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Challenging The Cholesterol Myth

U.S. physicians and health professionals demand
an independent review of statin therapy.

by Marjorie Mazel Hecht

Copyright © 2005 21st Century Science Associates

The latest guidelines of the National Cholesterol Education Program (NCEP) of the National Institutes of Health, issued in July 2004, would have millions more Americans taking statin drugs to reduce their risk of heart disease from cholesterol. But the evidence on which the new guidelines were based has come into question by the medical community—and for good reason: The studies behind the new guidelines don’t show what the NCEP says they show, and statin drugs don’t lower most peoples risk of heart disease.

On September 23, 2004, 35 prominent physicians, epidemiologists, and other scientists wrote to the heads of the National Institutes of Health, the National Heart, Lung and Blood Institute, and the National Cholesterol Education Program to urge and independent review of the guidelines on which the new recommendations are based: “There is strong evidence to suggest that an objective, independent re-evaluation of the scientific evidence from the five new studies of statin therapy would lead to different conclusions than those presented by the current National Cholesterol Education Program,” the letter states.

Among the signers of the letter are John Abramson, M.D., Clinical Instructor, Primary Care, Harvard Medical School; R. James Barnard, Ph.D., Professor, Department of Physiological Science at UCLA,; Christopher Gardner, Ph.D., Assistant Professor of Medicine, Stanford University; Jerome R. Hoffman, M.D., Professor of Medicine, UCLA School of Medicine; Marion Nestle, Ph.D., Paulette Goddard Professor of Nutrition, Food Studies, and Public Health, New York University; David L. Brown, M.D., Professor of Medicine and Epidemiology, Albert Einstein College of Medicine and Director, Interventional Cardiology, Beth Israel Medical Center; and the Center for Science in the Public Interest.

The letter notes that eight of the nine authors of the July recommendations have financial ties to statin manufacturers, including Pfizer, Merck, Bristol-Meyers Squibb, and AstraZeneca, a fact that was not made known when the recommendations were first published in the journal Circulation. "Such conflicts," the letter states, "certainly could affect authors' judgment and undermine public confidence in the report.”

“But like surrogate endpoints in clinical studies, the conflicts are a diversion from the most important Question: Are these lower LDL [low-density lipoproteins, or "bad" cholesterol] targets justified by the scientific evidence?"

The authors outline four major objections to the NCEP interpretation of the data. First, the letter states, "We believe the evidence does not support extending these guidelines to women who are at moderately high risk of CVD cardiovascular disease (so-called 'primary prevention')." Not one of the six studies used “provides significant evidence to support” the claim that “statins reduce the risk of heart disease in moderately high risk women under the age of 65.”

Second, the letter states, "We believe the evidence does not support extending these guidelines to older persons who are at risk of CVD (primary prevention)." There were nine studies involved, and not one of them "provided significant evidence that statins protect senior citizens without heart disease." The authors of the letter note that those above 65 and treated with a statin "did not experience significantly fewer heart attacks and strokes. But they did develop 25 percent more new cancers than the people in the control group (statistically significant)."

Third, the authors state: "We believe the evidence in the five latest clinical trials for extending these guidelines to primary prevention of coronary heart disease in patients with diabetes is mixed." They note that for 250 diabetic patients treated with a statin, in one study, "one death was prevented each year"—but four times as many lives would be saved if those sedentary diabetic patients would become physically active. "The relative importance of statin therapy and routine exercise was not mentioned in the NCEP recommendations," the authors note.

Fourth, the authors state that one study, designated as ALLHAT, "did not show a benefit from more than tripling the number of people taking statins (as recommended by the 2001 and 2004 NCEP updates). . . . The results show that tripling the number of people taking statins . . . provides no additional benefit—not to those older or younger, male or female, with or without diabetes, with or without heart disease, and among those without heart disease, not to those with LDL-cholesterol higher or lower than 130 mg/dL, The only group that derived any significant benefit from more statins was African-Americans, who had fewer episodes of heart disease, but not fewer deaths. . . ."

In conclusion, the authors state: "The American people are poorly served when government-sanctioned clinical recommendations, uncritically amplified by the media, misdirect attention and resources to expensive medical therapies that may not be scientifically justified, Only an independent review, totally free from conflicts of interest, can restore public confidence by determining if that has happened in this case. We therefore request that you move expeditiously to appoint such a panel and provide it with the resources needed to conduct the review."

The Fat Wars

This latest battle over cholesterol takes place after more than 40 years of propaganda—unsubstantiated by scientific evidence—that a low-fat, low-cholesterol diet will lower your risk of heart disease. One of the principal investigators in the famous Framingham Study of heart disease, George v. Mann, M.D., called this "the great diet-heart scam," and "the greatest scientific deception of our times." Mann devoted much of his career to promoting the truth—as opposed to the officially sponsored fiction, and he named the names of those in the medical profession who preferred their funding from the corn oil companies to telling the truth. These doctors, including Harvard's famed Frederick Stare, shamelessly spread the line that polyunsaturated vegetable fats were good for your heart, while animal fats, like butter and lard, were bad. As Mann characterized those scientists who accepted the diet-heart idea: "Fearing to lose their soft-money funding, the academicians who should speak up and stop this wasteful anti-science are strangely quiet. Their silence has delayed a solution for coronary heart disease by a generation."

Mann organized a conference on the issue in November 1991 in Washington, D.C. In the invitation to the conference he wrote: "Hundreds of millions of tax dollars are wasted by the bureaucracy and the self-interested Heart Association. Segments of the food industry play the game for profits. Research on the true causes and prevention is stifled by denying funding to the 'unbelievers.' This meeting will review the data and expose the rascals."1

In an article in Nutrition Today magazine, Mann wrote: "Those who manipulate data do not appreciate that understanding the nature of things cannot be permanently distorted—the true explanations cannot be permanently ignored. Inexorably, truth is revealed and deception is exposed . . . In due time, truth will come out. This is the relieving grace in this sorry sequence."

Although more than a decade has passed since Mann made these statements, the truth is still waiting to "come out."


An article by George Mann, "The Great Diet-Heart Scam," appeared in the May-June 1989 issue of 21st Century Science & Technology magazine. [A very small group of Americans, less than one-half of one percent, inherit a familial trait that causes very high blood cholesterol levels and can lead to premature death. Individuals with that genetic trait need specialized medical therapy and the comments in these articles do not apply.]

