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The Ultimate Guide to the Natural Management of High Cholesterol and Cardiovascular Risk Factors

by Dr. James Meschino, DC, MS, ROHP


In recent years statin drugs have become a popular drug of choice to address hypercholesterolemia in both the primary and secondary prevention of coronary heartdisease and other vascular problems. Although studies of large populations have shown that the use of various statin drugs produce a significant decline in blood cholesterol with accompanying reductions in myocardial infarction and other cardiovascular events, there are associated risk factors and unanswered safety questions associated with their use. In the majority of cases of hypercholesterolemia the benefit-to risk-analysis suggests that aggressive dietary intervention (with exercise) should be the first intervention to lower cholesterol into the desirable range (below 150 mg/dL), followed, if necessary, by supplementation with gum guggul and/or policosanol, then bile acid sequestrants, and finally a statin drug, in this sequence. Persistent elevation of triglyceride and/or low HDL levels in conjunction with hypercholesterolemia may require the judicious concurrent use of niacin and/or a fibric acid derivative medication.


Primum Non Nocere ‘‘ (first do no harm)” is one of the principal precepts taught to all medical and alternative healthcare students and practitioners. It reminds a practitioner that he or she must consider the possible harm that any intervention might do. It is most often mentioned when debating use of an intervention with an obvious chance of harm but a less certain chance of benefit. On a practical basis, it prompts practitioners to initate treatment beginning with interventions with the best known benefit-to-risk ratio, and proceeding, when necessary, to include interventions that are efficacious, but less safe or where the safety of an intervention is less well established.

With respect to the management of hypercholesterolemia the evidence suggests that in the majority of cases (approximately 90% of cases) the first line of treatment should involve aggressive dietary treatment involving a low saturated fat and cholesterol diet, with additional emphasis on cholesterol lowering foods and supplements containing soluble dietary fiber. In some cases a plant-based diet, exclusively, is the best option. Therapeutic lifestyle change should also include, in most cases, adherence to regular endurance exercise training, which further helps to lower total and LDL-cholesterol, raise HDL- cholesterol, reduces triglycerides and encourages central and peripheral cardiovascular adaptations that are beneficial in regards to lowering overall cardiovascular disease risk. (Mayers, 2003, pp. 2-5), (Sheppard & Balady, 1999, pp. 963-972) When aggressive therapeutic lifestyle change does not produce sufficient cholesterol lowering outcomes (achieving a total fasting cholesterol level below 150 mg/dL) then daily supplementation with gum guggul and/or policosanol, two natural health products, represent the next steps in the treatment protocol, according to evidence-based, benefit- to-risk ratio analysis.
Failure of these interventions to produce a desired result requires consideration of a bile acid sequestrant drug to further reduce blood cholesterol. If all of these interventions fail, after a proper test period (approximately 6-9 months), or patient compliance with aggressive lifestyle change is inadequate, then the treatment protocol justifiably may proceed to include the use of cholesterol-loweing statin drugs (HMG-CoA reductase inhibitors). Statin drugs may also be considered earlier in the course of treatment in cases of established familial hypercholesterolemia, where initial fasting cholesterol levels exceed 300 mg per dL, or in cases where coronary or other cardiovascular events may be imminent.
Finally, other drugs, such as niacin and fibric acid derivatives deserve consideration when aggresssive therapeutic lifestyle change has not brought about sufficient reductions in triglycerides levels (target level is less than 1.13 mmol/L or100 mg/dL) and/or HDL levels remain low (target level for men is above 1.17 mmol/L or 45 mg/dL, and in
women target levels are above 1.42 mmol/L or 55 mg/dL) in patients who have other major risk factors for coronary heart disease.
Unfortunately, the recent trend has been to rely upon statin drugs as the first line of treatment in the management of hypercholesterolemia, with little regard for diet, exercise, soluble fiber supplementation, and the use of bile acid sequestrants. A review of the literature suggests that this approach is inappropriate from a benefit-to-risk ratio standpoint, and that health practitioners would be best advised to follow the treatment protocol outlined in this paper,which provides a prudent, evidence-based guideline to the pharmacotherapeutic management of hypercholesterolemia.

The Ultimate Guide to the Natural Management of High Cholesterol and Cardiovascular Risk Factors

- by Dr. James Meschino, DC, MS, ROHP

The Ultimate Guide to the Natural Management of High Cholesterol and Cardiovascular Risk Factors

Dr. James Meschino, 


Cardiovascular Disease Statistics And Major Risk Factors

Cardiovascular disease is the leading cause of death in both men and women in the United States, and is a major cause of death in most developed countries. According to the Centers for Disease Control and Prevention (CDC), approximately 70 million people in the United States have heart disease, and approximately 930,000 people die from the condition each year. Heart disease contributes to approximately 40% of all deaths. Although often considered a man’s disease, according to the American Heart Association, cardiovascular disease accounts for more deaths in women per year in the United States than the next six causes of death combined. (Heart Disease)
From 1989 to 1999, the death rate from coronary artery disease declined 24%. This decline was mainly attributed to modest improvements in dietary and exercise practices, reduction in smoking, as well as better management of hypertension and hypercholesterolemia and medical care, in general. With respect to smoking cessation, according to the World Health Organization, the risk of coronary artery disease decreases by 50% in the first year after quitting. In the past two to three decades there has been more than a 20% decline in cigarette smoking among Americans. The most recent studies indicate that US 

adults who are current smokers didn’t budge
between 2004 and 2005, holding steady at just under 21%. However, that figure had been decreasing slowly for the past 8 years. (Mariolis, et al, 2006, pp. 1145-1151)
Strong evidence also exists to indicate that a decline in blood cholesterol levels reduces risk of heart disease. There has been a modest decline in the blood levels of American over the past three decades due to voluntary dietary changes, and since the 1980’s clinical studies using drug and/ or dietary interventions to lower cholesterol have demonstrated that lowering cholesterol reduces risk of heart disease as both a primary and secondary intervention for this disease. (Kashyap, ML, 1997, pp. 517-23), (Ornish, et al., 1983, pp. 54-9), (Esselstyn, Jr., 2001, pp. 171-177) In the United States the

average adult’s total cholesterol is between 210 and 220 mg/dL and the average daily intake of saturated fat (a major stimulus to hepatic cholesterol synthesis) is 50-70 grams per day (in many cases exceeding 100 gms). In countries where saturated fat intake is very low, blood cholesterol levels are below 150 mg/dL and coronary heart disease incidence is virtually zero. These facts will be revisited as a feature theme of this discussion (Castelli & Griffin, 1988, pp. 44- 56)

Numerous major risk factors for heart disease have been identified, which stem from genetic, gender, age and environmental influences. More specifically, these include increasing age, gender (males develop CHD at a younger age and more men die from this disease than women), ethnicity, hypertension, hypercholesterolemia, diabetes, smoking, inactivity, and obesity (particularly android obesity). Other factors are also associated with increased risk of cardiovascular disease, but their significance and prevalence have not yet been precisely determined (i.e. stress, alcohol consumption, hyperhomocysteineima). (Pearson, et al., 2002, pp. 388-391), (Boushey, Beresford, Omenn & Motulsky, 1995, pp. 1049-1057) Some experts suggest that 10% of the population’s coronary artery disease risk appears to be attributable to hyperhomocysteinemia, but further studies are warranted to confirm this value. In most cases hyperhomocysteinemia results from sub-optimal intakes of folic acid, and/or vitamin B12 and vitamin B6. Folic acid and vitamin B12 provide an essential methyl group to recycle homocysteine back to methionine. Methionine is further converted to S-adenosyl methionine, which donates its methyl group (originally acquired from folic acid) to many chemical reactions within the cell, such as those required for DNA synthesis. With loss of its methyl group S-adenosyl methionine once again becomes homocysteine. In cases of sub-optimal intake of folic acid and/or vitamin

B12 and vitamin B6, homocysteine levels accumulate intracellularly. At certain threshold level homocysteine leaks out of the cell to enter the blood stream. In the blood stream high levels of homocysteine cause damage to the endothelial lining (endothelial cell desquamation) of blood vessels, creating sites for atherosclerosis to develop. It also causes vasoconstriction of blood vessels, and increases monocyte binding to the vessel wall. In this instance monocytes are transformed into macrophage cells, which ingest LDL-cholesterol, ever expanding into foam cells, which form an important component of atherosclerotic plaque. Homocysteine may also cause oxidation of LDL cholesterol. Oxidized LDL-cholesterol has been shown to be more atherogenic than non-oxidized LDL-cholesterol, via the uncontrolled LDL-cholesterol (oxidized LDL-cholesterol) uptake by macrophages at the site of atherosclerotic plaque formation. A fasting homocysteine blood level above 6.3 micromoles per liter is associated with increased risk for vascular disease. Studies show that supplementation with folic acid, vitamin B12 and vitamin B6 can lower homoscysteine levels to an appreciable degree in many patients with hyperhomocysteinemia. Vitamin B6 is also required for homocysteine recycling in that vitamin B6 is a co-factor in the reaction that converts homocysteine to cystathionine, which can be further converted to the importation sulfur-containing amino acids serine and cysteine. (Boushey, Beresford, Omenn & Motulsky, 1995b, pp. 1049-1057), (Woodside, Yarnell, M., Young & Marmon, 1998, pp. 858-66), (Rimm, et al., 1998, pp. 359-66)

Increasing age –

the risk of heart disease increases as individuals gets older. In general, beginning at 45 for men and age 55 for women the risk of developing heart diseases increases progressively and dramatically,

Male sex (gender) —

Men have a greater risk of heart attack than women, and they have attacks earlier in life. Even after menopause, when women’s death rate from heart disease increases, the death rate in women is still less than in their male counterparts.

Heredity (including Race) —

Children of parents with heart disease are more likely to develop it themselves. African Americans have more severe high blood pressure than Caucasians and a higher risk of heart disease. Heart disease risk is also higher among Mexican Americans, American Indians, native Hawaiians and some Asian Americans. This is partly due to higher rates of obesity and diabetes. Most people with a strong family history of heart disease have one or more other risk factors for the disease (i.e. hypertension, hypercholesterolema, diabetes)

Tobacco smoke —

Smokers have an increased risk of coronary heart disease that is 2–4 times that of non smokers. Cigarette smoking is a powerful independent risk factor for sudden cardiac death in patients with coronary heart disease; smokers have about twice the risk of non smokers.

High blood pressure —

High blood pressure increases the heart’s workload, causing the heart to thicken and become stiffer. It also increases risk of stroke, heart attack, kidney failure and congestive heart failure. When high blood pressure exists with obesity, smoking, high blood cholesterol levels or diabetes, the risk of heart attack or stroke increases several times.

Physical inactivity —

An inactive lifestyle is an established risk factor for coronary heart disease. Regular, moderate-to-vigorous physical activity helps prevent heart and blood vessel disease via a number of central and peripheral adaptations. Exercise can also help control other risk factors such as blood cholesterol, triglycerides, diabetes and obesity, as well as help lower blood pressure in some hypertensive patients.

Obesity and overweight —

People who have excess body fat (especially central obesity – android obesity) are more likely to develop heart disease and stroke even if they have no other risk factors. Excess weight increases strain on the heart. It is often associated with hypertension, hypercholesterolemia, hypertriglyceridema and lower levels of HDL. (Pearson, et al., 2002, pp. 388-391) Central obesity is very metabolically active fat, which implies that free fatty acids are easily released to the bloodstream from abdominal adipose tissue. These free fatty acids can be taken up by the liver and re-circulated back to the blood stream within very low density lipoproteins (VLDL). In turn, higher VLDL levels produce higher circulating triglyceride levels as well as its remnant particle (the LDL-C), which results in higher circulating levels of LDL- cholesterol as well. Android obesity also increases risk of diabetes by increasing insulin resistance. The most recent evidence suggests that waist circumference is a better predictor of cardiovascular disease risk than is body mass index. More specifically a waist circumference greater than 35.6 inches (89 cm) for men and 33.2 inches (83 cm) for women, is strongly associated with high lipid levels, high blood pressure and glucose intolerance. (Zhu, et al., 2005, pp. 409-15)

Diabetes mellitus —

Diabetes seriously increases risk of developing cardiovascular disease. Even when glucose levels are under control, diabetes increases the risk of heart disease and stroke, but to a lesser degree than occurs when blood sugar is not well controlled. About 75% of patients with diabetes die from heart or blood vessel diseases.

