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Transcript of MIASMATIC EVALUATION OF HYPERLIPIDEMIA
i
MIASMATIC EVALUATION OF HYPERLIPIDEMIA
by
Dr SHEENA K.N
Dissertation Submitted to
Rajiv Gandhi University of Health Sciences, Karnataka, Bangalore
In partial fulfillment of
the requirements for the degree of
Doctor of Medicine in
Organon of Medicine and Homoeopathic Philosophy
Under the guidance of
Dr ROSHAN PINTO
DEPARTMENT OF ORGANON OF MEDICINE AND
HOMOEOPAT HIC PHILOSOPHY,
FATHE R MULLE R HOMOEOPAT HIC MEDICAL COLLEGE,
DERALAKATTE, MANGALORE
2011
ii
CERTIFICATE BY THE GUIDE
This is to cert ify that the dissertat ion ent it led “MIASMATIC
EVALUATION OF HYPERLIPIDEMIA” is a bonafide research work done by
Dr SHEENA K.N under my guidance and supervision dur ing the year
2008 – 2011, in part ia l fulfillment o f t he requirement for the award o f the
degree o f “DOCTOR OF MEDICINE” (ORGANON OF MEDICINE
AND HOMOEOPATHIC PHILOSOPHY) .
I have sat isfied myself regarding the authent icit y o f her
observat ions noted in this dissertat ion and it conforms to the standards o f
Rajiv Gandhi Universit y o f Healt h Sciences, Karnataka, Bangalore. It has
not been submit ted (part ial or full) for the award o f any other Degree or
Dip loma.
Dr ROSHAN PINTO Date : M D (H O M )
Place: Mangalore Professor , Depar tment of
Organon of Medicine and
Homoeopathic Philosophy,
Father Muller Homoeopathic Medica l
College and Hospita l,
Deralakat te, Mangalore
iii
DECLARATION BY THE CANDIDATE
I hereby declare t hat this dissertat ion ent it led “MIASMATIC
EVALUATION OF HYPERLIPIDEMIA” is a bonafide and genuine research
work carr ied out by me, under the guidance o f Dr ROSHAN PINTO ,
Professor, Department o f Organon o f medicine and Homoeopathic
Philo sophy, dur ing the year 2008–2011, in part ial fulfi llment o f
requirement for the award o f DOCTOR OF MEDICINE (ORGANON OF
MEDICINE AND HOMOEOPATHIC PHILOSOPHY) .
I have not previously submit ted this work (part ial or full) to any
other universit y for the award o f any other Degree or Diploma.
Date:
Place: Mangalore Dr SHEENA K.N
iv
ENDORSEMENT BY THE HOD, PRINCIPAL/
HEAD OF THE INSTITUTION
This is to cert ify t hat the dissertat ion ent it led “MIASMATIC
EVALUATION OF HYPERLIPIDEMIA” is a bonafide research work carr ied
out by Dr SHEENA K.N under t he guidance and supervis ion o f
Dr ROSHAN PINTO dur ing the year 2008 – 2011, in part ial fulfillment
of the requirement for the award o f the degree o f “DOCTOR OF
MEDICINE” (ORGANON OF MEDICINE AND HOMOEOPATHIC
PHILOSOPHY) .
We have sat isfied regarding the authent ic it y o f her observat ions
noted in this dissertat ion and it conforms the standards o f Rajiv Gandh i
Universit y o f Health Sciences, Karnataka, Bangalore. It has not been
submit ted (part ial or full) for the award of any other Degree or Diploma.
HEAD OF THE DEPARTMENT PRINCIPAL
Dr SHIVAPRASAD K. Dr SRINATH RAO BSc, MD (HOM) MD (HOM)
Professor, HOD, Professor, HOD, Dept . of Organon o f Medic ine and Dept.of Materia Medica, Homoeopathic Philo sophy, Fr. Muller Homoeopathic, Fr. Muller Homoeopathic Medical Medical College, College, Deralakatte, Mangalore Deralakatte, Mangalore
Date: Date:
v
Place: Manga lore P lace: Manga lore
COPYRIGHT
Declaration by the Candidate
I hereby declare that the Rajiv Gandhi University of Health
Sciences, Karnataka, Bangalore shall have the r ights to preserve, use
and disseminate this dissertat ion / thesis in pr int or elect ronic format for
academic / research purpose.
Date:
Place: Mangalore Dr SHEENA K.N
© Rajiv Gandhi University of Health Sciences, Karnataka
vi
Acknowledgement
I consider this as my privilege to thank the Almighty God, who is
responsible for everything in my l i fe, and give him all the glory for the accomplishment of my post graduate studies. I thank him for helping me to
achieve this task through the following persons who have been of immense help and source of encouragement in my endeavor .
I would l ike to express my sincere and hear tfel t thanks to my respected teacher and guide Dr Roshan Pinto , Professor, Department of Organon of
Medicine and Homoeopathic Philosophy for providing me expert guidance, constructive advice, freedom of thought, personal attention, t imely support and encouragement throughout my post graduate course and during the dissertation
work. It is my good fortune to do this work under his guidance.
It is my privilege to express sincere grati tude to Rev. Fr Patrick Rodrigues, Director, FMCI and Rev. Fr Wilfred Prakash D’souza ,
Administrator of Fr. Muller Homoeopathic Medical college, Mangalore for providing me an opportunity and adequate facil i t ies to carry out this work to my satisfaction in this reputed insti tution.
I would l ike to express my grati tude to Dr Shashi Kant Tiwari former
principal, who is and was a real source of inspiration and also Dr Srinath Rao, Principal, Father Muller Homoeopathic Medical College for his support while
persuing my studies.
I express my sincere thanks to Dr Shivaprasad K , Vice principal and Head of the Department of Organon of Medicine and Homoeopathic Philosophy, for his constant support , care and encouragement.
I also express my grati tude to Dr M. K. Kamath , PG Co-ordinator and
Head of the Department of Medicine, who was the man behind most acti vi t ies of the postgraduates, guiding us to perfection.
vii
I owe my sincere grati tude for all the help, and cooperation that I have received from my colleagues of various departments of FMHMC of whick I
cannot withhold the names of few l i ke Dr Jacintha Monteiro, Dr Deena Monteiro, Dr Deepa Rebello, Dr Prabhukiran and Dr Joseph Thomas.
I must thank all my batchmates especially Dr Shalini and Dr Rekha for
their companionship, co operation and t imely help which considerably eased my task. I at tribute part of my success and st rength to them.
A word of grati tude to Mr Suresh and Dr Shripathi Kalluraya for t eaching statist ical application and research help ing to formulate the Research
Methodologies for my synopsis and carry out the statist ical work of my thesis.
I thank all the members of non-teaching staff of Fr. Muller Homoeopathic Medical College, especially l ibrary staff for their prompt service and the staff of out patient department and clinical laboratory who has
provided me with the case material required for the study.
I would have never accomplished my goal without the encouragement and prayers of my parents Mr K. Narayanan & Mrs Rajalakshmi Narayanan and
my brother Mr Sreeji th who is a world of encouragement and understanding to me. Special regards I carry in my heart for my husband Mr Salin Kumar and my beloved son Vaishak Salin for their love and co -operation in every aspect
of my l i fe.
Last but not the least , my sincere thanks to all the Patients on whom the study was conducted and MicroBits , Kankanady for taking pains for the
successful and t imely completion of this work.
I thank all the persons who have directly or indirectly influenced me for the better outcome of this work.
Place: Mangalore
Date: Dr SHEENA K.N
viii
Affectionately
Dedicated To…
My Family
ix
LIST OF ABBREVIATIONS
< : Aggravation
> : Amelioration
α : Alpha
ACTH : Adrenocorticotrophic hormone
AMP : Adenosine mono phosphate
APD : Acid peptic disease
Apo : Apoprotein
ASCVD : Artherosclerotic cardio vascular disease
ATP : Adenosine Tri phosphate
Av : Aversion
β : Beta
CAD : Coronary artery disease
CETP : Cholesteryl ester transfer protein
Chol : Total cholesterol
Co A : Co enzyme A
CP : Characteristic particulars
Cr : Craving
CVA : Cerebrovascular accident
DALY : Disability adjusted life year
DM : Diabetes Mellitus
DM : Dominant miasm
x
FA : Fatty acid
F/H : Family history
FM : Fundamental miasm
HDL : High density lipoproteins
HMG : Hydroxy methyl glutaryl
HS : At bed time
IDL : Intermediate density lipoprotein
LCAT : Lecithin cholesteryl acyl transferase
LDL : Low density lipoprotein
LPL : Lipoprotein lipase
MG : Mental generals
NAD : No abnormality detected
NADPH : Nicotinamide adenine dinucleotide phosphate
PG : Physical generals
P/H : Past history
Pkt : Packet
PVD : Peripheral vascular disease
S : Same
SCR : Standardized case record
TG : Triglyceride
TAG : Triacyl glycerol
VLDL : Very Low density lipoprotein
WHO : World Health Organization
xi
ABSTRACT
Background: Hyperlipidemia is regarded as a highly modifiable risk factor for
cardiovascular disease due to the influence of cholesterol on atherosclerosis. It results
from genetic predisposition interacting with an individual diet & lifestyle. Any defect in
the synthesis, transport or excretion of the lipids causes a rise in their level in plasma
which becomes a risk factor for coronary heart disease which is one of the major cause of
death in the present day.
Objective :
1. To study the different types of hyperlipidemia
2. To assess the role of miasm in hyperlipidemia and know the effectiveness of
constitutional method of treatment which includes the miasmatic background of
the individual.
Methods:
A total number of 30 cases were taken randomly for the study. The cases with
deviated serum lipid i.e. Cholesterol > 200mg/ dl, Triglycerides > 150mg/dl, LDL >
130mg/ dl or HDL <40mg/ dl were selected. For the assessment of the clinical status
before and after the treatment, scoring was done which is mentioned in the annexure-1.
The score before and after the treatment was considered and ‘t’ test was applied.
Results:
Among the 30 cases, a prevalence of hyperlipidemia was found in the age group
between 35 - 45 yrs. Maximum incidence of hyperlipidemia is seen in sedentary working
individuals. Sycotic expression was found to be dominating in both fundamental and
xii
dominant miasm. Constitutional treatment with general management showed
effectiveness in the treatment of hyperlipidemia
Conclusion:
This study provides an evidence to say that there is reduction in the disease
intensity scores after the homoeopathic constitutional treatment with properly planned
general management including diet and exercise. Therefore a combination of
constitutional homoeopathic treatment and general management is effective in the
treatment of hyperlipidemia.
Key words:
Hyperlipidemia, constitutional treatment, general management, diet, exercise,
serum lipid levels.
xiii
TABLE OF CONTENTS
S. No. TOPIC PAGE No.
1 INTRODUCTION 1
2 AIMS AND OBJECTIVES 4
3 REVIEW OF LITERATURE 5
4 METHODOLOGY 77
5 RESULTS 81
6 DISCUSSION 95
7 CONCLUSION 100
8 SUMMARY 102
9 BIBLIOGRAPHY 103
10 ANNEXURES
ANNEXURE – 1 107
ANNEXURE – 2 108
ANNEXURE – 3 118
xiv
LIST OF TABLES
Table No. TITLES PAGE NO.
1 Fredrickson classification of hyperlipidemia 30
2 Miasmatic evaluation criteria 67
3 Distribution of cases according to age group 81
4 Distribution of cases according to sex 81
5 Distribution of cases according to religion 83
6 Case distribution according to physical activity 83
7 Case distribution according to fundamental miasm 85
8 Case distribution according to dominant miasm 85
9 Case distribution according to type of hyperlipidemia 87
10 Case distribution according to constitutional remedies 88
11 Case distribution according to the improvement 90
12 Statistical analysis 91
xv
LIST OF FIGURES
Figure No.
TITLE PAGE No.
1 Lipid Digestion 7
2 Lipid degradation 7
3 Fat absorption 9
4 Fat metabolism 12
5 Source and fate of Triglycerols 14
6 Source and fate of cholesterol 17
7 Composition of Lipoprotein 22
8 Transport of Lipids 25
9 Diet pyramid 50
10 Natural sources reducing hyperlipidaemia 52
11 Case distribution according to age group 82
12 Case distribution according to sex 82
13 Case distribution according to religion 84
14 Case distribution according to physical activity 84
15 Case distribution according to fundamental miasm 86
16 Case distribution according to dominant miasm 86
17 Case distribution according to type of hyperlipidemia 89
18 Case distribution according to constitutional remedies 89
19 Case distribution according to the effectiveness of treatment 90
20 Distribution of all cases according to pre and post treatment analysis 94
i
Introduction
1
INTRODUCTION
Raised or abnormal levels of lipids & lipoproteins in the blood has become a
common clinical problem of the century which has turned out to be a challenge to the
physician. In today’s world most deaths are attributable to non communicable diseases &
over half of these are a result of cardiovascular diseases. Heart disease & stroke are first
& second cause of death in developed countries. WHO has drawn attention to the fact
that coronary heart disease is our “modern epidemic”.
Today there is a vast body of evidence showing the triangular relationship between
habitual diet, blood cholesterol & coronary heart disease. It is a well established fact that
a persistently high cholesterol level in blood can precipitate a cardiac event.
Hyperlipidemia is a rise in plasma cholesterol, triglyceride or both. It is regarded
as a highly modifiable risk factor for cardiovascular disease due to the influence of
cholesterol on atherosclerosis. Genetic factors are the most important determinants of a
given individual’s triglycerides & LDL levels besides the westernized life styles which
emphasize on rich food & sedentary living.
The ability of a remedy to eradicate inborn tendency of disease is not possible by
considering only symptom similarity of presenting disease. It needs much deeper
understanding of disease from evolution point of view. Such an effort from Master
Hahnemann resulted in the concept of miasms which was one among the many mysteries
of homoeopathy till recently. However genetic mapping raises the hope of understanding
miasms.
2
Any tendency to disease or destruction which can be recognized in man derives
from a structural anomaly which imprints its characteristics on him. The expression
varies in different individuals according to constitution, hereditary disposition,
education, habit, mode of life, diet, occupation, tendencies of the mind, morals, etc;
which together constitutes the miasm.
Miasm is a sort of taint, hereditary or acquired, which lies dormant in the human
system but is reactivated by circumstantial pathogens and helps to bring about
disequilibrium in vital force which in general parlance is called disease. It is a unique
complex phenomenon which acts by prolonging the disease and or by obstructing the
process of cure, even though a true similimum has been prescribed. If utilized with our
principle it shows natural way towards cure. Unless we understand the phenomena of
acting and basic miasms, it will not be possible to find the true similimum for the
eradication of the disease. The phenomenon of recurrence of the disease will be there to
torment the patient and to tax the physician.
Medical science has advanced by leaps & bounds from the time of Dr Samuel
Hahnemann regarding etiology, pathophysiology & management of chronic disease. A
homoeopath should keep in pace with this ongoing advances & renew his sources &
literature without deviating from the basic principles put down by Dr Hahnemann.
Experiments were conducted all time to find cause of disease to benefit the sick.
Exact cause is seldom found. But these studies can give information regarding correlation
between two phenomena. If understood, they provide the basic path towards inference.
In present scenario medical practice is purely based on scientific experimentation &
inferential statistics. Hence it is a necessity to have a scientific vision of truth.
3
To cure a person does not mean only to free him from his present suffering, or
alleviate his suffering; but also to preserve him and spare him from future sufferings.
Evaluation of the miasm in an individual followed by antimiasmatic treatment can help in
the prevention of the progress and complication of the disease.
This study is an attempt towards assessing the predisposing miasm in
hyperlipidemia and thereby establish the specific miasmatic preponderance in the
expression of a chronic disease and its antimiasmatic treatment as specified by
Dr Hahnemann which may help to abort or prevent disease progress.
1
Objectives
4
OBJECTIVES
1. To study the different types of hyperlipidemia
2. To assess the role of miasm in hyperlipidemia and know the effectiveness of
constitutional method of treatment which includes the miasmatic background of
the individual
4
Review of Literature
5
REVIEW OF LITERATURE
Lipids derived from the Greek word Lipos which means fat is the chief
concentrated storage form of energy besides their role in cellular structure & various
other biological function. They are heterogeneous group of compounds regarded as
organic substances relatively insoluble in water, soluble in organic solvents like alcohol.1
Classification1
1) Simple – Esters of fatty acids with alcohol
Fats & oils - Esters of FA with glycerol
Waxes – Esters of FA with alcohol
2) Complex (Compound) – Esters of FA with alcohols containing additional groups
such as phosphate, nitrogenous base, carbohydrate, protein etc
Phospholipids – Contains phosphoric acid & frequently a nitrogenous base
in addition to alcohol & FA
Glycolipids – Contains carbohydrate, Nitogenous base & FA
Lipoprotein – Mononuclear complexes of lipids with proteins
Other complex lipids – Sulfolipids, Aminolipids, Lipopolysacharrides
3) Derived lipids – Derivatives obtained on hydrolysis of simple & complex which have
the characteristics of lipids like Glycerol, FA, Ketone bodies, steroid hormones etc
4) Miscellaneous lipids – Large number of compounds possessing the characteristics of
Lipids
5) Neutral lipids – Uncharged lipids like Mono, Di and Triacylglycerol, Cholesterol,
Chloesteryl esters
6
Digestion of dietary lipid1,2,3
There is a considerable variation in the daily consumption of lipids which mostly
depends on economic status & dietary habits.
Several chemical compounds in food and in the body classified as lipids includes
(1) Neutral fat, also known as triglycerides; (2) Phospholipid (3) Cholesterol; and (4) a
few others of less importance.2
Large lipid particles to a negligible amount are broken down into smaller with
lipolytic enzyme, lingual lipase. Released short chain FA can be directly absorbed from
stomach wall & enter portal vein.4
For effective digestion of lipids emulsification occurs in small intestine by
detergent action of bile salts, surfactant action of degraded lipids & mechanical mixing
due to peristalsis. Bile contains a large quantity of bile salts as well as the phospholipid
lecithin, the major function of which is to make the fat globules readily fragmentable.
Powerful lipase of the pancreatic juice & enteric lipase in the enterocytes of the
small intestine hydrolyze & break down long chain & short chain FA of TAG into alpha
& beta monoglycerides , glycerol & FA.
Lipid esterase in pancreatic juice in presence of bile acids acts on monoacyl
glycerol, cholesteryl esters etc to give FA.
Cholesterol esterase in pancreatic juice either catalyzes the esterification of free
cholesterol with FA or cleaves cholesteryl esters to cholesterol & free FA. Both the
cholesterol esters and the phospholipids are hydrolyzed to free the fatty acids by the
enzyme cholesterol ester hydrolase and phospholipase A2 in the pancreatic secretion
respectively.2
7
Fig. 1: Lipid Digestion
Fig.2: Lipid degradation 5
8
Transport of digested fat across the membrane of intstinal villous layer into intestinal
epithelial cells occur by simple diffusion through cell membrane. Within the intestinal
epithelial cells alpha monoglycerides are further hydrolyzed by intestinal lipase to free
FA & glycerol.1
Absorption2,3
Absorption from the small intestine each day consists100 or more grams of fat.
The bile salt micelles which are small spherical, cylindrical globules composed of 20 to
40 molecules of bile salt, act as a transport medium to carry the monoglycerides and free
fatty acids to the brush borders of the intestinal epithelial cells. There the monoglycerides
and free FA are absorbed into the blood. But the bile salts themselves are released back
into the chyme to be used again for this “ferrying” process. The bile salt micelles play the
same role in “ferrying” free cholesterol and phospholipid molecule.2
Glycerol, phospholipid, short chain, medium chain & unsaturated FA are
absorbed directly to portal vein & is taken to liver. Some absorbed FA enter into lymph
of lacteals which passes through thoracic duct to systemic circulation
Free FA in intestinal wall are reincorporated into TG after activation. This cannot
pass to lymphatics & hence enter the lymph as minute, dispersed droplets called
chylomicrons which are lipoprotein complex composed of largely TG, cholesterol,
phopholipid & specific apo protein. The chylomicrons enter lymphatic vessels and are
then transported upward through the thoracic duct and emptied into the circulating
venous blood at the juncture of the jugular and subclavian veins to enter into systemic
circulation.1
9
Cholesterol is absorbed from intestine in free form. Esterification takes place
within intestinal mucosal cell. Most of the cholesterol and phospholipids absorbed from
the gastrointestinal tract enter the chylomicrons.
Some amount of fat, not hydrolyzed completely in intestinal lumen can combine
with bile salts and absorbed as micelles into lymphatic channels.
Some of lysophospholipid are resynthesised to phospholipid again by mucosal
cell while few are incorporated in VLDL in intestinal mucosal cell.
Fig.3: Fat absorption5
10
Metabolism1,2,5
Lipids constitute about 15% – 20 % of body weight in human.
Plasma lipids includes TAG, Cholesterol, Phospholipid, free FA, & Glycerol
TAG ( Neutral fat ) are the most abundant lipids comprising 80% - 90% of body
lipids. Most of the TAG are stored in adipose tissue & serve as energy reserves of the
body. It acts as an insulating material for maintaining body temperature. They are also
utilized by muscle, liver, heart etc as per needs of the body.