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[Coronary heart disease, atherosclerosis, heart attacks, strokes, high blood pressure, type-2 diabetes, obesity, senile dementia, Alzheimer’s and similar age-related diseases are not new, but they were rare prior to 1900. They are now epidemic. Before 1900 sugar was a luxury item, readily obtainable to only the wealthy few. The average American now consumes 120 pounds of sugar per year. The major sources of dietary fat before 1900 were from butter, lard, coconut oil, and olive oil. Those foods have been greatly reduced. Since then, dietary oils have been subjected to a chemical process called hydrogenation to prevent them from smoking during cooking, to allow them to spread like butter, and to avoid rancidity during storage. Hydrogenation produces trans fats, which contribute to those diseases. Hydrogenation also virtually destroys two of the essential dietary fatty acids required for life and health. People in industrialized nations now consume 40 pounds or more per year of new types of fats, that were never before a part of the human diet. If diet contributes to disease, it is these changes that must be at fault.]

Link to more information related to this subject

Link to more information abut Heart Disease

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The Role of Cholesterol and Diet In Heart Disease

by Alice Ottoboni, Ph.D. and Fred Ottoboni, M.P.H., Ph.D.

Copyright © 2005 21st Century Science Associates

Shortly after World War II, the increasing incidence of coronary heart disease1 prompted the medical community, with government support, to initiate a massive and long-term study of what might possibly be the cause. The study, known as the Framingham Study, enrolled a large number of families whose diets, lifestyles, and environments were surveyed and their medical and laboratory findings routinely recorded. After several years, it was noted that there was a positive association between blood cholesterol levels and incidence of heart attacks.

During this same period, nutrition pioneer Ancel Keys and his wife, Margaret, discovered a regional culinary tradition they named the Mediterranean diet. Convinced that this diet, which was considered low in animal fats, protected against coronary heart disease, they set out to obtain statistics on deaths from coronary heart disease and fat consumption from countries that had such statistics. They found strong associations between the two in six countries. These associations were taken as proof of cause and effect and, with support of the cholesterol-heart disease suggestion from the Framingham Study, gave rise to the lipid hypothesis, also referred to as the cholesterol hypothesis, for coronary heart disease.

The research of Ancel Keys and his colleagues became widely publicized and popular. The nutrition community enthusiastically adopted the lipid hypothesis, and clinical and epidemiological research in the field proliferated. The lipid hypothesis was accepted as fact by the medical community, and, in 1956, representatives of the American Heart Association presented the hypothesis on national television. The public was informed that the cause of coronary heart disease was butter, lard, beef, and eggs. The diet recommended by the American Heart Association replaced these traditional foods with vegetable seed oils, margarine, chicken, bread, and cereals. This was the birth of the heart-healthy diet that soon became formalized in the government-sponsored low-fat, high-carbohydrate dietary policy that was adopted and followed by millions of Americans for over fifty years.

An in-depth examination of the body of literature on which the government-sponsored dietary policy was founded reveals serious flaws in experimental design and data evaluation. The most flawed of the studies that introduced the lipid hypothesis was that of Ancel Keys. Although Keys presented data from six countries that had statistics on heart attack deaths and fat consumption, there were actually over twenty that had such statistics available at the time. Why did Keys exclude the latter data? The fact is that the countries excluded did not show the same association between fat consumption and deaths from heart attacks. In a thoughtful analysis in The Cholesterol Myths; Swedish physician Uffe Ravnskov clearly explained that if Keys had included data from all 22 countries, support for Keys's hypothesis would have been weak. Ravnskov went on to conclude that, based on a thorough review of all relevant scientific literature, the lipid-cholesterol hypothesis is a fallacy.

During the next two decades, many nutrition studies investigated the diet/heart connection. Unfortunately, the epidemiological competence of many investigators left much to be desired. In numerous studies, only fat consumption of participants was recorded, to the exclusion of all other diet components. To their credit, a few scientists reported that people who consumed high levels of saturated fat also consumed high levels of sugar. They implicated sugar as the major dietary cause of coronary heart disease with convincing data correlating coronary heart disease to sugar consumption, but their data were ignored. By this time, the direction of research was firmly controlled by proponents of the lipid hypothesis, which already had been expanded to include dietary cholesterol as a culprit.

Even in face of the general acceptance of the lipid hypothesis, a number of scientists were skeptical, claiming that, despite the numerous studies of population groups in many countries, epidemiological methods had not identified the causes of cardiovascular diseases. An extensive review of the literature prior to 1977, including data from the massive Framingham Study, confirmed that the information available concerning the impact of diet on cardiovascular disease did not produce a clear picture of cause and effect. Thus, long after the public was urged to change its dietary habits, the true causes of cardiovascular diseases were still obscure.

Despite this confusing situation, it is apparent that sometime before 1970, those responsible for food policy in the United States had decided that dietary fat, particularly saturated fat and cholesterol, was the cause of high cholesterol, high blood pressure, and coronary heart disease. As a result, the low-fat, high-carbohydrate, "heart-healthy" diet sponsored by the government was adopted by millions of Americans. Thus those who governed national dietary policy more than 30 years ago directed a whole nation, using a flawed road map, down a dietary path they promised would lead to a healthier life. The map seems to have been drawn using the simplistic but faulty logic that the fat and cholesterol that clogs arteries must have come from the fat and cholesterol in the diet. That this logic is not founded on scientific fact is easily demonstrated by the biochemistry of fat and cholesterol synthesis found even in college textbooks.

Proponents of the lipid hypothesis argue that some patients have success in lowering blood cholesterol on a very low-fat Pritikin-like diet that eliminates animal fats. This is true, but not because the diet is very low in fat, but because it is very low in calories. If a body has no calories in excess of its daily energy requirements, it cannot have calories to divert to cholesterol synthesis. Further, Pritikin-like diets are not useful as a long-term strategy because, being very low in fat, they tend to be deficient in protein and essential fatty acids and because lowering blood cholesterol, per se, does not prevent coronary heart disease.

What Is Cholesterol?

Cholesterol is the principal sterol (steroid alcohol) in higher animals, and is an indispensable constituent of all cells and fluids of the body. It is a large, complex chemical present in the lipid fraction of the diet in combination with the true fats—the fatty acids and their triglycerides. Because the true fats are the most prevalent and familiar lipids in the diet, the term fat has become synonymous with lipid in nutrition vocabulary, with the result that cholesterol is often erroneously classed as a fat.

Cholesterol comprises up to 50 percent of cell membrane lipids, where its function is to regulate membrane flexibility. In addition to other vital biochemical and physiological functions, cholesterol is the starting point for the synthesis of several groups of very important biochemicals, including the male and female sex hormones, vitamin D, and the bile acids.

Cholesterol is transported in the blood in combination with specialized proteins. These combinations form lipid-protein molecules of varying density, hence the familiar LDLs and HDLs (low-density and high-density lipoproteins) that are routinely measured in medical examinations. In general, LDL transports cholesterol to all parts of the body where it is needed. Because one of these needs is to deposit cholesterol over inflamed arterial lesions, LDL has been labeled as “bad." This designation is unfortunate because the deposition is a mechanism to protect against further damage, rather than a cause of damage. Conversely, HDL is labeled “good" because it carries cholesterol away from the body for eventual disposal.

