Management of hyperlipidemia

Tieraona Low Dog ; Riley, David. Alternative Therapies in Health and Medicine 9.3
(May/Jun 2003): 28-40; quiz 41.

Abstract
TranslateAbstract

Coronary heart disease (CHD) is one of the most prevalent diseases that can be prevented
through necessary changes in lifestyle, diet, the use of botanicals and dietary supplements, and
the use of treatment strategies. One of the main causes of CHD is atherosclerosis brought about
by the excess fat and cholesterol in the body. Riley presents an education activity for physicians
that explore treatment options for CHD.

Full text
TranslateFull text

A therosclerosis is the major cause of coronary heart disease and one of the leading causes of
death in the United States. While genetic variables contribute to the development of the disease
in some individuals, the real tragedy is the fact that many deaths could be prevented by eating a
low fat diet, exercising regularly, not smoking and maintaining a healthy body weight. New
medical research is evaluating the interplay between plaque formation in atherosclerosis and
inflammation with new evidence suggesting that C-reactive protein-a marker for inflammation-
may be of primary importance in evaluating risks in heart disease. This section will focus
primarily on the use of therapeutic lifestyle changes and the current state of evidence for diet,
botanicals, and nutritional supplements that are commonly used for the prevention and treatment
of coronary heart disease (CHD).

LIPIDS

Cholesterol and triglycerides comprise the major plasma lipids found in the body and are
essential for human health. Cholesterol can be synthesized by the liver or absorbed through the
intestine from dietary sources. It is an important component of cell membranes and serves as a
precursor to bile acids and steroid hormones. Since lipids are not water-soluble, they must be
transported in the blood in specialized complexes, called lipoproteins, which contain both lipid
and specialized proteins (apolipoproteins). There are three major classes of lipoproteins: low
density lipoproteins (LDL), high-density lipoproteins (HDL), and very low-density lipoproteins
(VLDL). Another lipoprotein class, intermediate density lipoprotein (IDL), falls somewhere
between VLDL and LDL and is included in the LDL measurement.
Triglycerides are the most prevalent form of fat in the human diet. Triglycerides are esters
consisting of a glycerol molecule coupled to three fatty acid residues of varying carbon chain
lengths and degrees of saturation. Triglycerides of plant origin (most, not all) are liquid at room
temperature and are termed "polyunsaturates." Animal triglycerides are generally solid at room
temperature and are termed "saturated."

During digestion, triglycerides are hydrolyzed to form monoglycerides and fatty acids that are
subsequently absorbed into the intestinal epithelium and then re-synthesized into triglycerides.
Triglycerides are found in all plasma lipoproteins but are the major lipid component of those
lipoproteins with a density less than 1.019 kg/L. These include chylomicrons, chylomicron
remnants, VLDL and IDL.

The Role of Low Density Lipoproteins in Coronary Heart Disease

Accumulating evidence over the past forty years has linked elevated total cholesterol and LDL
cholesterol (LDL-C), and low HDL cholesterol (HDL-C) with the development of coronary heart
disease (CHD). LDL-C is the major contributor to total cholesterol concentration in humans,
accounting for one-half to two-thirds of plasma cholesterol. It contains a single apolipoprotein,
apo B-100 (apo B). LDL-C is thought to be the major atherogenic lipoprotein and is the primary
target of cholesterol lowering drug therapy.

New guidelines have been issued for what are considered "optimal" levels of LDL-C. These
recommendations can be found in the Third Report of the Expert Panel on Detection, Evaluation,
and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) that was issued
through the National Institutes of Health National Heart, Lung and Blood Institute in 2001.1
Researchers have found that any LDL-C level above 100 mg/dL appears to be atherogenic.
Based upon this finding, the following targets have been recommended. Values should be based
upon a lipid profile drawn after a 9-12 hour fast.

What does this all mean? The new recommendations are to be used as "guidelines." It is
important to treat each individual according to his or her own personal risk. The major risk factors
that should be considered, include:

* Cigarette smoking

* Low HDL cholesterol (less than 40 mg/dL)

* Age (men =/> 45 years; women =/> 55 years)

* Hypertension (BP =/> 140/90, or taking anti-hypertensive medication)

* Family history of a male first degree relative with CHD before age 55 or a female first degree
relative with CHD before age 65.

The Framingham Point Scores for Men and Women are important tools for predicting the 10-year
risk of CHD for both men and women.2 Points are given for various risk factors with the total
number providing a 10-year risk for developing CHD. Determining the 10-year risk allows
practitioners to determine what target should be set for each individual.

Anyone who already has existing peripheral artery disease, clinical CHD or symptomatic carotid
artery disease should have a target goal of < 100 mg/dL of LDL-C. However, if one has 0-1 risk
factors, than the LDL-C goal remains at <160 mg/dL, while those with 2+ risk factors should have
a target LDL-C of < 130 mg/dL.

The Role of Serum Triglycerides in Coronary Heart Disease

Elevated triglyceride concentrations in the fasting state are of clinical importance in a number of
conditions. It is well known that severely elevated triglyceride levels (>1,000 mg/dL) pose a
significant risk for developing of abdominal pain and pancreatitis. However, the relationship
between elevated serum triglycerides and CHD has been debated for many years. Because
elevation of triglycerides often occurs in association with obesity, cigarette smoking,
hypertension, and diabetes-it has been difficult to determine if it is the "triglyceride" part of this
complex equation that puts individuals at increased risk of CHD. The evidence now seems clear
that elevated triglycerides increase one's risk for developing CHD. Recent meta-analyses have
shown that elevated trigylcerides are an independent risk factor for heart disease.3,4 It appears
that the triglyceride-rich lipoproteins associated with atherosclerosis are the remnant lipoproteins,
which include VLDL and IDL.5

Elevation of triglycerides and low levels of HDL-C are extremely common in patients with obesity,
insulin resistance and type II diabetes. The elevation of triglycerides in individuals with insulin
resistance is primarily due to an overproduction, and clearance in some instances, of VLDL.6
Moderate exercise improves insulin sensitivity and reduces triglyceride concentrations, making it
an important part of the overall treatment plan.7 Diet, weight loss and omega-3 fatty acids should
also be considered as part of a therapeutic lifestyle approach to elevated triglycerides.