High blood cholesterol —

Studies consistently show that as blood cholesterol rises, risk of coronary heart disease also rises. This is true in regards to total cholesterol and especially with respect to LDL-cholesterol. Higher HDL-cholesterol levels are associated with reduced risk of cardiovascular disease. An individual’s cholesterol level is affected by age, sex, heredity and diet. (Pearson, et al., 2002, pp. 388-391).

This paper discusses the known impact of blood cholesterol on coronary heart disease and presents an evidence-based lifestyle and pharmacotherapeutic model to help Americans attain and maintain optimal levels of blood cholesterol in regards to the primary and secondary prevention of heart disease, while at the same time reducing risk of adverse side effects associated with cholesterol-lowering drugs and natural pharmacological agents (the use of natural supplements). The pharmacotherapeutic model presented in this paper differs from that proposed by the National Research Council, National Cholesterol Education Program and The American Heart Association, for reasons that will be highlighted and supported throughout the discussion. As noted above, other risk factors in addition to the control of blood cholesterol require attention in the primary and secondary prevention of coronary heart disease. However, much of the controversy about this disease centers around the levels of cholesterol that are most desirable to achieve and which interventions are the most efficient and safest to achieve these optimal blood cholesterol levels.

Lipoprotein Physiology And Metabolism

High levels of total cholesterol and LDL-cholesterol are a major risk factor for the development of coronary heart disease, whereas higher levels of HDL-cholesterol is associated with decreased risk of this disease. As such, this discussion begins with a review of lipoprotein physiology and metabolism as a means to appreciate the steps involved in the development of hypercholesterolemia and the mechanisms of action through which hypocholesterolemic drugs and nutritional agents can help to keep cholesterol within the safe and optimal range.
Following the ingestion of dietary triglycerides, containing long-chain fatty acids (saturated fatty acids), chylomicrons produced in the intestinal mucosa carry these reassembled triglycerides into the thoracic lymph duct to the blood stream. They are removed from plasma with a half-life of 5-15 minutes. Most of the triglyceride is hydrolyzed by lipoprotein lipase in the capillary bed of adipose tissue and muscle. ApoC-II, an activator of lipoprotein lipase, is acquired by chylomicrons by a transfer of the ApoC-II peptide from circulation plasma high- density lipoprotein (HDL). After removal of some of the triglyceride, chylomicron remnants are rapidly taken up and cleared by the liver.
In response to the presence of long chain saturated fatty acids in the liver, the liver secretes into the blood stream a large very-low-density lipoprotein(VLDL). Its core consists mostly of triglyceride synthesized in the liver with a smaller amount of cholesterol esters. VLDL’s display on their surface two predominant proteins, Apoprotein B-100 and E, both of which can be bound by low-density lipoprotein (LDL) receptors. The VLDL serves to transport endogenously synthesized triglyceride to body storage tissues and organs that utilize these lipids for energy storage (ie. adipose cells) or as a substrate for metabolic reactions, (ie. muscle cells). In this instance the major precursors for triglyceride synthesis are glucose and plasma free fatty acids. The synthesis of VLDL can be stimulated by the over feeding of carbohydrates or proteins, by the ingestion of dietary saturated fats, and by a variety of metabolic stimuli that cause an increase in plasma free fatty acids. The ingestion of saturated fat, in particular, appears to exert the strongest dietary influence upon the formation of more cholesterol-rich VLDLs for reasons that will be discussed shortly. However, not all saturated fats are equal in their cholesterol raising effects (which is beyond the scope of this paper). It is suffice to say that in general the over consumption of saturated fat is a major contributing factor to the outcome of undesirable blood cholesterol levels (and ratios) in as much as 90% of all cases of hypercholesterolemia.

 Once secreted into the blood stream from the liver VLDLs are catabolized fairly rapidly with a half-life of 6-12 hours. When a VLDL particle reaches the capillaries of adipose tissue or of muscle, its triglyceride is extracted. The result is a new kind of remnant particle, decreased in size and enriched in cholesteryl esters, but retaining its two Apoproteins; it is called intermediate-density lipoprotein, or IDL.

In human beings about half of the IDL particles are removed from the circulation quickly – within from two to six hours of their formation – because they bind very tightly to liver cells, which extract their cholesterol to make new VLDL and bile acids. Tight binding is attributable to Apoprotein E, whose affinity for LDL receptors on liver cells is greater than that of Apoprotein B-100’s lower affinity for LDL receptor sites on body cells. The IDLs that remain in the circulation slowly become LDL cholesterol lipoproteins as they give up additional trigycerides to adipose and muscle tissue. As well the Apoprotein E dissociates from the IDL in its transformation into LDL- cholesterol. The LDL particles have a much longer life span than IDL particles as they (LDL) circulate for an average of two and a half days before binding to LDL receptors in the liver and in other tissues.

A major reason for this is that LDL no longer possesses Apoprotein E, and thus has less affinity for LDL receptors on liver and other body cells. As such, its clearance from the circulation is slower. As LDL circulates throughout the vascular system it easily becomes incorporated into the arterial plaque, accelerating the atherosclerotic process and further encouraging thrombus formation.

To review, LDLs are a remnant particle of VLDL catabolism. Approximately fifty percent of the LDL particle is cholesterol. Recent studies suggest that LDL may be the biologic vehicle to provide cholesterol to the cell for feedback inhibition. To review this mechanism we should understand that cholesterol in the body is obtained from the diet and is also synthesized in the liver or the intestinal mucosa for release in association with lipoproteins. In the adult, other than liver and intestinal cells, most cells in the body, with the exception of endocrine glands,

do not demonstrate active cholesterol synthesis, (the synthesis of cholesterol beginning with the condensation of two Acetyl CoA molecules to yield Acetoacetyl CoA, which goes on to form beta hydroxy-beta Methylglutaryl CoA, the basic substrate for cholesterol synthesis).
As LDL circulates in the blood stream with its rich supply of cholesterol it has the opportunity to bind to receptors clustered in specialized regions where the cell membrane is indented to form craters known as coated pits. Once bound to these cellular receptors the LDL particle is pinched off and carried into the cell as membrane-bounded sacs called endocytic vesicles. The affinity of apoprotein B-100 attracts the LDL particle to the receptors site of the host cell and through this described mechanism of receptor-mediated endocytosis, the LDL particle is taken into the cell as an intracellular particle where it binds to a lysosome, a sac filled with digestive enzymes. Some of the enzymes break down the LDL’s coat, exposing the cholesteryl ester core. Another enzyme clips off the fatty acid tails of the cholesteryl esters, liberating unesterified cholesterol. All cells in the body incorporate cholesterol into newly synthesized surface membranes. In certain specialized cells the cholesterol extracted from LDL has other roles. In the adrenal gland and in the ovary, for instance, it is converted into the steroid hormones cortisol and estradiol , respectively. Some of the cholesterol arriving in the liver from LDL is converted into bile acids, which have a digestive function in the intestine.
On the subject of cholesterol feedback inhibition, the presence of unesterified cholesterol in the cell modulates three processes. First, by turning off the enzyme HMG CoA reductase, it reduces the cell’s ability to make its own cholesterol and thus cholesterol synthesis from within the cell is turned off. Second, the incoming LDL derived cholesterols promotes the storage of cholesterol in the cell by activating an enzyme called lecithin: cholesterol Acyltransferase (ACAT). This enzyme reattaches a fatty acid to excess cholesterol molecular, making cholesteryl esters that are deposited in storage lipid droplets. Third, and most significant concerning cardiovascular function, the accumulation of cholesterol within the cell drives a feedback mechanism that makes the cell stop synthesizing new LDL receptors (a glycoprotein coded in the cell’s ribosome). Cells thereby adjust their complement of LDL receptors such that enough cholesterol is brought in to meet their varying demands but not enough to overload them. Therefore, if excess LDL is circulating in the blood stream and the body cells have satisfied their cholesterol needs, the body cells, in turn, reduce the number of LDL receptors that are synthesized and delivered to the cell surface. In this instance a decreased clearance of LDL from the blood stream occurs. As a result, the individual demonstrates higher levels of circulating LDL-cholesterol, which puts them at increased risk for the development of atherosclerosis. 

Thus, an important strategy in the prevention of coronary heart disease requires that an individual consume amounts of saturated fat (and cholesterol) that result in LDL levels that are not associated with the development of atherosclerosis. In most cases this requires limiting saturated fat and cholesterol intake to levels well below those presently consumed by the average American.

Interestingly, seventy-five percent of the receptor-mediated removal of LDL takes place in the liver. Most tissues are found to have some receptors, but those of the liver, adrenal gland and ovary, which are the organs with particularly large requirements for cholesterol, have the highest concentration of receptors. (Brown & Goldstein, 1984, pp. 58-66), (Breckenridge & Patten, 1980, pp.
345-359), (Ernest & Levy, 1984, pp. 724-739),
(Krause & Mahan, 1984, pp. 546-599)
Epidemiologic surveys done in many countries over the past 50 years have uniformly shown that atherosclerosis becomes severe as the mean LDL level rises in a population. With few exceptions, studies indicate that populations consuming small amounts of animal fats (as in Japan and Yugoslavia) have low cholesterol levels. Populations with a high intake of such fats (as in eastern Finland ) have high levels of serum cholesterol. Subsequent studies, (to those of Ancel Keys reported from 1958-1968) of many different populations have confirmed Keys’ findings: high LDL levels are the rule in the populations that consume a large part of their calories as fats (predominantly saturated fats) from meat and dairy products. (Gordon, Kannel, Castelli & Dauber, 1981, pp. 1128- 1131), (Key, 1970, pp. 11-1211), (Cheraskin, Rigsdorf & Clark, 1970, pp. 250-301), (Lipid Research Clinical trials and their effect on medical therapy: The Multiple Risk Factor Intervention Trial., 1984).

Early intervention trials involving dietary modification and first generation lipid lowering drugs (not statin drugs) demonstrated that a decline in cholesterol levels (as well as an increase in HDL levels) reduced risk of coronary events. For instance, the Lipid Research Clinics Coronary Primary Prevention Trial concluded that a 1% decrease in total serum cholesterol corresponded with a 2-3% decrease in risk of coronary artery disease. 18 The Helsinki Heart Study yielded similar results. (Frick, et al., 1983, pp. 1237-45), (Manninen, et al., 1988, pp. 641-

The Important Relationship Between Bile Acids And Cholesterol

Upon the ingestion of dietary fats, bile acids (originally formed in the liver from cholesterol) are secreted into the small intestine, where they emulsify dietary fats. Having done their work, many bile acids are reabsorbed from the intestine, returned to the bloodstream, taken up by the liver and again secreted into the upper intestine. This recycling of bile acids ordinarily limits the liver’s need for cholesterol, and thus, down- regulates the production of LDL receptors, resulting in higher levels of circulating LDL-cholesterol.

