Anda di halaman 1dari 158

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
DE PART ME NT OF O RGAN ON OF ME DICINE AND HOMOE OPAT HIC P HI LO SOP HY, FAT HE R M ULLE R HOMOE O PAT HIC ME DICA L COL LE GE , DE RA LAKAT T E , MANGAL ORE

2011
i

CERTIFICATE BY THE GUIDE


This is t o cert ify t hat t he d issert at io n ent it led MIASMATIC EVALUATION OF HYPERLIPIDEMIA is a bo nafid e research wo rk do ne by Dr SHEENA K .N und er my gu id ance and sup er visio n dur ing t he year 2008 201 1, in part ia l fu lfillment o f t he requ ir ement fo r t he award o f t he degree o f DO CTOR O F MEDICINE (ORGANON OF MEDICINE AND HOMOEOPATH IC PH ILOSOPH Y) . I have sat isfied myself reg ard ing t he aut hent icit y of her

o bser vat io ns no t ed in t his d issert at io n and it co nfo r ms t o t he st and ards o f Rajiv Gand hi Univer sit y o f Healt h Sciences, Kar nat aka, Bang alo re. It has no t been su bmit t ed (p art ial o r fu ll) fo r t he award o f any o t her Degr ee o r Dip lo ma.

Dr ROSHAN PINTO Date : Place: Mang alo re


MD (HOM)

Pr of ess or , D epar tment of Or ganon of M edicine a nd Homo eopathic Philos op hy, Father Muller H omo eopathic M edica l College a nd H osp ital ,

Deralak at t e, Mangalo r e

ii

DECLARATION BY THE CANDIDATE

her eby declare t hat

t his d issert at io n

ent it led

MIASMATIC

EVALUATION OF HYPERLIPIDEMIA is a bo nafide and g enu ine research wo rk carr ied o ut by me, u nd er t he gu idance o f Dr ROSHAN PINTO, Pro fesso r, Philo so p hy, Depart ment d ur ing t he o f Organo n year of med icine in and Ho mo eo pat hic fu lfillment of

20 0820 11,

p art ial

requ ir ement fo r t he award o f DOCTOR OF MEDICINE (ORGANON O F MEDICINE AND HOMOEOPATH IC PH ILOSO PHY) . I have no t previo u sly su b mit t ed t his wo rk (part ial o r fu ll) t o an y ot her u niver sit y fo r t he award o f any o t her Degree o r Dip lo ma.

Date: Place: Mang alo re Dr SHEENA K .N

iii

ENDORSEMENT BY THE HOD, PRINCIPAL/ HEAD OF THE INSTITUTION


This is t o cert ify t hat t he d issert at io n ent it led MIASMATIC EVALUATION OF HYPERLIPIDEMIA is a bo nafid e research wo rk carr ied o ut by Dr SHEENA K .N u nder t he gu idance and super vis io n o f Dr ROSHAN PINTO d ur ing t he year 20 08 2011, in part ial fu lfillment o f t he req u irement fo r t he award o f t he degree o f DO CTOR O F MEDICINE (ORGANON O F MEDICINE AND HOMOEO PATH IC PHILOSO PHY). We have sat isfied reg ard ing t he aut hen t ic it y o f her o bser vat io ns no t ed in t his d issert at io n and it co nfo r ms t he st and ards o f Rajiv Gand h i Universit y o f Healt h S ciences, Kar nat aka, Bangalo re. It has no t been su bmit t ed (part ial o r fu ll) fo r t he award o f a ny o t her Degree o r Dip lo ma.

HEAD O F THE DEPARTMENT Dr SHIVAPRASAD K . BSc, M D (H OM ) Professor, HOD, Dept . o f Organo n o f Med ic ine and Ho mo eo pat hic P hilo so ph y, Fr. Muller Homoeopathic Medical College, Deralakatte, Mangalore

PRINCIPAL Dr SRINATH RAO


MD (HOM)

Professor, HOD, Dept.of Materia Medica, Fr. Mu ller Ho mo eo pat hic, Medical College, Deralakatte, Mangalore

Dat e:
iv

Dat e:

P lace: Manga lo re

P lace: Manga lo re

COPYRIGHT

Declaration by the Candidate

I hereb y declare t hat t he Rajiv Gand hi University of H ea lth Sciences, K arnata ka, Bangalo re shall have t he r ig ht s t o preserve, u se and d isseminat e t his d issert at io n / t hesis in pr int o r elect ro nic fo r mat fo r acad emic / research purpo se.

Date: Place: Mang alo re Dr SHEENA K .N

Rajiv Gandhi University o f Hea lth Sciences, K arnata ka

Acknowledgement

I consid er this as my privileg e to thank the Almight y God, who is responsible for ever ything in my life, an d give him all the glory for th e accom plishment of m y post graduat e studies. I thank him for h elping me t o achieve this task thro ugh the follo wing perso ns who have b een of imm ense hel p and source of enco uragem ent in my end eavor . I would like to expr ess m y sin cer e and h ear tfelt thanks to my resp ect ed teach er and guide Dr Rosha n Pinto, Prof essor, Department of Organon of Medicin e and Homo eopathic Philosoph y f or providing me exp ert guidan ce, constructive advi ce, freedom of thought, per sonal attention, timely support and encourag em ent throughout m y post graduat e course and during the diss ertation work. It is my good fortune to do this wor k under his guidance. It is m y pri vileg e to express sincere gra titude to R ev. Fr P atrick Rodrigues, Director, FMCI and Rev. Fr Wilfred Prakash Dsouza, Administrator of Fr. Muller Homo eopathic Medi cal coll ege, Man galore fo r providing m e an opportunity and ad equat e f acilities to carry out this wor k to my satisfaction in this reputed institution. I would like to expr ess my gratitude to Dr Shashi Kant Tiwari former principal, who is and was a real source of inspiration and also Dr Srinath Rao, Prin cipal, Father Muller Homo eopathic Med ical College for his support whil e persuing my studies. I express m y sincere than ks to Dr Shivapr asad K , Vice prin cipal and Head of the Departm ent of Organon of Medi cine and Homo eopathic Philosophy, for his constant support, care and encouragement. I also express my gratitud e to Dr M. K. Kamath, PG Co-ordinator an d Head of th e D epartm ent of M edicin e, wh o wa s the man behind most acti vities of the postgraduates, guiding us to perfection.

vi

I o we m y sin cer e gratitude for all the help, and coop eration that I have received from my coll eagues of various d epartments of FMH MC of whick I cannot withhold th e nam es of few li ke D r Jacint ha Mont eiro, Dr Deena Monteiro, Dr Deepa Rebello, Dr Prabhukira n and Dr Josep h Tho mas. I must than k all my batchmates es pecially Dr Shalini and Dr Rekha for their companions hip, co operation and tim ely help which considerabl y eas ed my task. I attribute part of my success and st rength to them. A wor d of gratitud e to Mr Suresh and D r Shripathi Kalluraya for t eachin g statistical application and r esear ch h elp ing to formulat e th e R esear ch Methodologi es for my synopsis and carry ou t the statistical wor k of my thesis. I thank all the m emb ers of no n-t eaching staff of Fr. Mull er

Homoeopathi c M edical Colleg e, esp ecially library staff for th eir promp t service and th e staff o f out patient depart ment and clini cal laboratory who ha s provided m e with the cas e material requir ed for the study. I would hav e n ever a ccom plished my go al without th e encourag em ent an d prayers of my par ents Mr K. Naraya na n & Mrs Rajalakshmi Naraya na n and my brother Mr Sreejith who is a world of en couragement and un derstanding to me. Special reg ards I carr y in my heart for my husb and Mr Salin Kumar and my b eloved son Vaishak Salin for their love and co -operation in every aspect of my life. Last but not the least, my sin cer e tha nks to all th e Patients o n whom th e study was conduct ed and MicroBits, Kan kanady for takin g pains for the successful and timely compl etion of this wor k. I thank all th e p ersons who have directly or indirectly influ enced m e fo r the better outco me of this work.