The Role of High-Density Lipoproteins in CHD

HDL-C normally makes up 20-30% of the total serum cholesterol and is often referred to as the
"good" cholesterol, as high levels have been shown to be a strong, independent inverse predictor
of CHD risk. As total cholesterol levels increase and HDL-C levels decrease, the incidence of
myocardial infarction rises (Wilson, 1990). The good news is that for every 1% increase in HDL-
C, there is a 2-3 % decrease in CHD risk.8

There are numerous medications that can raise HDL-C, including niacin and the fibrates. While
estrogen replacement therapy increases HDL-C in postmenopausal women, this effect is
modified by some progestin therapies.9 Synthetic progestins have been shown to reverse or
eliminate the beneficial effects of estrogen on lipid profiles. In the Postmenopausal
Estrogen/Progestin Interventions (PEPI) trial, HDL-C levels were significantly higher in the
conjugated equine estrogen (CEE) + micronized progesterone (MP) group compared to the CEE
+ medroxyprogesterone acetate (MPA) group.10 A 1985 Swedish study included 58
postmenopausal women who received 2 mg oral estradiol daily for 3 months followed by an
additional 3 month course of 2 mg estradiol daily + 10 mg MPA, 200 mg MP, or 20 mg
levonorgestrel given for 20 days of each menstrual cycle. There was a significant decrease in
HDL-C in the groups receiving estradiol plus MPA or levonorgestrel. No change in HDL was
noted in the group receiving estradiol with MP.11 Two other trials have shown similar
results.12,13

The Role of Homocysteine

Homocysteine, an intermediate amino acid formed during the metabolism of methionine, has
been shown to be an independent, modifiable risk factor for cardiovascular disease.14 Plasma
homocysteine is normally </=12 [mu]mol/L. When elevated, homocysteine can play a role in the
development of cardiovascular disease. It should be duly noted that a number of patients with
established coronary artery disease have relatively normal lipid values and hyperhomocystinemia
(levels >/=15 mcmol/L). Researchers have noted that reductions in homocysteine levels that
occurred after cardiac rehabilitation and exercise training were shown to lead to a 20% to 30%
reduction in overall coronary artery disease risk.15 Furthermore, abnormal homocysteine
concentrations are prevalent in patients with diabetes16 and obesity,17 although its relationship
with excess cardiovascular morbidity is not yet clear.

The three vitamins necessary to metabolize homocysteine are folic acid and vitamins B6 and
B12. When homocysteine levels are elevated it may be due to a deficiency of folic acid, vitamin
B12, and to a lesser extent, vitamin B6.18 Vitamin B6 is found in meat, poultry, fish, legumes,
peanuts, walnuts, oats, brown rice, and whole wheat. Vitamin B12 is found only in animal
products and supplements. Folic acid can be found in citrus fruits, tomatoes, green leafy
vegetables, asparagus, broccoli, yeast, lentils, beans, eggs, beef, organ meats, whole grains,
and enriched cereals.18 The diet should provide an adequate intake of these nutrients, or if
lacking, a supplement should be administered.
At this time it seems prudent to lower elevated homocysteine levels as a secondary preventative
measure in patients with coronary artery disease. To measure homocysteine, total fasting
plasma homocysteine levels are recommended. Levels of serum folic acid, vitamins B6 and B12
and creatinine should be measured at the same time as homocysteine.

TREATMENT STRATEGIES

This section will not address the use of pharmaceutical/prescription drug therapies for the
treatment of hyperlipidemia. However, it is essential to recognize the important contribution the
newer cholesterol-lowering medications have made in the treatment of CHD. In 1980, resins and
niacin were the most commonly used lipid-lowering medications. By 1985, fibrates had caused a
decline in the use of niacin and resins and by 1989; 3-hydroxy-3-methylglutaryl-coenzyme A
reductase inhibitor (HMG-CoA) statin drugs had replaced fibrates as the most heavily used lipid-
lowering medications.19 By the mid-to-latter 1990s, several landmark trials provided clear
evidence that lipid-lowering therapy decreases cardiovascular events, including mortality. These
studies included the Scandinavian Simvastatin Survival Study [4S], the West of Scotland
Coronary Prevention Study (WOSCOPS), and the Air Force/Texas Coronary Atherosclerosis
Prevention Study.

Dietary Intervention

Heart healthy diets should be considered one of the primary therapeutic lifestyle interventions for
patients with any level of risk for CHD. Prevention always trumps treatment. The diet should
emphasize fruits and vegetables; fat-free and low-fat dairy products; cereal and grain products;
legumes and nuts; and fish, poultry, and lean meats. Eating five to seven servings of fresh fruits
and vegetables can be hard for many people to obtain in this fast-food culture; however, these
foods provide fiber and essential nutrients with low calories. Researchers have demonstrated
that diets high in fruit and vegetable intake reduce the risk for developing heart disease, stroke,
and hypertension.20,21

Whole grain products provide the body with complex carbohydrates, fiber and other essential
nutrients. Populations that consume a diet high in grain and fiber have been shown to decrease
risk of cardiovascular disease. Complex carbohydrates (bread, cereal, pasta) should be chosen
over simple carbohydrates. Soluble fibers, such as pectin, oat, and psyllium, have been shown to
reduce LDL-C and total cholesterol levels.

Saturated Fat and Trans-Fatty Acids

Individuals with moderate to high risk of CHD should limit their cholesterol intake to less than 200
mg/d and saturated fat should not make up more than 7% of the total daily calories. Individuals
with low risk of CHD should limit their cholesterol intake to 300 mg/d and saturated fat should be
limited to 10% of the total daily calories. Saturated fat is the predominant fat found in animal
products (i.e., beef, pork, egg yolks, dairy products, poultry) and in coconut and palm oil.
Although shellfish and eggs are high in cholesterol, they are low in saturated fat. Contrary to
popular belief, studies have shown that eating shellfish and eggs does not significantly affect
LDL-C levels.22,23

In addition to saturated fat, individuals should reduce their consumption of trans-fatty acids.
Vegetable oils contain one or more double bonds between carbon atoms. When hydrogen is
added to vegetable oils so that the fat becomes solid at room temperature (margarine), the
hydrogens are added on in the "trans" position, or on the opposite sides of the longitudinal axis of
the double bond Trans-fatty acids increase LDL-C and triglycerides in the diet.24

Trans-fatty acids are found in baked goods, fried foods, fast foods, restaurant fare, margarine,
and other products made with hydrogenated fat. In general, both saturated fat and trans-fatty
acid intake should be limited to less than 10% of the total daily calories. It is essential that
individuals do not substitute high-sugar, nutrient-poor, calorie-dense foods when attempting to
lose weight or reduce fat in the diet.

In summary, saturated fatty acids, trans-unsaturated fatty acids are the primary food components
that raise LDL-C and should be reduced in the diet, and substituted with polyunsaturated and
monounsaturated fatty acids.

