A REVIEW OF HYPERLIPIDEMIA AND MEDICINAL PLANTS

Abstract

ABSTRACT
Hyperlipidemia has been ranked as one of the greatest risk factors contributing to prevalence and severity of coronary heart diseases. Coronary heart disease, stroke, atherosclerosis and hyperlipidemia are the primary cause of death. The elevation of serum total cholesterol and low density lipoprotein (LDL) cholesterol has been reported as a primary risk factor
for cardiovascular disease. Hyperlipidemia is a condition when abnormally high levels of lipids i.e. the fatty substances are found in the blood. Hypolipidemic drugs are extensively used as prophylactic agents to prevent such atherosclerosis induced disorders. But these hypolipidemic drugs are not free from adverse effects. Many plant derivatives and domestic remedies have been screened for their hypolipidemic action. More than 70 medicinal plants have been documented to have significant hypolipidemic action. During the last decade, an increase in the use of medicinal plants has been observed in metropolitan areas of developed countries. Medicinal plants play a major role in hypolipidemic activity. The advantages of herbal medicines reported are effectiveness, safety, affordability and acceptability.This review focus on hyperlipidemia and the role of plants used for the treatment of hyperlipidemia.

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ABSTRACT
Hyperlipidemia has been ranked as one of the greatest risk factors contributing to prevalence and severity of coronary
heart diseases. Coronary heart disease, stroke, atherosclerosis and hyperlipidemia are the primary cause of death. The
elevation of serum total cholesterol and low density lipoprotein (LDL) cholesterol has been reported as a primary risk factor
for cardiovascular disease. Hyperlipidemia is a condition when abnormally high levels of lipids i.e. the fatty substances are
found in the blood. Hypolipidemic drugs are extensively used as prophylactic agents to prevent such atherosclerosis induced
disorders. But these hypolipidemic drugs are not free from adverse effects. Many plant derivatives and domestic remedies
have been screened for their hypolipidemic action. More than 70 medicinal plants have been documented to have
significant hypolipidemic action. During the last decade, an increase in the use of medicinal plants has been observed in
metropolitan areas of developed countries. Medicinal plants play a major role in hypolipidemic activity. The advantages of
herbal medicines reported are effectiveness, safety, affordability and acceptability.This review focus on hyperlipidemia and
the role of plants used for the treatment of hyperlipidemia.
Keywords Atherosclerosis, hyperlipidemia, herbal drugs, lipids, obesity.
1. INTRODUCTION
Hyperlipidemia is a condition when abnormally high levels of lipids i.e.the fatty substance are found in the
blood.This condition is also called hypercholesterolemia/hyperlipoproteinemia
1
.Human body is complex machinery and for
maintaining the homeostasis of various organ and organ system.Any undesirable change will disturb the balance resulting in
diseased state
2
.Lipids are fats in the blood stream,commonly divided into cholesterol and triglycerides. Cholesterol
circulates in the bloodstream and is involved in the structure and function of cells.Triglycerides(TG) are best viewed as
energy that is either used immediately or stored in fat cells.TG are manufactured in the liver from the foods or by being
absorbed from the intestine
3
.Virchow in 19
th
century who identified cholesterol crystals in atherosclerotic lesion and stated
that endothelial cell injury initiates atherogenesis
2
.In a modification of this hypothesis it was proposed that the endothelium
normally influences the behaviour of arterial smooth muscle cells by providing a barrier to the passage of plasma
proteins,and that the major effect of haemodynamic or other factors that injure endothelium is to reduce the effectiveness of
the barrier
4
.Arteries are normally smooth and unobstructed on the inside, but in case of increased lipid level, a sticky
substance called plaque is formed inside the walls of arteries. This leads to reduced blood flow, leading to stiffening and
narrowing of the arteries. It has been proved that elevated plasma levels of cholesterol and of LDL are responsible for
atherosclerosis in man, and epidemiological data suggests that elevated plasma levels of HDL have a protective effect
5
.
2. CLASSIFICATION OF LIPID CONCENTRATIONS
The cholesterol along with some other types of fats cannot be dissolved in the blood. Moreover, in order to be
transported to and from cells, they have to be specially carried by certain molecules called lipoproteins, which consist of an
outer layer of protein with an inner core of cholesterol and triglycerides
6,7
.In addition, the lipoproteins have been found
essential for cholesterol to move around the body.The lipids can be classified as TC, triglycerides, LDL, HDL and very low
density lipoprotein (VLDL) cholesterol.
Total cholesterol
According to guidelines of National Cholesterol Education Program (NCEP), TC concentrations below 200 mg/dL
have been regarded as desirable, whereas, concentrations greater than 240 mg/dL are referred to as hyperlipidemic.
A REVIEW OF HYPERLIPIDEMIA AND MEDICINAL PLANTS
Dhaliya Salam. A, Surya A. S, Dawn V Tomy, Dr. Betty Carla, Dr. Arun Kumar*, Dr. C. Sunil*
St. Joseph’s College of Pharmacy, Cherthala, Kerala, India.