However, soluble dietary fiber, and/or cholesterol resin drugs, bind to bile acids (and cholesterol) within the intestinal lumen and drag them out of the body via the fecal route. In this instance liver cells sense a relative deficiency of bile acids and, in turn, increase the number of LDL receptors on their surface. This increases clearance of LDL from the circulation. Further, the loss of bile acids via the fecal route encourages more rapid conversion of hepatic cholesterol to be converted into bile acids, which in turn, are also excreted via the fecal route in the presence of continued ingestion of soluble dietary fiber and/or bile acid sequestrant drugs. Thus, the net effect of a low saturated fat and cholesterol diet, in combination with a diet high in soluble dietary fiber (and/or the co-administration of a bile acid sequestrant drug), both reduce the synthesis of LDL and enhances the clearance of LDL from the circulation (as well as the excretion of excess cholesterol from the body in the form of bile acids), thereby lowering serum levels of total and LDL cholesterol. (Anderson & Gustafson, 1988, pp. 749-53), (Edmunds & Mayhew, pp. 312-25),
(Kingsley, CM, 1992, pp. 147-160)

The Ultimate Guide to the Natural Management of High Cholesterol and Cardiovascular Risk Factors

- by Dr. James Meschino, DC, MS, ROHP

The Ultimate Guide to the Natural Management of High Cholesterol and Cardiovascular Risk Factors

Dr. James Meschino, 


Genetic Influence On Blood Cholesterol Levels

The relationship between dietary factors, elevated LDL-cholesterol, and subsequent development of cardiovascular disease has been the subject of many recent investigations. Evidence strongly implicates faulty dietary behaviors in the majority of cases of hypercholesterolemia. However, in 5-10 percent of hypercholesterolemic cases genetic problems are the root cause. In 1939 Carl Muller of the Oslo Community Hospital in Norway identified an inborn error of metabolism causing high blood cholesterol levels and heart attacks in young people. In this instance Muller demonstrated that the absence of the LDL receptor, due to decreased or impaired production of the receptor by the cell’s genetic code, resulted in high levels of circulating LDL-cholesterol.

This condition he identified as familial hypercholesterolemia(FH). A milder form of this condition (heterozygous form) was identified by two Americans in the 1960’s, named A.V. Khachadurian and D. Fredrickson. This form is quite common amongst most ethnic groups: about one in 500 people in most ethnic groups. Their plasma LDL level is twice the normal value (even before birth) and without treatment they begin to experience heart attacks by the time they are 35. Among people under 60 who have heart attacks, one in 20 has heterozygous FH.

Homozygous FH individuals (about one in a million) have a circulating LDL level more than six times higher than normal. In these patients heart attacks can occur at the age of two and are inevitable by the age of 20 unless aggressive treatment is undertaken. It is notable that these children and young adults have none of the risk factors for atherosclerosis other than an elevated LDL level. They have normal blood pressure, do not smoke and do not have a high blood glucose level.

 A gene on chromosome 19, called the LDLR gene, controls the production of these receptors. Familial hypercholesterolaemia is due to a mutation of the LDLR gene that changes the way the receptors develop, either in number or structure. The mutation for familial hypercholesterolemia is not always the same. Depending on the particular sit

that has undergone mutation, the LDL receptor may not be synthesized at all, or it may be synthesized but then fail to be transported to the cell surface, or the receptor may fail to bind LDL, or the receptors fail to cluster in coated pits. In the case of FH, blood cholesterol levels are elevated by two mechanisms. First, the lack of LDL cholesterol clearance from the blood stream due to faulty LDL receptor production or function causes a rise on LDL blood levels. Second, the lack of cholesterol entering the cell via LDL receptor-mediated endocytosis results in the cell overproducing its own cholesterol, as feedback inhibition via HMG CoA reductase cannot be turned off by the entrance LDL-cholesterol into the cell. 

The excess production of cholesterol promotes its excretion into the bloodstream (elevated lipoprotein secretion), which serves to further elevate blood cholesterol levels. Clinical evidence is quite clear that very few people with familial hypercholesterolaemia are able to reduce their cholesterol levels by diet and lifestyle changes alone. Most will need special

cholesterol-lowering drugs. (Brown & Goldstein, 1984, pp. 58-66), http://www.betterhealth.vic.

  • If one parent has one mutated gene and one normal gene in the pair, each child of this parent has a 50 per cent chance of inheriting the mutated gene. The risk of developing early coronary artery disease depends on the gender of the child:
  • Around 50 per cent of males who inherit the genetic mutation from this parent will develop coronary artery disease before the age of 50 years.
  • All of the affected male children of this parent will develop heart disease by the age of 70 years.
  • About 85 per cent of affected male children of this parent will have a heart attack before the age of 60 years.
  • Around 12 per cent of females who inherit the genetic mutation from this parent will develop coronary artery disease before the age of 50 years, and 74 per cent by the age of 70 years.

If both parents carry the mutated gene, each child has a 25 per cent chance of inheriting both the genes containing mutations. In this case, the child will develop a severe form of coronary artery disease very early in life, perhaps while still in childhood. This form of familial hypercholesterolaemia is resistant to treatment. Despite medical intervention, the risk of heart attack remains high. Symptoms can include patches of excess cholesterol collecting in the skin, particularly at the elbows, knees and buttocks. 


Familial combined hyperlipidemia (FCHL) affects an estimated one in 10 Americans with premature heart disease, making it a leading contributor to death and disability in our society. This figure also implies that in 90% of individuals with high cholesterol the cause is not primarily due to genetic factors.

(http://www.betterhealth.vic.gov.au/bhcv2/bhcarticles. nsf/pages/Cholesterol_genetic_factors?open) Extending this further, reports indicate that 50- 55% of Americans have cholesterol within an undesirable range (above 200 mg/dL – although I will argue that this figure should be 180 mg/dL and more ideally 150 mg/dL). Based on these findings, 90% of Americans with high cholesterol do not have this problem for genetic reasons, but rather due to faulty dietary and lifestyle practices. (Edmunds & Mayhew, pp. 312- 25), (Castelli, et al., 1986, pp. 2835-8)

One final consideration is that some cases of hypercholesterolemia and/or hypertriglyceridemia are a consequence of an underlying disorder or may be a side effect of certain medications. For instance, elevated triglyceride levels may be secondary to diabetes mellitus, Cushing’s syndrome, uremia, nephritic syndrome, acute hepatitis, systemic lupus, monoclonal gammopathies, acute myocardial infarction, sepsis and excessive burns, or induced by alcohol, thiazide diuretics, beta-blockers, glucocorticoids, estrogen or retinoid drugs. Hypercholesterolemia may be secondary to Cushing’s syndrome, hypothyroidism, anorexia nervosa, nephritic syndrome, primary biliary cirrhosis, or induced by thiazide drugs, progestins, anabolic steroids or retinoid drugs. As such, health practitioners must screen for these underlying causes of hyperlipidemia, based upon the patient’s history and presenting signs, symptoms and laboratory findings, in cases where hyperlipidemia is identified.

In short, health practitioners should be cognizant of the genetic factors that may contribute to hypercholesterolemia (and other lipid disorders), as well as disorders and drugs that can produce secondary hyperlipidemia. Screening for these factors involves taking a proper history, performing a thorough physical examination, listening carefully for clues as the patient reports their symptoms, and identifying any drugs the patient is taking that may be contributing to their hyperlipidemic state. However, even given these factors, the majority of hypercholesterolemia cases are not caused by genetic factors, co-morbidity issues or the side effects of concurrent medications. (Edmunds & Mayhew, pp. 312-25)

Cholesterol Cut Off Points And The Desirable Range

The National Research Council, in its 1989 report “Diet and Health,” recommended an upper limit of total cholesterol of 200 mg/dL, even though a number of the scientists felt that a greater reduction would confer additional health benefits. However, the committee felt that setting the cut-off too low would merely frustrate the public. The council also suggested that if the upper level were set at 200 mg/dL, most Americans would achieve a total cholesterol level of 150 mg/dL or less. (National Research Council (US) Committee on Diet & Health, 1989) That has not occurred. Most Americans and their physicians feel “safe” with a cholesterol total of up to 200 mg/dL. However, the evidence suggests otherwise. In the Framingham study, 35% of ischemic heart disease occurred in patients with total cholesterol levels between 150 and 200 mg/dL. (Castelli, 1996, pp. 61-64) In the CARE study, the average total cholesterol level in patients with a history of heart attack was 209 mg/dL. (Sacks, et al., 1996, pp. 1001-1009)

Dr. Scott Grundy, chairman of the NCEP, proclaimed a number of years ago that 90% of heart attacks could be prevented if the population’s cholesterol was 150 mg/dL or less - a figure identical to that hoped for by the National Research Council in 1989. (Esselstyn, Jr., 2001, pp. 171-177)


Decisions pertaining to appropriate cut off points for blood cholesterol were augmented between the years 2001 and 2004, based on more recent findings from cholesterol lowering studies involving statin drugs. These recommendations primarily address LDL-cholesterol levels rather than total cholesterol levels. A short history of these events is worth highlighting. The Adult Treatment Panel III (ATP III) of the National Cholesterol Education Program issued an evidence-based set of guidelines on cholesterol management in 2001. Since the publication of ATP III, a number of major clinical trials of statin therapy with clinical end points have been published. These trials addressed issues that were not examined in previous clinical trials of cholesterol-lowering therapy. The trials confirm the benefit of cholesterol-lowering therapy in high-risk patients and support the ATP III treatment goal of low-density lipoprotein cholesterol (LDL-C) <100 mg/dL. They also support the inclusion of patients with diabetes in the high-risk category and confirm the benefits of LDL-lowering therapy in these patients. They further confirm that older persons benefit from therapeutic lowering of LDL-C. The major modifications stemming from these more recent studies included the following:

  1. 1
    In high-risk persons, the recommended LDL-C goal is <100 mg/dL, but when risk is very high, an LDL-C goal of <70 mg/dL is a therapeutic option.
  2. 2
    The above therapeutic option extends also to patients at very high risk who have a baseline LDL-C <100 mg/dL.
  3. 3
    When a high-risk patient has high triglycerides or low high-density lipoprotein cholesterol (HDL-C), consideration can be given to combining a fibrate or nicotinic acid with an LDL- lowering drug.
  4. 4
    For moderately high-risk persons (2+ risk factors and 10-year risk 10% to 20%), the recommended LDL-C goal is <130 mg/dL, but an LDL-C goal <100 mg/dL is a therapeutic option on the basis of recent trial evidence. The latter option extends also to moderately high-risk persons with a baseline LDL-C of 100 to 129 mg/dL. \
  5. 5
    When LDL-lowering drug therapy is employed in high-risk or moderately high-risk persons, it is advised that intensity of therapy be sufficient to achieve at least a 30% to 40% reduction in LDL-C levels.
  6. 6
    Any person at high risk or moderately high risk who has lifestyle-related risk factors (eg, obesity, physical inactivity, elevated triglycerides, low HDL-C, or metabolic syndrome) is a candidate for therapeutic lifestyle changes to modify these risk factors regardless of LDL-C level.
  7. 7
    For people in lower-risk categories, recent clinical trials do not modify the goals and cutpoints of therapy. (Grundy, Cleeman, Merz & Brewer, Jr., 2004, p. 763)

How To Achieve A Cholesterol Level Below 150 mg/dL

In light of recent recommendations from ATP III and the overall findings from the Framingham Heart Study, the evidence suggests that achieving a fasting blood cholesterol below 150 mg/dL confers the greatest degree of prevention against heart disease. As doctor Castelli points out, in 40 years of the Framingham study there has not been one single heart attack in anyone with a total cholesterol under 150 mg/dL. Dr. William Castelli is the third person to hold the post of medical director of the Framingham Study. The Framingham Heart study also reveals that approximately 90% of all coronary deaths could be prevented if total cholesterol was kept below 182 mg/dL, systolic blood pressure was under 120 mmHg, and no smoking or diabetes was present. The Framingham Heart Study began in 1948 under the jurisdiction of the National Heart, Lung and Blood Institute, in which every two years the 5,000 volunteer participants are monitored for a host of risk factors for heart disease. The Framingham study strongly identifies that hypertension, smoking and a fasting blood cholesterol above 150 mg/dL are significant risk factors for heart disease. (http://www.pbs. org/saf/1104/features/castelli4.htm)