Place: Mangalore Date: Dr SHEENA K.N

vii

Affectionately Dedicated To My Family

viii

LIST OF ABBREVIATIONS

< > ACTH AMP APD Apo ASCVD ATP Av CAD CETP Chol Co A CP Cr CVA DALY DM DM

: : : : : : : : : : : : : : : : : : : : :

Aggravation Amelioration Alpha Adrenocorticotrophic hormone Adenosine mono phosphate Acid peptic disease Apoprotein Artherosclerotic cardio vascular disease Adenosine Tri phosphate Aversion Beta Coronary artery disease Cholesteryl ester transfer protein Total cholesterol Co enzyme A Characteristic particulars Craving Cerebrovascular accident Disability adjusted life year Diabetes Mellitus Dominant miasm
ix

FA F/H FM HDL HMG HS IDL LCAT LDL LPL MG NAD NADPH PG P/H Pkt PVD S SCR TG TAG VLDL WHO

: : : : : : : : : : : : : : : : : : : : : : :

Fatty acid Family history Fundamental miasm High density lipoproteins Hydroxy methyl glutaryl At bed time Intermediate density lipoprotein Lecithin cholesteryl acyl transferase Low density lipoprotein Lipoprotein lipase Mental generals No abnormality detected Nicotinamide adenine dinucleotide phosphate Physical generals Past history Packet Peripheral vascular disease Same Standardized case record Triglyceride Triacyl glycerol Very Low density lipoprotein World Health Organization
x

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
xi

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.

xii

TABLE OF CONTENTS

S. No. 1 2 3 4 5 6 7 8 9 10 INTRODUCTION

TOPIC

PAGE No. 1 4 5 77 81 95 100 102 103

AIMS AND OBJECTIVES REVIEW OF LITERATURE METHODOLOGY RESULTS DISCUSSION CONCLUSION SUMMARY BIBLIOGRAPHY ANNEXURES ANNEXURE 1 ANNEXURE 2 ANNEXURE 3

107 108 118

xiii

LIST OF TABLES

Table No. 1 2 3 4 5 6 7 8 9 10 11 12

TITLES Fredrickson classification of hyperlipidemia Miasmatic evaluation criteria Distribution of cases according to age group Distribution of cases according to sex Distribution of cases according to religion Case distribution according to physical activity Case distribution according to fundamental miasm Case distribution according to dominant miasm Case distribution according to type of hyperlipidemia Case distribution according to constitutional remedies Case distribution according to the improvement Statistical analysis

PAGE NO. 30 67 81 81 83 83 85 85 87 88 90 91

xiv

LIST OF FIGURES

Figure No. 1 Lipid Digestion 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 Lipid degradation Fat absorption Fat metabolism

TITLE

PAGE No. 7 7 9 12 14 17 22 25 50 52 82 82 84 84 86 86 89 89 90 94

Source and fate of Triglycerols Source and fate of cholesterol Composition of Lipoprotein Transport of Lipids Diet pyramid Natural sources reducing hyperlipidaemia Case distribution according to age group Case distribution according to sex Case distribution according to religion Case distribution according to physical activity Case distribution according to fundamental miasm Case distribution according to dominant miasm Case distribution according to type of hyperlipidemia Case distribution according to constitutional remedies Case distribution according to the effectiveness of treatment Distribution of all cases according to pre and post treatment analysis

xv

Introduction
i

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 todays 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 individuals 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.

Any tendency to disease or destruction which can be recognized in man derives from a varies in structural anomaly which imprints its characteristics on him. The expression 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.
2

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

Objectives
1

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

Review of Literature
4

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
5

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
6

Fig. 1: Lipid Digestion

Fig.2: Lipid degradation 5


7

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

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


9

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 - 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
10

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, -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 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 acetylCoA molecules formed by -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 -hydroxybutyric acid, and minute quantities are converted into acetone The acetoacetic acid, -hydroxybutyric
11

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, 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


12

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 -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.

13

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


14

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.

15

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
16

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


17

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.

18

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.

19

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
20

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
21

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

22

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 esterrich 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.

23

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

24

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


25

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 receptormediated 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.

26

HYPERLIPIDEMIA
Cardiovascular disease are responsible for 25% & Cerebrovascular disease for 19% of DALYs 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
27

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
28

Diabetes mellitus Cushings 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

29

Table 1:Fredrickson classification of hyperlipidaemia 13 Type Type I Synonym Buerger Gruetz syndrome. Primary hyperlipoproteinemia or Familial chylomicronemia Biochemical alterations Decreased lipoprotein lipase or altered Apo C II Serum alterations Elevated chylomicron

Type IIa

Polygenic hypercholesterolemia or Familial hypercholesterolemia Combined hyperlipidemia

LDL receptor deficiency

Elevated LDL only

Type IIb

Decreased LDL receptor and increased Apo B Defect in Apo E synthesis Increased VLDL production and decreased elimination Increased VLDL production and decreased LDL

Elevated LDL, VLDL and Triglycerides Increased IDL Increased VLDL

Type III Type IV

Familial dysbetalipoproteinemia Endogenous hyperlipemia

Type V

Familial hypertriglyceridemia

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)

30

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
31

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 highcaloric, 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 band. Ratio of VLDL to total plasma TG > 0.30 is consistent
32

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
33

inheritance and has a high penetrance 90% of parent and 50% of the patients 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 receptorbinding 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 receptormediated 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

34

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
35

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.
36

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 firstdegree 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

37

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.
38

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 apoBcontaining 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

39

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

40

low in obesity. Weight loss is often associated with a reduction of plasma apoBcontaining 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
41

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
42

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 Gierkes 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 oestrogencontaining 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
43

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
44

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 makeup 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

45

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 HDL cholesterol Triglycerides LDL cholesterol TC/HDL Ratio LDL/HDL Ratio : : : : : : <200mg/dL >40mg/dL <150mg/dL <130mg/dL <3.0 indicates low risk,3.0-5.0 indicates high risk. 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
46

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
47

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
48

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 bodyweight 13 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.

49

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
50

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

51

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


52

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 eradication23 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
53

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
54

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. Hahnemanns 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
55

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
56

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 30 The word Miasmoriginated 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 patients life & can be
57

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
58

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. Hahnemanns 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

59

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
60

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 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 miasm responsible for

61

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 parents 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
62

more profoundly. Using Hahnemanns powerful theory we can treat a miasmatic state before pathology emerges & we can prevent the transmission of parents 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
63

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 Psora Sycosis - Tubercular - Syphilis.29 Prodrome -

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

64

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

65

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

66

Table 2: Miasmatic evaluation criteria 24,26, 29,31,38,39 Psora / Sensitising Sycotic / Constructive / Inco ordination Anxiety. Fear. Restless. Suspicious. Jealousy. Mental Nervous. Irritable. Tendency to harm / exploit Generals Timid. Perversion. others. Hyperworkoholics. Tendency to commit evil. Hypergreedy. Cross. No deep mental Irritable. No spiritual concentration / sacred outlook, not influenced by thoughts. Hyporeasoning. moral doctrine or religion. Impractical thoughts. Insanity. Inclined to commit Hypoconfidence. crime. Mischevous, Bent Philosopher. Builds castles upon misdeeds. Born in air. Indolent. criminal. Revengeful, devoid Aversion to work ,bath, of all sense of rhiteousness. keep things clean. Untidy. Thinks of their own ailment. Lack of discipline. Time Suppress ailments / passs too fast/ too slow symptoms. Brooding over Repugnance to & fatigue on things. Self condemnation. mental & physical exertion. Fixed ideas. Lack of self Wants to lie down. confidence. Suicidal Sensitive to odour. tendency with proper cause. Alert. Quick. Active. Slow. Sluggish. Intelligence Unable to control or Incoordination of thoughts disappearance of thoughts. and perception.