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However, epidemiological evidence suggests that the risk of cardiac events decreases as TC levels fall approximately to 150
mg/dL. Moreover, TC should be less than 180 mg/dL for children
8-10
.
Triglyceride
Triglycerides are another type of fat that is carried in the blood by VLDL. The excess calories, alcohol or sugar in the
body get converted into triglycerides and stored in fat cells throughout the body
11
.The triglyceride concentration less than
150 mg/dL is regarded as normal, wheras, concentrations of 200-499 mg/dL are considered as high. Moreover,
concentrations of 500 mg/dL or higher are considered dangerous for the development and progression of various CVDs
9
.
LDL cholesterol
LDL is commonly known as the bad cholesterol, which is produced by the liver and carry cholesterol and other lipids
from the liver to different areas of the body like muscles, tissues, organs and heart. The high levels of LDL indicate much
more cholesterol in the blood stream than necessary and hence, increase the risk of heart disease
8,12
.According to NCEP
guidelines, LDL cholesterol concentrations below 100mg/dL are considered optimal, whereas concentrations in the range of
160-189 mg/dL are considered to the higher side.However, increasing evidence supports that normal human LDL cholesterol
concentration can be as low as 50 to 70 mg/dL
9
.Moreover, it has been comprehensively seen that the risk of CVDs decreases
as LDL cholesterol concentration decreases.
HDL cholesterol
HDL is commonly referred to as the good cholesterol, which is produced by the liver to carry cholesterol and other
lipids from tissues back to the liver for degradation
13
.High levels of HDL cholesterol have been considered as a good
indicator of a healthy heart. The concentrations of 60 mg/dL or higher have been considered as optimal, whereas, HDL
concentrations below 40 mg/dL are considered as major risk factor for CVDs. However, HDL is often interpreted in the
context of TC and LDL concentrations, and hence may be regarded as less significant when LDL is low
9,13
.
VLDL Cholesterol
VLDL is similar to LDL cholesterol in the sense that it contains mostly fat and not much protein. VLDL cholesterol is
the lipoproteins that carry cholesterol from the liver to organs and tissues in the body
14
.They are formed by a combination of
cholesterol and triglycerides. Moreover, VLDLs are heavier than LDL, and are also associated with atherosclerosis and heart
disease
14
.
3. MECHANISM OF LIPID TRANSPORT

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Lipids are insoluble in water. Hence, they are transported around the body as lipoproteins. Lipids originate from two
sources: endogenous lipids, synthesized in the liver, and exogenous lipids, ingested and processed in the intestine.
Approximately 7% of body’s cholesterol circulates in plasma in the form of low density lipoproteins (LDL). The level of
plasma cholesterol is influenced by its synthesis and catabolism in which liver plays a crucial role
15
.
4. TYPES OF HYPERLIPIDEMIA
Hyperlipidemia can be broadly divided into:
Primary;hyperlipidemia is due to Single gene defect:
It is familial and called as monogenic or genetic.
Polygenic gene defect
Multiple genetic defect, dietary and physical activity are caused due to it.
TYPE DISORDER CAUSE OCCURANCE ELEVATED
PLASMA
LIPOPROTEIN
I.
Familial lipoprotein
lipase deficiency
Genetic Very rare Chylomicrons
II
a
Familial
hypercholesterolemia
Genetic Less common LDL
II
b
Polygenic
hypercholesterolemia
Multifactorial Commonest LDL
III Familial
dysbetalipoproteinemia
Genetic Rare IDL,Chylomicrons
Remnants
IV Hypertriglyceridemia
Multifactorial
Genetic
Common VLDL
V Familial combined
hyperlipidemia
Genetic Less common VLDL,LDL
LDL-low density lipoprotein,VLDL-very low density lipoprotein,IDL-intermediate density lipoprotein
16
.

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Table 1.TYPES OF PRIMARY HYPERLIPIDEMIA
16
SECONDARY HYPERLIPIDEMIA
It is associated with diabetes, myxoedema, nephritic syndrome, chronic alcoholism, with use of drugs like corticosteroids,
oral contraceptives, Beta blockers
17
TYPE
REASONS
Hypercholesterolemia
• Hypothyroidism
• Anorexia nervosa
• Acute intermittent porphyria
• Obstructive liver disease
• Nephrotic syndrome
• Drugs:Progestins,thiazide diuretics,glucocorticoids,
betablockers,isotretinion,protease
inhibitors,cyclosporine,mirtazapine,sirolimus.
Hypertriglyceridemia
• Obesity
• Pregnancy
• Lipodystrophy
• Acute hepatitis
• Diabetis mellitus
• Ileal bypass surgery
• Glycogen storage disease
• Systemic lupus erythematosus
• Monoclonal gammopathy: multiple myeloma
• Drugs:Alcohol,estrogens,isotretinoin,beta
blockers,glucocorticoids,bile-acid
resins,thiazides,asparaginase,interferons,azole
antifungals,mirtazapine,anabolic
steroids,sirolimus,bexarotene.

