i

MIASMATIC EVALUATION OF HYPERLIPIDEMIA

by

Dr SHEENA K.N

Dissertation Submitted to

Rajiv Gandhi University of Health Sciences, Karnataka, Bangalore

In partial fulfillment of

the requirements for the degree of

Doctor of Medicine in

Organon of Medicine and Homoeopathic Philosophy

Under the guidance of

Dr ROSHAN PINTO

DEPARTMENT OF ORGANON OF MEDICINE AND

HOMOEOPAT HIC PHILOSOPHY,

FATHE R MULLE R HOMOEOPAT HIC MEDICAL COLLEGE,

DERALAKATTE, MANGALORE

2011

ii

CERTIFICATE BY THE GUIDE

This is to cert ify that the dissertat ion ent it led “MIASMATIC

EVALUATION OF HYPERLIPIDEMIA” is a bonafide research work done by

Dr SHEENA K.N under my guidance and supervision dur ing the year

2008 – 2011, in part ia l fulfillment o f t he requirement for the award o f the

degree o f “DOCTOR OF MEDICINE” (ORGANON OF MEDICINE

AND HOMOEOPATHIC PHILOSOPHY) .

I have sat isfied myself regarding the authent icit y o f her

observat ions noted in this dissertat ion and it conforms to the standards o f

Rajiv Gandhi Universit y o f Healt h Sciences, Karnataka, Bangalore. It has

not been submit ted (part ial or full) for the award o f any other Degree or

Dip loma.

Dr ROSHAN PINTO Date : M D (H O M )

Place: Mangalore Professor , Depar tment of

Organon of Medicine and

Homoeopathic Philosophy,

Father Muller Homoeopathic Medica l

College and Hospita l,

Deralakat te, Mangalore

iii

DECLARATION BY THE CANDIDATE

I hereby declare t hat this dissertat ion ent it led “MIASMATIC

EVALUATION OF HYPERLIPIDEMIA” is a bonafide and genuine research

work carr ied out by me, under the guidance o f Dr ROSHAN PINTO ,

Professor, Department o f Organon o f medicine and Homoeopathic

Philo sophy, dur ing the year 2008–2011, in part ial fulfi llment o f

requirement for the award o f DOCTOR OF MEDICINE (ORGANON OF

MEDICINE AND HOMOEOPATHIC PHILOSOPHY) .

I have not previously submit ted this work (part ial or full) to any

other universit y for the award o f any other Degree or Diploma.

Date:

Place: Mangalore Dr SHEENA K.N

iv

ENDORSEMENT BY THE HOD, PRINCIPAL/

HEAD OF THE INSTITUTION

This is to cert ify t hat the dissertat ion ent it led “MIASMATIC

EVALUATION OF HYPERLIPIDEMIA” is a bonafide research work carr ied

out by Dr SHEENA K.N under t he guidance and supervis ion o f

Dr ROSHAN PINTO dur ing the year 2008 – 2011, in part ial fulfillment

of the requirement for the award o f the degree o f “DOCTOR OF

MEDICINE” (ORGANON OF MEDICINE AND HOMOEOPATHIC

PHILOSOPHY) .

We have sat isfied regarding the authent ic it y o f her observat ions

noted in this dissertat ion and it conforms the standards o f Rajiv Gandh i

Universit y o f Health Sciences, Karnataka, Bangalore. It has not been

submit ted (part ial or full) for the award of any other Degree or Diploma.

HEAD OF THE DEPARTMENT PRINCIPAL

Dr SHIVAPRASAD K. Dr SRINATH RAO BSc, MD (HOM) MD (HOM)

Professor, HOD, Professor, HOD, Dept . of Organon o f Medic ine and Dept.of Materia Medica, Homoeopathic Philo sophy, Fr. Muller Homoeopathic, Fr. Muller Homoeopathic Medical Medical College, College, Deralakatte, Mangalore Deralakatte, Mangalore

Date: Date:

v

Place: Manga lore P lace: Manga lore

COPYRIGHT

Declaration by the Candidate

I hereby declare that the Rajiv Gandhi University of Health

Sciences, Karnataka, Bangalore shall have the r ights to preserve, use

and disseminate this dissertat ion / thesis in pr int or elect ronic format for

academic / research purpose.

Date:

Place: Mangalore Dr SHEENA K.N

© Rajiv Gandhi University of Health Sciences, Karnataka

vi

Acknowledgement

I consider this as my privilege to thank the Almighty God, who is

responsible for everything in my l i fe, and give him all the glory for the accomplishment of my post graduate studies. I thank him for helping me to

achieve this task through the following persons who have been of immense help and source of encouragement in my endeavor .

I would l ike to express my sincere and hear tfel t thanks to my respected teacher and guide Dr Roshan Pinto , Professor, Department of Organon of

Medicine and Homoeopathic Philosophy for providing me expert guidance, constructive advice, freedom of thought, personal attention, t imely support and encouragement throughout my post graduate course and during the dissertation

work. It is my good fortune to do this work under his guidance.

It is my privilege to express sincere grati tude to Rev. Fr Patrick Rodrigues, Director, FMCI and Rev. Fr Wilfred Prakash D’souza ,

Administrator of Fr. Muller Homoeopathic Medical college, Mangalore for providing me an opportunity and adequate facil i t ies to carry out this work to my satisfaction in this reputed insti tution.

I would l ike to express my grati tude to Dr Shashi Kant Tiwari former

principal, who is and was a real source of inspiration and also Dr Srinath Rao, Principal, Father Muller Homoeopathic Medical College for his support while

persuing my studies.

I express my sincere thanks to Dr Shivaprasad K , Vice principal and Head of the Department of Organon of Medicine and Homoeopathic Philosophy, for his constant support , care and encouragement.

I also express my grati tude to Dr M. K. Kamath , PG Co-ordinator and

Head of the Department of Medicine, who was the man behind most acti vi t ies of the postgraduates, guiding us to perfection.

vii

I owe my sincere grati tude for all the help, and cooperation that I have received from my colleagues of various departments of FMHMC of whick I

cannot withhold the names of few l i ke Dr Jacintha Monteiro, Dr Deena Monteiro, Dr Deepa Rebello, Dr Prabhukiran and Dr Joseph Thomas.

I must thank all my batchmates especially Dr Shalini and Dr Rekha for

their companionship, co operation and t imely help which considerably eased my task. I at tribute part of my success and st rength to them.

A word of grati tude to Mr Suresh and Dr Shripathi Kalluraya for t eaching statist ical application and research help ing to formulate the Research

Methodologies for my synopsis and carry out the statist ical work of my thesis.

I thank all the members of non-teaching staff of Fr. Muller Homoeopathic Medical College, especially l ibrary staff for their prompt service and the staff of out patient department and clinical laboratory who has

provided me with the case material required for the study.

I would have never accomplished my goal without the encouragement and prayers of my parents Mr K. Narayanan & Mrs Rajalakshmi Narayanan and

my brother Mr Sreeji th who is a world of encouragement and understanding to me. Special regards I carry in my heart for my husband Mr Salin Kumar and my beloved son Vaishak Salin for their love and co -operation in every aspect

of my l i fe.

Last but not the least , my sincere thanks to all the Patients on whom the study was conducted and MicroBits , Kankanady for taking pains for the

successful and t imely completion of this work.

I thank all the persons who have directly or indirectly influenced me for the better outcome of this work.

Place: Mangalore

Date: Dr SHEENA K.N

viii

Affectionately

Dedicated To…

My Family

ix

LIST OF ABBREVIATIONS

< : Aggravation

> : Amelioration

α : Alpha

ACTH : Adrenocorticotrophic hormone

AMP : Adenosine mono phosphate

APD : Acid peptic disease

Apo : Apoprotein

ASCVD : Artherosclerotic cardio vascular disease

ATP : Adenosine Tri phosphate

Av : Aversion

β : Beta

CAD : Coronary artery disease

CETP : Cholesteryl ester transfer protein

Chol : Total cholesterol

Co A : Co enzyme A

CP : Characteristic particulars

Cr : Craving

CVA : Cerebrovascular accident

DALY : Disability adjusted life year

DM : Diabetes Mellitus

DM : Dominant miasm

x

FA : Fatty acid

F/H : Family history

FM : Fundamental miasm

HDL : High density lipoproteins

HMG : Hydroxy methyl glutaryl

HS : At bed time

IDL : Intermediate density lipoprotein

LCAT : Lecithin cholesteryl acyl transferase

LDL : Low density lipoprotein

LPL : Lipoprotein lipase

MG : Mental generals

NAD : No abnormality detected

NADPH : Nicotinamide adenine dinucleotide phosphate

PG : Physical generals

P/H : Past history

Pkt : Packet

PVD : Peripheral vascular disease

S : Same

SCR : Standardized case record

TG : Triglyceride

TAG : Triacyl glycerol

VLDL : Very Low density lipoprotein

WHO : World Health Organization

xi

ABSTRACT

Background: Hyperlipidemia is regarded as a highly modifiable risk factor for

cardiovascular disease due to the influence of cholesterol on atherosclerosis. It results

from genetic predisposition interacting with an individual diet & lifestyle. Any defect in

the synthesis, transport or excretion of the lipids causes a rise in their level in plasma

which becomes a risk factor for coronary heart disease which is one of the major cause of

death in the present day.

Objective :

1. To study the different types of hyperlipidemia

2. To assess the role of miasm in hyperlipidemia and know the effectiveness of

constitutional method of treatment which includes the miasmatic background of

the individual.

Methods:

A total number of 30 cases were taken randomly for the study. The cases with

deviated serum lipid i.e. Cholesterol > 200mg/ dl, Triglycerides > 150mg/dl, LDL >

130mg/ dl or HDL <40mg/ dl were selected. For the assessment of the clinical status

before and after the treatment, scoring was done which is mentioned in the annexure-1.

The score before and after the treatment was considered and ‘t’ test was applied.

Results:

Among the 30 cases, a prevalence of hyperlipidemia was found in the age group

between 35 - 45 yrs. Maximum incidence of hyperlipidemia is seen in sedentary working

individuals. Sycotic expression was found to be dominating in both fundamental and

xii

dominant miasm. Constitutional treatment with general management showed

effectiveness in the treatment of hyperlipidemia

Conclusion:

This study provides an evidence to say that there is reduction in the disease

intensity scores after the homoeopathic constitutional treatment with properly planned

general management including diet and exercise. Therefore a combination of

constitutional homoeopathic treatment and general management is effective in the

treatment of hyperlipidemia.

Key words:

Hyperlipidemia, constitutional treatment, general management, diet, exercise,

serum lipid levels.

xiii

TABLE OF CONTENTS

S. No. TOPIC PAGE No.

1 INTRODUCTION 1

2 AIMS AND OBJECTIVES 4

3 REVIEW OF LITERATURE 5

4 METHODOLOGY 77

5 RESULTS 81

6 DISCUSSION 95

7 CONCLUSION 100

8 SUMMARY 102

9 BIBLIOGRAPHY 103

10 ANNEXURES

ANNEXURE – 1 107

ANNEXURE – 2 108

ANNEXURE – 3 118

xiv

LIST OF TABLES

Table No. TITLES PAGE NO.

1 Fredrickson classification of hyperlipidemia 30

2 Miasmatic evaluation criteria 67

3 Distribution of cases according to age group 81

4 Distribution of cases according to sex 81

5 Distribution of cases according to religion 83

6 Case distribution according to physical activity 83

7 Case distribution according to fundamental miasm 85

8 Case distribution according to dominant miasm 85

9 Case distribution according to type of hyperlipidemia 87

10 Case distribution according to constitutional remedies 88

11 Case distribution according to the improvement 90

12 Statistical analysis 91

xv

LIST OF FIGURES

Figure No.

TITLE PAGE No.

1 Lipid Digestion 7

2 Lipid degradation 7

3 Fat absorption 9

4 Fat metabolism 12

5 Source and fate of Triglycerols 14

6 Source and fate of cholesterol 17

7 Composition of Lipoprotein 22

8 Transport of Lipids 25

9 Diet pyramid 50

10 Natural sources reducing hyperlipidaemia 52

11 Case distribution according to age group 82

12 Case distribution according to sex 82

13 Case distribution according to religion 84

14 Case distribution according to physical activity 84

15 Case distribution according to fundamental miasm 86

16 Case distribution according to dominant miasm 86

17 Case distribution according to type of hyperlipidemia 89

18 Case distribution according to constitutional remedies 89

19 Case distribution according to the effectiveness of treatment 90

20 Distribution of all cases according to pre and post treatment analysis 94

i

Introduction

1

INTRODUCTION

Raised or abnormal levels of lipids & lipoproteins in the blood has become a

common clinical problem of the century which has turned out to be a challenge to the

physician. In today’s world most deaths are attributable to non communicable diseases &

over half of these are a result of cardiovascular diseases. Heart disease & stroke are first

& second cause of death in developed countries. WHO has drawn attention to the fact

that coronary heart disease is our “modern epidemic”.

Today there is a vast body of evidence showing the triangular relationship between

habitual diet, blood cholesterol & coronary heart disease. It is a well established fact that

a persistently high cholesterol level in blood can precipitate a cardiac event.

Hyperlipidemia is a rise in plasma cholesterol, triglyceride or both. It is regarded

as a highly modifiable risk factor for cardiovascular disease due to the influence of

cholesterol on atherosclerosis. Genetic factors are the most important determinants of a

given individual’s triglycerides & LDL levels besides the westernized life styles which

emphasize on rich food & sedentary living.

The ability of a remedy to eradicate inborn tendency of disease is not possible by

considering only symptom similarity of presenting disease. It needs much deeper

understanding of disease from evolution point of view. Such an effort from Master

Hahnemann resulted in the concept of miasms which was one among the many mysteries

of homoeopathy till recently. However genetic mapping raises the hope of understanding

miasms.

2

Any tendency to disease or destruction which can be recognized in man derives

from a structural anomaly which imprints its characteristics on him. The expression

varies in different individuals according to constitution, hereditary disposition,

education, habit, mode of life, diet, occupation, tendencies of the mind, morals, etc;

which together constitutes the miasm.

Miasm is a sort of taint, hereditary or acquired, which lies dormant in the human

system but is reactivated by circumstantial pathogens and helps to bring about

disequilibrium in vital force which in general parlance is called disease. It is a unique

complex phenomenon which acts by prolonging the disease and or by obstructing the

process of cure, even though a true similimum has been prescribed. If utilized with our

principle it shows natural way towards cure. Unless we understand the phenomena of

acting and basic miasms, it will not be possible to find the true similimum for the

eradication of the disease. The phenomenon of recurrence of the disease will be there to

torment the patient and to tax the physician.

Medical science has advanced by leaps & bounds from the time of Dr Samuel

Hahnemann regarding etiology, pathophysiology & management of chronic disease. A

homoeopath should keep in pace with this ongoing advances & renew his sources &

literature without deviating from the basic principles put down by Dr Hahnemann.

Experiments were conducted all time to find cause of disease to benefit the sick.

Exact cause is seldom found. But these studies can give information regarding correlation

between two phenomena. If understood, they provide the basic path towards inference.

In present scenario medical practice is purely based on scientific experimentation &

inferential statistics. Hence it is a necessity to have a scientific vision of truth.

3

To cure a person does not mean only to free him from his present suffering, or

alleviate his suffering; but also to preserve him and spare him from future sufferings.

Evaluation of the miasm in an individual followed by antimiasmatic treatment can help in

the prevention of the progress and complication of the disease.

This study is an attempt towards assessing the predisposing miasm in

hyperlipidemia and thereby establish the specific miasmatic preponderance in the

expression of a chronic disease and its antimiasmatic treatment as specified by

Dr Hahnemann which may help to abort or prevent disease progress.

1

Objectives

4

OBJECTIVES

1. To study the different types of hyperlipidemia

2. To assess the role of miasm in hyperlipidemia and know the effectiveness of

constitutional method of treatment which includes the miasmatic background of

the individual

4

Review of Literature

5

REVIEW OF LITERATURE

Lipids derived from the Greek word Lipos which means fat is the chief

concentrated storage form of energy besides their role in cellular structure & various

other biological function. They are heterogeneous group of compounds regarded as

organic substances relatively insoluble in water, soluble in organic solvents like alcohol.1

Classification1

1) Simple – Esters of fatty acids with alcohol

Fats & oils - Esters of FA with glycerol

Waxes – Esters of FA with alcohol

2) Complex (Compound) – Esters of FA with alcohols containing additional groups

such as phosphate, nitrogenous base, carbohydrate, protein etc

Phospholipids – Contains phosphoric acid & frequently a nitrogenous base

in addition to alcohol & FA

Glycolipids – Contains carbohydrate, Nitogenous base & FA

Lipoprotein – Mononuclear complexes of lipids with proteins

Other complex lipids – Sulfolipids, Aminolipids, Lipopolysacharrides

3) Derived lipids – Derivatives obtained on hydrolysis of simple & complex which have

the characteristics of lipids like Glycerol, FA, Ketone bodies, steroid hormones etc

4) Miscellaneous lipids – Large number of compounds possessing the characteristics of

Lipids

5) Neutral lipids – Uncharged lipids like Mono, Di and Triacylglycerol, Cholesterol,

Chloesteryl esters

6

Digestion of dietary lipid1,2,3

There is a considerable variation in the daily consumption of lipids which mostly

depends on economic status & dietary habits.

Several chemical compounds in food and in the body classified as lipids includes

(1) Neutral fat, also known as triglycerides; (2) Phospholipid (3) Cholesterol; and (4) a

few others of less importance.2

Large lipid particles to a negligible amount are broken down into smaller with

lipolytic enzyme, lingual lipase. Released short chain FA can be directly absorbed from

stomach wall & enter portal vein.4

For effective digestion of lipids emulsification occurs in small intestine by

detergent action of bile salts, surfactant action of degraded lipids & mechanical mixing

due to peristalsis. Bile contains a large quantity of bile salts as well as the phospholipid

lecithin, the major function of which is to make the fat globules readily fragmentable.

Powerful lipase of the pancreatic juice & enteric lipase in the enterocytes of the

small intestine hydrolyze & break down long chain & short chain FA of TAG into alpha

& beta monoglycerides , glycerol & FA.

Lipid esterase in pancreatic juice in presence of bile acids acts on monoacyl

glycerol, cholesteryl esters etc to give FA.

Cholesterol esterase in pancreatic juice either catalyzes the esterification of free

cholesterol with FA or cleaves cholesteryl esters to cholesterol & free FA. Both the

cholesterol esters and the phospholipids are hydrolyzed to free the fatty acids by the

enzyme cholesterol ester hydrolase and phospholipase A2 in the pancreatic secretion

respectively.2

7

Fig. 1: Lipid Digestion

Fig.2: Lipid degradation 5

8

Transport of digested fat across the membrane of intstinal villous layer into intestinal

epithelial cells occur by simple diffusion through cell membrane. Within the intestinal

epithelial cells alpha monoglycerides are further hydrolyzed by intestinal lipase to free

FA & glycerol.1

Absorption2,3

Absorption from the small intestine each day consists100 or more grams of fat.

The bile salt micelles which are small spherical, cylindrical globules composed of 20 to

40 molecules of bile salt, act as a transport medium to carry the monoglycerides and free

fatty acids to the brush borders of the intestinal epithelial cells. There the monoglycerides

and free FA are absorbed into the blood. But the bile salts themselves are released back

into the chyme to be used again for this “ferrying” process. The bile salt micelles play the

same role in “ferrying” free cholesterol and phospholipid molecule.2

Glycerol, phospholipid, short chain, medium chain & unsaturated FA are

absorbed directly to portal vein & is taken to liver. Some absorbed FA enter into lymph

of lacteals which passes through thoracic duct to systemic circulation

Free FA in intestinal wall are reincorporated into TG after activation. This cannot

pass to lymphatics & hence enter the lymph as minute, dispersed droplets called

chylomicrons which are lipoprotein complex composed of largely TG, cholesterol,

phopholipid & specific apo protein. The chylomicrons enter lymphatic vessels and are

then transported upward through the thoracic duct and emptied into the circulating

venous blood at the juncture of the jugular and subclavian veins to enter into systemic

circulation.1

9

Cholesterol is absorbed from intestine in free form. Esterification takes place

within intestinal mucosal cell. Most of the cholesterol and phospholipids absorbed from

the gastrointestinal tract enter the chylomicrons.

Some amount of fat, not hydrolyzed completely in intestinal lumen can combine

with bile salts and absorbed as micelles into lymphatic channels.

Some of lysophospholipid are resynthesised to phospholipid again by mucosal

cell while few are incorporated in VLDL in intestinal mucosal cell.

Fig.3: Fat absorption5

10

Metabolism1,2,5

Lipids constitute about 15% – 20 % of body weight in human.

Plasma lipids includes TAG, Cholesterol, Phospholipid, free FA, & Glycerol

TAG ( Neutral fat ) are the most abundant lipids comprising 80% - 90% of body

lipids. Most of the TAG are stored in adipose tissue & serve as energy reserves of the

body. It acts as an insulating material for maintaining body temperature. They are also

utilized by muscle, liver, heart etc as per needs of the body.

