Disease Review

DISEASE REVIEW OF MEDORAGA

Hyperlipidema or Dyslipidemia involves abnormally elevated levels of any or
all lipids and /or lipoproteins in the blood i.e., elevation of plasma cholesterol,
triglycerides, low or high density lipo protein. A linear relation exists between lipid
levels & cardio vascular risks; hence there is a great emphasis in the treatment of
dyslipidemia. The term Hyperlipidema or Dyslipidemia can be correlated with
Medodhtugata vyadhi / santharpana janya vyadhi as per Ayurvedic literature.
According to Ayurvedic classics, it is caused by derangement of Agni which leads to
aama which in turn causes Medodhatwagnimandya and uttarothara dhatu poshana does
not occur which leads to accumulation of medodhatu in the srotas. It gives rise to
various disorders of meda origin. In modern it can be referred as Hyperlipidema or
Dyslipidemia.
HISTORICAL REWIEW
SAMHITA KALA (2000 B.C-1300 A.D)
The main classical text of this era is Charaka, Sushruta &Vagbhata
samhitha.Brihatrayies explains sneha and snehapradhana aharas helps in the formation
of medapradoshaja vyadhis.

Charaka samhitha :( 2 B.C) 1

Charaka mentioned medodosha in Charaka Sutrastana 21st chapter “Ashta

Ninditiya Purusha” (eight despicable personalities), Its causative factors are mainly
exogenous and hereditary.
Sushruta Samhitha (2 AD) 2
Susrutacharya mentioned about production of medas from rasa datu leads to obesity.
Madhava Nidana (7th A.D.)3
Madhava Nidana has elaborated the pathophysiology of this disease on the basis
of fat tissue.
Sharangadhara Samhita (13th AD)4
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In this text sveda has been mentioned as Upadathu of Meda and described
sthaulya as Medo dosha janya vyadi.

Bhavaprakasha Samhitha (16th A.D)5

In this text Bhavamishra mentioned that Medodathu is increased in the body due
to lack of exercise etc and detailed study about the aetiogenesis, signs and symptoms and
treatment aspects of Medoroga.
Chakrapani (11th century)6
Acharya Chakradatta has compile the original thoughts of Brihattrayi and
presented with their own views under the heading of Medorogadhikar.In the line of
treatment of sthaulya he has commented that Guru Property helps to alleviate Kshudha
while Aptharpana property helps to reduce Meda.

MEDOROGA7
Introduction
Lipids in the body can be correlated with Medodathu, Vasa, and Majjadhatu;
these are in the normal condition. But when they are in disturbed state disease occurs
and can be termed as Rasa Raktha Snehavridhi or Medodushti (Hyperlipidemia).This
medas deposited in Stayi and Asthayi forms. The Asthayi forms of Medas are found in
Raktha Dhatu and which is the Cholesterol, Triglycerides and some are transported by
Lipoproteins. Sthayi forms can be found in Adipose tissue.
SYNONYMS OF MEDHOROGA
SYNONYMS CA.S SU.S KA.S AS.S AS.H M.N SHA.S B.P Y.R
Medoroga - + - + + + + + +
Medo dosha + - - - + - + + +
Medovriddhi - - - - - - - + +
Medovikara - - - - - - - + -
Medogada - - - - - - + + -
Medapusti - - - - - - - - +
Atipushti - - - + - - - + -
Pushti + + + + - - + + +
Upachaya + + + + + - + + +
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Jatharya - + - - - - - - -
Brimhatva + - + + + - - - -
Medadushti - - - - - - - - +

NIDANA OF MEDOOGA8
All Acharya stressed up on the role of imbalanced diet sedentary habits
for the etiology of manifestation of the Medoroga or Santarpanajanya vyadhis.
Aharaja factors
Includes atisampoorana (over eating) adhyasana (repeated eating), Madhura
guru sheeta dravyaahara (sweet heavy and cold foods), Sleshma dravya ahara,
atimadyasevana (excess alcohol consumption)
Viharaja factors
Divaswapna (day sleep), Avyayama (lack of excercise), achintana
(lack of thinking),Harshanityatva(exhilaration),and sedentary habits.
Anyanidana: Excess Use of therapeutic measures.