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Hypocholesterolemia
• Malnutrition
• Malabsorption
• Chronic liver disease
• Myeloproliferative diseases
• Chronic infectious diseases:AIDS,tuberculosis
Low HDL
• Malnutrition
• Obesity
• Drugs:anabolicsteroids,probucol,isotretinoin,progestins.
Table 2. Types and Reasons
5. CAUSES OF HYERLIPIDEMIA
The main cause of hyperlipidemia includes changes in lifestyle habits in which risk factor is mainly poor diet i.e with a fat
intake greater than 40 percent of total calories, saturated fat intake greater than 10 percent of total calories; and cholesterol
intake greater than 300 milligrams per day or treatable medical conditions
18
.The abnormal cholesterol levels are the result of
an unhealthy lifestyle including taking high-fat diet and other lifestyle factors like being overweight, smoking heavy alcohol
use and lack of exercise. Other factors include diabetes, kidney disease, pregnancy, and an underactive thyroid gland
19
.
Other illnesses that may elevate cholesterol levels include polycystic ovary syndrome and kidney disease. The higher levels
of female hormones like estrogen, have been noted to increase or change cholesterol levels. In addition, drugs like diuretics,
beta-blockers and medicines used to treat depression have also been reported to raise cholesterol levels
20
. Another
modifying factors in the development and progression of hyperlipidemia are age and gender. It has been shown that

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cholesterol levels rise as the person gets older
21-23
. Heredity has also been a modifying factor for the progression of
hyperlipidemia as it has been noted that the genes partly determine the amount of cholesterol body makes
24
.
Other factors that cause hyperlipdemia without any prevalence information includes the following
18
.
Berardinelli-Seip congenital lipodystrophy – hyperlipidemia
A rare genetic disorder having heptomegaly, loss genetic disorder characterized by diabetes mellitus, loss of body fat,
hepatomegaly, enlarged genitals, increased skeletal growth and other abnormalities
25
Berardinelli-Seip congenital lipodystrophy, type 1 – hyperlipidemia
A rare genetic disorder caused by a defect on the AGPAT2 gene on chromosome 9q34.3
26
characterized by early-onset
diabetes mellitus, loss of body fat, serious insulin resistance, high blood triglycerides and fatty liver
Berardinelli-Seip congenital lipodystrophy, type 2 – hyperlipidemia
A rare genetic disorder caused by a defect on the BSCL2 gene on chromosome 11q13 by early-onset diabetes mellitus,
loss of body fat, serious insulin resistance, high blood triglycerides and fatty liver
27
.
Cholestasis
It is a condition the bile flow from the liver to the duodenum is blocked. It is of two types first one is caused by
mechanical blockage in the duct system which occur from a gallstone or malignancy and other type is metabolic cholestasis,
in which disturbances in bile formation occur because of genetic defects or acquired as a side effect of many medications
28
Chromosome 15q, deletion:
A rare chromosomal disorder which occurs because of deletion of genetic material from the long arm of chromosome
15
29
.
Neuropathy, hereditary motor and sensory, Okinawa type:
A dominantly inherited, slow-progressing motor and sensory nerve disease which primarily involves the proximal
muscles (i.e. the muscles closest to the trunk of the body)
30
.
Chronic renal failure
Metabolic syndrome
Nephrotic syndrome – hyperlipidemia
6. PATHOPHYSIOLOGY OF HYPERLIPIDEMIA
• The pathophysiology of hyperlipidemia can be studied under two headins, i.e., primary hyperlipidemia and
secondary hyperlipidemia. The pathophysiology of primary hyperlipidemia involve that the idiopathic
hyperchylomicronemia defect in lipid metabolism leads to hypertriglyceridemia and hyperchylomicronemia which
is caused by a defect in lipoprotein lipase activity or the absence of the surface apoprotein CII
31
.Moreover,
hyperchylomicronemia in cats with autosomal recessive defect in lipoprotein lipase (LPL) activity showed the
occurrence of primary hyperlipidemia
32
.
•
In secondary hyperlipidemia, the postprandial absorption of chylomicrons from the gastrointestinal tract occurs 30-
60 min after ingestion of a meal containing fat that may increase serum triglycerides for 3-10 hours
33
.The diabetes
mellitus patients have been noted to possess low LPL activity which further caused high synthesis of VLDL
cholesterol by the liver ultimately leading to hyperlipidemia. Moreover, hypothyroidism-induced low LPL activity
and lipolytic activity has been noted to reduce hepatic degradation of cholesterol to bile acids. Furthermore,
hyperadrenocorticism increased the synthesis of VLDL by the liver causing both hypercholesterolemia and
hypertriglyceridemia
34,35
.Liverdisease hypercholesterolemia has been noted to be caused by reduced excretion of