After absorption, most of the TAG in chylomicrons are removed from the

circulating blood as they pass through the capillaries of adipose tissue or the liver which

contain large quantities of hormone sensitive enzyme lipoprotein lipase. This enzyme

hydrolyzes the TG of chylomicrons releasing FA and glycerol. Complete degradation of

TAG to glycerol & free FA is lipolysis. The FA, being highly miscible with the

membranes of the cells, immediately diffuse into the fat cells of the adipose tissue and

into the liver cells where they are converted to acyl co A & reesterified into TG, with new

glycerol being supplied by the metabolic processes of the storage cells. Acyl Co A can be

obtained from dietary, FA synthesis, or TG circulating in chylomicron & VLDL. It also

occurs from α- glycerophosphate obtained from glucose oxidation & conversion of

glycerol

Fat that has been stored in the adipose tissue is to be used elsewhere in the body

to provide energy transported mainly in the form of free FA. This is achieved by

hydrolysis of the triglycerides back into FA and glycerol. Free FA released in lipolysis

enter circulation & are transported bound to albumin which enters various tissues &

utilized for energy.8

11

Glycerol produced in lipolysis is transported to liver where it is activated to

glycerol – 3 – phosphate which may be used for the synthesis of TAG & phospholipids. It

may also enter glycolysis.

TG continually undergoes synthesis ( Esterification ) & breakdown( Lipolysis )

within tissue. Resultant of these two process determines the magnitude of free FA pool in

adipose tissue & this in turn will determine the level of free FA circulating in blood

When rate of reesterification is less than rate of lipolysis, free FA accumulate & diffuses

into plasma & raises the level of free FA in plasma.6

When the amount of glucose available to the fat cell is inadequate, one of the

glucose breakdown products, α-glycerophosphate, is also available in insufficient

quantities, a hormone-sensitive cellular lipase can be activated, which promote rapid

hydrolysis of TG.

Large increase in free FA concentration in the blood occurs when rate of

utilization of fat for cellular energy also increase as in cases of starvation and in diabetes,

where the person derives little or no metabolic energy from carbohydrates.

95 % of energy obtained from fat comes by β oxidation of FA which occur only

in the mitochondria. Transport into the mitochondria is a carrier mediated process that

uses carnitine as the carrier substance. Once inside the mitochondria, FA split away from

carnitine and are degraded and oxidized which involves successive cleavage. The acetyl-

CoA molecules formed by β-oxidation of FA, enter immediately into the citric acid cycle

liberating large amounts of ATP. When excessive amounts of lipids are being used for

energy, part of the acetoacetic acid is also converted into β-hydroxybutyric acid, and

minute quantities are converted into acetone The acetoacetic acid, β-hydroxybutyric

12

acid, and acetone diffuse freely through the liver cell membranes and are transported by

the blood to the peripheral tissues. Here they again diffuse into the cells, where reverse

reactions occur and acetyl-CoA molecules are formed. These in turn enter the citric acid

cycle and are oxidized for energy. The concentrations of acetoacetic acid, β-

hydroxybutyric acid, and acetone occasionally rise to levels many times above normal in

the blood and interstitial fluids causing a condition called ketosis.3

Fig.4: Fat metabolism5

13

Plasma TG are derived from intestinal dietary fat during absorption & otherwise

from liver. In fasting state the FA is derived from adipose cell in minute quantities.TG

are taken up by the liver & a portion is reexcreted as VLDL and transported to the

adipose tissue, where they are stored.

Synthesis of TAG from Carbohydrates and Proteins7

Whenever a greater quantity of carbohydrates or proteins enters the body than can

be used immediately for energy or can be stored, the excess is rapidly converted into TG

which are secreted as lipoproteins.

Regulation of TAG synthesis8

Inactive form of lipase is activated by cyclic AMP dependent protein kinase to

activate lipase. Epinephrine, norepinephrine, glucagon, thyroxine, ACTH etc enhance the

activity of adenylate cyclase & thus increase lipolysis.

Insulin decreases cyclic AMP levels & thereby inactivate lipase. When no insulin

is available, as occurs in serious diabetes mellitus, fats are poorly synthesized. Here

glucose does not enter the fat and liver cells satisfactorily, so that little of the acetyl-CoA

and NADPH needed for fat synthesis can be derived from glucose. More over lack of

glucose in the fat cells greatly reduces the availability of α-glycerophosphate, which also

makes it difficult for the tissues to form TG.

During exercise, as a result of sympathetic stimulation, release of epinephrine and

norepinephrine by the adrenal medullae which directly activate hormone-sensitive

triglyceride lipase, present in abundance in the fat cells, causes rapid breakdown of TG

and mobilization of FA.

14

Stress causes corticotropin to be released by the anterior pituitary gland, and this

causes the adrenal cortex to secrete extra quantities of glucocorticoids thereby activating

the same hormone-sensitive triglyceride lipase. Growth hormone has a similar but weaker

effect in activating hormone-sensitive lipase

Thyroid hormone causes rapid mobilization of fat, which is believed to result

indirectly from an increased overall rate of energy metabolism in all cells of the body

under the influence of this hormone.3

Fig.5: Source and fate of Triacylglycerols 5

15

Cholesterol is animal sterol comprising 2gm / Kg body weight. It is a structural

component of cell membrane & precursor for synthesis of all steroids. 1 It is an essential

ingredient in the structure of lipoprotein. Being a poor conductor of electricity, it helps to

insulate nerve fibres. Vitamin D 3 is synthesized from 7 – dehydrocholesterol.6

The most abundant nonmembranous use of cholesterol in the body is to form

cholic acid in the liver. 80 % of cholesterol is converted into cholic acid. This is

conjugated with other substances to form bile salts, which promote digestion and

absorption of fats. A small quantity of cholesterol is used by the adrenal glands to form

adrenocortical hormones, the ovaries to form progesterone and estrogen, and the testes to

form testosterone.

A large amount of cholesterol is precipitated in the corneum of the skin which

along with other lipids, makes the skin highly resistant to the absorption of water soluble

substances and to the action of many chemical agents, because cholesterol and the other

skin lipids are highly inert to acids and to many solvents that might otherwise easily

penetrate the body. Also, these lipid substances help prevent water evaporation from the

skin. 3

FA can get esterified to form cholesterol esters and transported to liver as

cholesteryl esters for oxidation which helps in regulating cholesterol level in body fluids.

About 70 % of the cholesterol in the lipoproteins of the plasma is in the form of

cholesterol esters.

16

Synthesis of Cholesterol5

Cholesterol, is present in the diets of all people, and it can be absorbed slowly

from the gastrointestinal tract into the intestinal lymph. It is highly fat soluble but only

slightly soluble in water. Besides the cholesterol absorbed from the gastrointestinal tract,

called exogenous cholesterol, a greater quantity is formed in the cells of the body, called

endogenous cholesterol which circulates in the lipoproteins of the plasma formed by the

liver in majority, as well as from other cells of the body. Cholesterol in diet absorbed

from intestine in company with other lipids are incorporated into chylomicrons & to

some extent into LDL. Absorbed cholesterol is excreted in bile as bile salts after

conversion to bile acids. This is partly reabsorbed.

Regulation of cholesterol synthesis7

An increase in the amount of cholesterol ingested each day increases the plasma

concentration slightly. The rising concentration of cholesterol inhibits the most essential

enzyme for endogenous synthesis of cholesterol, 3-hydroxy-3-methylglutaryl CoA

reductase, thus providing an intrinsic feedback control system to prevent an excessive

increase in plasma cholesterol concentration.

Hormonal control is done by glucagon & glucocorticoids which favour formation

of inactive HMG co A reductase & thus reduce cholesterol synthesis.

Lack of insulin or thyroid hormone increases the blood cholesterol concentration,

whereas excess thyroid hormone decreases the concentration. These effects are probably

caused mainly by changes in the degree of activation of specific enzymes responsible for

the metabolism of lipid substances. Fasting and bile acids reduces activity of enzyme

thereby reducing cholesterol synthesis

17

A highly saturated fat diet increases blood cholesterol concentration 15 to 25%

due to increased fat deposition in the liver, which then provides increased quantities of

acetyl-CoA in the liver cells for the production of cholesterol whereas ingestion of fat

containing highly unsaturated FA usually depresses the blood cholesterol concentration a

slight to moderate amount.

Unabsorbed cholesterol in the intestine is acted upon by intestinal bacteria &

excreted as faecal sterols. Certain vegetables contain plant sterols which inhibit

reabsorption of cholesterol.

Fig.6: Source and fate of cholesterol 5

18

Phospholipids and Cholesterol Phospholipids: The major types of body phospholipids

are lecithins, cephalins, and sphingomyelin. Although the chemical structures of

phospholipids are somewhat variant, their physical properties are similar. They are all

lipid soluble and forms an important constituent of lipoproteins in the blood and are

essential for the formation and function of most of these. In their absence, serious

abnormalities of transport of cholesterol and other lipids can occur.2

Thromboplastin, which is needed to initiate the clotting process, is composed

mainly of one of the cephalins.6

Large quantities of sphingomyelin are present in the nervous system which acts as

an electrical insulator in the myelin sheath around nerve fibers. Phospholipids are donors

of phosphate radicals when these radicals are needed for different chemical reactions in

the tissues.

The most important of all the functions of phospholipids is participation in the

formation of structural elements such as in cell membranes and intracellular membranes

throughout the body.6

Synthesisof Phospholipids.2

Phospholipids are synthesized in essentially all cells of the body from

phosphatidic acid & 1, 2 diacyl glycerol. Probably 90 % are formed in the liver cells;

substantial quantities are also formed by the intestinal epithelial cells during lipid

absorption from the gut. The lipase causes hydrolysis of phospholipid releasing FA to be

stored in the cells.

19

LIPOPROTEINS1,2,9

In the post absorptive state, after all the chylomicrons have been removed from

the blood, more than 95% of all the lipids in the plasma are in the form of lipoprotein

which are macromolecular complexes of lipids with protein, containing TG, cholesterol,

phospholipids, and fat-soluble vitamins. They transport lipids through body fluids

(plasma, interstitial fluid, and lymph) to and from tissues. The total concentration of

lipoproteins in the plasma averages about 700 mg per 100 ml of plasma with Cholesterol

180 mg/dl, Phospholipids 160mg/dl, Triglycerides 160mg/dl and Protein 200mg/dl.

Based on their relative densities and seperation by electrophoresis it is classified as

1) Chylomicron are synthesized in the small intestine in the course of fat absorption

& in liver and transport dietary TAG to various tissues. They consist of highest

(99%) quantity of lipid mostly TAG besides about 9% phospholipids, 3%

cholesterol & lowest concentration (1%) of protein apoprotein B - 48. They have

least density and is largest in size. Nascent chylomicron with apo C II & apo E

derived from HDL forms chylomicron. Chylomicron formation fluctuates with the

load of TG absorbed.

2) Very low density lipoproteins (VLDL) which contain high concentrations of

TAG and moderate concentrations of both cholesterol and phospholipids are

produced in liver & intestine. It helps transport of endogeneously synthesised

TAG. Nascent VLDL with apo B 100 rich in TAG & cholesterol, with apo CII &

apo E donated by circulating HDL forms VLDL.

20

3) Intermediate-density lipoproteins (IDL) are VLDL from which a share of the

TG has been removed, so that the concentrations of cholesterol and phospholipids

are increased.

4) Low-density lipoprotein (LDL) are derived from IDL in the course of VLDL

metabolism, by the removal of almost all the TG, leaving an especially high

concentration of cholesterol and a moderately high concentration of

phospholipids. Apo E is returned to HDL. Thereby LDL contains high cholesterol

& less TAG. It transports cholesterol from liver to other tissues. Most important

function of LDL is to supply cholesterol to extrahepatic tissues by binding to the

specific receptor pits on cell membrane which is recognized by apo B 100. Defect

in LDL receptor causes elevation of plasma LDL & hence plasma cholesterol.

5) High-density lipoproteins (HDL) contains a high concentration of protein

(about50%) but much smaller concentrations of cholesterol and phospholipids.

Mostly synthesized in liver, it transports cholesterol from peripheral tissues to

liver. Free nacsent HDL is synthesized in liver which contain free cholesterol,

phospholipid & apoprotein. HDL accepts free cholesterol from other lipoprotein

in circulation & cell membrane of peripheral tissue which undergoes LCAT

catalysed esterification.

6) FA complexed with albumin

Each lipoprotein class comprises a family of particles that vary slightly in density,

size, migration during electrophoresis, and protein composition. The density of a

lipoprotein is determined by the amount of lipid and protein per particle. HDL is

the smallest and most dense lipoprotein, whereas chylomicrons and VLDL are the

21

largest and least dense lipoprotein particles Most TG is transported in

chylomicrons or VLDL, and most cholesterol is carried as cholesteryl esters in

LDL and HDL .They function as transport vehicles for lipids in blood plasma &

deliver the lipid components to various tissue for utilization. VLDL transport TG

synthesized in the liver mainly to the adipose tissue, whereas the other

lipoproteins are especially important in the different stages of phospholipid and

cholesterol transport from the liver to the peripheral tissues or from the periphery

back to the liver.9

Structure9,10

Lipoprotein consists of a neutral lipid core with TAG or cholesteryl ester,

sorrounded by a coat shell of hydrophilic lipids like phospholipids, unesterified

cholesterol and apoprotein that interact with body fluids. Polar amphiphilic portion are

exposed on surface so that it is soluble in aqueous solution.

Apoprotein is the protein component of lipoprotein which acts as its structural

component. It recognizes the cell membrane surface receptors, facilitates transfer of

lipids between lipoprotein classes & between lipoprotein & cells. It activates enzymes

involved in lipoprotein metabolism.

ApoA-I, which is synthesized in the liver and intestine, is found on virtually all

HDL particles. ApoA-II is the second most abundant HDL apolipoprotein and is found on

approximately two-thirds of all HDL particles. ApoB is the major structural protein of

chylomicrons, VLDL, IDL, and LDL; one molecule of apoB, either apoB-48

(chylomicrons) or apoB-100 (VLDL, IDL, or LDL), is present on each lipoprotein

particle. The human liver makes only apoB-100, and the intestine makes apoB-48. ApoE

22

present in multiple copies on chylomicrons, VLDL and IDL plays a critical role in the

metabolism and clearance of TG rich particles. Three apolipoproteins of the C-series

(apoC-I, -II, and -III) also participate in the metabolism of TG rich lipoproteins.

Fig.7: Composition of Lipoprotein 10

23

Metabolism & transport of lipoproteins

Transport of dietary lipids (Exogenous pathway) 9,10

Dietary cholesterol and retinol are esterified by the addition of a FA in the

enterocyte to form cholesteryl esters and retinyl esters, respectively. Longer-chain FA

are incorporated into TG and packaged with apoB-48, cholesteryl esters, retinyl esters,

phospholipids, and cholesterol to form chylomicrons. Nascent chylomicrons are secreted

into the intestinal lymph and delivered directly to the systemic circulation, where they are

extensively processed by peripheral tissues before reaching the liver. Apoprotein C-II on

chylomicron, binds to specific receptors in adipose tissue, skeletal muscle, cardiac muscle

and the liver and allows the endothelial enzyme, LPL, to remove most of the TG from the

particle and liberating free FA and glycerol. The released free FA are taken up by

adjacent myocytes or adipocytes and either oxidized or reesterified and stored as TG.

Some free FA bind with albumin and are transported to other tissues, especially the liver.

ApoC-II, is transferred to circulating chylomicrons or returned to HDL.

The chylomicron particle progressively shrinks in size as the hydrophobic core is

hydrolyzed and the hydrophilic lipids (cholesterol and phospholipids) on the particle

surface are transferred to HDL. The resultant smaller, more cholesterol ester–rich

particles are referred to as chylomicron remnants. The remnant particles are rapidly

removed from the circulation by receptors on hepatocytes in a process that requires apo

E. Consequently, few, if any, chylomicrons are present in the blood after a 12-h fast,

except in individuals with disorders of chylomicron metabolism.

24

Cholesteryl esters form an integral part of HDL. From peripheral tissue

cholesterol is trapped in HDL by a reaction catalysed by LCAT, transported to liver for

degradation and excretion .The process is known as reverse cholesterol transport

Cholesterol ester transfer protein synthesised in liver, facilitates exchange of

components between different lipoprotein & thereby transfer cholesterol esters from HDL

to VLDL or LDL in exchange for TAG.

Transport of hepatic lipids (Endogenous pathway)9,10

The endogenous pathway of lipoprotein metabolism refers to the hepatic secretion

and metabolism of VLDL to IDL and LDL.

The cholesterol in LDL accounts for 70% of the plasma cholesterol in most

individuals. Approximately 70% of circulating LDLs are cleared by LDL receptor–

mediated endocytosis in the liver

Long-chain FA are esterified into TAG and incorporated into VLDL, which has

aoprotein B-100 as an essential component. Apoproteins C-II and E are incorporated later

into VLDL by transfer from HDL particles. As they pass round the circulation, VLDL

particles bind through apoprotein C-II allowing TG to be progressively removed by LPL

in the capillary endothelium. As VLDL remnants undergo further hydrolysis, they

continue to shrink in size, which contain similar amounts of cholesterol and TG leaving a

particle, now depleted of TG and apoprotein C-II, called an intermediate-density

lipoprotein (IDL) particle which have apoprotein B-100 and apoprotein E molecules on

the particle surface. Most IDL particles bind to liver LDL receptors through the

apoprotein E molecule and are then catabolized.11

25

The liver removes approximately 40 to 60% of VLDL remnants and IDL. The

remainder of IDL is remodeled by hepatic lipase to form LDL. During this process, most

of the TG in the particle is hydrolyzed and all apolipoproteins except apoB-100 are

transferred to other lipoproteins.

LDL particles become Lp(a) lipoproteins as a result of the linkage of apoprotein

(a) to aproprotein B-100. Raised levels of Lp(a) lipoprotein is a risk factor for

cardiovascular disease. The HDL particle transports cholesterol away from the periphery

and may transfer it indirectly to other particles such as VLDL in the circulation or deliver

its cholesterol directly to the liver.11

Fig. 8: Transport of Lipids 10

26

HDL metabolism and reverse cholesterol transport 9

All nucleated cells synthesize cholesterol but only hepatocytes can efficiently

metabolize and excrete cholesterol from the body. The predominant route of cholesterol

elimination is by excretion into the bile, either directly or after conversion to bile acids.

Cholesterol in peripheral cells is transported from the plasma membranes of

peripheral cells to the liver by an HDL-mediated process termed reverse cholesterol

transport. Nascent HDL particles are synthesized by the intestine and the liver. The newly

formed discoidal HDL particles contain apoA-I and phospholipids (mainly lecithin) but

rapidly acquire unesterified cholesterol and additional phospholipids from peripheral

tissues via transport by the membrane protein ATP-binding cassette protein A1

(ABCA1). Once incorporated in the HDL particle, cholesterol is esterified by LCAT a

plasma enzyme associated with HDL. As HDL acquires more cholesteryl ester it

becomes spherical, and additional apolipoproteins and lipids are transferred to the

particles from the surfaces of chylomicrons and VLDL during lipolysis. HDL cholesteryl

esters are transferred to apo B containing lipoproteins in exchange for TG by the CETP.

The cholesteryl esters are then removed from the circulation by LDL receptor–mediated

endocytosis. HDL cholesterol can also be taken up directly by hepatocytes via the

scavenger receptor class BI (SR-BI), a cell-surface receptor that mediates the selective

transfer of lipids to cells.

27

HYPERLIPIDEMIA

Cardiovascular disease are responsible for 25% & Cerebrovascular disease for

19% of DALY’s lost due to non communicable disease in southeast Asian region

countries. More than half the patients with angiographically confirmed premature

coronary heart disease have a familial lipoprotein disorder which represents the most

common genetic dyslipidaemia with a prevalence of 1 – 2 %. Familial combined

hyperlipidemia characterized by elevated levels of cholesterol or TG or both is estimated

to cause 10 – 20 % of premature coronary heart disease and 10 % of myocardial

infarction.12

The abnormal levels of TG and or cholesterol in plasma are consequent to excess

of substrate leading to more production, defective transport, delayed peripheral clearance,

reduced utilization of Lipoprotein or their intermediaries, or combinations of these

abnormalities. The causes responsible for such lipid disorders could be primary, i.e. an

inherent genetic (monogenic or polygenic) defect of lipid-Lipoprotein-Apo metabolism

or more commonly secondary to certain diseases.13

Classification of Hyperlipidemia due to disorders of lipoprotein metabolism 9,13

1. Primary disorders of Apo B containing lipoprotein catabolism causing elevated

plasma cholesterol levels ( Known etiology)

Lipoprotein lipase and Apo C - II deficiency / Familial chylomicronemia

Hepatic lipase deficiency

Familial dysbetalipoproteinemia

Familial hypercholesterolemia

28

Familial defective Apo – B 100

Autosomal recessive hypercholesterolemia

Wolman disease

Cholesteryl ester storage disease

Sitosterolemia

2. Primary disorders of Apo – B containing lipoprotein metabolism ( Unknown

etiology)

Familial hypertriglyceridemia

Familial combined hyperlipidemia

Polygenic hypercholesterolemia

3. Genetic disorder of HDL metabolism (Known etiology)

Apo A – I deficiency

Apo A- I mutation

LCAT deficiency

CETP deficiency

4. Primary disorders of HDL metabolism

Primary hypoalphalipoproteinemia

Familial hyperalphalipoproteinemia

5. Secondary disorders of hyperlipidaemia

Obesity

Hypothyroidism

Nephrotic syndrome

Chronic liver disease

29

Diabetes mellitus

Cushing’s syndrome

Drugs

Excessive alcohol consumption

Glycogen storage disease

Systemic lupus erythematosus

Hypopituitarism

Pregnancy

Pancreatitis

Irrespective of the underlying mechanism of lipid disorder, the biochemical

abnormalities will manifest as hypertriglyceridaemia, hypercholesterolaemia or a

combination of both. Raised TG levels suggest an increase in VLDL and or Chylomicron

levels while an isolated rise in cholesterol indicates rise in LDL level. Considering the

raised levels of TG, cholesterol or both and the Lipoprotein molecule which is in excess

in the circulation, hyperlipoproteinaemias have been classified by Fredrickson into five

major groups.13

30

Table 1:Fredrickson classification of hyperlipidaemia 13

Type Synonym Biochemical alterations

Serum alterations

Type I Buerger Gruetz syndrome. Primary hyperlipoproteinemia or Familial chylomicronemia

Decreased lipoprotein lipase or altered Apo C II

Elevated chylomicron

Type IIa Polygenic hypercholesterolemia or Familial hypercholesterolemia

LDL receptor deficiency

Elevated LDL only

Type IIb Combined hyperlipidemia Decreased LDL receptor and increased Apo B

Elevated LDL, VLDL and Triglycerides

Type III Familial dysbetalipoproteinemia

Defect in Apo E synthesis

Increased IDL

Type IV Endogenous hyperlipemia Increased VLDL production and decreased elimination

Increased VLDL

Type V Familial hypertriglyceridemia Increased VLDL production and decreased LDL

Increased VLDL and chylomicrons

Primary disorders of apob-containing lipoprotein catabolism causing

Elevated plasma cholesterol levels (known etiology)9

Single-gene defects can result in the accumulation of specific classes of

lipoprotein particles. Mutations in genes encoding key proteins in the metabolism and

clearance of apoB-containing lipoproteins cause type I (chylomicronemia), type II

(elevations in LDL) and type III (elevations in IDL)

31

Lipoprotein Lipase and ApoC-II Deficiency (Familial Chylomicronemia Syndrome;

Type I Hyperlipoproteinemia) is an autosomal recessive in inheritance pattern and has

a population frequency of one in a million. Multiple mutations in the LPL and apoC-II

genes cause these diseases. Genetic deficiency of either LPL required for the hydrolysis

of TG or apoC-II which acts as a cofactor for LPL in chylomicrons and VLDL, results in

impaired lipolysis and profound elevations in plasma chylomicrons. These produce

greatly elevated TG concentrations owing to the persistence of chylomicrons in the

circulation. They also have elevations in plasma VLDL. The chylomicrons persist in the

circulation for days which are normally delipidated and removed from the circulation

within 12 h of the last meal. Hence fasting TG levels are almost invariably 1000 mg/dL.

