The Cholesterol Paradigm: Beware of the Side Effects of Anti-Cholesterol Drugs

An Interview with Sheldon Zerden, Part 2

VitaminConn

Written By:
Richard A. Passwater, Ph.D.
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Last month, we chatted with Sheldon Zerden about his new book, The Cholesterol Paradigm: The Greatest Health Scam of the Century. We discussed many of the fallacies of the Cholesterol Diet–Heart Hypothesis including four lines of evidence; any one of which is sufficient to disprove the cholesterol theory.

• One thousand persons in the Framingham Study were examined with a dietary review. There was no relation between dietary habits and high blood cholesterol (cholesterolemia).

• Two thousand persons in the Tecumseh Study were given 24-hour diet recall interviews. Levels of serum (blood) lipids (cholesterol, triglycerides, etc.) were found unrelated to dietary practice.

• The Finnish Trial based on 29,217 person-years with subjects 34 to 64 years of age showed no effect of the treatment diet on total mortality.

• In clinical trials with drugs used to reduce high blood cholesterol (cholesterolemia), no drugs for the management of high blood cholesterol (cholesterolemia) were proven completely safe and efficacious.

This month, we will chat about the hazards of the statin family of anti-cholesterol drugs.

As frequent guest in this column, cardiologist Dr. Stephen Sinatra remarked in his newsletter, “Though you wouldn’t know it was based on today’s obsession with cholesterol levels, cardiology has been slowly veering away from the narrow view of cholesterol as a primary cause of heart disease. Cardiologists are slowly accepting that it’s inflammation of arterial tissue that leads to heart disease and most strokes. The field is realizing that although cholesterol plays a role in the biochemical process that creates damage in arterial walls—which, in turn, leads to plaque, occlusions and clots—it’s a relatively minor one. In other words, they’ve realized that even though they may find cholesterol at the scene of the crime, it’s not necessarily the perpetrator” (“Let’s Clear Up the Cholesterol Confusion Once and For All,” Heart, Health & Nutrition, p. 3, August 2008).

Yes, there is cholesterol in the plaque (deposits). But, it is not there because it has been eaten or because there is a high amount of it in the blood. It is not a simple matter of cholesterol creeping into the artery walls as mud settles to the bottom of a river. If that were the case, we would expect to see deposits form in the feet first and also form in the veins.

The evidence that Sheldon Zerden presented last month, which is conveniently ignored by the drug pushers and real-food substitute marketers, is that dietary cholesterol is not related to heart disease, nor is blood cholesterol level.

Passwater: Millions of people are lowering their blood cholesterol levels with statin drugs. Are the side effects really as rare as the pharmaceutical companies claim in the ads?

Zerden: The answer is no! One statin (Baycol) was taken off the market after two years of rhabdomyolysis (muscle breakdown) deaths. Dr. Duane Graveline is an expert on statin side effects. He suffered four amnesia episodes after taking four different statins for 10 years.

SolgarPasswater: Dr. Graveline has an excellent Web site on statin side effects (www.spacedoc.net). He points out that when a statin lowers blood cholesterol, it is, at the same time, reducing the synthesis of coenzyme Q10, dolichols, selenoproteins, Rho, glutathione and normal phosphorylation by a similar amount. This is the cause of the thousands of side effect reports largely unknown to the medical community. He has written three books on the side effects of statin drugs.

Zerden: Dr. M.F. Muldoon finds that some cognitive deterioration can be found in most statin users (23). Coenzyme Q10 (ubiquinone) levels plummet when statins are initiated. Neuropeptide formation is damaged by statin use, which is responsible for depression, irritability, hostility, aggressiveness, road rage behavior, accidents and suicides.

Passwater: Wow! Several scientists and physicians have emphasized in my columns many times over the years that anyone taking statins should also take coenzyme Q10 supplements. But, are statins really necessary in the first place?

Zerden: The forces of greed have ignored the science that argues against the use of statin drugs. A major study published in The Lancet by Drs. John Abramson and Jonathan Wright offers the following conclusion: “We have pooled the data from eight randomized trials that compared statins with a placebo in primary prevention populations at increased risk (24). Our analysis suggests that lipid-lowering statins should not be prescribed for true primary prevention in women of any age or for men older than 69 years. High-risk men aged 30–69 years should be advised that about 50 patients need to be treated for five years to prevent one event (heart attack). In our experience, many men presented with this evidence do not choose to take a statin.”

Passwater: That fits well with the remarks by Dr. Kilmer McCully of homocysteine fame. He reports on www.spacedoc.net/kilmer_mccully_cholesterol_2, “In an analysis of six major statin trials (EXCEL, 4S, WOSCOPS, CARE, AFCAPS, LIPID), the reduction of cardiovascular mortality ranged from –19% to –41% when expressed as relative risk reduction, but from –0.12% to –3.5% when expressed as absolute risk reduction. This statistical manipulation to make the results more impressive illustrates Mark Twain’s aphorism: There are lies, damn lies, and statistics. Thus, a multi-billion dollar drug industry depends upon using misleading interpretations of statistics showing trivial differences between treated and control groups.”