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cholesterol in the bile. Furthermore, in nephrotic syndrome, the common synthetic pathway for albumin and
cholesterol causes low oncotic pressure ultimately leading to enhanced cholesterol synthesis
36
.
• The response-to-injury hypothesis states that risk factors such as oxidized LDL, mechanical injury to the
endothelium, excessive homocysteine, immunologic attack, or infection-induced changes in endothelial and intimal
function lead to endothelial dysfunction and a series of cellular interactions that culminate in atherosclerosis. The
eventual clinical outcomes may include angina, myocardial infarction, arrhythmias, stroke, peripheral arterial
disease, abdominal aortic aneurysm, and sudden death.
• Atherosclerotic lesions are thought to arise from transport and retention of plasma LDL through the endothelial cell
layer into the extracellular matrix of the subendothelial space. Once in the artery wall, LDL is chemically modified
through oxidation and nonenzymatic glycation. Mildly oxidized LDL then recruits monocytes into the artery wall.
These monocytes then become transformed into macrophages that accelerate LDL oxidation.
• Oxidized LDL provokes an inflammatory response mediated by a number of chemoattractants and cytokines (e.g.,
monocyte colony-stimulating factor, intercellular adhesion molecule, platelet-derived growth factor, transforming
growth factors, interleukin-1, interleukin-6).
• Repeated injury and repair within an atherosclerotic plaque eventually leads to a fibrous cap protecting the
underlying core of lipids, collagen, calcium, and inflammatory cells such as T lymphocytes. Maintenance of the
fibrous plaque is critical to prevent plaque rupture and subsequent coronary thrombosis.
• The extent of oxidation and the inflammatory response are under genetic control, and primary or genetic
lipoprotein disorders are classified into six categories for the phenotypic description of hyperlipidemia. The types
and corresponding lipoprotein elevations include the following: I (chylomicrons), IIa (LDL), IIb (LDL + very low
density lipoprotein, or VLDL), III (intermediate-density lipoprotein, or IDL); IV (VLDL), and V (VLDL +
chylomicrons). Secondary forms of hyperlipidemia also exist, and several drug classes may elevate lipid levels (e.g.,
progestins, thiazide diuretics, glucocorticoids, β blockers, isotretinoin, protease inhibitors, cyclosporine,
mirtazapine, sirolimus).
• The primary defect in familial hypercholesterolemia is the inability to bind LDL to the LDL receptor (LDL-R) or,
rarely, a defect of internalizing the LDL-R complex into the cell after normal binding. This leads to lack of LDL
degradation by cells and unregulated biosynthesis of cholesterol, with totalcholesterol and LDL-C being inversely
proportional to the deficit in LDL receptors
37
.
7. CLINICAL MANIFESTATIONS
• Familial hypercholesterolemia is characterized by a selective elevation in plasma LDL and deposition of LDL-
derived cholesterol in tendons (xanthomas) and arteries (atheromas).
• Familial lipoprotein lipase deficiency is characterized by a massive accumulation of chylomicrons and a
corresponding increase in plasma triglycerides or a type I lipoprotein pattern. Presenting manifestations include
repeated attacks of pancreatitis and abdominal pain, eruptive cutaneous xanthomatosis, and hepatosplenomegaly
beginning in childhood. Symptom severity is proportional to dietary fat intake, and consequently to the elevation of
chylomicrons. Accelerated atherosclerosis is not associated with this disease.
• Patients with familial type III hyperlipoproteinemia develop the following clinical features after age 20: xanthoma
striata palmaris (yellow discolorations of the palmar and digital creases); tuberous or tuberoeruptive xanthomas
(bulbous cutaneous xanthomas); and severe atherosclerosis involving the coronary arteries, internal carotids, and
abdominal aorta.
• Type IV hyperlipoproteinemia is common and occurs in adulthood primarily in patients who are obese, diabetic,
and hyperuricemic and do not have xanthomas. It may be secondary to alcohol ingestion and can be aggravated by
stress, progestins, oral contraceptives, thiazides, or β blockers.