LPL and apoC-II deficiency is usually present in childhood with recurrent acute

pancreatitis. Opalescent retinal blood vessels are (lipemia retinalis) seen. Eruptive

xanthomas, which are small yellowish-white papules, often appear in clusters on the

back, buttocks, and extensor surfaces of the arms and legs. These typically painless skin

lesions may become pruritic as they regress. Hepatosplenomegaly results from the uptake

of circulating chylomicrons by reticuloendothelial cells in the liver and spleen. Some

patients with persistent and pronounced chylomicronemia never develop any of these

symptoms. Premature ASCVD has not been consistently demonstrated to be a feature.

Investigation shows profoundly reduced LPL activity. The presence of chylomicrons

floating like cream on top of fasting plasma suggests this diagnosis

Hepatic Lipase Deficiency is a very rare autosomal recessive disorder due to deficiency

of HL which hydrolyzes TG and phospholipids in remnant lipoproteins and HDL. It is

characterized by elevated plasma cholesterol and TG due to the accumulation of

32

lipoprotein remnants. HDL-C is normal or elevated. The diagnosis is confirmed by

measuring HL activity in post-heparin plasma.

Familial Dysbetalipoproteinemia (Type III Hyperlipoproteinemia or Familial broad

disease) is transmitted as a single gene defect that encodes the structure of Apo E,

causing variations in ApoE which is present in multiple copies on chylomicron and

VLDL remnants and mediates their removal via hepatic lipoprotein receptors.

Interference with its ability to bind lipoprotein receptors, leads to partial catabolism of

VLDL. This is characterized by a mixed hyperlipidemia due to the accumulation of

remnant lipoprotein particles. It is associated with slightly higher LDL-C level. A high-

caloric, high-fat diet, diabetes mellitus, obesity, hypothyroidism, renal disease, estrogen

deficiency, alcohol use, or the presence of another genetic form of hyperlipidemia can

precipitate hyperlipoproteinemia.

Usually presents in adulthood with xanthomas and premature coronary and

peripheral vascular disease. Xanthomas can be as Tuberoeruptive xanthomas which begin

as clusters of small papules on the elbows, knees, or buttocks and can grow to the size of

small grapes or Palmar xanthoma (alternatively called xanthomata striata palmaris) which

are orange-yellow discolorations of the creases in the palms.

Plasma cholesterol and TG are elevated to a relatively similar degree to reach 500

mg/dL The triglycerides tends to be greater than cholesterol later. Premature ASCVD

with severe CAD, PVD and stroke are seen in patients even as early as the third decade of

life.13

FDBL is diagnosed by lipoprotein electrophoresis in which remnant lipoprotein

accumulate in a broad β band. Ratio of VLDL to total plasma TG > 0.30 is consistent

33

with diagnosis of FDBL. Protein methods (apoE phenotyping) or DNA-based methods

(apoE genotyping) can be performed to confirm homozygosity for apoE2. Other

mutations in apoE can also cause this condition.

Familial Hypercholesterolemia (FH) is very rare autosomal co dominant disorder

caused by around 750 mutations in the LDL receptor gene causing no LDL receptors in

the liver. This leads to delayed catabolism of LDL and its precursor particles from the

blood, resulting in increased rates of LDL production. It is characterized by elevated

plasma LDL-C with normal TG. Total cholesterol levels are usually 500 mg/dL - 1000

mg/dL.

Most patients with homozygous FH present in childhood with cutaneous

xanthomas on the hands, wrists, elbows, knees, heels, or buttocks. Arcus cornea is

usually present and some patients have xanthelasmas. Accelerated atherosclerosis is a

devastating complication of homozygous FH and can result in disability and death in

childhood. The diagnosis can be confirmed by obtaining a skin biopsy and measuring

LDL receptor activity in cultured skin fibroblasts or by quantifying the number of LDL

receptors on the surfaces of lymphocytes using cell-sorting technology.

Heterozygous FH caused by the inheritance of one mutant LDL receptor allele

occurs in approximately 1 in 500 persons worldwide, making it one of the most common

single gene disorders. It is characterized by elevated plasma LDL-C 200 to 400 mg/dL

and normal TG levels. They present with hypercholesterolemia from birth, and can be

detected in the cord blood. The disease is often detected in adulthood, on routine

screening, appearance of tendon xanthomas, or the premature development of

symptomatic coronary atherosclerotic disease. Since the disease is codominant in

34

inheritance and has a high penetrance 90% of parent and 50% of the patient’s siblings

are usually hypercholesterolemic. The family history is frequently positive for premature

ASCVD on one side of the family, particularly among male relatives. Corneal arcus is

common, and tendon xanthomas involving the dorsum of the hands, elbows, knees, and

especially the Achilles tendons are present in 75% of patients. FH heterozygotes with

elevated plasma Lp(a)appear to be at greater risk for cardiovascular complications.

Untreated men with heterozygous FH have a 50% chance of having MI before age 60.

Although the age of onset of atherosclerotic heart disease is later in women with FH,

coronary disease is significantly more common in women with FH than in the general

female population. No definitive diagnostic test for heterozygous FH is available.

Familial Defective ApoB-100 (FDB) is a dominantly inherited disorder. As a

consequence of the mutation in LDL receptor–binding domain of apoB-100, LDL binds

the LDL receptor with reduced affinity and is removed from the circulation at a reduced

rate. The disease is characterized by elevated plasma LDL-C levels with normal TG,

tendon xanthomas, and an increased incidence of premature ASCVD.

Autosomal Recessive Hypercholesterolemia (ARH) is a rare disorder due to mutations

in a protein involved in LDL receptor–mediated endocytosis in the liver. Clinically it is

characterized by hypercholesterolemia, tendon xanthomas, and premature CAD.

Wolman Disease is an autosomal recessive disorder caused by complete deficiency of

lysosomal acid lipase. Failure to hydrolyze the neutral lipids, results in their accumulation

within cells. The disease presents within the first weeks of life with hepatosplenomegaly,

steatorrhea, adrenal calcification, and failure to thrive. The disease is usually fatal within

35

the first year of life and can be diagnosed by measuring acid lipase activity in fibroblasts

or liver tissue biopsy specimens

Cholesteryl Ester Storage Disease is a less severe form of genetic disorder in which

there is low, but detectable, acid lipase activity. Patients with this disorder sometimes

present in childhood with hepatomegaly and a mixed hyperlipidemia, due to elevations in

the levels of plasma LDL and VLDL. Other patients present later in life with hepatic

fibrosis, portal hypertension, or with premature atherosclerosis.

Sitosterolemia is a rare autosomal recessive disease caused by mutations in one of two

members of the ATP - binding cassette transporter family. Due to mutation in these genes

the intestinal absorption of plant sterols is increased and biliary excretion of the sterols is

reduced, resulting in increased plasma levels of sitosterol and other plant sterols. Patients

with sitosterolemia can have either normal or elevated plasma levels of cholesterol.

Irrespective of the plasma cholesterol level, these patients develop cutaneous and

tendon xanthomas as well as premature atherosclerosis. Episodes of hemolysis,

presumably secondary to the incorporation of plant sterols into the red blood cell

membrane, are a distinctive clinical feature of this disease. Sitosterolemia is confirmed by

demonstrating an elevated plasma sitosterol level.

Primary disorders of ApoB-containing lipoprotein metabolism (Unknown

etiology)9,13

Familial Hypertriglyceridemia (FHTG,) is a relatively common (1 in 500) autosomal

dominant disorder of unknown etiology. An increased VLDL production, impaired

VLDL catabolism, or a combination of the two causes elevation of VLDL (Type IV

hyperlipoproteinemia). Some patients with FHTG have a more severe form of

36

hyperlipidemia in which both VLDL and chylomicrons are elevated (type V

hyperlipidemia), as these two classes of lipoproteins compete for the same lipolytic

pathway. Increased intake of simple carbohydrates, obesity, insulin resistance, alcohol

use, or estrogen treatment, all of which increase VLDL synthesis, can precipitate the

development of chylomicronemia, severe hypertriglyceridaemia and pancreatitis It is

characterized by moderately elevated plasma TG with more modest elevations in

cholesterol. FHTG does not appear to be associated with increased risk of ASCVD in

many families. Clinically xanthomas are lacking. The diagnosis of FHTG is suggested by

the triad of elevated plasma TG 250 to 1000 mg/dL, normal or only mildly increased

cholesterol levels > 250 mg/ dL, and reduced plasma HDL-C. Plasma LDL-C is

generally not increased and is often reduced due to defective metabolism of the TG-rich

particles. The identification of other first-degree relatives with hypertriglyceridemia is

useful in making the diagnosis.

Familial Combined Hyperlipidemia (FCHL) multiple lipoprotein-type

hyperlipidaemia, It is of an autosomal dominant inherence. The molecular etiology of

FCHL is unknown but is likely to involve defects in several different genes. FCHL is the

most common primary lipid disorder, occurring in approximately 1 in 200 persons.

Approximately 20% of patients who develop CAD before age 60 have FCHL. It is

characterized by moderate elevation of plasma TG and cholesterol and reduced plasma

HDL-C. The affected family members typically have one of three possible phenotypes:

(1) elevated plasma LDL-C, (2) elevated plasma TG and VLDL-C, or (3) elevated plasma

LDL-C and VLDL-C. A classic feature of FCHL is that the lipoprotein phenotype can

switch among these phenotypes with changing patterns of lipids in the blood.

37

FCHL has no typical physical signs. They can manifest in childhood but is

sometimes not fully expressed until adulthood. Visceral obesity, glucose intolerance,

insulin resistance, hypertension, and hyperuricemia are often present. These patients do

not develop xanthomas The levels of apoB are disproportionately high relative to plasma

LDL-C due to the presence of small dense LDL.

A mixed dyslipidemia with plasma TG levels between 200 and 800 mg/dL,

cholesterol levels between 200 and 400 mg/dL, and HDL-C levels >40 mg/dL and a

family history of hyperlipidemia and or premature CAD suggests the diagnosis of FCHL.

An elevated plasma apoB level supports this diagnosis.

Polygenic Hypercholesterolemia This is the most prevalent form of

hypercholesterolaemia. It is characterized by hypercholesterolemia with a normal plasma

TG in the absence of secondary causes of hypercholesterolemia. Only 10% of first-

degree relatives are hypercholesterolemic. Xanthomas are absent.

Genetic disorders of HDL metabolism

Mutations in certain genes encoding critical proteins in HDL synthesis and

catabolism cause marked variations in plasma HDL-C levels. Genetic forms of

hypoalphalipoproteinemia (low HDL-C) are not always associated with accelerated

atherosclerosis.

ApoA-I Deficiency and ApoA-I Mutations is seen with complete genetic deficiency of

apoA-I due to mutations in the apoA-I gene resulting in the virtual absence of HDL from

the plasma. Because apoA-I is required for LCAT function, plasma and tissue levels of

free cholesterol are increased, leading to development of corneal opacities and plantar

38

xanthomas. Clinically apparent coronary atherosclerosis typically appears between the

fourth and seventh decade.

Mutations in the apoA-I gene has low plasma HDL . But are rare. Other than

corneal opacities, most of them have no clinical sequelae. A few specific mutations in

apoA-I cause systemic amyloidosis and the mutant apoA-I has been found as a

component of the amyloid plaque.

Tangier Disease is a rare autosomal codominant form of low plasma HDL-C caused by

mutations in the gene encoding ATP-binding cassette transporter 1 gene (ABCA1), a

cellular transporter that facilitates efflux of unesterified cholesterol and phospholipids

from cells to apoA-I and plays a critical role in the generation and stabilization of the

mature HDL particle. In its absence, HDL is rapidly cleared from the circulation. Patients

with Tangier disease have plasma HDL-C levels < 5 mg/dL and extremely low

circulating levels of apoA-I.

The disease is associated with cholesterol accumulation in the reticuloendothelial

system, resulting in hepatosplenomegaly and pathognomonic enlarged, grayish yellow or

orange tonsils. An intermittent peripheral neuropathy (mononeuritis multiplex) or a

sphingomyelia like neurologic disorder can also be seen in this disorder. Tangier disease

is associated with premature atherosclerotic disease, but the risk is not very high which

may be attributed to the low plasma LDL-C seen in this condition.

LCAT Deficiency is a rare disorder caused by mutations in LCAT enzyme which

mediates the esterification of cholesterol ,the deficiency of which impairs the formation

of mature HDL particles and leads to rapid catabolism of circulating apoA-I causing great

increase in the proportion of free cholesterol in circulating lipoproteins.

39

Progressive corneal opacification due to the deposition of free cholesterol in the

lens, very low plasma HDL-C < 10 mg/dL, and variable hypertriglyceridemia are

characteristic of both complete deficiency (classic LCAT deficiency) and partial

deficiency (fish-eye disease) types. Complete LCAT deficiency is characterized by a

hemolytic anemia and progressive renal insufficiency that eventually leads to end-stage

renal disease. Despite the extremely low plasma levels of HDL-C and apoA-I, premature

ASCVD is not a feature of either complete or partial LCAT deficiency. The diagnosis can

be confirmed by assaying LCAT activity in the plasma.

CETP Deficiency occurs with mutations in the gene encoding CETP which facilitates the

transfer of cholesteryl esters among lipoproteins, especially from HDL to apoB-

containing lipoproteins in exchange for triglycerides causing a high HDL-C condition.

Homozygous deficiency of CETP, results in very high plasma HDL-C > 150 mg/dL due

to accumulation of large, cholesterol-rich HDL particles while heterozygotes for CETP

deficiency have only modestly elevated HDL-C. The relationship of CETP deficiency to

risk of ASCVD remains a matter of debate.

Primary disorders of HDL metabolism 9,11 The gene defect is not known

Primary Hypoalphalipoproteinemia / Familial hypoalphalipoproteinemia is the most

common inherited cause with a low plasma HDL-C level with relatively normal

cholesterol and TG levels. It is an autosomal dominant disease. The metabolic etiology

of this disease appears to be primarily accelerated catabolism of HDL and its

apolipoproteins. Several cases have been described in association with an increased

incidence of premature ASCVD

40

Familial Hyperalphalipoproteinemia Familial hyperalphalipoproteinemia has a

dominant inheritance pattern. Plasma HDL-C is usually > 80 mg/dL in affected women

and > 70 mg/ dL in affected men. The genetic basis of primary

hyperalphalipoproteinemia is not known, and the condition may be associated with

decreased risk of CAD.

Secondary disorders of lipoprotein metabolism9, 11

Significant changes in plasma levels of lipoproteins are seen in a variety of

diseases. These constitute the vast majority of cases with hyperlipidaemia met in clinical

practice.

Change-over to modern low-fibre, high-fat and refined carbohydrate diet is

probably the major cause for the high prevalence of Type IV and Type IIb

hyperlipidaemias seen in urban societies of India which are highly atherogenic and thus

are considered as the first reversible risk factor of ASCVD. Dietary control of fat intake

along with n-3FA supplementations is necessary to alleviate this type of

hyperlipidaemia.13

Obesity is frequently, though not invariably, accompanied by hyperlipidemia. The

increase in adipocyte mass and accompanying decrease in insulin sensitivity associated

with obesity have multiple effects on lipid metabolism. More free FA are delivered from

the expanded adipose tissue to the liver where they are re-esterified in hepatocytes to

form TG, which are packaged into VLDL for secretion into the circulation. High dietary

intake of simple carbohydrates also drives hepatic production of VLDL, leading to

increases in VLDL and or LDL in some obese individuals. Plasma HDL-C tends to be

41

low in obesity. Weight loss is often associated with a reduction of plasma apoB-

containing lipoproteins and an increase of plasma HDL-C.

Diabetes Mellitus Patients with type 1 diabetes mellitus are generally not hyperlipidemic

if they are under good glycemic control. Diabetic ketoacidosis is frequently accompanied

by hypertriglyceridemia due to increased hepatic influx of free FA from adipose tissue.

The hypertriglyceridemia responds dramatically to administration of insulin.

Patients with type 2 diabetes mellitus are usually dyslipidemic, even if under

relatively good glycemic control. The high levels of insulin and insulin resistance

associated with type 2 diabetes causes (1) a decrease in LPL activity resulting in reduced

catabolism of chylomicrons and VLDL, (2) an increase in the release of free FA from the

adipose tissue, (3) an increase in FA synthesis in the liver, and (4) an increase in hepatic

VLDL production. They have several lipid abnormalities, including elevated plasma TG

(due to increased VLDL and lipoprotein remnants), elevated dense LDL, and decreased

HDL-C. In some diabetic patients, especially those with a genetic defect in lipid

metabolism, the TG can be extremely elevated. Elevated plasma LDL-C level in diabetic

indicate the development of diabetic nephropathy. Patients with lipodystrophy, who have

profound insulin resistance, have markedly elevated VLDL and chylomicrons.

Thyroid Disease Hypothyroidism is associated with elevated plasma LDL-C primarily

due to a reduction in hepatic LDL receptor function and delayed clearance of LDL.

Thyroxin has a permissive role in stimulating the key enzymes like LPL and LCAT in

circulation. Therefore in patients with hypothyroidism there is decreased catabolism of

VLDL and IDL which causes accumulation of cholesterol and TG in circulation, having

an increased circulating IDL. Some are mildly hypertriglyceridemic > 300 mg/dL. Type

42

IIa and sometimes Type IIb with lower levels of HDL2 is the dyslipidaemia seen in

untreated patients with hypothyroidism. The profile is highly atherogenic.13

Renal Disorders Nephrotic syndrome is associated with hyperlipoproteinemia, which is

usually mixed but can manifest as hypercholesterolemia or hypertriglyceridemia alone. It

appears to be due to a combination of increased hepatic production and decreased

clearance of VLDL, with increased LDL production.

TG lipolysis and remnant clearance are both reduced in patients with renal

failure. Patients with renal transplants are usually hyperlipidemic due to

immunosuppression drugs

Liver Disorders: Liver being the principal site of formation and clearance of

lipoproteins, liver diseases can profoundly affect plasma lipid levels in a variety of ways.

Hepatitis due to infection, drugs, or alcohol is often associated with increased VLDL

synthesis and mild to moderate hypertriglyceridemia. Cholestasis is associated with

hypercholesterolemia as it blocks the major excretory pathway by which cholesterol is

excreted.But in chronic liver disease an abnormal lipoprotein is synthesised and secreted

by the liver, called lipoprotein X, over and above diversion of cholesterol to the systemic

circulation, producing a peculiar type of hypercholesterolaemia. However, in acute liver

cell failure, there is decreased synthesis of LCAT and so slower catabolism of VLDL

producing Type IV hyperlipidaemia.13

Severe hepatitis and liver failure are associated with dramatic reductions in

plasma cholesterol and TG due to reduced lipoprotein biosynthetic capacity.