Dr. McCully also states, “In the even more massive Lipid Research Clinics (LRC) trial, 4,000 participants with very high cholesterol levels were selected from almost half a million men. After lowering cholesterol levels for seven years by the resin cholestyramine, fatal heart attack figures were 1.7% (in the treated group) compared with 2.3% (in the placebo group), a difference of 0.6%, or 12 individuals. The investigators expressed these differences as relative risk reductions of 19% and 30% by throwing out the denominators of their fractions.”

What a trick! Note how a small absolute reduction in events gets translated into a much larger relative reduction through the magic of taking a ratio of a ratio.

The JUPITER (Justification for the Use of Statins in Prevention: An Intervention Trial Evaluating Rosuvastatin [Crestor]) study examined the ability of Crestor to reduce inflammation by studying C-reactive protein (CRP). CRP is an independent predictor of heart attacks. Well, the study suggested it did, but the control group had a disproportionate percentage of metabolic syndrome or people having a family history of heart disease. This is a serious flaw. However, the absolute reduction of cardiac events among the group taking Crestor was low and would occur only after years of taking the statin. If the statin reduces inflammation, that is good, but it doesn’t reflect on the cholesterol question. What is disturbing is that the group taking Crestor either saw their blood sugar levels rise or were newly diagnosed with diabetes.

How can we force the U.S. Food and Drug Administration (FDA) to release the adverse event reports on the statin drugs? Do we have to sue the FDA for this information?

Zerden: Thanks for mentioning the JUPITER Study. I discuss it thoroughly in my book. To address your question, that answer is given to me in an e-mail from Professor Joel M. Kauffman of Philadelphia, PA. He quotes from his book, Malignant Medical Myths: “You have to use the Freedom of Information Act and have your senators or representatives threaten the FDA for not responding.”

Tom Scherer, a civil rights activist, was started on Simvastatin (Zocor in the USA) and he developed myalgia and chronic fatigue. He e-mailed me on July 28, 2004 that he obtained data from the FDA under the Freedom of Information Act, however it required Congressional intercession. The data obtained were on adverse event reports actually reported from November 1997 through May 14, 2004 on Simvastatin. The data showed 11,589 individual adverse event reports, of which over 416 resulted in death! There were more than four adverse events per patient, 49,350 in all.

Passwater: Is there any validity at all to the Cholesterol Diet–Heart Hypothesis?

Zerden: The answer to this question is summed up beautifully by Dr. Uffe Ravnskov in his book, The Cholesterol Myths: “If a scientific hypothesis is sound, it must agree with all observations. A hypothesis is not like a sports event, where the team with the greatest number of points wins the game. Even one observation that does not support a hypothesis is enough to disprove it. The proponents of a scientific idea have the burden of proof on their shoulders. The opponent does not have to present an alternative idea; his task is only to find weakness in the hypothesis. If there is only one proof against it, one proof that cannot be denied and that is based on reliable scientific observations, the hypothesis must be rejected. And the Cholesterol Diet–Heart idea is filled with features that have repeatedly been proven false.”

Passwater: Well, you are preaching to the choir here. The responsibility of the scientists is to first confirm any observation, then set about trying to disprove the hypothesis, rather than attempting to confirm it. The scientist must try to figure out what would prove the hypothesis wrong and then set out to conduct that experiment. Instead, today, many scientists try to keep their funds rolling in by repeating similar studies that they believe will add to the confirmation. They look for ways to find supporting evidence. This is totally unscientific; 1,000 studies of the same event only confirms that event, not the hypothesis. Finding a few more ways that support the hypothesis merely ignores the possibility that the hypothesis is wrong and only prolongs the inevitable and wastes money. But, it builds careers. The hypothesis must be attacked and defended in order to be proven. To do otherwise is to waste time and money, but that is what many so-called scientists do today—make a career out of repeating the same event instead of trying to test the validity of the hypothesis.

First, the Cholesterol Diet–Heart Hypothesis proponents dictated “Don’t eat cholesterol.” Then, they wanted everyone to add a cup of corn oil (polyunsaturated fats) to their daily diet. Next, it was increase the polyunsaturated-to-saturated fat ratio, then cut back on all fats, then take resins to prevent absorption of cholesterol, and finally take statin drugs. All of this without observing meaningful decreases in death rate. As for blood cholesterol levels, it went from total cholesterol to “bad cholesterol” (LDL) ratio, to “good cholesterol” (HDL) to “bad cholesterol” level to LDL-c and apolipoprotein b and apolipoprotein a levels. None of these measures are dependent on cholesterol or fats in the diet. But, they are running out of excuses. As you so elegantly elucidate in your book, the Cholesterol Diet–Heart Hypothesis has failed at every test, therefore it is invalid.