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• Type V is characterized by abdominal pain, pancreatitis, eruptive xanthomas, and peripheral polyneuropathy. These
patients are commonly obese, hyperuricemic, and diabetic; alcohol intake, exogenous estrogens, and renal
insufficiency tend to be exacerbating factors. The risk of atherosclerosis is increased with this disorder
38
.
8. DIAGNOSIS OF HYPERLIPIDEMIA
• The National Cholesterol Education Program recommends that a fasting lipoprotein profile (FLP) including
total cholesterol, LDL, HDL, and triglycerides should be measured in all adults 20 years of age or older at
least once every 5 years.
• Measurement of plasma cholesterol (which is about 3% lower than serum determinations), triglyceride, and
HDL levels after a 12-hour or longer fast is important, because triglycerides may be elevated in nonfasted
individuals; total cholesterol is only modestly affected by fasting.
• Two determinations, 1 to 8 weeks apart, with the patient on a stable diet and weight, and in the absence of acute
illness, are recommended to minimize variability and to obtain a reliable baseline. If the total cholesterol is greater
than 200 mg/dL, a second determination is recommended, and if the values are more than 30 mg/dL apart, the
average of three values should be used.
• After a lipid abnormality is confirmed, major components of the evaluation are the history (including age, gender,
and, if female, menstrual and estrogen replacement status), physical examination, and laboratory investigations.
• A complete history and physical examination should assess (1) presence or absence of cardiovascular risk factors or
definite cardiovascular disease in the individual; (2) family history of premature cardiovascular disease or lipid
disorders; (3) presence or absence of secondary causes of hyperlipidemia, including concurrent medications; and (4)
presence or absence of xanthomas, abdominal pain, or history of pancreatitis, renal or liver disease, peripheral
vascular disease, abdominal aortic aneurysm, or cerebral vascular disease (carotid bruits, stroke, or transient
ischemic attack).
• Diabetes mellitus is now regarded as a CHD risk equivalent. That is, the presence of diabetes in patients without
known CHD is associated with the same level of risk as patients without diabetes but having confirmed CHD.
• If the physical examination and history are insufficient to diagnose a familial disorder, then agarose-gel lipoprotein
electrophoresis is useful to determine which class of lipoproteins is affected. If the triglyceride levels are below 400
mg/dL and neither type III hyperlipidemia nor chylomicrons are detected by electrophoresis, then one can calculate
VLDL and LDL concentrations: VLDL = triglyceride/5; LDL = total cholesterol - (VLDL + HDL). Initial testing uses
total cholesterol for case finding, but subsequent management decisions should be based on LDL.
• Because total cholesterol is composed of cholesterol derived from LDL, VLDL, and HDL, determination of HDL is
useful when total plasma cholesterol is elevated. HDL may be elevated by moderate alcohol ingestion (fewer than
two drinks per day), physical exercise, smoking cessation, weight loss, oral contraceptives, phenytoin, and
terbutaline. HDL may be lowered by smoking, obesity, a sedentary lifestyle, and drugs such as β blockers.
• Diagnosis of lipoprotein lipase deficiency is based on low or absent enzyme activity with normal human plasma or
apolipoprotein C-II, a cofactor of the enzyme
39
.
To have a low risk of heart disease, your desirable lipid levels are
1
• LDL less than 130 mg/dL or < 70 if you have established diagnosis of diabetes
• HDL greater than 40 mg/dL (men) or 50 mg/dL (women);
• Total cholesterol less than 200 mg/dL; and
• Triglycerides less than 200 mg/dL or 150 if you have established heart disease or diabetes.

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9. TREATMENT
• The National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) recommends that a fasting
lipoprotein profile and risk factor assessment be used in the initial classification of adults. There are three categories
of risk that modify the goals and modalities of LDL-lowering therapy. The highest risk category is having known
CHD or CHD risk equivalents; the risk for major coronary events is equal to or greater than that for established
CHD (i.e., more than 20% per 10 years, or 2% per year). The intermediate category includes two or more risk factors,
in which the 10-year risk for CHD is 20% or less. The lowest risk category is persons with zero to one risk factor,
which is usually associated with a 10-year risk of CHD of less than 10%
39
.
Over the past few years guidelines for the use of lipid-lowering therapy have become more aggressive following the
results of major trials showing mortality benefit for the use of statins. Most guidelines recommend statin treatment for a
patient with CAD with a 10-year risk that is greater than 20% (high risk) once a trial of dietary therapy has been
unsuccessful. However, treatment can be cost effective with a 10-year risk of 10%. The goals of therapy are the reduction of
LDL cholesterol levels and the level of initiation of therapeutic lifestyle change (TLC) and proper drug therapy are for adults
and children. While these goals are surrogate end points, the primary reason to institute TLC and drug therapy is to reduce
the risk first or recurrent events such as MI, angina, heart failure, ischemic stroke, or other forms of peripheral arterial
disease such as carotid stenosis or abdominal aortic aneurysm
1
.
Treatment therapy involves two approaches
1
:
• Non-pharmacological therapy
• Pharmacological therapy
Non pharmacological therapy
The objectives of dietary therapy are to decrease the intake of total fat, saturated fatty acids
(i.e., saturated fat), and cholesterol progressively and to achieve a desirable body weight.
• Reduced saturated fat intake to 7 percent of daily calories;
• Reduced total fat intake to 25 to 35 percent of daily calories;
• Limited dietary cholesterol to less than 200 mg per day;
• Eating 20 to 30 g a day of soluble fiber, which is found in oats, peas, beans, and certain fruits; and
• Increased intake of plant stanols or sterols, substances found in nuts, vegetable oils, corn and rice, to 2 to 3 g daily.
Other foods that can help control cholesterol include cold-water fish, such as mackerel, sardines, and salmon. These fish
contain omega-3 fatty acids that may lower triglycerides. Soybeans found in tofu and soy nuts and many meat substitutes
contain a powerful antioxidant that can lower LDL
1
.
Pharmacological therapy
CLASSIFICATION OF DRUGS
15
;
1. HMG-CoA reductase inhibitors (Statins): Lovastatin, Simvastatin, Pravastatin, Atorvastin, Rosuvastin.
2. Bile acid sequestrants (Resins): Cholestyramine, Colestipol.
3. Activate lipoprotein lipase (Fibric acid derivatives): Clofibrate, Gemfibrozil, Benzafibrate and Fenofibrate.
4. Inhibit lipolysis and triglyceride synthesis: Nicotinic acid.
5. Others: Ezetimibe, Gugulipid.