In regards to achieving a fasting blood cholesterol below 150 mg/dL Castelli contends that all persons, with exception of the 5-10% of hypercholesterolemic patients who have familial hypercholesterolemia (genetic cases) could achieve this desirable blood cholesterol level upon adopting a vegetarian diet. However, most people are able to achieve levels below 180 mg/dL and often below 150 mg/dL with adoption of a low fat diet (no more than 7-15 grams 

of saturated fat and no more than 150-200 mg of cholesterol ingestion per day). Castelli himself was able to reduce his total blood cholesterol from 270 to 190 mg/ dL and raised his HDL-cholesterol from 49 to 63 mg/dL simply through the adoption of a low fat diet (as presented above) and daily exercise. Most physicians would recommend drug therapy for patients with a total fasting cholesterol of 270 mg/dL. (http://www.pbs. org/saf/1104/features/castelli4.htm)
Other researchers have arrived at similar conclusions. Dr. Dean Ornish showed that the combination of daily exercise, with daily stress reduction and diet with less

than 10% calories from fat was sufficient to lower LDL-cholesterol by an average of 37.4% within two months. This group of high-risk patients also experienced a 90% reduction in frequency of angina episodes. (Ornish, et al., 1983, pp. 54-9)
More recently a small, but significant clinical trial by Dr. Caldwell Esselstyn Jr. of the Cleveland Clinic Foundation showed that a plant-based diet in conjunction with cholesterol- reducing medication eliminated progression of coronary artery disease over a 12-year period in patients with triple-vessel disease. Most of the 18 patients had experienced an earlier failed intervention of bypass surgery or angioplasty. All patients who maintained the diet achieved the cholesterol goal of less than 150 mg/ dL and had no recurrent coronary events during the 12 years. At 5 years, angiography was repeated in most cases. By analysis of the stenosis percentage none had progression of disease, and 70% had selective regression. 

These data are compelling when one considers that the same group had experienced more than 49 coronary events during the 8 years before this study. (Rosamond, et al., 1998, pp. 861-867)

The evidence strongly suggests that attaining a fasting blood cholesterol below 150 mg/dL is the desirable goal for both the primary and secondary prevention of coronary heart disease. The problem is that health officials have not provided the public with accurate information about what blood level of cholesterol to achieve and what dietary program to employed to achieve the optimal protection against the number one cause of death in America. The basic diet favored by National Cholesterol Education Program, and other government agencies, contains not only grains, legumes, vegetables, and fruit, but also oil, low-fat milk and milk products, butter, cheese, poultry, lean meat, and fish. It allows for up to 30% of calories to be provide by fat. Unfortunately, there is no evidence to support the notion that by eating such a diet one can achieve a cholesterol level of 150 mg/dL or avoid coronary artery disease. (Esselstyn, Jr., 2001, pp. 171-177)


The evidence strongly suggests that attaining a fasting blood cholesterol below 150 mg/dL is the desirable goal for both the primary and secondary prevention of coronary heart disease. The problem is that health officials have not provided the public with accurate information about what blood level of cholesterol to achieve and what dietary program to employed to achieve the optimal protection against the number one cause of death in America. The basic diet favored by National Cholesterol Education Program, and other government agencies, contains not only grains, legumes, vegetables, and fruit, but also oil, low-fat milk and milk products, butter, cheese, poultry, lean meat, and fish. It allows for up to 30% of calories to be provide by fat. Unfortunately, there is no evidence to support the notion that by eating such a diet one can achieve a cholesterol level of 150 mg/dL or avoid coronary artery disease. (Esselstyn, Jr., 2001, pp. 171-177)


The Food Guide Pyramid, the familiar geometric symbol used to promote the recommendations by the U.S. Department of Agriculture and the Department of Health and Human Services, is laden with dairy products, animal products, and oils, which are the essential building blocks for coronary artery disease. In addition, from a design standpoint, the choice of a pyramid is potentially confusing and misleading. Some viewers may be led to believe that the foods at the

the compensation sources of the US Dietary Guidelines Committee. Six of the eleven committee members, including the chairman, were found to have relationships with the meat, dairy, or egg industry. Ties to industry and politics result in conflict within our private and governmental health institutions, compromising the accuracy of their public message. (Esselstyn, Jr., 2001, pp. 171-177)
In short the American people have not been provided with inaccurate information about how to lower their cholesterol into the optimal range with respect to the prevention of heart disease. As Dr. Esselstyn suggests, even though many people might find a plant-based diet initially difficult to follow,

top (meats, sweets, and fatty foods) are the most helpful, when in fact they are the most harmful. To avoid such sources of confusion, it is suggested that the geometric figures be eliminated and promote three simple food categories: safe, condiments, and unsafe. (Esselstyn, Jr., 2001, pp. 171-177)


There is emerging evidence that government agencies that issue dietary recommendations to the public have been influenced by lobbying groups and have not based their recommendations upon the best available scientific information.


Anygrouppromotingdietaryguidelinesfor the public should base its decisions upon science and not politics or economics. However, the USDA has been subjected to intensive industry lobbying, which compromises its capacity to be fair and objective.

As recently as October, 2000, the Physicians Committee for Responsible Medicine successfully litigated the USDA to ascertain

every patient with the diagnosis of coronary artery disease should at the least be offered the option of this potentially curative arrest and reversal approach.


At the same time, experts such as Dr. Castelli point out that a vegetarian diet is not required in most cases, as many people are able to achieve a cholesterol level below 150 mg/dL by following a low fat diet that may include, in addition to plant-based foods, reasonable amounts of low fat dairy products, chicken breast, turkey breast, Cornish hen, and small amounts of soft margarine, olive oil, and low fat treats such as angel food cake. (Castelli & Griffin, 1988b, pp. 44- 56)


TheMediterraneandietandmonounsaturated oils have become unjustifiably popular because of the Lyon Diet Heart Study. No studies of monounsaturated oils have shown them to arrest and reverse coronary disease. The Lyon study did show a slower rate of progression, but this is hardly an acceptable goal. In a study of patients with coronary

disease, Blankenhorn actually showed the reverse, that disease progressed as rapidly in patients on a monounsaturated diet as it did in those on a saturated fat diet. (de Lorgeril M, Salen, Martin JL, Deloye & Mamelle, 1999, pp. 779-785), (Blankenhorn, Johnson, Mack, El Zein HA & Vailas, 1990, pp. 1646-1652)
In response to the confusion about diet, cholesterol and heart disease, the expert faculty at the First National Conference on the Elimination and Prevention of Coronary Artery Disease issued a new set of recommendations:

  1. 1
    Present nutritional guidelines of government and national health organizations do not provide a maximal opportunity either to arrest or to prevent coronary artery disease.
  2. 2
    The optimal diet consists of grains, legumes, vegetables, and fruit, with <10%-15% of its calories coming from fat.
    This diet minimizes the likelihood of stroke, obesity, hypertension, type II diabetes, and cancers of the breast, prostate, colon, rectum, uterus, and ovary. There are no known adverse effects of such a diet when mineral and vitamin contents are adequate.
  3. 3
    Children and adolescents require major attention to develop early habits of optimal nutrition. Schools should assume a significant leadership role in achieving this goal.
  4. 4
    Speculation about the degree of public compliance with a low-fat diet must not alter the accuracy of the recommendations. (Esselstyn, Jr., 1998, pp. 2T-4T)

More recently, the Portfolio Diet proposed by Dr. David Jenkins and fellow researchers has taken center stage as a means to lower cholesterol in hypercholesterolemic individuals using therapeutic lifestyle changes (TLC). This diet is essentially a low fat diet with special focus on foods that contain known agents to lower cholesterol (viscous fiber, soy protein, almonds and plant sterols). This diet has demonstrated a remarkable ability to significantly reduce total cholesterol and LDL cholesterol to a degree comparable to the use of first-generation statin drug, within patients recruited for the same study. (Jenkins, et al., 2006, pp. 582-91)

The Ultimate Guide to the Natural Management of High Cholesterol and Cardiovascular Risk Factors

- by Dr. James Meschino, DC, MS, ROHP

The Ultimate Guide to the Natural Management of High Cholesterol and Cardiovascular Risk Factors

Dr. James Meschino, 


A Proposed Model For The Pharmacological And Lifestyle Management of Patients With Hypercholesterolemia

 (Total Fasting Cholesterol above 150 mg/dL)

The evidence presented above suggests that anyone experiencing a fasting blood cholesterol level above 150 mg/dL is at risk for premature development of coronary heart disease. The question then becomes what are the safest and most effective interventions to bring about a drop in total cholesterol to below 150 mg/dL in Americans who have levels above this threshold. As with all therapies the risk- to-benefit ratio must be addressed when making clinical decisions affecting the lives of individuals. As such, the following proposal examines the efficacy and safety of various approaches to managing hypercholesterolemia and makes evidence-based recommendations regarding the use of combined nutrition, supplementation and pharmacological interventions, based on a staging process that is determined by severity of the problem as well as patient compliance and response to treatment.

 1. Dietary Intervention

A. National Cholesterol Education Program Step I And Step II Diets

The National Cholesterol Education Program recommends its Step I and Step II Diet as a means to reduce cholesterol. However, clinical studies indicate that the cholesterol-lowering effect of these diets is unlikely to help hypercholesterolemic patients achieve a blood level below 150 mg/dL in the majority of cases. Only modest reductions of total and LDL-cholesterol have been noted using these interventions. For example the commonly cited beFIT study tested whether teaching the NCEP step II diet (<30% of calories from total fat and <7% from saturated fat) is an effective therapy in hypercholesterolemic women and men with or without elevated triglycerides after 6 months. Hypercholesterolemic subjects had two LDL cholesterol measurements above the age- and sex-specific 75th percentile, and combined hyperlipidemic subjects additionally had similarly elevated triglyceride.

Six months after diet instruction, 178 women and 231 men reported total and saturated fat intakes of approximately 25% and
7.5% kcal. LDL cholesterol was reduced in women (7.6% and 8.1%) and men (8.8% and 8.1%)
with hypercholesterolemia and combined hyperlipidemia, respectively, but was not different by sex or lipid disorder. Candidates for drug therapy were reduced from between 27% and 37% to 20%. HDL cholesterol was significantly decreased in women (-6.4% and -4.7%) but not in men (-1.3% and -2.7%).


Studies such as this lead many physicians to believe that dietary change can at best produce only an 8% reduction in blood cholesterol compared to cholesterol reductions between 20-40
% (approximately) available from the use of statin drugs. In the words of David Jenkins et al ‘‘the apparent ineffectiveness of conventional dietary strategies to reduce serum cholesterol by comparison with statins has reduced enthusiasm for diet as a therapeutic option’’. (Jenkins, et al., 2006, pp. 582-91) Further, based on recent evidence, physicians are being encouraged to prescribe statin drugs in patients with mildly elevated blood cholesterol levels (200- 221 mg/dL) even in younger individuals where no other risk factors for heart disease are present. (Downs, et al., 1998, pp. 1615-22) As a result, many physician pay little attention to educating their patients
about diet (as they feel it does not have a significant impact on cholesterol reduction) and opt to recommend statin drugs as first line of therapy for hypercholesterolemia, even in mild to moderate cases, and in patients with no other risk factors coronary disease. Recommendations arising from the The Heart Protection Study (by the Medical Research Council (MRC) and the British Heart Foundation in the United Kingdom) are a good example of this trend. (Mihaylova, et al., 2005, pp. 1779-85)


In recent years a number of dietary nutrients and specific nutritional programs have demonstrated impressive results in regards to the use of dietary intervention as first line therapy for hypercholesterolemia.