Monounsaturated Fats

It is well-known that in areas of the world where olive oil is used as the primary cooking oil there
is less coronary heart disease. Commonly referred to as the Mediterranean diet, studies have
shown that diets low in saturated fat and rich in monounsaturated fats have a beneficial effect
upon endothelial function and lipid status.25 The Mediterranean diet can be described as the
dietary pattern found in the olive growing areas of the Mediterranean region, at least up until the
1960s. Generally speaking, these diets consisted not only of generous amounts of olive oil but
were also rich in fruits, vegetables, complex carbohydrates, fish and moderate amounts of wine.

Monounsaturated fatty acids have been shown to reduce LDL-C, but not HDL-C, when they are
substituted for saturated fat in the diet. High intakes of polyunsaturated fatty acids found in other
vegetable oils have been shown to reduce HDL-C levels, about a 1% reduction for every 2% of
total calories in which polyunsaturated fatty acids replace saturated or monounsaturated fatty
acids.26 When the diet is changed to provide 10% saturated, 18% monounsaturated, and 10
percent polyunsaturated fat with a total of 250 mg/d of cholesterol, HDL-C levels were not
reduced.27 Interesingly, strict vegetarians typically have been shown to have 12% lower HDL-C
levels than control nonvegetarians and 7% lower values than lactovegetarians.

Soy Protein and Isoflavones

Soy is rich in isoflavones, provides a beneficial source of fiber and is naturally low in saturated fat
and cholesterol. A 1995 a meta-analysis of 38 clinical trials involving soy concluded that
consumption of soy protein, in place of animal protein, significantly lowers total cholesterol, LDL-
C and triglycerides. No change in HDL-C was noted.28 Recent studies have shown that 20-50
g/d of soy protein reduces LDL-C in patients with mild elevations of cholesterol who are following
a low saturated fat diet.29,30

In October 1999, the FDA formally approved a health claim that allows foods containing 6.25 g of
soy protein per serving (assuming 4 servings, or 25 g/d soy protein) to make the claim that the
food reduces the risk of heart disease on their label.(Available at:
http://circ.ahajournals.org/math/ge.gif.) A more recent review concluded that soy isoflavones had
no little cholesterol lowering effect and that a better understanding of the pharmacokinetics and
bioavailability of individual isoflavones was needed.32

Fish and the Omega-3 Fatty Acids

A growing body of evidence derived from epidemiological studies and clinical trials has
consistently demonstrated that fish oil has a beneficial effect upon triglycerides and reduces the
risk for a variety of cardiovascular events. Clinical trials such as the Diet and Reinfarction Trial
and the Indian Experiment of Infarct Survival, have demonstrated a reduction in cardiac death
rates and in the incidence of cardiac symptoms in patients receiving fish oil.33 A recent meta-
analysis of 11 trials (15,806 patients) published between 1966 and 1999 concluded that omega-3
fatty acid-enriched diets reduced the risk of nonfatal myocardial infarction, fatal myocardial
infarction, and sudden death in patients with coronary heart disease.34 The American Heart
Association now recommends eating at least two servings of fish per week, especially salmon.

The beneficial fatty acids found in fish oil are eicosapentaenoic (EPA) and docosahexaenoic
(DHA) acids. These fatty acids exert multiple actions that have a positive affect on vascular
function. These include improved endothelial function through stimulation of nitric oxide, changes
in vascular tone via actions on selective ion channels, and maintenance of vascular integrity.35
EPA has several anti-thrombotic actions, including the inhibition of platelet activating factor,36
prostaglandin 12 and thromboxane A2, prostaglandins involved in platelet aggregation and
vasoconstriction.37 And finally, studies have shown that omega-3 fatty acids prevent neointima
formation by making smooth muscle cells less responsive to TXA2 induced proliferation of
smooth muscle cells.38 All in all, adding coldwater fish to the diet seems like a wise idea for most
folks. For those who don't care for the taste of fish, fish oil supplements are available on the
market.

The amount of omega-3 fatty acids needed to lower serum triglycerides is approximately 1 g/d,
which can easily be provided by adding fish to the diet. Administering as little as 0.21 g EPA and
0.12 g DHA per day of omega 3 fatty acids in fish oil supplements, has been shown to
significantly lower serum triglycerides in hyperlipidemics.39 A recent Cochrane systematic review
that found that fish oil supplementation reduced triglycerides in patients with type-2 diabetes but
also raised LDL-C, especially those on high doses of fish oil. No beneficial or adverse effects on
glycemic control were noted.40 Patients with primarily elevation of triglycerides would seem to
benefit from the addition of fish oil supplementation, however, those with elevation of LDL-C and
triglycerides may be better off with combination therapy. The use of dietary interventions with
lipid-lowering medications may offer a superior treatment, than either treatment alone, in patients
with mixed forms of hyperlipidemia.

A randomized, controlled crossover trial was conducted over a 10 month period in 120 previously
untreated hypercholesterolemic men aged 35-64 years living in Finland.41 After a 4- 6-week
placebo run-in period, participants were randomly assigned to a habitual diet (n = 60) or dietary
treatment group (n = 60), and each of these groups was further randomized in a double-blind
crossover fashion to receive simvastatin (20 mg/d) or placebo, each for 12 weeks (n = 30 in each
group). The main goals of the dietary treatment were to reduce intake of saturated and trans-fats
to no more than 10% of total calories by replacing them partly with monounsaturated and
polyunsaturated fats rich in omega-3 fatty acids. Dietary treatment decreased levels of total
cholesterol by 7.6% (P<.001), LDL cholesterol by 10.8% (P<.001), HDL cholesterol by 4.9% (P
=.01), apolipoprotein B by 5.7% (P =.003), serum insulin by 14.0% (P =.02), and alpha-
tocopherol by 3.5% (P =.04). Simvastatin decreased levels of total cholesterol by 20.8%, LDL
cholesterol by 29.7%, triglycerides by 13.6%, apolipoprotein B by 22.4%, alpha-tocopherol by
16.2%, beta-carotene by 19.5%, and ubiquinol-10 by 22.0% (P<.001 for all) and increased levels
of HDL cholesterol by 7.0% (P<.001) and serum insulin by 13.2% (P =.005). There were no
changes in glucose levels in any group. The authors concluded, "A modified Mediterranean-type
diet rich in omega-3 fatty acids efficiently potentiated the cholesterol-lowering effect of
simvastatin, counteracted the fasting insulin-elevating effect of simvastatin, and, unlike
simvastatin, did not decrease serum levels of beta-carotene and ubiquinol-10."