Tubercular / Reactive 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.

Syphilitic / destructive 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.

Very bright, intelligent & sharp, or slow & dull totally. Lack of concentration

Slow to react. Careless mistakes. Arithmetical calculation difficult.

67

Memory

Weakness of memory. But studious.

Absentmindedness. Slow thought and speech. General loss of memory. Cannot find words. Cruel- Mental torture. Quarellsome. Mean minded & concealing. Fear of making mistakes

Inability or slow in comprehension. Highly keen.

Impaired memory. Total forgetfulness.

Behaviour

Decietful behavior.

Some cruelty due to dissatisfaction. Fearless. Fear of dogs, dark

Violent, cold blooded murderers. Fear of people. Panicky terror Introvert. Escapes from self & others. Aversion to company. Constantly dwell on suicide. Merciless with no sympathy. Irresponsible, lacks sense of duty. Perverted sexual cravings. Insensitive mentally and physically.

Fear

Fear of strangers, death, disease, future. Aversion to people & company. Dreads to be alone Internally extremely selfish. Hide & seek nature. Tendency to dishonesty, wickedness. Oversensitive mentally & physically.

Social relation

Extroverts

Morose. Sullen. Does not like advices. Likes company Unrestrained & uncontrollable passions of life. Easily forms intense emotional bonds. Intense sexual desire. Hypersensitive.

Attitude

Selfish & possessive with a tendency to conceal.

Sensitivity

Like barometer to storm or rain.

68

Metabolism

Pathology

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 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

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

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. Produces destructive Early suppuration and delayed disorders everywhere. healing. Scars breakdown. Ulceration from early phase of disease. Degeneration. Deviation anything perverted.

69

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 Hyperactive. Dramatic development of symptoms

Excess manifested by hypertrophy, hyperplasia, neoplasia, hypersecretion, hypersensitivity, hyperthermia, hyperactivity Hydrogenoid. Greenish or
greenish yellow, jelly like, catarrhal purulent discharges

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

Disorganised digestion deformities, fragility.


Putrid, offensive, pus like discharges. Little

subjective symptoms. Less desire, craving, aversion & feelings.

with fishbrine odour. Hypertension, Restless. Deposition. Reflects more objective symptoms with less subjective symptom

cold very easily Reflects many subjective symptom. Mental, emotional, pathological & destructive

Pace of action

Extremely Slow & insidious onset & recovery

Depend on preponderance of psora / syphilitic miasms. Moderate or Rapid

Rapid or Insidious

70

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. Metabolic disorders Hyperlipidemia, hyperurecemia, chronic pelvic inflammatory disease. After effects of immunization , injection, blood transfusion, excessive food intake. Suppression of pathological elimination & proliferation

< 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.

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

71

Constitutional Appearance Face

Lean thin, Active

Obese.Flabby, sluggish. Stout, Overnourished. Dropsical. Oily skin

Lean thin. Narrow chest

Thin, wrinkled, looks old for his age. Greasy. High cheek bones & rough skin. Dry & wrinkled like old person.Thick lips Sensitive to changes either heat or cold Offensive < all complaints

Inverted pyramid Yellow sallow, pale, earthy complexion. Eyes sunken

Pale ,round, fair smooth, clear skin & waxy smooth complexion. Sunken eyes, flushed cheeks. Thin lips. Extremely chilly Profuse

Thermal Perspiration

Generally chilly Profuse, offensive, during sleep Insatiable hunger Sweet, Sour, Spicy, Salty. Oily, Fried, Indigestible Unnatural substances like chalk, clay, Hot food. Milk, cold food

Hot On forehead during sleep. Copious. Discomfort after eating

Appetite Craving

Increased

Decreased Stimulants like alcohol, tea, coffee, very spicy. Indigestible.Cold food

Alcohol, Beer, Pungent, Well Indigestible things, Potatoes, seasoned, Salty food. Tea, Tobacco, Meat, Salt, Greasy, fatty food. Things which make them sick. Very hot / really cold Meat, milk, wine, spices Meat

Aversion

Meat, animal food, less spicy food Dysentry

Bowels

Constipation

Diarrhoea

Alternating diarrhea and constipation

72

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. Mutation in gene Secondary to nephritic syndrome

Etiology

Unknown cause Increased intake of fat, Secondary to alcoholism, drugs, hepatic infections

Pathology

Defective metabolism of fat Deficiency in apoprotein or enzymes.

Mutation in gene. Hepatic cholestasis. Enzyme disorders Secondary to auto immune disease like SLE, endocrine disorders like DM, hypothyroidism, Cushings syndrome. Defect in receptors, enzyme activity. Deposition of cholesterol & lipoprotein in the wall of blood vessels

Mutation in gene

Defect in receptors, enzymes

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
73

Recurrent pancreatitis. Intermittent peripheral neuropathy

Lack of apoprotein, receptors, enzyme activity Atheromatous plaque resulting in complication of haemorrhage, thromboembolic phenomena Accelerated atherosclerosis Premature CAD, Stroke, PVD Haemolysis

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. nitac. phos. Plb. Plb-i. Polyg-a. rad-br. rauw. Sec. sil. solid. spartin-s. Stront-c. Stront-i. strophh. 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. MURPHYS 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. argn. Arn. ars. Ars-i. Aur. aur-br. Aur-i. aur-m-n. Bar-c. bar-i. bar-m. bell-p. benz-ac. cact. cal-

74

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. BOERICKES 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. Kalii. 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.

75

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
76

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.

77

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.

78

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.

79

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
80

RESULTS
Table 3: Distribution of cases according to age group Age group 25-35 35-45 45-55 55-65 65-75 No. of cases 7 10 4 7 2 Percentage 23.33 33.3 13.3 23.3 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 Male Female Total

No. of case 12 18 30

Percentage 40 60 100

Out of 30 patients studied, 12 cases (40%) were males and 18 cases (60%) were females.

81

Case distribution according to age group


35 30 25 20 15 10 5 0 25-35 35-45 45-55 55-65 65-75 7 4 13.3 10 7 2 6.6 23.33 23.3 No. of cases Percentage 33.3

Age group
Fig.11: Case distribution according to age group

Distribution of cases according to sex


Males 12 40% Females 18 60%

Fig.12: Case distribution according to sex

82

Table 5: Case distribution according to religion Religion Hindu Christian Muslim Total No of cases 8 14 8 30 Percentage 26.6 46.6 26.6 100

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 each26.66%).

Table 6: Case distribution according to physical activity Physical activity Sedentary Moderate Severe Total No of cases 16 14 0 30 Percentage 53.33 46.6 0 100

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.