B. The Addition Of Soluble Dietary Fiber

Dating back to 1988, Dr. James Anderson and Nancy Gustafson (MS.RN) published data showing the an impressive number of clinical trials demonstrate that daily consumption of approximately 60-120 gm of oat bran (dry measure) or 100-130 gm of dried beans can reduce serum cholesterol by approximately 12-20% in hypercholesterolemic patients. These foods contain soluble dietary fibers, which encourage the excretion of cholesterol and bile acids via the
fecal route and increase production of short chain fatty acid production in the large bowel. These short chain fatty acids may produce further cholesterol lowering effects by inhibiting cholesterol synthesis in the liver. (Anderson & Gustafson, 1988, pp. 749-53)

Supplementation with psyllium husk fiber and ground flaxseed has also been shown to reduce cholesterol levels. Soluble fibers, including those from psyllium husk, have been shown to augment the cholesterol- lowering effects of a low-fat diet in persons with hypercholesterolemia.
As evidence of this, the US Food and Drug Administration recently authorized the use of health claims on food products containing soluble fiber from psyllium that state that they are associated with a decreased risk of coronary heart disease. The meta-analysis conducted by Dr. James W Anderson has helped to more precisely define the hypolipidemic effects and safety of psyllium

when used as an adjunct to a low-fat diet in men and women with hypercholesterolemia. The 8 studies in the meta-analysis included a total of 384 and 272 subjects receiving psyllium or cellulose placebo, respectively. All studies evaluated the hypocholesterolemic effects of
10.2 g psyllium per day, adjunctive to a low-fat diet for eight weeks or longer in individuals with mild-to-moderate hypercholesterolemia. The addition of psyllium to a low fat diet was implemented after a low-fat diet lead-in phase lasting a minimum of eight weeks. Results showed that consumption of 10.2 g psyllium per day lowered serum total cholesterol by 4%, LDL cholesterol by 7%, and the ratio of apolipoprotein (apo) B to apo A-I by 6%, relative to placebo in subjects already consuming a low-fat diet, with no effect on serum HDL or triacylglycerol concentrations. (Anderson, et al., 2000, pp. 472-479)


Studies also reveal that the daily ingestion of 40-50 gm of ground flaxseed can lower total blood cholesterol by up to 10 percent in people with high cholesterol levels. Ground flaxseed has also been shown to lower LDL-cholesterol by approximately 15 percent and concentrations of lipoprotein (a) [Lp(a)] by 7 percent. Lp(a). As with psyllium husk fiber, flaxseeds contain significant levels of cholesterol-lowering soluble fiber. (Arjmandi, et al., 1998, pp. 1203-1214), (Jenkins, et al., 1999, pp. 395-402), (Prasad, et al., 1998, pp. 367-375)


As well, supplementation with a viscous fiber blend containing glucomannan and xanthan, marketed as PGX, has shown that it is able to reduce blood cholesterol by 21.7 mg/dL and LDL by 14 mg/dL when study subjects took one gram of glucomannan before each meal. (Walsh DE, Yaghoubian V, Behforooz A, 1984, pp. 289-93) (Walsh, Yaghoubian & Behforooz, 1984, pp. 289-93), (Vuksan V, Breitman & Sievenpiper, 2004)

C. Aggressive Therapeutic Diets For Hypercholesterolemia

As mentioned above, The Ornish Program (developed by Dr. Dean Ornish M.D.) has been shown to produce a 37.4% reduction in LDL-cholesterol in patients with known cardiovascular disease. A hallmark aspect of this program includes a total fat intake of less than 10% of total calories (compared to 30% permitted by the NCEP). (Ornish, et al., 1983, pp. 54-9)
More recently the portfolio diet, proposed by David Jenkins et al, showed that a diet that includes combinations of cholesterol lowering functional foods (recently recommended by the NCEP and the AHA), could reduce cholesterol levels to the same or similar extent as statin 

drugs in hypercholesterolemic patients. The portfolio diet is a vegetarian diet that emphasizes cholesterol lowering foods including: margarine enriched with plant esters providing 1.0 gm plant sterols per 1000 kcal diet; viscous fibers and psyllium (approximately 10 gm/1000kcal from oats (4.24 gm), barley

(1.36 gm), and psyllium (4.15 gm); 100-200 gm of okra and eggplant providing additional viscous fiber (total .61 gm), eaten every second day; soy protein (21.4 gm/1000 kcal) provided as soy milk and soy meat analogues including soy burgers, soy dogs, and soy deli slices; whole almonds (14 gm/1000 kcal). The other two groups in the study followed either a standard low fat/high fiber diet or the standard low fat/high fiber diet plus 20 mg of lovastatin daily.

The results showed that after four weeks individuals following the standard low fat/high fiber diet showed an average LDL-cholesterol reduction of approximately 8.5%; individuals following the low fat/high fiber diet plus 20 mg of lovastatin showed a 33 % reduction (approximately) in LDL-cholesterol and the group assigned to the portfolio diet showed a reduction in LDL- cholesterol of approximately 30%. The study by Jenkins et al provides clear evidence that aggressive dietary therapy alone can produce a cholesterol lowering effect equal, or similar, to that of statin drugs (approximately 30%). (Jenkins, et al., 2006, pp. 582-91)


As previously mentioned, the plant-based diet proposed by Dr. Esselstyn M.D. has demonstrated significant cholesterol lowering effects on a subpopulation of patients not taking cholesterol lowering medication, and in coronary heart disease patients with base line total cholesterol levels as low as 156 mg/dL and LDL levels at 97 mg/dL. After 32 months of dietary therapy only (no drugs, no stress reduction, no exercise) one of the patients showed a decline in total cholesterol from 156 mg/dL to 89 mg/dL and an LDL reduction from 97 mg/dL to 38 mg/dL. (Esselstyn, Jr., 1998b, pp. 2T-4T)


Based upon the efficacy and safety of diet therapy, patients with fasting blood cholesterol levels above 150 mg/dL and patients with established coronary heart disease (and diabetics) should be educated about the importance of aggressive dietary therapy to their long-term survival. Although many patients may not comply with an exclusively plant-based diet or a diet that allows only 10% calories from fat, the importance of these dietary modifications should be sufficiently stressed to mobilize patients to make the most extensive dietary modifications they are capable of, and to comply to the best of their ability with these recommendations. Further, these patients should be instructed to consume at least ½ cup of beans (high fiber varieties such as red kidney beans and chick peas) each day, as well as supplementing with 10 gm of psyllium husk fiber and 50 gm of ground flaxseed. They may also consider taking 1 gm of PGX (viscous fiber blend) prior to each meal to aid in cholesterol reduction and glucose regulation.


If aggressive dietary therapy does not achieve the desired result (fasting total cholesterol of 150 mg/dL) after a three-week trial, then additional supplementation should follow for the next 12 weeks. The additional supplementation program should include gum guggul and policosanol.

2. Additional Supplementation Program To Lower Cholesterol

Gum guggul and policosanol, two natural health supplement products, have been shown to reduce total and LDL cholesterol in a number of clinical trials involving hypercholesterolemic patients. However, a recent clinical trial published in the American Journal of Clinical Nutrition has shed some doubt about the efficacy of policosanol this regard. (Kassis & Jones,
06, pp. 1003-8)

Gum guggul or gugulipid is derived from the mukul myrrh tree, which is native to India. Upon injury, the tree exudes a yellowish gum resin known as gum guggul, gugulipid or guggulu. The trees are tapped during the winter to acquire these oleoresin compounds that have been used extensively by Ayurevedic (Indian medical system) physicians for centuries to treat a wide variety of disorders. The most scientifically proven application for the use of gugulipid pertains to its ability to lower blood cholesterol, triglycerides, and improve the LDL to HDL- cholesterol ratio in patients with hypercholesterolemia and related lipid disorders


Gugulipid was granted approval in India for marketing as a lipid-lowering drug in June 1986. Studies show that it lowers total cholesterol, LDL –cholesterol, while elevating HDL–cholesterol levels. It appears that guggulsterones increase the uptake of LDL –cholesterol from the blood by the liver. Studies in humans demonstrate that guggulsterone can produce a cholesterol reduction of 14-27%, in 4-12 weeks, and a 22-30% drop in blood triglyceride levels, in patients with hypercholesterolemia and/or hypertriglyceridemia. A striking feature is its lack of toxicity. Unlike other cholesterol lowering drugs, the administration of gugulipid has not revealed any significant side effects, liver damage or toxicity, in human or animal studies to date. At least three well-controlled double-blind trials have shown that the oral administration of 75 – 100 mg of guggulsterone per day can significantly lower cholesterol and triglycerides, and improve the LDL to HDL-cholesterol ratio. (Agarwal, et al., 1986, pp. 626-634), (Nityanand, Srivastava & Asthana, 1989, pp. 321-328), (Singh, et al., 1990, pp. 37-44)

Policosanol is a natural compound derived from sugar cane wax, which has been shown to significantly reduce high cholesterol in human and animal studies. It also has been shown to reduce platelet stickiness, improving blood flow and aiding patients with intermittent claudication and non-insulin dependent diabetes mellitus. Policosanol is a mixture of higher primary aliphatic alcohols isolated from sugar cane wax, whose main component is octacosanol.

A review of the clinical trials using policosanol to lower cholesterol levels in humans appeared in the American Heart Journal in 2002. A review of the available peer- reviewed journal publications revealed that policosanol, at doses of 10 to 20 mg per day lowers total cholesterol by 17% to 21% and low-density lipoprotein (LDL) cholesterol by 21% to 29%, and raises high-density lipoprotein (HDL, the good cholesterol) cholesterol by 8% to 15%. Daily doses of 10 mg of policosanol have been shown to be equally effective in lowering total and LDL cholesterol as the same dose of simvastatin or pravastatin. Doses of policosanol above 10 mg produce anticoagulant effects and thus, should doses above 10 mg per day should be used judiciously in patients prone to bleeding disorders and in those taking other anti- coagulant agents. In these cases monitoring of the INR is warranted.


Long-term studies with policosanol in humans have not shown any significant side effects and is this supplement is associated with a safer profile than statin drugs to date. (Gouni- Berthold & Berthold, 2002, pp. 356-65), (Prat, Mar1999, pp. 286-94), (Canetti, et al., 1995, pp. 159-65), (Mirkin, et al., 2001, pp. 31-41)


There are other cholesterol-lowering supplements available, but their safety profile is cause for concern. Garlic extract supplements, containing 4,000 mcg of allicin (a disulfide compound) has been shown to lower cholesterol to a modest degree (approximately 9%). However, it exerts marked anticoagulant effects and has been associated with documented bleeding disorders when taken alone or in combination with anticoagulant drugs. (Warshafsky, et al., 1993, pp. 599-605), (McNeill, 1993, pp. 97-110), (Rose, Croissant, Parliament & Levin, 1990, pp. 880-2)


Red yeast rice is natural source of lovastatin, which is an HMG CoA reductase inhibitor, exerting statin drug effects on the suppression of hepatic cholesterol synthesis. Studies indicate that supplementation with red yeast rice products (i.e. Cholestin) can reduce LDL cholesterol by 22% in 12 weeks, at a daily dosage of 2.4 gms of product (yielding 10 mg of lovastatin). Due to their physiological effects red yeast rice supplements have the potential to produce the same or similar adverse side effects as regulated statin drugs. Some of these side effects can be very serious and life threatening. Until the safety of these products is better established they should not be included in the conservative or natural management of hypercholesterolemia. (Havel, 1999, pp. 175-6), (Heber & Yip, 1999,
pp. 231-6)


As noted above, if the patient does achieve a fasting blood cholesterol below 150 mg/dL within the first three months of aggressive (or the best effort they can put forth in this regard) dietary measures, then the addition of gum guggul (yielding 75 mg of guggulsterone content daily) and 10 mg of policosanol should be added to the treatment protocol for the ensuing three month period (dietary measures remain in place).