After absorption, most of the TAG in chylomicrons are removed from the
circulating blood as they pass through the capillaries of adipose tissue or the liver which
contain large quantities of hormone sensitive enzyme lipoprotein lipase. This enzyme
hydrolyzes the TG of chylomicrons releasing FA and glycerol. Complete degradation of
TAG to glycerol & free FA is lipolysis. The FA, being highly miscible with the
membranes of the cells, immediately diffuse into the fat cells of the adipose tissue and
into the liver cells where they are converted to acyl co A & reesterified into TG, with new
glycerol being supplied by the metabolic processes of the storage cells. Acyl Co A can be
obtained from dietary, FA synthesis, or TG circulating in chylomicron & VLDL. It also
occurs from α- glycerophosphate obtained from glucose oxidation & conversion of
glycerol
Fat that has been stored in the adipose tissue is to be used elsewhere in the body
to provide energy transported mainly in the form of free FA. This is achieved by
hydrolysis of the triglycerides back into FA and glycerol. Free FA released in lipolysis
enter circulation & are transported bound to albumin which enters various tissues &
utilized for energy.8
11
Glycerol produced in lipolysis is transported to liver where it is activated to
glycerol – 3 – phosphate which may be used for the synthesis of TAG & phospholipids. It
may also enter glycolysis.
TG continually undergoes synthesis ( Esterification ) & breakdown( Lipolysis )
within tissue. Resultant of these two process determines the magnitude of free FA pool in
adipose tissue & this in turn will determine the level of free FA circulating in blood
When rate of reesterification is less than rate of lipolysis, free FA accumulate & diffuses
into plasma & raises the level of free FA in plasma.6
When the amount of glucose available to the fat cell is inadequate, one of the
glucose breakdown products, α-glycerophosphate, is also available in insufficient
quantities, a hormone-sensitive cellular lipase can be activated, which promote rapid
hydrolysis of TG.
Large increase in free FA concentration in the blood occurs when rate of
utilization of fat for cellular energy also increase as in cases of starvation and in diabetes,
where the person derives little or no metabolic energy from carbohydrates.
95 % of energy obtained from fat comes by β oxidation of FA which occur only
in the mitochondria. Transport into the mitochondria is a carrier mediated process that
uses carnitine as the carrier substance. Once inside the mitochondria, FA split away from
carnitine and are degraded and oxidized which involves successive cleavage. The acetyl-
CoA molecules formed by β-oxidation of FA, enter immediately into the citric acid cycle
liberating large amounts of ATP. When excessive amounts of lipids are being used for
energy, part of the acetoacetic acid is also converted into β-hydroxybutyric acid, and
minute quantities are converted into acetone The acetoacetic acid, β-hydroxybutyric
12
acid, and acetone diffuse freely through the liver cell membranes and are transported by
the blood to the peripheral tissues. Here they again diffuse into the cells, where reverse
reactions occur and acetyl-CoA molecules are formed. These in turn enter the citric acid
cycle and are oxidized for energy. The concentrations of acetoacetic acid, β-
hydroxybutyric acid, and acetone occasionally rise to levels many times above normal in
the blood and interstitial fluids causing a condition called ketosis.3
Fig.4: Fat metabolism5
13
Plasma TG are derived from intestinal dietary fat during absorption & otherwise
from liver. In fasting state the FA is derived from adipose cell in minute quantities.TG
are taken up by the liver & a portion is reexcreted as VLDL and transported to the
adipose tissue, where they are stored.
Synthesis of TAG from Carbohydrates and Proteins7
Whenever a greater quantity of carbohydrates or proteins enters the body than can
be used immediately for energy or can be stored, the excess is rapidly converted into TG
which are secreted as lipoproteins.
Regulation of TAG synthesis8
Inactive form of lipase is activated by cyclic AMP dependent protein kinase to
activate lipase. Epinephrine, norepinephrine, glucagon, thyroxine, ACTH etc enhance the
activity of adenylate cyclase & thus increase lipolysis.
Insulin decreases cyclic AMP levels & thereby inactivate lipase. When no insulin
is available, as occurs in serious diabetes mellitus, fats are poorly synthesized. Here
glucose does not enter the fat and liver cells satisfactorily, so that little of the acetyl-CoA
and NADPH needed for fat synthesis can be derived from glucose. More over lack of
glucose in the fat cells greatly reduces the availability of α-glycerophosphate, which also
makes it difficult for the tissues to form TG.
During exercise, as a result of sympathetic stimulation, release of epinephrine and
norepinephrine by the adrenal medullae which directly activate hormone-sensitive
triglyceride lipase, present in abundance in the fat cells, causes rapid breakdown of TG
and mobilization of FA.
14
Stress causes corticotropin to be released by the anterior pituitary gland, and this
causes the adrenal cortex to secrete extra quantities of glucocorticoids thereby activating
the same hormone-sensitive triglyceride lipase. Growth hormone has a similar but weaker
effect in activating hormone-sensitive lipase
Thyroid hormone causes rapid mobilization of fat, which is believed to result
indirectly from an increased overall rate of energy metabolism in all cells of the body
under the influence of this hormone.3
Fig.5: Source and fate of Triacylglycerols 5
15
Cholesterol is animal sterol comprising 2gm / Kg body weight. It is a structural
component of cell membrane & precursor for synthesis of all steroids. 1 It is an essential
ingredient in the structure of lipoprotein. Being a poor conductor of electricity, it helps to
insulate nerve fibres. Vitamin D 3 is synthesized from 7 – dehydrocholesterol.6
The most abundant nonmembranous use of cholesterol in the body is to form
cholic acid in the liver. 80 % of cholesterol is converted into cholic acid. This is
conjugated with other substances to form bile salts, which promote digestion and
absorption of fats. A small quantity of cholesterol is used by the adrenal glands to form
adrenocortical hormones, the ovaries to form progesterone and estrogen, and the testes to
form testosterone.
A large amount of cholesterol is precipitated in the corneum of the skin which
along with other lipids, makes the skin highly resistant to the absorption of water soluble
substances and to the action of many chemical agents, because cholesterol and the other
skin lipids are highly inert to acids and to many solvents that might otherwise easily
penetrate the body. Also, these lipid substances help prevent water evaporation from the
skin. 3
FA can get esterified to form cholesterol esters and transported to liver as
cholesteryl esters for oxidation which helps in regulating cholesterol level in body fluids.
About 70 % of the cholesterol in the lipoproteins of the plasma is in the form of
cholesterol esters.
16
Synthesis of Cholesterol5
Cholesterol, is present in the diets of all people, and it can be absorbed slowly
from the gastrointestinal tract into the intestinal lymph. It is highly fat soluble but only
slightly soluble in water. Besides the cholesterol absorbed from the gastrointestinal tract,
called exogenous cholesterol, a greater quantity is formed in the cells of the body, called
endogenous cholesterol which circulates in the lipoproteins of the plasma formed by the
liver in majority, as well as from other cells of the body. Cholesterol in diet absorbed
from intestine in company with other lipids are incorporated into chylomicrons & to
some extent into LDL. Absorbed cholesterol is excreted in bile as bile salts after
conversion to bile acids. This is partly reabsorbed.
Regulation of cholesterol synthesis7
An increase in the amount of cholesterol ingested each day increases the plasma
concentration slightly. The rising concentration of cholesterol inhibits the most essential
enzyme for endogenous synthesis of cholesterol, 3-hydroxy-3-methylglutaryl CoA
reductase, thus providing an intrinsic feedback control system to prevent an excessive
increase in plasma cholesterol concentration.
Hormonal control is done by glucagon & glucocorticoids which favour formation
of inactive HMG co A reductase & thus reduce cholesterol synthesis.
Lack of insulin or thyroid hormone increases the blood cholesterol concentration,
whereas excess thyroid hormone decreases the concentration. These effects are probably
caused mainly by changes in the degree of activation of specific enzymes responsible for
the metabolism of lipid substances. Fasting and bile acids reduces activity of enzyme
thereby reducing cholesterol synthesis
17
A highly saturated fat diet increases blood cholesterol concentration 15 to 25%
due to increased fat deposition in the liver, which then provides increased quantities of
acetyl-CoA in the liver cells for the production of cholesterol whereas ingestion of fat
containing highly unsaturated FA usually depresses the blood cholesterol concentration a
slight to moderate amount.
Unabsorbed cholesterol in the intestine is acted upon by intestinal bacteria &
excreted as faecal sterols. Certain vegetables contain plant sterols which inhibit
reabsorption of cholesterol.
Fig.6: Source and fate of cholesterol 5
18
Phospholipids and Cholesterol Phospholipids: The major types of body phospholipids
are lecithins, cephalins, and sphingomyelin. Although the chemical structures of
phospholipids are somewhat variant, their physical properties are similar. They are all
lipid soluble and forms an important constituent of lipoproteins in the blood and are
essential for the formation and function of most of these. In their absence, serious
abnormalities of transport of cholesterol and other lipids can occur.2
Thromboplastin, which is needed to initiate the clotting process, is composed
mainly of one of the cephalins.6
Large quantities of sphingomyelin are present in the nervous system which acts as
an electrical insulator in the myelin sheath around nerve fibers. Phospholipids are donors
of phosphate radicals when these radicals are needed for different chemical reactions in
the tissues.
The most important of all the functions of phospholipids is participation in the
formation of structural elements such as in cell membranes and intracellular membranes
throughout the body.6
Synthesisof Phospholipids.2
Phospholipids are synthesized in essentially all cells of the body from
phosphatidic acid & 1, 2 diacyl glycerol. Probably 90 % are formed in the liver cells;
substantial quantities are also formed by the intestinal epithelial cells during lipid
absorption from the gut. The lipase causes hydrolysis of phospholipid releasing FA to be
stored in the cells.
19
LIPOPROTEINS1,2,9
In the post absorptive state, after all the chylomicrons have been removed from
the blood, more than 95% of all the lipids in the plasma are in the form of lipoprotein
which are macromolecular complexes of lipids with protein, containing TG, cholesterol,
phospholipids, and fat-soluble vitamins. They transport lipids through body fluids
(plasma, interstitial fluid, and lymph) to and from tissues. The total concentration of
lipoproteins in the plasma averages about 700 mg per 100 ml of plasma with Cholesterol
180 mg/dl, Phospholipids 160mg/dl, Triglycerides 160mg/dl and Protein 200mg/dl.
Based on their relative densities and seperation by electrophoresis it is classified as
1) Chylomicron are synthesized in the small intestine in the course of fat absorption
& in liver and transport dietary TAG to various tissues. They consist of highest
(99%) quantity of lipid mostly TAG besides about 9% phospholipids, 3%
cholesterol & lowest concentration (1%) of protein apoprotein B - 48. They have
least density and is largest in size. Nascent chylomicron with apo C II & apo E
derived from HDL forms chylomicron. Chylomicron formation fluctuates with the
load of TG absorbed.
2) Very low density lipoproteins (VLDL) which contain high concentrations of
TAG and moderate concentrations of both cholesterol and phospholipids are
produced in liver & intestine. It helps transport of endogeneously synthesised
TAG. Nascent VLDL with apo B 100 rich in TAG & cholesterol, with apo CII &
apo E donated by circulating HDL forms VLDL.
20
3) Intermediate-density lipoproteins (IDL) are VLDL from which a share of the
TG has been removed, so that the concentrations of cholesterol and phospholipids
are increased.
4) Low-density lipoprotein (LDL) are derived from IDL in the course of VLDL
metabolism, by the removal of almost all the TG, leaving an especially high
concentration of cholesterol and a moderately high concentration of
phospholipids. Apo E is returned to HDL. Thereby LDL contains high cholesterol
& less TAG. It transports cholesterol from liver to other tissues. Most important
function of LDL is to supply cholesterol to extrahepatic tissues by binding to the
specific receptor pits on cell membrane which is recognized by apo B 100. Defect
in LDL receptor causes elevation of plasma LDL & hence plasma cholesterol.
5) High-density lipoproteins (HDL) contains a high concentration of protein
(about50%) but much smaller concentrations of cholesterol and phospholipids.
Mostly synthesized in liver, it transports cholesterol from peripheral tissues to
liver. Free nacsent HDL is synthesized in liver which contain free cholesterol,
phospholipid & apoprotein. HDL accepts free cholesterol from other lipoprotein
in circulation & cell membrane of peripheral tissue which undergoes LCAT
catalysed esterification.
6) FA complexed with albumin
Each lipoprotein class comprises a family of particles that vary slightly in density,
size, migration during electrophoresis, and protein composition. The density of a
lipoprotein is determined by the amount of lipid and protein per particle. HDL is
the smallest and most dense lipoprotein, whereas chylomicrons and VLDL are the
21
largest and least dense lipoprotein particles Most TG is transported in
chylomicrons or VLDL, and most cholesterol is carried as cholesteryl esters in
LDL and HDL .They function as transport vehicles for lipids in blood plasma &
deliver the lipid components to various tissue for utilization. VLDL transport TG
synthesized in the liver mainly to the adipose tissue, whereas the other
lipoproteins are especially important in the different stages of phospholipid and
cholesterol transport from the liver to the peripheral tissues or from the periphery
back to the liver.9
Structure9,10
Lipoprotein consists of a neutral lipid core with TAG or cholesteryl ester,
sorrounded by a coat shell of hydrophilic lipids like phospholipids, unesterified
cholesterol and apoprotein that interact with body fluids. Polar amphiphilic portion are
exposed on surface so that it is soluble in aqueous solution.
Apoprotein is the protein component of lipoprotein which acts as its structural
component. It recognizes the cell membrane surface receptors, facilitates transfer of
lipids between lipoprotein classes & between lipoprotein & cells. It activates enzymes
involved in lipoprotein metabolism.
ApoA-I, which is synthesized in the liver and intestine, is found on virtually all
HDL particles. ApoA-II is the second most abundant HDL apolipoprotein and is found on
approximately two-thirds of all HDL particles. ApoB is the major structural protein of
chylomicrons, VLDL, IDL, and LDL; one molecule of apoB, either apoB-48
(chylomicrons) or apoB-100 (VLDL, IDL, or LDL), is present on each lipoprotein
particle. The human liver makes only apoB-100, and the intestine makes apoB-48. ApoE
22
present in multiple copies on chylomicrons, VLDL and IDL plays a critical role in the
metabolism and clearance of TG rich particles. Three apolipoproteins of the C-series
(apoC-I, -II, and -III) also participate in the metabolism of TG rich lipoproteins.
Fig.7: Composition of Lipoprotein 10
23
Metabolism & transport of lipoproteins
Transport of dietary lipids (Exogenous pathway) 9,10
Dietary cholesterol and retinol are esterified by the addition of a FA in the
enterocyte to form cholesteryl esters and retinyl esters, respectively. Longer-chain FA
are incorporated into TG and packaged with apoB-48, cholesteryl esters, retinyl esters,
phospholipids, and cholesterol to form chylomicrons. Nascent chylomicrons are secreted
into the intestinal lymph and delivered directly to the systemic circulation, where they are
extensively processed by peripheral tissues before reaching the liver. Apoprotein C-II on
chylomicron, binds to specific receptors in adipose tissue, skeletal muscle, cardiac muscle
and the liver and allows the endothelial enzyme, LPL, to remove most of the TG from the
particle and liberating free FA and glycerol. The released free FA are taken up by
adjacent myocytes or adipocytes and either oxidized or reesterified and stored as TG.
Some free FA bind with albumin and are transported to other tissues, especially the liver.
ApoC-II, is transferred to circulating chylomicrons or returned to HDL.
The chylomicron particle progressively shrinks in size as the hydrophobic core is
hydrolyzed and the hydrophilic lipids (cholesterol and phospholipids) on the particle
surface are transferred to HDL. The resultant smaller, more cholesterol ester–rich
particles are referred to as chylomicron remnants. The remnant particles are rapidly
removed from the circulation by receptors on hepatocytes in a process that requires apo
E. Consequently, few, if any, chylomicrons are present in the blood after a 12-h fast,
except in individuals with disorders of chylomicron metabolism.
24
Cholesteryl esters form an integral part of HDL. From peripheral tissue
cholesterol is trapped in HDL by a reaction catalysed by LCAT, transported to liver for
degradation and excretion .The process is known as reverse cholesterol transport
Cholesterol ester transfer protein synthesised in liver, facilitates exchange of
components between different lipoprotein & thereby transfer cholesterol esters from HDL
to VLDL or LDL in exchange for TAG.
Transport of hepatic lipids (Endogenous pathway)9,10
The endogenous pathway of lipoprotein metabolism refers to the hepatic secretion
and metabolism of VLDL to IDL and LDL.
The cholesterol in LDL accounts for 70% of the plasma cholesterol in most
individuals. Approximately 70% of circulating LDLs are cleared by LDL receptor–
mediated endocytosis in the liver
Long-chain FA are esterified into TAG and incorporated into VLDL, which has
aoprotein B-100 as an essential component. Apoproteins C-II and E are incorporated later
into VLDL by transfer from HDL particles. As they pass round the circulation, VLDL
particles bind through apoprotein C-II allowing TG to be progressively removed by LPL
in the capillary endothelium. As VLDL remnants undergo further hydrolysis, they
continue to shrink in size, which contain similar amounts of cholesterol and TG leaving a
particle, now depleted of TG and apoprotein C-II, called an intermediate-density
lipoprotein (IDL) particle which have apoprotein B-100 and apoprotein E molecules on
the particle surface. Most IDL particles bind to liver LDL receptors through the
apoprotein E molecule and are then catabolized.11
25
The liver removes approximately 40 to 60% of VLDL remnants and IDL. The
remainder of IDL is remodeled by hepatic lipase to form LDL. During this process, most
of the TG in the particle is hydrolyzed and all apolipoproteins except apoB-100 are
transferred to other lipoproteins.
LDL particles become Lp(a) lipoproteins as a result of the linkage of apoprotein
(a) to aproprotein B-100. Raised levels of Lp(a) lipoprotein is a risk factor for
cardiovascular disease. The HDL particle transports cholesterol away from the periphery
and may transfer it indirectly to other particles such as VLDL in the circulation or deliver
its cholesterol directly to the liver.11
Fig. 8: Transport of Lipids 10
26
HDL metabolism and reverse cholesterol transport 9
All nucleated cells synthesize cholesterol but only hepatocytes can efficiently
metabolize and excrete cholesterol from the body. The predominant route of cholesterol
elimination is by excretion into the bile, either directly or after conversion to bile acids.
Cholesterol in peripheral cells is transported from the plasma membranes of
peripheral cells to the liver by an HDL-mediated process termed reverse cholesterol
transport. Nascent HDL particles are synthesized by the intestine and the liver. The newly
formed discoidal HDL particles contain apoA-I and phospholipids (mainly lecithin) but
rapidly acquire unesterified cholesterol and additional phospholipids from peripheral
tissues via transport by the membrane protein ATP-binding cassette protein A1
(ABCA1). Once incorporated in the HDL particle, cholesterol is esterified by LCAT a
plasma enzyme associated with HDL. As HDL acquires more cholesteryl ester it
becomes spherical, and additional apolipoproteins and lipids are transferred to the
particles from the surfaces of chylomicrons and VLDL during lipolysis. HDL cholesteryl
esters are transferred to apo B containing lipoproteins in exchange for TG by the CETP.
The cholesteryl esters are then removed from the circulation by LDL receptor–mediated
endocytosis. HDL cholesterol can also be taken up directly by hepatocytes via the
scavenger receptor class BI (SR-BI), a cell-surface receptor that mediates the selective
transfer of lipids to cells.
27
HYPERLIPIDEMIA
Cardiovascular disease are responsible for 25% & Cerebrovascular disease for
19% of DALY’s lost due to non communicable disease in southeast Asian region
countries. More than half the patients with angiographically confirmed premature
coronary heart disease have a familial lipoprotein disorder which represents the most
common genetic dyslipidaemia with a prevalence of 1 – 2 %. Familial combined
hyperlipidemia characterized by elevated levels of cholesterol or TG or both is estimated
to cause 10 – 20 % of premature coronary heart disease and 10 % of myocardial
infarction.12
The abnormal levels of TG and or cholesterol in plasma are consequent to excess
of substrate leading to more production, defective transport, delayed peripheral clearance,
reduced utilization of Lipoprotein or their intermediaries, or combinations of these
abnormalities. The causes responsible for such lipid disorders could be primary, i.e. an
inherent genetic (monogenic or polygenic) defect of lipid-Lipoprotein-Apo metabolism
or more commonly secondary to certain diseases.13
Classification of Hyperlipidemia due to disorders of lipoprotein metabolism 9,13
1. Primary disorders of Apo B containing lipoprotein catabolism causing elevated
plasma cholesterol levels ( Known etiology)
Lipoprotein lipase and Apo C - II deficiency / Familial chylomicronemia
Hepatic lipase deficiency
Familial dysbetalipoproteinemia
Familial hypercholesterolemia
28
Familial defective Apo – B 100
Autosomal recessive hypercholesterolemia
Wolman disease
Cholesteryl ester storage disease
Sitosterolemia
2. Primary disorders of Apo – B containing lipoprotein metabolism ( Unknown
etiology)
Familial hypertriglyceridemia
Familial combined hyperlipidemia
Polygenic hypercholesterolemia
3. Genetic disorder of HDL metabolism (Known etiology)
Apo A – I deficiency
Apo A- I mutation
LCAT deficiency
CETP deficiency
4. Primary disorders of HDL metabolism
Primary hypoalphalipoproteinemia
Familial hyperalphalipoproteinemia
5. Secondary disorders of hyperlipidaemia
Obesity
Hypothyroidism
Nephrotic syndrome
Chronic liver disease
29
Diabetes mellitus
Cushing’s syndrome
Drugs
Excessive alcohol consumption
Glycogen storage disease
Systemic lupus erythematosus
Hypopituitarism
Pregnancy
Pancreatitis
Irrespective of the underlying mechanism of lipid disorder, the biochemical
abnormalities will manifest as hypertriglyceridaemia, hypercholesterolaemia or a
combination of both. Raised TG levels suggest an increase in VLDL and or Chylomicron
levels while an isolated rise in cholesterol indicates rise in LDL level. Considering the
raised levels of TG, cholesterol or both and the Lipoprotein molecule which is in excess
in the circulation, hyperlipoproteinaemias have been classified by Fredrickson into five
major groups.13
30
Table 1:Fredrickson classification of hyperlipidaemia 13
Type Synonym Biochemical alterations
Serum alterations
Type I Buerger Gruetz syndrome. Primary hyperlipoproteinemia or Familial chylomicronemia
Decreased lipoprotein lipase or altered Apo C II
Elevated chylomicron
Type IIa Polygenic hypercholesterolemia or Familial hypercholesterolemia
LDL receptor deficiency
Elevated LDL only
Type IIb Combined hyperlipidemia Decreased LDL receptor and increased Apo B
Elevated LDL, VLDL and Triglycerides
Type III Familial dysbetalipoproteinemia
Defect in Apo E synthesis
Increased IDL
Type IV Endogenous hyperlipemia Increased VLDL production and decreased elimination
Increased VLDL
Type V Familial hypertriglyceridemia Increased VLDL production and decreased LDL
Increased VLDL and chylomicrons
Primary disorders of apob-containing lipoprotein catabolism causing
Elevated plasma cholesterol levels (known etiology)9
Single-gene defects can result in the accumulation of specific classes of
lipoprotein particles. Mutations in genes encoding key proteins in the metabolism and
clearance of apoB-containing lipoproteins cause type I (chylomicronemia), type II
(elevations in LDL) and type III (elevations in IDL)
31
Lipoprotein Lipase and ApoC-II Deficiency (Familial Chylomicronemia Syndrome;
Type I Hyperlipoproteinemia) is an autosomal recessive in inheritance pattern and has
a population frequency of one in a million. Multiple mutations in the LPL and apoC-II
genes cause these diseases. Genetic deficiency of either LPL required for the hydrolysis
of TG or apoC-II which acts as a cofactor for LPL in chylomicrons and VLDL, results in
impaired lipolysis and profound elevations in plasma chylomicrons. These produce
greatly elevated TG concentrations owing to the persistence of chylomicrons in the
circulation. They also have elevations in plasma VLDL. The chylomicrons persist in the
circulation for days which are normally delipidated and removed from the circulation
within 12 h of the last meal. Hence fasting TG levels are almost invariably 1000 mg/dL.