Synthesis of cholesterol occurs in virtually all cells of the body, including the walls of arteries, but the major portion is synthesized by liver cells. Synthesis is controlled by mechanisms that turn the process on and off, depending on the body's needs. Under normal circumstances, the body produces no more cholesterol than its life processes require. Excess cholesterol is excreted from the body by the liver, via the gallbladder, into the small intestine, and eliminated with the feces.

Despite considerable scientific data showing that high blood cholesterol and heart attacks do not have a causal relationship, but rather are co-symptoms of an unhealthful dietary regime, the nutritional and medical communities continue to insist that high blood cholesterol is dangerous and must be reduced. This fixation on cholesterol as a marker for coronary heart disease makes it essential that patients, and potential patients who are concerned for their long-term health, not only understand the significance of blood cholesterol, but also know how diet is responsible for high blood cholesterol levels.

Diet and Cholesterol

Dietary cholesterol, which is present only in foods from animal sources, is poorly absorbed from the intestines. Cholesterol in foods donot cause a significant increase in a person's normal level of blood cholesterol, despite misinformation to the contrary. Very high intakes of dietary cholesterol may increase blood cholesterol levels a few percent, but intakes below 800 milligrams a day have little impact. This is because healthy individuals maintain relatively constant levels of blood cholesterol regardless of the quantity of cholesterol in the diet. The amount of cholesterol the body synthesizes is reduced by whatever quantity of cholesterol is absorbed from the intestinal tract. The more cholesterol in the diet, the less cholesterol the body makes. The human body is a very energy-saving machine in all aspects of its biochemistry, not just in cholesterol synthesis. It does not waste energy in making what is provided by an outside source.

The biosynthesis of cholesterol is governed primarily by the hormone insulin, the secretion of which depends on the blood glucose level, which derives largely from dietary sugar and starch. Starch is broken down to glucose, which is absorbed into the body where it causes release of insulin from the pancreas. Then, in a series of about 10 biochemical reactions called glycolysis, glucose yields acetyl Coenzyme-A (ACA). Sugar is absorbed into the body where it splits in two, to yield glucose and fructose. The glucose half goes to ACA via glycolysis, but fructose bypasses glycolysis and goes directly to ACA.

A major function of ACA is to provide energy for life processes, but it is also a precursor of other important biochemicals, including cholesterol and fats. There are two multi-step pathways for ACA. One goes through HMG Coenzyme-A (HMG) to cholesterol, and the other goes to body fat. Both of these pathways require insulin to proceed. In brief, the amount of glucose in the blood dictates the amount of insulin produced by the pancreas, and this insulin, in turn, directs ACA to go to cholesterol and body fat.

When the blood glucose level drops, as with low-carbohydrate diets, the insulin level falls and the pancreas secretes its complement hormone glucagon. This leads to a shift in metabolic pattern to one that spares glucose for its critical homeostatic role in blood. In this glucagon-governed pattern, the glucose required to maintain blood glucose levels is made from amino acids provided by protein. To further spare glucose from being diverted to provide energy, glucagon causes the release of fat from stored body fat, and converts it to HMG through ACA. Then, instead of HMG going to cholesterol, it is converted to ketone bodies, which are used to provide energy.

The metabolic pathway for a diet balanced in nutrients results in two stages: After a full meal, insulin release dominates, leading to increases in fat and cholesterol. Several hours later, when dietary nutrients are not available and hunger pangs occur, low blood glucose and low blood insulin cause glucagon release, which promotes breakdown of body fat for energy and energy-releasing ketone bodies.

Even though dietary cholesterol does not cause a significant increase in normal cholesterol levels, imbalances of other nutrients in the diet, such as sugar and starch, can force the body to synthesize more cholesterol than it requires; Such dietary imbalances override the cholesterol-synthesizing control mechanisms, and cause the body itself to overproduce cholesterol by release of insulin and via the HMG CoA pathway. This excess production of cholesterol results in an abnormal increase in blood cholesterol.

High levels of blood cholesterol are the result of long-term dietary excesses of sugars and starches. The sugars are provided by soft drinks, candy, and sweet bakery products; and the starches are provided by bread, cereals, potatoes, and pastas. The medical significance of high blood cholesterol for coronary heart disease in the absence of arteriosclerosis can be debated, but there is no doubt that high blood cholesterol is a warning signal that the diet is laying the foundation for coronary ,heart disease. A diet that causes high blood cholesterol promotes obesity, insulin resistance, and chronic inflammation, all of which are powerful risk factors for coronary heart disease, in addition to other chronic debilitating diseases.

Why is the public so ill-informed on the subject of cholesterol? Many studies published in scientific journals over the past decades have been critical of the lipid hypothesis. These journals, unfortunately, are not usually read by the general public. The mass media, which is the principal source of medical and health information for most people, does not publish information that is counter to the dictates of the establishment. Thus, there has been little recognition by the average citizen that a cholesterol controversy exists in the scientific community.

The public owes a debt of gratitude to Uffe Ravnskov for his role in bringing serious questions about the need for, and dangers of, cholesterol treatment to public attention. Dr. Ravnskov, a Swedish physician and researcher, became concerned about the scientific inaccuracies and mis-statements put forth by the anti-cholesterol campaign when it was introduced in Sweden in 1989. As a result, Dr. Ravnskov devoted himself to communicating the scientific facts about cholesterol to patients and potential patients through articles, books, and the Internet. Dr. Ravnskov's writings explain, in lay language, the myths concerning the relationship between cholesterol and coronary heart disease.

The Role of Homocysteine

At this point, arteriosclerosis and atherosclerosis require definition. Arteriosclerosis refers to hardening of the arteries. It is observed as toughened areas that often contain calcium deposits called plaques. Atherosclerosis refers to an advanced form of arteriosclerosis that is characterized by deposits of cholesterol, fats, and blood clots within the arterial plaques. This distinction is basic to an understanding of the role of nutrients in the' development and progression of coronary heart disease.

Arteriosclerosis appears to be a necessary precondition for atherosclerosis. When arteriosclerotic lesions occur, the body deposits cholesterol in the lesion to heal and protect it from further damage. Arteriosclerosis has no relationship to blood cholesterol level. Cholesterol deposition occurs in arteriosclerotic lesions regardless of how low the blood cholesterol level is, and it does not deposit in healthy vessels regardless of how high the cholesterol level is. This explains the seeming paradox of why some people with low cholesterol suffer heart attacks and some people with high cholesterol do not. The explanation can be found in the role of homocysteine.