The shame or crime is that so much time, brain-power and money has been wasted on a theory that was scientifically disproven decades ago. Only the vested interest of the fundraisers, natural food replacements (such as trans-fat margarines and egg substitutes) and drug companies kept it alive.

Even Big Pharma appears to have secretly given up on it even as they peddle their drugs. That is why they have switched from cholesterol-lowering studies to inflammation-reduction studies with the statins. Even then, there is no meaningful lowering of the death rate and they seem to be abandoning this line of study as well. I doubt if anyone can con the National Institute of Health into funding more expensive large-scale studies in the $500-million to $1-billion range, and I doubt if Big Pharma will invest its own money in more large studies. They must realize that better results can be obtained through better nutrition, especially with vitamins and minerals. Recently, Pfizer—the manufacturer of the statin, Lipitor—announced it will no longer develop medicine to prevent or treat atherosclerotic heart disease (25).

However, many of our readers will need more information before they can discard what they have been led to believe by so many commercials and fundraisers. Your new book contains many more facts and clear explanations. Is it available yet and if so, how can our readers get a copy?

Zerden: The book will be available through all major stores, and can be ordered from cholesterolparadigm@gmail.com or axnoon@yahoo.com. The first printing was set to go to press last month.

Passwater: Since the Cholesterol Diet-Heart Hypothesis is wrong and both dietary and blood cholesterol and fats are not the cause of heart attacks, and cardiovascular exercises do not prevent heart disease, is there something that we should focus on? How about anti-inflammatory diets or Mediterranean-style diets? What advice do you offer to reduce the risk of heart attacks?

Zerden: The individual has the responsibility to eat an optimal diet with the best nutrition possible. In addition, he should supplement his diet with those minerals and vitamins that are still lacking. The best diet does not have everything we need to be in the best of health. Exercise is also important.

That is the best way to achieve a quality of life and provide the basis for an extended lifespan.

Passwater: Well, Dr. Ann Louise Gittleman states that your new book is “must reading for all of us who have been given distorted and misguided message that cholesterol is unequivocally bad in the food and blood stream. Like fine cream, the TRUTH always rises to the top and I predict that this book will be a runaway best seller.”

Some of the points we tried to bring out are that:

1. Dietary cholesterol is not the cause of heart disease. Moderation and variety of diet are important. It is more important to eat a nourishing balanced diet, rich in fish and fish oils and vitamins, than it is to fear eating cholesterol (cholesterolphobia). Vegetarians should consider algae or microorganism sources of EPA and DHA rather than rely solely on ALA.

2. There are many risk factors for coronary heart disease much more important than blood levels of cholesterol and more emphasis should be placed on these more meaningful risk factors.

Cholesterol in plaque does play a role in CHD, but it is not directly related to dietary cholesterol intake, except in the minor number of people with genetic polymorphisms (hereditary familial hyperlipidemia).

3. Antioxidant nutrients protect arteries and lipoproteins and reduce cholesterol plaque formation. Niacin, fish oil, tocotrienols and other nutrients favorably reduce existing cholesterol plaque.

Niacin has been shown to reduce mortality and nonfatal myocardial infarction (MI) in large clinical trials. For example, in the Coronary Drug Project, patients with a history of MI were randomized to receive niacin (n = 1,119) or placebo (n = 2,789) for 5 years. The risk of MI was significantly reduced in patients receiving niacin at 5 years, but niacin had no significant effect on mortality at this time point. However, in a 10-year follow-up of patients in this study (15 years after the study was initiated), mortality was significantly lower in patients who had been treated with niacin than in those who had received placebo.

In mid-November 2009, a time-released niacin formulation (Niaspan) was shown to be effective in reducing artery plaque, whereas the cholesterol- lowering drugs (Zetia and Vytorin) were not.

4. Statin drugs may have benefits such as anti-inflammation. Statins do lower blood cholesterol, but at a price of damaging many health pathways. Studies of statins have not shown that statins’ ability to lower cholesterol results in a meaningful ability to reduce overall death, except in a minor mathematically significant (but not health significant) manner. Some statins do reduce inflammation and this can lower heart disease risk in some risk populations. The physician should decide who might benefit from this reduction in inflammation and prescribe accordingly. However, any prescription for a statin should be accompanied by the advice to also consume CoQ10 supplements.

5. Statins reduce CoQ10 production and cause serious side effects in addition to the well-known rhabdomyolysis. Other health risks include cognitive decline, myositis, myalgia, pain, drowsiness and possibly cancer.