83

Case distributions according to religion

Muslim

26.6 8 46.6 14 26.6 8 Percentage No of cases

Christian

Hindu

20

40

60

Fig.13: Case distribution according to religion

Case distribution according to physical acitivity


53.33 60 40 20 0 Sedentary Moderate 16 14 0 46.6 No of cases Percentage 0 Percentage No of cases Severe

Fig.14: Case distribution according to physical activity

84

Table 7: Case distribution according to fundamental miasm Miasm Fundamental miasm No. of cases Psora Sycosis Syphilitic Tubercular Sycosyphilitic Psora syco Total 0 16 1 1 11 1 30 Percentage 0 53.3 3.3 3.3 36.6 3.3 100

Table 8: Case distribution according to dominant miasm Dominant miasm Miasm Psora Sycosis Syphilitic Tubercular Psorasyco Total No. of cases 8 16 0 1 5 30 Percentage 26.6 53.3 0 3.3 16.6 100

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
85

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

Case distribution according to fundamental miasm


100 53.3 50 16 0 1 3.3 0 3.3 36.6 30 3.3 No of cases 0 30 Percentage o No of cases 0 100 100

Fig.15: Case distribution according to fundamental miasm

Case distribution according to dominant miasm


1 3% 5 17% 8 27%

Psora Sycosis Syphilitic Tubercular Psorasyco

16 53%

Fig.16: Case distribution according to dominant miasm


86

Table 9: Case distribution according to the type of hyperlipidemia Type of Hyperlipidemia Familial hyper cholesterolemia Polygenic hypercholesterolemia Familial combined hyperlipidemia CETP deficiency Familial chylomicronemia Hepatic lipasedeficiency Secondary hyperlipidemia Total No of cases

Percentage 13.3 20 33.3 3.3 3.3 6.6 16.6 100

4 7 10 1 1 2 5 30

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%) .

87

Table 10: Case distribution according to constitutional remedies

Name of the remedy Calcarea carb Lycopodium Medorrhinum Natrum mur Nux Vomica Phosphorus Pulsatilla Sepia Sulphur Total

No of cases 4 10 1 2 1 4 4 2 2 30

Percentage 13.3 33.3 3.3 6.6 3.3 13.3 13.3 6.6 6.6 100

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.

88

Fig.17: Case distribution according to the type of hyperlipidemia

Case distribution according to constitutional remedies


35 30 25 No of cases 20 15 10 5 0 0 2 4 1 4 13.3 10 3.3 2 6.6 3.3 4 1 6 8 4 2 2 10 13.3 13.3 6.6 6.6 Percentage 33.3

Fig.18: Case distribution according to constitutional remedies


89

Table 11: Case distribution according to the effectiveness of treatment Effectiveness Improved Not improved Total No of cases 26 4 30 Percentage 86.6 13.3 100

86.6 90 80 70 60 50 40 30 20 10 0 Improved Not improved 4 No of cases 26 13.3 percentage No of cases percentage

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.

90

THE EXPLANATION OF THE STATISTICAL TOOLS AND TECHNIQUES Table 12: Statistical analysis table

Sl.No 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

X 15 11 6 11 12 17 16 22 15 15 14 23 9 7 18 7 19 14 13 19 29 20 6 10 15 14 15 17 9 4 Mean X =422

Y 5 7 1 4 15 4 11 31 13 10 6 17 5 7 14 2 12 4 0 16 16 15 1 4 9 13 13 13 2 4 Mean Y = 274

(X - Y)=Z 10 4 5 7 -3 13 5 -9 2 5 8 6 4 0 4 5 7 10 13 3 13 5 5 6 6 1 2 4 7 0 Mean Z =148

_ Z 5.07 -0.93 0.07 2.07 -7.93 8.07 0.07 -13.93 -2.93 0.07 3.07 1.07 -0.93 -4.93 -0.93 0.07 2.07 5.07 8.07 -1.93 8.07 0.07 0.07 1.07 1.07 -3.93 -2.93 -0.93 2.07 -4.93

_ (Z Z)2 25.70 0.86 0.00 4.28 62.88 65.12 0.00 194.04 8.58 0.00 9.42 1.14 0.86 24.30 0.86 0.00 2.28 25.70 65.12 3.72 65.12 0.00 0.00 1.14 1.14 15.44 8.58 0.86 4.28 24.30 Mean _ (Z Z)2 = 617.87

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
91

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

92

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.

93

35

30

25

20 Scoring before 15 Scoring after

10

0 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

Fig.20: Distribution of all cases according to pre and post treatment analysis using scoring char
94

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 andt 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%).

95

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.
96

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. Fishers 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.

97

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 couldnt 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.
98

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.

99

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.

100

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
101

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

102

Bibliography
103

BIBLIOGRAPHY
1. Sathyanarayana U, Chakrapani U. Biochemistry. 3rded. Kolkata: Books & Allied (P) Ltd; 2006. p. 28, 29, 285 7 2. Arthur C Guyton, Jhon E Hall. Text book of medical physiology. 11thed. Pennsylvania: Elsevier Saunders; 2006. p. 811, 812, 840 850 3. Tortora G. J, Derrickson B. Principles of anatomy and physiology.12thed. USA: John Wiley & Sons, Inc; 2009. p. 954, 990-3 4. Chatterjea M N, Rana Shinde. Text book of medical biochemistry.7thed. New Delhi: Jaypee brothers, Medical publishers (P) Ltd; 2007. p. 416-426 5. Agamemnon Despopou, Stefen Silbernagl. Colour atlas of physiology. 5thed. New York: Thieme; 2003. p. 252 - 7 6. Vasudevan D M, Sreekumari. Text book of biochemistry. 5thed. New Delhi: Jaypee brothers, Medical publishers (P) Ltd; 2007. p. 129 162 7. Robert K Murray, Darryl K Granner, Peter A Mayes, Victor W Rodwell. Harpers illustrated biochemistry. 26thed. USA: Mc Graw Hill; 2003. p. 205 228 8. Devlen Thomas M. Text book of biochemistry with clinical correlation. 6thed. USA: A John wiley and sons inc.publication; 2006. p.662, 666, 676-691,707-717 9. Kasper D L, Braunwald E, Fauci A S, Hauser, Longo, Jameson. Harrisons principles of internal medicine.17thed. USA: Mc Graw Hill; 2008. p. 2416-2427 10. J Koolman K H, Roehm. Colour atlas of biochemistry. 2nded. New York: Thieme; 2005. p. 162 172
103

11.

Kumar P & Clark M. Clinical medicine. 6thed. USA: Elsevier Saunders publication; 2005. p. 1137 1143

12.

Park K. Parks text book of preventive and social medicine. 19thed. Jabalpur: Banarsidas Bhanot publishers; 2008. p. 302-7, 314

13.

Shah N S, Paulanand M, Acharya N, Vidya N, Bichile SR, Karnad R Dilip. API text book of medicine. 7th ed. Mumbai: The Association of physicians of India; 2006. p. 250 7

14.

Fischbach Frances, Marshall Barnett, Dunning. A manual of laboratory and diagnostic test. 7thed. USA: Lippincott Williams and Wilkins; 2004. p. 421

15.