The theory that homocysteine is intimately involved in cardiovascular disease was proposed by Kilmer McCully, a Harvard physician and research scientist, more than 30 years ago. Homocysteine, formed in the body from the amino acid methionine, plays a valuable biochemical role in normal, healthy metabolism; however, like many otherwise valuable biochemicals, homocysteine does damage when its normal metabolism is disrupted. In the case of homocysteine, the metabolic disruption is caused by deficiencies of three B vitamins, B6, B12, and folic acid, which give rise to excessive levels in the blood. High blood homocysteine damages the walls of arteries and causes them to thicken, lose their elasticity, and form plaques and blood clots: This condition is the arteriosclerosis that predisposes to atherosclerotic diseases, including heart attacks and strokes.

There is ample clinical evidence to support the suggestion that homocysteinemia is a far more accurate predictor of coronary heart disease than is a high cholesterol level. However, because these findings are in conflict with the dogma that cholesterol and fats cause coronary heart disease, they are apparently unacceptable to the medical establishment Today, clinical laboratories have the ability to measure homocysteine levels as part of routine blood analyses, yet such analyses are rarely requested in medical practice.

Why is it that medical practice essentially ignores the role of homocysteine in coronary heart disease and stresses the importance of cholesterol? Both biochemicals are amenable to being kept within normal values by diet; homocysteine with supplementation of the appropriate B vitamins and cholesterol with a low sugar and starch diet. Further, high blood homocysteine is a valid risk factor for coronary heart disease, whereas high blood cholesterol is no more than a questionable risk factor, except perhaps when accompanied by arteriosclerosis. Thus, the obvious answer to the question is that there are no drugs that can lower blood homocysteine, but there are drugs that can lower blood cholesterol. These are the drugs known as statins.

Treatment of Heart Disease

The statin drugs are a class of compounds, commonly referred to as cholesterol pills, which include such trade names as CrestorTM, LipitorTM, MevacorTM, and ZocorTM. Although slightly different in structure, all statins lower blood cholesterol by inhibiting the biochemical conversion of HMG to mevalonic acid (MVA), which, in turn, is converted by a series of biochemical reactions to cholesterol.

As with most drugs, the statins have side effects—unanticipated biochemical reactions incidental to the desired one. Side effects mayor may not be harmful. One harmful reaction of the statins is the inhibition of the body's ability to manufacture Coenzyme Q-10 (CoQ-10). MVA is not only a precursor of cholesterol but also a precursor of CoQ-10. Thus, by inhibiting biosynthesis of cholesterol, statins also inhibit biosynthesis of CoQ-10.

CoQ-10 has a complex structure that can accept or donate electrons in biochemical reactions. This ability makes it an essential coenzyme partner for a number of enzymes that store or release energy in biochemical reactions. All cells require CoQ-10 to provide energy for metabolic processes. Heart tissues have a much greater energy demand and, hence, a much greater need for CoQ-10 than most other tissues in the body. Thus, because of this great demand for energy, symptoms of CoQ-10 deficiency are often related to the heart, primarily as congestive heart failure. It is ironic that statin drugs, which are medications prescribed to prevent coronary heart disease, can themselves cause heart disease by creating a deficiency of a biochemical essential for good heart health. Other important symptoms of CoQ-10 deficiency are muscle pains, fatigue, and a general lack of energy.

The New Cholesterol Guidelines

Proof of the fact that the medical establishment is fully committed to the cholesterol hypothesis is the publication of the "New Cholesterol Guidelines" for the nation's doctors by the National Heart, Lung, and Blood Institute (NHLBI) of the National Institutes of Health (NIH) in May of 2001. These guidelines are major clinical practice guidelines for the prevention and management of high cholesterol in adults. The stated goals of the new guidelines are to reduce the prevalence of high blood cholesterol, better identify people at high risk, and reduce the risk of coronary heart disease.

The impetus for the guidelines was the fact that, despite the decades-long pursuit of the heart-healthy diet by many Americans, coronary heart disease had finally become the number one killer in the U.S., striking down about 500,000 people each year—primarily by heart attack. The guidelines lower the laboratory value for blood cholesterol that would trigger statin drug therapy, and modify conventional dietary recommendations to urge more rigorous reduction of dietary cholesterol and saturated fats.

NHLBI estimated in 2001 that, under the new guidelines, the number of Americans on low-saturated-fat, low-cholesterol dietary treatment would increase from about 52 million to about 65 million, and the number who are prescribed cholesterol-lowering drugs would increase from about 13 million to about 36 million. The guidelines advise physicians that, because Americans at high risk for a heart attack are too often not identified and, as a result, do not receive sufficiently aggressive treatment, cholesterol-lowering drugs should be employed when diet and exercise do not sufficiently lower blood cholesterol.

These new guidelines were presented to the public as if written and promulgated by NIH, a branch of the U.S. Government. But the facts are that the new guidelines were approved and issued by the National Cholesterol Education Program (NCEP), a nongovernmental organization operating under the aegis of, and with the support of, the NHLBI. A subgroup of the NCEP, called the Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults, actually wrote the new guidelines. It is noteworthy that the Expert Panel was composed primarily of experts from the drug industry.

Despite the fact that the process by which the guidelines were written may seem proper to most people, it was not. This process bypassed government codes aimed at ensuring that standards, guidance documents, and rules approved and promulgated by government agencies have been considered in open meetings and are free of bias. The approach used by NCEP suggests a strategy in which special interests used the stature and credibility of a government agency to promote faulty science that supports the sale of low-fat, low-cholesterol foods and certain prescription drugs. It is ethically wrong and seemingly illegal for a private group, ostensibly sponsored by the federal government, to be given the responsibility for formulating and approving guidelines that will become standards of good practice for all of the physicians in our country.

Within days of the publication of the 2001 guidelines, public interest groups raised questions about the influence of drug manufacturers. It was estimated that the guidelines could put about 18 percent of the entire U.S. population on statin drugs, which would have the effect of tripling sales of these products to nearly $30 billion per year. Aside from a potential windfall for drug companies, a grave concern is for the impact the guidelines will have on both the practice of medicine and the long-term health of Americans. Will physicians see the guidelines as the product of the latest government research? Will they prescribe more statin drugs and tell their patients to try harder to follow a low-saturated-fat, low-cholesterol diet? Will lawyers and judges use these guidelines as standards of good practice in legal controversies?

Some answers are now forthcoming. Since the promulgation of the guidelines, skyrocketing sales of statin drug constitute very good evidence that the nation's medical professionals are responding to them. This increase in statin drug sales indicates that doctors are promoting the heart-healthy diet, increasing blood cholesterol testing, and prescribing statins. Thus, the folly of a half-century is continued and reinforced. But faulty science inevitably has its price. Heart disease will continue unabated and better approaches to controlling coronary heart disease will very likely continue to be marginalized.