Patients who have undergone organ transplant surgery often develop dyslipidemia due to the
chronic administration of corticosteroids and cyclosporine medications. Dietary interventions
should be recommended and supported. However, if diet is not sufficient for corrected the
dyslipidemia, combined treatment with low-dose pravastatin and fish oil has been shown to be
more effective than pravastatin treatment alone for improving the lipid profiles after renal
transplantation.42

A note of caution: mercury levels in fish can range from 10-1,000 parts per billion. Mercury finds
its way into rivers, lakes, and oceans from coal-burning power plants and other industrial sources
and is known to cause learning disabilities and developmental delays. Eat fish high in omega-3
fatty acids that are least likely to contain mercury, such as tuna and salmon. One 3-ounce
serving of salmon contains approximately 1.2-1.5 grams of omega-3 fatty acids. High-mercury
content fish such as king mackerel and shark should be avoided, especially by pregnant women
and children.

The Role of Plant Sterols in Controlling Cholesterol

While cholesterol is the sterol of mammalian cells, phytosterols are the sterols produced by
plants. While plant sterols are similar to the structure of cholesterol, they differ by possessing a
methyl or ethyl group in their side chains, making them poorly absorbed. Plant derived sterols
have been shown to decrease total cholesterol levels for more than fifty years. While their
success as pharmaceutical agents were never fully realized due to the introduction of more
powerful drugs, plant sterols have now become part of a public health strategy for maintaining
healthy lipid levels by adding them to foods, such as margarine and salad dressing.

Due to their structural similarity with cholesterol, phytosterols impair intestinal absorption of
cholesterol, resulting in a 10-15% reduction in LDL-C with daily intakes of 2-3 grams.43 The
ability of plant sterols to displace cholesterol from micelles in the small intestine is part of the
mechanism that inhibits cholesterol absorption.44 It appears that esterification of these sterols
increases their solubility in fat and their efficacy in lowering LDL-C45 and most products on the
market today are esterified to unsaturated fatty acids (sterol esters) or saturated fat (stanol
esters). Studies have shown that both products work equally well in reducing LDL-C,46 but
neither offer any reduction in triglycerides or increase in HDL-C.

Patients taking cholesterol-lowering medications may experience additional benefit when

consuming phytosterol rich margarines or spreads. A recent study of 167 patients stable on statin
medications for at least 3 months found a further reduction of total cholesterol by 12% at 8
weeks, compared with a reduction in the placebo group of 5% (P <0.0001) and a reduction of
LDL-C of 17% compared with a 7% reduction in the placebo group (P<0.0001).47

The use of phytosterol rich margarines and spreads do not seem to adversely affect the taste of
food and extensive toxicological studies have failed to reveal any significant harmful side effects
with the use of these "functional" foods.43 It should be noted, however, that there are reports of
decreased serum levels of b-carotene, a-tocopherol, and/or lycopene as a result of eating foods
that contain stanol and sterol esters. Additional supplementation of these nutrients may be
necessary. Plant sterols are recommended by both the American Heart Association and the
National Cholesterol Education Program Expert Panel as adjunct therapy for the reduction of
low-density lipoprotein.

Alcohol

The evidence is convincing that the moderate consumption of alcohol (one to two drinks per day)
reduces insulin resistance, lowers blood pressure and increases HDL-C.48 A recent meta-
analysis found strong and consistent evidence linking moderate alcohol intake with increased
HDL-C and apolipoprotein AI levels, as well as lower concentrations of fibrinogen. The authors
calculated an overall predicted 24.7% reduction in risk of coronary heart disease associated with
an intake of 30 g of alcohol a day owing to changes in these markers."49

Exactly what type of alcohol offers the best protection against cardiovascular disease is still
being debated. Some researchers believe that it is the ethanol itself that is beneficial,50 while
others contend that red wine that offers the most benefit.51 While the verdict is still not in, a
recent review of the clinical and experimental evidence suggests that red wine may offer greater
cardiovascular protection than other types of alcoholic beverages.52 This protection is believed
to be due to the antioxidant, vasorelaxant and antithrombotic properties of the polyphenolic
compounds present in wine.53 These polyphenolic compounds, such as resveratrol, have been
shown to prevent lipoprotein oxidation in vitro,54 however, animal studies of the effects of
resveratrol on atherosclerosis are conflicting.

What are the down sides to alcohol consumption? In addition to those that are well known, such
as fetal alcohol syndrome, alcoholism and hypertension, it should be noted that even moderate
amounts of alcohol can increase triglyceride levels. Research has also shown that those who
consume more than three drinks per day are more likely to experience harm than benefit.55
There is an increased risk of breast cancer in women who consume 2 or more servings of
alcohol per day, making a number of specialists opt to recommend limiting women to 1 serving of
alcohol per day.56 In summary, those who enjoy a glass of wine with dinner should be
encouraged to consider it a part of a healthy lifestyle, while those who abstain from alcohol for
personal reasons should not be encouraged to start drinking. And remember, the antioxidant
compounds found in wine can also be found in grape juice.57

Weight Loss

Obesity is often associated with elevated triglycerides and low levels of HDL-C.26 It is currently
postulated that elevation of triglycerides leads to increased catabolism of triglyceride rich HDL-C,
resulting in lower levels of HDL-C.6 Weight loss in most obese individuals tends to increase
plasma HDL-C levels, as well as decreasing triglyceride levels.58 However, it is important to note
that low fat diets often reduce, or fail to increase, HDL-C levels. One should replace saturated fat
with monounsaturated fats in any weight loss program designed to increase HDL-C.59

The Framingham Study demonstrated that HDL-C in tobacco smokers averaged 13 percent less
than that of nonsmokers.60 The physiologic effects of smoking tobacco include endothelial injury,
lower HDL-C, impaired exercise performance, and altered oxygen delivery.61 Discontinuation of
cigarette smoking has been shown to result in a 3- to 4-mg/dL increase in HDL-C.48

DIETARY SUPPLEMENTS

Niacin

Niacin, nicotinic acid, may be used to reduce serum cholesterol and triglycerides. It is currently
the most effective drug available for raising HDL-C62 and has been shown to reduce coronary
death and non-fatal myocardial infarction.63

Three grams per day of immediate-release niacin reduces LDL-C levels by an average of 20% to
25%, while doses of 1 g/d have been shown to raise HDL-C levels by 15-20%. An extended
release prescription product is available, Niaspan (KOS), which has been shown to lower LDL-C
by 15% to 20% at its maximum dose of 2 g/d. Both the extended release and the immediate
release niacin products taken at doses as low as 1 g/d reduce triglyceride concentrations by 20%
to 35%.1 The major limitation to the use of niacin as a lipid-lowering agent is its side effect
profile, which includes flushing with both immediate- and extended-release products. Taking a
baby aspirin 30 minutes before taking niacin can minimize this effect. Alcohol and hot liquids tend
to intensify the flushing, so avoiding these substances when taking the daily dose of niacin is
advisable.