At the end of the second three-month period, if blood cholesterol objectives are not achieved, then the addition of a bile acid sequestrant drug should be considered as an addition to the treatment protocol.

3. Bile Acid Sequestrant Drugs

Bile acid sequestrants are the safest drugs available for treatment of hypercholesterolemia. These drugs are copolymers that function as anion-exchange resins in the intestinal lumen. As such, they bind to bile acids in the intestinal lumen promoting their excretion via the fecal route (in much the same way as soluble fiber acts to lower cholesterol). Bile acid sequestrants thus lower cholesterol by increasing excretion of bile acids (a precursor of cholesterol synthesis),by enhancing the conversion of cholesterol to bile acids in the liver (which face elimination via the fecal route) and by increasing LDL receptor expression on liver cells (thereby increasing cholesterol clearance from the bloodstream as hepatic cells sense a deficiency of cholesterol due to the accelerated conversion of cholesterol to bile acids).These drugs provide the best results when taken 30-60 minutes before meals. Bile acid sequestrants (for example
8 gram/day of Cholestyramine) can lower

LDL cholesterol by 10%-15 %. Higher doses (24 gram/day of cholestyramine) can lower LDL cholesterol by approximately 25%. Side effects of bile acids sequestants are not of a serious nature and include constipation, abdominal pain, bloating, vomiting, diarrhea, weight loss, and flatulence.

Bile acid sequestrants can bind to and decrease the absorption of other drugs, such as warfarin (Coumadin), thyroid hormones (Synthroid, Levoxyl), digoxin (Lanoxin), thiazide diuretics (Hydrodiuril, Oretic, Dyazide, Maxzide), and many others. Therefore, these medications should be taken 1 hour before or 4-6 hours after the administration of a bile acid sequestrant. Bile acid sequestrants reduces the absorption of vitamin A, D, E, and K. Long-term use may thus cause a deficiency of vitamin A, D, E, and
K. Note that these drugs are contraindicated in patients with complete biliary obstruction and hypersensitivity to either cholestyramine or colesipol. (Edmunds & Mayhew, pp. 312- 25), (Bays & Dujovne, 1992, pp. 162-193)

The patient should once again be evaluated after three months of combination treatment involving aggressive dietary therapy, gum guggul and policosanol supplementation, and a bile acid sequestrant drug. If they achieve a total cholesterol goal below 150 mg/dL, but show signs of high triglycerides and/or low HDL levels then the addition of niacin or a fibric acid derivative to the treatment protocol deserves consideration, especially in patients with other major risk factors for coronary heart disease (i.e. diabetes, metabolic syndrome, hypertension, smoking, hyperhomocysteinemia).

4. Niacin

Niacin is one of the most effective antihyperlidemic agents at lowering triglycerides and increasing HDL. It has similar LDL lowering ability as bile acid sequestrants, but its safety profile is not as impressive. The main limitation to its use is flushing. Slow release niacin produces less of a flushing effect but is shown to be more hepatotoxic and thus, is not recommended. Niacin is believed to act on hormone- sensitive lipase, leading to inhibition of free fatty acid release from adipose tissue. This, in turn, reduces synthesis of VLDL in the liver, and in turn, a reduction in LDL. It may also increase the activity of lipoprotein lipase, which hastens the clearance of triglycerides from the bloodstream. The mechanism underlying its ability to raise HDL is unclear, however HDL elevations of 15-35% can be expected with niacin doses of 500-1000 mg, three times per day (1,000 mg, three times per day is the dose to titrate up to). Niacin should be taken immediately following meals. To reduce flushing patients should be instructed not to ingest niacin with hot beverages, and if necessary, may use 325 mg of aspirin to reduce flushing, pruritis, warm sensations and tingling.

Contraindications to the use of niacin include hypersensitivity to niacin, active liver disease or gallbladder disease, active peptic ulcer, pregnancy or lactation. Niacin use may cause liver damage and has been associated with jaundice and hepatotoxicity. As such, liver function tests should be performed at baseline and at 6 and 12 weeks after beginning therapy and periodically (twice yearly) thereafter. If used in combination with a statin drug or fibric acid derivative drug (i.e. Genfrozil or Fenofibrate) liver function tests should be monitored more frequently due to greater potential for liver damage. Myopathy may also occur in patients using niacin as well as elevations in creatine kinase. Niacin also worsens glycemic control, thus it use in metabolic syndrome and diabetes (two conditions where high triglycerides and low HDL commonly occur) may be of concern. In these cases glucose monitoring is recommended. Niacin has been shown to aggravate peptic ulcers and hyperuricemia and thus it is not recommended for patients with active ulcers and used with caution in patients with a history of gout. (Edmunds & Mayhew, pp. 312-25), (Bays & Dujovne, 1992, pp. 162-193)

In some cases whereniacinis contraindicated the use of fibric acid derivative drugs may be an acceptable alternative to lower triglycerides and elevate HDL. (Edmunds & Mayhew, pp. 312-25), (Bays & Dujovne, 1992, pp. 162-193)

It is worth pointing out that regular physical activity (and weight loss) also produces significant reductions in triglycerides and an elevation of HDL. As such, endurance exercise in conjunction with the dietary strategies outlined above appears to be a safer intervention for many (but not all) hypertriglyceridemia patients than is the ingestion of high dose niacin. (Mayers, 2003, pp. 2-5), (Sheppard & Balady, 1999, pp. 963-972)

5. Fibric Acid Derivatives



Fibric acid derivatives (i.e. Gemfibrozil, Fenofibrate) are highly effective at lowering triglycerides and elevating HDL. These drugs can be used in patients with gout because they promote the urinary loss of uric acid. These drugs are thought to work by increasing lipoprotein lipase activity (hence, clearing triglycerides from the circulation) and suppressing free fatty acid release from adipose tissue (similar to the effects of niacin).It may also increase apoprotein A-1 synthesis, which may account for its ability to raise HDL levels. Similar to the effects of niacin, these drugs typically reduce triglycerides by 20-50% and raise HDL by 10-15%. Fenofibrate can reduce LDL-cholesterol 20-25% in some cases. These drugs are best taken twice daily 30 minutes before meals.

These drugs are contraindicated in cases of hepatic dysfunction as they may cause hepatotoxicity and in biliary cirrhosis and gallbladder disease, as they may also cause cholelithiasis. They are contraindicated in cases of severe renal dysfunction and in cases of hypersensitivity to gemfibrozil. When gemfibrozil is administered alone or when co-administered with statin drugs there is an increased potential for myositis or rhabdomyolysis. The use of these drugs requires monitoring of liver enzymes, (i.e.AST,ALT), particularly serum transaminases on the same frequency as noted above in regards to the use of niacin. (Edmunds & Mayhew, pp. 312-25), (Bays & Dujovne, 1992, pp. 162-193) Fibric acid derivatives are generally well tolerated. Side effects include indigestion, nausea, abdominal pain and flatulence. Rare side effects include rash, fever, atrial fibrillation with palpitations, weight gain, muscle aches, headaches, drowsiness, anemia and low white blood cell count. A study by the World Health Organization examining the effects of clofibrate (an early fibric acid derivative drug) suggested that clofibrate therapy may increase overall mortality, especially in regards to increased risk of intestinal cancers, while at the same time decreasing cardiovascular mortality. (Bays & Dujovne, 1992, pp. 162-193) No subsequent reports have suggested increased overall mortality or intestinal cancer risk from the commonly prescribed current generation of fibric acid derivatives (gemfibrozil-Lopid, fenofibrate-Tricor). (Edmunds & Mayhew, pp. 312-25) Gemfibrozil can displace other medications from their carrier protein, such as oral hypoglycemics. This results in increased levels of free drug and, in this case, increases the hypoglycaemic effect. This drug may also potentiate the action of warfarin through the same action. As such, glucose and prothrombin monitoring are important when gemfibrozil is co-administered with these drugs. Large clinical studies have shown that gemfibrozil reduces cardiovascular in patients with high triglyceride and low HDL levels. The usual dose of gemfibrozil is 300 or 600 mg, twice per day. Doses should be taken before breakfast and the evening meal. (Bays & Dujovne, 1992, pp. 162-193)

If the use of aggressive dietary therapy (with exercise where applicable), supplementation with gum guggul and policosanol and the use of bile acid sequestrants do not lower fasting blood cholesterol to below 150 mg/dL within the 9-month stage-in trial period reviewed above, then the use of statin drugs is a final measure by which to further lower cholesterol in these patients. Unfortunately, the recent trend has been to use statin drugs as the first line of therapy with virtual abandonment of the other effective and safe interventions presented in this paper. Although the cholesterol lowering effects of statin drugs is quite impressive there are certain known risks and uncertainties attached to their use that are cause for concern at this time. The following discussion highlights the potential dangers associated with over use and abuse of statin drugs, which is underway in our society.

6. Statin Drugs

To understand the mechanism of action that enables statin drugs to lower cholesterol it is important to first review the steps in cholesterol synthesis: Acetyl- CoA – Acetoacetyl CoA,
-HMG-CoA (beta hydroxy- beta Methylglutaryl CoA) – Mevalonate – Mevolanate Pyrophosphate – Isopentenyl Pyrophosphate – Geranyl Pyrophosphate – Famesyl Pyrophosphate – Squalene

– Cholesterol. Note also that Femesyl Pyrophosphate is a precursor for the synthesis of coenzyme Q10 as well as dolichol. Coenzyme Q10 is an essential co-factor in cellular energy production and possesses fat-soluble antioxidant properties. Dolichol is an important molecule in protein synthesis regulation. Thus, inhibiting the synthesis of mevolanate, which is the function of statin drugs, also impairs the synthesis of coenzyme Q10 and dolichol. (Folkers & Yamamura, 1984)


Statin drugs are HMG-CoA reductase inhibitors in that they are reversible, competitive inhibitors of HMG-CoA reductase, the rate-limiting enzyme that converts hydroxymethyl glutaric acid (HMG-CoA) to mevalonate in the chain of reactions that leads to cholesterol synthesis in the liver. As such, these drugs decrease cholesterol synthesis in the liver, even in situations when the liver would otherwise produce cholesterol, as is the case with VLDL synthesis when saturated fat arrives in the liver from the intestinal tract or when released from adipose tissue. In this regard statin drugs suppress normal functioning within the liver, which is likely a good thing in cases of familial hypercholesterolemia (where the normal feedback mechanism of cholesterol synthesis inhibition is abnormal), but may be undesirable in other circumstances. The danger is that saturated fats, normally excreted by liver cells in VLDL, may accumulate in the liver and eventually damage liver cells. Evidence of liver cell damage involves the appearance of abnormally high liver enzymes in the bloodstream.