The "New Cholesterol Guidelines" ignore the adverse effects of excess dietary carbohydrates on heart health, despite the fact that, in reaching their conclusions, the authors acknowledged the fact that the 40-year use of the heart-healthy diet was accompanied by concurrent increases in the coronary heart disease that this particular diet was supposed to prevent. Then, in the face of these irrefutable facts, they recommended that Americans intensify their use of the heart-healthy diet. Such disregard for both facts and logic is not a rational outcome of scientific deliberation. When you see water running uphill, look for a pump!

What Do You Do Now?

As a beginning, accept the fact that your health is your personal responsibility; Do not assume, as many people do, that caring for your health is your doctor's task alone. Your doctor is concerned about your health, but you are only one of his many patients to whom he must devote his professional thoughts and concerns. He does not have time to be your alter ego, even if he could. Remember, no matter how much you depend on your doctor to provide you with good health, it is only you, not he, who will suffer the heart attack.

Make your doctor a partner in your health by becoming an informed health care consumer, and learn some basics of nutrition and its relationship to coronary heart disease. Reading and study will help you explain why an excess of glucose-releasing foods (sugar and starch) and an imbalance of essential fatty acids are two of the most important nutritional causes of modern nutritional diseases.

It is important for you to be informed, because your doctor is not an expert in nutrition and probably knows little more about it than an informed layman. His knowledge of nutrition most likely came from nutrition academia, which is the arbiter of nutrition knowledge and defender of the lipid-cholesterol hypothesis. Thus, your doctor may not be aware of the biochemistry involved, and so, instead of recommending a low-carbohydrate diet, he will tell you to eliminate animal fats, and perhaps even red meat, as recommended by the "New Cholesterol Guidelines."

Along with your doctor, make your pharmacist a part of your health care team, especially if you are taking any prescription medications. As with nutrition, your doctor is not an expert in drug action. His knowledge of drug action comes from the pharmaceutical salespeople who explain how a drug works and what its side effects are. However, drug companies are not required to warn doctors about depletion of nutrients by a drug, or to include this hazard on drug labels. Thus, deficiency-caused health problems are often misdiagnosed because most doctors are not sufficiently aware of such problems.

On the other hand, pharmacists are knowledgeable not only in mechanisms of drug action, but also in mechanisms of action of natural and synthetic non-drug chemicals, including vitamins, minerals, herbs, miscellaneous supplements, and a wide variety of substances not intended for human consumption. Your pharmacist is an indispensable member of your health care team who, if you are taking statin drugs, can advise you about their depletion of CoQ-10.

Granted, reading and study will take effort, but it will be worth it because it is your health and that of your loved ones you are protecting. Be assured that nutrition is not an esoteric discipline; no one has a monopoly on knowledge of nutritional science, and no one has a monopoly on the ability to understand why the human body is not a simple furnace that will thrive on any fuel. It is a living organism dependent on countless complex biochemical reactions. It requires its own special fuel, a diet composed of a proper balance of specific proteins, fats, and carbohydrates, plus a host of other nutrients.

Finally, if you already have heart disease or any of the other modern nutritional diseases, take comfort in the fact that the human body is a very forgiving creature and will respond favorably to good nutrition, even after decades of abuse. And keep in mind as you study and learn-there are no drugs that can cure a nutritional disease!

Note: 1. Heart disease is a catch-all for a wide and varied group of afflictions of the heart that compromise its ability to perform adequately its job of pumping blood to all parts of the body to deliver nutrients and remove waste products. The heart disease that is the most common cause of cardiovascular disability and death, better known as a heart attack, is referred to as coronary heart disease (CHD), and is the subject of this discussion.

The authors are long-time public health scientists, now retired. This article is adapted from their book, The Modern Nutritional Diseases: Heart Disease, Stroke, Type-2 Diabetes, Obesity, Cancer, and How to Prevent Them, published in 2002 by Vincente Books, Sparks, Nevada, P.O. Box 50704, Sparks, NV 89435. The cover price is $29.95. The publisher sells this book directly by mail order for $19.95 with free shipping in the USA, with payment by check (made out to Vincente Books, Inc).

Recommended Reading

Robert C. Atkins, Dr: Atkins' New Diet Revolution (New York, N.V.: Avon Books, Inc., 1999). This book contains a wealth of information on the causes and dangers of obesity. It describes a dietary program for safely returning to normal weight and health,

Robert C. Atkins, Vita-Nutrient Solution (New York, N.Y.. Fireside, Simon & Schuster,1999). Aptly subtitled "Nature's Answer to Drugs," this book presents detailed information on the use of nutritional supplements in the treatment of many chronic illnesses.

Mary D. and Michael R. Eades, Protein Power (New York: Bantam Books, 1999). This book is based on the Eades's long and successful medical practice specializing in weight loss and control using a 40:30:30 (carbohydrate: protein: fat) diet plan.

Mary G. Enig, Know Your Fats (Silver Spring, Md.: Bethesda Press, 2000). An important source of accurate nutritional information on fats, oils, and cholesterol, this book contains difficult-to-find information for saturated, trans, and unsaturated fat composition of several hundred foods.

Duane Graveline, Lipitor; Thief of Memory: Statin Drugs and the Misguided War on Cholesterol (Havelford, Penna.: Infinity Publishing, 2004). The physician-author describes the devastating cognitive side effects of a statin drug that he suffered.

Kilmer and Martha McCully, The Heart Revolution (New York: HarperCollins Publishers, 1999). This book describes the role of homocysteine In cardiovascular disease and how vitamins B6, B12, and folic acid prevent its damaging effects.

Michael T. Murray, Encyclopedia of Nutritional Supplements (Rocklin, Calif.: Prima Publishing, 1996). This book contains a wealth of information, including deficiency symptoms, recommended dosages, uses, benefits, safety issues, and interactions, for many supplements.

Alice and Fred Ottoboni, The Modern Nutritional Diseases (Heart Disease, Stroke, Type-2 Diabetes, Obesity, Cancer) and How to Prevent Them (Sparks, Nev.: Vincente Books Inc., 2002).

Uffe Ravnskov, The Cholesterol Myths: Exposing the Fallacy that Saturated Fat and Cholesterol Cause Heart Disease (Washington, D.C.: New Trends Publishing, Inc., 2000). The physician-author explains the scientific facts concerning the true relationship between cholesterol and heart disease-essential for anyone taking statin drugs.

Ray Sahelian, All About Coenzyme Q-10 (Garden City Park, N.Y.: Avery Publishing Group, 1998). This is an important and informative small book about this vital coenzyme inhibited by statins.

Barry Sears, The Omega Rx Zone: The Miracle of New High-Dose Fish Oil (New York: Regan Books, HarperCollins Publishers, Inc., 2002). This book explains in easy-to-read language the functions and importance of essential fatty acids.