Niacin is sometimes combined with statin medication in patients with low HDL. A 3 year double-
blind, placebo controlled study of 160 adults with atherosclerosis and low HDL-C found that a
combination of simvastatin and niacin improved HDL-C levels, caused artery blockages to
recede and significantly lowered heart complications compared to placebo.64 In the study,
patients received either a combination of simvastatin and niacin alone, antioxidants alone
(vitamins E, C, beta-carotene and selenium), simvastatin-niacin plus antioxidants, or placebo.
Over 3 years, those taking the simvastatin-niacin were 60% to 90% less likely than placebo
patients to have a heart attack or stroke, require angioplasty or to die from causes related to
heart disease. This study found that the group receiving the combination plus antioxidants had
less of an increase in their HDL-C, leading researchers to question the wisdom of combining
antioxidants with statin therapy. At the time, the most that can be said from this arm of the study,
is that this particular combination of antioxidants appeared to blunt some of the benefit of the
simvastatin-niacin therapy. It should not be extrapolated to all patient populations and other statin
treatments at this time.

As liver function tests may transiently rise, niacin should not be taken by anyone with acute liver
disease. Sustained-release niacin has also been associated with severe liver toxicity when given
in doses above 2 grams daily. Niacin can worsen glycemic control in patients with diabetes and
aggravate gouty arthritis.

Policosanols

Policsanols are a mixture of alcohols usually extracted from sugar can wax or beeswax and
composed primarily of octacosanol. They have demonstrated effectiveness in the treatment of
Type II hypercholesterolemia and have been shown to be safe in studies that have run for more
than three years. At doses of up to 20 mg per day policosanols have lowered total cholesterol
and low-density lipoprotein (LDL) cholesterol by more than 20% and raised high-density
lipoprotein cholesterol (HDL) by up to 15%. This is roughly equivalent to the effects noted in
clinical trials involving patients treated with simvastatin or pravastatin. Triglyceride levels have
not been shown to be influenced by treatment with policosanols. In vitro studies suggest that
policosanols may inhibit hepatic cholesterol synthesis and animal studies support the theory that
LDL breakdown may be increased.65

BOTANICAL THERAPIES USED FOR HYPERLIPIDEMIA Red Yeast Rice (Monascus

purpureus)

The product sold as red yeast rice is prepared from cooked, non-glutinous white rice fermented
by the yeast Monascus purpureus, which is then sterilized, dried, ground and encapsulated. Red
yeast rice is a dietary staple in many Asian countries, with typical dietary consumption ranging
from 14 to 55 g/d.66 In addition to its medicinal properities, red yeast rice has been used to make
rice wine and as a food preservative for maintaining the color and taste of fish and meat.67

The primary active ingredient in red yeast rice is thought to be monacolin K (also known as
mevinolin and lovastatin). Monacolin K inhibits the enzyme that initiates cholesterol biosynthesis,
HMG-CoA reductase. It is highly unlikely that the small amount of monacolin K present in red
yeast rice fully accounts for the beneficial effects on lipids seen in clinical trials, as it is present at
only 0.2%. Red yeast rice also contains other potential lipid-lowering agents, such as ten other
monacolin analogs, omega-3 fatty acids, isoflavones, and plant sterols (ss-sitosterol,
campesterol, stigmasterol, and sapogenin).68

A randomized double-blind, placebo-controlled study of 83 men and women found that those
taking 2.4 g/d red yeast rice significantly lowered their cholesterol from 250 mg/dL to 208 mg/dL
(17%) after eight weeks compared to controls.66 LDL-C levels dropped from 173 to 134 (22%),
triglycerides dropped from 133 to 118 (12%), while HDL-C remained the same. Dietary intake
was monitored, and there were no significant differences between the two groups in total
calories, total fat, saturated fat, monounsaturated fat, polyunsaturated fat or fiber. No changes in
liver function tests or other serious adverse events were reported.

A pilot trial of red yeast rice was conducted with 14 individuals with dyslipidemia related to
human immunodeficiency virus (HIV). Patients were randomly assigned to receive either 1,200
mg/d of red yeast rice or placebo for 8 weeks in a double-blind fashion. At the conclusion of the
trial there was a statistically significant reduction in total cholesterol (P=0.01) and LDL-CC
(P=0.01) in the group receiving red yeast rice compared to placebo. No changes were noted in
HDL-C or triglycerides and no adverse effects were reported.69

A recent study of commercial red yeast rice products found that there is tremendous variation in
quality between products. Findings from clinical trials demonstrating significant and clinically
relevant cholesterol reduction using a defined Chinese red yeast rice preparation (Cholestin)
cannot be generalized to other commercially available preparations that do not contain the same
levels and profile of monacolins. Citrinin, a toxic fermentation by-product, was found at
measurable concentrations in 7 of the 9 preparations.70

It should be noted that the proprietary red yeast rice product used in the clinical trials, Cholestin,
is no longer available as a dietary supplement in the US. The FDA claimed that the manufacturer
was selling "lovastatin," a patented lipid-lowering drug sold by Merck. After several years of
battling it out in court, Pharmanex lost the fight and Cholestin was removed from sale, though,
other red yeast rice products (of questionable quality) can still be found on the shelves of health
food stores. From a cost perspective, the consumer definitely got the raw end of the deal on this
one. The current cost for cholesterol-lowering drugs is roughly $120-300 per month, with an
average cost of $187 per month.71 The red yeast rice product used in the clinical trials costs
roughly $25-35 per month.