Mcphee J. Stephen, Papadakis A. Maxine,Tierney M. Lawrence. 2008 Current medical diagnosis and treatment. 47thed. USA: Mc Graw Hill; 2008. p. 1074 76

16. 17. 18. 19. 20. 21. 22.

http://www.pubmed.org hyperlipidemia. Accessed on 6th September 2008 http://www.wikepedia.com hyperlipidemia. Accessed on 6th September 2008 http// emedicine.medscape.com/article/overview HDL. 4th October 2010 http://www.ehow.com/about foods-control-cholesterol.html.10th October 2010 http://www.American Heart.org. Accessed on 8th September 2008 http://www.womensheart.org/Nutrition/mediterranean.asp&usg.10th October 2010 Das Devlina, Vimala R and Das Nilanjana. Functional foods of natural origin - An overview. Indian journal of natural products and resources. June 2010, Vol 1; p. 137 - 9

23.

Hahnemann Samuel. Organon of medicine. 6th ed. New Delhi: B Jain publishers Pvt Ltd; Reprint1998. p. 94, 166-172.

104

24.

Hahnemann Samuel. The chronic diseases. VlI reprint ed. New Delhi: B Jain Publishers (P) Ltd; 1995. p. 6,45-7,83,107

25.

Allen J H. The Chronic miasms psora and pseudopsora. Reprint ed. New Delhi: B Jain Publishers (P) Ltd; 1998. p. 9-50, 59, 67, 84, 89, 90, 100-109

26.

Sarkar B.K. Organon of medicine (5th & 6th ed). 8th ed. Calcutta: M. Bhattacharyya and co (P) Ltd; 1984. p. 162 8, 346 - 371.

27. 28.

http://www.similimum.com/organon of medicine. Accessed on 15th October 2010 Dudgeon R E. Lectures on the theory and practice of homoeopathy. Reprint ed. New Delhi: B Jain publishers (P) Ltd; 2001. p. 242-301

29.

Dhawale M L. Hahnemanian totality symposium Part II Area c. 2nded. Mumbai: Institute of clinical research; 2000. p. c-1- c-96

30.

Dhawale M L. Principles and practice of homoeopathy. 3rded. Bombay: Institute of clinical research; 2000. p. 28,306-312

31.

Mandal Biman. Miasmatic Diagnosis in homoeopathy. 1sted. Kolkata: New central Book Agency (P) Ltd; 2003. p. 18-20,22-4,39-44,56-61,79-88

32.

Schepper Luc De. Hahnemannian Text book of classical homoeopathy for the proffessional. 1st Revised ed. New Delhi: B Jain Publishers (P) Ltd; p. 355 - 397

33.

Patel P. Ramanlal. Chronic miasm in homoeopathy and their cure with classification of their rubric/symptoms in Dr .Kents repertory. 1st ed. Kottayam: Hahnemann book house; 1996. p. 6, 7, 75.

34.

Ortega PS. Notes on the miasms or hahnemanns chronic diseases. 1st English ed. New Delhi: National homoeopathic pharmacy; 1980. p. 53-5, 63, 69-72,75-8.

105

35.

Kent James Taylor. Lectures on homoeopathic philosophy. Reprint ed. New Delhi: B Jain Publishers Pvt. Ltd; 2002. p. 114-139

36.

Close Stuart. The genius of homoeopathy lectures and essays on homoeopathy. Reprint ed. New Delhi: B. Jain Publishers PVT Ltd; 2004. p. 87-111

37.

Roberts H.A. The principles and art of cure by homoeopathy. reprint ed. New Delhi: B Jain publishers; 1996. p.180-241

38.

Banerjee S K. Miasmatic diagnosis practical tips with clinical comparisons. reprint ed. New Delhi: B. Jain publishers (P) Ltd; 1998. p. 1-19, 59-61, 98, 99.

39.

Speight Phyllis. A comparison of the chronic miasms. reprint ed. New Delhi: B Jain Publishers (P) Ltd; 1994. p. 2-9,40-1

40.

Schroyens Fredricks. Synthesis repertorium homeopathicum syntheticum. 9.1 ed. New Delhi: B Jain publishers (P) Ltd; 2007. p. 172,1924,1971,1896

41.

Murphy Robin. Homoeopathic medical repertory. 1sted. New Delhi: Indian books & Periodical Syndicate; 1994. p.160

42.

William Boericke. Pocket manual of homoeopathic materia medica and repertory. 9thed. New Delhi: B. Jain publishers (p) Ltd; 2002. p. 29, 76, 84, 96, 106, 176, 199, 149, 238, 305, 310,524,528,613,614,629,666,853

43.

Clarke J H. A dictionary of practical materia medica, vol-1. Reprint ed. New Delhi: B Jain publishers; 1996. p. 507,605,

44.

Vithoulkas George. Homoeopathy medicine for the new millennium. 26thed. New york: Arco publishing; 2000. p. 32,36

45.

Choudhury H. Indications of miasm. 2nd ed. New Delhi: B Jain publishers; 2005. p. 9-13, 29-39, 31-4, 36-42, 50-2,
106

54-6,

62,

71-3,

77-88,

98,

99

Annexures
103

ANNEXURE 1 SCORING CHART

Sl. No 1 2 3 4 5 6 7 8 9 10 11

Cholesterol, mg/dl <200 200 - 225 225 - 250 250 - 275 275 - 300 300 - 325 325 - 350 350 - 375 375 - 400 400 425 >425

Score

Triglycerides, mg/dl <150 150 - 175 175 - 200 200 - 225 225 - 250 250 - 275 275 - 300 300 - 325 325 - 350 350 - 375 >375

Score

LDL, mg/dl <130 130 - 135 135 - 140 140 - 145 145 - 150 150 - 155 155 - 160 160 - 165 165 - 170 170 - 175 >175

Score

HDL, mg/dl >40 40 - 38 38 - 36 36 - 34 34 - 32 32 - 30 30 - 28 28 - 26 26 - 24 24 - 22 <22

Score

0 1 2 3 4 5 6 7 8 9 10

0 1 2 3 4 5 6 7 8 9 10

0 1 2 3 4 5 6 7 8 9 10

0 1 2 3 4 5 6 7 8 9 10

107

ANNEXURE 2 DETAILED CASE STUDY


PRELIMINARY DATA Name Age Sex Occupation Education Religion Address : : : : : : : Mr S B 41 yrs Male Govt Employee Graduate Hindu Neeleshwaram SCR No. Date Physician : : : 57123 26-06-10 Dr. MK

CHIEF COMPLAINT No 1. LOCATION Rectum Since 5 6 yrs SENSATION Hard stool Difficult to pass Burning2 Bleeding Hair fall, Dandruff Powdery scales Slight itching MODALITY < spicy food, fried food, Non Veg CONCOMITANT

2.

Head Scalp Since 5 6 yrs

< after stool < 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.

108

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 Mother Brother - Expired following some liver disease - Hypercholesterolemia, Haemorrhoids Haemorrhoids

TREATMENT HISTORY Allopathic treatment for Haemorrhoids. PATIENT AS A PERSON Appearance Appetite Craving Aversion Perspiration Bowel Bladder Thermal Sleep : : : : : : Stocky Good Meat, sweets Nil Normal Hard

: 5 - 6/day : : Chilly (C4H) Good Company desire Doesnt like contradiction


109

Mental generals :

Doesnt like to share Superficial relation

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 Temperature 74/min, regular, good volume and vessel wall not palpable. Afebrile at the time of examination 18/min 120/80 mm of Hg. ( Right arm supine position)

Respiratory rate Blood pressure 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

110

INVESTIGATIONS DONE Serum cholesterol - 282 mg/dl TG 166 mg/ dl LDL 156 mg/dl HDL 32 mg/dl PROVISIONAL DIAGNOSIS External Haemorrhoids Hard stool difficult to pass Burning Bleeding after stool < spicy food Alopecia areata Hair loss Familial hypercholesterolemia Raised serum cholesterol, TG and LDL. Low HDL

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 doesnt get angry fast and deslikes contradiction. He has fear of dark from childhood. His memory is weak but active thinking and clear perception.