Barry Sears, The Anti-Aging Zone (New York: Regan Books, HarperCollins Publishers, Inc., 1999). Sears discusses here the mechanisms of aging and how a 40:30:30 (carbohydrate: protein: fat) diet affords anti-aging benefits.

Diana Schwartzbein, The Schwartzbein Principle (Deerfield Beach, Fla.: Health Communication, Inc., 1999). This book presents numerous case histories in which chronic debilitating diseases were controlled or reversed by diet and lifestyle changes.

Artemis Simopoulos and Jo Robinson, The Omega Diet (New York: HarperCollins Publishers, Inc., 1999). This book is valuable for an understanding of the tremendously important role the essential fatty acids play in all phases of life.

Technical References

J.P. Bantle et al.,"Effects of Dietary Fructose on Plasma Lipid in Healthy Subjects," Am. J. Clin. Nutr, Vol. 72, No.5, pp. 1128-34, (2000).

M. Cesari, B.W.H.J. Penninx, A.B. Newman, et al. "Inflammatory Markers and the Onset of Cardiovascular Events: Results of the Health ABC study," Circulation, Vol. 108, pp. 2317-2322 (2003).

M.G. Enig, "More on Coronary Heart Disease: The Dietary Sense and Nonsense," N. Engl. J. Med., Vol. 331, No.9, p. 615 (1994).

P.H. Langsjoen and A.M. Langsjoen, "The Clinical Use of HMG CoA-reductase Inhibitors and the Associated Depletion of Coenzyme a10: A review of Animal and Human Publications," BioFactors Vol. 18, pp. 101-11 (2003).

Langsjoen PH, Langsjoen AM. "Overview of the Use of CoQ-10 in Cardiovascular Disease," BioFactors, Vol. 9, Nos. 24, pp. 273-284 (1999).

A.J. Olszewski and K.S. McCully, "Fish Oil Decreases Serum Homocysteine in Hyperlipemic Men," Coron. Art. Dis., Vol. 4, pp. 53-60 (1993).

A.J. Olszewski, W.B. Szostak, M. Bialkowska, S. Rudnicki, and K.S. McCully, "Reduction of Plasma Lipid and Homocysteine Levels by Pyridoxine, Folate, Cobalamin, Choline, Riboflavin, and Troxerutin in Atherosclerosis," Atherosclerosis, Vol. 75, pp. 1-9 (1989).

M. Rauchhaus, A.L. Clark, W. Doehner, et al. "The Relationship between Cholesterol and Survival in Patients with Chronic Heart Failure," J. Am. CoIl. Cardiol., Vol. 42, No.11, pp. 1933-1940 (2003).

U. Ravnskov, "High Cholesterol May Protect against Infections and Atherosclerosis," a. J. Med., Vol. 96, pp. 927-34 (2003).

Ravnskov U. "Statins As the New Aspirin: Conclusions from the Heart Protection Study Were Premature," Brit. Med. J., Vol. 324, p. 789 (2002).

Ravnskov U. "A Hypothesis Out-of-date: The Diet-heart Idea," J. Clin. Epidemiol., Vol. 55, No.11, pp. 1057-63 (2002). Same issue: "Dissenr by W.S.Weintraub and "Reply" by U. Ravnskov.

U. Ravnskov, C. Allan, D. Atrens, M.G. Enig, et al. "Studies of Dietary Fat and Heart Disease," Science, Vol. 295, pp. 1464-65 (2002).

U. Ravnskov and M.C. Sutter, "Aggressive Lipid-Iowering Therapy and Regression of Coronary Atheromata," JAMA, Vol. 292, p. 38, (2004).

Sutter MC. "Blood Cholesterol Is Not Causally Related to Atherosclerosis, Cardiovasc. Res., Vol. 28, p. 575 (1994).

Sutter MC. "Assigning Causation in Disease: Beyond Koch's Postulates," Persp. in Bioi. and Med., Vol. 39, pp. 581-592 (1996).

E. Vos and S.C. Cunnane, "Alpha-linolenic Acid, Linoleic Acid, Coronary Artery Disease and Overall Mortality," Am: J. Clin. Nutt:, Vol. 77, pp. 521-2 (2003).

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Cholesterol Is Not a Health Marker

Copyright © 2005 21st Century Science Associates

A physician and educator explains that the focus on cholesterol is driven by commercial interests, not health; it's where the money is to be made.

Dr. Abramson is a Clinical Instructor in Primary Care at Harvard Medical School, and the author of Overdosed America: The Broken Promise of American Medicine, published in September 2004 by HarperCollins. He was interviewed by Managing Editor of 21st Century Science and Technology, Marjorie Mazel Hecht, November 2004.

Question: From your research analysis, what do you see as the relationship of cholesterol to heart disease and overall mortality?

Data from the Framingham Heart Study were published in 1993 in the Archives of Internal Medicine. They show that cholesterol is positively correlated with overall mortality through age 40. There is no relationship between cholesterol and overall mortality between ages 50 and 70, and there's a negative relationship between cholesterol and mortality at age 80, So the lower the cholesterol, the higher the mortality at age 80.

Question: So, if we're talking about people over 50. Once people reach 50, there's not a correlation between overall mortality and cholesterol.

There is a correlation between mortality from heart disease and cholesterol until people reach age 70, and then the relationship goes away.

Question:  So, there's a correlation between heart disease mortality and cholesterol up to age 70....

There's no evidence that cholesterol increases the overall risk of mortality, once age 50 is reached. And no evidence that cholesterol increases the risk of heart disease mortality, once age 70 is reached.

Question: But for the people in between, what do you tell them? What does this mean for the people in their 40s, 50s, and 60s, who are told that they need a cholesterol-lowering drug?

There are two separate issues here. One is: What does the evidence show about the benefits of cholesterol lowering.

There is no evidence from randomized controlled studies, that lowering cholesterol with statin drugs is beneficial to women who don't have heart disease or diabetes. Similarly, there's no evidence from randomized controlled studies that lowering cholesterol for people over age 65, without heart disease or diabetes, is beneficial. But the 2001 Cholesterol Guidelines from the National Cholesterol Education Program recommended an increase from 13 million to 36 million Americans taking statins. Most of that increase was for primary prevention. Most of those people don't have heart disease or diabetes.

Question: How do you define heart disease, just to be clear?

Having had a heart attack, or symptoms from blockage of the coronary arteries—angina.

Question: So, if you haven't had a heart attack, and there's no evidence of blockage of your arteries. . . if you are a woman, there is no evidence that you get a benefit from cholesterol-lowering with statin drugs. And for men, what would you say?

For men at elevated risk, there is evidence of benefit, of reduction of the risk of heart attack and cardiovascular mortality.

Question: How do you define an elevated risk?