Adverse Side Effects From Statin Drugs

A known side effect of statin drugs is liver damage with high circulating levels of liver enzymes

(i.e. ALT, AST). Standard textbooks of pharmacology, and other published sources suggest that less than 1% of patients demonstrate liver function tests greater than three times the upper limit of normal during therapy. (Edmunds & Mayhew, pp. 312-25), (Bays & Dujovne, 1992, pp. 162-193)

Drug companies indicate that the side effects associated with statin drugs is low; approximately 1-2% for serious muscle damage and liver dysfunction (usually represented as an increase in liver enzyme laboratory tests). Nevertheless, many physicians who prescribe these drugs indicate otherwise. A survey by a prominent American cardiologist suggests that muscle aches and weakness occur in approximately 30% of patients who take statins. The survey further suggest that patients who take a statin drug, often develop annoying, sometimes incapacitating muscle aches and weakness that abruptly stop when they discontinue use of the drug, and return when drug use is resumed. In light of this evidence some physicians associated with the Life Extension Foundation and the American Academy of Anti-Aging Medicine suggest that it may be better to regard statin therapy as a solution only after other natural alternatives have been exhausted. Their advice to the public suggests that if a doctor prescribes a statin drug the patient should delay initiation of the drug treatment until they have had the opportunity, for two to three months, to try aggressive dietary therapy (i.e. portfolio diet plan) and natural cholesterol- and LDL-lowering supplements. For patients already taking statin drugs they suggest not to stop using the drug abruptly, but rather to wean the patient off the drug. Doing so abruptly carries a small but real risk of activating previously silent coronary plaque. Instead, they advise adding natural supplements while the patient is taking the statin agent. (with the exception of red yeast rice) (Davis, 2004)

In addition to risk of liver damage and muscle pain, rare cases of life threatening rhabdomyolysis with acute renal failure secondary to myoglobinuria have occurred with statin use. Rhabdomyolysis is a condition in which large numbers of skeletal muscle cells die, causing massive amounts of muscle proteins, myoglobin, to enter the bloodstream. The muscle proteins become trapped in the kidneys where they interfere with the kidneys’ normal filtering process, leading to potentially fatal kidney damage and renal failure. Symptoms of Rhabdomyolysis include:

Muscle pain
(in specific muscles or throughout the body)




Nausea or

Dark Urine

As such, patients taking these drugs are instructed to report immediately unexplained muscle pain, fever, tenderness or weakness. Therapy should be discontinued if markedly elevated creatinine phosphokinase levels are present. (Edmunds & Mayhew, pp. 312-25)

Initially approved in 1997, Baycol (cerivastatin) was a member of a class of cholesterol lowering drugs known as “statins. Baycol was recalled in August 2001 after reports of over 100 deaths worldwide due to rhabdomyolysis. Problems with Baycol were reported most frequently when it was used at higher doses, when used in elderly patients, and particularly, when used with another lipid-lowering drug called Lopid (gemfibrozil). (Psaty & Burke, 2006, pp. 1753-1755)

The prescription drug Crestor, also known as rosuvastatin, is a statin drug produced by AstraZeneca. Crestor was approved by the U.S. Food and Drug Administration in August 2003, after much delay due to safety concerns. Despite questions about safety AstraZeneca aggressively marketed Crestor, spending over $1 billion to promote Crestor in its first year. The manufacturer has marketed Crestor as a “super statin”, claiming that it lowers harmful cholesterol levels better than other competing statins. During clinical trials, seven patients using Crestor developed the life threatening disease rhabdomyolysis. Clinical trials of Crestor revealed the presence of muscle proteins and microscopic blood in the urine. In addition, damaged muscle cells release large amounts of potassium that may result in abnormal heart rhythms that can lead to heart attack.

Safety concerns prompted AstraZeneca to withdraw the 80 mg. dose of Crestor and many critics still express concern over the 40 mg dose. In May 2004, AstraZeneca, wrote doctors in Britain urging them to start patients on a mere 10-milligram dose of Crestor because of concerns about the muscle-destroying condition, rhabdomyolysis.

U.S. Researchers reported that cholesterol-lowering drug Crestor has more than double the side effects, including deaths, of rival statin drugs. The study found that the rate of adverse events among Crestor users in the study was 2.2 times higher than patients taking Zocor (simvastatin) and 6.8 times higher than patients taking Lipitor (atorvastatin). Serious side effects include muscle damage known as myopathy, including a severe form known as rhabdomyolysis.

Despite the report, the American Heart association which published the study in its journal Circulation, said the drug was still generally safe if prescribed properly and that patients should not panic or stop taking the drug

Public Citizen, a consumer watchdog group, had submitted a petition to the FDA in March 2005 urging the FDA to ban the drug. The petition was rejected.

Evidence such as this calls into question the safety of statin drugs as a whole, and prompts concerns about the safety of long term use of these drugs, for which they are intended. (http://www.drugrecalls.com/crestor.html)

As well, some authorities indicate that statin drugs have not been adequately tested on women and that some evidence suggests that these drugs may increase breast cancer risk in females. Analysis of women participating in the Sentara Health Plan suggested that young women (median age 57.6), who are treated with statins, may be at increased risk for the development of breast cancer. This large study involved 8344 female statin users, who took these drugs for a mean of 9.3 months. (Mortimer, Axelrod & Zimbro, ASCO Annual Meeting 2003) The CARE trial and the AFCAPS/TexCAPS study have also suggested that statin drugs may increase risk of breast cancer. (Downs, et al., 1998b, pp. 1615-22), (Szucs, et al., 1998, pp. 319-29) Other critics cite the adverse effects that statin drugs have on coenzyme Q10 (CoQ10) synthesis, which in turn, may increase risk of congestive heart failure. As noted above, the synthesis of CoQ10 shares the same pathway as that of cholesterol synthesis. As such, HMG-CoA reductase inhibition has been shown to result in decreased CoQ10 production and plasma CoQ10 levels. (Watts GF, et al., 1993, pp. 1055- 7)


CoQ10 is an essential component of the electron transfer system in the mitochondria. More specifically, it functions to shuttle hydrogen electrons from NAD to cytochrome b, facilitating the release of energy required to re-couple ADP with inorganic phosphate in the synthesis of ATP. As such, CoQ10 is an integral part of the bioenergetic system that enables cells to produce adequate amounts of ATP through aerobic pathways. ATP is the primary fuel required to power the body’s metabolic reactions, maintain optimal function of cells and sustain life. A deficit in ATP synthesis can compromise any number of energy-dependent cellular functions and hasten the onset of dysfunction and if severe enough, cell death. A decrease in ATP reduces energy availability at a cellular level and is associated with the development of congestive heart failure, Parkinson’s disease, compromised immune function, muscle pain and dysfunction and other problems. 62, (Langsjoen, et al. 1994, pp. 165-175), (Shults, 2003, pp. 1917-21)


As indicated by Kitamura (1984) and Folkers (1985), the depletion of CoQ10 appears to be well tolerated in younger and healthier patients, particularly in the short term. However, data reveals that that CoQ10 depletion has detrimental cardiac effects in humans with pre-existing cardiac dysfunction and has shown similar effects in animal testing, particularly with older animals. CoQ10 is known to be deficient in congestive heart failure (CHF) with the degree of deficiency in blood and cardiac tissue correlating with severity of the CHF. Normal whole blood levels of CoQ10 are in the range of 1.0 gm/ml (plus of minus 0.2 gm/ml) with deficiency in the range of 0.6 gm/ ml (plus or minus 0.2 gm/ml). (Kitamura, et al., 1984, pp. 243-252), (Folkers, Vadhanavikit & Mortenson, 1985, pp. 901-4) It is also known that CoQ10 levels decline after the age of 40. (Kalen, Appelkvist & Dallner, 1989, pp. 579-84)

Pepe et al, (2001) presented evidence at the American Heart Association Scientific Sessions in Anaheim that patients undergoing by pass surgery may be more susceptible to statin- induced lowering of CoQ10 cardiac tissue levels, as well as elderly patients taking statin drugs. (Pepe, et al., 2001, p. 521) As pointed out by Dr. Peter Langsjoen M.D. F.A.C.C. (and CoQ10 researcher), approximately 4.8 million Americans are diagnosed with congestive heart failure. Half or those patients will die within five years. Each year there are an estimated 400,000 new cases of CHF. He
suggests that statin drugs may be a significant contributing cause of the recent epidemic of this disease in the US.

He further points out that large-scale statin trials excluded patients with NYHA class III and NYHA class IV heart failure such that long term safety of statins in patients with CHF has not been established. He concludes by stating that all prescribing physicians should be notified that statin drugs produce a depletion in CoQ10, which in settings of pre-existing CoQ10 deficiency, such as CHF, and aging, has the ability to markedly worsen mycocardial function. He and other CoQ10 researchers also recommend the co- administration of 100-200 mg CoQ10 when statin drugs are prescribed. This is not yet a common practice among US physicians at this time. They recommend that a black box warning should be present in the labelling for statin sold in the United States, which reads as follows: HMG-CoA reductase inihibitors block the endogenous biosynthesis of an essential co-factor, coenzyme Q10, required for energy production. A deficiency of coenzyme Q10 is associated with impairment of myocardial function, with liver dysfunction and with myopathies (including cardiomyopathy and congestive heart failure). All patients taking HMG-CoA reductase inihibitors should therefore be advised to take 100 to 200 mg per day of supplemented coenzyme Q10. On July 8, 2002, within the letter entitled Statin- Induced Cardiomyopathy, Dr. Langsjoen wrote the following as part of the citizen’s petition letter on statin drugs, which was sent, along with accompanying research, to the Food and Drug Administration,

“Statins kill people - lots of people - and they wound many, many more. All patients taking statins become depleted in Coenzyme Q10 (CoQ10), eventually - those patients who start with a relatively low CoQ10 levels (the elderly and patients with heart failure) begin to manifest signs/symptoms of CoQ10 deficiency relatively rapidly - in 6 to 12 months. Younger, healthier people who’s only “illness” is the non- illness “hypercholesterolemia” can tolerate statins for several years before getting into trouble with fatigue, muscle weakness and soreness (usually with normal muscle enzyme CPK tests) and most ominously - heart failure.

In my practice of 17 years in Tyler, Texas, I have seen a frightening increase in heart failure secondary to statin usage, “statin cardiomyopathy”. Over the past five years, statins have become more potent, are being prescribed in higher doses, and are being used with reckless abandon in the elderly and in patients with “normal” cholesterol levels. We are in the midst of a CHF epidemic in the US with a dramatic increase over the past decade. Are we causing this epidemic through our zealous use of statins? In large part I think the answer is yes. We are now in a position to witness the unfolding of the greatest medical tragedy of all time - never before in history has the medical establishment knowingly (Merck & Co., Inc. has two 1990 patents combining CoQ10 with statins to prevent CoQ10 depletion and attendant side effects) created a life threatening nutrient deficiency in millions of otherwise healthy people, only to then sit back with arrogance and horrific irresponsibility and watch to see what happens - as I see two to three new statin cardiomyopathies per week in my practice, I cannot help but view my once great profession with a mixture of sorrow and contempt.’’ (http://www.redflagsdaily.com/ features/2002_july08P.html)

A large Danish study also indicated that statin users have a higher risk for the development of polyneuropathy, with risk increasing the longer the patient used the drug. (Gaist, Jeppesen U, Garcia Rodriguez LA, Hallas & Sindrup, 2002, pp. 1333-7)

The Ultimate Guide to the Natural Management of High Cholesterol and Cardiovascular Risk Factors

- by Dr. James Meschino, DC, MS, ROHP

The Ultimate Guide to the Natural Management of High Cholesterol and Cardiovascular Risk Factors

Dr. James Meschino, 


Proven Benefits Of Statin Drugs In The Prevention of Cardiovascular Disease

In terms of the benefits related to the use of statin drugs it is well established that statin drugs produce a significant reduction in total cholesterol and LDL cholesterol. Reductions in total cholesterol are in the range of 22-42% and reductions for LDL cholesterol are in the range of 27-55%. Statin drugs also have a modest effect on raising HDL and lowering triglyceride blood levels. Overall, statin drugs have been shown to reduce risk of heart attack by approximately 30% over five years of treatment. 