Thank you for writing the book and for sharing the information with our readers. It may be life-saving information for many if they shift their emphasis from cholesterol to the many scientifically well-supported risk factors. WF

Dr. Richard Passwater is the author of more than 40 books and 500 articles on nutrition. He is the vice president of research and development for Solgar, Inc. Dr. Passwater has been WholeFoods Magazine’s science editor and author of this column since 1984. More information is available on his Web site, www.drpasswater.com

References
1. D.J. McNamara, “Dietary Cholesterol and Atherosclerosis,” Biochim. Biophys. Acta 1529 (1–3), 310–320 (2000).
2. E.R. Pinckney and R.L. Smith, “Statistical Analysis of Lipid Research Clinics Program,” Lancet 1 (8531), 503–504 (1987).
3. K.A. Oster, “The Decline of Common Sense and the Ascent of Computerized Non-sense in Medicine,” J. Appl. Nutr. 10–15 (1975).
4. G.V. Mann, “Diet-Heart: End of an Era,” N. Engl. J. Med. 297 (12), 644–650 (1977).
5. H.E. Garrett, et al., “Serum Cholesterol Values in Patients Treated Surgically for Atherosclerosis,” JAMA 189 (9), 655–659 (1964).
6. K. McCulley, “Cholesterol, Part 2” www.spacedoc.net/kilmer_mccully_cholesterol_2, accessed November 11, 2009.
7. M.S. Brown and J.L. Goldstein, “Lowering Plasma Cholesterol by Raising LDL Receptors,” N. Engl. J. Med. 305 (9), 515–517 (1981).
8. T.B. Newman and S.B. Hulley, “Carcinogenicity of Lipid-Lowering Drugs,” JAMA 275 (1), 55–60 (1996).
9. G. Rose, et al., “Colon Cancer and Blood-Cholesterol,” Lancet 1 (7850), 181–183 (1974).
10. J.J. Sadler, B.C. Strain and M.J. Caballero, Eds., Encyclopedia of Human Nutrition (San Diego, CA, Academic Press, 1999).
11. H.N. Ginsberg, et al., “A Dose-Response Study of the Effects of Dietary Cholesterol on Fasting and Postprandial Lipid and Lipoprotein Metabolism in Healthy Young Men,” Arterioscler. Thromb. 14 (4), 576–586 (1994).
12. F.A. Kummerow, et al., “The Influence of Egg Consumption on the Serum Cholesterol Level in Human Subjects,” Am. J. Clin. Nutr. 30 (5), 664–673 (1977).
13. G.J. Slater, et al., Nutr. Rept. Intl. 14, 249 (1996).
14. H.A. Kahn, “Change in Serum Cholesterol Associated with Changes in the United States Civilian Diet, 1909–1965,”Am. J. Clin. Nutr. 23 (7), 879–882 (1970).
15. G.V. Mann, Ed.. Coronary Heart Disease: The Dietary Sense and Nonsense: An Evaluation by Scientists (London, UK, Janus, 1993).
16. C. Mudd, Cholesterol and Your Health: The Great American Rip-off (Oklahoma City, OK, Amer Lite Co., 1990).
17. M.L. Burr and P.M. Sweetnam, “Vegetarianism, Dietary Fiber, and Mortality,” Am. J. Clin. Nutr. 36 (5), 873–877 (1982).
18. C.V. Felton et al., “Dietary Polyunsaturated Fatty Acids and Composition of Human Aortic Plaques,” Lancet, 344 (8931), 1195–1196 (1994).
19. C.C. Seltzer, (1991). “The Framingham Heart Study Shows No Increases in Coronary Heart Disease Rates from Cholesterol Values of 205 to 264 mg%,” G. Ital. Cardiol. 21 (6), 683.
20. B.D. Forette, et al., “Cholesterol as a Risk Factor for Mortality in Elderly Women,” Lancet 1 (8643), 868–870 (1989).
21. A. Siegel, et al., “Effect of Marathon Running on Inflammatory and Hemostatic Markers,” Amer. J. Card. 88 (8), 15 (2001).
22. F.A. Kummerow, “Viewpoint on the Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation and Treatment of High Blood Cholesterol in Adults,” J. Am. Coll. Nutr. 12 (1), 2–13 (1993).
23. M.F. Muldoon, et al., “Randomized Trial of the Effects of Simvastatin on Cognitive Functioning in Hypercholesterolemic Adults,” Am. J. Med. 117 (11), 823–829 (2004).
24. J. Abramson and J.M. Wright, “Are Lipid-Lowering Guidelines Evidence-Based?” Lancet 369 (9557), 168–169 (2007).
25. “Pfizer to Cut R&D Jobs, Retreat from Heart-Drug Research,” Wall Street Journal, Sept. 30, 2008, http://blogs.wsj.com/health/2008/09/30/pfizer-to-cut-rd-jobs-retreat-from-heart-drug-research/.

Published in WholeFoods Magazine, Jan. 2010