The original studies included in the WOSCOP1 looked at men with LDL-cholesterol levels2 averaging 192.2 They lived in Western Scotland, which has among the highest rates of heart disease in the world. And then the other study that was included in the 2001 guidelines was the AFCAS/TexCAPS study,3 which looked at lowering cholesterol in a broader population with an average LDL level of 150. And the difference in the results of those two studies is telling. In the WOSCOPS study, there was a 31 percent reduction in cardiovascular events and a 22 percent reduction in overall mortality, which just missed being statistically significant.

But in the AFCAPS study, the relative risk reduction in cardiovascular disease was 37 percent in the people who took the statin. But there was not a statistically significant reduction in cardiovascular mortality, and there were actually slightly more deaths overall in the people who took the statin than in the people who took the placebo. And the most important finding from this study is virtually unknown, which is, that there were equal numbers of serious illnesses in the people who took the statins and the people who took the placebo—serious illness being defined as something that causes hospitalization, death, or a new diagnosis of cancer.

So, in the AFCAPS study, it looks like you're trading cardiovascular diseases for other diseases, and not improving overall health.

The important issue here, is that if you go backwards, and apply the cholesterol guidelines for primary prevention, that were developed on the basis of the WOSCOPS and AFCAPS studies, about 85 percent of the men in the AFCAPS study qualify for statins based on the guidelines that were made using that study. But when you look at the overall benefit, you see that you're not saving any lives, and it looks like you're simply trading cardiovascular disease for other disease.

Question: So what did the statins do? Suppress the immune system?

We don't know. I wouldn't jump to a conclusion. I'd leave it a black box.

Question: But there are so many black boxes in this whole area.

Exactly. That's what I've been doing for the last three years—trying to recalculate, and figure out whether the cholesterol recommendations are based on good evidence or not. And I think as a clinician, somebody who comes in, and who fits the WOSCOP study—say a man comes in with an LDL of 192, I can say to him, "Look, if I treat 100 men like you with a statin drug, in two years, I will prevent one heart attack, and in 5 1/2 years, I will prevent one death. So, do you want to take a statin? And the person can make his decision, yes or no. I'm not saying it's a foregone conclusion. Many people would want to take the statin, and others would choose not to. As long as the person understands the risks and benefits, I would support either decision.

But if I say to a person with 150 LDL, "If I treat 100 people like yourself with a statin, in 2 1/2 years we'll prevent one cardiovascular event, but it will be replaced by another serious illness, and there is no reduction in your overall risk of mortality," I doubt that a lot of people would opt for the statin.

An additional problem is that the National Cholesterol Education Program focused virtually all our attention on lowering cholesterol with drugs. Yet, we find out that exercise and diet are much more important in preventing heart disease and improving overall health. The important point is that when we talk about exercise, diet, not smoking, drinking in moderation, and maintaining a healthy body weight, those are very weak ways to lower cholesterol—they are not very effective at lowering cholesterol at all, but they are very effective ways to reduce our risk of heart disease, and to improve our overall health.

So, many people, even the most educated people and the best educated doctors, have been focused so on cholesterol, that they think lifestyle changes are being recommended because they will lower cholesterol; but it's not lowering cholesterol that's the goal, it's improving health. And then when you go back to the original Framingham data, that we started the interview with, you see that cholesterol isn't the end-all and be-all.

In fact, there was a study published in the Journal of the American Medical Association about a month ago that looked at the results of following 7,300 women for 31 years, in Chicago, previously healthy women. It's like the Framingham Heart Study—women weren't included in the study if they had heart disease or major cardiogram changes. And it looked at the contribution of various risk factors to overall mortality: blood pressure, diabetes, smoking, cholesterol, race, and minor cardiogram changes. The contribution of cholesterol to overall mortality for these women was 0.00.

Question: So we have an area which people are very scared about, but which is a black box, still to me. We know certain things, but how do you explain this to the ordinary person?. . .

Well, I think it's pretty simple, that the information that's coming at doctors and patients about cholesterol, is getting pushed forward primarily by commercial interests for its commercial value. It's not about improving our health.

Question: It's pushing drugs—very high priced drugs.

High priced and potentially dangerous drugs.

Question: So, what would you recommend for someone who has high cholesterol, and who is at risk for, or already has a heart condition?

Let's separate the Question: first, someone who has high cholesterol and is at risk for heart disease. In the new guidelines, that would be that they have two or more risk factors, that their chance of having heart disease in the next 10 years is 10 to 20 percent, and their LDL-cholesterol is 130 and above, before July 2004 [when the new guidelines were adopted] or 100 or above after July 2004.

Let's separate it out for men and women, under and over 65. For women, there's no evidence that lowering their cholesterol with drugs is going to be beneficial. But there is very good evidence that exercising routinely, eating a healthy diet, not smoking, drinking in moderation, and maintaining a healthy body weight, reduces their risk of developing heart disease by 83 percent.

Now that's a headline, to me—an 83 percent reduction in risk of heart disease. Whereas the statin has zero percent reduction in heart disease. So, it's very clear to me what women should do.

For men who are at significant risk of heart disease, taking a statin may help to reduce the risk of heart disease, but it's very important to remember that each of the other lifestyle changes is probably more important than taking a statin, and combined, they are far more important.

For people over 65, who don't have heart disease or diabetes, we don't have significant evidence from randomized controlled studies that taking a statin drug decreases their risk of heart disease or their overall mortality rate. But we do have very good evidence—just recently a study published in JAMA [Journal of the American Medical Association], showing that elderly folks who exercise routinely, eat a Mediterranean-style diet, don't smoke, and drink in moderation, have only 35 percent the mortality rate of people who don't do those things.

So, those lifestyle issues are very important for those elderly folks. But taking a statin drug, we don't have evidence [that it decreases mortality]. We do have evidence, however, that people 70 or older, who take a statin drug, develop significantly more cancer.

Question: Why do you think there is such a difference between men and women under 65?

Well, women have much lower rates of heart disease prior to menopause and in the years immediately following menopause. So there's probably something that's protective about women's hormonal environment, that we don't quite understand, that makes women's heart disease different from men, until they get into older age. And it's not simply the estrogen and progesterone, because the HERS study4 showed us that even though hormone replacement therapy reduces "bad" cholesterol and improves "good" cholesterol, it doesn't reduce the risk of heart disease.

Cholesterol is given far too much weight as a health marker. And the disparity in the HERS study, really points it out: that lowering "bad" cholesterol and increasing "good" cholesterol, doesn't necessarily improve the risk of heart disease. It's more complicated than that.

Cholesterol levels are what we call a surrogate end point. They are not a health marker. They are not a health outcome. But because the money is to be made in getting people to believe that lowering cholesterol is the important health outcome, that's what patients and doctors have become focused on.