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Table 3. Drugs and their actions
HMG-CoA Reductase Inhibitors (Atorvastatin, Fluvastatin, Lovastatin, Pravastatin, Rosuvastatin, Simvastatin)
• Statins inhibit 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, interrupting the conversion of
HMG-CoA to mevalonate, the rate-limiting step in de novo cholesterol biosynthesis. Reduced synthesis of LDL
andenhanced catabolism of LDL mediated through LDL receptors appear to be the principal mechanisms for lipid-
lowering effects.
• When used as monotherapy, statins are the most potent total and LDL cholesterol-lowering agents and among the
best tolerated. Total and LDL cholesterol are reduced in a dose-related fashion by 30% or more when added to
dietary therapy.
• Combination therapy with a statin and BAR is rational as numbers of LDL receptors are increased, leading to greater
degradation of LDL cholesterol; intracellular synthesis of cholesterol is inhibited; and enterohepatic recycling of bile
acids is interrupted.
• Combination therapy with a statin and ezetimibe is also rational because ezetimibe inhibits cholesterol absorption
across the gut border and adds 12% to 20% further reduction when combined with a statin or other drugs.
• Constipation occurs in fewer than 10% of patients taking statins. Other adverse effects include elevated serum
aminotransferase levels (primarily alanine aminotransferase), elevated creatine kinase levels, myopathy, and rarely
rhabdomyolysis.

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Bile Acid Resins (Cholestyramine, Colestipol, Colesevelam)
• The primary action of bile acid resins (BARs) is to bind bile acids in the intestinal lumen, with a concurrent
interruption of enterohepatic circulation of bile acids, which decreases the bile acid pool size and stimulates hepatic
synthesis of bile acids from cholesterol. Depletion of the hepatic pool of cholesterol results in an increase in
cholesterol biosynthesis and an increase in the number of LDL receptors on the hepatocyte membrane, which
stimulates an enhanced rate of catabolism from plasma and lowers LDL levels. The increase in hepatic cholesterol
biosynthesis may be paralleled by increased hepatic VLDL production and, consequently, BARs may aggravate
hypertriglyceridemia in patients with combined hyperlipidemia.
• BARs are useful in treating primary hypercholesterolemia (familial hyper- cholesterolemia, familial combined
hyperlipidemia, type IIa hyperlipoproteinemia).
• Gastrointestinal complaints of constipation, bloating, epigastric fullness, nausea, and flatulence are most commonly
reported. These adverse effects can be managed by increasing fluid intake, modifying the diet to increase bulk, and
using stool softeners.
• The gritty texture and bulk may be minimized by mixing the powder with orange drink or juice. Colestipol may
have better palatability than cholestyramine because it is odorless and tasteless. Tablet forms should help improve
adherence with this form of therapy.
• Other potential adverse effects include impaired absorption of fat-soluble vitamins A, D, E, and K; hypernatremia
and hyperchloremia; gastrointestinal obstruction; and reduced bioavailability of acidic drugs such as warfarin,
nicotinic acid, thyroxine, acetaminophen, hydrocortisone, hydrochlorothiazide, loperamide, and possibly iron. Drug
interactions may be avoided by alternating administration times with an interval of 6 hours or greater between the
BAR and other drugs.
Fibric Acids (Gemfibrozil, Fenofibrate, Clofibrate)
• Fibrate monotherapy is effective in reducing VLDL, but a reciprocal rise in LDL may occur and total cholesterol
values may remain relatively unchanged. Plasma HDL concentrations may rise 10% to 15% or more with fibrates.
• Gemfibrozil reduces the synthesis of VLDL and, to a lesser extent, apolipoprotein B with a concurrent increase in
the rate of removal of triglyceride-rich lipoproteins from plasma. Clofibrate is less effective than gemfibrozil or
niacin in reducing VLDL production.
• Gastrointestinal complaints occur in 3% to 5% of patients, rash in 2%, dizziness in 2.4%, and transient elevations in
transaminase levels and alkaline phosphatase in 4.5% and 1.3%, respectively. Clofibrate and, less commonly,
gemfibrozil may enhance the formation of gallstones.
• A myositis syndrome of myalgia, weakness, stiffness, malaise, and elevations in creatine kinase and aspartate
aminotransferase may occur and seems to be more common in patients with renal insufficiency.
• Fibrates may potentiate the effects of oral anticoagulants, and the international normalized ratio (INR) should be
monitored very closely with this combination.
Niacin
• Niacin (nicotinic acid) reduces the hepatic synthesis of VLDL, which in turn leads to a reduction in the synthesis of
LDL. Niacin also increases HDL by reducing its catabolism.
• The principal use of niacin is for mixed hyperlipidemia or as a second-line agent in combination therapy for
hypercholesterolemia. It is a first-line agent or alternative for the treatment of hypertriglyceridemia and diabetic
dyslipidemia.

