha Orientalia ; 2003. p.275.

190. Bhaishajyaratnavali, Chapter 5, Shloka 1286-1287. Edited by Ambikadatta Shastry, 15th edn. Varanasi : Choukambha Sanskritha Sansthana ; 2002 p.130-131.

191. Prof. P.V. Sharma, Dravyaguna vignana, Vol- II. 16th edn. Varanasi : Choukambha Bharati Academy ; 1995. P.275-278.

192. Ibid, p335-336

193. Ibid, p359-361

194. Ibid, p331-335

195. Ibid, p800-804

196. Ibid, p753-758

197. Ibid, p 239-241

198. Ibid, p758-760

199. Ibid, p 370-372

200. Ibid, p 162-165

Bibliography - 163


201. Ibid, p 616-617

202. Ibid, p 664-666

203. Ibid, p 141-143

204. Ibid, p 39-41

205. Bhavamishra,Bhavaprakasha Nighantu. Edited by G.S. Pande. , 6th edn. Varanasi : Choukambha Bharati Academy ; 1982. p.266-267.

206. Prof. P.V. Sharma, Dravyaguna vignana, Vol- II. 16th edn. Varanasi : Choukambha Bharati Academy ; 1995. P. 120-123.

207. Kokate CK, Purohit AP, Gokhale SB, Pharmocognocy. 1st edn. Pune : Publisher Dinesh Furia Niroli prakashana ; 1990. p. 242-243.

Bibliography - 164

DEPARTMENT OF POST GRADUTE STUDIES IN PANCHAKARMA D.G.M.C. GADAG.

SPECIAL CASE SHEAT PROFORMA FOR “ THE STUDY OF AROHANA SNHEHAPANA AND ITS EFFECT ON SAMEDARAKTA WITH SPECIAL

REFERANCE TO HYPERLIPIDAEMIA AND NORMAL LIPID VALUES.”

GUIDE : DR. P. SHIVARAMUDU. DR. VARSHA.S.KULKARNI. M.D. (AYU) M.D.SCHOLAR CO-GUIDE : DR. S.H.DODDAMANI. M.D. (AYU) 1. Name of the patient : 2. Father’/Husband’ Name : 3. Age : Sl. No. : 4. Sex : O.P.D. No. : Male Female 5. Religion : I.P.D. No. : Hindu Muslim Christen Others

6. Education : D O.A : D.O.D : M UM 7. Marital Status : 8. Occupation :

Labour Student Executive Sedentary

9. Economic status :

Poor Middle Cl High Cl

10. Address : Ph. No. : Mail I.D : PIN

A Hyperlipidaemic B Narmolipidaemic

10. Group : Increased

abnormality Decreased

abnormality Normal Limits Variable

11. Result :

CONSENT

I am fully educated with the disease and treatment there by I got satisfied whole heartedly. I accept for the medicinal trial over me.

Investigator signature Patient’s signature

1) PRADHANA VEDANA (MAIN COMPLAINTS):

Laxanas Before Treatment After Treatment

Chala Spik, Sthana, Udara Krichravyavayata Dourbalya Dourghandhyata Swedadhikyata

2) ANUBHANDHI VEDANA (ASSOCIATED COMPLAINTS) :

Lakshanas P/A Duration Atikshudha Atipipasa Atinidra Gadgadhatwa Javoparodha Soukumarata Krathana Ayurhasa

3. POORVA VYADHI VRUTTANTA (PAST HISTORY) : 4. KULA VRUTTANTA ( FAMILY HISTORY) : Father Husband / Wife Mother Children Brother Sister If anybody in the family suffering from

Hyperlipidaemia Hypertension

5. VAYAKTIK VRUTTANTA ( PERSONAL HISTORY) :

A) AHARA

AHARA Alpa Sama Atipramana

FOOD Veg Mixed

DOMINANT RASA IN DIET Madhu Amla Lavan Katu Tikta Kashaya GUNA Snigda Sheeta Guru Ushna DIETIC HABIT Samashana Vishamashana Adhyashana OTHER

B) VIHARA NATURE OF WORK Manual Sedentory Labour Travelling Day Night

Sleep time Sound Disturbed Day / Night SLEEP

VYAYAMA No Occasionally Every Day C) VYASANA

Alcohol Smoking Tobacco Chewing Any other

Quantity Quantity Quantity Quantity

VYASANA Duration Duration Duration Duration

D) JATARAGNI Jataragni Mandagni Teekhanagni Vishamagni

E) RUTUSHRAVA VRUTTANTA

Rutushrava vruttanta Prasootika Vruttanta

Issues Abortion Operation Age of menarche Menapause

Artava pravrithi

If the patient female

Day Sama Alpa Adhik

6) ASTHASTHANA PAREEKSHA:

Nadi ( Pulse) Shabda Mootra Jihwa Mala Drik Akruti Sparash (Temp)

7. SAMANYA PAREEKSHA: B.P. R.Rate H.Rate Height

Before Treatment After Treatment Weight

Body mass index = Weight in Kg . Height in meter2

8. a) DASHAVIDHA PAREEKSHA:

Shareerik V P K VP PK KV Sama Prakruti Manasika S R T SR ST TR Sama Sarataha Pravara Madhyama Avara Samhananataha Pravara Madhyama Avara Pramanataha Pravara Madhyama Avara Satmyataha Pravara Madhyama Avara Satwataha Pravara Madhyama Avara Ahara Shakti Abhyavaharana

Pravara Madhyama Avara

Shakti Jeerana Shakti

Pravara Madhyama Avara

Vyayama Shakti Pravara Madhyama Avara Vayataha Bala Madhyama Vriddha Vikrutitaha VIKRUTITAHA PAREEKSHA. * Nidana ------- * Roopa -------- b) SYSTEMIC EXAMINATION * Gastro-intestinal System ------- * Respiratory System ------ * Cardio Vascular System ------

* Nervous System ------

9. LABORATORY INVESTIGATION:

a. SPECIAL INVESTIGATIONS

Serum Lipid Profile Pre Test Post Test Changes Observed

1. Serum Cholesterol mg/dl mg/dl mg/dl 2. Triglycerides mg/dl mg/dl mg/dl 3. HDL mg/dl mg/dl mg/dl 4. LDL mg/dl mg/dl mg/dl 5. VLDL mg/dl mg/dl mg/dl

b. OTHER INVESTIGATIONS

HB % TC DC ESR FBS RBS Urine (R) Alb Sug Micr

10. CHIKITSA PATRIKA :

AMAPACHANA -------- Amapachana by 3-6gm Panchakola choorna before food with hot water till Niramavasta seen (3-7 days)

SNEHAPANA

Sneha used ------- Murchita Tilataila Anupana -------- Ushnajala

PRADHANA KARMA

Day/Date I II III IV V VI VII Sneha matra Pana kala (time of sneha administration)

Agnipradurbhava kala Total time taken for Sneha Jeerna

• OBSERVATION OF JEERYMANA LAXANAS Laxanas I Time II Time III Time IV Time V Time VI Time VII Time

Shiroruja Bhrama Lalasrava Murcha Angasada Klama Trishna Daha Arati

• SNEHA JEERNA LAXANAS

Laxanas I Time II Time III Time IV Time V Time VI Time VII Time

Jeeryamana lakshana Prashama

Shareera Laghuta Kshudha pravrutti Trishna Pravrutti Udgara Shuddhi Anya

• OBSERVATION OF SAMYAK SNIDHA LAXANAS

Laxanas I Time II Time III Time IV Time V Time VI Time VII Time Vatanulomana Agnideepti Purish snigdhata Asamahata varchas Twak snigdhata Anga laghavata Gatra mardhavata Snehodwega Klama Shaithilya

ASAMYAK SNIGDHA LAKSHANAS

Asnigdha Lakshanas – Ruksha Purisha/ Grathita Purisha/ Apravaguna Vata/ Mrdu Pakta/ Kharatva/ Raukshyata. Ati Snigdha Lakshana – Panduta/ Gaurava/ Jadya/ Tandra/ Aruchi/ Utklesha/ Purishasya Avipakvata. SNEHAPANA VYAPAT

Tandra/ Utklesha/ Anaha/ Jvara/ Stambha/ Visanmyatha/ Kushta/ Pandu/ Kandu/ Shopha/ Arsha/ Aruchi/ Trishna/ Grahani

Dosha/ Staimitya/ Vakyanigraha/ Shula/ Ama Pradosha.

• DAILY DIET CHART DURING SNEHAPANA

Day Anna Kala Kind of (Anna) Food I II III IV V VI VII

Advised for follow up treatment: 1. Vishram kala (Abhyanga & Sweda) : 2. Shodhana karma : Signature of Co - Guide Signature of Guide

snehapana samedarakta pk002-gdg

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