Garlic (Allium sativum)

Garlic is perhaps the best known of the lipid-lowering herbs amongst the lay public. The lipid
lowering effects of garlic have been demonstrated in both animal studies and human clinical
trials. A number of meta-analyses have been performed over the years, demonstrating a
reduction in total cholesterol of 5-12%.72-75 While the evidence does support a small but
statistically significant decrease in lipid levels at 3 months follow-up, pooled analyses of placebo-
controlled trials failed to demonstrate significant reductions of total cholesterol at six months. The
recent report by the Agency for Healthcare Research and Quality (AHRQ) concluded "it is not
clear if statistically significant positive short-term effects-but negative longer term effects-are due
to: systematic differences in studies that have longer or shorter follow-up durations; fewer longer
term studies; or time-dependent effects of garlic."76

Most studies suggest a possible short-term benefit of garlic on lipid levels, insignificant effects on
blood pressure, and no effect on glucose levels. The trials are difficult to assess, as a whole,
given their short duration and the unpredictable release and inadequate definition of active
constituents in the garlic preparations used in the studies. Most garlic supplements are
standardized on allicin potential and are enteric-coated to prevent gastric acid inactivation of the
allicin-producing enzyme, alliinase. A recent evaluation of garlic powder tablets used in clinical
trials (1989-1997) found that the there was great variation in the amount of allicin released when
subject to the United States Pharmacopoeia (USP) acid disintegration test (724A). Older batches
were found to be more resistant to acid-disintegration and released three times more allicin (44%
vs 15% of their potential, P<0.001) than newer lots. Conflicting trial results may be the result of
lower amounts of bioavailable allicin in some products.77 Another study found that 23 out of 24
brands tested released only 15% of their allicin potential when subjected to the USP testing
method. To assure greater bioavailability, garlic powder supplements should no longer be
standardized to allicin potential, but on dissolution allicin release.78 Until test products can be
assured of containing and making bioavailable the key active constituents in garlic-conducting
and evaluating clinical trials will be extremely difficult to do.

The benefits of long-term garlic consumption may have more to do with cardiovascular benefits
other than simply lowering lipids. Garlic has been shown to have mild anti-hypertensive,79
antiarrhythmic,80,81 antithrombotic and antiatherogenic activity. The latter properties are due to
inhibition of platelet aggregation, inhibition of cholesterol biosynthesis and enhancing
fibrinolysis.80,81 The lipid lowering effects of garlic are though to be due to inhibition of HMG-
CoA reductase84 and increased catabolism of fatty acid containing lipids, especially
triglycerides.85 Garlic oil, aged garlic, fresh garlic, and garlic powder have been shown to inhibit
platelet aggregation via interference with the cyclooxygenase mediated thromboxane synthesis
pathway.86 Raw garlic inhibited cyclooxygenase activity non-competitively and irreversibly.87
After 26 weeks of garlic consumption, there was roughly an 80% reduction in serum
thromboxane in healthy male volunteers eating 3 grams fresh garlic daily.87 Cooked garlic has a
lower inhibitory effect upon platelet aggregation than raw garlic.88

The antiatherogenic activity of garlic has been demonstrated in a clinical study conducted in
Europe. A four-year study was conducted with 152 men and women diagnosed with advanced
plaque accumulation and one other cardiac risk factor (high cholesterol, hypertension). Patients
were randomized to take 900 mg. garlic (Kwai) or placebo for forty-eight months. Ultrasound was
used to measure plaque in carotid and femoral arteries at 0, 16, 36, and 48 months. At 48
months: a 2.6% reduction in plaque volume was noted in the garlic group, compared to a 15.6%
increase in the placebo group.89 While encouraging, methodological limitations prevent any
concrete conclusions.

Potential adverse effects of garlic that should be noted by health care practitioners include cases
of postoperative bleeding during augmentation mammaplasty90 and transurethral resection of
the prostate91 in patients taking garlic prior to surgery. There is also a report of spontaneous
spinal epidural hematoma.92 Evidence is lacking for a direct interaction of warfarin with garlic.
Three cases of hemorrhage with garlic have been reported but none of the patients were taking
warfarin.93 It is well known, however, that anti-platelet agents can increase the risk of major
bleeding when combined with warfarin. Practitioners should be watchful of patients on warfarin
who consume generous amounts of garlic.

Fresh garlic and dried garlic powder are probably the best preparations for patient use, as
commercial garlic powder tablets can provide differing clinical results.[function of]In conclusion,
garlic appears to have a mild, yet beneficial, effect upon the cardiovascular system and should
be considered part of a heart healthy diet when making therapeutic lifestyle changes. The lipid-
lowering effects are mild and may not be sustained, thus garlic should be not be considered a
primary therapy for patients with moderate to severe forms of dyslipidemia.

Guggul (Commiphora mukul)

The guggul tree grows in dry areas of India, Pakistan and Afghanistan. For thousands of years,
healers have tapped the trees to make medicines used to control weight and to treat other
ailments. Since the 1960's, research has focused upon its lipid-lowering activity and today it is an
approved lipid-lowering agent in India. While it is known that guggul appears to prevent oxidation
of LDL,94 more recent research seems to indicate that the guggulsterones (4,17(20)-
pregnadiene-3, 16-dione) found in guggul are highly efficacious antagonists of the farnesoid X
receptor (FXR), a nuclear hormone receptor that is activated by bile acids. The FXR receptor
controls cholesterol by regulating the level of bile acids in the body. Blocking the action of FXR
helps the body rid itself of more cholesterol. Guggulsterone treatment decreased hepatic
cholesterol in mice fed a high cholesterol diet, but was not effective in mice without the FXR
receptor.95

Older studies have demonstrated a reduction in total serum cholesterol, LDL-C, VLDL and
triglycerides, with an increase in HDL-C.96-97 One trial found guggul to be as effective as
clofibrate in reducing cholesterol levels,98 while another study of 61 patients with
hypercholesterolemia found 50 mg guggulsterones BID to be superior to placebo in reducing
lipids over a 24-week period. Guggul decreased total cholesterol levels by 11.7%, LDL-C by
12.5%, triglycerides by 12.0%, with no change noted in HDL-C.99
While intriguing, these studies suffer from methodological flaws that make any definitive
conclusion about lipid-lowering effects premature. However, given the in vitro, animal and human
data, this herb warrants further study as it may prove to be a beneficial, well-tolerated and cost-
effective treatment for dysplipidemia.

The purified, standardized extract of the plant is much better tolerated than the raw herb, which
was reported to cause numerous side effects including abdominal pain, diarrhea and skin rash.
Most extracts are standardized to 5% guggulsterone content and the therapeutic dose is 500 mg.
taken three times per day, so as to provide 25 mg guggulsterone TID.

Side effects reported in clinical trials were minor and included diarrhea, mild nausea, headache,
and restlessness.99 Guggul is contraindicated during pregnancy due to purported uterine
stimulating properties.100 Guggul has been reported to reduce the effectiveness of propranolol
and diltiazem.101

Globe Artichoke (Cynara scolymus)

Artichoke leaf has been used as a treatment for dyspepsia since ancient times. More recently,
researchers have found that the leaf extract has lipid-lowering activity. In vitro research seems to
indicate that the mechanism of action appears to be an indirect inhibition of HMG-CoA
reductase.84 While there are likely multiple active constituents, luteolin exerted the highest
inhibitory potency and effectively blocked the stimulation of cholesterol biosynthesis by insulin.
Artichoke extracts also enhance biliary cholesterol excretion,102 which may also contribute to its
lipid lowering effects.