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• Niacin has many common adverse drug reactions; most of the symptoms and biochemical abnormalities seen do
not require discontinuation of therapy.
• Cutaneous flushing and itching appear to be prostaglandin mediated and can be reduced by taking aspirin 325 mg
shortly before niacin ingestion. Taking the niacin dose with meals and slowly titrating the dose upward may
minimize these effects. Concomitant alcohol and hot drinks may magnify the flushing and pruritus from niacin, and
they should be avoided at the time of ingestion. Gastrointestinal intolerance is also a common problem.
• Potentially important laboratory abnormalities occurring with niacin therapy include elevated liver function tests,
hyperuricemia, and hyperglycemia. Niacin-associated hepatitis is more common with sustained-release
preparations, and their use should be restricted to patients intolerant of regular-release products. Niacin is
contraindicated in patients with active liver disease, and it may exacerbate preexisting gout and diabetes.
• Nicotinamide should not be used in the treatment of hyperlipidemia because it does not effectively lower
cholesterol or triglyceride levels.
Ezetimibe
• Ezetimibe interferes with the absorption of cholesterol from the brush border of the intestine, a novel mechanism
that makes it a good choice for adjunctive therapy. It is approved as both monotherapy and for use with a statin.
The dose is 10 mg once daily, given with or without food. When used alone, it results in an approximate 18%
reduction in LDL cholesterol. When added to a statin, ezetimibe lowers LDL by about an additional 12% to 20%. A
combination product (Vytorin) containing ezetimibe 10 mg and simvastatin 10, 20, 40 or 80 mg is available.
Ezetimibe is well tolerated; approximately 4% of patients experience gastrointestinal upset. Because cardiovascular
outcomes with ezetimibe have not been evaluated, it should be reserved for patients unable to tolerate statin
therapy or those who do not achieve satisfactory lipid lowering with a statin alone.
Fish Oil Supplementation.
• Diets high in omega-3 polyunsaturated fatty acids (from fish oil), most commonly eicosapentaenoic acid (EPA),
reduce cholesterol, triglycerides, LDL, and VLDL and may elevate HDL cholesterol.
• Fish oil supplementation may be most useful in patients with hypertrigly- ceridemia, but its role in treatment is
not well defined.
•
Complications of fish oil supplementation such as thrombocytopenia and bleeding disorders have been noted,
especially with high doses (EPA, 15 to 30 g/day)
40
10. HERBAL MEDICINES
Hyperlipidemia associated lipid disorders are considered to cause the atherosclerotic cardiovascular disease
41
.The
main aim of treatment in patients with hyperlipidemia is to reduce the risk of developing ischemic heart disease or the
occurrence of further cardiovascular or cerebrovascular disease
42
.The consumption of synthetic drugs leads to
hyperuricemia, diarrhoea, nausea, myositis, gastric irritation, flushing, dry skin and abnormal liver function. The medicinal
plants play a major role in hypolipidemic activity
43
. The advantages of herbal medicines reported are effectiveness,safety,
affordability and acceptability.Due to less communication means, poverty, ignorance and unavaila-bility of modern health
facilities, most people especially rural people are still forced to practice traditional medicines for their common day
ailments. Most of these people form the poorest link in the trade of medicinal plants
44
.
Over the past decade, herbal medicine has become a topic of global importance, making an impact on both world
health and international trade. Medicinal plants continue to play a central role in the healthcare system of large proportions
of the world’s population
45
. This is particularly true in developing countries, where herbal medicine has a long and
uninterrupted history of use. Continuous usage of herbal medicine by a large proportion of the population in the developing
countries is largely due to the high cost of Western Pharmaceuticals and Healthcare
46
.

