In recent years, medical practitioners have increasingly relied on statin drugs (HMG CoA reductase inhibitors), such as atorvastatin, lovastatin, fluvastatin, pravastatin, and rosuvastin, as a primary method to reduce high cholesterol.
Drug companies indicate that the incidence of significant side effects associated with statin drugs is low: approximately 1 percent to 2 percent for serious muscle damage and liver dysfunction (usually represented as an increase in liver enzyme laboratory tests).7 However, some physicians who prescribe these drugs indicate that side effects are much more common. A survey by a prominent American cardiologist suggests muscle aches and weakness occur in approximately 30 percent of patients who take statins. The survey further suggested 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.4
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 normal filtering process, leading to potential fatal kidney damage and renal failure.
Symptoms of rhabdomyolysis include:
- muscle pain (in specific muscles or throughout the body);
- nausea or vomiting; and
- dark urine.
As such, patients taking these drugs are instructed to report unexplained muscle pain, fever, tenderness or weakness immediately.7
Some researchers and clinicians suggest statin drugs also increase the risk of congestive heart failure, as statin drugs reduce the body's synthesis of coenzyme Q10, which is required for energy production within cardiac muscle.26 Some human studies also show a higher incidence of breast cancer in female statin drug users compared to non-users.17,25 A large Danish study indicated that statin users have a higher risk for the development of polyneuropathy, with the risk increasing the longer the patient uses the drug.9 From the available evidence, it appears that the safety profile of statin drugs has not been fully established and that many questions remain unanswered regarding health problems which may arise from their long-term use. Moreover, some of these side effects are very serious and life-threatening and, by some counts, occur in an alarmingly high percentage of patients. As such, some physicians encourage patients to use more natural interventions (diet, soluble fiber and natural supplements, other than red yeast rice), as their first efforts to lower cholesterol; and to use statin drugs as a last resort and/or use them only in very high-risk patients.4
A review of the available research suggests that in regard to benefit-to-risk analysis, the first intervention to lower cholesterol should be aggressive dietary therapy (and in most cases, endurance exercise) for the majority of cases of hypercholesterolemia; followed, if necessary, by supplementation with gum guggul and/or policosanol (natural cholesterol-lowering health products), then bile acid sequestrant drugs, 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. However, it should be noted that aerobic exercise is a highly useful means to lower triglycerides and raise HDL cholesterol,16,24 which in some cases can eliminate the need for high-dose niacin and fibric-acid-derivative drugs. (Both of these drugs carry risk of liver damage.)
Many patients consulting chiropractors and other alternative practitioners ask our advice about the safety of cholesterol-lowering medications (particularly statin drugs) prescribed by their physicians. This article highlights the dietary approach practitioners should encourage patients to follow in order to lower cholesterol levels. Aggressive dietary therapy and exercise represent the primary measures to lower cholesterol unless hypercholesterolemia is due to genetic factors (only 5 percent to 10 percent of hypercholesterolemic cases result primarily from genetic influences); there has been a previous cardiovascular event; or hypercholesterolemia is secondary to another health problem (Cushing's syndrome, hypothyroidism, anorexia nervosa, nephritic syndrome, primary biliary cirrhosis), or induced by thiazide drugs, progestins, anabolic steroids or retinoid drugs.7,11
Dietary Measures to Lower Cholesterol
In light of recent recommendations from Adult Treatment Panel III (in regard to hypercholesterolemia) and the overall findings from the Framingham Heart Study, the evidence suggests that achieving a fasting blood cholesterol level below 150 mg/dL confers the greatest degree of prevention against heart disease. As Dr. W.P. Castelli points out, in 40 years of the Framingham study, there has not been one single heart attack in anyone with total cholesterol under 150 mg/dL. The Framingham Heart Study also reveals that approximately 90 percent of all coronary deaths could be prevented if total cholesterol were kept below 182 mg/dL, systolic blood pressure were kept under 120 mmHg, and no smoking or diabetes were present. The Framingham Heart Study began in 1948 under the jurisdiction of the National Heart, Lung and Blood Institute. Every two years, the study monitors 5,000 volunteers for a host of risk factors for heart disease.12