LPL and apoC-II deficiency is usually present in childhood with recurrent acute
pancreatitis. Opalescent retinal blood vessels are (lipemia retinalis) seen. Eruptive
xanthomas, which are small yellowish-white papules, often appear in clusters on the
back, buttocks, and extensor surfaces of the arms and legs. These typically painless skin
lesions may become pruritic as they regress. Hepatosplenomegaly results from the uptake
of circulating chylomicrons by reticuloendothelial cells in the liver and spleen. Some
patients with persistent and pronounced chylomicronemia never develop any of these
symptoms. Premature ASCVD has not been consistently demonstrated to be a feature.
Investigation shows profoundly reduced LPL activity. The presence of chylomicrons
floating like cream on top of fasting plasma suggests this diagnosis
Hepatic Lipase Deficiency is a very rare autosomal recessive disorder due to deficiency
of HL which hydrolyzes TG and phospholipids in remnant lipoproteins and HDL. It is
characterized by elevated plasma cholesterol and TG due to the accumulation of
32
lipoprotein remnants. HDL-C is normal or elevated. The diagnosis is confirmed by
measuring HL activity in post-heparin plasma.
Familial Dysbetalipoproteinemia (Type III Hyperlipoproteinemia or Familial broad
disease) is transmitted as a single gene defect that encodes the structure of Apo E,
causing variations in ApoE which is present in multiple copies on chylomicron and
VLDL remnants and mediates their removal via hepatic lipoprotein receptors.
Interference with its ability to bind lipoprotein receptors, leads to partial catabolism of
VLDL. This is characterized by a mixed hyperlipidemia due to the accumulation of
remnant lipoprotein particles. It is associated with slightly higher LDL-C level. A high-
caloric, high-fat diet, diabetes mellitus, obesity, hypothyroidism, renal disease, estrogen
deficiency, alcohol use, or the presence of another genetic form of hyperlipidemia can
precipitate hyperlipoproteinemia.
Usually presents in adulthood with xanthomas and premature coronary and
peripheral vascular disease. Xanthomas can be as Tuberoeruptive xanthomas which begin
as clusters of small papules on the elbows, knees, or buttocks and can grow to the size of
small grapes or Palmar xanthoma (alternatively called xanthomata striata palmaris) which
are orange-yellow discolorations of the creases in the palms.
Plasma cholesterol and TG are elevated to a relatively similar degree to reach 500
mg/dL The triglycerides tends to be greater than cholesterol later. Premature ASCVD
with severe CAD, PVD and stroke are seen in patients even as early as the third decade of
life.13
FDBL is diagnosed by lipoprotein electrophoresis in which remnant lipoprotein
accumulate in a broad β band. Ratio of VLDL to total plasma TG > 0.30 is consistent
33
with diagnosis of FDBL. Protein methods (apoE phenotyping) or DNA-based methods
(apoE genotyping) can be performed to confirm homozygosity for apoE2. Other
mutations in apoE can also cause this condition.
Familial Hypercholesterolemia (FH) is very rare autosomal co dominant disorder
caused by around 750 mutations in the LDL receptor gene causing no LDL receptors in
the liver. This leads to delayed catabolism of LDL and its precursor particles from the
blood, resulting in increased rates of LDL production. It is characterized by elevated
plasma LDL-C with normal TG. Total cholesterol levels are usually 500 mg/dL - 1000
mg/dL.
Most patients with homozygous FH present in childhood with cutaneous
xanthomas on the hands, wrists, elbows, knees, heels, or buttocks. Arcus cornea is
usually present and some patients have xanthelasmas. Accelerated atherosclerosis is a
devastating complication of homozygous FH and can result in disability and death in
childhood. The diagnosis can be confirmed by obtaining a skin biopsy and measuring
LDL receptor activity in cultured skin fibroblasts or by quantifying the number of LDL
receptors on the surfaces of lymphocytes using cell-sorting technology.
Heterozygous FH caused by the inheritance of one mutant LDL receptor allele
occurs in approximately 1 in 500 persons worldwide, making it one of the most common
single gene disorders. It is characterized by elevated plasma LDL-C 200 to 400 mg/dL
and normal TG levels. They present with hypercholesterolemia from birth, and can be
detected in the cord blood. The disease is often detected in adulthood, on routine
screening, appearance of tendon xanthomas, or the premature development of
symptomatic coronary atherosclerotic disease. Since the disease is codominant in
34
inheritance and has a high penetrance 90% of parent and 50% of the patient’s siblings
are usually hypercholesterolemic. The family history is frequently positive for premature
ASCVD on one side of the family, particularly among male relatives. Corneal arcus is
common, and tendon xanthomas involving the dorsum of the hands, elbows, knees, and
especially the Achilles tendons are present in 75% of patients. FH heterozygotes with
elevated plasma Lp(a)appear to be at greater risk for cardiovascular complications.
Untreated men with heterozygous FH have a 50% chance of having MI before age 60.
Although the age of onset of atherosclerotic heart disease is later in women with FH,
coronary disease is significantly more common in women with FH than in the general
female population. No definitive diagnostic test for heterozygous FH is available.
Familial Defective ApoB-100 (FDB) is a dominantly inherited disorder. As a
consequence of the mutation in LDL receptor–binding domain of apoB-100, LDL binds
the LDL receptor with reduced affinity and is removed from the circulation at a reduced
rate. The disease is characterized by elevated plasma LDL-C levels with normal TG,
tendon xanthomas, and an increased incidence of premature ASCVD.
Autosomal Recessive Hypercholesterolemia (ARH) is a rare disorder due to mutations
in a protein involved in LDL receptor–mediated endocytosis in the liver. Clinically it is
characterized by hypercholesterolemia, tendon xanthomas, and premature CAD.
Wolman Disease is an autosomal recessive disorder caused by complete deficiency of
lysosomal acid lipase. Failure to hydrolyze the neutral lipids, results in their accumulation
within cells. The disease presents within the first weeks of life with hepatosplenomegaly,
steatorrhea, adrenal calcification, and failure to thrive. The disease is usually fatal within
35
the first year of life and can be diagnosed by measuring acid lipase activity in fibroblasts
or liver tissue biopsy specimens
Cholesteryl Ester Storage Disease is a less severe form of genetic disorder in which
there is low, but detectable, acid lipase activity. Patients with this disorder sometimes
present in childhood with hepatomegaly and a mixed hyperlipidemia, due to elevations in
the levels of plasma LDL and VLDL. Other patients present later in life with hepatic
fibrosis, portal hypertension, or with premature atherosclerosis.
Sitosterolemia is a rare autosomal recessive disease caused by mutations in one of two
members of the ATP - binding cassette transporter family. Due to mutation in these genes
the intestinal absorption of plant sterols is increased and biliary excretion of the sterols is
reduced, resulting in increased plasma levels of sitosterol and other plant sterols. Patients
with sitosterolemia can have either normal or elevated plasma levels of cholesterol.
Irrespective of the plasma cholesterol level, these patients develop cutaneous and
tendon xanthomas as well as premature atherosclerosis. Episodes of hemolysis,
presumably secondary to the incorporation of plant sterols into the red blood cell
membrane, are a distinctive clinical feature of this disease. Sitosterolemia is confirmed by
demonstrating an elevated plasma sitosterol level.
Primary disorders of ApoB-containing lipoprotein metabolism (Unknown
etiology)9,13
Familial Hypertriglyceridemia (FHTG,) is a relatively common (1 in 500) autosomal
dominant disorder of unknown etiology. An increased VLDL production, impaired
VLDL catabolism, or a combination of the two causes elevation of VLDL (Type IV
hyperlipoproteinemia). Some patients with FHTG have a more severe form of
36
hyperlipidemia in which both VLDL and chylomicrons are elevated (type V
hyperlipidemia), as these two classes of lipoproteins compete for the same lipolytic
pathway. Increased intake of simple carbohydrates, obesity, insulin resistance, alcohol
use, or estrogen treatment, all of which increase VLDL synthesis, can precipitate the
development of chylomicronemia, severe hypertriglyceridaemia and pancreatitis It is
characterized by moderately elevated plasma TG with more modest elevations in
cholesterol. FHTG does not appear to be associated with increased risk of ASCVD in
many families. Clinically xanthomas are lacking. The diagnosis of FHTG is suggested by
the triad of elevated plasma TG 250 to 1000 mg/dL, normal or only mildly increased
cholesterol levels > 250 mg/ dL, and reduced plasma HDL-C. Plasma LDL-C is
generally not increased and is often reduced due to defective metabolism of the TG-rich
particles. The identification of other first-degree relatives with hypertriglyceridemia is
useful in making the diagnosis.
Familial Combined Hyperlipidemia (FCHL) multiple lipoprotein-type
hyperlipidaemia, It is of an autosomal dominant inherence. The molecular etiology of
FCHL is unknown but is likely to involve defects in several different genes. FCHL is the
most common primary lipid disorder, occurring in approximately 1 in 200 persons.
Approximately 20% of patients who develop CAD before age 60 have FCHL. It is
characterized by moderate elevation of plasma TG and cholesterol and reduced plasma
HDL-C. The affected family members typically have one of three possible phenotypes:
(1) elevated plasma LDL-C, (2) elevated plasma TG and VLDL-C, or (3) elevated plasma
LDL-C and VLDL-C. A classic feature of FCHL is that the lipoprotein phenotype can
switch among these phenotypes with changing patterns of lipids in the blood.
37
FCHL has no typical physical signs. They can manifest in childhood but is
sometimes not fully expressed until adulthood. Visceral obesity, glucose intolerance,
insulin resistance, hypertension, and hyperuricemia are often present. These patients do
not develop xanthomas The levels of apoB are disproportionately high relative to plasma
LDL-C due to the presence of small dense LDL.
A mixed dyslipidemia with plasma TG levels between 200 and 800 mg/dL,
cholesterol levels between 200 and 400 mg/dL, and HDL-C levels >40 mg/dL and a
family history of hyperlipidemia and or premature CAD suggests the diagnosis of FCHL.
An elevated plasma apoB level supports this diagnosis.
Polygenic Hypercholesterolemia This is the most prevalent form of
hypercholesterolaemia. It is characterized by hypercholesterolemia with a normal plasma
TG in the absence of secondary causes of hypercholesterolemia. Only 10% of first-
degree relatives are hypercholesterolemic. Xanthomas are absent.
Genetic disorders of HDL metabolism
Mutations in certain genes encoding critical proteins in HDL synthesis and
catabolism cause marked variations in plasma HDL-C levels. Genetic forms of
hypoalphalipoproteinemia (low HDL-C) are not always associated with accelerated
atherosclerosis.
ApoA-I Deficiency and ApoA-I Mutations is seen with complete genetic deficiency of
apoA-I due to mutations in the apoA-I gene resulting in the virtual absence of HDL from
the plasma. Because apoA-I is required for LCAT function, plasma and tissue levels of
free cholesterol are increased, leading to development of corneal opacities and plantar
38
xanthomas. Clinically apparent coronary atherosclerosis typically appears between the
fourth and seventh decade.
Mutations in the apoA-I gene has low plasma HDL . But are rare. Other than
corneal opacities, most of them have no clinical sequelae. A few specific mutations in
apoA-I cause systemic amyloidosis and the mutant apoA-I has been found as a
component of the amyloid plaque.
Tangier Disease is a rare autosomal codominant form of low plasma HDL-C caused by
mutations in the gene encoding ATP-binding cassette transporter 1 gene (ABCA1), a
cellular transporter that facilitates efflux of unesterified cholesterol and phospholipids
from cells to apoA-I and plays a critical role in the generation and stabilization of the
mature HDL particle. In its absence, HDL is rapidly cleared from the circulation. Patients
with Tangier disease have plasma HDL-C levels < 5 mg/dL and extremely low
circulating levels of apoA-I.
The disease is associated with cholesterol accumulation in the reticuloendothelial
system, resulting in hepatosplenomegaly and pathognomonic enlarged, grayish yellow or
orange tonsils. An intermittent peripheral neuropathy (mononeuritis multiplex) or a
sphingomyelia like neurologic disorder can also be seen in this disorder. Tangier disease
is associated with premature atherosclerotic disease, but the risk is not very high which
may be attributed to the low plasma LDL-C seen in this condition.
LCAT Deficiency is a rare disorder caused by mutations in LCAT enzyme which
mediates the esterification of cholesterol ,the deficiency of which impairs the formation
of mature HDL particles and leads to rapid catabolism of circulating apoA-I causing great
increase in the proportion of free cholesterol in circulating lipoproteins.
39
Progressive corneal opacification due to the deposition of free cholesterol in the
lens, very low plasma HDL-C < 10 mg/dL, and variable hypertriglyceridemia are
characteristic of both complete deficiency (classic LCAT deficiency) and partial
deficiency (fish-eye disease) types. Complete LCAT deficiency is characterized by a
hemolytic anemia and progressive renal insufficiency that eventually leads to end-stage
renal disease. Despite the extremely low plasma levels of HDL-C and apoA-I, premature
ASCVD is not a feature of either complete or partial LCAT deficiency. The diagnosis can
be confirmed by assaying LCAT activity in the plasma.
CETP Deficiency occurs with mutations in the gene encoding CETP which facilitates the
transfer of cholesteryl esters among lipoproteins, especially from HDL to apoB-
containing lipoproteins in exchange for triglycerides causing a high HDL-C condition.
Homozygous deficiency of CETP, results in very high plasma HDL-C > 150 mg/dL due
to accumulation of large, cholesterol-rich HDL particles while heterozygotes for CETP
deficiency have only modestly elevated HDL-C. The relationship of CETP deficiency to
risk of ASCVD remains a matter of debate.
Primary disorders of HDL metabolism 9,11 The gene defect is not known
Primary Hypoalphalipoproteinemia / Familial hypoalphalipoproteinemia is the most
common inherited cause with a low plasma HDL-C level with relatively normal
cholesterol and TG levels. It is an autosomal dominant disease. The metabolic etiology
of this disease appears to be primarily accelerated catabolism of HDL and its
apolipoproteins. Several cases have been described in association with an increased
incidence of premature ASCVD
40
Familial Hyperalphalipoproteinemia Familial hyperalphalipoproteinemia has a
dominant inheritance pattern. Plasma HDL-C is usually > 80 mg/dL in affected women
and > 70 mg/ dL in affected men. The genetic basis of primary
hyperalphalipoproteinemia is not known, and the condition may be associated with
decreased risk of CAD.
Secondary disorders of lipoprotein metabolism9, 11
Significant changes in plasma levels of lipoproteins are seen in a variety of
diseases. These constitute the vast majority of cases with hyperlipidaemia met in clinical
practice.
Change-over to modern low-fibre, high-fat and refined carbohydrate diet is
probably the major cause for the high prevalence of Type IV and Type IIb
hyperlipidaemias seen in urban societies of India which are highly atherogenic and thus
are considered as the first reversible risk factor of ASCVD. Dietary control of fat intake
along with n-3FA supplementations is necessary to alleviate this type of
hyperlipidaemia.13
Obesity is frequently, though not invariably, accompanied by hyperlipidemia. The
increase in adipocyte mass and accompanying decrease in insulin sensitivity associated
with obesity have multiple effects on lipid metabolism. More free FA are delivered from
the expanded adipose tissue to the liver where they are re-esterified in hepatocytes to
form TG, which are packaged into VLDL for secretion into the circulation. High dietary
intake of simple carbohydrates also drives hepatic production of VLDL, leading to
increases in VLDL and or LDL in some obese individuals. Plasma HDL-C tends to be
41
low in obesity. Weight loss is often associated with a reduction of plasma apoB-
containing lipoproteins and an increase of plasma HDL-C.
Diabetes Mellitus Patients with type 1 diabetes mellitus are generally not hyperlipidemic
if they are under good glycemic control. Diabetic ketoacidosis is frequently accompanied
by hypertriglyceridemia due to increased hepatic influx of free FA from adipose tissue.
The hypertriglyceridemia responds dramatically to administration of insulin.
Patients with type 2 diabetes mellitus are usually dyslipidemic, even if under
relatively good glycemic control. The high levels of insulin and insulin resistance
associated with type 2 diabetes causes (1) a decrease in LPL activity resulting in reduced
catabolism of chylomicrons and VLDL, (2) an increase in the release of free FA from the
adipose tissue, (3) an increase in FA synthesis in the liver, and (4) an increase in hepatic
VLDL production. They have several lipid abnormalities, including elevated plasma TG
(due to increased VLDL and lipoprotein remnants), elevated dense LDL, and decreased
HDL-C. In some diabetic patients, especially those with a genetic defect in lipid
metabolism, the TG can be extremely elevated. Elevated plasma LDL-C level in diabetic
indicate the development of diabetic nephropathy. Patients with lipodystrophy, who have
profound insulin resistance, have markedly elevated VLDL and chylomicrons.
Thyroid Disease Hypothyroidism is associated with elevated plasma LDL-C primarily
due to a reduction in hepatic LDL receptor function and delayed clearance of LDL.
Thyroxin has a permissive role in stimulating the key enzymes like LPL and LCAT in
circulation. Therefore in patients with hypothyroidism there is decreased catabolism of
VLDL and IDL which causes accumulation of cholesterol and TG in circulation, having
an increased circulating IDL. Some are mildly hypertriglyceridemic > 300 mg/dL. Type
42
IIa and sometimes Type IIb with lower levels of HDL2 is the dyslipidaemia seen in
untreated patients with hypothyroidism. The profile is highly atherogenic.13
Renal Disorders Nephrotic syndrome is associated with hyperlipoproteinemia, which is
usually mixed but can manifest as hypercholesterolemia or hypertriglyceridemia alone. It
appears to be due to a combination of increased hepatic production and decreased
clearance of VLDL, with increased LDL production.
TG lipolysis and remnant clearance are both reduced in patients with renal
failure. Patients with renal transplants are usually hyperlipidemic due to
immunosuppression drugs
Liver Disorders: Liver being the principal site of formation and clearance of
lipoproteins, liver diseases can profoundly affect plasma lipid levels in a variety of ways.
Hepatitis due to infection, drugs, or alcohol is often associated with increased VLDL
synthesis and mild to moderate hypertriglyceridemia. Cholestasis is associated with
hypercholesterolemia as it blocks the major excretory pathway by which cholesterol is
excreted.But in chronic liver disease an abnormal lipoprotein is synthesised and secreted
by the liver, called lipoprotein X, over and above diversion of cholesterol to the systemic
circulation, producing a peculiar type of hypercholesterolaemia. However, in acute liver
cell failure, there is decreased synthesis of LCAT and so slower catabolism of VLDL
producing Type IV hyperlipidaemia.13
Severe hepatitis and liver failure are associated with dramatic reductions in
plasma cholesterol and TG due to reduced lipoprotein biosynthetic capacity.
Alcohol: Regular alcohol consumption has a variable effect on plasma lipid levels. The
most common effect of alcohol is to increase plasma TG levels. Excess of alcohol intake
43
induces FA synthesis in the liver causing suppression of FA oxidation. Excess of free FA
combines with glycerol and thus excess of VLDL is secreted. Further, there is also slower
degradation of Chylomicron and so Type V hyperlipidaemia occurs in these patients.13
The usual lipoprotein pattern seen with alcohol consumption is type IV (increased
VLDL), but persons with an underlying primary lipid disorder may develop severe
hypertriglyceridemia (type V) if they drink alcohol. Regular alcohol use is also associated
with a mild to moderate increase in plasma levels of HDL-C
Glycogen Storage Diseases Other rarer causes of secondary hyperlipidemias include
glycogen storage diseases such as von Gierke’s disease, which is caused by mutations in
glucose-6-phosphatase. The inability to mobilize hepatic glucose during fasting results in
hypoinsulinemia and increased release of free FA from adipose tissue. Hepatic FA
synthesis is also increased, resulting in fat accumulation in the liver and increased VLDL
secretion. The hyperlipidemia associated with this disease can be very severe
Autoimmune diseases (SLE, dysglobulinaemias) produce autoantibodies which form
complexes with either the enzymes like LPL or with the Apo of the circulating
lipoprotein and slows down their catabolism, producing varieties of dyslipidaemias.13
Cushing Syndrome: Glucocorticoid excess is associated with increased VLDL synthesis
and hypertriglyceridemia causing mild elevations in plasma LDL-C in Cushing
Syndrome.