Alcohol: Regular alcohol consumption has a variable effect on plasma lipid levels. The

most common effect of alcohol is to increase plasma TG levels. Excess of alcohol intake

43

induces FA synthesis in the liver causing suppression of FA oxidation. Excess of free FA

combines with glycerol and thus excess of VLDL is secreted. Further, there is also slower

degradation of Chylomicron and so Type V hyperlipidaemia occurs in these patients.13

The usual lipoprotein pattern seen with alcohol consumption is type IV (increased

VLDL), but persons with an underlying primary lipid disorder may develop severe

hypertriglyceridemia (type V) if they drink alcohol. Regular alcohol use is also associated

with a mild to moderate increase in plasma levels of HDL-C

Glycogen Storage Diseases Other rarer causes of secondary hyperlipidemias include

glycogen storage diseases such as von Gierke’s disease, which is caused by mutations in

glucose-6-phosphatase. The inability to mobilize hepatic glucose during fasting results in

hypoinsulinemia and increased release of free FA from adipose tissue. Hepatic FA

synthesis is also increased, resulting in fat accumulation in the liver and increased VLDL

secretion. The hyperlipidemia associated with this disease can be very severe

Autoimmune diseases (SLE, dysglobulinaemias) produce autoantibodies which form

complexes with either the enzymes like LPL or with the Apo of the circulating

lipoprotein and slows down their catabolism, producing varieties of dyslipidaemias.13

Cushing Syndrome: Glucocorticoid excess is associated with increased VLDL synthesis

and hypertriglyceridemia causing mild elevations in plasma LDL-C in Cushing

Syndrome.

Drugs A variety of drugs have been identified to interfere with lipid metabolism either

directly or indirectly and cause dyslipidaemias. The most important are the oestrogen-

containing OCP which can enhance VLDL production from liver and produce

hypertriglyceridaemia This problem gets aggravated if the woman has some undetected

metabolic, hormonal or genetic defect related to lipid metabolism.13

44

MANAGEMENT OF HYPERLIPIDEMIA

Early detection and early control of high cholesterol in a person is an important

step in reducing the development and progression of coronary heart disease and

atherosclerosis. Lowering plasma cholesterol by diet and drugs slows and may even

reverse the progression of atherosclerotic lesions and the complications they cause

The demonstration that lipid-lowering therapy significantly reduces the clinical

complications of ASCVD has brought the diagnosis and treatment of these disorders

into the domain of the general internist. The metabolic consequences associated with

changes in diet and lifestyle have increased the number of hyperlipidemic individuals

who could benefit from lipid-lowering therapy.13 Most patients with hyperlipidaemia are

asymptomatic and have no clinical signs. Many are discovered during the screening of

high-risk individuals 11

Guidelines for the screening and management of lipid disorders have been

provided by an expert Adult Treatment Panel (ATP) convened by the National

Cholesterol Education Program (NCEP) of the National Heart Lung and Blood Institute.

The NCEP ATPIII guidelines published in 2001 recommend that all adults over age 20

have plasma levels of cholesterol, TG, LDL-C, and HDL-C measured after a 12-hr

overnight fast.9

Selective screening of people at high risk of cardiovascular disease should be

undertaken, to include those with:

A family history of coronary heart disease (especially below 50 years of age)

A family history of lipid disorders

The presence of a xanthoma

45

The presence of xanthelasma or corneal arcus before the age of 40 years

Obesity

Diabetes mellitus

Hypertension

Acute pancreatitis

Those undergoing renal replacement therapy

Serum cholesterol concentration does not change significantly after a meal and as

a screening test, a random blood sample is sufficient. If the total cholesterol concentration

is raised, HDL cholesterol, TG, and LDL cholesterol concentrations should be quantitated

on a fasting sample. If a test for hypertriglyceridaemia is needed, a fasting blood sample

is mandatory 11

Multiple epidemiologic studies have demonstrated a strong relationship between

serum cholesterol and CAD. Randomized controlled clinical trials have unequivocally

documented that lowering plasma cholesterol reduces the risk of clinical events due to

atherosclerosis. Since both hypertriglyceridemia and low plasma levels of HDL-C confer

higher ASCVD risk, the NCEP ATPIII recommends more aggressive therapy to lower

the plasma LDL-C in patients with these dyslipidemias.9

Hyperlipidaemia results from genetic predisposition interacting with an

individual's diet.11 Studies show the role of the environment rather than the genetic make-

up of a population. Data from The Multiple Risk Factor Intervention Trial (MRFIT) have

shown that although cardiovascular risk rises progressively as total cholesterol

concentration increases the risk increase is modest for individuals with no other

46

cardiovascular risk factors. With each additional risk factor the effect produced by the

same difference in cholesterol concentration becomes greatly magnified.11

Reference values 14,15

Normal values vary with age, diet, sex and geographic regime.

Recommended levels of lipoproteins in Indian population are :

Total cholesterol : <200mg/dL

HDL cholesterol : >40mg/dL

Triglycerides : <150mg/dL

LDL cholesterol : <130mg/dL

TC/HDL Ratio : <3.0 indicates low risk,3.0-5.0 indicates high risk.

LDL/HDL Ratio : 1.5-3.5mg/dL

Nonpharmacologic Treatment 11,13

Therapeutic Lifestyle Changes (TLC) includes a cholesterol-lowering diet (TLC diet),

physical activity, and weight management for anyone whose LDL is above goal.

Dietary and life-style intervention

Studies have reported only modest cholesterol lowering benefits of diet therapy.

The effect of diet therapy varies among individuals. Some have striking reduction in LDL

upto 25 – 30% whereas others will have clinically important increase. Moreover diets

very low in total fat or in saturated fat may lower HDL as much as LDL. Low fat, high

carbohydrate diet may result in reduction in HDL.

Still diet control is the cornerstone of therapy in the management of

hyperlipidaemias. Modification of life-style, which includes food habits, cessation of

47

smoking, cutting down alcoholic beverages, weight control and regular exercises, is not

only necessary to attain eulipaemia but is the first step in the management of

hyperlipidaemias.

Frequent snacks and canned or commercially available precooked food (junk

food) should be abandoned as they are rich in fats and cream as well as refined

carbohydrates.

Alcohol supplies empty calories; its intake should be restricted to social purposes

in a patient with dyslipidaemia and in others should not exceed 30 g/day

. Dietary protein should be such that its fat content is low, viz., dried beans, peas

and pulses, chicken-breast, lean meat, low-fat dairy products and game birds and animals.

The diet should contain adequate amount of natural soluble fibres derived from

oats and barley, certain fruits such as oranges apples,and pears and vegetables such as

brussels sprouts and carrots.13,16

Substitution of saturated fat with monounsaturates and polyunsaturates

Most polyunsaturated fats come from vegetable oils, whereas most saturated fat

comes from meat and dairy products. Monounsaturated oils, particularly olive oil, and

polyunsaturated oils such as sunflower, safflower, corn and soya oil, should be used

instead of saturated fat-rich alternatives. Hydrogenation increases saturation and adds

trans FA which are as bad as saturated fat. Turkey breast and chicken breast are literally

free of cholesterol as soon as the skin is removed.11,17

Reduce the dietary cholesterol intake. Liver, offal and fish roes should be avoided.

Although eggs and prawns are rich in cholesterol their total contribution to the body's

cholesterol pool is small and they can still be part of a balanced lipid-lowering diet.11

48

In the hypercholesterolemic patient, dietary saturated fat and cholesterol should be

restricted. Dairy products and meat are the principal sources of saturated fat in the diet.

Fish and poultry with fat and skin removed should be substituted for this. Meat products

including sausages and reconstituted meats should be avoided since the concentration of

fat is unknown and often high. Baking and grilling of meats reduces the fat content and is

preferred to frying. Do not add fat in the cooking and serving process. Low-fat or cottage

cheese and skimmed or semi-skimmed milk should be substituted for the standard full-fat

varieties. Pastries and cakes contain large quantities of fat and should be avoided.

Similarly, refined carbohydrates like maida and maida preparations should be avoided

while carbohydrates with high-fibre content are preferred.11

Certain foods and dietary additives are associated with modest reductions in

plasma cholesterol levels. Plant stanol and sterol interfere with cholesterol absorption

from the intestine by competing for space in the micelles that deliver lipid to the mucosal

cells of the gut. and reduce plasma LDL-C levels by 10 to 15% when taken three times

per day. They are largely unabsorbed and excreted in the stool.9

For patients who are hypertriglyceridemic, the intake of simple sugars should

also be curtailed. For severe hypertriglyceridemic restriction of total fat intake is critical.

The most widely used diet to lower the LDL-C level is the “Step 1 diet”

developed by the American Heart Association. Most patients have a relatively modest

(10%) decrease in plasma levels of LDL-C on a step I diet in the absence of any

associated weight loss. In this diet no more than 30% of total calorie is provided by fat

and less than 10% of total calories is provided by saturated fat. Monounsaturated fats

should contribute 10% to 15% and polyunsaturated fats should contribute 10% or less of

49

the total daily energy intake. Cholesterol intake should be less than 300 mg/dl. Further

reduction in fat intake is unacceptable to many patients. 9

Weight loss and exercise: The treatment of obesity, if present, can have a

favorable impact on plasma lipid levels. Plasma TG and LDL levels tend to fall and

HDL levels tend to increase in obese persons who lose weight. Aerobic exercise has a

very modest elevating effect on plasma levels of HDLC. Gradual reduction protocols

along with dietary restrictions have to be implemented to achieve an ideal bodyweight13

A reduced fat diet, which is more realistic, only affects those levels if

accompanied by weight loss. Cutting fat without losing weight actually increase TG

levels and decrease HDL.18 Eating more calories than body needs, whether from fat or

carbohydrates, will be stored as fat. Hence the aim should be to lower total calorie intake

than total fat intake.19

Eating small amounts of fat can keep from overindulging on total calories.

Dietary fat causes our bodies to produce a hormone that tells intestines to slow down the

emptying process so that fullness is felt and are less likely to overeat.20 Moreover without

some fat in the diets, body could not make nerve cells and hormones or absorb fat soluble

vitamins. In any type of secondary hyperlipidaemia, the primary care envisages

correction of the underlying cause which has induced hyperlipidaemia.

50

Fig. 9: Diet pyramid 21

Natural sources reducing hyperlipidemia 18,20

Along with getting plenty of fiber, there are foods that will help in promoting the

lowering of cholesterol as well as herbs that can further reduce cholesterol.

Carrots, apples and the white layer inside of citrus rinds containing pectin are

advantageous to lowering cholesterol levels

Avocado, which is very high in fat, has unexpectedly become a cholesterol reducer

Beans are high in fiber and low in cholesterol

51

Garlic and onions in daily diet lower cholesterol and is also credited with lowering

blood pressure.

Cayenne pepper (Capsicum minimum) and other plants that contain the phenolic

compound capsaicin have a well demonstrated effect in lowering blood cholesterol levels,

as does the widely used spice Fenugreek.

Caraway is another aromatic spice with demonstrable cholesterol lowering properties.

Strawberry reduces oxidative damage to LDL while mainaining reduction in blood

lipids.

Soyaprotein decreases total cholesterol, LDL and Triglycerides

Green leafy vegetables, pulses, legumes, root vegetables, and unprocessed ereals,

help reduce circulating lipid concentrations.

Olive oil contains polyunsaturated fats that help to lower LDL levels while increasing

levels of HDL, or "good" cholesterol.

Nuts such as walnuts, almonds, hazelnuts and pistachios have polyunsaturated fatty acids

prominently, which can reduce blood cholesterol levels.

Chinese red yeast rice (which contains lovastatin) can have modest cholesterol-lowering

effects.

Polyphenolic substance derived from cocoa powder contribute to reduction in LDL and

elevation in HDL and suppression of oxidized LDL and thereby reduces atherogenesis

Peanut and peanut butter lowers cholesterol and reduces CHD risk

Flavonoid rich dark chocolate has beneficial effect on endothelial function

Cinnamon has blood-thinning properties that can help lower cholesterol levels

52

Marine fish oils containing long chain omega – 3 FA eicosapentaenoic acid ( EPA ) and

docosahexaenoic acid ( DHA ) have potential role in reducing plasma levels of

cholesterol and TG and thereby reducing incidence of CAD . Fatty fish, such as salmon,

tuna and mackerel, is an excellent source of omega-3 FA, and the American Heart

Association recommends getting at least two servings of fatty fish each week for

cholesterol management and general heart health.

Flaxseed and canola oil also contain some omega-3 fatty acid

Fig. 10: Natural sources reducing hyperlipidemia 19,20,21,22

53

UNDERSTANDING OF MIASM

§78 “The true natural chronic diseases are those that arise from a chronic miasm,

which when left to themselves, and unchecked by the employment of those remedies that

are specific for them, always go on increasing and growing worse, notwithstanding the

best mental and corporeal regimen, and torment the patient to the end of his life with ever

aggravated sufferings. These are the most numerous and greatest scourges of the human

race; for the most robust constitution, the best regulated mode of living and the most

vigorous energy of the vital force are insufficient for their eradication”23

Hyperlipidemia belongs to the true natural chronic disease as specified by

Hahnemann in §78 where even the best regulated mode of living with diet therapy and

weight loss may not reduce the disease symptom which is presented as only a rise in

serum lipid level unless complicated. Literature itself says that studies have reported only

modest cholesterol lowering benefits by diet therapy, the effect of which varies among

individuals.

In “The chronic diseases” Hahnemann says - “All chronic diseases of mankind,

even those left to themselves, not aggravated by a perverted treatment, show, as said,

such a constancy and perseverance, that as soon as they have developed and have not

been thoroughly healed by the medical art, they evermore increase with the years, and

during the whole of man's lifetime; and they cannot be diminished by the strength

belonging even to the most robust constitution. Still less can they be overcome and

extinguished. Thus they never pass away of themselves, but increase and are aggravated

even till death. They must therefore all have for their origin and foundation constant

54

chronic miasms, whereby their parasitical existence in the human organism is enabled to

continually rise and grow”.24

A constitutional remedy which includes the chronic miasm becomes the right

antimiasmatic remedy to expel this potentiality of the individual affected unfavourably by

certain stigmata which result from either hereditary factors (inherited) or previous

indiscretion of the patient (acquired). An evaluation of the predisposing miasm of the

individual, paves the path to select the right antimiasmatic remedy, the administration of

which not only relieves him of his disease but also prevents the predisposition to the

miasmatic tendency.25

Hence hyperlipidemia which is a true natural chronic disease requires an

antimiasmatic remedy for the true anhilation of the disease besides the diet and lifestyle

management.

In the “Organon of Medicine” Samuel Hahnemann separated the origin of disease

into two categories, the exciting and fundamental causes, and related them very closely to

the susceptibility of the physical constitution.

§5 says “Useful to the physician in assisting him to cure are the particulars of the

most probable exciting cause of the acute disease as well as the most significant points in

the complete history of the chronic disease, to enable him to discover its fundamental

cause, which is generally due to a chronic miasm. In these investigations, the

ascertainable physical constitution of the patient (especially when the disease is chronic),

his moral and intellectual character, his occupation, mode of living and habits, his social

and domestic relations, his age, sexual function, etc., are to be taken into

consideration.”26

55

Hahnemann taught that the susceptibility to the exciting factors lies in the

fundamental cause which is attributed to the chronic miasms.27 Thus it resolves itself into

the fact that the only and supreme influence which determines its action and its

development in any human being is an inheritance of the above mentioned chronic

miasms the effects of which are passed from one generation to the next and caused

predispositions to certain disease syndromes. This invisible potentiality in some form is

imposed upon the life of every unborn child in some degree,often to such an extent as to

destroy the new life or drive it from its living house by its invisible expelling powers. 25

Since the dawn of medical history there has been a constant search for the causes

of the acute and chronic diseases that afflict humanity. This quest made great advances

when the ancient Greek physician, Hippocrates, taught that all diseases were caused by

the predisposition inherent in the innate constitution and its susceptibility to a

constellation of causation rather than any one single effect. In the Greek philosophy

disease is caused by an interdependent set of circumstances which disrupts the natural

ebb and flow of the pneuma (vital force) within the organism. Hahnemann’s pathology is

based on dynamical theory of disease i.e. Disease is primarily a morbid dynamic

functional disturbance of vital principle 27

Disease is nothing more than changes in the general state of the human economy,

which declare themselves as symptoms; or, in other words; disease is but the influence of

some subversive force, acting in conjunction with the life force, subverting the action and

changing the physiological momentum. It is a modified mode of motion, a vibratory

change. The suffering of the immaterial vital principle which animates the interior of our

bodies, when morbidly disturbed, produces symptoms in the organism that are manifest

56

and these morbidly produced symptoms constitute what is known as disease in all its

multiplied forms, whether functional or structural.25

The father, then, we say, of all sickness of whatever nature it may be, is, directly

or indirectly, a subversive force whose action is co-existent with the life force. Therefore,

through this co-existent action we may have any conceivable anatomical, physiological or

histological imperfection which manifest as mental, moral or even spiritual

imperfection.28

The chief feature in pathology is a constant factor in all persons attacked by the

same malady, which has furnished the name of said malady. Yet there is a characteristic

difference in each individual case that gives it its individuality, causing it to differ from

all other cases. The symptoms vary according to the peculiarity of the individual's

original constitution, his hereditary predisposition, the different faults of his education

and his habits, his mode of life and diet, his occupations, his mental pursuits, his

morality, etc. No lesion or pathological condition is the first cause of any disease, for the

disease process precedes them all, and the true cause always lies in the disturbed or

distressed life force itself.25

The natural tendency of life force, is to assert itself & thus restore the state to

harmony. The disease is held back often by that natural physiological resistance that each

organism is endowed with and other conditions favorable to the development of health

and strength such as physical training, climate, diet, fresh air, etc. It is the same

stupendous potentiality that gives the wonderful manifestations in life, so in disease. Here

the life potential combines with the miasmatic potential Thus in chronic diseases vital

force was impeded by miasms & natural process of recovery & cure were interfered The

57

tendency of the disease in these patients was to progress relentlessly and leads to chronic

relapsing states of ill health difficult to cure.30

Hahnemann sought an explanation for the frequent relapses he observed in certain

patients with chronic complaints whom he treated according to his system To him it

gradually became clear that such chronic conditions cannot be cured by the vital force

alone, nor by any manipulation of diet or life habits. He then launched into exhaustive

inquiries of all such chronic cases to see if any common denominator could be found to

explain the deep & invisible weakness which predisposed to their chronic condition – A

weakness which Hahnemann termed miasm. These weakness were transmitted from one

generation to next according to his investigations which included whenever possible,

interviews with the ancestors of chronic disease patients. All these observations were

published in “The chronic diseases” 3300

The word “Miasm”originated from Greek word “Miasma” which is derived from

“Miasmatos” from “Miainien” meaning stain, pollution, defilement.31 Term “Miasm”

was employed by him to indicate a defect in the constitution which interfered with the

process of recovery & cure.30 Miasms are states or conditions which pollutes the human

organism with unhealthy tendencies which when taken into the organism, may set up a

specific disease. They are dynamic disease producing powers or an invisible polluting

substance which once it gains entrance, overpowers the Vital force & pollutes the whole

system producing true natural chronic diseases & predispose human beings to acute

disease which can only be known through their actions & functions 32. Each miasm

creates a weakness or a tendency to a particular group of disease. If not eradicated with a

suitable antimiasmatic remedy, it will persist through out the patient’s life & can be

58

transmitted to others especially to children. Kent called it predisposition, a state,

dyscrasia or diathesis.32 It acts by prolonging the disease and or by obstructing the

process of cure, even though a true similimum has been prescribed. Chronic miasms are

thus the fundamental causes of diseases and the diseases caused by them are the effects.31

The new phenomena, or that which is supposed to be new disease, is nothing

more than the daily workings of the miasm, or the further development of miasmatic

action, the forward movement of a perverted life action, a miasmatic revelation of that

unknown force. Idiosyncrasy, dyscrasia, predisposition, and even certain forms of

temperament are all climaxes of perversion or change, and stand forth as the finished

work within the organism of the action of chronic miasm. The nature and character of the

disease depends wholly on the form of the miasm and the character of the bond with the

life; therefore, the study of disease becomes a study into the nature of the miasm present

in the organism and the degree of its activity. The true pathognomonic symptoms of a

given case are those that cover the existing active miasm. In this way our therapeutic

grouping becomes a miasmatic one and not a pathological one 25

Hahnemann observed them in greater detail, classified them, in three broad

groups with definite attribute & predisposition. He observed a close association between

these groups & the diseases of itch, syphilis & gonorrhoea which were rampant in those

times. A detailed clinical study of these patients enabled him to describe in detail the

characteristic symptoms of these groups & also indicate their disease potentials. He

evolved a similar grouping of remedies which helped in curing them. Thus he classified

the drugs in Materia medica also into three like groups employing the same attributes.

Understanding the innate constitution is fundamental to homoeopathic treatment because

59

it holds the keys to an individual's susceptibility as well as the inherited effects of the

chronic miasms. On the basis of law of similars, he directed physician to ensure that the

selected remedy belonged to similar group.30

The diseases are built accordingly on four different plans – Occupational / drug

disease, Psora, sycosis & syphilis.

In all human beings we will find a portion of all three pathological characteristics.

Yet one will always be dominant, preponderant, modulating & determining more strongly

the biological structures as well as those of soul &character – Dominant miasm.