In regard to achieving a fasting blood cholesterol below 150 mg/dL, Dr. Castelli contends that all people, with the exception of 5 percent to 10 percent 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). Dr. 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), along with daily exercise. Most physicians would recommend drug therapy for patients with total fasting cholesterol of 270 mg/dL.12
Other researchers have arrived at similar conclusions. Dr. Dean Ornish showed that the combination of daily exercise, daily stress reduction and a strict diet (with less than 10 percent of calorie intake from fat) was sufficient to lower LDL cholesterol by an average of 37.4 percent within two months. This group of high-risk patients also experienced a 90 percent reduction in frequency of angina episodes.18
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 five years, angiography was repeated in most cases. By analysis of the stenosis percentage, none had any progression of the disease and 70 percent had selective regression. This data is compelling when one considers that the same group had experienced more than 49 coronary events during the eight years before this study.21
The evidence strongly suggests that attaining a fasting blood cholesterol level 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 the ideal blood level of cholesterol or the dietary program that will achieve optimal protection against the number-one cause of death in America. The basic diet favored by the National Cholesterol Education Program and other government agencies contains not only grains, legumes, vegetables and fruit, but also oil, dairy products, poultry, lean meat and fish. It allows for up to 30 percent of calories to be provided by fat. Unfortunately, there is no evidence that by eating such a diet, one can achieve a cholesterol level of 150 mg/dL or avoid coronary artery disease.8
There is emerging evidence that government agencies which issue dietary recommendations to the public have been influenced by lobbying groups, and have not based their recommendations upon the best available scientific information. Any group promoting dietary guidelines for the public should base its decisions on science, 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 against the USDA to ascertain the compensation sources of the U.S. Dietary Guidelines Committee. Six of the 11 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.8
In short, the American people have not been provided with accurate 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, every patient with the diagnosis of coronary artery disease should at 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.2
The Mediterranean diet and monounsaturated 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, et al., 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.1,5
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 drugs within patients recruited for the same study.13
What If Diet Therapy Fails?
If dietary therapy (and aerobic exercise) fail to reduce blood cholesterol to below 150 mg/dL, the practitioners should consider the addition of psyllium husk fiber (10 gm per day) and/or ground flaxseed (50 gm per day), as well as two natural cholesterol-lowering supplements, gum guggul and policosanol. (To read two of my previous DC articles on these supplements, search online at www.chiroweb.com/columnist/meschino.) If these natural interventions do not achieve the intended outcome for blood cholesterol after a six-month trial (diet and exercise for three months, followed by another three months of diet and exercise, with the addition of psyllium husk fiber, ground flaxseed, gum guggul and policosanol), then the addition of a bile acid sequestrant drug for the ensuing three months deserves consideration as the safest next step to lower cholesterol. If all of these interventions fail to result in fasting blood cholesterol level below 180 mg/dL (in non-smokers, non-diabetics and non-hypertensive patients), a statin drug may be considered.
Unfortunately, many physicians currently use statin drugs as the first resort, not the last resort, in cases of hypercholesterolemia. This appears to be contrary to benefit-to-risk analysis in the majority of cases. As such, alternative health care practitioners should be aware of the efficacy and risks pertaining to cholesterol-lowering interventions, as a means to provide hypercholesterolemic patients with accurate information regarding the use of appropriate dietary modifications, supplements and medications.
- Blankenhorn DH, Johnson RL, Mack WJ, El Zein HA, Vailas LI. The influence of diet on the appearance of new lesions in human coronary arteries. JAMA, 1990;263(12):1646-1652.
- Castelli WP, Griffin G. How to help patients cut down on saturated fat: A simple strategy. PostGraduate Medicine, 1988a;84(3):44-56.
- Collins R, Armitage J, Parish S, Sleigh P, Peto R. MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 5,963 people with diabetes: a randomised placebo-controlled trial. Lancet, 2003;361(9374):2005-16.