Drugs A variety of drugs have been identified to interfere with lipid metabolism either
directly or indirectly and cause dyslipidaemias. The most important are the oestrogen-
containing OCP which can enhance VLDL production from liver and produce
hypertriglyceridaemia This problem gets aggravated if the woman has some undetected
metabolic, hormonal or genetic defect related to lipid metabolism.13
44
MANAGEMENT OF HYPERLIPIDEMIA
Early detection and early control of high cholesterol in a person is an important
step in reducing the development and progression of coronary heart disease and
atherosclerosis. Lowering plasma cholesterol by diet and drugs slows and may even
reverse the progression of atherosclerotic lesions and the complications they cause
The demonstration that lipid-lowering therapy significantly reduces the clinical
complications of ASCVD has brought the diagnosis and treatment of these disorders
into the domain of the general internist. The metabolic consequences associated with
changes in diet and lifestyle have increased the number of hyperlipidemic individuals
who could benefit from lipid-lowering therapy.13 Most patients with hyperlipidaemia are
asymptomatic and have no clinical signs. Many are discovered during the screening of
high-risk individuals 11
Guidelines for the screening and management of lipid disorders have been
provided by an expert Adult Treatment Panel (ATP) convened by the National
Cholesterol Education Program (NCEP) of the National Heart Lung and Blood Institute.
The NCEP ATPIII guidelines published in 2001 recommend that all adults over age 20
have plasma levels of cholesterol, TG, LDL-C, and HDL-C measured after a 12-hr
overnight fast.9
Selective screening of people at high risk of cardiovascular disease should be
undertaken, to include those with:
A family history of coronary heart disease (especially below 50 years of age)
A family history of lipid disorders
The presence of a xanthoma
45
The presence of xanthelasma or corneal arcus before the age of 40 years
Obesity
Diabetes mellitus
Hypertension
Acute pancreatitis
Those undergoing renal replacement therapy
Serum cholesterol concentration does not change significantly after a meal and as
a screening test, a random blood sample is sufficient. If the total cholesterol concentration
is raised, HDL cholesterol, TG, and LDL cholesterol concentrations should be quantitated
on a fasting sample. If a test for hypertriglyceridaemia is needed, a fasting blood sample
is mandatory 11
Multiple epidemiologic studies have demonstrated a strong relationship between
serum cholesterol and CAD. Randomized controlled clinical trials have unequivocally
documented that lowering plasma cholesterol reduces the risk of clinical events due to
atherosclerosis. Since both hypertriglyceridemia and low plasma levels of HDL-C confer
higher ASCVD risk, the NCEP ATPIII recommends more aggressive therapy to lower
the plasma LDL-C in patients with these dyslipidemias.9
Hyperlipidaemia results from genetic predisposition interacting with an
individual's diet.11 Studies show the role of the environment rather than the genetic make-
up of a population. Data from The Multiple Risk Factor Intervention Trial (MRFIT) have
shown that although cardiovascular risk rises progressively as total cholesterol
concentration increases the risk increase is modest for individuals with no other
46
cardiovascular risk factors. With each additional risk factor the effect produced by the
same difference in cholesterol concentration becomes greatly magnified.11
Reference values 14,15
Normal values vary with age, diet, sex and geographic regime.
Recommended levels of lipoproteins in Indian population are :
Total cholesterol : <200mg/dL
HDL cholesterol : >40mg/dL
Triglycerides : <150mg/dL
LDL cholesterol : <130mg/dL
TC/HDL Ratio : <3.0 indicates low risk,3.0-5.0 indicates high risk.
LDL/HDL Ratio : 1.5-3.5mg/dL
Nonpharmacologic Treatment 11,13
Therapeutic Lifestyle Changes (TLC) includes a cholesterol-lowering diet (TLC diet),
physical activity, and weight management for anyone whose LDL is above goal.
Dietary and life-style intervention
Studies have reported only modest cholesterol lowering benefits of diet therapy.
The effect of diet therapy varies among individuals. Some have striking reduction in LDL
upto 25 – 30% whereas others will have clinically important increase. Moreover diets
very low in total fat or in saturated fat may lower HDL as much as LDL. Low fat, high
carbohydrate diet may result in reduction in HDL.
Still diet control is the cornerstone of therapy in the management of
hyperlipidaemias. Modification of life-style, which includes food habits, cessation of
47
smoking, cutting down alcoholic beverages, weight control and regular exercises, is not
only necessary to attain eulipaemia but is the first step in the management of
hyperlipidaemias.
Frequent snacks and canned or commercially available precooked food (junk
food) should be abandoned as they are rich in fats and cream as well as refined
carbohydrates.
Alcohol supplies empty calories; its intake should be restricted to social purposes
in a patient with dyslipidaemia and in others should not exceed 30 g/day
. Dietary protein should be such that its fat content is low, viz., dried beans, peas
and pulses, chicken-breast, lean meat, low-fat dairy products and game birds and animals.
The diet should contain adequate amount of natural soluble fibres derived from
oats and barley, certain fruits such as oranges apples,and pears and vegetables such as
brussels sprouts and carrots.13,16
Substitution of saturated fat with monounsaturates and polyunsaturates
Most polyunsaturated fats come from vegetable oils, whereas most saturated fat
comes from meat and dairy products. Monounsaturated oils, particularly olive oil, and
polyunsaturated oils such as sunflower, safflower, corn and soya oil, should be used
instead of saturated fat-rich alternatives. Hydrogenation increases saturation and adds
trans FA which are as bad as saturated fat. Turkey breast and chicken breast are literally
free of cholesterol as soon as the skin is removed.11,17
Reduce the dietary cholesterol intake. Liver, offal and fish roes should be avoided.
Although eggs and prawns are rich in cholesterol their total contribution to the body's
cholesterol pool is small and they can still be part of a balanced lipid-lowering diet.11
48
In the hypercholesterolemic patient, dietary saturated fat and cholesterol should be
restricted. Dairy products and meat are the principal sources of saturated fat in the diet.
Fish and poultry with fat and skin removed should be substituted for this. Meat products
including sausages and reconstituted meats should be avoided since the concentration of
fat is unknown and often high. Baking and grilling of meats reduces the fat content and is
preferred to frying. Do not add fat in the cooking and serving process. Low-fat or cottage
cheese and skimmed or semi-skimmed milk should be substituted for the standard full-fat
varieties. Pastries and cakes contain large quantities of fat and should be avoided.
Similarly, refined carbohydrates like maida and maida preparations should be avoided
while carbohydrates with high-fibre content are preferred.11
Certain foods and dietary additives are associated with modest reductions in
plasma cholesterol levels. Plant stanol and sterol interfere with cholesterol absorption
from the intestine by competing for space in the micelles that deliver lipid to the mucosal
cells of the gut. and reduce plasma LDL-C levels by 10 to 15% when taken three times
per day. They are largely unabsorbed and excreted in the stool.9
For patients who are hypertriglyceridemic, the intake of simple sugars should
also be curtailed. For severe hypertriglyceridemic restriction of total fat intake is critical.
The most widely used diet to lower the LDL-C level is the “Step 1 diet”
developed by the American Heart Association. Most patients have a relatively modest
(10%) decrease in plasma levels of LDL-C on a step I diet in the absence of any
associated weight loss. In this diet no more than 30% of total calorie is provided by fat
and less than 10% of total calories is provided by saturated fat. Monounsaturated fats
should contribute 10% to 15% and polyunsaturated fats should contribute 10% or less of
49
the total daily energy intake. Cholesterol intake should be less than 300 mg/dl. Further
reduction in fat intake is unacceptable to many patients. 9
Weight loss and exercise: The treatment of obesity, if present, can have a
favorable impact on plasma lipid levels. Plasma TG and LDL levels tend to fall and
HDL levels tend to increase in obese persons who lose weight. Aerobic exercise has a
very modest elevating effect on plasma levels of HDLC. Gradual reduction protocols
along with dietary restrictions have to be implemented to achieve an ideal bodyweight13
A reduced fat diet, which is more realistic, only affects those levels if
accompanied by weight loss. Cutting fat without losing weight actually increase TG
levels and decrease HDL.18 Eating more calories than body needs, whether from fat or
carbohydrates, will be stored as fat. Hence the aim should be to lower total calorie intake
than total fat intake.19
Eating small amounts of fat can keep from overindulging on total calories.
Dietary fat causes our bodies to produce a hormone that tells intestines to slow down the
emptying process so that fullness is felt and are less likely to overeat.20 Moreover without
some fat in the diets, body could not make nerve cells and hormones or absorb fat soluble
vitamins. In any type of secondary hyperlipidaemia, the primary care envisages
correction of the underlying cause which has induced hyperlipidaemia.
50
Fig. 9: Diet pyramid 21
Natural sources reducing hyperlipidemia 18,20
Along with getting plenty of fiber, there are foods that will help in promoting the
lowering of cholesterol as well as herbs that can further reduce cholesterol.
Carrots, apples and the white layer inside of citrus rinds containing pectin are
advantageous to lowering cholesterol levels
Avocado, which is very high in fat, has unexpectedly become a cholesterol reducer
Beans are high in fiber and low in cholesterol
51
Garlic and onions in daily diet lower cholesterol and is also credited with lowering
blood pressure.
Cayenne pepper (Capsicum minimum) and other plants that contain the phenolic
compound capsaicin have a well demonstrated effect in lowering blood cholesterol levels,
as does the widely used spice Fenugreek.
Caraway is another aromatic spice with demonstrable cholesterol lowering properties.
Strawberry reduces oxidative damage to LDL while mainaining reduction in blood
lipids.
Soyaprotein decreases total cholesterol, LDL and Triglycerides
Green leafy vegetables, pulses, legumes, root vegetables, and unprocessed ereals,
help reduce circulating lipid concentrations.
Olive oil contains polyunsaturated fats that help to lower LDL levels while increasing
levels of HDL, or "good" cholesterol.
Nuts such as walnuts, almonds, hazelnuts and pistachios have polyunsaturated fatty acids
prominently, which can reduce blood cholesterol levels.
Chinese red yeast rice (which contains lovastatin) can have modest cholesterol-lowering
effects.
Polyphenolic substance derived from cocoa powder contribute to reduction in LDL and
elevation in HDL and suppression of oxidized LDL and thereby reduces atherogenesis
Peanut and peanut butter lowers cholesterol and reduces CHD risk
Flavonoid rich dark chocolate has beneficial effect on endothelial function
Cinnamon has blood-thinning properties that can help lower cholesterol levels
52
Marine fish oils containing long chain omega – 3 FA eicosapentaenoic acid ( EPA ) and
docosahexaenoic acid ( DHA ) have potential role in reducing plasma levels of
cholesterol and TG and thereby reducing incidence of CAD . Fatty fish, such as salmon,
tuna and mackerel, is an excellent source of omega-3 FA, and the American Heart
Association recommends getting at least two servings of fatty fish each week for
cholesterol management and general heart health.
Flaxseed and canola oil also contain some omega-3 fatty acid
Fig. 10: Natural sources reducing hyperlipidemia 19,20,21,22
53
UNDERSTANDING OF MIASM
§78 “The true natural chronic diseases are those that arise from a chronic miasm,
which when left to themselves, and unchecked by the employment of those remedies that
are specific for them, always go on increasing and growing worse, notwithstanding the
best mental and corporeal regimen, and torment the patient to the end of his life with ever
aggravated sufferings. These are the most numerous and greatest scourges of the human
race; for the most robust constitution, the best regulated mode of living and the most
vigorous energy of the vital force are insufficient for their eradication”23
Hyperlipidemia belongs to the true natural chronic disease as specified by
Hahnemann in §78 where even the best regulated mode of living with diet therapy and
weight loss may not reduce the disease symptom which is presented as only a rise in
serum lipid level unless complicated. Literature itself says that studies have reported only
modest cholesterol lowering benefits by diet therapy, the effect of which varies among
individuals.
In “The chronic diseases” Hahnemann says - “All chronic diseases of mankind,
even those left to themselves, not aggravated by a perverted treatment, show, as said,
such a constancy and perseverance, that as soon as they have developed and have not
been thoroughly healed by the medical art, they evermore increase with the years, and
during the whole of man's lifetime; and they cannot be diminished by the strength
belonging even to the most robust constitution. Still less can they be overcome and
extinguished. Thus they never pass away of themselves, but increase and are aggravated
even till death. They must therefore all have for their origin and foundation constant
54
chronic miasms, whereby their parasitical existence in the human organism is enabled to
continually rise and grow”.24
A constitutional remedy which includes the chronic miasm becomes the right
antimiasmatic remedy to expel this potentiality of the individual affected unfavourably by
certain stigmata which result from either hereditary factors (inherited) or previous
indiscretion of the patient (acquired). An evaluation of the predisposing miasm of the
individual, paves the path to select the right antimiasmatic remedy, the administration of
which not only relieves him of his disease but also prevents the predisposition to the
miasmatic tendency.25
Hence hyperlipidemia which is a true natural chronic disease requires an
antimiasmatic remedy for the true anhilation of the disease besides the diet and lifestyle
management.
In the “Organon of Medicine” Samuel Hahnemann separated the origin of disease
into two categories, the exciting and fundamental causes, and related them very closely to
the susceptibility of the physical constitution.
§5 says “Useful to the physician in assisting him to cure are the particulars of the
most probable exciting cause of the acute disease as well as the most significant points in
the complete history of the chronic disease, to enable him to discover its fundamental
cause, which is generally due to a chronic miasm. In these investigations, the
ascertainable physical constitution of the patient (especially when the disease is chronic),
his moral and intellectual character, his occupation, mode of living and habits, his social
and domestic relations, his age, sexual function, etc., are to be taken into
consideration.”26
55
Hahnemann taught that the susceptibility to the exciting factors lies in the
fundamental cause which is attributed to the chronic miasms.27 Thus it resolves itself into
the fact that the only and supreme influence which determines its action and its
development in any human being is an inheritance of the above mentioned chronic
miasms the effects of which are passed from one generation to the next and caused
predispositions to certain disease syndromes. This invisible potentiality in some form is
imposed upon the life of every unborn child in some degree,often to such an extent as to
destroy the new life or drive it from its living house by its invisible expelling powers. 25
Since the dawn of medical history there has been a constant search for the causes
of the acute and chronic diseases that afflict humanity. This quest made great advances
when the ancient Greek physician, Hippocrates, taught that all diseases were caused by
the predisposition inherent in the innate constitution and its susceptibility to a
constellation of causation rather than any one single effect. In the Greek philosophy
disease is caused by an interdependent set of circumstances which disrupts the natural
ebb and flow of the pneuma (vital force) within the organism. Hahnemann’s pathology is
based on dynamical theory of disease i.e. Disease is primarily a morbid dynamic
functional disturbance of vital principle 27
Disease is nothing more than changes in the general state of the human economy,
which declare themselves as symptoms; or, in other words; disease is but the influence of
some subversive force, acting in conjunction with the life force, subverting the action and
changing the physiological momentum. It is a modified mode of motion, a vibratory
change. The suffering of the immaterial vital principle which animates the interior of our
bodies, when morbidly disturbed, produces symptoms in the organism that are manifest
56
and these morbidly produced symptoms constitute what is known as disease in all its
multiplied forms, whether functional or structural.25
The father, then, we say, of all sickness of whatever nature it may be, is, directly
or indirectly, a subversive force whose action is co-existent with the life force. Therefore,
through this co-existent action we may have any conceivable anatomical, physiological or
histological imperfection which manifest as mental, moral or even spiritual
imperfection.28
The chief feature in pathology is a constant factor in all persons attacked by the
same malady, which has furnished the name of said malady. Yet there is a characteristic
difference in each individual case that gives it its individuality, causing it to differ from
all other cases. The symptoms vary according to the peculiarity of the individual's
original constitution, his hereditary predisposition, the different faults of his education
and his habits, his mode of life and diet, his occupations, his mental pursuits, his
morality, etc. No lesion or pathological condition is the first cause of any disease, for the
disease process precedes them all, and the true cause always lies in the disturbed or
distressed life force itself.25
The natural tendency of life force, is to assert itself & thus restore the state to
harmony. The disease is held back often by that natural physiological resistance that each
organism is endowed with and other conditions favorable to the development of health
and strength such as physical training, climate, diet, fresh air, etc. It is the same
stupendous potentiality that gives the wonderful manifestations in life, so in disease. Here
the life potential combines with the miasmatic potential Thus in chronic diseases vital
force was impeded by miasms & natural process of recovery & cure were interfered The
57
tendency of the disease in these patients was to progress relentlessly and leads to chronic
relapsing states of ill health difficult to cure.30
Hahnemann sought an explanation for the frequent relapses he observed in certain
patients with chronic complaints whom he treated according to his system To him it
gradually became clear that such chronic conditions cannot be cured by the vital force
alone, nor by any manipulation of diet or life habits. He then launched into exhaustive
inquiries of all such chronic cases to see if any common denominator could be found to
explain the deep & invisible weakness which predisposed to their chronic condition – A
weakness which Hahnemann termed miasm. These weakness were transmitted from one
generation to next according to his investigations which included whenever possible,
interviews with the ancestors of chronic disease patients. All these observations were
published in “The chronic diseases” 3300
The word “Miasm”originated from Greek word “Miasma” which is derived from
“Miasmatos” from “Miainien” meaning stain, pollution, defilement.31 Term “Miasm”
was employed by him to indicate a defect in the constitution which interfered with the
process of recovery & cure.30 Miasms are states or conditions which pollutes the human
organism with unhealthy tendencies which when taken into the organism, may set up a
specific disease. They are dynamic disease producing powers or an invisible polluting
substance which once it gains entrance, overpowers the Vital force & pollutes the whole
system producing true natural chronic diseases & predispose human beings to acute
disease which can only be known through their actions & functions 32. Each miasm
creates a weakness or a tendency to a particular group of disease. If not eradicated with a
suitable antimiasmatic remedy, it will persist through out the patient’s life & can be
58
transmitted to others especially to children. Kent called it predisposition, a state,
dyscrasia or diathesis.32 It acts by prolonging the disease and or by obstructing the
process of cure, even though a true similimum has been prescribed. Chronic miasms are
thus the fundamental causes of diseases and the diseases caused by them are the effects.31
The new phenomena, or that which is supposed to be new disease, is nothing
more than the daily workings of the miasm, or the further development of miasmatic
action, the forward movement of a perverted life action, a miasmatic revelation of that
unknown force. Idiosyncrasy, dyscrasia, predisposition, and even certain forms of
temperament are all climaxes of perversion or change, and stand forth as the finished
work within the organism of the action of chronic miasm. The nature and character of the
disease depends wholly on the form of the miasm and the character of the bond with the
life; therefore, the study of disease becomes a study into the nature of the miasm present
in the organism and the degree of its activity. The true pathognomonic symptoms of a
given case are those that cover the existing active miasm. In this way our therapeutic
grouping becomes a miasmatic one and not a pathological one 25
Hahnemann observed them in greater detail, classified them, in three broad
groups with definite attribute & predisposition. He observed a close association between
these groups & the diseases of itch, syphilis & gonorrhoea which were rampant in those
times. A detailed clinical study of these patients enabled him to describe in detail the
characteristic symptoms of these groups & also indicate their disease potentials. He
evolved a similar grouping of remedies which helped in curing them. Thus he classified
the drugs in Materia medica also into three like groups employing the same attributes.
Understanding the innate constitution is fundamental to homoeopathic treatment because
59
it holds the keys to an individual's susceptibility as well as the inherited effects of the
chronic miasms. On the basis of law of similars, he directed physician to ensure that the
selected remedy belonged to similar group.30
The diseases are built accordingly on four different plans – Occupational / drug
disease, Psora, sycosis & syphilis.
In all human beings we will find a portion of all three pathological characteristics.
Yet one will always be dominant, preponderant, modulating & determining more strongly
the biological structures as well as those of soul &character – Dominant miasm.
Characteristic guiding symptoms from present condition of patient is linked with
earlier development depicted in past history & family history – Fundamental miasm.29
The term “Psora” originated from Hebrew word “Tsorat” meaning “A groove”, “a
fault”, “a pollution”, “a stigma”, an itch derived from Latin & Greek. It is a condition of
man, a condition that favours diseases.31
The term “Sycosis” came from the Greek word “Fig”. Hahnemann’s term for
constitutional effects of gonorrhoea primarily manifested by condylomatous or
cauliflower like growth on skin. Morbid conditions developed as a result of suppressed
chronic gonorrhoea, inherited gonorroeal poison or repeated vaccination. produces a
chronic miasmatic state, sycosis.31
Syphilis is the constitutional state engendering perversion which includes
destruction degeneration and aggressiveness.31
Tubercular miasm or pseudopsora denotes combination of hereditary taints of
psora & syphilis.31
60
The life force is in the pathological business and is prepared to manufacture any
pathological formation depending upon the nature of the internal exciting or acting
miasm. If the miasm be psoric we have psoric manifestations. If it be sycotic, we have
sycotic pathology; and if syphilitic, we have the polymorphic pathological presentations
of that miasm; or, if we have the miasm syphilis and psora combined, we have the
multiplied changes and infinite destructive processes known as tubercular pathology. The
disturbances are in accordance with the existing active miasm, modified by previous
heredity or miasmatic states of the organism.25
Miasms have always separate entity. They cannot be mixed together.