SAMPRAPTHI GHATAKAS9
Udbhavastana - Amashaya
Sanchar - Rasayani
Adhishtana - Whole body.
Vyatka - Whole body
Dosha - Tridosha, Samanavayu, Apanavayu, Vyanavayu Pachaka pitha
Srotas - Annavaha, Rasavaha, Mamsavaha, Medovaha.
Sroto dushti - Agnimandya Medodhatvagni mandhya, Jadaragnimandhya
Ama - Medodhatugata
STHANA AND SWARUPA OF MEDHO DHATU
MEDODHATU
POSHAKA(mobile in nature) POSHAKA(mobile in nature)
It circulated in whole body along with It circulated in whole body along with
Gatiyuktha rasa–rakta dath for nourishing Gatiyuktha rasa–rakta dathu for nourishing
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the Poshya Meda Dhatu. the Poshya Meda Dhatu.

According to Modern science it can be According to Modern science it can be
correlated with cholesterol and lipids, correlated with cholesterol and lipids,
which are present in circulating blood. which are present in circulating blood.

Karma of Medhodhatu
According to Sushruta samhitha- Sneha, Sweda, Dridhatva and Atipushti are the
functions of medodhatu.
According to Ashtanga samgraham- Netra and Gatrasnigdhata are the functions of
medadhatu Snehana is the main function of Medhodhatu and with Sneha property it
helps to keep luster of skin, hair, eye, etc.
MEDHOVAHA SROTAS
The channels which give nutrition to the Medhodhatu and the vessels carrying the
nutritive material up to the site of Medodhatu can be considered as Medo vaha
Srotas(It carries nutrition from the preceeding Dhatu i.e. Mamsa (Poshaka) to Medo
dhatu).
SADHYAASADHYATA
Medoroga is a Krichrasadhya vyadhi.

CHIKITSA10
1) Nidana Parivarjana
2) Samshodana
3) Samsamana
NIDANA PARIVARJANA
This is the first line of treatment of any disease and it is the most important line
of treatment of Medovyadi also. This indicates that the root of samprapti process ie.,
Nidana must be avoided for the best management of disease.Aharatmaka,
Viharatmaka, manas and others are comes under nidana which are responsible for the
disease should be avoided.
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SAMSHODHANA THERAPY
Shodhana means Apakarshana of Dosha. The therapies in which the vitiated Doshas are
eliminated after mobilizing them from the body is known as Shodhana therapy.
SAMSAMANA THERAPY
The therapy, which could not excrete the dosha from the body, but suppresses
the vitiated dosha and simultaneously brings equilibrium to imbalance of Dosha, is
called as Samsamana. Langhana and Rukshana can be administrated for Samsamana
purpose in staulya.
Chikitsa can be implemented through seven different ways.
 Deepana
 Marutasevana
 Kshudha Nigraha
 Pachana
 Atapa sevana
 vyayama
PATHYA- APATHYA11
AHARA PATHYA APATHYA
Suka Dhanya Purana Shali,Kodrava, Godhuma,Naveena
(Creal grain) Shyamak,Yava,Laja,Nivara. Dhanya
(Shali)
Shami Dhanya Mudga,Rajamasha,Kulatha,Chanaka, Masha,Tila
Adaki
Shaka Varga Patola,Shigru,Mulaka ,Surasa. Kanda,Shaka,Madhura.
(Vegitables)
Phala Varga Kapitha,Jambu,Amalaki,Bhibitaki, Madhura phala
(Fruits) Haritaki,Marica,Pippali,Eranda.
Drava varga Madhu,Takra,Shilajatu. Ksheera
LIPIDS: 12
Lipids constitute a heterogeneous group of compounds, which are relatively
insoluble in water, but freely soluble in non-polar organic solvents like benzene,
chloroform,ether,acetone etc.They are of great importance to the body as the chief
 Disease Review

concentrated storage forms of energy, besides their role in cellular structure and various
other biochemical functions.
PLASMA LIPIDS13:
Main plasma lipids are:-
 Cholesterol and its esters.
 Triglycerides.
 Phospholipids.
 Non-Esterified fatty acids.
Cholesterol and its esters:
Cholesterol is synthesized in most of the body tissue of the body except CNS
(Wilson, 1968) about 6mg of cholesterol circulates in the plasma. There are two source
of cholesterol, 300mg/day comes from dietary source and about 800mg/day comes from
endogenous synthesis. The cholesterol pool is maintained by a steady state by the
excretion of an equal amount of cholesterol daily. About 800mg/day is lost through
faeces and 25mg/dl as bile acids. The remaining 50mg is used for hormone production or

excreted through skin(Paul‟s Samuel,1983).Cholesterol exists in plasma in two forms