Characteristic guiding symptoms from present condition of patient is linked with

earlier development depicted in past history & family history – Fundamental miasm.29

The term “Psora” originated from Hebrew word “Tsorat” meaning “A groove”, “a

fault”, “a pollution”, “a stigma”, an itch derived from Latin & Greek. It is a condition of

man, a condition that favours diseases.31

The term “Sycosis” came from the Greek word “Fig”. Hahnemann’s term for

constitutional effects of gonorrhoea primarily manifested by condylomatous or

cauliflower like growth on skin. Morbid conditions developed as a result of suppressed

chronic gonorrhoea, inherited gonorroeal poison or repeated vaccination. produces a

chronic miasmatic state, sycosis.31

Syphilis is the constitutional state engendering perversion which includes

destruction degeneration and aggressiveness.31

Tubercular miasm or pseudopsora denotes combination of hereditary taints of

psora & syphilis.31

60

The life force is in the pathological business and is prepared to manufacture any

pathological formation depending upon the nature of the internal exciting or acting

miasm. If the miasm be psoric we have psoric manifestations. If it be sycotic, we have

sycotic pathology; and if syphilitic, we have the polymorphic pathological presentations

of that miasm; or, if we have the miasm syphilis and psora combined, we have the

multiplied changes and infinite destructive processes known as tubercular pathology. The

disturbances are in accordance with the existing active miasm, modified by previous

heredity or miasmatic states of the organism.25

Miasms have always separate entity. They cannot be mixed together.

Manifestation of a disease are generally limited to one miasm at a time Only the

miasmatic states of different miasms may intermingle. These are mixed miasmatic

states.31

Some of the most complicated disease, difficult to cure, represent the combination

of all three miasms. Any structural change occurs only when other miasms supervene on

psoric base. In such a combination, the propensity to the development of disease is

enhanced considerably. And it is here that a simple cause becomes a complex thing,

difficult to understand or analyze, as new coloring is given to the symptomatology, as

well as to the pathological groupings, as they partake in part of the nature of the

combined miasms. It is dreadful to contemplate such a condition of things as is present on

the earth today. Almost every man is polluted with this disease; and it is more difficult to

cure diseases at the present time where the physicians resort to palliatives and

suppressive measures. The study of these cases is difficult. But it is greatly simplified by

a thorough knowledge and understanding of the miasms.29

61

The three miasms represent three broad constitutional types which indicate

different susceptibilities to the development of illness. A detailed study in three planes –

emotional, intellectual & physical enables us to identify the miasm responsible for

illness.29

The physical signs of a person are fundamental to the treatment of chronic

disorders because the constitution and temperament shows the effects of the inherited

miasms. We must get beyond relying solely on the personal or family history to uncover

miasms. The miasms are present in the very symptomatology of the client. The

syndromes produced by the miasms point to the fundamental cause even if it cannot be

traced in the case taking to a specific etiological factor.27

Each of the chronic miasms have their own characteristic signs that are an integral

part of the totality of the symptoms. The reality of miasm in a patient is always expressed

by signs & symptoms the patient produces which permit the individual expression of

characteristics of miasm which allow to determine, recognize & wholly handle the patient

individuality It is these symptom pictures that clue the homoeopath into which miasms

are present within the constitution of the individual. Thus the etiology points to the

symptoms and the symptoms point to the etiology. This is how the homoeopath

understands which miasmic layers are dormant, latent and active. All of these factors

point to the proper anti-miasmic remedies.29

H. C. Allen in his classic, ‘The Chronic Miasms’ says “You cannot follow the

evolution of the curative process; you cannot even prescribe intelligently the proper diet

for a patient, unless you know the basic miasm. Of course the diseases that are present

62

will help you to some extent, but you have no surety unless you know the underlying

basic disturber of the disordered life” 27

We can not select the most similar remedy possible unless the phenomena of the

acting and basic miasms is understood; for the true similar is always based upon the

existing basic miasms, whether we be conscious or unconscious of the fact. The curative

remedy is but the pathopoesis of a certain pathogenesis of an existing miasm.32

The progress of a case cannot be watched without a definite knowledge of these

disease forces (miasms), with their mysterious, but persistent, progressions, pauses, rests,

forward movements, retreats and attacks along unfamiliar lines, and of whose multiplied

modes of action we have taken no cognizance. If we become acquainted with the

character of miasm, their history and action upon the life of the organism, we are able to

follow these processes and able to give a prognosis as to the probable outcome in a given

case of disease; for the character of the miasm gives us the character of the affection of

the disease formula. In that way we are able to head off the new developments and new

processes that come upon unexpectedly.29

Miasmatic theory could be considered the true genetic theory, since miasm are

transmitted to children. Children inherit from each parent particular sensitivities in

particular organs & the resulting disorder in the child is either an accurate copy of one

parent’s disorder or a compounding of disorders inherited from both the parents. It also

provides something analogous genetic therapy, since the inherited miasm can be treated

& the genetic transmission halted protecting future generations.32

When the miasms are latent the symptoms are mainly transient. But as the miasm

becomes active, it produces constant, more serious symptoms which effect the vital force

63

more profoundly. Using Hahnemann’s powerful theory we can treat a miasmatic state

before pathology emerges & we can prevent the transmission of parent’s susceptibility to

children. This is true preventive medicine.32

Miasmatic trump cards are the best to prove supremacy of homoeopathy among

other methods of treatment in chronic & incurable illness with a stamp of unknown

cause(s). For better generation we have to study chronic miasms & treat the people

homoeopathically. We can study miasmatic medicines to improve future generation

through a long course of treatment. With homoeopathic knowledge & understanding

miasmatic disease we can improve mentally & physically near & dear relatives

Find the chronic miasms, treat them well & let us live in peace & harmony 33

True homeopathy can be likened to organic gardening, where a weak soil is

carefully tended and strengthened so that its fruits will proliferate with vitality and in

such a way that weeds, bugs, and blights, etc. are discouraged.

MIASMATIC CLEAVAGE OF HYPERLIPIDEMIA

The miasms are destructive in every way, of both mind and body and they tear at

the very spirit of man. It is disorganizing disease that fills the state and we cannot meet

these conditions intelligently until we recognize the ancient origin of disease and

undertake its extermination on the basis of miasm.

The environmental factors, may be the causative modalities or maintaining cause

which modifies disease response in its progression from psora to syphilis. A critical

analysis of these response and final resultant expressed at different levels of organization

and areas leads to the four categories of constitution with distinct predisposition to the

64

development of characteristic disease response. This division, first attempted by

Hahnemann was modified in the light of clinical experience and re interpreted in the light

of present day understanding of ramification and expression, internal as well as external

of disease. The Hanemanian totality is an evolutionary one spreading itself in space

through the four miasmatic expressions.29

A number of progressive as well as increasing abnormalities in the biochemic

balance of the system are produced by the onward slaught of disease, leaving the system

progressively vulnerable to further damage. By a study of the physiological function

along with correlates from biochemistry, these various mechanisms are understood and

their implications in terms of cellular susceptibility and sensitivity is essential for

understanding of the totality of functions of the entire system.29

Concepts of general and special pathology when carefully correlated with the

clinical evolution and expression of the disease gives clinically useful standard of time

which can be correlated with the operations of environmental factors. It is possible to

correlate and interpret all these observations in relation to Hahnemmanian theory of

miasms and dyscrasia which can be generalized as time expression. It allows to evolve a

continuous specific spectrum – Constitution (Normality) - Diathesis - Prodrome -

Psora Sycosis - Tubercular - Syphilis.29

An alert observation is required in a fast moving clinical situation and to interpret

the totality furnishing the requisite guidance correctly in terms of miasmatic

interpretation. Constitutional homoeopathic prescribing will demand the use of a diverse

type from various lab investigations, clinicopathological as well as radiological.29

65

From the natural pathological evolution of hyperlipidemia, it is evident that

though initially the only symptom is raised serum lipid profile, with time, it leads to an

end stage of vascular complications causing widespread destruction of several systems of

the body including vital organs.

An increased parasympathetic tone leads to an overall decrease in the activity of

the endocrines which is reflected in an increase in the anabolic process and decrease in

the catabolism, a reduction in the overall turnover, retention, accumulation of cholesterol,

aberration in lipid metabolism leading to deposits of cholesterol and lipoprotein in the

wall of blood vessels causing narrowing of the vessels.29

Properly applied constitutional treatment in the process of cure should not

terminate at the disappearance of presenting symptoms but extend further towards the

idealistic point of positive health by the removal of entire abnormal susceptibility so that

all tendency to recurrence is eliminated.

Constitution results from the interaction between genetic factors and the

environmental factors to give its peculiar reactivities to the environmental circumstances

which tend to drive ahead the individual in a characteristic manner unfolding a tendency

to favour expression favouring one miasm over the rest.29

Hahnemann directs that the similarity be established at the level of disease (§ 6 )

taking into account the qualitative characteristics along with causation, inclusive of

hereditary and predispositions utilizing signs and symptoms as the only discernible

evidence of the totality of expression of the disorder within the phenomena of the

disease.34

66

Miasmatic study of a disease can be assessed by taking into account in a

meticulous manner, the full details of the troubles experienced by the patient inclusive of

various treatments administered, its suppressive effects which must have lead to the

consequence of a protracted state of ill health, continued to attract noxious environmental

influences to produce a complex diseased state.29,35

Observations leads us to the concept of the fundamental miasm indicated by

family history of disease as well as the personal past history as the hereditary, genetic

predisposition is reinforced by the past illness. The dominant miasm is deduced from the

prominent expressions of disease at the time of observation.29,36

The clinical investigation should clearly incorporate the time dimension in all its

aspects and the expression (subjective or objective) demarcated fully with location,

sensation, modalities and concomitant and origin, duration and progress with reference to

the levels of intelligence, emotional and physical, as well as areas ( tissue, organ or

system) along with environment factors (work, family and social circle). Only then the

miasmatic expressions and the dynamic background of the patient can be appreciated. 29

Thereby the miasmatic basis of the hyperlipidemia, which do not express any

clinical symptom of the disease other than a rise in the serum lipid levels, unless

complicated is studied through ,Family and Past history, Causation, Mental generals,

Physical generals, Pathological stage of disease and Symptomatology of the disease

67

Table 2: Miasmatic evaluation criteria 24,26, 29,31,38,39

Psora / Sensitising Sycotic / Constructive / Inco ordination

Tubercular / Reactive Syphilitic / destructive

Mental Generals

Anxiety. Fear. Restless. Nervous. Irritable. Timid. Perversion. Tendency to commit evil. No deep mental concentration / sacred thoughts. Hyporeasoning. Impractical thoughts. Hypoconfidence. Philosopher. Builds castles in air. Indolent. Aversion to work ,bath, keep things clean. Untidy. Lack of discipline. Time passés too fast/ too slow Repugnance to & fatigue on mental & physical exertion. Wants to lie down. Sensitive to odour.

Suspicious. Jealousy. Tendency to harm / exploit others. Hyperworkoholics. Hypergreedy. Cross. Irritable. No spiritual outlook, not influenced by moral doctrine or religion. Insanity. Inclined to commit crime. Mischevous, Bent upon misdeeds. Born criminal. Revengeful, devoid of all sense of rhiteousness. Thinks of their own ailment. Suppress ailments / symptoms. Brooding over things. Self condemnation. Fixed ideas. Lack of self confidence. Suicidal tendency with proper cause.

Dissatisfaction. Lack of tolerance. Changeable. Anger. Irritable. Quarrelsome. Crave & perversions for things that will harm them. Indifferent. Unconcerned about his sufferings. Hopeful of recovery. Willing to take risks & undertake ventures.

Destructive. Cannot explain his symptoms. Lack of self confidence. Keeps dippression to himself. Dull. Stupid. Idiocy. Ignorance. Stubborn. Obstinate. Melancholic.Gloomy Closemouthed, answers in monosyllables. Desire to be in solitude. Disgust of life. Desire to escape. Lack of self confidence. Suicidal tendency without proper cause.

Intelligence Alert. Quick. Active. Unable to control or disappearance of thoughts.

Slow. Sluggish. Incoordination of thoughts and perception.

Very bright, intelligent & sharp, or slow & dull totally. Lack of concentration

Slow to react. Careless mistakes. Arithmetical calculation difficult.

68

Memory Weakness of memory. But studious.

Absentmindedness. Slow thought and speech. General loss of memory. Cannot find words.

Inability or slow in comprehension. Highly keen.

Impaired memory. Total forgetfulness.

Behaviour Decietful behavior. Cruel- Mental torture. Quarellsome. Mean minded & concealing.

Some cruelty due to dissatisfaction.

Violent, cold blooded murderers.

Fear Fear of strangers, death, disease, future.

Fear of making mistakes Fearless. Fear of dogs, dark

Fear of people. Panicky terror

Social relation Aversion to people & company. Dreads to be alone

Extroverts

Morose. Sullen. Does not like advices. Likes company

Introvert. Escapes from self & others. Aversion to company.

Attitude Internally extremely selfish. Hide & seek nature. Tendency to dishonesty, wickedness.

Selfish & possessive with a tendency to conceal.

Unrestrained & uncontrollable passions of life. Easily forms intense emotional bonds. Intense sexual desire.

Constantly dwell on suicide. Merciless with no sympathy. Irresponsible, lacks sense of duty. Perverted sexual cravings.

Sensitivity Oversensitive mentally & physically.

Like barometer to storm or rain.

Hypersensitive. Insensitive mentally and physically.

69

Metabolism Excessive demands for all supplies of nature but poor digestion & metabolism. More active catabolism than anabolism. Nutritional troubles resulting from defective metabolism of formative elements. Poor development or disproportionate accumulation of fat.. Disturbed water metabolism resulting in increased thirst, dryness of tissues. Inadequate utilisation in mineral metabolism. Loss of minerals

Disturbs pigment metabolism, endocrinal system. Increase in anabolic process & decrease in catabolism. A reduction in overall turnover. Retention, accumulation of cholesterol, aberration in lipid metabolism.

Poor in bone, flesh & blood Depletion, drainage & wasting disease. Loss of vital fluids (Diarrhoea, urine, sweat, bleeding) . Increased catabolism & decreased anabolism. Rapid physical waste.

Disturbs metabolism of mineral elements & produces deficient growth

Pathology Produces only functional disturbances manifested by hypersensitivity, itching, irritation, burning leading to congestion & inflammation. Never produces any structural damage. Spasms, paroxysmic phenomena & neuro vegetative manifestations

Physical & mental inco ordination. Physical overgrowth, uncontrolled proliferation at the cost of other. Infiltration in the form of warts, condylomata, tumours, fibrous tissue.

Rapid response to any stimuli. Early suppuration and delayed healing. Scars breakdown.

Produces destructive disorders everywhere. Ulceration from early phase of disease. Degeneration. Deviation – anything perverted.

70

Characteristic

Nature of disease

Deficiency or lack of inhibition, all cells & organs producing an insufficiency, functional deficiency, lack of productivity – Hypotension, Atrophy, Hypoplasia Anemia, Weakness. Hypoimmunity, Dryness, Lack of assimilation. Thin, watery, acrid serous discharges. Hypersusceptibility. Mental & Physical irritation. Deficiency disorders. Reflects many subjective symptoms. Little or no objective symptoms. Desires, aversion, intolerance are prominent

Excess manifested by hypertrophy, hyperplasia, neoplasia, hypersecretion, hypersensitivity, hyperthermia, hyperactivity Hydrogenoid. Greenish or greenish yellow, jelly like, catarrhal purulent discharges with fishbrine odour. Hypertension, Restless. Deposition. Reflects more objective symptoms with less subjective symptom

Haemorrhages. Allergies. Alternation & periodicity. Changeableness. Confusing vague symptoms. Craves things which make them sick. Depletion. Thick greenish or yellowish green discharges with smell of old cheese. Catches cold very easily Reflects many subjective symptom. Mental, emotional, pathological & destructive

Disorganised digestion deformities, fragility. Putrid, offensive, pus like discharges. Little subjective symptoms. Less desire, craving, aversion & feelings.

Pace of action Hyperactive. Dramatic development of symptoms

Extremely Slow & insidious onset & recovery

Depend on preponderance of psora / syphilitic miasms. Moderate or Rapid

Rapid or Insidious

71

Modalities < Standing, Cold, Morning, Movement, Between sunrise & set, Mental excitement, Worry, Grief, Anxiety, Fear, Noise, Strong smells, Before menses.

> Warmth, Scratching, Crying, Eating, Rest, Natural discharges, Appearance of suppressed skin eruption.

<Rest, Damp, Rainy, Humid, Thunderstorm, Change of weather, Meat, Abnormal discharges, Anger, Irritability

> Slow motion, Stretching, Dry weather, Lying on stomach, Pressure, Suppressed normal discharge, When wart, fibrous growth appear. Breaking open of old ulcers, sores, gonorrhoeal discharges, scars.

< Thunderstorm, Milk, Night, Fruits, Oily food, Closed room, Pressure, Excitement, Physical & mental exertion, Artificial light, Anger, After sleep.

>Dry weather, Open air, Day time, External heat, Travel Outbreak of an old ulcer, diarrhoea, offensive foot or axillary sweat, nose bleeding, gonorrhoeal symptoms.

< Sunset to sunrise, Movement, Extremes of temperature, At sea side, Thunderstorm, Warmth, Natural discharges

>Sunrise to sunset, Change of position, Abnormal discharge. Winter, Cold weather

History of Suppression of skin eruptions & physiological eliminations. Repeated attacks of acute infectious diseases. Stress – emotional & Psychological.

Metabolic disorders – Hyperlipidemia, hyperurecemia, chronic pelvic inflammatory disease. After effects of immunization , injection, blood transfusion, excessive food intake. Suppression of pathological elimination & proliferation

Tuberculosis, Whooping cough, Bronchitis, BA, Bronchopneumonia.Tendency to hay fever, common cold. Suppression of physiological & pathological elimination, foot sweat, skin eruption Recurrent infection

Suppression of pathological elimination Psychosis, incidence of suicide, CVA, MI Repeated abortion, IUD. Infertility, Degenerative diseases

72

Constitutional Appearance

Lean thin, Active Obese.Flabby, sluggish. Stout, Overnourished.

Lean thin. Narrow chest

Thin, wrinkled, looks old for his age.

Face Inverted pyramid Yellow sallow, pale, earthy complexion. Eyes sunken

Dropsical. Oily skin Pale ,round, fair smooth, clear skin & waxy smooth complexion. Sunken eyes, flushed cheeks. Thin lips.

Greasy. High cheek bones & rough skin. Dry & wrinkled like old person.Thick lips

Thermal

Generally chilly

Hot

Extremely chilly

Sensitive to changes either heat or cold Perspiration

Profuse, offensive, during sleep

On forehead during sleep. Copious.

Profuse

Offensive < all complaints

Appetite

Insatiable hunger

Discomfort after eating

Increased

Decreased

Craving

Sweet, Sour, Spicy, Salty. Oily, Fried, Indigestible Unnatural substances like chalk, clay, Hot food.

Alcohol, Beer, Pungent, Well seasoned, Salty food.

Indigestible things, Potatoes, Tea, Tobacco, Meat, Salt, Greasy, fatty food. Things which make them sick. Very hot / really cold

Stimulants like alcohol, tea, coffee, very spicy. Indigestible.Cold food

Aversion

Milk, cold food

Meat, milk, wine, spices

Meat

Meat, animal food, less spicy food

Bowels

Constipation

Diarrhoea Alternating diarrhea and constipation

Dysentry

73

Particulars of Hyperlipidemia Family history

May or may not have a F/H of hyperlipidemia

F/H of hyperlipidemia, atherosclerosis, CAD etc

F/H of hyperlipidemia

Strong F/H of hyperlipidemia, early CAD, stroke etc.

Etiology

Unknown cause Increased intake of fat, Secondary to alcoholism, drugs, hepatic infections

Mutation in gene. Hepatic cholestasis. Enzyme disorders Secondary to auto immune disease like SLE, endocrine disorders like DM, hypothyroidism, Cushing’s syndrome.

Mutation in gene

Mutation in gene Secondary to nephritic syndrome

Pathology Defective metabolism of fat Deficiency in apoprotein or enzymes.

Defect in receptors, enzyme activity. Deposition of cholesterol & lipoprotein in the wall of blood vessels

Defect in receptors, enzymes

Lack of apoprotein, receptors, enzyme activity Atheromatous plaque resulting in complication of haemorrhage, thromboembolic phenomena

Clinical Manifestations

No manifestations with only serum changes Pancreatitis. Reversible with diet & life style changes

Lipemia retinalis Hepatomegaly, Hepatic fibrosis, Spleenomegaly, hypertension, Xanthoma, Xanthelesma, Atherosclerosis, Enlarged tonsils

Recurrent pancreatitis. Intermittent peripheral neuropathy

Accelerated atherosclerosis Premature CAD, Stroke, PVD Haemolysis

74

HYPERLIPIDEMIA IN REPERTORY

The rubrics specifically related to hyperlipidemia seen in repertories are

SYNTHESIS 9.1 40

Generals – Hyperlipidemia - all-s, aur, calc, calc-f, chel, chin, chion, chr-ac, colch, cortiso,

ferr-i, hydr, lec, med, nux-v, perh-mal, tarax, thuj, thyreotr, vanad, zing

Generals – Arteriosclerosis - adren. Am-i. am-van. aml-ns. ant-ar. arg-n. Arn. ars. Ars-i.

asar. aster. Aur. aur-br. Aur-i. aur-m-n. Bar-c. bar-i. bar-m. bell-p. benz-ac. cact. cal-ren.

Calc. calc-ar. calc-f. card-m. chinin-s. chlol. con. crat. Cupr. ergot. fl-ac. form. form-ac. fuc.

Glon. hed. hyper. iod. kali-bi. Kali-i. kali-sal. kres. lach. lith-c. mag-f. mand. naja Nat-i. nit-

ac. phos. Plb. Plb-i. Polyg-a. rad-br. rauw. Sec. sil. solid. spartin-s. Stront-c. Stront-i. stroph-

h. sumb. syph. Tab. thlas. thyr. Vanad. Visc. zinc-p.