An older study of seventeen outpatients with familial Type IIa or Type IIb hyperlipoproteinemia
was undertaken to determine the efficacy of cynarin for lowering lipids in this population. The
patients were treated with either 250 mg or 750 mg of cynarin for three months. There were no
significant changes noted in serum cholesterol and triglyceride levels.103 Of course, this study
used an isolated constituent from artichoke, which, at least according to recent in vitro data, is
not the main lipid-lowering agent.

A recent randomized, placebo controlled multi-center trial examined the efficacy and tolerability
of 450 mg per tablet artichoke dry extract (drug/extract ratio 25-35:1, aqueous extract, CY450)
versus placebo for the treatment of hyperlipidemia. The study enrolled 143 adult patients with
initial total cholesterol of greater than 280 mg/dl and randomized them to receive either 1,800 mg
artichoke dry extract per day or placebo for 6 weeks. Changes of total cholesterol and LDL-
cholesterol from baseline to the end of treatment showed a statistically significant superiority (P =
0.0001) of artichoke dry extract over placebo. The decrease of total cholesterol in the CY450
group was 18.5% compared to 8.6% in the placebo group. LDL-cholesterol decrease in the
CY450 group was 22.9% and 6.3% for placebo. LDL/HDL ratio showed a decrease of 20.2% in
the CY450 group and 7.2% in the placebo group. No adverse events were noted in the study.104

The adverse effect profile for artichoke in the literature is very good. The only contraindication at
this time is for use in those with bile duct obstruction. This is due to the choleretic activity of the
extract.

Flavonoid Rich Herbs

Flavonoids are responsible for the colors of flowers, fruit, and sometimes leaves and a wide
variety of flavonoid classes may be found amongst fruits, vegetables and beverages, such as tea
and wine. Flavonoids have biological properties that have been shown to promote health and
help reduce the risk of disease. Flavonoids possess anti-oxidant, anti-neoplastic and anti-
inflammatory activity; extend the activity of vitamin C, and exert positive effects upon the
cardiovascular system.105,106 Polyphenolic flavonoids are thought to reduce the risk of
coronary artery disease through the inhibition of platelet aggregation, reducing injury from
ischemia and reperfusion, reducing plasma cholesterol levels and/or through the inhibition of LDL
oxidation.107,108 For instance, licorice extract (free of glycyrrhizinic acid, the component
associated with water retention and hypertension) and the isoflavane glabridin, a major
polyphenolic compound found in licorice, were both shown to markedly inhibit LDL oxidation in
10 normolipidemic individuals during one study.109

Diets that are rich in plant polyphenols, such as red wine or tea, are thought to offer a beneficial
effect upon the cardiovascular system. The following herbs are rich in flavonoids that, when
regularly consumed in the diet, may offer some cardiovascular protection. More rigorous
research is required before any formal recommendations can be made regarding treatment,
however, enough preliminary data exists to suggest that these spices should be considered part
of a healthy heart diet.

Tea (Camellia sinensis)

Tea is second only to water as the most common drink in the world. Green tea from Camellia
sinensis has been shown to lower plasma cholesterol in animal models of
hypercholesterolemia.110 Prospective studies have suggested that the polyphenolic flavonoids
in tea may exert a protective effect against cardiovascular disease. A potential mechanism put
forth for such an effect has been inhibition of lipid peroxidation by polyphenolic antioxidants.
However, a recent study challenges this hypothesis as the polyphenolic compounds from tea
failed to inhibit in vivo lipid peroxidation.111 Other researchers have suggested that tea
increases the expression of the hepatic LDL-C receptor, a cell surface protein involved in the
control of plasma cholesterol,112 and increases the fecal excretion of bile acids and
cholesterol.113 The purported beneficial effects might also be explained by the ability of green
tea catechins and gallate esters to reduce intestinal cholesterol absorption and inhibit platelet
aggregation.

A meta-analysis of tea consumption in relation to stroke, myocardial infarction, and all coronary
heart disease was conducted based on 10 cohort studies and seven case-control studies.114
The authors concluded that, "The incidence rate of myocardial infarction is estimated to decrease
by 11% with an increase in tea consumption of 3 cups per day (fixed-effects relative risk estimate
= 0.89, 95% confidence interval: 0.79, 1.01) (1 cup = 237 ml). However, evidence of bias toward
preferential publication of smaller studies that suggest protective effects urges caution in
interpreting this result." The study-specific effect estimates for stroke and coronary heart disease
were found to be too heterogeneous to allow for summarization.

The authors clearly point out the limitations of their findings. When evaluating studies, they found
that many failed to precisely identify the type of tea being used or consumed-studies referring to
the test item simply as "tea." This represents a significant problem with evaluating the evidence
as "tea" actually represents a very heterogeneous group of beverages, which can include
fermented black tea, half fermented oolongs, unfermented green tea, and sweetened or
unsweetened ice tea, and other very distinct herbal teas.

Also lacking in most studies was how the tea was prepared. How long was the herb steeped and
was milk added to the beverage? These are important questions that must be adequately
addressed as these variables can affect the content of the tea.114

Turmeric (Curcuma longa)

Turmeric is a member of the ginger family and has been used as a spice for millennia. The
rhizome contains 0.3-5.4% curcumin, the substance that gives turmeric its lovely orange-yellow
color. Curcumin has been shown to possess anti-inflammatory, anti-oxidant and lipid-lowering
effects. Animal studies have shown that rats fed 0.2 g curcuminoids per 100 g diet experience a
reduction in total cholesterol and triglycerides when compared to control animals.115 Other
studies have confirmed the lipid-lowering effects of curcumin in animals.116,117 The lipid-
lowering effects are thought to be due to alterations in fatty acid metabolism, or through
enhancing the conversion of cholesterol to bile acids. It is important to note that no human
clinical trials could be found to confirm the lipid lowering effects of curcumin, or turmeric, and
what dose would be necessary for efficacy.