–Free cholesterol(20-40%) and Esterified cholesterol(60-80%).In human,60-70%

cholesterol is transported by LDL,20-30%by HDL and 5-10%by VLDL.
Functions:
Present in every cell of the body and is part of cell membrane.
Endocrine glands such as adrenals, ovaries and testes store cholesterol for conversion
into the hormones like estrogens, cortisones, aldosterone etc.It prevents toxins from
entering into the cells. It is closely related to the defensive mechanism of the body. It is
observed that during acute infection blood cholesterol falls and tends to rise during
recovery.
It also needed for synthesis of vitamin D and to form cell membrane and to insulate
nerves.
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2. Triglycerides:
Triglycerides are esters of three fatty acids and glycerol. It can be both
exogenously and endogenously derived. The exogenous TG is derived from diet and it
circulates in the blood in the form of chylomicrons.The endogenous form is
synthesized in the liver and mostly constitutes the TG presents in VLDL (Frederickson
1965).
Uses:They provide energy for different metabolic processes.
3. Phospholipids:
These forms come under conjugated lipids which contain glycerol and fatty acid
with some specific substance.E.g.Lecithin .Phospholipids constitute 25%LDL and 30%
HDL.
Uses: They are an important constituent of lipoproteins are essential for the formation of
some of them. They participate in the formation of structural elements i.e. membranes.
4:Non-Essential fatty acids:
They are important sources of energy. The amount of free fatty acid circulating in
plasma are insignificant i.e. 8-20mg/day out of a total of 400-800mg of total lipids.
Lipoproteins:
Cholesterol and triglycerides are hydrophilic and require to be transported
through the aqueous environment of plasma. For this they form a family with
special protein called lipoproteins. These lipid protein particles are called as lipoproteins.
Depending upon density (by ultra centrifugation) or on the electrophoresis mobility,
the lipoproteins in plasma are classified in to 5 major varieties;
a) Chylomicrons.
b) Very low-density lipoproteins (VLDL) or pre -beta lipoproteins
c) Intermediate density lipoproteins (IDL) or broad-beta lipoproteins d) Low density
lipoproteins (LDL) or beta lipoproteins.
e) High density lipoproteins (HDL) or alpha lipoproteins.
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Lipid Transport In Body14

a) Exogenous Pathway (That is transport of dietary lipids):-through chylomicrons.
b)Endogenous Pathway (i.e. transport of synthesized lipids):-through lipoproteins. a)
Exogenous pathway:
It is responsible for the digestion and tissue dissemination of dietary fats. In the
intestinal mucosa all of dietary TG and 50% of cholesterol are taken up by the
intestinal cells (enterocytes)after combination with bile salts to form water soluble
micelles. They are incorporated with chylomicrons and secreted into intestinal lymphatic
to reach blood stream via thoracic duct.TG component is removed by enzyme
lipoprotein lipase located on the endothelial surface of capillary beds in adipose
tissue and cardiac and skeletal muscles.
From here the apolipoproteins and phospholipids is shed to form the precursor of HDL
and the remnant cholesterol which is taken up by the hepatic LDL receptor to be used for
the synthesis of bile acid and VLDL and some are excreted into bile.
b) Endogenous Pathway:
It conveys lipids from liver to the peripheral tissue back to the liver. It is divided in to
2 subsystems
1) The Apo B-100 lipo protein system: - Transport of triglycerides, cholesterol, etc.
from liver to other tissues through VLDL&LDL.
2) The Apo A-1 lipoprotein system:-Reverse cholesterol transport through HDL,
from other tissue to liver.
LDL
LDL amounts for 2/3 of plasma cholesterol. Thus when liver and extra hepatic
tissue require more cholesterol they increase the number of LDL receptors in the cell
surface and remove LDL from plasma(75%).25%LDL is removed by peripheral tissues
like adrenals and gonads which have LDL receptors.
In 1985 ,Goldstein and Brown were awarded the Nobel Price for the
 Disease Review