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Herbal medicines have been main source of primary healthcare in all over the world. From ancient times, plants
have been catering as rich source of effective and safe medicines. Today according to the WHO as many as 80 % of world
populations are still dependent on traditional medicines. Herbal medicines are finished, labeled medicinal products that
contain as active ingredients, aerial or under ground part of plants or other plant materials, or combination thereof, whether
in the crude state or as plant preparations. Medicines containing plant materials combined with chemically defined active
substances, including chemically defined isolated constituents of plants are not considered to be herbal medicines
47
.
Chemical principles from natural sources have become much simpler and have contributed significantly to the
development of new drugs from medicinal plants
48
. The valuable medicinal properties of different plants are due to presence
of several constituents i.e. saponins, tannins, alkaloids, alkenyl phenols, glycol-alkaloids, flavonoids, sesquiterpenes
lactones, terpenoids and phorbol esters
49
. Among them some are act as synergistic and enhance the bioactivity of other
compounds.
The Indian subcontinent is a vast repository of medicinal plants that are used in traditional medical treatments
50
. In
India, around 15000 medicinal plants have been recorded
51
however traditional communities are using only 7,000 - 7,500
plants for curing different diseases
52-54
. The medicinal plants are listed in various indigenous systems such as Siddha (600),
Ayurveda (700), Amchi (600), Unani (700) and Allopathy (30) plant species for different ailments
55
. According to another
estimate 17,000 species of medicinal plants have been recorded out of which, nearly 3,000 species are used in medicinal
field
56
. The Indian Vedas also describes the widespread use of herbal products and aqueous extract of different plant parts
for curing different diseases. Maximum 30% of root part of medicinal plant is used in different practices in comparison to
other plant parts
57
. Medicinal plant based drug industries is progressing very fast in India but it is best with a number of
problems.
Currently used hypolipidemic drugs are associated with so many adverse effects and withdrawal is associated with
rebound phenomenon which is not seen with herbal preparations. Plant parts or plant extract are sometimes even more
potent than known hypolipidemic drugs. This indicates that the research has stopped with just reporting the effect of plant
derivates and the findings are not translated into clinical research. Taking these finding forward is mandatory to develop
new drugs in this area. Hence further research into identifying the active principle, conducting preclinical studies & if
possible clinical studies is needed
58
. Here are some plants which showed antilipidemic activity.
SERIAL
No.
BOTANICAL
NAME
FAMILY PARTS USED REFERENCES
1
Amaranthus
Spinosus
59
Amaranthaceae Leaves Girija et.al
2
Glycyrrhiza
Glabra
60
Fabaceae Root
Nishant et.al
3
Withania
Somnifera
60
Solanaceae Root
Nishant et.al

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4 Chlorophytum
Borivilianum
60
Liliaceae Root
Nishant et.al
5 Moringa oleifera
61
Moringaceae Leaves,root,seeds Rajanandh MG et al
6 Sphaeranthus indicus
62
Asteraceae Flower heads
V V Pandey et al
7 Rhinacanthus
nasutus
63
Acanthaceae Whole plant
Brahma Srinivas et al
8
Pithecellobium
Dulce benth
64
.
Leguminosae Fresh leaves Sundar Rajan et al
9
Hibiscus cannabinus
65
Malvaceae Fresh mature leaves Shivali et al
10
Sapindus
emarginatus
66
Sapindaceae Pericarp Srikanth et al
11
Eclipta prostrata
67
Asteraceae Plant juice R.Dandapani
12
Sesbania grandiflora
68
Fabaceae Leaves Saravanakumar et al
13
Lycium barbarum
69
Solanaceae Fruit Qiong Luo et al

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14
Ougeinia oojeinensis
70
Fabaceae Bark Velmurugan et al
15
Randia dumetorum
71
Rubiaceae Fruit Piyush et al
16
Luffa aegyptiaca
72
cuccurbitaceae Fruit Abdul Hameed et al
17 Bauhinia purpurea
73
Fabaceae Leaves Lakshmi et al
18 Psidium guajava
74
Myrtaceae Leaves Shubhangi et al
19 Piliostigma
thonningii
75
Leaves Dasofunjo et al
20 Crotalaria juncea
76
Fabaceae Leaves K.Harikumar et al
Table 4. PLANTS WITH ANTIHYPERLIPIDEMIC ACTIVITY
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