111

FIRST PRESCRIPTION: 1. Phosphorous 200 1 Pkt x HS 2. No 40 pills 404 x 2 weeks Follow Up Criteria 1) Hyperlipidemia 2) Hard stool 3) Burning 4) Bleeding 5) Hairfall 6) Dandruff MIASMATIC EXPRESSION Sector F/H Psora Sycosis M Haemorrhoids, hypercholesterolemia B - Haemorrhoids P/H Mentals -----Weak Memory Fear of dark Likes company Superficial relations. Does not share with others Appearance- Stocky Cr-Meat Thermally chilly Hairfall, Burning pain,Bleeding
112

Tubercular

Syphilis F Premature death due to liver disease -----

Physicals Characteristic particulars

Bowels -hard Cr- Sweet

ESSENTIAL EVOLUTIONARY TOTALITY Pt Good Pt Good Pt Good di sp os iti on Likes company Superficial relation Doesnt like to share Deslikes contradiction Fear of dark Memory weak Craving Meat, Sweets Thermally Chilly Bowels Hard
Sycosis

family pr ed FM Sycotic - Syphilitic is po DM Tubercular sit io n

Pt Good

family

society

Pt Good Pt Good

society
Syphilis

work

work

Mingles with every one Maintains good relation


Tubercular

Hyperlipidaemia Hard stool

D i a t h

Burning Bleeding < after stool < spicy food Hair fall

Psora

D i s e a s e s

Familial hypercholesterolemia External Haemorrhoids Alopecia areata

113

CONSTITUTIONAL TOTALITY MENTAL GENERALS Mingles easily with people Likes Company Superficial relations Doesnt 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

114

General management Patient was advised systematically regarding dietary management and also general guide lines regarding exercise. FOLLOW UPS DATE 10. 07 .10 1 2 3 > SYMPTOM CHANGES 4 > 5 6 < 7 8 9 10 RX 1. SL pkt (1P) HS 2. No 40 pills 404 x 2 wks 1 2 3 > 4 > 5 6 < 7 8 9 10 RX 1. Phos 200 (1P) H S2. No 2 . No 40 pills 404 x 2 wks . RX 1. SL pkt (1P) HS 2 . No 40 pills 404 x 2 wks 1 2 3 > 4 > 5 6 < 7 8 9 10 RX 1. SL pkt (1P) HS 2. No 40 pills 404 x 2 wks PRESCRIPTION

> 24.07.10

Serum cholesterol 226 mg/dl TG 138mg/dl LDL 123 mg/dl HDL 35 mg/dl 1 2 3 > 4 > 5 6 7 8 9 10

> > 7. 08. 10

Generally feels better

> >

Generals good 21. 08. 10

115

1 4.09-10 >

2 >

3 >

4 >

5 -

6 -

10

RX 1. SL pkt (1P) HS 2. No 40 pills 404 x 2 wks

1 > 18.09.10

2 >

3 >

4 >

5 -

6 -

10

RX 1. SL pkt (1P) HS 2. No 40 pills 404 x 4 wks

Generals good

SCORING

Sl No

Serum lipid levels

Scoring before treatment 4 1 6 4 15

Scoring after treatment 2 0 0 3 5

1. 2. 3. 4.

Cholesterol Triglycerides LDL HDL Total

116

INVESTIGATIONS REPORTS BEFORE AND AFTER TREATMENT

117

ANNEXURE 3 MASTER CHART

Sl. no

Particulars Of the Patient

Clinical Diagnosis

Past And Family History

Investigations

Totality

Miasms

Remedy

Duration of treatment

Result Scoring B A
5 Improved

Before
1 Name: Mr S B Age : 41 yrs Sex : M Occu : Govt employee Relegion :Hindu Add : Neeleshwar SCR No : 57123 Familial hypercholest erolemia External Haemorrhoid s Alopecia areata Mother Hypercholes terolemia, Haemorrhoi ds Father Expired due to liver disease Brother Haemorrhoi ds Mother Epilepsy Father Bronchial asthma, DM, Died following Renal failure Brother DM Chol 282mg/ dl TG166mg/ dl LDL 156mg/ dl HDL32mg/ dl Chol255mg/ dl TG 138mg/ dl LDL 168mg/ dl HDL 47mg/ dl

After
Chol 226mg/ dl TG 138mg/ dl LDL 123mg/ dl HDL 35mg/ dl Chol 232mg/ dl TG 106mg/ dl LDL155mg/ dl HDL56mg/ dl MG: Fear of dark, Likes company, Doesnt like contradiction, Doesnt like to share, weak memory PG: Stocky appearance Cr Sweets, meat Chilly patient CP: Bleeding < spicy food Hairfall< summer

FM
SycoSyphil

DM
Tub Phos 200 3 mths

15

Name: Mrs K M Age :40 yrs Sex:F Occu: Housewife Relegion: Muslim Add :Kumbla SCR No: 43325

Familial combined hyperlipidem iaAllergic rhinitis

MG Brooding, Suppressed emotion, Weeping when alone, Hasty, Doesnt 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

SycoSyphil

Psora

Natrum Mur 30

5 mths

11

Improved

118

Sl. no

Particulars Of The Patient

Clinical Diagnosis

Past And Family History


Mother Osteoarthr itis Father Expired of MI

Investigations Totality Before


Chol250mg/ dl TG 66mg/ dl LDL 148 mg/ dl HDL89mg/ dl

Miasms

Remedy

Duration of treatment

Scoring

Result

After
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 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

FM
SycoSyphil

DM
Syco Puls 200, 1M 4mths 6

B
1

A
Improved

Name: Mrs Y Age : 41 yrs Sex: F Occu: Housewife Relegion: Hindu Add :Ullal SCR No: 14392

CETP deficiency Osteoarthritis Calcanean spur Hypertension

Name: Mr M Age : 35yrs Sex: M Occu: Driver Relegion: Muslim Add : Payyannur SCR No: 48619

Familial chylomicronem ia LRTI Tension headache Hypertension

Mother Bronchial asthma Father Died of MI

Chol 223mg/ dl TG425mg/ dl LDL 129mg/ dl HDL50mg/ dl

Chol 198mg/ dl TG 280mg/ dl LDL 101mg/ dl HDL 41mg/ dl

SycoSyphil

Psora

Sulph 200

5mths

11

Improved

119

Sl. no

Particulars Of The Patient

Clinical Diagnosis

Past And Family History


P/H Appendici tis Father Hypertens ion

Investigations Totality Before


Chol 235mg/ dl TG 86mg/ dl LDL176mg/ dl HDL42mg/ dl Chol 310mg/ dl TG 130mg/ dl LDL 157mg/ dl HDL 27mg/ dl

Miasms

Remedy

Duration of treatment

Scoring

Result

After
Chol324mg/ dl TG122mg/ dl LDL234mg/ dl HDL46mg/ dl Chol 149mg/ dl TG 113mg/ dl LDL 95mg/ dl HDL 31mg/ 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 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

FM
Syco

DM
Psora Lyco 200 4 mths

B
12

A
15 Not Improved

Name: Mr J P Age : 27 Yrs Sex:M Occu: Attendar Relegion :Christian Add : Manjeshwar SCR No: 9154

Polygenic hypercholester olemia Sinusitis APD

Name: Mrs N Age : 37 Sex: F Occu Housewife: Relegion: Hindu Add : Bejai SCR No: 54279