- Old people in – bar-c, stroph-h

Generals – Diabetis mellitus – accompanied by arteriosclerosis – aur, chlorpr,plb, syzyg

Mind – memory weakness – arteriosclerotic disease with - plb.

MURPHY’S REPERTORY 41

Blood - Blood vessels, general – atheroma- aur-m. bell. brom. Calc. Calc-f. caps. Graph.

kali-i. Lac-ac. Lach. lyc. phos. Plb. Sil. sulph.

- elderly people, in Lach.

- morbus brightii, in ph-ac.

- obese persons, in- caps.

Blood – Blood vessels, general – arteriosclerosis - adren. am-i. am-van. aml-ns. ant-ar. arg-

n. Arn. ars. Ars-i. Aur. aur-br. Aur-i. aur-m-n. Bar-c. bar-i. bar-m. bell-p. benz-ac. cact. cal-

75

ren. Calc. calc-ar. calc-f. card-m. chinin-s. chlol. con. crat. Cupr. ergot. fl-ac. form. form-ac.

fuc. Glon. hed. hyper. iod. Kali-i. kali-sal. kres. lach. lith-c. mag-f. mang. naja Nat-i. nit-ac.

phos. Plb. Plb-i. Polyg-a. rad-br. rauw. Sec. sil. solid. Stront-c. Stront-i. stroph-h. sumb. Tab.

thlas. thyr. Vanad. Visc. zinc-p.

BOERICKE’S REPERTORY 42

Circulatory system - Arteries - Atheroma of arteries - adren. Am-i. am-van. ant-ar. arn.

ars. Ars-i. aur. Aur-i. aur-m-n. Bar-c. bar-m. cact. calc-f. chinin-s. con. crat. ergot. Glon. Kali-

i. kali-sal. lach. lith-c. Nat-i. phos. plb. Plb-i. Polyg-a. sec. stront-c. Stront-i. stroph-h. sumb.

thyroiod. Vanad.

SPECIFIC THERAPEUTICS 42,43. As in any other disease, the remedy that encompasses

the diseased state of the constitutional expression at all levels, body, mind and spirit, termed

as constitutional remedy which necessarily coincides with the miasmatic expression of the

individual is the approach to hyperlipidemia. Inspite there are certain remedies specifically

related to hyperlipidemia clinically proven to bring down serum lipid levels as well as

remove the pathological deposition of lipids on arterial walls.

Allium Sativum – Adapted to fleshy subjects. Patients who eat a great deal more especially

meat than they drink.

Arnica – Marked effect on blood. Fatty heart and hypertrophy.

Arsenicum iodatum – Senile heart, fatty degeneration, Arteriosclerosis.

Aurum metallicum – Develops in the organism by attacking the blood. Deterioration of

body fluids. Arteriosclerosis with high blood pressure.

Baryta carb – Useful in general degenerative changes, especially in coats of arteries.Acts on

the muscular coats of heart and vessels. Arterial fibrosis. Blood vessels soften and

degenerate.

76

Calc flour – Arteriosclerosis.

Cardus marianus – Has specific relation to vascular system. Abuse of alcoholic beverages

especially beer.

Cholesterinum – Obstinate hepatic engorgements. Gallstones.

Crataegus – Arteriosclerosis. Said to have a solvent power upon crustaceous and calcareous

deposits in arteries.

Glonoine – Sciatica in atheromatous subjects.

Graphites – Tendency to obesity. Aids absorption of cicatricial tissue.

Plumbum metallicum – A great drug of general sclerotic condition. Hypertension and

arteriosclerosis.

Plumbum iodatum - Arteriosclerosis

Polygonum aviculare – In material doses of tincture found useful especially in

arteriosclerosis

Strontia – Arteriosclerosis. High blood pressure with flushed face, pulsating arteries

Strontia iodat - Arteriosclerosis

Tabacum – Produces high tension and arteriosclerosis of coronary arteries

Vanadium – Arteriosclerosis. Fatty heart. Atheroma of arteries of brain and liver

76

Methodology

77

METHODOLOGY

Source of data

This study was conducted on the patients who reported to the outpatient

department of Fr. Muller Homoeopathic Medical College and Hospital, Deralakatte, as

well as from Kankanady and peripheral centres. Patients belonging to age group of 25 to

75 years were considered for the study. Both the sexes were included belonging to

various socioeconomic group. A total number of 30 cases were taken randomly for the

study. The cases with elevated serum Cholesterol > 200mg/ dl, Triglycerides > 150mg/dl,

LDL > 130mg/ dl or HDL <40mg/ dl were selected The inclusion and exclusion criteria

were followed as given later.

Methods of collection of data

The data was collected by purposive sampling technique as per the inclusion

criteria and processed in a Standardized Case Record (SCR). Processing includes analysis

and synthesis of the case which were done as per the guidelines and principles of

Homoeopathy.

The potency selection and repetition of the dose were done according to the

demand of the case, such as Acute or Chronic, Susceptibility, Vitality and Suppression (if

any), Changes in structural and functional level, and the degree of correspondence to the

remedies. Follow up in each case was planned for a minimum of 3 months.

During the follow up each case was evaluated according to the scoring criteria,

which includes the serum lipoprotein levels before and after treatment.

78

Inclusion criteria:

All cases with hyperlipidemia between the age group 25 yrs and 75yrs, from both

sexes would be selected.

Subjects who have diagnosed of hyperlipidemia based on clinical history, clinical

presentation, clinical examination and blood investigation.

Exclusion criteria:

Subjects below 25 years and above 75 years

Subjects with serious complications like Myocardial infarction, Stroke etc.

The method used for this study is a clinical method for the confirmation. The

results obtained have been statistically analyzed and evaluated. No controls have been

kept for the study. All cases were treated after detailed history taking, with the help of

S.C.R., in which the complete symptomatology of patients (clinical presentation and

individual symptoms) and the investigation reports were recorded.

Selection of medicine in each case was based on the data such as etiological

factors, qualified mentals, physical generals, concomitants, characteristic particulars,

repertorial approach and clinical indications from different authorities. Potencies ranging

from 30 to 1M (centesimal scale) have been used in this study. Repetition and change of

potency and remedy were done as and when needed, according to the Homoeopathic

principles. In between the period of medications, all the patients were kept under placebo

continuously.

79

Follow ups:

Majorities of the patients were reviewed, on a fortnightly basis, to assess the

subjective and objective changes. Each case was followed for a minimum of 3 – 6 months

from the commencement of treatment.

The abbreviations used in the follow up were:

S – No change or same

< - Aggravation of clinical features

> Amelioration of clinical features

0 – Disappearance of clinical features

G – good

N – Normal

R – Regular etc.

Diet and Regimen

All the patients were explained and educated about the importance of low calorie

diet and physical exercises as per the need. Instructions were given to avoid other

medicinal agents during the treatment.

Assessment of Effectiveness

Effectiveness of the treatment was assessed on the basis of

1. Serum lipid profile

2. For the effective assessment and evaluation, disease intensity scores were also

maintained.

80

After completion of treatment, disease intensity of the post treatment scores were

compared with the pre treatment disease intensity score and statistically evaluated.

Notes: For disease intensity scores refer appendix: 1

Plan for Data Analysis

Data has been analysed by using descriptive statistics and the results have been

presented by using frequency table, percentage, pie diagram, and graphs. The

significance of treatment effect based on different homoeopathic therapeutic strategies

are tested using ‘t’ test.

80

Results

81

RESULTS

Table 3: Distribution of cases according to age group

Age group No. of cases Percentage

25-35 7 23.33

35-45 10 33.3

45-55 4 13.3

55-65 7 23.3

65-75 2 6.6

In this study maximum prevalence of Hyperlipidemia were found in the age

group of 35 to 45 years (10 cases – 33.33%). Followed by 25 to 35 and 55 to 65 years of

age group (7 case in each group – 23.33%) and 45 to 55 years of age group (4 cases –

13.3%). Minimum prevalence is found in 65 to 75 years age group (2 cases 6.6%).

Table 4: Distribution of cases according to sex

Sex No. of case Percentage

Male 12 40

Female 18 60

Total 30 100

Out of 30 patients studied, 12 cases (40%) were males and 18 cases (60%) were females.

82

Fig.11: Case distribution according to age group

Fig.12: Case distribution according to sex

0

5

10

15

20

25

30

35

25-35 35-45 45-55 55-65 65-75

710

47

2

23.33

33.3

13.3

23.3

6.6

No. of cases

Percentage

Case distribution according to age group

Age group

Males12

40%

Females18

60%

Distribution of cases according to sex

83

Table 5: Case distribution according to religion

Religion No of cases Percentage

Hindu 8 26.6

Christian 14 46.6

Muslim 8 26.6

Total 30 100

Out of 30 cases maximum prevalence of Hyperlipidemia was found in Christians

(14 cases – 46.66%). Hindus and Muslims shared equal prevalence of (8 cases each-

26.66%).

Table 6: Case distribution according to physical activity

Physical activity No of cases Percentage

Sedentary 16 53.33

Moderate 14 46.6

Severe 0 0

Total 30 100

Among 30 patients included in this clinical study, majority 16 cases (53.3 %)

were found to have sedentary life with minimal physical activity. The rest were patients

with moderate physical activity 14 cases (46.6%). There were no patients with severe

physical activity.

84

Fig.13: Case distribution according to religion

Fig.14: Case distribution according to physical activity

0 20 40 60

Hindu

Christian

Muslim

8

14

8

26.6

46.6

26.6

Percentage

No of cases

Case distributions according to religion

No of cases

Percentage0

20

40

60

SedentaryModerate

Severe

1614

0

53.3346.6

0

No of cases

Percentage

Case distribution according to physical acitivity

85

Table 7: Case distribution according to fundamental miasm

Miasm Fundamental miasm

No. of cases Percentage

Psora 0 0

Sycosis 16 53.3

Syphilitic 1 3.3

Tubercular 1 3.3

Sycosyphilitic 11 36.6

Psora syco 1 3.3

Total 30 100

Table 8: Case distribution according to dominant miasm

Miasm

Dominant miasm

No. of cases Percentage

Psora 8 26.6

Sycosis 16 53.3

Syphilitic 0 0

Tubercular 1 3.3

Psorasyco 5 16.6

Total 30 100

Sycotic expression is well marked and found to be dominating in both

fundamental and dominant miasm with 16 cases (53.3%). Syco syphilitic expression

stands next with 11 (36.6%) in fundamental miasm and Psora with 8 (26.6%) in

dominant miasm. Tubercular, Syphilitic and Psora-sycotic comprises 1 each (3.3%) in

fundamental miasm. Psora comprises 8 (26.6%) and Psorasycotic 5 (16.6%) cases in

86

dominant miasm. Only one case gives Tubercular expression (3.3%) in dominant miasm.

There is no expression from Psoric miasm in fundamental miasm and syphilitic miasm in

dominant miasm

Fig.15: Case distribution according to fundamental miasm

Fig.16: Case distribution according to dominant miasm

No of cases 0

0

50

100

161 0

30

100

30

53.3

3.3 3.3

36.6

3.3

100

No of cases 0

Percentage o

Case distribution according to fundamental miasm

827%

1653%

1 3%

517% Psora

Sycosis

Syphilitic

Tubercular

Psorasyco

Case distribution according to dominant miasm

87

Table 9: Case distribution according to the type of hyperlipidemia

Type of Hyperlipidemia No of cases Percentage

Familial hyper cholesterolemia 4 13.3

Polygenic hypercholesterolemia 7 20

Familial combined hyperlipidemia 10 33.3

CETP deficiency 1 3.3

Familial chylomicronemia 1 3.3

Hepatic lipasedeficiency 2 6.6

Secondary hyperlipidemia 5 16.6

Total 30 100

Among 30 patients included in this clinical study, majority (10 cases-33.3 %)

were found to be having Familial combined hyperlipidemia. Polygenic hyperlipidemia

was next with 7 cases (23.3%).This was followed by Secondary hyperlipidemia and

Familial hypercholesterolemia with 5(16.6%) and 4 (13.3%) cases respectively. The rest

were of Hepatic lipase deficiency (2cases – 6.6%), CETP deficiency (1case – 3.3%) and

Familial chylomicronemia(1case – 3.3%) .

88

Table 10: Case distribution according to constitutional remedies

Name of the remedy No of cases Percentage Calcarea carb 4 13.3

Lycopodium 10 33.3

Medorrhinum 1 3.3

Natrum mur 2 6.6

Nux Vomica 1 3.3

Phosphorus 4 13.3

Pulsatilla 4 13.3

Sepia 2 6.6

Sulphur 2 6.6

Total 30 100

Out of 30 cases, Lycopodium was used as a constitutional remedy in 10 cases (33.3%).

Calcarea carb, Phosphorous and Pulsatilla were used as constitutional remedy in 4 cases

(13.3%) each. Sepia, Sulphur and Natrum mur were used as constitutional in 2 cases

(6.6%) each.1 case (3.3%) each was treated with Nux vomica and Medorrhinum.

89

Fig.17: Case distribution according to the type of hyperlipidemia

Fig.18: Case distribution according to constitutional remedies

4

10

1 2 1

4 42 2

13.3

33.3

3.3

6.6

3.3

13.3 13.3

6.6 6.6

0

5

10

15

20

25

30

35

0 2 4 6 8 10

No of cases

Percentage

Case distribution according to constitutional remedies

90

Table 11: Case distribution according to the effectiveness of treatment

Effectiveness No of cases Percentage

Improved 26 86.6

Not improved 4 13.3

Total 30 100

Fig.19: Case distribution according to the effectiveness of treatment

Out of 30 cases, 26 ( 86,6%) showed improvement in the serum lipid profile.

Following the guidelines all through the proforma, the status of the patient is assessed

and substantiated under two criteria according to the score, based on serum lipid level.

No of cases

percentage

0

10

20

30

40

50

60

70

80

90

Improved

26

4

86.6

13.3

No of cases

percentage

Not improved

91

THE EXPLANATION OF THE STATISTICAL TOOLS AND TECHNIQUES

Table 12: Statistical analysis table

X - Score before treatment Z - Mean difference Y - Score after treatment

Mean X = 422/30 = 14.07 Mean Y = 274/30 = 9.13 Mean Z = 148/30 = 4.93

Sl.No X Y (X - Y)=Z _ Z

_ (Z – Z)2

1 15 5 10 5.07 25.70 2 11 7 4 -0.93 0.86 3 6 1 5 0.07 0.00 4 11 4 7 2.07 4.28 5 12 15 -3 -7.93 62.88 6 17 4 13 8.07 65.12 7 16 11 5 0.07 0.00 8 22 31 -9 -13.93 194.04 9 15 13 2 -2.93 8.58 10 15 10 5 0.07 0.00 11 14 6 8 3.07 9.42 12 23 17 6 1.07 1.14 13 9 5 4 -0.93 0.86 14 7 7 0 -4.93 24.30 15 18 14 4 -0.93 0.86 16 7 2 5 0.07 0.00 17 19 12 7 2.07 2.28 18 14 4 10 5.07 25.70 19 13 0 13 8.07 65.12 20 19 16 3 -1.93 3.72 21 29 16 13 8.07 65.12 22 20 15 5 0.07 0.00 23 6 1 5 0.07 0.00 24 10 4 6 1.07 1.14 25 15 9 6 1.07 1.14 26 14 13 1 -3.93 15.44 27 15 13 2 -2.93 8.58 28 17 13 4 -0.93 0.86 29 9 2 7 2.07 4.28 30 4 4 0 -4.93 24.30

Mean X =422

Mean Y = 274

Mean Z =148 Mean _

(Z – Z)2 = 617.87

92

A. Question to be answered: is there any significant difference between the scores

taken before and after the treatment.

B. Null hypothesis: there is no significant difference between the scores before and

after the treatment.

C. Standard error of the mean differences: the mean of the differences

Z = Z/n = 148/30 = 4.93

The estimation of the population standard deviation is given by the formula

SZ = √ (Z –Z) 2 / n-1

= √ 617.87 / 29

= √ 21.31

= 4.62

The estimation of the standard error is calculated by using the formula

= SZ /√n

= 4.62 /√30

= 4.62/ 5.47

= 0.84

D. Critical ratio is calculated using the formula : t = Z /Sz /√n

= 4.93 / 0.84

= 5.85

93

E. Compare with the tabled values:

The test statistic ‘t’ follows student ‘t’ distribution with n-1(29) degrees of

freedom. Here, tabled value of ‘t’ at 5% level of significance is 2.045 and 1% level of

significance is 2.756 for 29 degrees of freedom. Since the calculated value is 5.85 which

is greater than the tabled at 5% &1%, we reject the Null Hypothesis.

Inference: This study provides an evidence to say that there is reduction in the disease

intensity scores after the homoeopathic treatment based on constitutional treatment and

general management. Therefore the Homeopathic constitutional medicines are effective

in treating hyperlipidemia.

94

Fig.20: Distribution of all cases according to pre and post treatment analysis using scoring char

0

5

10

15

20

25

30

35

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30

Scoring before

Scoring after

95

Discussion

95

DISCUSSION

Hyperlipidemia, which is the raised or abnormal levels of lipids & lipoproteins in

the blood has become a great health hazard, especially in developed countries which has

turned out to be a challenge to the physician. It contributes to high morbidity and

remains a major cause of high mortality in our country.

The current study is done for the better understanding of different types of

hyperlipidemia, to assess the role of miasm in hyperlipidaemia and its management

through general and constitutional homoeopathic treatment.

This study was conducted in patients who reported to the outpatient department of

Fr. Muller Homoeopathic Medical College and Hospital at Deralakatte, as well as from

Kankanady and peripheral centres.

A total number of 30 cases were taken randomly for the study. The cases with

deviated serum lipid i.e. Cholesterol > 200mg/ dl, Triglycerides > 150mg/dl, LDL >

130mg/ dl or HDL <40mg/ dl were selected. The inclusion and exclusion criteria were

followed strictly. For the assessment of the clinical status before and after the treatment

the score was used which is mentioned in the annexure-1. The score before and after the

treatment was considered and‘t’ test was applied.

Prevalence of hyperlipidemia is more frequent among the age group 35-45 years

i.e. 10 (33.33%) cases. Followed by 25 to 35 and 55 to 65 years of age group (7 case in

each group – 23.33%) and 45 to 55 years of age group (4 cases – 13.3%). Minimum

prevalence is found in 65 to 75 years of age group (2 cases 6.6%).

96

Osteoarthritis, hypertension and fibroid uterus in females are the most common

associated complaints observed in the study.

Among the 30 cases selected females 18 (33.33%) were found to be dominating

than the males 12 (40%). Of the different cases selected for study, maximum number of

cases reported from patients with Christian background i.e. around 14 (46.66%). Hindus

and Muslims shared equal prevalence of (8 cases each- 26.66%).

All 30 cases selected were analyzed and graded based on their occupation as

severe , moderate, and sedentary workers. At the end of the study it was concluded from

the data aggregated that maximum incidence of hyperlipidemia is seen in sedentary

working individuals at a rate of 16 (53.33%) cases out of 30. The rest were patients with

moderate physical activity 14 (46.6%), There were no patients with severe physical

activity.

Only 5 (16.6%) out of 30 cases in their background presented with a family

history of Hyperlipidemia, MI or stroke in previous generations recent or remote where

as 25 (83.3%) of cases did not present with the family history.

According to the miasmatic evaluation of the 30 cases taken for the study it was

found that sycotic expression to be dominating in both fundamental and dominant

miasm with 16 (53.33%) cases. Sycosyphilitic expression stands next with 11(36.6%) for

fundamental miasm and Psora with 8 (26.6%) cases for dominant miasm. Tubercular,

Syphilitic and Psora-sycotic comprises 1 each (3.3%) in fundamental miasm. Psora

comprises 8 (26.6%) and Psorasycotic 5(16.6%) cases in dominant miasm. Only one

case gives Tubercular expression (3.3%) in dominant miasm. There is no expression from

Psoric miasm in fundamental miasm and syphilitic miasm in dominant miasm.

97

Among 30 patients included in this clinical study, majority 10 (33.33%) cases

were diagnosed as Familial combined hyperlipidemia. Polygenic hyperlipidemia was next

with 7 cases (23.3%).This was followed by Secondary hyperlipidemia and Familial

hypercholesterolemia with 5(16.6%) and 4 (13.3%) cases respectively. The rest were of

Hepatic lipase deficiency (2cases – 6.6%), CETP deficiency (1case – 3.3%) and Familial

chylomicronemia(1case – 3.3%) .

After evaluating each case, a constitutional remedy was prescribed. Evaluation

of these prescribed constitutional remedies helps us to know thee most commonly used

remedies. Maximum occurrence was taken by Lycopodium which is given in 10 cases

with a percentage of 33.33% and followed by other remedies like Phosphorous, Calcarea

carb and Pulsatilla in 4 cases(13.33%)each. Sepia, Sulphur and Natrum mur were used as

constitutional in 2 cases (6.6%) each.1 case (3.3%) each was treated with Nux vomica

and Medorrhinum..

Out of 30 cases, 200th potency was selected for the first prescription in

maximum cases 27 (90%). 30th potency was given in 2 cases (6.66%).10M potency was

given in 1case (3.33%).

For the assessment of effectiveness of homoeopathic treatment, disease intensity

scores before and after treatment were statistically evaluated with ‘t’ test and which is

found significant. Fisher’s exact test is used to find out any association between

Hyperlipidemia and Constitutional medicines and the value obtained after statistical

evaluation indicated that there is an association between the disease and constitutional

medicine of the patient.

98

Evaluation of the serum lipid levels before and after the treatment revealed that

there is improvement before and after treatment.