discovery of LDL receptors .This regulation of hepatic LDL receptor pathway is

dominant mechanism for controlling LDL levels in humans .The ability to modulate
hepatic LDL receptor number by diet and therapeutic agents form the basis of most
current techniques to lower LDL levels and for this reason subjects with homozygous
hypercholesterolemia who completely lack LDL receptor do not respond to any
hypolipidaemic drugs used at present(Brown and Goldstein1986).
HDL
HDL is synthesized in the liver as discoidal particles. They contain free
cholesterol and phospholipids and Apolipoproteins.
VLDL and IDL
Liver secretes VLDL in to blood. They are acted upon by endothelial lipoprotein
lipase similar to chylomicrons. The released fatty acids are stored in adipose tissue and
muscle .So the function of VLDL is to transport triglycerides from liver to adipose tissue
and muscle. The remnant called the intermediate density lipoprotein (IDL), which has
more cholesterol than triglycerides. Half of the IDL is taken back by the liver cells
through attachment to another type of LDL receptor. From this, triglycerides molecules
are gradually released leading to formation of LDL.

DYSLIPIDEMIA / HYPERLIPIDEMA

Dyslipidemia15 is a metabolic disorder in which the abnormal levels of Lipids

like Cholesterol, Triglycerides or Fat phospholipids in the blood. Most dyslipidemias are

Hyperlipidemia16 ie., an elevation of lipids in blood and there is a deposition of

esterified cholesterol in the wall of arteries .It can cause narrowing and blockage of
arteries and produce mainly heart disease while other diseases include CVD,Renal
disease, Liver disease, Peripheral vascular disease. Hyperlipidemia is not a single disease
but a range of disorder, with a variety of metabolic disorders, even environmental as well
as genetic factors.
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FREDERICKSON’S CLASSIFICATION OF HYPERLIPIDAEMIA17

Primary Hyperlipidemia is classified into-type I, IIa, IIb, III, IV, &V. They may
be only hypercholesterolemia (type IIa)or only Hypertriglyceridemia(type I,IV&V)or
both (combined form)(type II b & III).
Hyperlipoproteinemia type I
Type I Hyperlipoproteinemia exists in several forms.
Lipoprotein lipase deficiency (Type Ia): due to a deficiency of lipoprotein lipase (LPL)
or altered apolipoproteins C2, resulting in elevated chylomicrons.The particles that
transfer fatty acids from the digestive tract to the liver.
Familial apoprotein CII deficiency (Type Ib): a condition caused by a lack of
lipoprotein lipase activator.
Lipoprotein lipase (Type Ic) :Chyomicronemia
Type I Hyperlipoproteinemia usually presents in childhood with eruptive xantomata
and abdominal colic .
Complication :Retinal vein occlusion, acute pancreatitis, organomegaly, and lipaemia
retinalis.
Hyperlipoproteinemia type II
Hyperlipoproteinemia type II, by far the most common form ,is further classified
into type IIa and type IIb depending mainly on whether there is elevation in the
triglyceride level in addition to LDL cholesterol.
Hyperlipoproteinemia type III
This form is due to high chylomicrons and IDL(Intermediate density
lipoprotein).Also known as broad beta disease or dysbeta lipoproteinemia,the most
common cause for this form is the presence of ApoE E2/E2 genotype.
Hyperlipoproteinemia type IV
Familial Hypertriglyceridemia is an autosomal dominant condition
occurring in approximately1%of the population.
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Hyperlipoproteinemia type V
Hyperlipoproteinemia type V is very similar to type I, but with high VLDL in
addition to chylomicrons.
It is also associated with glucose intolerance and hyperuricemia.
Acquired (Secondary)
Acquired Hyperlipidemia often mimic primary forms of Hyperlipidemia and can
have similar consequences. They may result in the increased risk of premature
atherosclerosis or when associated with marked Hypertriglyceridemia ,may lead to
pancreatitis and other complications of the Chyomicronemia syndrome .
The most common cause of acquired Hyperlipidemia are:-
a) Diabetes mellitus.
b) Use of drugs such as diuretics, beta blockers, and estrogens.
c) Other conditions leading to acquired Hyperlipidemia include
d) Hypothyroidism
e) Renal failure
f) Nephrotic syndrome g) Alcohol usage
h) Some endocrine disorders and metabolic disorders