Manifestation of a disease are generally limited to one miasm at a time Only the
miasmatic states of different miasms may intermingle. These are mixed miasmatic
states.31
Some of the most complicated disease, difficult to cure, represent the combination
of all three miasms. Any structural change occurs only when other miasms supervene on
psoric base. In such a combination, the propensity to the development of disease is
enhanced considerably. And it is here that a simple cause becomes a complex thing,
difficult to understand or analyze, as new coloring is given to the symptomatology, as
well as to the pathological groupings, as they partake in part of the nature of the
combined miasms. It is dreadful to contemplate such a condition of things as is present on
the earth today. Almost every man is polluted with this disease; and it is more difficult to
cure diseases at the present time where the physicians resort to palliatives and
suppressive measures. The study of these cases is difficult. But it is greatly simplified by
a thorough knowledge and understanding of the miasms.29
61
The three miasms represent three broad constitutional types which indicate
different susceptibilities to the development of illness. A detailed study in three planes –
emotional, intellectual & physical enables us to identify the miasm responsible for
illness.29
The physical signs of a person are fundamental to the treatment of chronic
disorders because the constitution and temperament shows the effects of the inherited
miasms. We must get beyond relying solely on the personal or family history to uncover
miasms. The miasms are present in the very symptomatology of the client. The
syndromes produced by the miasms point to the fundamental cause even if it cannot be
traced in the case taking to a specific etiological factor.27
Each of the chronic miasms have their own characteristic signs that are an integral
part of the totality of the symptoms. The reality of miasm in a patient is always expressed
by signs & symptoms the patient produces which permit the individual expression of
characteristics of miasm which allow to determine, recognize & wholly handle the patient
individuality It is these symptom pictures that clue the homoeopath into which miasms
are present within the constitution of the individual. Thus the etiology points to the
symptoms and the symptoms point to the etiology. This is how the homoeopath
understands which miasmic layers are dormant, latent and active. All of these factors
point to the proper anti-miasmic remedies.29
H. C. Allen in his classic, ‘The Chronic Miasms’ says “You cannot follow the
evolution of the curative process; you cannot even prescribe intelligently the proper diet
for a patient, unless you know the basic miasm. Of course the diseases that are present
62
will help you to some extent, but you have no surety unless you know the underlying
basic disturber of the disordered life” 27
We can not select the most similar remedy possible unless the phenomena of the
acting and basic miasms is understood; for the true similar is always based upon the
existing basic miasms, whether we be conscious or unconscious of the fact. The curative
remedy is but the pathopoesis of a certain pathogenesis of an existing miasm.32
The progress of a case cannot be watched without a definite knowledge of these
disease forces (miasms), with their mysterious, but persistent, progressions, pauses, rests,
forward movements, retreats and attacks along unfamiliar lines, and of whose multiplied
modes of action we have taken no cognizance. If we become acquainted with the
character of miasm, their history and action upon the life of the organism, we are able to
follow these processes and able to give a prognosis as to the probable outcome in a given
case of disease; for the character of the miasm gives us the character of the affection of
the disease formula. In that way we are able to head off the new developments and new
processes that come upon unexpectedly.29
Miasmatic theory could be considered the true genetic theory, since miasm are
transmitted to children. Children inherit from each parent particular sensitivities in
particular organs & the resulting disorder in the child is either an accurate copy of one
parent’s disorder or a compounding of disorders inherited from both the parents. It also
provides something analogous genetic therapy, since the inherited miasm can be treated
& the genetic transmission halted protecting future generations.32
When the miasms are latent the symptoms are mainly transient. But as the miasm
becomes active, it produces constant, more serious symptoms which effect the vital force
63
more profoundly. Using Hahnemann’s powerful theory we can treat a miasmatic state
before pathology emerges & we can prevent the transmission of parent’s susceptibility to
children. This is true preventive medicine.32
Miasmatic trump cards are the best to prove supremacy of homoeopathy among
other methods of treatment in chronic & incurable illness with a stamp of unknown
cause(s). For better generation we have to study chronic miasms & treat the people
homoeopathically. We can study miasmatic medicines to improve future generation
through a long course of treatment. With homoeopathic knowledge & understanding
miasmatic disease we can improve mentally & physically near & dear relatives
Find the chronic miasms, treat them well & let us live in peace & harmony 33
True homeopathy can be likened to organic gardening, where a weak soil is
carefully tended and strengthened so that its fruits will proliferate with vitality and in
such a way that weeds, bugs, and blights, etc. are discouraged.
MIASMATIC CLEAVAGE OF HYPERLIPIDEMIA
The miasms are destructive in every way, of both mind and body and they tear at
the very spirit of man. It is disorganizing disease that fills the state and we cannot meet
these conditions intelligently until we recognize the ancient origin of disease and
undertake its extermination on the basis of miasm.
The environmental factors, may be the causative modalities or maintaining cause
which modifies disease response in its progression from psora to syphilis. A critical
analysis of these response and final resultant expressed at different levels of organization
and areas leads to the four categories of constitution with distinct predisposition to the
64
development of characteristic disease response. This division, first attempted by
Hahnemann was modified in the light of clinical experience and re interpreted in the light
of present day understanding of ramification and expression, internal as well as external
of disease. The Hanemanian totality is an evolutionary one spreading itself in space
through the four miasmatic expressions.29
A number of progressive as well as increasing abnormalities in the biochemic
balance of the system are produced by the onward slaught of disease, leaving the system
progressively vulnerable to further damage. By a study of the physiological function
along with correlates from biochemistry, these various mechanisms are understood and
their implications in terms of cellular susceptibility and sensitivity is essential for
understanding of the totality of functions of the entire system.29
Concepts of general and special pathology when carefully correlated with the
clinical evolution and expression of the disease gives clinically useful standard of time
which can be correlated with the operations of environmental factors. It is possible to
correlate and interpret all these observations in relation to Hahnemmanian theory of
miasms and dyscrasia which can be generalized as time expression. It allows to evolve a
continuous specific spectrum – Constitution (Normality) - Diathesis - Prodrome -
Psora Sycosis - Tubercular - Syphilis.29
An alert observation is required in a fast moving clinical situation and to interpret
the totality furnishing the requisite guidance correctly in terms of miasmatic
interpretation. Constitutional homoeopathic prescribing will demand the use of a diverse
type from various lab investigations, clinicopathological as well as radiological.29
65
From the natural pathological evolution of hyperlipidemia, it is evident that
though initially the only symptom is raised serum lipid profile, with time, it leads to an
end stage of vascular complications causing widespread destruction of several systems of
the body including vital organs.
An increased parasympathetic tone leads to an overall decrease in the activity of
the endocrines which is reflected in an increase in the anabolic process and decrease in
the catabolism, a reduction in the overall turnover, retention, accumulation of cholesterol,
aberration in lipid metabolism leading to deposits of cholesterol and lipoprotein in the
wall of blood vessels causing narrowing of the vessels.29
Properly applied constitutional treatment in the process of cure should not
terminate at the disappearance of presenting symptoms but extend further towards the
idealistic point of positive health by the removal of entire abnormal susceptibility so that
all tendency to recurrence is eliminated.
Constitution results from the interaction between genetic factors and the
environmental factors to give its peculiar reactivities to the environmental circumstances
which tend to drive ahead the individual in a characteristic manner unfolding a tendency
to favour expression favouring one miasm over the rest.29
Hahnemann directs that the similarity be established at the level of disease (§ 6 )
taking into account the qualitative characteristics along with causation, inclusive of
hereditary and predispositions utilizing signs and symptoms as the only discernible
evidence of the totality of expression of the disorder within the phenomena of the
disease.34
66
Miasmatic study of a disease can be assessed by taking into account in a
meticulous manner, the full details of the troubles experienced by the patient inclusive of
various treatments administered, its suppressive effects which must have lead to the
consequence of a protracted state of ill health, continued to attract noxious environmental
influences to produce a complex diseased state.29,35
Observations leads us to the concept of the fundamental miasm indicated by
family history of disease as well as the personal past history as the hereditary, genetic
predisposition is reinforced by the past illness. The dominant miasm is deduced from the
prominent expressions of disease at the time of observation.29,36
The clinical investigation should clearly incorporate the time dimension in all its
aspects and the expression (subjective or objective) demarcated fully with location,
sensation, modalities and concomitant and origin, duration and progress with reference to
the levels of intelligence, emotional and physical, as well as areas ( tissue, organ or
system) along with environment factors (work, family and social circle). Only then the
miasmatic expressions and the dynamic background of the patient can be appreciated. 29
Thereby the miasmatic basis of the hyperlipidemia, which do not express any
clinical symptom of the disease other than a rise in the serum lipid levels, unless
complicated is studied through ,Family and Past history, Causation, Mental generals,
Physical generals, Pathological stage of disease and Symptomatology of the disease
67
Table 2: Miasmatic evaluation criteria 24,26, 29,31,38,39
Psora / Sensitising Sycotic / Constructive / Inco ordination
Tubercular / Reactive Syphilitic / destructive
Mental Generals
Anxiety. Fear. Restless. Nervous. Irritable. Timid. Perversion. Tendency to commit evil. No deep mental concentration / sacred thoughts. Hyporeasoning. Impractical thoughts. Hypoconfidence. Philosopher. Builds castles in air. Indolent. Aversion to work ,bath, keep things clean. Untidy. Lack of discipline. Time passés too fast/ too slow Repugnance to & fatigue on mental & physical exertion. Wants to lie down. Sensitive to odour.
Suspicious. Jealousy. Tendency to harm / exploit others. Hyperworkoholics. Hypergreedy. Cross. Irritable. No spiritual outlook, not influenced by moral doctrine or religion. Insanity. Inclined to commit crime. Mischevous, Bent upon misdeeds. Born criminal. Revengeful, devoid of all sense of rhiteousness. Thinks of their own ailment. Suppress ailments / symptoms. Brooding over things. Self condemnation. Fixed ideas. Lack of self confidence. Suicidal tendency with proper cause.
Dissatisfaction. Lack of tolerance. Changeable. Anger. Irritable. Quarrelsome. Crave & perversions for things that will harm them. Indifferent. Unconcerned about his sufferings. Hopeful of recovery. Willing to take risks & undertake ventures.
Destructive. Cannot explain his symptoms. Lack of self confidence. Keeps dippression to himself. Dull. Stupid. Idiocy. Ignorance. Stubborn. Obstinate. Melancholic.Gloomy Closemouthed, answers in monosyllables. Desire to be in solitude. Disgust of life. Desire to escape. Lack of self confidence. Suicidal tendency without proper cause.
Intelligence Alert. Quick. Active. Unable to control or disappearance of thoughts.
Slow. Sluggish. Incoordination of thoughts and perception.
Very bright, intelligent & sharp, or slow & dull totally. Lack of concentration
Slow to react. Careless mistakes. Arithmetical calculation difficult.
68
Memory Weakness of memory. But studious.
Absentmindedness. Slow thought and speech. General loss of memory. Cannot find words.
Inability or slow in comprehension. Highly keen.
Impaired memory. Total forgetfulness.
Behaviour Decietful behavior. Cruel- Mental torture. Quarellsome. Mean minded & concealing.
Some cruelty due to dissatisfaction.
Violent, cold blooded murderers.
Fear Fear of strangers, death, disease, future.
Fear of making mistakes Fearless. Fear of dogs, dark
Fear of people. Panicky terror
Social relation Aversion to people & company. Dreads to be alone
Extroverts
Morose. Sullen. Does not like advices. Likes company
Introvert. Escapes from self & others. Aversion to company.
Attitude Internally extremely selfish. Hide & seek nature. Tendency to dishonesty, wickedness.
Selfish & possessive with a tendency to conceal.
Unrestrained & uncontrollable passions of life. Easily forms intense emotional bonds. Intense sexual desire.
Constantly dwell on suicide. Merciless with no sympathy. Irresponsible, lacks sense of duty. Perverted sexual cravings.
Sensitivity Oversensitive mentally & physically.
Like barometer to storm or rain.
Hypersensitive. Insensitive mentally and physically.
69
Metabolism Excessive demands for all supplies of nature but poor digestion & metabolism. More active catabolism than anabolism. Nutritional troubles resulting from defective metabolism of formative elements. Poor development or disproportionate accumulation of fat.. Disturbed water metabolism resulting in increased thirst, dryness of tissues. Inadequate utilisation in mineral metabolism. Loss of minerals
Disturbs pigment metabolism, endocrinal system. Increase in anabolic process & decrease in catabolism. A reduction in overall turnover. Retention, accumulation of cholesterol, aberration in lipid metabolism.
Poor in bone, flesh & blood Depletion, drainage & wasting disease. Loss of vital fluids (Diarrhoea, urine, sweat, bleeding) . Increased catabolism & decreased anabolism. Rapid physical waste.
Disturbs metabolism of mineral elements & produces deficient growth
Pathology Produces only functional disturbances manifested by hypersensitivity, itching, irritation, burning leading to congestion & inflammation. Never produces any structural damage. Spasms, paroxysmic phenomena & neuro vegetative manifestations
Physical & mental inco ordination. Physical overgrowth, uncontrolled proliferation at the cost of other. Infiltration in the form of warts, condylomata, tumours, fibrous tissue.
Rapid response to any stimuli. Early suppuration and delayed healing. Scars breakdown.
Produces destructive disorders everywhere. Ulceration from early phase of disease. Degeneration. Deviation – anything perverted.
70
Characteristic
Nature of disease
Deficiency or lack of inhibition, all cells & organs producing an insufficiency, functional deficiency, lack of productivity – Hypotension, Atrophy, Hypoplasia Anemia, Weakness. Hypoimmunity, Dryness, Lack of assimilation. Thin, watery, acrid serous discharges. Hypersusceptibility. Mental & Physical irritation. Deficiency disorders. Reflects many subjective symptoms. Little or no objective symptoms. Desires, aversion, intolerance are prominent
Excess manifested by hypertrophy, hyperplasia, neoplasia, hypersecretion, hypersensitivity, hyperthermia, hyperactivity Hydrogenoid. Greenish or greenish yellow, jelly like, catarrhal purulent discharges with fishbrine odour. Hypertension, Restless. Deposition. Reflects more objective symptoms with less subjective symptom
Haemorrhages. Allergies. Alternation & periodicity. Changeableness. Confusing vague symptoms. Craves things which make them sick. Depletion. Thick greenish or yellowish green discharges with smell of old cheese. Catches cold very easily Reflects many subjective symptom. Mental, emotional, pathological & destructive
Disorganised digestion deformities, fragility. Putrid, offensive, pus like discharges. Little subjective symptoms. Less desire, craving, aversion & feelings.
Pace of action Hyperactive. Dramatic development of symptoms
Extremely Slow & insidious onset & recovery
Depend on preponderance of psora / syphilitic miasms. Moderate or Rapid
Rapid or Insidious
71
Modalities < Standing, Cold, Morning, Movement, Between sunrise & set, Mental excitement, Worry, Grief, Anxiety, Fear, Noise, Strong smells, Before menses.
> Warmth, Scratching, Crying, Eating, Rest, Natural discharges, Appearance of suppressed skin eruption.
<Rest, Damp, Rainy, Humid, Thunderstorm, Change of weather, Meat, Abnormal discharges, Anger, Irritability
> Slow motion, Stretching, Dry weather, Lying on stomach, Pressure, Suppressed normal discharge, When wart, fibrous growth appear. Breaking open of old ulcers, sores, gonorrhoeal discharges, scars.
< Thunderstorm, Milk, Night, Fruits, Oily food, Closed room, Pressure, Excitement, Physical & mental exertion, Artificial light, Anger, After sleep.
>Dry weather, Open air, Day time, External heat, Travel Outbreak of an old ulcer, diarrhoea, offensive foot or axillary sweat, nose bleeding, gonorrhoeal symptoms.
< Sunset to sunrise, Movement, Extremes of temperature, At sea side, Thunderstorm, Warmth, Natural discharges
>Sunrise to sunset, Change of position, Abnormal discharge. Winter, Cold weather
History of Suppression of skin eruptions & physiological eliminations. Repeated attacks of acute infectious diseases. Stress – emotional & Psychological.
Metabolic disorders – Hyperlipidemia, hyperurecemia, chronic pelvic inflammatory disease. After effects of immunization , injection, blood transfusion, excessive food intake. Suppression of pathological elimination & proliferation
Tuberculosis, Whooping cough, Bronchitis, BA, Bronchopneumonia.Tendency to hay fever, common cold. Suppression of physiological & pathological elimination, foot sweat, skin eruption Recurrent infection
Suppression of pathological elimination Psychosis, incidence of suicide, CVA, MI Repeated abortion, IUD. Infertility, Degenerative diseases
72
Constitutional Appearance
Lean thin, Active Obese.Flabby, sluggish. Stout, Overnourished.
Lean thin. Narrow chest
Thin, wrinkled, looks old for his age.
Face Inverted pyramid Yellow sallow, pale, earthy complexion. Eyes sunken
Dropsical. Oily skin Pale ,round, fair smooth, clear skin & waxy smooth complexion. Sunken eyes, flushed cheeks. Thin lips.
Greasy. High cheek bones & rough skin. Dry & wrinkled like old person.Thick lips
Thermal
Generally chilly
Hot
Extremely chilly
Sensitive to changes either heat or cold Perspiration
Profuse, offensive, during sleep
On forehead during sleep. Copious.
Profuse
Offensive < all complaints
Appetite
Insatiable hunger
Discomfort after eating
Increased
Decreased
Craving
Sweet, Sour, Spicy, Salty. Oily, Fried, Indigestible Unnatural substances like chalk, clay, Hot food.
Alcohol, Beer, Pungent, Well seasoned, Salty food.
Indigestible things, Potatoes, Tea, Tobacco, Meat, Salt, Greasy, fatty food. Things which make them sick. Very hot / really cold
Stimulants like alcohol, tea, coffee, very spicy. Indigestible.Cold food
Aversion
Milk, cold food
Meat, milk, wine, spices
Meat
Meat, animal food, less spicy food
Bowels
Constipation
Diarrhoea Alternating diarrhea and constipation
Dysentry
73
Particulars of Hyperlipidemia Family history
May or may not have a F/H of hyperlipidemia
F/H of hyperlipidemia, atherosclerosis, CAD etc
F/H of hyperlipidemia
Strong F/H of hyperlipidemia, early CAD, stroke etc.
Etiology
Unknown cause Increased intake of fat, Secondary to alcoholism, drugs, hepatic infections
Mutation in gene. Hepatic cholestasis. Enzyme disorders Secondary to auto immune disease like SLE, endocrine disorders like DM, hypothyroidism, Cushing’s syndrome.
Mutation in gene
Mutation in gene Secondary to nephritic syndrome
Pathology Defective metabolism of fat Deficiency in apoprotein or enzymes.
Defect in receptors, enzyme activity. Deposition of cholesterol & lipoprotein in the wall of blood vessels
Defect in receptors, enzymes
Lack of apoprotein, receptors, enzyme activity Atheromatous plaque resulting in complication of haemorrhage, thromboembolic phenomena
Clinical Manifestations
No manifestations with only serum changes Pancreatitis. Reversible with diet & life style changes
Lipemia retinalis Hepatomegaly, Hepatic fibrosis, Spleenomegaly, hypertension, Xanthoma, Xanthelesma, Atherosclerosis, Enlarged tonsils
Recurrent pancreatitis. Intermittent peripheral neuropathy
Accelerated atherosclerosis Premature CAD, Stroke, PVD Haemolysis
74
HYPERLIPIDEMIA IN REPERTORY
The rubrics specifically related to hyperlipidemia seen in repertories are
SYNTHESIS 9.1 40
Generals – Hyperlipidemia - all-s, aur, calc, calc-f, chel, chin, chion, chr-ac, colch, cortiso,
ferr-i, hydr, lec, med, nux-v, perh-mal, tarax, thuj, thyreotr, vanad, zing
Generals – Arteriosclerosis - adren. Am-i. am-van. aml-ns. ant-ar. arg-n. Arn. ars. Ars-i.
asar. aster. Aur. aur-br. Aur-i. aur-m-n. Bar-c. bar-i. bar-m. bell-p. benz-ac. cact. cal-ren.
Calc. calc-ar. calc-f. card-m. chinin-s. chlol. con. crat. Cupr. ergot. fl-ac. form. form-ac. fuc.
Glon. hed. hyper. iod. kali-bi. Kali-i. kali-sal. kres. lach. lith-c. mag-f. mand. naja Nat-i. nit-
ac. phos. Plb. Plb-i. Polyg-a. rad-br. rauw. Sec. sil. solid. spartin-s. Stront-c. Stront-i. stroph-
h. sumb. syph. Tab. thlas. thyr. Vanad. Visc. zinc-p.
- Old people in – bar-c, stroph-h
Generals – Diabetis mellitus – accompanied by arteriosclerosis – aur, chlorpr,plb, syzyg
Mind – memory weakness – arteriosclerotic disease with - plb.
MURPHY’S REPERTORY 41
Blood - Blood vessels, general – atheroma- aur-m. bell. brom. Calc. Calc-f. caps. Graph.
kali-i. Lac-ac. Lach. lyc. phos. Plb. Sil. sulph.
- elderly people, in Lach.
- morbus brightii, in ph-ac.
- obese persons, in- caps.