Curcumin inhibits platelet aggregation mediated by the platelet agonists: epinephrine, ADP,
platelet-activating factor, collagen, and arachidonic acid.118 Adverse effects are minor but can
include gastrointestinal disturbances and contact dermatitis. Patients with gallstones or bile duct
obstruction should avoid this herb, as curcumin has been shown, by ultrasound examination, to
induce contraction of the gallbladder in humans.119

While turmeric is commonly used as a spice, most research has been conducted on the isolated
curcuminoids. The dose generally recommended is 400-600 mg TID. At this time, the addition of
turmeric to the diet may be considered part of a heart healthy diet for those who enjoy the flavor
of this spice, however, it is premature to recommend curcumin as a primary treatment for
hyperlipidemia.

Ginger (Zingiber officinale)

Ginger is a commonly used culinary herb. It has been used for thousands of years in China and
India for medicinal purposes. In vitro research has shown that constituents within ginger have an
inhibitory effect upon cholesterol biosynthesis.120 Animal studies have also demonstrated lipid-
lowering activity with ginger via enhancing the activity of hepatic cholesterol-7-hydroxylase, the
rate-limiting enzyme in bile acids biosynthesis, thereby stimulating cholesterol conversion to bile
acids, an important mechanism for eliminating cholesterol from the body.121 A study in rabbits
found that an orally administered ethanolic extract of ginger (200 mg/kg) reduced lipids after 10
weeks of being fed a cholesterol rich diet. The authors found, at this dose, ginger produced
similar results as gemfrimbrozil.122

In contrast to the in vitro and animal data, a clinical trial involving patients with coronary artery
disease, 4 grams per day dried ginger powder for 3 months failed to inhibit ADP- and
epinephrine-induced platelet aggregation, alter fibrinolytic activity, or effect blood lipids or blood
sugar.123 It should be noted, however, that a single dose of 10 g powdered ginger administered
to these patients produced a significant reduction in platelet aggregation.

Standardized ginger extract had no significant effects on coagulation parameters or on warfarin-

induced changes in blood coagulation in rats.124 Evidence is lacking for a direct interaction
between warfarin and ginger.93 When ginger is used as a spice or at doses of 3 grams per day
or less, there should be little concern for interaction with this category of medication.

Administration of 6 g dried ginger powder increased exfoliation of gastric surface epithelial cells
in human test subjects. This dose may cause gastric irritation and is potentially ulcerogenic. It is
recommended that consumption be less than 6 g/d dried ginger. Patients treated with ginger
have reported flatulence and heartburn but the rhizome should be considered quite safe when
used as a spice in food.

Hawthorn (Crataegus laevigata)

Hawthorn is a fruit-bearing shrub that has a long and distinguished history as a medicinal agent.
It has been used primarily to treat digestive and cardiovascular disorders. Most contemporary
research of hawthorn has focused on its use in treating a variety of cardiovascular conditions.
The cardiovascular effects are believed to be the result of positive inotropic activity, ability to
increase the integrity of the blood vessel wall and improve coronary blood flow, and positive
effects on oxygen utilization. Flavonoids are postulated to account for the majority of these
effects.

Hawthorn has been shown to reduce cholesterol in rabbits fed a high cholesterol diet.125-126
This study found that supplementation of hawthorn fruit did not affect the activities of HMG-CoA
reductase or cholesterol 7alpha-hydroxylase (CH) but it did suppress the activity of intestinal acyl
CoA:cholesterol acyltransferase (ACAT) (p < 0.05). The authors conclude that the lipid lowering
effects of hawthorn may be due, at least in part, to the inhibition of cholesterol absorption
mediated by down-regulation of intestinal ACAT activity.

Though hawthorn is often found in dietary supplements designed to reduce cholesterol, there are
no human clinical trials to review to determine if the fruit, leaves or flowers lower lipids humans,
and if they do-to what extent and at what dose. Hawthorn appears to have a low level of toxicity,
however, practitioners should be aware of potential interaction with certain medications.
Hawthorn preparations may potentiate the activity of cardiac glycoside medications such as
digitalis.100 Hawthorn exerts a positive inotropic effect that is not caused by phosphodiesterase
inhibition or a beta-sympathomimetic effect, as the L-type calcium current is not affected.127 The
positive inotropic action of hawthorn appears to be cAMP-independent, similar to cardiac
glycosides,128 which may explain an additive effect when the herb is taken with digitalis.
Crataegus extract blocks repolarizing potassium currents in ventricular myocytes, similar to the
action of class III antiarrhythmic drugs and might be the basis of the antiarrhythmic effects
described for hawthorn.127

OTHER BOTANICALS

Bishop's Weed (Ammi visnaga)

The fruit of this plant have been used since ancient times for its medicinal effects. Papyrus
writings from Egypt describe the use of Ammi visnaga for the treatment of asthma, painful kidney
stones and angina. Khellin has been shown to exert lipid-lowering effects in animal studies.128 A
study of khellin in 20 non-obese men with normal lipid levels found a significant increase in HDL-
cholesterol levels, although, total cholesterol and triglyceride concentrations remained
unchanged. Unfortunately, nausea and vomiting were responsible for the withdrawal of four
volunteers, and elevation of liver enzymes caused the withdrawal of an additional two
participants.129 These side effects are not generally noted with standardized preparations of the
whole fruit.

Visnadin dilates the coronary vessels and brings about an increase in coronary circulation.130
The German Commission E approved the use of Ammi visnaga for the treatment of mild anginal
symptoms. Standardized preparations of this herb may be useful for mid angina, especially in
those patients who do not tolerate nitroglycerin. Generally, standardized extracts are
recommended that provide an equivalent of 20 mg khellin per day.

Sidebar

InnoVision Communications is accredited by the Accreditation Council for Continuing Medical

Education to provide continuing medical education for physicians. This education activity consists
of a journal article in the May 2003 issue of Alternative Therapies in Health and Medicine. The
participant should study the article, then complete the self-evaluation at the end of the activity.
The activity and self-evaluation are expected to take a maximum of 1 hour.

DESCRIPTION

Coronary heart disease (CHD) is the one of the most prevalent diseases in the US. It is also one
of the most preventable. This lesson explores the treatment of CHD through changes in lifestyle,
dietary modifications, and the use of botanicals and dietary supplements.

OBJECTIVES

Upon completion of this article, participants will be able to do the following:

1. Discuss the role of lipoproteins, triglycerides, and homocysteines in CHD.

2. Examine the effect of lifestyle and diet on cholesterol levels.

3. Identify dietary supplements and botanicals that have shown efficacy in reducing risk-factors
for CHD, and explain their mechanism of action, benefits, and possible side-effects.

Sidebar

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http://www.alternative-therapies.com and selecting the Continuing Education option.

References
References

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http://mv.ezproxy.com.ezproxy.lib.rmit.edu.au/projects/slpprojectlayout4.asp?p=20.

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AuthorAffiliation