Polygenic hypercholester olemia Varicose veins

P/H Bronchial asthma, Chikungu nya Mother DM Expired

Syco

Syco

Puls 200

3 mths

17

Improved

120

Sl. no

Particulars Of The Patient

Clinical Diagnosis

Past And Family History


P/H Eczema Bronchial asthma since 15 yrs Father DM, Hypertens ion Mother DM, Hypertens ion Mother DM

Investigations Totality Before


Chol 271mg/ dl TG 124mg/ dl LDL 212mg/ dl HDL 35mg/ dl

Miasms

Remedy

Duration of treatment

Scoring

Result

After
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

FM
Syco

DM
Syco Lyco 200 4mths

B
16

A
11 Improved

Name: Mrs L R Age :42yrs Sex: F Occu: Lecturer Relegion: Christian Add : Bendore SCR No:54604

Polygenic hypercholester olemia Hypertension

Name: Mr H Age : 32yrs Sex: M Occu: Clerk Relegion: Muslim Add :Urumanai SCR No: 9504

Familial combined hyperlipidemia Functional impotency

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

121

Sl. no

Particulars Of The Patient

Clinical Diagnosis

Past And Family History

Investigations Totality Before After

Miasms

Remedy

Duration of treatment

Scoring

Result

FM

DM

Name:Mrs G M Age :44yrs Sex:F Occu: Housewife Relegion: Christian Add :Kannur SCR No:57489

Polygenic hypercholester olemia Osteoarthritis Sinusitis

P/H Bronchial asthma, Chikungu nya Father Bronchial asthma

Chol 287mg/ dl TG175mg/ dl LDL210mg/ dl HDL42mg/ dl

Chol269mg / dl TG146mg / dl LDL195mg / dl HDL45mg/ 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 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

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 hyperlipidemia Diabetic cataract APD

P/H- DM since 14 yrs Night blindness at 5yrs Mother DM, Hypertens ion, Stroke

Chol234mg/ dl TG200mg/ dl LDL 161mg/ dl HDL 33mg/ dl

Chol228mg / dl TG 163mg / dl LDL 156mg / dl HDL 40mg/ dl

SycoSyphil

Syco

Phos 200

5 mths

15

10

Improved

122

Sl. no

Particulars Of The Patient

Clinical Diagnosis

Past And Family History


Father died of peptic ulcer Mother died of Tuberculo sis

Investigations Totality Before


Chol 258mg/ dl TG 203mg/ dl LDL 168mg/ dl HDL 50mg/ dl

Miasms

Remedy

Duration of treatment

Scoring

Result

After
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

FM
Tub

DM
Syco Nux Vom 200 3 mths

B
14 6

A
Improved

11

Name: Mr K Age : 44 yrs Sex: M Occu: Executive officer Relegion: Hindu Add : Mangalore SCR No: 56928

Familial combined Hyperlipidemia Cholecystolithi asis

12

Name :Mr B Age : 58 yrs Sex: M Occu: Railway Guard Relegion: Hindu Add : Ottappalam SCR No: 55073

Secondary hyperlipidemia Hypertension 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

Chol238mg / 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

123

Sl. no

Particulars Of The Patient

Clinical Diagnosis

Past And Family History


Mother Hypertens ion

Investigations Totality Before


Chol241mg/ dl TG222mg/ dl LDL149mg/ dl HDL48mg/ dl Chol267mg/ dl TG 197mg/ dl LDL 139mg/ dl HDL 89mg/ dl

Miasms

Remedy

Duration of treatment

Scoring

Result

After
Chol224mg / dl TG 207mg / dl LDL 130mg / dl HDL 53mg/ dl Chol 257mg / dl TG 187mg / dl LDL 138mg / dl HDL 82mg/ 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 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

FM
Syco

DM
Syco Phos 200 3 mths 9

B
5

A
Impeoved

13

Name: Mrs L S Age : 48 yrs Sex: F Occu: Housewife Relegion: Christian Add : Bantwala SCR No: 57290

Familial combined hyperlipidemia Cholecystolithi asis

14

Name: Sr T Age : 43yrs Sex: F

Occu: Accountant Relegion: Christian Add :Deralakatte SCR No: 14010

Familial combined hyperlipidemia Allergic rhinitis, Arthritis Calcanean spur

P/H Fibroid uterus Mother DM Father DM, Hypertens ion Grand father DM, Hypertens ion

Syco

PsoraSyco

Sepia 200

5 mths

Not Improved

124

Sl. No

Particulars Of The Patient

Clinical Diagnosis

Past And Family History


Grand father DM, Hypertens ion, Osteoarthr itis Father Hypertens ion

Investigations Totality Before


Chol273mg/ dl TG197mg/ dl LDL199mg/ dl HDL34mg/ dl Chol212mg/ dl TG 166mg/ dl LDL 134mg/ dl HDL 36mg/ dl

Miasms

Remedy

Duration of treatment

Scoring

Result

After
Chol268mg / dl TG 156mg / dl LDL179 mg/ dl HDL 42mg/ dl Chol 198mg / dl TG 152mg / dl LDL 127mg / dl HDL 40mg/ dl MG Stress , Anxiety,Irritable, Controls anger, Contradiction <, Likes consolation, Likes company, Hasty decision, Adequate confidence, Weak memory PG Stocky appearance Perspiration of feet CrFried food, Av- Leafy Veg Hot patient CP 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

FM
Syco

DM
Psora Lyco30, 200 12mths

B
18

A
14 Improved

15

Name: Mr M Age : 44 yrs Sex:M Occu: Airlines officer Relegion: Christian Add : Panjim SCR No: 33269

Familial hypercholester olemia Migraine

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 Hypertens ion since 15yrs Fibroid uterus Mother Hypertens ion

Syco

Syco

Lyco 200

7 mths

Improved

125

Sl. No

Particulars Of The Patient

Clinical Diagnosis

Past And Family History

Investigations
Totality

Miasms

Remedy

Duration of treatment

Scoring

Result

Before
17 Name: Mrs K H Age: 57 yrs Sex: F Occu: Housewife Relegion: Muslim Add : Valencia SCR No: 56804 Familial combined hyperlipide mia Migraine, Cholelithia sis P/H Fibroid uterus Mother Cardiac failure Brother Renal failure Sister - DM, Hypertension Chol281mg/ dl TG349mg/ dl LDL163mg/ dl HDL50mg/ dl

After
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 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

FM SycoSyphil

DM PsoraSyco Lyco 200 4 mths

B
19 12

A
Improved

18

Name: Mr C Age : 63 yrs Sex: M Occu: Lab assistant Relegion: Hindu Add : Mangalore SCR No: 55419

Secondary hyperlipide mia Grade I Renal parenchym al disease, Cholecystol ithiasis Grade II BPH

P/H Hydrocoele at the age of 28 yrs, Hypertension since 5 yrs FatherHypertension Mother- DM, Hypertension, Osteoarthritis BrotherHypertension

Chol247mg/ dl TG 127mg/ dl LDL 183mg/ dl HDL 37mg/ dl

Chol209mg / dl TG113mg / dl LDL144mg / dl HDL44mg/ dl

Syco

Syco

Calc carb 10 M

10mths

14

Improved

126

Sl. No

Particulars Of The Patient

Clinical Diagnosis

Past And Family History

Investigations
Totality

Miasms

Remedy

Duration of treatment

Scoring

Result

Before
19 Name: Mrs A M Age : 50 yrs Sex: F Occu: Lab assistant Relegion: Christian Add : Surathkal SCR No: NITK 06 Polygenic hyperchole sterolemia Varicose veins Osteoarthrit is Cervical spondylosis P/H Eczema in childhoodBro nchial asthma since 20 yrs Cerebral infarction Chol251mg/ dl TG102mg/ dl LDL186mg/ dl HDL44mg/ dl