Blood – Blood vessels, general – arteriosclerosis - adren. am-i. am-van. aml-ns. ant-ar. arg-
n. Arn. ars. Ars-i. Aur. aur-br. Aur-i. aur-m-n. Bar-c. bar-i. bar-m. bell-p. benz-ac. cact. cal-
75
ren. Calc. calc-ar. calc-f. card-m. chinin-s. chlol. con. crat. Cupr. ergot. fl-ac. form. form-ac.
fuc. Glon. hed. hyper. iod. Kali-i. kali-sal. kres. lach. lith-c. mag-f. mang. naja Nat-i. nit-ac.
phos. Plb. Plb-i. Polyg-a. rad-br. rauw. Sec. sil. solid. Stront-c. Stront-i. stroph-h. sumb. Tab.
thlas. thyr. Vanad. Visc. zinc-p.
BOERICKE’S REPERTORY 42
Circulatory system - Arteries - Atheroma of arteries - adren. Am-i. am-van. ant-ar. arn.
ars. Ars-i. aur. Aur-i. aur-m-n. Bar-c. bar-m. cact. calc-f. chinin-s. con. crat. ergot. Glon. Kali-
i. kali-sal. lach. lith-c. Nat-i. phos. plb. Plb-i. Polyg-a. sec. stront-c. Stront-i. stroph-h. sumb.
thyroiod. Vanad.
SPECIFIC THERAPEUTICS 42,43. As in any other disease, the remedy that encompasses
the diseased state of the constitutional expression at all levels, body, mind and spirit, termed
as constitutional remedy which necessarily coincides with the miasmatic expression of the
individual is the approach to hyperlipidemia. Inspite there are certain remedies specifically
related to hyperlipidemia clinically proven to bring down serum lipid levels as well as
remove the pathological deposition of lipids on arterial walls.
Allium Sativum – Adapted to fleshy subjects. Patients who eat a great deal more especially
meat than they drink.
Arnica – Marked effect on blood. Fatty heart and hypertrophy.
Arsenicum iodatum – Senile heart, fatty degeneration, Arteriosclerosis.
Aurum metallicum – Develops in the organism by attacking the blood. Deterioration of
body fluids. Arteriosclerosis with high blood pressure.
Baryta carb – Useful in general degenerative changes, especially in coats of arteries.Acts on
the muscular coats of heart and vessels. Arterial fibrosis. Blood vessels soften and
degenerate.
76
Calc flour – Arteriosclerosis.
Cardus marianus – Has specific relation to vascular system. Abuse of alcoholic beverages
especially beer.
Cholesterinum – Obstinate hepatic engorgements. Gallstones.
Crataegus – Arteriosclerosis. Said to have a solvent power upon crustaceous and calcareous
deposits in arteries.
Glonoine – Sciatica in atheromatous subjects.
Graphites – Tendency to obesity. Aids absorption of cicatricial tissue.
Plumbum metallicum – A great drug of general sclerotic condition. Hypertension and
arteriosclerosis.
Plumbum iodatum - Arteriosclerosis
Polygonum aviculare – In material doses of tincture found useful especially in
arteriosclerosis
Strontia – Arteriosclerosis. High blood pressure with flushed face, pulsating arteries
Strontia iodat - Arteriosclerosis
Tabacum – Produces high tension and arteriosclerosis of coronary arteries
Vanadium – Arteriosclerosis. Fatty heart. Atheroma of arteries of brain and liver
76
Methodology
77
METHODOLOGY
Source of data
This study was conducted on the patients who reported to the outpatient
department of Fr. Muller Homoeopathic Medical College and Hospital, Deralakatte, as
well as from Kankanady and peripheral centres. Patients belonging to age group of 25 to
75 years were considered for the study. Both the sexes were included belonging to
various socioeconomic group. A total number of 30 cases were taken randomly for the
study. The cases with elevated serum Cholesterol > 200mg/ dl, Triglycerides > 150mg/dl,
LDL > 130mg/ dl or HDL <40mg/ dl were selected The inclusion and exclusion criteria
were followed as given later.
Methods of collection of data
The data was collected by purposive sampling technique as per the inclusion
criteria and processed in a Standardized Case Record (SCR). Processing includes analysis
and synthesis of the case which were done as per the guidelines and principles of
Homoeopathy.
The potency selection and repetition of the dose were done according to the
demand of the case, such as Acute or Chronic, Susceptibility, Vitality and Suppression (if
any), Changes in structural and functional level, and the degree of correspondence to the
remedies. Follow up in each case was planned for a minimum of 3 months.
During the follow up each case was evaluated according to the scoring criteria,
which includes the serum lipoprotein levels before and after treatment.
78
Inclusion criteria:
All cases with hyperlipidemia between the age group 25 yrs and 75yrs, from both
sexes would be selected.
Subjects who have diagnosed of hyperlipidemia based on clinical history, clinical
presentation, clinical examination and blood investigation.
Exclusion criteria:
Subjects below 25 years and above 75 years
Subjects with serious complications like Myocardial infarction, Stroke etc.
The method used for this study is a clinical method for the confirmation. The
results obtained have been statistically analyzed and evaluated. No controls have been
kept for the study. All cases were treated after detailed history taking, with the help of
S.C.R., in which the complete symptomatology of patients (clinical presentation and
individual symptoms) and the investigation reports were recorded.
Selection of medicine in each case was based on the data such as etiological
factors, qualified mentals, physical generals, concomitants, characteristic particulars,
repertorial approach and clinical indications from different authorities. Potencies ranging
from 30 to 1M (centesimal scale) have been used in this study. Repetition and change of
potency and remedy were done as and when needed, according to the Homoeopathic
principles. In between the period of medications, all the patients were kept under placebo
continuously.
79
Follow ups:
Majorities of the patients were reviewed, on a fortnightly basis, to assess the
subjective and objective changes. Each case was followed for a minimum of 3 – 6 months
from the commencement of treatment.
The abbreviations used in the follow up were:
S – No change or same
< - Aggravation of clinical features
> Amelioration of clinical features
0 – Disappearance of clinical features
G – good
N – Normal
R – Regular etc.
Diet and Regimen
All the patients were explained and educated about the importance of low calorie
diet and physical exercises as per the need. Instructions were given to avoid other
medicinal agents during the treatment.
Assessment of Effectiveness
Effectiveness of the treatment was assessed on the basis of
1. Serum lipid profile
2. For the effective assessment and evaluation, disease intensity scores were also
maintained.
80
After completion of treatment, disease intensity of the post treatment scores were
compared with the pre treatment disease intensity score and statistically evaluated.
Notes: For disease intensity scores refer appendix: 1
Plan for Data Analysis
Data has been analysed by using descriptive statistics and the results have been
presented by using frequency table, percentage, pie diagram, and graphs. The
significance of treatment effect based on different homoeopathic therapeutic strategies
are tested using ‘t’ test.
80
Results
81
RESULTS
Table 3: Distribution of cases according to age group
Age group No. of cases Percentage
25-35 7 23.33
35-45 10 33.3
45-55 4 13.3
55-65 7 23.3
65-75 2 6.6
In this study maximum prevalence of Hyperlipidemia were found in the age
group of 35 to 45 years (10 cases – 33.33%). Followed by 25 to 35 and 55 to 65 years of
age group (7 case in each group – 23.33%) and 45 to 55 years of age group (4 cases –
13.3%). Minimum prevalence is found in 65 to 75 years age group (2 cases 6.6%).
Table 4: Distribution of cases according to sex
Sex No. of case Percentage
Male 12 40
Female 18 60
Total 30 100
Out of 30 patients studied, 12 cases (40%) were males and 18 cases (60%) were females.
82
Fig.11: Case distribution according to age group
Fig.12: Case distribution according to sex
0
5
10
15
20
25
30
35
25-35 35-45 45-55 55-65 65-75
710
47
2
23.33
33.3
13.3
23.3
6.6
No. of cases
Percentage
Case distribution according to age group
Age group
Males12
40%
Females18
60%
Distribution of cases according to sex
83
Table 5: Case distribution according to religion
Religion No of cases Percentage
Hindu 8 26.6
Christian 14 46.6
Muslim 8 26.6
Total 30 100
Out of 30 cases maximum prevalence of Hyperlipidemia was found in Christians
(14 cases – 46.66%). Hindus and Muslims shared equal prevalence of (8 cases each-
26.66%).
Table 6: Case distribution according to physical activity
Physical activity No of cases Percentage
Sedentary 16 53.33
Moderate 14 46.6
Severe 0 0
Total 30 100
Among 30 patients included in this clinical study, majority 16 cases (53.3 %)
were found to have sedentary life with minimal physical activity. The rest were patients
with moderate physical activity 14 cases (46.6%). There were no patients with severe
physical activity.
84
Fig.13: Case distribution according to religion
Fig.14: Case distribution according to physical activity
0 20 40 60
Hindu
Christian
Muslim
8
14
8
26.6
46.6
26.6
Percentage
No of cases
Case distributions according to religion
No of cases
Percentage0
20
40
60
SedentaryModerate
Severe
1614
0
53.3346.6
0
No of cases
Percentage
Case distribution according to physical acitivity
85
Table 7: Case distribution according to fundamental miasm
Miasm Fundamental miasm
No. of cases Percentage
Psora 0 0
Sycosis 16 53.3
Syphilitic 1 3.3
Tubercular 1 3.3
Sycosyphilitic 11 36.6
Psora syco 1 3.3
Total 30 100
Table 8: Case distribution according to dominant miasm
Miasm
Dominant miasm
No. of cases Percentage
Psora 8 26.6
Sycosis 16 53.3
Syphilitic 0 0
Tubercular 1 3.3
Psorasyco 5 16.6
Total 30 100
Sycotic expression is well marked and found to be dominating in both
fundamental and dominant miasm with 16 cases (53.3%). Syco syphilitic expression
stands next with 11 (36.6%) in fundamental miasm and Psora with 8 (26.6%) in
dominant miasm. Tubercular, Syphilitic and Psora-sycotic comprises 1 each (3.3%) in
fundamental miasm. Psora comprises 8 (26.6%) and Psorasycotic 5 (16.6%) cases in
86
dominant miasm. Only one case gives Tubercular expression (3.3%) in dominant miasm.
There is no expression from Psoric miasm in fundamental miasm and syphilitic miasm in
dominant miasm
Fig.15: Case distribution according to fundamental miasm
Fig.16: Case distribution according to dominant miasm
No of cases 0
0
50
100
161 0
30
100
30
53.3
3.3 3.3
36.6
3.3
100
No of cases 0
Percentage o
Case distribution according to fundamental miasm
827%
1653%
1 3%
517% Psora
Sycosis
Syphilitic
Tubercular
Psorasyco
Case distribution according to dominant miasm
87
Table 9: Case distribution according to the type of hyperlipidemia
Type of Hyperlipidemia No of cases Percentage
Familial hyper cholesterolemia 4 13.3
Polygenic hypercholesterolemia 7 20
Familial combined hyperlipidemia 10 33.3
CETP deficiency 1 3.3
Familial chylomicronemia 1 3.3
Hepatic lipasedeficiency 2 6.6
Secondary hyperlipidemia 5 16.6
Total 30 100
Among 30 patients included in this clinical study, majority (10 cases-33.3 %)
were found to be having Familial combined hyperlipidemia. Polygenic hyperlipidemia
was next with 7 cases (23.3%).This was followed by Secondary hyperlipidemia and
Familial hypercholesterolemia with 5(16.6%) and 4 (13.3%) cases respectively. The rest
were of Hepatic lipase deficiency (2cases – 6.6%), CETP deficiency (1case – 3.3%) and
Familial chylomicronemia(1case – 3.3%) .
88
Table 10: Case distribution according to constitutional remedies
Name of the remedy No of cases Percentage Calcarea carb 4 13.3
Lycopodium 10 33.3
Medorrhinum 1 3.3
Natrum mur 2 6.6
Nux Vomica 1 3.3
Phosphorus 4 13.3
Pulsatilla 4 13.3
Sepia 2 6.6
Sulphur 2 6.6
Total 30 100
Out of 30 cases, Lycopodium was used as a constitutional remedy in 10 cases (33.3%).
Calcarea carb, Phosphorous and Pulsatilla were used as constitutional remedy in 4 cases
(13.3%) each. Sepia, Sulphur and Natrum mur were used as constitutional in 2 cases
(6.6%) each.1 case (3.3%) each was treated with Nux vomica and Medorrhinum.
89
Fig.17: Case distribution according to the type of hyperlipidemia
Fig.18: Case distribution according to constitutional remedies
4
10
1 2 1
4 42 2
13.3
33.3
3.3
6.6
3.3
13.3 13.3
6.6 6.6
0
5
10
15
20
25
30
35
0 2 4 6 8 10
No of cases
Percentage
Case distribution according to constitutional remedies
90
Table 11: Case distribution according to the effectiveness of treatment
Effectiveness No of cases Percentage
Improved 26 86.6
Not improved 4 13.3
Total 30 100
Fig.19: Case distribution according to the effectiveness of treatment
Out of 30 cases, 26 ( 86,6%) showed improvement in the serum lipid profile.
Following the guidelines all through the proforma, the status of the patient is assessed
and substantiated under two criteria according to the score, based on serum lipid level.
No of cases
percentage
0
10
20
30
40
50
60
70
80
90
Improved
26
4
86.6
13.3
No of cases
percentage
Not improved
91
THE EXPLANATION OF THE STATISTICAL TOOLS AND TECHNIQUES
Table 12: Statistical analysis table
X - Score before treatment Z - Mean difference Y - Score after treatment
Mean X = 422/30 = 14.07 Mean Y = 274/30 = 9.13 Mean Z = 148/30 = 4.93
Sl.No X Y (X - Y)=Z _ Z
_ (Z – Z)2
1 15 5 10 5.07 25.70 2 11 7 4 -0.93 0.86 3 6 1 5 0.07 0.00 4 11 4 7 2.07 4.28 5 12 15 -3 -7.93 62.88 6 17 4 13 8.07 65.12 7 16 11 5 0.07 0.00 8 22 31 -9 -13.93 194.04 9 15 13 2 -2.93 8.58 10 15 10 5 0.07 0.00 11 14 6 8 3.07 9.42 12 23 17 6 1.07 1.14 13 9 5 4 -0.93 0.86 14 7 7 0 -4.93 24.30 15 18 14 4 -0.93 0.86 16 7 2 5 0.07 0.00 17 19 12 7 2.07 2.28 18 14 4 10 5.07 25.70 19 13 0 13 8.07 65.12 20 19 16 3 -1.93 3.72 21 29 16 13 8.07 65.12 22 20 15 5 0.07 0.00 23 6 1 5 0.07 0.00 24 10 4 6 1.07 1.14 25 15 9 6 1.07 1.14 26 14 13 1 -3.93 15.44 27 15 13 2 -2.93 8.58 28 17 13 4 -0.93 0.86 29 9 2 7 2.07 4.28 30 4 4 0 -4.93 24.30
Mean X =422
Mean Y = 274
Mean Z =148 Mean _
(Z – Z)2 = 617.87
92
A. Question to be answered: is there any significant difference between the scores
taken before and after the treatment.
B. Null hypothesis: there is no significant difference between the scores before and
after the treatment.
C. Standard error of the mean differences: the mean of the differences
Z = Z/n = 148/30 = 4.93
The estimation of the population standard deviation is given by the formula
SZ = √ (Z –Z) 2 / n-1
= √ 617.87 / 29
= √ 21.31
= 4.62
The estimation of the standard error is calculated by using the formula
= SZ /√n
= 4.62 /√30
= 4.62/ 5.47
= 0.84
D. Critical ratio is calculated using the formula : t = Z /Sz /√n
= 4.93 / 0.84
= 5.85
93
E. Compare with the tabled values:
The test statistic ‘t’ follows student ‘t’ distribution with n-1(29) degrees of
freedom. Here, tabled value of ‘t’ at 5% level of significance is 2.045 and 1% level of
significance is 2.756 for 29 degrees of freedom. Since the calculated value is 5.85 which
is greater than the tabled at 5% &1%, we reject the Null Hypothesis.
Inference: This study provides an evidence to say that there is reduction in the disease
intensity scores after the homoeopathic treatment based on constitutional treatment and
general management. Therefore the Homeopathic constitutional medicines are effective
in treating hyperlipidemia.
94
Fig.20: Distribution of all cases according to pre and post treatment analysis using scoring char
0
5
10
15
20
25
30
35
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30
Scoring before
Scoring after
95
Discussion
95
DISCUSSION
Hyperlipidemia, which is the raised or abnormal levels of lipids & lipoproteins in
the blood has become a great health hazard, especially in developed countries which has
turned out to be a challenge to the physician. It contributes to high morbidity and
remains a major cause of high mortality in our country.
The current study is done for the better understanding of different types of
hyperlipidemia, to assess the role of miasm in hyperlipidaemia and its management
through general and constitutional homoeopathic treatment.
This study was conducted in patients who reported to the outpatient department of
Fr. Muller Homoeopathic Medical College and Hospital at Deralakatte, as well as from
Kankanady and peripheral centres.
A total number of 30 cases were taken randomly for the study. The cases with
deviated serum lipid i.e. Cholesterol > 200mg/ dl, Triglycerides > 150mg/dl, LDL >
130mg/ dl or HDL <40mg/ dl were selected. The inclusion and exclusion criteria were
followed strictly. For the assessment of the clinical status before and after the treatment
the score was used which is mentioned in the annexure-1. The score before and after the
treatment was considered and‘t’ test was applied.
Prevalence of hyperlipidemia is more frequent among the age group 35-45 years
i.e. 10 (33.33%) cases. Followed by 25 to 35 and 55 to 65 years of age group (7 case in
each group – 23.33%) and 45 to 55 years of age group (4 cases – 13.3%). Minimum
prevalence is found in 65 to 75 years of age group (2 cases 6.6%).
96
Osteoarthritis, hypertension and fibroid uterus in females are the most common
associated complaints observed in the study.
Among the 30 cases selected females 18 (33.33%) were found to be dominating
than the males 12 (40%). Of the different cases selected for study, maximum number of
cases reported from patients with Christian background i.e. around 14 (46.66%). Hindus
and Muslims shared equal prevalence of (8 cases each- 26.66%).
All 30 cases selected were analyzed and graded based on their occupation as
severe , moderate, and sedentary workers. At the end of the study it was concluded from
the data aggregated that maximum incidence of hyperlipidemia is seen in sedentary
working individuals at a rate of 16 (53.33%) cases out of 30. The rest were patients with
moderate physical activity 14 (46.6%), There were no patients with severe physical
activity.
Only 5 (16.6%) out of 30 cases in their background presented with a family
history of Hyperlipidemia, MI or stroke in previous generations recent or remote where
as 25 (83.3%) of cases did not present with the family history.
According to the miasmatic evaluation of the 30 cases taken for the study it was
found that sycotic expression to be dominating in both fundamental and dominant
miasm with 16 (53.33%) cases. Sycosyphilitic expression stands next with 11(36.6%) for
fundamental miasm and Psora with 8 (26.6%) cases for dominant miasm. Tubercular,
Syphilitic and Psora-sycotic comprises 1 each (3.3%) in fundamental miasm. Psora
comprises 8 (26.6%) and Psorasycotic 5(16.6%) cases in dominant miasm. Only one
case gives Tubercular expression (3.3%) in dominant miasm. There is no expression from
Psoric miasm in fundamental miasm and syphilitic miasm in dominant miasm.
97
Among 30 patients included in this clinical study, majority 10 (33.33%) cases
were diagnosed as Familial combined hyperlipidemia. Polygenic hyperlipidemia was next
with 7 cases (23.3%).This was followed by Secondary hyperlipidemia and Familial
hypercholesterolemia with 5(16.6%) and 4 (13.3%) cases respectively. The rest were of
Hepatic lipase deficiency (2cases – 6.6%), CETP deficiency (1case – 3.3%) and Familial
chylomicronemia(1case – 3.3%) .
After evaluating each case, a constitutional remedy was prescribed. Evaluation
of these prescribed constitutional remedies helps us to know thee most commonly used
remedies. Maximum occurrence was taken by Lycopodium which is given in 10 cases
with a percentage of 33.33% and followed by other remedies like Phosphorous, Calcarea
carb and Pulsatilla in 4 cases(13.33%)each. Sepia, Sulphur and Natrum mur were used as
constitutional in 2 cases (6.6%) each.1 case (3.3%) each was treated with Nux vomica
and Medorrhinum..
Out of 30 cases, 200th potency was selected for the first prescription in
maximum cases 27 (90%). 30th potency was given in 2 cases (6.66%).10M potency was
given in 1case (3.33%).
For the assessment of effectiveness of homoeopathic treatment, disease intensity
scores before and after treatment were statistically evaluated with ‘t’ test and which is
found significant. Fisher’s exact test is used to find out any association between
Hyperlipidemia and Constitutional medicines and the value obtained after statistical
evaluation indicated that there is an association between the disease and constitutional
medicine of the patient.
98
Evaluation of the serum lipid levels before and after the treatment revealed that
there is improvement before and after treatment.
The result is understood after evaluating the scored values before and after
treatment. Value obtained is 5.85, which is more than the tabled value of 2.045. Hence
null hypothesis is rejected.
Inference: From the study it is clear that homoeopathic constitutional treatment is
effective in the treatment of hyperlipidemia with a well planned general management.
LIMITATIONS:
1. Hyperlipidemia is a chronic disorder requiring long-term management for desired
results. As the study has the time limit, it was not possible to observe the patients
for longer periods.
2. Some good cases couldn’t be included in this study because of discontinuation of
treatment in between the study.
3. This is a restricted sample design, in which only 30 cases were studied. Chances
of sampling error are increased with small sample size and hence the conclusions
based on those cases have limited implications. Generalization of the result is
difficult to emphasize.
4. Hyperlipidemia is observed in increasing number of population. But many are
not aware of the consequences. Most of the cases reported with other complaints
and were detected of hyperlipidaemia on screening.
5. Repeated serum analysis was not done in all the cases. Hence there is possibility
of incompleteness in the study.