In the widely publicized Scandinavian Simvastatin Survival Study, 4,444 participants took the simvastatin drug (Zocor®) or a placebo. Heart attacks and death decreased from 28% in the placebo group to 19% in the simvastatin group. The Scandinavian study and similar trials solidly bolster the argument that statins reduce LDL and thereby lower the risk of heart attacks in people who have suffered prior heart attacks, as well as in people at risk for a first heart attack. (Pedersen, etal., 1998, pp. 1453-60), (Collins, Armitage, Parish, Sleigh & Peto, 2003, pp. 2005-16), (Heart Protection Study Collaborative Group, 2002, pp. 2005-16), (LIPID Study Group, 1998, pp. 1349-57), (LIPID Study Group, 2002, pp. 1379-87), (Shepherd, et al., 1995, pp. 1301-7), (Sacks, et al., 1995, pp. 621-3) According to the most recent NCEP guidelines the indications for the use of statins have been broadened such that patients with modest elevations in total (200 – 220 mg/dL) and LDL-cholesterol levels are now being treated in hopes of favourably altering the incidence of stroke and myocardial infarction. According to Dr. Rory Collins, citing findings from the MRC/BHF study, even individuals with fasting blood cholesterol below 200 mg/dL and/or LDL below 120 mg/dL should be considered candidates for statin drug therapy. (http://www.ctsu.ox.ac.uk/~hps/) At present more than 200 million people worldwide meet the inclusion criteria for cholesterol-lowering treatment and at this time 25 million people are taking statin drugs for this problem. As one investment reporter put it, statin drugs ‘‘turn cholesterol into money.’’ Lipitor® alone brought Pfizer $9.2 billion in 2003, more than the company earned over several years in the early 1990s. (Pfizer) Industry estimates put total annual spending on statins at more than $22 billion. (Davis, 2004)

Statin drugs not only reduce the synthesis of cholesterol, but also increase cholesterol clearance from the blood steam. Reduced cholesterol synthesis results in a relative intracellular deficiency of cholesterol, prompting cells to increase their production of LDL receptors and their transport to the cell surface. The up-regulation of LDL receptors is a secondary compensatory response, which serves to further reduce blood cholesterol levels via the catabolic clearance of LDL-cholesterol. (Edmunds & Mayhew, pp. 312-25) Additionally, statin drugs also demonstrate anti-inflammatory effects (decreasing C-reactive protein), a stabilizing effect on arterial plaque, may increase nitric oxide bioavailability, and possess antioxidant properties, all of which may contribute to their anti-heart disease attributes. (Sukhova GK ; Williams JK ; Libby P, 2002, p. 1452), (Davignon, 2004, pp. 39-43)

Statin drugs typically start to work within 2 weeks, with maximal lipoprotein changes occurring 4 to 6 weeks after initiation. Serum lipoprotein concentrations typically return to baseline values within a similar period after drug discontinuation. This implies that statin therapy is a lifelong therapy. (Edmunds & Mayhew, pp. 312-25) Unfortunately, no one has been using these drugs long enough to know if they are safe to take for decades at a time. Given their propensity to cause liver, muscle and nerve damage there may be significant risks associated with lifelong statin therapy. (Langsjoen P. The clinical use of HMG-CoA reductase inhibitors), (http://www.redflagsdaily.com/features/2002_july08P.html)

Daily doses of 10,20,40 and 80 mg of statin drug therapy represents the common available treatment protocols. As a rule, higher doses produce greater declines in blood cholesterol. They are generally metabolized via the CYP 3A4 or CYP 2C9 phase I pathways, and most statin drugs are highly protein bound in the circulation (90-98%). In addition to the side effects mentioned above, in certain cases statin drugs cause photosensitivity and therefore, patients should be instructed to use sunscreens and limit prolonged sun exposure, or wear protective clothing until tolerance has been determined. Statin drugs are contraindicated in cases of active liver disease or unexplained elevation of transaminase. Pregnant and lactating women should also not be placed on these drugs. (Edmunds & Mayhew, pp. 312-25)


Fasting blood cholesterol above 150 mg/dL is associated with increased risk for coronary heart disease and other forms of cardiovascular disease. The evidence suggests that the majority of patients with hypercholesterolemia can be managed using aggressive dietary therapy with, in most cases, regular endurance exercise, as well as the inclusion of foods and supplements containing cholesterol lowering soluble dietary fiber. In regards to risk-to- benefit analysis, this approach represents an effective and safe first line of therapy in these cases. If this approach does not attain the desired result within 3-months the addition of gum guggul and/or policosanol supplementation appears to represent a safe and effective intervention to include for the ensuing 3-month period. If these efforts fail, then the addition of a bile acid sequestrant drug to this regiment represents the next line of therapy in regards to providing patients with the safest next step to employ. In cases where aggressive therapeutic lifestyle change and gum guggul and/or policosanol supplementation do not adequately address hypertriglyceridemia and/or low HDL levels in high-risk patients, then the inclusion of niacin or a fibric acid derivative drug warrants consideration to address these problems.

In the event that all of the previous measures fail to reduce cholesterol to below 150 mg/dL, the use of statin drugs deserves consideration. In cases of established familial hypercholesterolemia and in cases of hypercholesterolemia in patients facing a more imminent risk of myocardial infarction or stroke (i.e. previous heart attack or stroke, uncontrolled diabetes, unstable angina), then the introduction of a statin drug deserves consideration earlier in the treatment cycle.

However, in regards to the daily practice of medicine, in recent years statin drugs have become the first line treatment of choice to address hypercholesterolemia in both the primary and secondary prevention of coronary heart disease and other vascular problems. Although studies have shown significant declines in blood cholesterol with accompanying reductions in myocardial infarction and other cardiovascular events, statin drugs are associated with risk of serious and life-threatening liver, muscle and kidney damage. As well, statin drugs may contribute to the development of congestive heart failure via their adverse effects on coenzyme Q10 synthesis. Some evidence suggests that statin drugs may increase breast cancer risk in women.

Statin drugs are intended as a life long therapy, yet no one has used these drugs for a lifetime. As such, the true long-term safety profile, for which they are intended, is unknown at this time. One statin drug has already been recalled by the FDA due to safety issues and another (Crestor) is currently facing increasing criticism for similar reasons.

Until the long term safety of these drugs can be established to a more acceptable level, it would be wise to use these drugs only after safer, more well established cholesterol lowering lifestyle and drug interventions have been exhausted when managing a patient with hypercholesterolemia. Statin drugs should primarily be reserved for use in patients presenting with familial hypercholesterolemia and in cases where myocardial infarction or stroke are imminent concerns.


The argument regarding the safety of these drugs is not without substantiation. As mentioned, in their short history two statin drugs have already been either recalled or had significant warning attached to their use and dosage. A review drug recalls in the US in recent years demonstrates that many drugs are released into the marketplace before they are shown to have the safety assurance that the public deserves and expects. The following are recent examples of drug recalls following post-marketing surveillance:

  1. 1
    Baycol (cerivastatin) - Initially approved in 1997, this statin drug was voluntarily withdrawn in the summer of 2001 as discussed above.
  2. 2
    Seldane (terfenadine) – Initially introduced in 1985 this drug was with withdrawn in the late 1990s due to risk of fatal rhythm abnormalities. Allegra proved to be a safer treatment.
  3. 3
    Posicor (mibefradil) – This drug was taken off the market in 1998 because of its interactions with at least 25 drugs. It markedly increased the blood levels of those drugs, leading to potentially fatal side effects of the other medications.
  4. 4
    Duract (bromfenac) - This was a nonsteroidal anti-inflammatory drug that was withdrawn in 1998 after liver failure occurred in patients who took the short-term treatment for pain for more than the 10 days recommended in the labelling
  5. 5
    Propulsid (cisapride) was taken off the market in 2000 because of the risk of heart rhythm abnormalities, but it is still available
    under a special kind of investigational use. The drug is available to people with severely debilitating conditions for which the benefits may outweigh the risks and who meet specific clinical eligibility criteria.
  6. 6
    Fen-phen - The dangerous combination of the diet drugs fenfluramine, dexfenfluramine, and phentrimine, popularly known as fen-phen, have been linked to serious heart and lung problems. The drugs were manufactured by American Home Products (AHP), a subsidiary of Wyeth Pharmaceuticals, and widely sold under the brand names Redux (dexfenfluramine) and Podamin ® (fenfluramine). Despite noted safety concerns, the manufacturer, as well as doctors and diet clinics, aggressively marketed the fen-phen combination. As a result, over 6 million people used the diet drug ‘‘cocktail’’. The drugs were pulled off the market in 1997 when a report showed that as many as 30% of tested fen- phen users showed some heart valve damage. The U.S. Food And Drug Administration (FDA) received reports of 123 deaths in which fen- phen was identified and continues to regularly receive reports of heart valve disease linked to fen-phen. In addition to being linked to valvular heart disease, fen-phen has also been linked to primary pulmonary hypertension (PPH). PPH is a very rare, progressive and often, fatal lung condition where abnormally increased blood pressure occurs in the blood vessels in the lungs. Studies indicate that use of fen-phen increases one’s chance of developing PPH by as much as 30%.
  7. 7
    Vioxx - In June 2001, the Journal for the American Medical Association (JAMA) published a study reporting that use of Vioxx may lead to serious kidney problems. A separate article published later that year suggested Vioxx may significantly increase the risk of cardiovascular problems. On September 30, 2004, Merck & Co. announced an immediate recall of Vioxx after a clinical study indicated a significantly elevated risk of heart attacks, strokes, and other serious side effects
  8. 8
    Thalidomide – Although not a recent event, the thalidomide story further demonstrates that drugs are often approved and marketed before an adequate safety profile is established. Thalidomide was studied in the late 1950s as a sleeping pill and as a treatment for morning sickness in pregnancy, but was not marketed in the United States. The drug is well known for causing severe birth defects. It was approved in 1998, but it is only available under a very restricted distribution system to assure that fetuses are not exposed to it. Thalidomide is labeled for use to treat painful and disfiguring skin sores associated with Hansen’s disease (leprosy), but has other potentially important uses under development (http://www.drugrecalls. com/crestor.html), (Psaty & Burke, 2006, pp. 1753-1755), (Merck withheld info, 12/8/05), (New England Journal: Merck Concealed Data, 12/8/05) (Expression of Concern (editorial), 12/8/05), (Meadows, January-February 2002)

Lending support to the notion that drugs are often approved before their true safety is established, FDA reviewers from the Center For Drug Evaluation Research (CDER) recently expressed doubts about the way in which drugs are approved in the United States. According to the 2003 report of the Office of Inspector General of the Department of Health and Human Services, a survey of CDER reviewers revealed that 66% lacked confidence in the FDA’s safety monitoring of marketed prescription drugs, and 18% had felt pressure to approve a drug despite reservations about its quality, efficacy, or safety. In 2006, the Government Accountability Office found that the “FDA lacks clear and effective processes for making decisions about, and providing management oversight of, postmarket safety issues.” (Psaty & Burke, 2006, pp. 1753-1755)

To conclude, the long-term safety of statin drugs is not adequately known at this time for them enjoy the wide spread use that is currently underway in North America. This is important because patients are often encouraged from a young age to use these drugs daily as part a lifetime plan to help manage their hypercholesteolemic state. This paper has provided evidence that the non-statin drug approach to the management of hypercholesterolemia is most appropriate in the majority of cases from a standpoint of benefit-to-risk analysis. Clearly, physician and alternative healthcare practitioners should emphasize the importance of aggressive dietary therapy (including soluble fiber-containing foods and supplements) and a minimum of thirty minutes per day of aerobic exercise of at least moderate intensity, as the primary means to reduce blood cholesterol to below 150 mg/dL and improve other risk factors for cardiovascular disease (increase HDL, reduce triglycerides, improve aerobic fitness with associated central and peripheral adaptations, reduce blood pressure, reduce abdominal obesity and waist measurements, stress reduction, improve glucose and insulin regulation). To date, these interventions have not been addressed to the critical degree that is necessary to help patients avoid cardiovascular disease, which continues to be the leading cause of mortality in North America. From a benefit-to-risk analysis standpoint, therapeutic lifestyle change and the use, when necessary, of gum guggul and/or policosanol supplementation and/ or a bile acid sequestrant drug, represent the safest method of approaching this problem, and provide efficacy for the majority of patients with hypercholesterolemia.



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The Ultimate Guide to the Natural Management of High Cholesterol and Cardiovascular Risk Factors

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