After
Chol176mg / dl TG70mg/ dl LDL106mg / dl HDL56mg/ 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 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

FM Syco Syphil

DM Syco Puls 200 10mths

B
13 0

A
Improved

20

Name: Mrs B Age :60yrs Sex: F Occu: Housewife Relegion: Muslim Add : Kasargod SCR No: 5535

Polygenic hyperchole sterolemia 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

Chol412mg/ dl TG 98mg/ dl LDL 349mg/ dl HDL 44mg/ dl

Chol330mg / dl TG68mg/ dl LDL 275mg /dl HDL42mg/ dl

Syphil

Syco

Nat Mur 200

8mths

19

16

Improved

127

Sl. no

Particulars Of The Patient

Clinical Diagnosis

Past And Family History

Investigations Totality Before After


Chol276mg / dl TG 194mg / dl LDL196mg / dl HDL42 mg/ dl Chol296mg / dl TG 156mg / dl LDL 229mg / dl HDL 46mg/ 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 MG Irritable, Gets angry fast & shouts, Anticipatory anxiety about business, Doesnt 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

Miasms

Remedy

Duration of treatment

Scoring

Result

FM
Syco

DM
Syco Medorrhin 200 12 mths

B
29

A
16 Improved

21

Name: Mrs P B Age : 61 yrs Sex: F Occu: Housewife Relegion: Hindu Add : Padil SCR No: 1727

Familial hyperchole sterolemia Osteoarthrit is Cervical spondylosis

P/H Fibroid uterus, Hypertension since 14 yrs Hypothyroidis m since 5yrs Ganglion

Chol 346mg/ dl TG 206 mg/ dl LDL 287mg/ dl HDL18 mg/ dl Chol390mg/ dl TG 178mg/ dl LDL 315mg/ dl HDL 41mg/ dl

22

Name: Mr M S Age : 30yrs Sex: M Occu: Business Relegion: Muslim Add : Adur SCR No: 7994

Familial combined hyperlipide miaTension headache Flatulent dyspepsia Arthritis

FatherHypertension MotherHypertension, DM, Gastritis

Syco

Psora

Lyco 200, 1M

5mths

20

15

Improved

128

Sl. no

Particulars Of The Patient

Clinical Diagnosis

Past And Family History


P/H Jaundice, Lipoma

Investigations Totality Before


Chol 217mg/ dl TG 146mg/ dl LDL 148mg/ dl HDL 40mg/ dl Chol240mg/ dl TG208mg/ dl LDL 151mg/ dl HDL48mg/ dl

Miasms

Remedy

Duration of treatment

Scoring

Result

After
Chol 200mg / dl TG 139mg / dl LDL 128mg / dl HDL 45mg/ dl Chol 218mg / dl TG 160mg / dl LDL 138mg / dl HDL 48mg/ 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 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

FM
Syco

DM
Syco Lyco 200 5mths 6

B
1

A
Improved

23

Name: Mr A Age : 52 yrs Sex: M Occu: Bus conductor Relegion: Christian Add : Deralakatte SCR No: 8424

Secondary Hyperlipidemia Diabetis Mellitus

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, Tonsillitis Nasal polyp, Cervical lymphade nopathy, Valvular stenosis MotherDM BrotherDM, Cardiac disease

Syco

Syco

Lyco 200., 1M

5mths

10

Improved

129

Sl. no

Particulars Of The Patient

Clinical Diagnosis

Past And Family History

Investigations Totality Before After 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 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

Miasms

Remedy

Duration of treatment B

Scoring

Result

FM Syco Syphil

DM PsoraSyco Calc Carb 200 5mths

A 9 Improved

25

Name: Mrs A N Age : 35 yrs Sex: F Occu: Housewife Relegion: Hindu Add : Ballalbagh SCR No: 17102

Familial combined hyperlipidemia Tension headache Haemorrhoids Enterobiasis

P/H Malaria , Still birth delivery Mother Hypertens ion FatherHypertens ion, Epilepsy

Chol260mg/ dl TG 198mg/ dl LDL 177mg/ dl HDL 44mg/ dl

15

26

Name: Mrs C G Age : 55 yrs Sex: F Occu: Housewife Relegion: Christian Add : Ladyhill SCR No: 10548

Familial hypercholester olemia Migraine, Allergic rhinitis

P/H Chickenp ox MotherHypertens ion, Hyperchol esterolemi a, MI FatherExpired of Carcinom a thyroid

Chol270mg/ dl TG 147mg/ dl LDL 203mg/ dl HDL 38mg/ dl

Chol 253mg / dl TG 140mg / dl LDL 183mg / dl HDL 42mg/ dl

SycoSyphil

Psora

Sulphur 200

3mths

14

13

Improved

130

Sl. no

Particulars Of The Patient

Clinical Diagnosis

Past And Family History


P/H Hypertens ion since 10 yrs Father Carcinom a throat Sister IHD

Investigations Totality Before


Chol272mg/ dl TG186 mg/dl LDL 191mg/ dl HDL44mg/ dl

Miasms

Remedy

Duration of treatment

Scoring

Result

After
Chol259mg / 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 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

FM
SycoSyphil

DM
Syco Calcarea carb 200 4mths

B
15

A
13 Improved

27

Name: Mrs J D Age : 70 yrs Sex: F Occu: Housewife Relegion: Christian Add : Konaje SCR No: 16373

Familial combined hyperlipidemia Osteoarthritis

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 Pneumoni a Mother Fibroid uterus, Hypertens ion Fatherhypertensi on

Chol299mg/ dl TG208mg/ dl LDL207mg/ dl HDl51mg/ dl

Chol260mg / dl TG97mg/ dl LDL183mg /dl HDL58mg/ dl

Syco

Syco

Sepia 200

12mths

17

13

Improved

131

Sl. no

Particulars Of The Patient

Clinical Diagnosis

Past And Family History


Mother Filariasis, DM

Investigations Totality Before


Chol212mg/ dl TG200mg/ dl LDL140mg/ dl HDL32mg/ dl Chol205mg/ dl TG91mg/ dl LDL143mg/ dl HDL45mg/ dl

Miasms

Remedy

Duration of treatment

Scoring

Result

After
Chol188mg /dl TG171mg / dl LDL114mg / dl HDL40mg/ dl Chol200mg / dl TG90mg/ dl LDL141mg / dl HDL41mg 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 MG Stress, Irritable, gets angry fast, Shouts back, Optimistic, Confident PG Obese Perspiration increased in general, Appetite increased Thirst increased for cold water CrNon 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

FM
PsoraSyco

DM
Psora Lyco 200 3mths 9

B
2

A
Improved

29

Name: Mr A R Age : 30 yrs Sex: M Occu: Contractor Relegion: Muslim Add : Kallappu SCR No: 12984

Hepatic Lipase deficiency Obesity

30

Name: Mr P M Age : 29 yrs Sex: M

Occu: Merchant navy Relegion: Christian Add : Kulai SCR No: 17226

Polygenic hypercholester olemia Obesity Tension headache

Father Hypertens ion, DM

Syco

Psora

Calc carb 200

3mths

Not improved

132

133