6. There was no control group as such since the sample size was small.
99
7. In some cases few necessary details were lacking and the study is conducted
based on the available data.
RECOMMENDATIONS:
1. Bigger sample size with extended time of study would provide better result.
2. Improvised scales can be used, so that evaluation of the outcome of the study
would become more precise.
3. Same study can be conducted with the help of placebo controlled (single blind,
double blind) study.
4. An attempt to discover new techniques, closely monitoring the general
management of the patients.
100
Conclusion
100
CONCLUSION
1. Prevalence of hyperlipidemia is more frequently among the age group 35-45 years
i.e.10 cases (33.33%). cases reported to the study. This reproves the statement
that hyperlipidemia has its onset in the fourth decade.
2. Osteoarthritis, hypertension and fibroid uterus in females are the most common
associated complaints observed.
3. Females showed more prevalence i.e 18 cases (60%) out of 30 than the males
which can be due to the general prevalence in the inflow of female patients to the
OPD or due to purposive sampling.
4. Prevalence of hyperlipidemia shows maximum number of cases reported from
patients with Christian background i.e. around 14 (46.66%). Hindus and Muslims
shared equal prevalence of (8 cases each- 26.66%) Probably this result can be
attributed to the dietary factors noted in this community which serves as risk
factors or because the inflow of patients to the OPD is mainly of Christian
community.
5. At the end of the study it can be concluded from the data aggregated that
maximum incidence of hyperlipidemia is seen in sedentary working individuals at
a rate of 16 (53.33%) cases out of 30 and there were no patients with heavy
physical activity out of 30 reported to the study, indicating the lifestyle factors
and obesity as important factors that determine the severity of disease in
community.
101
6. According to the miasmatic evaluation of the 30 cases taken for the study sycosis
is presenting maximum predominance in fundamental as well as dominant miasm
in 16 (53.33%) cases. Complex miasms like Syco syphilitic expression stands
next11 (36.6%) for fundamental miasm, There is no expression from Psoric
miasm in fundamental miasm and syphilitic miasm in dominant miasm
7. Evaluation of the serum lipid profile before and after the treatment reveals that
there is improvement in 26 cases (86,66%) out of 30 cases
8. All the cases were worked out and the constitutional similimum was selected and
patients were observed on follow ups spaced at a gap of 2 weeks duration.
9. Along with the constitutional treatment general management in the form of diet
and exercise guidelines were given to the patient .
10. Lycopodium was the leading remedy at the constitutional level, proving the
general constitution of the remedy to be predisposed for hyperlipidemia
11. Potency selection was done based on the standardized guidelines in the SCR
according to the susceptibility and sensitivity of the patient.200th potency showed
maximum prevalance
12. According to the need of the cases some acute remedies were prescribed in
between.
13. The various statistical techniques applied proved the efficacy of the treatment.
.
101
Summary
102
SUMMARY
This study was conducted on patients with hyperlipidemia.
The objectives of the study were,
1. To study the different types of hyperlipidaemia
2. To assess the role of miasm in hyperlipidaemia and know the effectiveness of
constitutional method of treatment which includes the miasmatic background of
the individual .
A total of 30 cases were taken for study based on inclusion and exclusion criteria.
Majority of the cases were aged between 35-45years. Miasmatic evaluation of all
the cases revealed sycosis to have maximum predominance as fundamental as well as
dominant miasm. Constitutional medicines were given to all the patients and along with
that general management guidelines for diet and exercise guidelines were also explained.
Follow up analysis of the patients state was assessed with serum lipid profile.
Lycopodium as constitutional medicine had higher indications. 200th potency showed
wider indications. The study reveals that homoeopathic treatment with dietary and
exercise guidelines when strictly implemented is the best method of approaching
hyperlipidemia
103
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 son’s inc.publication; 2006. p.662, 666, 676-691,707-717
9. Kasper D L, Braunwald E, Fauci A S, Hauser, Longo, Jameson. Harrison’s
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
104
11. Kumar P & Clark M. Clinical medicine. 6thed. USA: Elsevier Saunder’s
publication; 2005. p. 1137 – 1143
12. Park K. Park’s 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. http://www.pubmed.org – hyperlipidemia. Accessed on 6th September 2008
17. http://www.wikepedia.com – hyperlipidemia. Accessed on 6th September 2008
18. http// emedicine.medscape.com/article/overview HDL. 4th October 2010
19. http://www.ehow.com/about foods-control-cholesterol.html.10th October 2010
20. http://www.American Heart.org. Accessed on 8th September 2008
21. http://www.womensheart.org/Nutrition/mediterranean.asp&usg.10th October 2010
22. 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.
105
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. http://www.similimum.com/organon of medicine. Accessed on 15th October 2010
28. 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 .Kent’s repertory. 1st ed. Kottayam:
Hahnemann book house; 1996. p. 6, 7, 75.
34. Ortega PS. Notes on the miasms or hahnemann’s chronic diseases. 1st English ed.
New Delhi: National homoeopathic pharmacy; 1980. p. 53-5, 63, 69-72,75-8.
106
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, 54-6, 62, 71-3, 77-88, 98, 99
103
Annexures
107
ANNEXURE – 1
SCORING CHART
Sl.
No
Cholesterol,
mg/dl Score
Triglycerides,
mg/dl Score
LDL,
mg/dl Score
HDL,
mg/dl Score
1 <200 0 <150 0 <130 0 >40 0
2 200 - 225 1 150 - 175 1 130 - 135 1 40 - 38 1
3 225 - 250 2 175 - 200 2 135 - 140 2 38 - 36 2
4 250 - 275 3 200 - 225 3 140 - 145 3 36 - 34 3
5 275 - 300 4 225 - 250 4 145 - 150 4 34 - 32 4
6 300 - 325 5 250 - 275 5 150 - 155 5 32 - 30 5
7 325 - 350 6 275 - 300 6 155 - 160 6 30 - 28 6
8 350 - 375 7 300 - 325 7 160 - 165 7 28 - 26 7
9 375 - 400 8 325 - 350 8 165 - 170 8 26 - 24 8
10 400 425 9 350 - 375 9 170 - 175 9 24 - 22 9
11 >425 10 >375 10 >175 10 <22 10
108
ANNEXURE – 2
DETAILED CASE STUDY
PRELIMINARY DATA
Name : Mr S B SCR No. : 57123
Age : 41 yrs Date : 26-06-10
Sex : Male Physician : Dr. MK
Occupation : Govt Employee
Education : Graduate
Religion : Hindu
Address : Neeleshwaram
CHIEF COMPLAINT
No LOCATION SENSATION MODALITY CONCOMITANT 1. Rectum
Since 5 – 6 yrs
Hard stool Difficult to pass Burning2 Bleeding
< spicy food, fried food, Non Veg < after stool
2. Head Scalp Since 5 – 6 yrs
Hair fall, Dandruff Powdery scales Slight itching
< combing < summer
HISTORY OF CHIEF COMPLAINT
The patient was apparently alright before 6yrs. The complaints started with hard
stools difficult to pass. Later bleeding started which was more after stool. The complaints
are more after spicy food, fried and non veg.
109
The patient also complains of hair fall which started around 5 yrs back. It is
accompanied with dandruff in the form of white powdery scales. Hair fall is more on
combing while Itching of scalp is more felt in summer
PAST HISTORY
Hypercholesterolemia since 2 - 3 years.
FAMILY HISTORY
Father - Expired following some liver disease
Mother - Hypercholesterolemia, Haemorrhoids
Brother - Haemorrhoids
TREATMENT HISTORY
Allopathic treatment for Haemorrhoids.
PATIENT AS A PERSON
Appearance : Stocky
Appetite : Good
Craving : Meat, sweets
Aversion : Nil
Perspiration : Normal
Bowel : Hard
Bladder : 5 - 6/day
Thermal : Chilly (C4H)
Sleep : Good
Mental generals : Company desire Doesn’t like to share
Doesn’t like contradiction Superficial relation
110
GENERAL PHYSICAL EXAMINATION
Well built and well nourished
Patient is well oriented with time place and person.
No signs of pallor, cyanosis, clubbing or icterus.
Vital signs:
Pulse - 74/min, regular, good volume and vessel wall not palpable.
Temperature - Afebrile at the time of examination
Respiratory rate - 18/min
Blood pressure - 120/80 mm of Hg. ( Right arm supine position)
Weight – 66 Kg
LOCAL EXAMINATION
External haemorrhoids 11 ‘ o clock position
No tenderness
No bleeding
SYSTEMIC EXAMINATION
Abdomen - NAD
Respiratory system - Vesicular breathe sounds
No added sounds
Cardiovascular system - S1 S2 heard
No murmurs
Central nervous system – NAD
111
INVESTIGATIONS DONE
Serum cholesterol - 282 mg/dl
TG – 166 mg/ dl
LDL– 156 mg/dl
HDL – 32 mg/dl
PROVISIONAL DIAGNOSIS
External Haemorrhoids Alopecia area’ta Familial hypercholesterolemia
Hard stool difficult to pass Hair loss Raised serum cholesterol, TG
Burning and LDL. Low HDL
Bleeding after stool
< spicy food
LIFE SPACE INVESTIGATION
The patient hails from a middle class family. Parents were agriculturists. Father
expired when the patient was 9 yrs old. By then his elder brothers were working and
hence did not face any financial constraints. His brothers are well settled. He got married
at the age of 28 yrs which was a love match and leads a happy life with one son and one
daughter.
He is affectionate, especially to his daughter. He likes to be in company of others
but does not go into deep relations nor does he like to share his feelings with others. He
doesn’t get angry fast and deslikes contradiction. He has fear of dark from childhood. His
memory is weak but active thinking and clear perception.
112
FIRST PRESCRIPTION:
1. Phosphorous 200
1 Pkt x HS
2. No 40 pills
4–0–4 x 2 weeks
Follow Up Criteria
1) Hyperlipidemia
2) Hard stool
3) Burning
4) Bleeding
5) Hairfall
6) Dandruff
MIASMATIC EXPRESSION
Sector Psora Sycosis Tubercular Syphilis
F/H M – Haemorrhoids, hypercholesterolemia
B - Haemorrhoids
F – Premature death due to liver disease
P/H ------ -----
Mentals Weak Memory
Fear of dark Likes company Superficial relations. Does not share with others
Physicals Bowels -hard Cr- Sweet
Appearance- Stocky Cr-Meat Thermally chilly
Characteristic particulars
Hairfall, Burning pain,Bleeding
113
ESSENTIAL EVOLUTIONARY TOTALITY
Pt family
Good predisposition
FM – Sycotic - Syphilitic
DM –Tubercular
Pt family
Good
Pt society
Good
Pt society
Good
Pt work
Good
Pt work
Good
disposition
Likes company Superficial relation
Doesn’t like to share Deslikes contradiction
Fear of dark Memory weak
Mingles with every one Maintains good relation
D i a t h D i s e a s e s
Craving – Meat, Sweets Thermally – Chilly
Bowels – Hard
Hyperlipidaemia
Hard stool
Burning
Bleeding < after stool
< spicy food
Hair fall
Familial hypercholesterolemia
External Haemorrhoids
Alopecia area’ta
Syphilis
Sycosis
Psora
Tubercular
114
CONSTITUTIONAL TOTALITY
MENTAL GENERALS
Mingles easily with people
Likes Company
Superficial relations
Doesn’t share
Deslikes contradiction
Weak memory
Fear of dark
PHYSICAL GENERALS
Caving for meat, sweets.
Thermally chilly
Bowels hard
CHARACTERISTIC PARTICULARS
Hyperlipidemia
Hard stool difficult to pass
Burning
Bleeding after stool < Spicy food
Hair fall,
Dandruff
MIASMATIC INTERPRETATION
Dominant miasm --- Tubercular
Fundamental miasm --- Sycosis - Syphilis
115
General management
Patient was advised systematically regarding dietary management and also
general guide lines regarding exercise.
FOLLOW UPS
DATE SYMPTOM CHANGES PRESCRIPTION
10. 07 .10
1 2 3 4 5 6 7 8 9 10 RX 1. SL pkt (1P)
H S
2. No 40 pills
4–0–4 x 2 wks
- - > > - <
24.07.10
1 2 3 4 5 6 7 8 9 10 RX
1. Phos 200 (1P) H S2. No 2 . No 40 pills
4–0–4 x 2 wks .
> - > > - <
Serum cholesterol – 226 mg/dl TG – 138mg/dl LDL – 123 mg/dl HDL – 35 mg/dl
7. 08. 10
1 2 3 4 5 6 7 8 9 10 RX 1. SL pkt (1P)
H S
2 . No 40 pills
4–0–4 x 2 wks
> > > > - -
Generally feels better
21. 08. 10
1 2 3 4 5 6 7 8 9 10 RX
1. SL pkt (1P) H S
2. No 40 pills
4–0–4 x 2 wks
> > > > - <
Generals – good
116
4.09-10
1 2 3 4 5 6 7 8 9 10 RX 1. SL pkt (1P)
H S 2. No 40 pills
4–0–4 x 2 wks
> > > > - -
18.09.10
1 2 3 4 5 6 7 8 9 10 RX
1. SL pkt (1P) H S
2. No 40 pills
4–0–4 x 4 wks
> > > > - -
Generals – good
SCORING
Sl No Serum lipid levels Scoring before treatment
Scoring after treatment
1. Cholesterol 4 2
2. Triglycerides 1 0
3. LDL 6 0
4. HDL 4 3
Total 15 5
117
INVESTIGATIONS REPORTS BEFORE AND AFTER TREATMENT
118
ANNEXURE 3
MASTER CHART
Sl. no
Particulars Of the Patient
Clinical Diagnosis
Past And Family History
Investigations Totality Miasms Remedy Duration of
treatment
Scoring
Result
Before After FM DM B A
1 Name: Mr S B Age : 41 yrs Sex : M Occu : Govt employee Relegion :Hindu Add : Neeleshwar SCR No : 57123
Familial hypercholesterolemia External Haemorrhoids Alopecia area’ta
Mother – Hypercholesterolemia, Haemorrhoids Father – Expired due to liver disease Brother - Haemorrhoids
Chol –282mg/dl TG- 166mg/ dl LDL – 156mg/dl HDL- 32mg/ dl
Chol – 226mg/dl TG – 138mg/ dl LDL – 123mg/dl HDL – 35mg/ dl
MG: Fear of dark, Likes company, Doesn’t like contradiction, Doesn’t like to share, weak memory PG: Stocky appearance Cr –Sweets, meat Chilly patient CP: Bleeding < spicy food Hairfall< summer
Syco- Syphil
Tub Phos 200 3 mths 15 5 Improved
2 Name: Mrs K M Age :40 yrs Sex:F Occu: Housewife Relegion: Muslim Add :Kumbla SCR No: 43325
Familial combined hyperlipidemiaAllergic rhinitis
Mother – Epilepsy Father – Bronchial asthma, DM, Died following Renal failure Brother -DM
Chol- 255mg/ dl TG – 138mg/ dl LDL – 168mg/ dl HDL 47mg/ dl
Chol – 232mg/ dl TG 106mg/ dl LDL- 155mg/ dl HDL- 56mg/ dl
MG – Brooding, Suppressed emotion, Weeping when alone, Hasty, Doesn’t like company, Good confidence PG – Stocky appearance Cr – Fish Av – Sweets, Ice cream, Hot patient CP – Sneezing < Dust, Cold air, Morning. Breathlessness < lying down, Night
Syco- Syphil
Psora Natrum Mur 30
5 mths
11 7 Improved
119
Sl. no
Particulars Of The Patient
Clinical Diagnosis
Past And
Family History
Investigations Totality
Miasms Remedy Duration of
treatment
Scoring Result
Before After FM DM B A
3 Name: Mrs Y
Age : 41 yrs Sex: F Occu: Housewife Relegion: Hindu Add :Ullal SCR No: 14392
CETP deficiency Osteoarthritis Calcanean spur Hypertension
Mother – Osteoarthritis Father – Expired of MI
Chol- 250mg/ dl TG – 66mg/ dl LDL – 148 mg/ dl HDL- 89mg/ dl
Chol – 225mg/ dl TG – 60mg/ dl LDL – 128mg/ dl HDL – 85mg / dl
MG: Mild, Likes company, Likes consolation Weak memory PG: Stocky appearance Decreased appetite Perspiration increased in general, Cr – Fish, Spicy Av – Veg Chilly patient CP: Joint pains pricking < before menses, exertion >Warmth, pressure Giddiness < getting up from sitting position
Syco- Syphil
Syco Puls 200, 1M
4mths 6 1 Improved
Name: Mr M Age : 35yrs Sex: M Occu: Driver Relegion: Muslim Add : Payyannur SCR No: 48619
Familial chylomicronemia LRTI Tension headache Hypertension
Mother – Bronchial asthma Father – Died of MI
Chol – 223mg/ dl TG- 425mg/ dl LDL – 129mg/ dl HDL- 50mg/ dl
Chol – 198mg/dl TG – 280mg/ dl LDL – 101mg/ dl HDL – 41mg/ dl
MG: Suppressed emotion, Arrogant, Introvert, Likes company, Sympathetic PG: stocky appearance Appetite decreased Thirst decreased Perspiration increased in general Cr- Shellfish Av- Meat Hot patient CP: Dry cough < after fried food, headache pricking < Tension, after sleep> pressure Chest burning < heavy food
Syco- Syphil
Psora Sulph 200 5mths 11 4 Improved
120
Sl. no
Particulars Of The Patient
Clinical Diagnosis
Past And
Family History
Investigations Totality
Miasms Remedy Duration of
treatment
Scoring Result
Before After FM DM B A
5 Name: Mr J P
Age : 27 Yrs Sex:M Occu: Attendar Relegion :Christian Add : Manjeshwar SCR No: 9154
Polygenic hypercholesterolemia Sinusitis APD
P/H Appendicitis Father – Hypertension
Chol – 235mg/dl TG -86mg/ dl LDL- 176mg/ dl HDL- 42mg/ dl
Chol- 324mg/dl TG- 122mg/ dl LDL- 234mg/ dl HDL- 46mg/ dl
MG: Anxiety about future Sensitive, Intolerant to contradiction. PG: Stocky appearance Cr - Non Veg, cold drinks. Av – Veg Hot patient CP: < Tension Abdomen fullness < spicy, Non Veg Head ache < Sun, exertion > Tight bandage
Syco Psora Lyco 200 4 mths 12 15 Not Improved
6 Name: Mrs N Age : 37 Sex: F Occu Housewife: Relegion: Hindu Add : Bejai SCR No: 54279
Polygenic hypercholesterolemia Varicose veins
P/H Bronchial asthma, Chikungunya Mother – DM Expired
Chol – 310mg/ dl TG – 130mg/ dl LDL – 157mg/ dl HDL – 27mg/ dl
Chol – 149mg/ dl TG – 113mg/ dl LDL – 95mg/ dl HDL– 31mg/ dl
MG – Shy, Sensitive, Obstinate, Likes to be in company PG – stocky appearance Perspiration increased on face,Hard stool, once in two days Av – Chicken Sour food disagrees Hot patient CP – Extremities pain, Burning < Exertion, morning > warmth, Massage
Syco Syco Puls 200 3 mths 17 4 Improved
121
Sl. no
Particulars Of The Patient
Clinical Diagnosis
Past And
Family History
Investigations Totality
Miasms Remedy Duration of
treatment
Scoring Result
Before After FM DM B A
7 Name: Mrs L R
Age :42yrs Sex: F Occu: Lecturer Relegion: Christian Add : Bendore SCR No:54604
Polygenic hypercholesterolemia Hypertension
P/H Eczema Bronchial asthma since 15 yrs Father – DM, Hypertension Mother – DM, Hypertension
Chol – 271mg/ dl TG – 124mg/ dl LDL – 212mg/ dl HDL – 35mg/ dl
Chol – 239mg/ dl TG – 112mg/ dl LDL – 174mg / dl HDL– 41mg/ dl
MG – Relegious, Emotional stress, Anxiety about children, Sympathetic, Suicidal thoughts PG – Obese Perspiration on face Cr – Sweets, fried food Av – Sour Hot patient
Syco Syco Lyco 200 4mths 16 11 Improved
8 Name: Mr H Age : 32yrs Sex: M Occu: Clerk Relegion: Muslim Add :Urumanai SCR No: 9504
Familial combined hyperlipidemiaFunctional impotency
Mother - DM
Chol – 465mg/dl TG – 180mg/ dl LDL – 374mg/ dl HDL – 55mg/ dl