The result is understood after evaluating the scored values before and after

treatment. Value obtained is 5.85, which is more than the tabled value of 2.045. Hence

null hypothesis is rejected.

Inference: From the study it is clear that homoeopathic constitutional treatment is

effective in the treatment of hyperlipidemia with a well planned general management.

LIMITATIONS:

1. Hyperlipidemia is a chronic disorder requiring long-term management for desired

results. As the study has the time limit, it was not possible to observe the patients

for longer periods.

2. Some good cases couldn’t be included in this study because of discontinuation of

treatment in between the study.

3. This is a restricted sample design, in which only 30 cases were studied. Chances

of sampling error are increased with small sample size and hence the conclusions

based on those cases have limited implications. Generalization of the result is

difficult to emphasize.

4. Hyperlipidemia is observed in increasing number of population. But many are

not aware of the consequences. Most of the cases reported with other complaints

and were detected of hyperlipidaemia on screening.

5. Repeated serum analysis was not done in all the cases. Hence there is possibility

of incompleteness in the study.

6. There was no control group as such since the sample size was small.

99

7. In some cases few necessary details were lacking and the study is conducted

based on the available data.

RECOMMENDATIONS:

1. Bigger sample size with extended time of study would provide better result.

2. Improvised scales can be used, so that evaluation of the outcome of the study

would become more precise.

3. Same study can be conducted with the help of placebo controlled (single blind,

double blind) study.

4. An attempt to discover new techniques, closely monitoring the general

management of the patients.

100

Conclusion

100

CONCLUSION

1. Prevalence of hyperlipidemia is more frequently among the age group 35-45 years

i.e.10 cases (33.33%). cases reported to the study. This reproves the statement

that hyperlipidemia has its onset in the fourth decade.

2. Osteoarthritis, hypertension and fibroid uterus in females are the most common

associated complaints observed.

3. Females showed more prevalence i.e 18 cases (60%) out of 30 than the males

which can be due to the general prevalence in the inflow of female patients to the

OPD or due to purposive sampling.

4. Prevalence of hyperlipidemia shows maximum number of cases reported from

patients with Christian background i.e. around 14 (46.66%). Hindus and Muslims

shared equal prevalence of (8 cases each- 26.66%) Probably this result can be

attributed to the dietary factors noted in this community which serves as risk

factors or because the inflow of patients to the OPD is mainly of Christian

community.

5. At the end of the study it can be concluded from the data aggregated that

maximum incidence of hyperlipidemia is seen in sedentary working individuals at

a rate of 16 (53.33%) cases out of 30 and there were no patients with heavy

physical activity out of 30 reported to the study, indicating the lifestyle factors

and obesity as important factors that determine the severity of disease in

community.

101

6. According to the miasmatic evaluation of the 30 cases taken for the study sycosis

is presenting maximum predominance in fundamental as well as dominant miasm

in 16 (53.33%) cases. Complex miasms like Syco syphilitic expression stands

next11 (36.6%) for fundamental miasm, There is no expression from Psoric

miasm in fundamental miasm and syphilitic miasm in dominant miasm

7. Evaluation of the serum lipid profile before and after the treatment reveals that

there is improvement in 26 cases (86,66%) out of 30 cases

8. All the cases were worked out and the constitutional similimum was selected and

patients were observed on follow ups spaced at a gap of 2 weeks duration.

9. Along with the constitutional treatment general management in the form of diet

and exercise guidelines were given to the patient .

10. Lycopodium was the leading remedy at the constitutional level, proving the

general constitution of the remedy to be predisposed for hyperlipidemia

11. Potency selection was done based on the standardized guidelines in the SCR

according to the susceptibility and sensitivity of the patient.200th potency showed

maximum prevalance

12. According to the need of the cases some acute remedies were prescribed in

between.

13. The various statistical techniques applied proved the efficacy of the treatment.

.

101

Summary

102

SUMMARY

This study was conducted on patients with hyperlipidemia.

The objectives of the study were,

1. To study the different types of hyperlipidaemia

2. To assess the role of miasm in hyperlipidaemia and know the effectiveness of

constitutional method of treatment which includes the miasmatic background of

the individual .

A total of 30 cases were taken for study based on inclusion and exclusion criteria.

Majority of the cases were aged between 35-45years. Miasmatic evaluation of all

the cases revealed sycosis to have maximum predominance as fundamental as well as

dominant miasm. Constitutional medicines were given to all the patients and along with

that general management guidelines for diet and exercise guidelines were also explained.

Follow up analysis of the patients state was assessed with serum lipid profile.

Lycopodium as constitutional medicine had higher indications. 200th potency showed

wider indications. The study reveals that homoeopathic treatment with dietary and

exercise guidelines when strictly implemented is the best method of approaching

hyperlipidemia

103

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103

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103

Annexures

107

ANNEXURE – 1

SCORING CHART

Sl.

No

Cholesterol,

mg/dl Score

Triglycerides,

mg/dl Score

LDL,

mg/dl Score

HDL,

mg/dl Score

1 <200 0 <150 0 <130 0 >40 0

2 200 - 225 1 150 - 175 1 130 - 135 1 40 - 38 1

3 225 - 250 2 175 - 200 2 135 - 140 2 38 - 36 2

4 250 - 275 3 200 - 225 3 140 - 145 3 36 - 34 3

5 275 - 300 4 225 - 250 4 145 - 150 4 34 - 32 4

6 300 - 325 5 250 - 275 5 150 - 155 5 32 - 30 5

7 325 - 350 6 275 - 300 6 155 - 160 6 30 - 28 6

8 350 - 375 7 300 - 325 7 160 - 165 7 28 - 26 7

9 375 - 400 8 325 - 350 8 165 - 170 8 26 - 24 8

10 400 425 9 350 - 375 9 170 - 175 9 24 - 22 9

11 >425 10 >375 10 >175 10 <22 10

108

ANNEXURE – 2

DETAILED CASE STUDY

PRELIMINARY DATA

Name : Mr S B SCR No. : 57123

Age : 41 yrs Date : 26-06-10

Sex : Male Physician : Dr. MK

Occupation : Govt Employee

Education : Graduate

Religion : Hindu

Address : Neeleshwaram

CHIEF COMPLAINT

No LOCATION SENSATION MODALITY CONCOMITANT 1. Rectum

Since 5 – 6 yrs

Hard stool Difficult to pass Burning2 Bleeding

< spicy food, fried food, Non Veg < after stool

2. Head Scalp Since 5 – 6 yrs

Hair fall, Dandruff Powdery scales Slight itching

< combing < summer

HISTORY OF CHIEF COMPLAINT

The patient was apparently alright before 6yrs. The complaints started with hard

stools difficult to pass. Later bleeding started which was more after stool. The complaints

are more after spicy food, fried and non veg.

109

The patient also complains of hair fall which started around 5 yrs back. It is

accompanied with dandruff in the form of white powdery scales. Hair fall is more on

combing while Itching of scalp is more felt in summer

PAST HISTORY

Hypercholesterolemia since 2 - 3 years.

FAMILY HISTORY

Father - Expired following some liver disease

Mother - Hypercholesterolemia, Haemorrhoids

Brother - Haemorrhoids

TREATMENT HISTORY

Allopathic treatment for Haemorrhoids.

PATIENT AS A PERSON

Appearance : Stocky

Appetite : Good

Craving : Meat, sweets

Aversion : Nil

Perspiration : Normal

Bowel : Hard

Bladder : 5 - 6/day

Thermal : Chilly (C4H)

Sleep : Good

Mental generals : Company desire Doesn’t like to share

Doesn’t like contradiction Superficial relation

110

GENERAL PHYSICAL EXAMINATION

Well built and well nourished

Patient is well oriented with time place and person.

No signs of pallor, cyanosis, clubbing or icterus.

Vital signs:

Pulse - 74/min, regular, good volume and vessel wall not palpable.

Temperature - Afebrile at the time of examination

Respiratory rate - 18/min

Blood pressure - 120/80 mm of Hg. ( Right arm supine position)

Weight – 66 Kg

LOCAL EXAMINATION

External haemorrhoids 11 ‘ o clock position

No tenderness

No bleeding

SYSTEMIC EXAMINATION

Abdomen - NAD

Respiratory system - Vesicular breathe sounds

No added sounds

Cardiovascular system - S1 S2 heard

No murmurs

Central nervous system – NAD

111

INVESTIGATIONS DONE

Serum cholesterol - 282 mg/dl

TG – 166 mg/ dl

LDL– 156 mg/dl

HDL – 32 mg/dl

PROVISIONAL DIAGNOSIS

External Haemorrhoids Alopecia area’ta Familial hypercholesterolemia

Hard stool difficult to pass Hair loss Raised serum cholesterol, TG

Burning and LDL. Low HDL

Bleeding after stool

< spicy food

LIFE SPACE INVESTIGATION

The patient hails from a middle class family. Parents were agriculturists. Father

expired when the patient was 9 yrs old. By then his elder brothers were working and

hence did not face any financial constraints. His brothers are well settled. He got married

at the age of 28 yrs which was a love match and leads a happy life with one son and one

daughter.

He is affectionate, especially to his daughter. He likes to be in company of others

but does not go into deep relations nor does he like to share his feelings with others. He

doesn’t get angry fast and deslikes contradiction. He has fear of dark from childhood. His

memory is weak but active thinking and clear perception.

112

FIRST PRESCRIPTION:

1. Phosphorous 200

1 Pkt x HS

2. No 40 pills

4–0–4 x 2 weeks

Follow Up Criteria

1) Hyperlipidemia

2) Hard stool

3) Burning

4) Bleeding

5) Hairfall

6) Dandruff

MIASMATIC EXPRESSION

Sector Psora Sycosis Tubercular Syphilis

F/H M – Haemorrhoids, hypercholesterolemia

B - Haemorrhoids

F – Premature death due to liver disease

P/H ------ -----

Mentals Weak Memory

Fear of dark Likes company Superficial relations. Does not share with others

Physicals Bowels -hard Cr- Sweet

Appearance- Stocky Cr-Meat Thermally chilly

Characteristic particulars

Hairfall, Burning pain,Bleeding

113

ESSENTIAL EVOLUTIONARY TOTALITY

Pt family

Good predisposition

FM – Sycotic - Syphilitic

DM –Tubercular

Pt family

Good

Pt society

Good

Pt society

Good

Pt work

Good

Pt work

Good

disposition

Likes company Superficial relation

Doesn’t like to share Deslikes contradiction

Fear of dark Memory weak

Mingles with every one Maintains good relation

D i a t h D i s e a s e s

Craving – Meat, Sweets Thermally – Chilly

Bowels – Hard

Hyperlipidaemia

Hard stool

Burning

Bleeding < after stool

< spicy food

Hair fall

Familial hypercholesterolemia

External Haemorrhoids

Alopecia area’ta

Syphilis

Sycosis

Psora

Tubercular

114

CONSTITUTIONAL TOTALITY

MENTAL GENERALS

Mingles easily with people

Likes Company

Superficial relations

Doesn’t share

Deslikes contradiction

Weak memory

Fear of dark

PHYSICAL GENERALS

Caving for meat, sweets.

Thermally chilly

Bowels hard

CHARACTERISTIC PARTICULARS

Hyperlipidemia

Hard stool difficult to pass

Burning

Bleeding after stool < Spicy food

Hair fall,

Dandruff

MIASMATIC INTERPRETATION

Dominant miasm --- Tubercular

Fundamental miasm --- Sycosis - Syphilis

115

General management

Patient was advised systematically regarding dietary management and also

general guide lines regarding exercise.

FOLLOW UPS

DATE SYMPTOM CHANGES PRESCRIPTION

10. 07 .10

1 2 3 4 5 6 7 8 9 10 RX 1. SL pkt (1P)

H S

2. No 40 pills

4–0–4 x 2 wks

- - > > - <

24.07.10

1 2 3 4 5 6 7 8 9 10 RX

1. Phos 200 (1P) H S2. No 2 . No 40 pills

4–0–4 x 2 wks .

> - > > - <

Serum cholesterol – 226 mg/dl TG – 138mg/dl LDL – 123 mg/dl HDL – 35 mg/dl

7. 08. 10

1 2 3 4 5 6 7 8 9 10 RX 1. SL pkt (1P)

H S

2 . No 40 pills

4–0–4 x 2 wks

> > > > - -

Generally feels better

21. 08. 10

1 2 3 4 5 6 7 8 9 10 RX

1. SL pkt (1P) H S

2. No 40 pills

4–0–4 x 2 wks

> > > > - <

Generals – good

116

4.09-10

1 2 3 4 5 6 7 8 9 10 RX 1. SL pkt (1P)

H S 2. No 40 pills

4–0–4 x 2 wks

> > > > - -

18.09.10

1 2 3 4 5 6 7 8 9 10 RX

1. SL pkt (1P) H S

2. No 40 pills

4–0–4 x 4 wks

> > > > - -

Generals – good

SCORING

Sl No Serum lipid levels Scoring before treatment

Scoring after treatment

1. Cholesterol 4 2

2. Triglycerides 1 0

3. LDL 6 0

4. HDL 4 3

Total 15 5

117

INVESTIGATIONS REPORTS BEFORE AND AFTER TREATMENT

118

ANNEXURE 3

MASTER CHART

Sl. no

Particulars Of the Patient

Clinical Diagnosis

Past And Family History

Investigations Totality Miasms Remedy Duration of

treatment

Scoring

Result

Before After FM DM B A

1 Name: Mr S B Age : 41 yrs Sex : M Occu : Govt employee Relegion :Hindu Add : Neeleshwar SCR No : 57123

Familial hypercholesterolemia External Haemorrhoids Alopecia area’ta

Mother – Hypercholesterolemia, Haemorrhoids Father – Expired due to liver disease Brother - Haemorrhoids

Chol –282mg/dl TG- 166mg/ dl LDL – 156mg/dl HDL- 32mg/ dl

Chol – 226mg/dl TG – 138mg/ dl LDL – 123mg/dl HDL – 35mg/ dl

MG: Fear of dark, Likes company, Doesn’t like contradiction, Doesn’t like to share, weak memory PG: Stocky appearance Cr –Sweets, meat Chilly patient CP: Bleeding < spicy food Hairfall< summer

Syco- Syphil

Tub Phos 200 3 mths 15 5 Improved

2 Name: Mrs K M Age :40 yrs Sex:F Occu: Housewife Relegion: Muslim Add :Kumbla SCR No: 43325

Familial combined hyperlipidemiaAllergic rhinitis

Mother – Epilepsy Father – Bronchial asthma, DM, Died following Renal failure Brother -DM

Chol- 255mg/ dl TG – 138mg/ dl LDL – 168mg/ dl HDL 47mg/ dl

Chol – 232mg/ dl TG 106mg/ dl LDL- 155mg/ dl HDL- 56mg/ dl

MG – Brooding, Suppressed emotion, Weeping when alone, Hasty, Doesn’t like company, Good confidence PG – Stocky appearance Cr – Fish Av – Sweets, Ice cream, Hot patient CP – Sneezing < Dust, Cold air, Morning. Breathlessness < lying down, Night

Syco- Syphil

Psora Natrum Mur 30

5 mths

11 7 Improved

119

Sl. no

Particulars Of The Patient

Clinical Diagnosis

Past And

Family History

Investigations Totality

Miasms Remedy Duration of

treatment

Scoring Result

Before After FM DM B A

3 Name: Mrs Y

Age : 41 yrs Sex: F Occu: Housewife Relegion: Hindu Add :Ullal SCR No: 14392

CETP deficiency Osteoarthritis Calcanean spur Hypertension

Mother – Osteoarthritis Father – Expired of MI

Chol- 250mg/ dl TG – 66mg/ dl LDL – 148 mg/ dl HDL- 89mg/ dl

Chol – 225mg/ dl TG – 60mg/ dl LDL – 128mg/ dl HDL – 85mg / dl

MG: Mild, Likes company, Likes consolation Weak memory PG: Stocky appearance Decreased appetite Perspiration increased in general, Cr – Fish, Spicy Av – Veg Chilly patient CP: Joint pains pricking < before menses, exertion >Warmth, pressure Giddiness < getting up from sitting position

Syco- Syphil

Syco Puls 200, 1M

4mths 6 1 Improved

Name: Mr M Age : 35yrs Sex: M Occu: Driver Relegion: Muslim Add : Payyannur SCR No: 48619

Familial chylomicronemia LRTI Tension headache Hypertension

Mother – Bronchial asthma Father – Died of MI

Chol – 223mg/ dl TG- 425mg/ dl LDL – 129mg/ dl HDL- 50mg/ dl

Chol – 198mg/dl TG – 280mg/ dl LDL – 101mg/ dl HDL – 41mg/ dl

MG: Suppressed emotion, Arrogant, Introvert, Likes company, Sympathetic PG: stocky appearance Appetite decreased Thirst decreased Perspiration increased in general Cr- Shellfish Av- Meat Hot patient CP: Dry cough < after fried food, headache pricking < Tension, after sleep> pressure Chest burning < heavy food

Syco- Syphil

Psora Sulph 200 5mths 11 4 Improved

120

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Particulars Of The Patient

Clinical Diagnosis

Past And

Family History

Investigations Totality

Miasms Remedy Duration of

treatment

Scoring Result

Before After FM DM B A

5 Name: Mr J P

Age : 27 Yrs Sex:M Occu: Attendar Relegion :Christian Add : Manjeshwar SCR No: 9154

Polygenic hypercholesterolemia Sinusitis APD

P/H Appendicitis Father – Hypertension

Chol – 235mg/dl TG -86mg/ dl LDL- 176mg/ dl HDL- 42mg/ dl

Chol- 324mg/dl TG- 122mg/ dl LDL- 234mg/ dl HDL- 46mg/ dl

MG: Anxiety about future Sensitive, Intolerant to contradiction. PG: Stocky appearance Cr - Non Veg, cold drinks. Av – Veg Hot patient CP: < Tension Abdomen fullness < spicy, Non Veg Head ache < Sun, exertion > Tight bandage

Syco Psora Lyco 200 4 mths 12 15 Not Improved

6 Name: Mrs N Age : 37 Sex: F Occu Housewife: Relegion: Hindu Add : Bejai SCR No: 54279

Polygenic hypercholesterolemia Varicose veins

P/H Bronchial asthma, Chikungunya Mother – DM Expired

Chol – 310mg/ dl TG – 130mg/ dl LDL – 157mg/ dl HDL – 27mg/ dl

Chol – 149mg/ dl TG – 113mg/ dl LDL – 95mg/ dl HDL– 31mg/ dl

MG – Shy, Sensitive, Obstinate, Likes to be in company PG – stocky appearance Perspiration increased on face,Hard stool, once in two days Av – Chicken Sour food disagrees Hot patient CP – Extremities pain, Burning < Exertion, morning > warmth, Massage

Syco Syco Puls 200 3 mths 17 4 Improved

121

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Particulars Of The Patient

Clinical Diagnosis

Past And

Family History

Investigations Totality

Miasms Remedy Duration of

treatment

Scoring Result

Before After FM DM B A

7 Name: Mrs L R

Age :42yrs Sex: F Occu: Lecturer Relegion: Christian Add : Bendore SCR No:54604

Polygenic hypercholesterolemia Hypertension

P/H Eczema Bronchial asthma since 15 yrs Father – DM, Hypertension Mother – DM, Hypertension

Chol – 271mg/ dl TG – 124mg/ dl LDL – 212mg/ dl HDL – 35mg/ dl

Chol – 239mg/ dl TG – 112mg/ dl LDL – 174mg / dl HDL– 41mg/ dl

MG – Relegious, Emotional stress, Anxiety about children, Sympathetic, Suicidal thoughts PG – Obese Perspiration on face Cr – Sweets, fried food Av – Sour Hot patient

Syco Syco Lyco 200 4mths 16 11 Improved

8 Name: Mr H Age : 32yrs Sex: M Occu: Clerk Relegion: Muslim Add :Urumanai SCR No: 9504

Familial combined hyperlipidemiaFunctional impotency

Mother - DM

Chol – 465mg/dl TG – 180mg/ dl LDL – 374mg/ dl HDL – 55mg/ dl

Chol – 448mg/dl TG – 170mg/ dl LDL – 394mg/ dl HDL– 20mg /dl

MG: Fear of dogs, Likes company PG: Stocky appearance Increased thirst, Scanty perspiration Cr – Veg Av – Fish, sweet Chilly patient CP: Premature ejaculation, Xanthoma Headache < evening, > sleep

Syco Psora - Syco

Phos 200, 1M

5mths 22 31 Not Improved

122

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Particulars Of The Patient

Clinical Diagnosis

Past And

Family History

Investigations Totality

Miasms Remedy Duration of

treatment

Scoring Result

Before After FM DM B A

9 Name:Mrs G M Age :44yrs Sex:F Occu: Housewife Relegion: Christian Add :Kannur SCR No:57489

Polygenic hypercholesterolemia Osteoarthritis Sinusitis

P/H Bronchial asthma, Chikungunya Father - Bronchial asthma

Chol – 287mg/ dl TG- 175mg/ dl LDL- 210mg/ dl HDL- 42mg/ dl

Chol-269mg/ dl TG- 146mg/ dl LDL-195mg/ dl HDL-45mg/ dl

MG – Mild, Indecisive, Weepy, Fear of thunderstorm, likes consolation PG – Stocky appearancePerspiration generally decreased, Thirst decreased Cr – Rice, Fish Av- Milk Hot patient CP – Joint pains < First movement > Rest Headache < Sun, Travelling, Afternoon > Tight bandage