- Davis W. Cholesterol and statin drugs: Separating hype from reality. Life Extension Magazine, November 2004.
- de Lorgeril M, Salen P, Martin JL, M. I., Deloye J, Mamelle N. Mediterranean diet, traditional risk factors, and the rate of cardiovascular complications after myocardial infarction. Circulation, 1999, 99, 779-785.
- Downs JR, et al. Primary prevention of acute coronary events with lovastatin in men and women with average cholesterol levels (Results of AFCAPS/TexCAPS). JAMA, 1998a;279(20):1615-22.
- Edmunds MW, & Mayhew (Eds.). Antihyperlipidemic Agents. Pharmacology for the Primary Care Provider, 2nd edition, pp. 312-25.
- Esselstyn CB. Resolving the Coronary Artery Disease Epidemic Through Plant-Based Nutrition. Preventive Cardiology, 2001; 4:171-177.
- Gaist D, Jeppesen U, A. M., Garcia Rodriguez LA, Hallas J, Sindrup SH. Statins and risk of polyneuropathy: a case-control study. Neurology, 2002;58:1333-7.
- Heart Protection Study Collaborative Group. MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high-risk individuals: a randomised placebo-controlled trial. Lancet, 2002;360 (9326):2005-16.
- Jenkins DJA, et al. Assessment of the longer-term effects of a dietary portfolio of cholesterol-lowering foods in hypercholesterolemia. Am J Clin Nutr, 2006;83:582-91.
- Long-Term Intervention with Pravastatin in Ischaemic Disease (LIPID) Study Group. Prevention of cardiovascular events and death with pravastatin in patients with coronary heart disease and a broad range of initial cholesterol levels. N Engl J Med, 1998;339(19):1349-57.
- Long-term Intervention with Pravastatin in Ischaemic Disease (LIPID) Study Group. Long-term effectiveness and safety of pravastatin in 9,014 patients with coronary heart disease and average cholesterol con centrations: the LIPID trial follow-up. Lancet, 2002; 359 vbb(9315):1379-87.
- Mayers J. Exercise and Cardiovascular Disease. Circulation, 2003;107:2-5.
- Mortimer JE, Axelrod R, Zimbro K. (ASCO Annual Meeting 2003). Effect of statins on breast cancer incidence: Findings from the Sentara Health Plan. Proc Am Soc Clin Oncol, 22.
- Ornish D, et al. Effects of stress management training and dietary changes in treatment of ischemic heart disease. JAMA, 1983;249:54-9.
- Pedersen TR, et al. Lipoprotein changes and reduction in the incidence of major coronary heart disease events in the Scandinavian Simvastatin Survival Study (4S). Circulation, 1998;97(15):1453-60.
- Pepe D, et al. A randomised, double-blind placebo controlled trial of preoperative Q10 therapy: Improved outcomes in coronary artery bypass surgery. Circulation, 2001, 104 (Suppl. 11), 521. (abstract)
- Rosamond WD, et al. Trends in the incidence of myocardial infarction and in mortality due to coronary heart disease, 1987 to 1994. N Eng J Med, 1998, 339 (13), 861-867.
- Sacks FM, Rouleau JL, Moye LA, et al. Baseline characteristics in the Cholesterol and Recurrent Events (CARE) trial of secondary prevention in patients with average serum cholesterol levels. Am J Cardiol, 1995;75(8):621-3.
- Shepherd J, Cobbe SM, Ford I, et al. Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. West of Scotland Coronary Prevention Study Group. N Engl J Med., 1995;333(20):1301-7.
- Sheppard R, Balady G. Exercise as Cardiovascular Therapy. Circulation, 1999;99:963-972.
- Szucs TD, et al. Pharmacoeconomic evaluation of pravastatin in the secondary prevention of coronary heart disease in patients with average cholesterol levels. An analysis for Germany based on the CARE study. Herz, 1998;23(5):319-29.
- Watts GF, C.C., et al. Plasma coenzyme Q10 (ubiquinone) concentrations in patients treated with simvastin. J Clin Pathol, 1993;46(11):1055-7.
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