Elevated cholesterol levels are generally classified18

Desirable: TC>200mg/dL, HDL<35mg/dL, LDL>130mg/dL
Borderline: TC >200-239, HDL<35mg /dL, LDL 131-160, and fewer than 2 risk
factors and without vascular disease.
High: presence of vascular disease and LDL≥ 160or TC≥240 mg/dL or HDL<35
mg/dL,or 2 or more risk factors.
An additional factor to consider is the total cholesterol /HDL ratio .The goal is to keep
the ratio below 5:1; the optimum ratio is 3.5:1.
DIAGNOSIS
Diagnosis of Hyperlipidemia is done via blood measurement of Cholesterol,
 Disease Review

Triglycerides, LDL, VLDL and HDL. LDL and VLDL can be measures indirectly by
applying the formula of FRIEDEWALD et al for calculation as
LDL=Total Cholesterol-HDL-VLDL
VLDL=Triglycerides/5 where all the values are measured in milligram per deciliter.
PARAMETERS
Most commonly used parameters in Hyperlipidemia are:
 1)Body Mass Index
 2)Waist circumference
 3)Waist/Hip ratio
 4)Relative weight(R W)
 5)Ponderal Index
 6)Skin fold thickness
 7)Age specific weight

MANAGAMENT OF HYPERLIPIDAEMIA:19
1.Dietary management;
A)To reduce meat and dairy products consumption.
B)Increase of vegetables, fruits and pulses in diet together with increased amount of
fish.
Weight Reduction: Weight should be in normal range as according to weight-height
chart.
Drug therapy: Along with diet and lifestyle changes drug can be administered.
Avoidance of substances: Smoking, alcohol etc
TREATMENT

ATORVASTATIN20
Statins are oral drugs used to improve cholesterol levels and decrease the risk
for a heart attack and stroke. Atorvastatin is a competitive inhibitor of HMG –COA
reductase .HMG –COA reductase catalyzes the reduction of3-hydroxy-3-
 Disease Review

methylglutaryl-coenzyme A to mevalonate, which is the rate-limiting step in hepatic

cholesterol biosynthesise.Inhibition of the enzyme decreases cholesterol synthesis,
increasing expression of low density lipoprotein receptors on hepatocytes.
Indications
Adjunct to diet in primary hypercholesterolemia (heterozygous familial and
non- familial) and mixed dyslipidemia (Type lla and llb)to reduce Total cholesterol,
LDL- cholesterol ,apo B and Triglycerides and to increase HDL-cholesterol. Adjunct to
diet in diet in treating elevated serum triglycerides (Type lV),Treatment of primary
dysbetalipoproteinemia,(Type lll).Adjunct to other lipid-lowering treatments in
homozygous familial hypercholesterolemia to reduce Total-cholesterol and LDL
cholesterol.LDL cholesterol &Apo B in patients 10-17 years of age with heterozygous
familial hypercholesterolemia if LDL cholesterol remains ≥ 190 mg/dL with either
family history of premature cardiovascular disease or if patients has at least 2 other
CVD risk factors. To reduce risk of MI, Stroke, and risk of revascularization procedures
in Adults risk. To reduce risk of MI and Stroke in patients with Type 2 diabetes and
risk, and angina in patients with clinically evident coronary heart disease.
Contraindications
Muscle damage due to Autoimmunity, Stroke caused by bleeding in the brain,
Liver failure, Liver problems, Kidney disease, serious muscle damage that may lead to
kidney failure. Recent operation, Loss of memory, High blood sugar, Abnormal liver
function tests, Injury, Pregnancy, A mother who is producing milk and breast feeding.
Side Effects
Severe allergic reactions, Itching, Difficult breathing or swallowing, Tightness
in the chest, Swelling of the- face, mouth,throat, tongue, lips etc, Burning, Numbness or
Tingling, Change in the amount of urine produced, Confusion , Memory problems,
Mental or mood problems, Muscle pain , Muscle weakness, weakness, Tenderness,
Frequent urination, joint pain , swelling of a tendon or joint, Persistent nausea, Loss of
appetite, Unusual tiredness.
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