Syco Psora - Syco

Puls 200 3 mths 15 13 Improved

10 Name: Mrs R D Age :58yrs Sex:F Occu: Housewife Relegion: Christian Add : Kulshekar SCR No:52832

Secondary hyperlipidemiaDiabetic cataract APD

P/H- DM since 14 yrs Night blindness at 5yrs Mother – DM, Hypertension, Stroke

Chol- 234mg/ dl TG- 200mg/dl LDL – 161mg/ dl HDL – 33mg/ dl

Chol- 228mg/ dl TG – 163mg/ dl LDL – 156mg/ dl HDL– 40mg/ dl

MG – Workaholic, Relegious, Mild, Sympathetic, Perfectionist, Fear of thunder & lightning, Anxiety about health PG – Stocky appearance, Perspiration increased generally Av – Spicy, Bitter Chilly patient CP – Distension of abdomen < Non Veg, Sweets

Syco- Syphil

Syco Phos 200 5 mths 15 10 Improved

123

Sl. no

Particulars Of The Patient

Clinical Diagnosis

Past And

Family History

Investigations Totality

Miasms Remedy Duration of

treatment

Scoring Result

Before After FM DM B A

11 Name: Mr K

Age : 44 yrs Sex: M Occu: Executive officer Relegion: Hindu Add : Mangalore SCR No: 56928

Familial combined Hyperlipidemia Cholecystolithiasis

Father died of peptic ulcer Mother died of Tuberculosis

Chol – 258mg/ dl TG – 203mg/ dl LDL – 168mg/ dl HDL – 50mg/ dl

Chol – 226mg/ dl TG – 182mg/ dl LDL – 139mg/dl HDL– 51mg/ dl

MG – Workaholic, Punctual, Leadership, Confident, Superiority, Bold PG – Stocky appearance Thirst increased Addiction – occasionally Alcohol Chilly patient CP – Right hypochondriac pain < after food

Tub Syco Nux Vom 200

3 mths 14 6 Improved

12 Name :Mr B Age : 58 yrs Sex: M Occu: Railway Guard Relegion: Hindu Add : Ottappalam SCR No: 55073

Secondary hyperlipidemiaHypertension Acute Bronchitis

P/H- DM since 18 yrs Chicken pox, 3yrs back Father – Died of Renal failure following DM Mother – Died of MI

Chol – 300mg/ dl TG – 147mg/ dl LDL – 248mg/ dl HDL – 23mg / dl

Chol- 238mg/ dl TG – 129mg/ dl LDL – 183mg/ dl HDL– 30mg/ dl

MG – Workoholic, Perfectionist, Irritable, Reacts for anger PG – Lean, Perspiration increased, Appetite increased, Thirst increased, Cr – Fish, Av – Meat, Hard Stools Hot patient CP – Dry cough < Night Breathlessness on distension of abdomen

Syco - Syphil

Syco Lyco200 8 mths 23 17 Improved

124

Sl. no

Particulars Of The Patient

Clinical Diagnosis

Past And

Family History

Investigations Totality

Miasms Remedy Duration of

treatment

Scoring Result

Before After FM DM B A

13 Name: Mrs L S

Age : 48 yrs Sex: F Occu: Housewife Relegion: Christian Add : Bantwala SCR No: 57290

Familial combined hyperlipidemia Cholecystolithiasis

Mother - Hypertension

Chol- 241mg/ dl TG- 222mg/ dl LDL- 149mg/dl HDL- 48mg/ dl

Chol- 224mg/ dl TG – 207mg/ dl LDL – 130mg/ dl HDL– 53mg/ dl

MG – Loquacious, Irritable, Gets angry fast, Likes consolation,Likes to share , Helps others, Memory weak PG- Obese, Perspiration increased in general Cr – Sweets, Ice cream Av- Spicy Pleasant dreams Chilly patient CP -

Syco Syco Phos 200 3 mths 9 5 Impeoved

14 Name: Sr T Age : 43yrs Sex: F Occu: Accountant Relegion: Christian Add :Deralakatte SCR No: 14010

Familial combined hyperlipidemiaAllergic rhinitis, Arthritis Calcanean spur

P/H Fibroid uterus Mother – DM Father – DM, Hypertension Grand father – DM, Hypertension

Chol- 267mg/ dl TG – 197mg/ dl LDL – 139mg/ dl HDL – 89mg/ dl

Chol – 257mg/ dl TG – 187mg/ dl LDL – 138mg/ dl HDL– 82mg/ dl

MG: Suppressed emotion, Likes company, fear of snakes & worms ,Irritable, Anger – reacts PG: Stocky appearance Cr – Sweets Av – Pungent,sour Perspiration on back Chilly patient CP: Sneezing < morning, dust Headache > Pressure, Night Joint pain < first movement

Syco Psora- Syco

Sepia 200 5 mths 7 7 Not Improved

125

Sl. No

Particulars Of The Patient

Clinical Diagnosis

Past And

Family History

Investigations Totality

Miasms Remedy Duration of

treatment

Scoring Result

Before After FM DM B A

15 Name: Mr M

Age : 44 yrs Sex:M Occu: Airlines officer Relegion: Christian Add : Panjim SCR No: 33269

Familial hypercholesterolemia Migraine

Grand father – DM, Hypertension, Osteoarthritis Father - Hypertension

Chol- 273mg/ dl TG- 197mg/ dl LDL- 199mg/ dl HDL- 34mg/ dl

Chol- 268mg/ dl TG – 156mg/ dl LDL- 179 mg/ dl HDL– 42mg/ dl

MG – Stress , Anxiety,Irritable, Controls anger, Contradiction <, Likes consolation, Likes company, Hasty decision, Adequate confidence, Weak memory PG – Stocky appearance Perspiration of feet Cr- Fried food, Av- Leafy Veg Hot patient CP -

Syco Psora Lyco30, 200

12mths 18 14 Improved

16 Name: Sr M B Age : 67 yrs Sex:F Occu: Teacher Relegion: Christian Add : Mangalore SCR No:56632

Hepatic lipase deficiency Osteoarthritis with Osteopenia

P/H – Filariasis Hypertension since 15yrs Fibroid uterus Mother - Hypertension

Chol- 212mg/ dl TG 166mg/ dl LDL – 134mg/ dl HDL – 36mg/ dl

Chol – 198mg/ dl TG – 152mg/ dl LDL – 127mg/ dl HDL– 40mg/ dl

MG – Sensitive, Friendly, Irritable, Controls anger. Likes to share, Likes company, Likes consolation, Fear of snakes & accidents PG – Stocky appearance Av- Cold food Cr- Hot & spicy food Dreams – Frightful, accidents Hot Patient CP – Joint pain shooting , Stiffness < morning, first movement > Hot application

Syco Syco Lyco 200 7 mths 7 2 Improved

126

Sl. No

Particulars Of The Patient

Clinical Diagnosis

Past And Family History

Investigations Totality

Miasms Remedy Duration of

treatment

Scoring Result

Before After FM DM B A

17 Name: Mrs K H

Age: 57 yrs Sex: F Occu: Housewife Relegion: Muslim Add : Valencia SCR No: 56804

Familial combined hyperlipidemia Migraine, Cholelithiasis

P/H – Fibroid uterus Mother – Cardiac failure Brother - Renal failure Sister - DM, Hypertension

Chol- 281mg/ dl TG- 349mg/ dl LDL- 163mg/ dl HDL- 50mg/ dl

Chol – 256mg/ dl TG – 297mg/ dl LDL – 143mg/ dl HDL– 54mg/ dl

MG – Brooding of past, Weepy, Grief, Anger on contradiction, Does not like consolation, likes company PG- Stocky appearance, Perspiration increased in general Cr- Fish Hot patient CP – Headache Burning, Radiadting to neck, Vomiting, Lachrymation < Sun, Travelling, Crowd, Tension, Talking Incontinence of urine

Syco- Syphil

Psora- Syco

Lyco 200 4 mths 19 12 Improved

18 Name: Mr C Age : 63 yrs Sex: M Occu: Lab assistant Relegion: Hindu Add : Mangalore SCR No: 55419

Secondary hyperlipidemia Grade I Renal parenchymal disease, Cholecystolithiasis Grade II BPH

P/H – Hydrocoele at the age of 28 yrs, Hypertension since 5 yrs Father- Hypertension Mother- DM, Hypertension, Osteoarthritis Brother- Hypertension

Chol- 247mg/ dl TG – 127mg/ dl LDL – 183mg/ dl HDL – 37mg/ dl

Chol- 209mg/ dl TG- 113mg/ dl LDL- 144mg/ dl HDL- 44mg/ dl

MG- Perfectionist, Confident PG – Stocky appearance Profuse general perspiration, offensive, yellow staining Cr- Fish Addiction – Smoking till 28yrs, Beer occasionally Chilly patient CP – Pricking pain in loin < Exertion

Syco Syco Calc carb 10 M

10mths 14 4 Improved

127

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Particulars Of The Patient

Clinical Diagnosis

Past And Family History

Investigations Totality

Miasms Remedy Duration of

treatment

Scoring Result

Before After FM DM B A

19 Name: Mrs A M

Age : 50 yrs Sex: F Occu: Lab assistant Relegion: Christian Add : Surathkal SCR No: NITK 06

Polygenic hypercholesterolemia Varicose veins Osteoarthritis Cervical spondylosis

P/H – Eczema in childhoodBronchial asthma since 20 yrs Cerebral infarction

Chol- 251mg/ dl TG- 102mg/ dl LDL- 186mg/ dl HDL- 44mg/ dl

Chol- 176mg/ dl TG- 70mg/ dl LDL- 106mg/ dl HDL- 56mg/ dl

MG – Mild, Weak memory, Inadequate confidence PG – Stocky appearance Appetite increased Thirst decreased profuse Perspiration Cr-Tea, Icecream, Sweets, Hot food, Fish, Spicy but disagreesAv- Oily food Ambhithermal CP – Aching pain of legs < Exertion, Standing Pricking pain & stiffness of joints < first movement > wam application

Syco - Syphil

Syco Puls 200 10mths 13 0 Improved

20 Name: Mrs B Age :60yrs Sex: F Occu: Housewife Relegion: Muslim Add : Kasargod SCR No: 5535

Polygenic hypercholesterolemia CAD APD

P/H – Haemorrhoids since 25 yrs Low back ache since 6 yrs Mother & 2 brothers died of cancer Brother died of MI Brother - Haemorrhoids

Chol- 412mg/ dl TG – 98mg/ dl LDL – 349mg/ dl HDL – 44mg/ dl

Chol- 330mg/ dl TG- 68mg/ dl LDL - 275mg/dl HDL- 42mg/ dl

MG – Irritable, Does not express /share, Suppressed emotion, Anxious about health, Weeps alone, Anger on contradiction, Fear of Snakes, Darkness, Robbers, Being alone, Weak memory PG – Stocky appearance Appetite decreased, Thirst decreased Cr- Fish, Sweet, Sour, Meat Unsatisfied stool Sleep disturbed Ambithermal CP- Breathlessness < Lying, Tension, Exertion Distension of abdomen < Early morning

Syphil Syco Nat Mur 200

8mths 19 16 Improved

128

Sl. no

Particulars Of The Patient

Clinical Diagnosis

Past And Family History

Investigations Totality

Miasms Remedy Duration of

treatment

Scoring Result

Before After FM DM B A

21 Name: Mrs P B

Age : 61 yrs Sex: F Occu: Housewife Relegion: Hindu Add : Padil SCR No: 1727

Familial hypercholesterolemia Osteoarthritis Cervical spondylosis

P/H – Fibroid uterus, Hypertension since 14 yrs Hypothyroidism since 5yrs Ganglion

Chol – 346mg/ dl TG - 206 mg/ dl LDL – 287mg/ dl HDL- 18 mg/ dl

Chol- 276mg/ dl TG - 194mg/ dl LDL- 196mg/ dl HDL- 42 mg/ dl

MG – Grief, Consolation <, Gets angry on contradiction Suppress anger PG – Stocky appearance Appetite decreased Perspiration increased in general Sleep disturbed by thoughts Cr- Fried Cannot tolerate fat Hot patient CP- Knee joint pain, Leg pain < Night

Syco Syco Medorrhin200

12 mths 29 16 Improved

22 Name: Mr M S Age : 30yrs Sex: M Occu: Business Relegion: Muslim Add : Adur SCR No: 7994

Familial combined hyperlipidemiaTension headache Flatulent dyspepsia Arthritis

Father- Hypertension Mother- Hypertension, DM, Gastritis

Chol- 390mg/ dl TG – 178mg/ dl LDL – 315mg/ dl HDL – 41mg/ dl

Chol- 296mg/ dl TG – 156mg/ dl LDL – 229mg/ dl HDL– 46mg/ dl

MG – Irritable, Gets angry fast & shouts, Anticipatory anxiety about business, Doesn’t like contradiction Likes company & consolation PG – Stocky appearance Perspiration increased, Appetite increased, Thirst increased Cr- Meat, egg, spicy Sleep disturbed with tension ,Increased sexual desire, Amorous dreams Addiction occasionally beer, Smoking Hot patient CP – General < 4-5 PM, Tension, Empty stomach Retrosternal burning < cold drinks, Egg > Hot drinks

Syco Psora Lyco 200, 1M

5mths 20 15 Improved

129

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Particulars Of The Patient

Clinical Diagnosis

Past And

Family History

Investigations Totality

Miasms Remedy Duration of

treatment

Scoring Result

Before After FM DM B A

23 Name: Mr A

Age : 52 yrs Sex: M Occu: Bus conductor Relegion: Christian Add : Deralakatte SCR No: 8424

Secondary HyperlipidemiaDiabetis Mellitus

P/H – Jaundice, Lipoma

Chol – 217mg/ dl TG – 146mg/ dl LDL – 148mg/ dl HDL – 40mg/ dl

Chol – 200mg/ dl TG – 139mg/ dl LDL – 128mg/ dl HDL– 45mg/ dl

MG – Stress, Perfectionist Likes company, Sensitive, Weepy, Irritable PG – Stocky appearance Perspiration decreased, Thirst increased Cr- Chicken, Fried, meat, fatty food, Pickle, milk Addiction – Alcohol, Smoking Chilly patient CP – Tingling & numbness of extremities < Night

Syco Syco Lyco 200 5mths 6 1 Improved

24 Name: Mrs J Age :36 yrs Sex: F Occu: Housewife Relegion: Muslim Add : Arkula SCR No: 3647

Secondary hyperlipidemia Osteoarthritis Cervical spondylosis Varicose veins Hypertension Diabitis Mellitus

P/H – Malaria, TonsillitisNasal polyp, Cervical lymphadenopathy, Valvular stenosis Mother- DM Brother- DM, Cardiac disease

Chol- 240mg/ dl TG- 208mg/ dl LDL – 151mg/ dl HDL-48mg/ dl

Chol – 218mg/ dl TG – 160mg/ dl LDL – 138mg/ dl HDL– 48mg/ dl

MG- Anxious about health, Perfectionist, Weepy, Yielding, Fear of being alone, Irritable, Short tempered, Shouts back, Likes company & Consolation PG – Obese Profuse, offensive perspiration, Thirst decreased, Cr- Chicken, Meat, Spicy Sleep disturbed, Dreams frightful, snakes Hot patient CP – Knee joint pricking pain < Exertion, Sitting > Continued motion Back pain < lying on back

Syco Syco Lyco 200., 1M

5mths 10 4 Improved

130

Sl. no

Particulars Of The Patient

Clinical Diagnosis

Past And Family History

Investigations Totality

Miasms Remedy Duration of

treatment

Scoring Result

Before After FM DM B A

25 Name: Mrs A N

Age : 35 yrs Sex: F Occu: Housewife Relegion: Hindu Add : Ballalbagh SCR No: 17102

Familial combined hyperlipidemiaTension headache Haemorrhoids Enterobiasis

P/H – Malaria , Still birth delivery Mother – Hypertension Father- Hypertension, Epilepsy

Chol- 260mg/ dl TG – 198mg/ dl LDL – 177mg/ dl HDL – 44mg/ dl

Chol – 237mg/ dl TG – 179mg/ dl LDL – 155mg/ dl HDL– 49mg/ dl

MG – Courageous, Cannot tolerate insults, Irritale, Shouts back. Dipressed, Fear of snakes, Tensed on silly matters PG – Stocky appearance Perspiration increased on neck & back, Thirst increased, Cr- Leafy veg, Sweets Dreams of falling down, Escaping Chilly patient CP – Headache throbbing < Crowd, Noise, Tension > Warmth, Rest Hard stool Burning < Chicken

Syco - Syphil

Psora- Syco

Calc Carb 200

5mths 15 9 Improved

26 Name: Mrs C G Age : 55 yrs Sex: F Occu: Housewife Relegion: Christian Add : Ladyhill SCR No: 10548

Familial hypercholesterolemia Migraine, Allergic rhinitis

P/H – Chickenpox Mother- Hypertension, Hypercholesterolemia, MI Father- Expired of Carcinoma thyroid

Chol- 270mg/ dl TG – 147mg/ dl LDL – 203mg/ dl HDL – 38mg/ dl

Chol – 253mg/ dl TG – 140mg/ dl LDL – 183mg/ dl HDL– 42mg/ dl

MG – Suppressed emotion, Grief, Relegious, Anxious about health, Fastidious, Likes company & consolation PG – Lean, Perspiration increased in general, Thirst increased, Cr- Warm Sleep unrefreshing Hot patient CP – Sneezing < Morning, Nose & eye itching Watery coryza Head heaviness < Morning > Vomiting

Syco- Syphil

Psora Sulphur 200

3mths 14 13 Improved

131

Sl. no

Particulars Of The Patient

Clinical Diagnosis

Past And

Family History

Investigations Totality

Miasms Remedy Duration of

treatment

Scoring Result

Before After FM DM B A

27 Name: Mrs J D

Age : 70 yrs Sex: F Occu: Housewife Relegion: Christian Add : Konaje SCR No: 16373

Familial combined hyperlipidemia Osteoarthritis

P/H – Hypertension since 10 yrs Father – Carcinoma throat Sister IHD

Chol- 272mg/ dl TG- 186 mg/dl LDL – 191mg/ dl HDL- 44mg/ dl

Chol- 259mg/ dl TG – 170mg/ dl LDL – 174mg/ dl HDL– 51mg/ dl

MG – Mild, Weepy, Consolation >, Memory weak PG – Stocky appearance Appetite decreased, Thirst decreased Perspiration increased on head Cr- Salt. Hard stools, Burning micturition Hot patient CP- Knee joint pain < Morning, walking, > Rest Pressure incontinence of urine

Syco- Syphil

Syco Calcarea carb 200

4mths 15 13 Improved

28 Name: Sr S Age : 58 yrs Sex: F Occu: Teacher Relegion: Christian Add :Mangalore SCR No: 18316

Familial combined hyperlipidemia Flatulent dyspepsia Cervical spondylosis Uterine fibroid

P/H – Typhoid Pneumonia Mother – Fibroid uterus, Hypertension Father- hypertension

Chol- 299mg/ dl TG- 208mg/ dl LDL- 207mg/ dl HDl- 51mg/ dl

Chol- 260mg/ dl TG- 97mg/ dl LDL- 183mg/dl HDL- 58mg/ dl

MG – Forsaken feeling, Insecurity, Sympathetic, Irritable, hates contradiction, Does not like consolation, Suppressed emotion, Fear of disease PG – Stocky appearance Perspiration increased on upper part of body, yellow staining Thirst increased Cr- Veg Av- Salt, Milk Hard difficult stool once in 2 days Urine difficult to control. Sleep disturbed Hot patient CP – Fullness in abdomen < Pork, Dal, Fish Neck pain < movement, Sitting straight

Syco Syco Sepia 200 12mths 17 13 Improved

132

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Particulars Of The Patient

Clinical Diagnosis

Past And

Family History

Investigations Totality

Miasms Remedy Duration of

treatment

Scoring Result

Before After FM DM B A

29 Name: Mr A R

Age : 30 yrs Sex: M Occu: Contractor Relegion: Muslim Add : Kallappu SCR No: 12984

Hepatic Lipase deficiency Obesity

Mother – Filariasis, DM

Chol- 212mg/ dl TG- 200mg/ dl LDL- 140mg/ dl HDL- 32mg/ dl

Chol- 188mg/dl TG- 171mg/ dl LDL- 114mg/ dl HDL- 40mg/ dl

MG- Irritable, Quarrelsome, Obstinate, Anxious, Contradiction <, Ambitious, Domonating, Fear of height PG – Obese Appetite increased, Thirst increased, Av- Veg Cr- Non Veg, Spicy. Hard stool Hot patient

Psora- Syco

Psora Lyco 200 3mths 9 2 Improved

30 Name: Mr P M Age : 29 yrs Sex: M Occu: Merchant navy Relegion: Christian Add : Kulai SCR No: 17226

Polygenic hypercholesterolemia Obesity Tension headache

Father – Hypertension, DM

Chol- 205mg/ dl TG- 91mg/ dl LDL- 143mg/ dl HDL- 45mg/ dl

Chol-200mg/ dl TG- 90mg/ dl LDL- 141mg/ dl HDL- 41mg dl

MG – Stress, Irritable, gets angry fast, Shouts back, Optimistic, Confident PG – Obese Perspiration increased in general, Appetite increased Thirst increased for cold water Cr- Non Veg Av- Salt Addiction – occasionally alcohol & smoking Hot patient CP- Weight gain Head ache throbbing, Pressure with perspiration < Walking > Rest Eye redness < Exposure to heat

Syco Psora Calc carb 200

3mths 4 4 Not improved

133