Chol – 448mg/dl TG – 170mg/ dl LDL – 394mg/ dl HDL– 20mg /dl
MG: Fear of dogs, Likes company PG: Stocky appearance Increased thirst, Scanty perspiration Cr – Veg Av – Fish, sweet Chilly patient CP: Premature ejaculation, Xanthoma Headache < evening, > sleep
Syco Psora - Syco
Phos 200, 1M
5mths 22 31 Not Improved
122
Sl. no
Particulars Of The Patient
Clinical Diagnosis
Past And
Family History
Investigations Totality
Miasms Remedy Duration of
treatment
Scoring Result
Before After FM DM B A
9 Name:Mrs G M Age :44yrs Sex:F Occu: Housewife Relegion: Christian Add :Kannur SCR No:57489
Polygenic hypercholesterolemia Osteoarthritis Sinusitis
P/H Bronchial asthma, Chikungunya Father - Bronchial asthma
Chol – 287mg/ dl TG- 175mg/ dl LDL- 210mg/ dl HDL- 42mg/ dl
Chol-269mg/ dl TG- 146mg/ dl LDL-195mg/ dl HDL-45mg/ dl
MG – Mild, Indecisive, Weepy, Fear of thunderstorm, likes consolation PG – Stocky appearancePerspiration generally decreased, Thirst decreased Cr – Rice, Fish Av- Milk Hot patient CP – Joint pains < First movement > Rest Headache < Sun, Travelling, Afternoon > Tight bandage
Syco Psora - Syco
Puls 200 3 mths 15 13 Improved
10 Name: Mrs R D Age :58yrs Sex:F Occu: Housewife Relegion: Christian Add : Kulshekar SCR No:52832
Secondary hyperlipidemiaDiabetic cataract APD
P/H- DM since 14 yrs Night blindness at 5yrs Mother – DM, Hypertension, Stroke
Chol- 234mg/ dl TG- 200mg/dl LDL – 161mg/ dl HDL – 33mg/ dl
Chol- 228mg/ dl TG – 163mg/ dl LDL – 156mg/ dl HDL– 40mg/ dl
MG – Workaholic, Relegious, Mild, Sympathetic, Perfectionist, Fear of thunder & lightning, Anxiety about health PG – Stocky appearance, Perspiration increased generally Av – Spicy, Bitter Chilly patient CP – Distension of abdomen < Non Veg, Sweets
Syco- Syphil
Syco Phos 200 5 mths 15 10 Improved
123
Sl. no
Particulars Of The Patient
Clinical Diagnosis
Past And
Family History
Investigations Totality
Miasms Remedy Duration of
treatment
Scoring Result
Before After FM DM B A
11 Name: Mr K
Age : 44 yrs Sex: M Occu: Executive officer Relegion: Hindu Add : Mangalore SCR No: 56928
Familial combined Hyperlipidemia Cholecystolithiasis
Father died of peptic ulcer Mother died of Tuberculosis
Chol – 258mg/ dl TG – 203mg/ dl LDL – 168mg/ dl HDL – 50mg/ dl
Chol – 226mg/ dl TG – 182mg/ dl LDL – 139mg/dl HDL– 51mg/ dl
MG – Workaholic, Punctual, Leadership, Confident, Superiority, Bold PG – Stocky appearance Thirst increased Addiction – occasionally Alcohol Chilly patient CP – Right hypochondriac pain < after food
Tub Syco Nux Vom 200
3 mths 14 6 Improved
12 Name :Mr B Age : 58 yrs Sex: M Occu: Railway Guard Relegion: Hindu Add : Ottappalam SCR No: 55073
Secondary hyperlipidemiaHypertension Acute Bronchitis
P/H- DM since 18 yrs Chicken pox, 3yrs back Father – Died of Renal failure following DM Mother – Died of MI
Chol – 300mg/ dl TG – 147mg/ dl LDL – 248mg/ dl HDL – 23mg / dl
Chol- 238mg/ dl TG – 129mg/ dl LDL – 183mg/ dl HDL– 30mg/ dl
MG – Workoholic, Perfectionist, Irritable, Reacts for anger PG – Lean, Perspiration increased, Appetite increased, Thirst increased, Cr – Fish, Av – Meat, Hard Stools Hot patient CP – Dry cough < Night Breathlessness on distension of abdomen
Syco - Syphil
Syco Lyco200 8 mths 23 17 Improved
124
Sl. no
Particulars Of The Patient
Clinical Diagnosis
Past And
Family History
Investigations Totality
Miasms Remedy Duration of
treatment
Scoring Result
Before After FM DM B A
13 Name: Mrs L S
Age : 48 yrs Sex: F Occu: Housewife Relegion: Christian Add : Bantwala SCR No: 57290
Familial combined hyperlipidemia Cholecystolithiasis
Mother - Hypertension
Chol- 241mg/ dl TG- 222mg/ dl LDL- 149mg/dl HDL- 48mg/ dl
Chol- 224mg/ dl TG – 207mg/ dl LDL – 130mg/ dl HDL– 53mg/ dl
MG – Loquacious, Irritable, Gets angry fast, Likes consolation,Likes to share , Helps others, Memory weak PG- Obese, Perspiration increased in general Cr – Sweets, Ice cream Av- Spicy Pleasant dreams Chilly patient CP -
Syco Syco Phos 200 3 mths 9 5 Impeoved
14 Name: Sr T Age : 43yrs Sex: F Occu: Accountant Relegion: Christian Add :Deralakatte SCR No: 14010
Familial combined hyperlipidemiaAllergic rhinitis, Arthritis Calcanean spur
P/H Fibroid uterus Mother – DM Father – DM, Hypertension Grand father – DM, Hypertension
Chol- 267mg/ dl TG – 197mg/ dl LDL – 139mg/ dl HDL – 89mg/ dl
Chol – 257mg/ dl TG – 187mg/ dl LDL – 138mg/ dl HDL– 82mg/ dl
MG: Suppressed emotion, Likes company, fear of snakes & worms ,Irritable, Anger – reacts PG: Stocky appearance Cr – Sweets Av – Pungent,sour Perspiration on back Chilly patient CP: Sneezing < morning, dust Headache > Pressure, Night Joint pain < first movement
Syco Psora- Syco
Sepia 200 5 mths 7 7 Not Improved
125
Sl. No
Particulars Of The Patient
Clinical Diagnosis
Past And
Family History
Investigations Totality
Miasms Remedy Duration of
treatment
Scoring Result
Before After FM DM B A
15 Name: Mr M
Age : 44 yrs Sex:M Occu: Airlines officer Relegion: Christian Add : Panjim SCR No: 33269
Familial hypercholesterolemia Migraine
Grand father – DM, Hypertension, Osteoarthritis Father - Hypertension
Chol- 273mg/ dl TG- 197mg/ dl LDL- 199mg/ dl HDL- 34mg/ dl
Chol- 268mg/ dl TG – 156mg/ dl LDL- 179 mg/ dl HDL– 42mg/ dl
MG – Stress , Anxiety,Irritable, Controls anger, Contradiction <, Likes consolation, Likes company, Hasty decision, Adequate confidence, Weak memory PG – Stocky appearance Perspiration of feet Cr- Fried food, Av- Leafy Veg Hot patient CP -
Syco Psora Lyco30, 200
12mths 18 14 Improved
16 Name: Sr M B Age : 67 yrs Sex:F Occu: Teacher Relegion: Christian Add : Mangalore SCR No:56632
Hepatic lipase deficiency Osteoarthritis with Osteopenia
P/H – Filariasis Hypertension since 15yrs Fibroid uterus Mother - Hypertension
Chol- 212mg/ dl TG 166mg/ dl LDL – 134mg/ dl HDL – 36mg/ dl
Chol – 198mg/ dl TG – 152mg/ dl LDL – 127mg/ dl HDL– 40mg/ dl
MG – Sensitive, Friendly, Irritable, Controls anger. Likes to share, Likes company, Likes consolation, Fear of snakes & accidents PG – Stocky appearance Av- Cold food Cr- Hot & spicy food Dreams – Frightful, accidents Hot Patient CP – Joint pain shooting , Stiffness < morning, first movement > Hot application
Syco Syco Lyco 200 7 mths 7 2 Improved
126
Sl. No
Particulars Of The Patient
Clinical Diagnosis
Past And Family History
Investigations Totality
Miasms Remedy Duration of
treatment
Scoring Result
Before After FM DM B A
17 Name: Mrs K H
Age: 57 yrs Sex: F Occu: Housewife Relegion: Muslim Add : Valencia SCR No: 56804
Familial combined hyperlipidemia Migraine, Cholelithiasis
P/H – Fibroid uterus Mother – Cardiac failure Brother - Renal failure Sister - DM, Hypertension
Chol- 281mg/ dl TG- 349mg/ dl LDL- 163mg/ dl HDL- 50mg/ dl
Chol – 256mg/ dl TG – 297mg/ dl LDL – 143mg/ dl HDL– 54mg/ dl
MG – Brooding of past, Weepy, Grief, Anger on contradiction, Does not like consolation, likes company PG- Stocky appearance, Perspiration increased in general Cr- Fish Hot patient CP – Headache Burning, Radiadting to neck, Vomiting, Lachrymation < Sun, Travelling, Crowd, Tension, Talking Incontinence of urine
Syco- Syphil
Psora- Syco
Lyco 200 4 mths 19 12 Improved
18 Name: Mr C Age : 63 yrs Sex: M Occu: Lab assistant Relegion: Hindu Add : Mangalore SCR No: 55419
Secondary hyperlipidemia Grade I Renal parenchymal disease, Cholecystolithiasis Grade II BPH
P/H – Hydrocoele at the age of 28 yrs, Hypertension since 5 yrs Father- Hypertension Mother- DM, Hypertension, Osteoarthritis Brother- Hypertension
Chol- 247mg/ dl TG – 127mg/ dl LDL – 183mg/ dl HDL – 37mg/ dl
Chol- 209mg/ dl TG- 113mg/ dl LDL- 144mg/ dl HDL- 44mg/ dl
MG- Perfectionist, Confident PG – Stocky appearance Profuse general perspiration, offensive, yellow staining Cr- Fish Addiction – Smoking till 28yrs, Beer occasionally Chilly patient CP – Pricking pain in loin < Exertion
Syco Syco Calc carb 10 M
10mths 14 4 Improved
127
Sl. No
Particulars Of The Patient
Clinical Diagnosis
Past And Family History
Investigations Totality
Miasms Remedy Duration of
treatment
Scoring Result
Before After FM DM B A
19 Name: Mrs A M
Age : 50 yrs Sex: F Occu: Lab assistant Relegion: Christian Add : Surathkal SCR No: NITK 06
Polygenic hypercholesterolemia Varicose veins Osteoarthritis Cervical spondylosis
P/H – Eczema in childhoodBronchial asthma since 20 yrs Cerebral infarction
Chol- 251mg/ dl TG- 102mg/ dl LDL- 186mg/ dl HDL- 44mg/ dl
Chol- 176mg/ dl TG- 70mg/ dl LDL- 106mg/ dl HDL- 56mg/ dl
MG – Mild, Weak memory, Inadequate confidence PG – Stocky appearance Appetite increased Thirst decreased profuse Perspiration Cr-Tea, Icecream, Sweets, Hot food, Fish, Spicy but disagreesAv- Oily food Ambhithermal CP – Aching pain of legs < Exertion, Standing Pricking pain & stiffness of joints < first movement > wam application
Syco - Syphil
Syco Puls 200 10mths 13 0 Improved
20 Name: Mrs B Age :60yrs Sex: F Occu: Housewife Relegion: Muslim Add : Kasargod SCR No: 5535
Polygenic hypercholesterolemia CAD APD
P/H – Haemorrhoids since 25 yrs Low back ache since 6 yrs Mother & 2 brothers died of cancer Brother died of MI Brother - Haemorrhoids
Chol- 412mg/ dl TG – 98mg/ dl LDL – 349mg/ dl HDL – 44mg/ dl
Chol- 330mg/ dl TG- 68mg/ dl LDL - 275mg/dl HDL- 42mg/ dl
MG – Irritable, Does not express /share, Suppressed emotion, Anxious about health, Weeps alone, Anger on contradiction, Fear of Snakes, Darkness, Robbers, Being alone, Weak memory PG – Stocky appearance Appetite decreased, Thirst decreased Cr- Fish, Sweet, Sour, Meat Unsatisfied stool Sleep disturbed Ambithermal CP- Breathlessness < Lying, Tension, Exertion Distension of abdomen < Early morning
Syphil Syco Nat Mur 200
8mths 19 16 Improved
128
Sl. no
Particulars Of The Patient
Clinical Diagnosis
Past And Family History
Investigations Totality
Miasms Remedy Duration of
treatment
Scoring Result
Before After FM DM B A
21 Name: Mrs P B
Age : 61 yrs Sex: F Occu: Housewife Relegion: Hindu Add : Padil SCR No: 1727
Familial hypercholesterolemia Osteoarthritis Cervical spondylosis
P/H – Fibroid uterus, Hypertension since 14 yrs Hypothyroidism since 5yrs Ganglion
Chol – 346mg/ dl TG - 206 mg/ dl LDL – 287mg/ dl HDL- 18 mg/ dl
Chol- 276mg/ dl TG - 194mg/ dl LDL- 196mg/ dl HDL- 42 mg/ dl
MG – Grief, Consolation <, Gets angry on contradiction Suppress anger PG – Stocky appearance Appetite decreased Perspiration increased in general Sleep disturbed by thoughts Cr- Fried Cannot tolerate fat Hot patient CP- Knee joint pain, Leg pain < Night
Syco Syco Medorrhin200
12 mths 29 16 Improved
22 Name: Mr M S Age : 30yrs Sex: M Occu: Business Relegion: Muslim Add : Adur SCR No: 7994
Familial combined hyperlipidemiaTension headache Flatulent dyspepsia Arthritis
Father- Hypertension Mother- Hypertension, DM, Gastritis
Chol- 390mg/ dl TG – 178mg/ dl LDL – 315mg/ dl HDL – 41mg/ dl
Chol- 296mg/ dl TG – 156mg/ dl LDL – 229mg/ dl HDL– 46mg/ dl
MG – Irritable, Gets angry fast & shouts, Anticipatory anxiety about business, Doesn’t like contradiction Likes company & consolation PG – Stocky appearance Perspiration increased, Appetite increased, Thirst increased Cr- Meat, egg, spicy Sleep disturbed with tension ,Increased sexual desire, Amorous dreams Addiction occasionally beer, Smoking Hot patient CP – General < 4-5 PM, Tension, Empty stomach Retrosternal burning < cold drinks, Egg > Hot drinks
Syco Psora Lyco 200, 1M
5mths 20 15 Improved
129
Sl. no
Particulars Of The Patient
Clinical Diagnosis
Past And
Family History
Investigations Totality
Miasms Remedy Duration of
treatment
Scoring Result
Before After FM DM B A
23 Name: Mr A
Age : 52 yrs Sex: M Occu: Bus conductor Relegion: Christian Add : Deralakatte SCR No: 8424
Secondary HyperlipidemiaDiabetis Mellitus
P/H – Jaundice, Lipoma
Chol – 217mg/ dl TG – 146mg/ dl LDL – 148mg/ dl HDL – 40mg/ dl
Chol – 200mg/ dl TG – 139mg/ dl LDL – 128mg/ dl HDL– 45mg/ dl
MG – Stress, Perfectionist Likes company, Sensitive, Weepy, Irritable PG – Stocky appearance Perspiration decreased, Thirst increased Cr- Chicken, Fried, meat, fatty food, Pickle, milk Addiction – Alcohol, Smoking Chilly patient CP – Tingling & numbness of extremities < Night
Syco Syco Lyco 200 5mths 6 1 Improved
24 Name: Mrs J Age :36 yrs Sex: F Occu: Housewife Relegion: Muslim Add : Arkula SCR No: 3647
Secondary hyperlipidemia Osteoarthritis Cervical spondylosis Varicose veins Hypertension Diabitis Mellitus
P/H – Malaria, TonsillitisNasal polyp, Cervical lymphadenopathy, Valvular stenosis Mother- DM Brother- DM, Cardiac disease
Chol- 240mg/ dl TG- 208mg/ dl LDL – 151mg/ dl HDL-48mg/ dl
Chol – 218mg/ dl TG – 160mg/ dl LDL – 138mg/ dl HDL– 48mg/ dl
MG- Anxious about health, Perfectionist, Weepy, Yielding, Fear of being alone, Irritable, Short tempered, Shouts back, Likes company & Consolation PG – Obese Profuse, offensive perspiration, Thirst decreased, Cr- Chicken, Meat, Spicy Sleep disturbed, Dreams frightful, snakes Hot patient CP – Knee joint pricking pain < Exertion, Sitting > Continued motion Back pain < lying on back
Syco Syco Lyco 200., 1M
5mths 10 4 Improved
130
Sl. no
Particulars Of The Patient
Clinical Diagnosis
Past And Family History
Investigations Totality
Miasms Remedy Duration of
treatment
Scoring Result
Before After FM DM B A
25 Name: Mrs A N
Age : 35 yrs Sex: F Occu: Housewife Relegion: Hindu Add : Ballalbagh SCR No: 17102
Familial combined hyperlipidemiaTension headache Haemorrhoids Enterobiasis
P/H – Malaria , Still birth delivery Mother – Hypertension Father- Hypertension, Epilepsy
Chol- 260mg/ dl TG – 198mg/ dl LDL – 177mg/ dl HDL – 44mg/ dl
Chol – 237mg/ dl TG – 179mg/ dl LDL – 155mg/ dl HDL– 49mg/ dl
MG – Courageous, Cannot tolerate insults, Irritale, Shouts back. Dipressed, Fear of snakes, Tensed on silly matters PG – Stocky appearance Perspiration increased on neck & back, Thirst increased, Cr- Leafy veg, Sweets Dreams of falling down, Escaping Chilly patient CP – Headache throbbing < Crowd, Noise, Tension > Warmth, Rest Hard stool Burning < Chicken
Syco - Syphil
Psora- Syco
Calc Carb 200
5mths 15 9 Improved
26 Name: Mrs C G Age : 55 yrs Sex: F Occu: Housewife Relegion: Christian Add : Ladyhill SCR No: 10548
Familial hypercholesterolemia Migraine, Allergic rhinitis
P/H – Chickenpox Mother- Hypertension, Hypercholesterolemia, MI Father- Expired of Carcinoma thyroid
Chol- 270mg/ dl TG – 147mg/ dl LDL – 203mg/ dl HDL – 38mg/ dl
Chol – 253mg/ dl TG – 140mg/ dl LDL – 183mg/ dl HDL– 42mg/ dl
MG – Suppressed emotion, Grief, Relegious, Anxious about health, Fastidious, Likes company & consolation PG – Lean, Perspiration increased in general, Thirst increased, Cr- Warm Sleep unrefreshing Hot patient CP – Sneezing < Morning, Nose & eye itching Watery coryza Head heaviness < Morning > Vomiting
Syco- Syphil
Psora Sulphur 200
3mths 14 13 Improved
131
Sl. no
Particulars Of The Patient
Clinical Diagnosis
Past And
Family History
Investigations Totality
Miasms Remedy Duration of
treatment
Scoring Result
Before After FM DM B A
27 Name: Mrs J D
Age : 70 yrs Sex: F Occu: Housewife Relegion: Christian Add : Konaje SCR No: 16373
Familial combined hyperlipidemia Osteoarthritis
P/H – Hypertension since 10 yrs Father – Carcinoma throat Sister IHD
Chol- 272mg/ dl TG- 186 mg/dl LDL – 191mg/ dl HDL- 44mg/ dl
Chol- 259mg/ dl TG – 170mg/ dl LDL – 174mg/ dl HDL– 51mg/ dl
MG – Mild, Weepy, Consolation >, Memory weak PG – Stocky appearance Appetite decreased, Thirst decreased Perspiration increased on head Cr- Salt. Hard stools, Burning micturition Hot patient CP- Knee joint pain < Morning, walking, > Rest Pressure incontinence of urine
Syco- Syphil
Syco Calcarea carb 200
4mths 15 13 Improved
28 Name: Sr S Age : 58 yrs Sex: F Occu: Teacher Relegion: Christian Add :Mangalore SCR No: 18316
Familial combined hyperlipidemia Flatulent dyspepsia Cervical spondylosis Uterine fibroid
P/H – Typhoid Pneumonia Mother – Fibroid uterus, Hypertension Father- hypertension
Chol- 299mg/ dl TG- 208mg/ dl LDL- 207mg/ dl HDl- 51mg/ dl
Chol- 260mg/ dl TG- 97mg/ dl LDL- 183mg/dl HDL- 58mg/ dl
MG – Forsaken feeling, Insecurity, Sympathetic, Irritable, hates contradiction, Does not like consolation, Suppressed emotion, Fear of disease PG – Stocky appearance Perspiration increased on upper part of body, yellow staining Thirst increased Cr- Veg Av- Salt, Milk Hard difficult stool once in 2 days Urine difficult to control. Sleep disturbed Hot patient CP – Fullness in abdomen < Pork, Dal, Fish Neck pain < movement, Sitting straight
Syco Syco Sepia 200 12mths 17 13 Improved
132
Sl. no
Particulars Of The Patient
Clinical Diagnosis
Past And
Family History
Investigations Totality
Miasms Remedy Duration of
treatment
Scoring Result
Before After FM DM B A
29 Name: Mr A R
Age : 30 yrs Sex: M Occu: Contractor Relegion: Muslim Add : Kallappu SCR No: 12984
Hepatic Lipase deficiency Obesity
Mother – Filariasis, DM
Chol- 212mg/ dl TG- 200mg/ dl LDL- 140mg/ dl HDL- 32mg/ dl
Chol- 188mg/dl TG- 171mg/ dl LDL- 114mg/ dl HDL- 40mg/ dl
MG- Irritable, Quarrelsome, Obstinate, Anxious, Contradiction <, Ambitious, Domonating, Fear of height PG – Obese Appetite increased, Thirst increased, Av- Veg Cr- Non Veg, Spicy. Hard stool Hot patient
Psora- Syco
Psora Lyco 200 3mths 9 2 Improved
30 Name: Mr P M Age : 29 yrs Sex: M Occu: Merchant navy Relegion: Christian Add : Kulai SCR No: 17226
Polygenic hypercholesterolemia Obesity Tension headache
Father – Hypertension, DM
Chol- 205mg/ dl TG- 91mg/ dl LDL- 143mg/ dl HDL- 45mg/ dl
Chol-200mg/ dl TG- 90mg/ dl LDL- 141mg/ dl HDL- 41mg dl
MG – Stress, Irritable, gets angry fast, Shouts back, Optimistic, Confident PG – Obese Perspiration increased in general, Appetite increased Thirst increased for cold water Cr- Non Veg Av- Salt Addiction – occasionally alcohol & smoking Hot patient CP- Weight gain Head ache throbbing, Pressure with perspiration < Walking > Rest Eye redness < Exposure to heat
Syco Psora Calc carb 200
3mths 4 4 Not improved
133