A really important study is the Lyon Diet Heart study—a randomized, controlled study—in which people who had heart attacks, were randomly assigned to eat a Mediterranean-style diet or a prudent post-heart-attack diet. The people who ate the Mediterranean diet had about a 70 percent reduction in their risk of heart disease, and about a 45 percent reduction in their death rate. So that's at least twice the benefit that we see patients, post-heart-attack treated with a statin (not that the two approaches can't be done at the same time). The important point here, is that the Mediterranean diet is very effective in preventing further heart disease and death, but it didn't lower people's cholesterol.

Question: The accompanying article by the Ottobonis, discusses how the intake of cholesterol in foods doesn't have a direct relationship to your body's cholesterol.

That's probably true, but type of food intake does have a big impact on your risk of heart disease.

Question: Yes, they also say that.

We've been sort of brainwashed into thinking that cholesterol is the most important health issue, but that's not true. That's where the money's to be made. ...

The facts that we know are that the Mediterranean diet works—and what about it works, I can't tell you. The jury is still out.

Question: Can you comment on the practice of using statistical data to determine medical diagnosis and treatment, instead of the traditional practice of an individual physician looking at an individual patient, and looking at the patient as a whole?

In the ideal, it would be a combination of the two. I think we have tipped way over into the biomedical model of medicine, where the unspoken underlying philosophy is that when we know more, the practice of medicine will be reduced to physics and chemistry.

Question: Or computer relationships. . .

Yes, and that that will be good medicine. What is very clear to me, is that our health is 70 or 80 percent of the way we live our lives, and the environment that we live our lives in. And, as a physician, if I want to help people to make the changes that will be far more effective, overall, than medical interventions, then I need to have a relationship with people, and understand what their own sources of meaning, and their own values are, why they want to be healthy, to help them make changes that are sustained, that will have far more impact on their health than taking medicines.

What's happening, all the things that we've talked about so far, is that probably about 80 percent about what doctors and patients believe to be true about medical care, is coming from commercial sources. So that we mostly believe that it's the medical care that's going to protect our health, and not how we live our lives. Now, what that 80 percent does, is rely very heavily on statistics. And I think you have to look at two parts of the question you are asking. And on the down-side of it, I'm in total agreement with you that the person has to be Sir William Osler, the first professor of medicine at Johns Hopkins, said it's more important to know what kind of person has a disease, than what kind of disease the person has.

Question: I think there is another component that has come in, and that is the cost-cutting one, which is forcing some of these statistical changes and HMOs.

But if you really wanted to cut costs, you'd go the other way.

Question: What I'm saying is that that is what's being done, the computerization of medicine is used to cut costs. . .

But I think it's the relentless dialectic of the marketplace.

Question: But the marketplace doesn't have a brain and doesn't make decisions. .

It just moves toward making more money.

Question: But it's the people who run it.

The length of visits has not gone down during the HMO period. In fact, the length of visits has actually gone up a minute or two. I entered private practice in 1982, and exited in 2002, 20 years later. So I saw these changes go on. Do you think when doctors were running around and collecting fees from each examining room, that they went slower, than when the HMO told them what they had to do?

Question: I think we had better medical care before the HMOs, put it that way.

Well, yes, but you can't blame it on the HMOs. . .I think that the HMOs are just along for the ride. It's the commercial intrusion, and the HMOs are a part of that. But it's the commercialization of medical knowledge that really underlies the whole thing. . . There are HMO excesses, I'm not disagreeing with what you are saying, but I think what's changed here is very important: that there's been a radical transformation in the purpose for which medical knowledge is developed and communicated. And that happened really in the 1990s.

In 1980, academic researchers turned up their noses at drug company money. President Reagan came in. Small government. Economic downturn. NIH money for clinical studies shrank, and academics had to turn to drug company money to do their research. But in 1991, still 80 percent of that commercially sponsored research was being done in universities, so the university researchers still had control of the study design, the data, and publication.

But then there was a radical transformation that proceeded after 1991. So that when you get to 2000, only 34 percent of that commercially sponsored research is being done at universities. The rest has been pulled out to for-profit research companies. The pharmaceutical companies now play the major role in designing studies. Most of the authors of the articles that are drug-company sponsored, don't get to see all the data from their own studies. They are only looking at the data that's getting parceled out to them by the drug companies.

Question: That's a very disgusting situation, in terms of the health of the nation.

It's huge, it's huge. So authors themselves are not seeing the data. They are submitting articles to journals when the drug companies let them. The drug companies are more likely to withhold from publication studies that won't help their sales. Then when you submit the articles to journals, even the best journals that are peer-reviewed, the peer reviewers don't get to see the data that the authors didn't get to see. So peer reviewers can't help us in this situation.

Question: Isn't it only recently that authors are disclosing financial links to the drug industry?

They've been disclosed, but that doesn't help at all. The situation we're in right now is that about 80 percent of our clinical research is coming from the drug companies, and even among the best of that research, the research that's selected to be in the Cochrane reviews, the odds are five times greater that commercially sponsored research will favor the drugs, than non-commercially sponsored research.

Question: So, really, we've lost our independent university- sponsored research capability in all this.

Right! Now it's 34 percent. But it's not just that it's only 34 percent. Drummond Rennie, the deputy editor of JAMA, said in 1999, that the academic institutions are so desperately trying to get that research money back, that it's a "race to the ethical bottom" among academic institutions. So now, they have to compete with the standards that for-profit research companies have, or they won't even get their 34 percent.

So the bottom line is that the purpose for which medical knowledge is produced and disseminated is no longer to improve the health of the American people. It's a corporate investment, and it's designed and carried out and publicized with the idea of improving the corporate bottom line.

Question: I think that's a good summary of the situation, in which to view all the things we've discussed. That's the thesis of your book.

Yes. What I've done is to show how the magician does his tricks: How this happened, and how we believe that this is the right way to run a health care system. My book discusses how our health-care system, which is spending $1.8 trillion ($500 billion of which is for unnecessary care, much of which is harmful to our health), how that can look to doctors and patients like the right way to practice medicine; that's really what the book is about.

Question: Meanwhile, if you look at things like infant mortality, the United States is sinking in this area. And if you look at other kinds of standard markers, where the U.S. once had a very fine health care system, leading in the world, now we are 14th or less among the nations of the world.

Out of 22 industrialized nations, we spend twice as much per capita, and we will live the shortest amount of time in good health.

Question: Something is wrong!

And infant mortality, which I go into in the book: the fact is that the concentration of neonatologists and neonatal beds for newborns, varies by a factor of four in the United States, with no benefit, once you have the minimum level. And when you compare the United States to other countries, we have twice as much neonatal intensive care capacity, but even looking at equivalent birth-weight babies, that doesn't buy us better survival statistics. So, what we're doing is spending twice as much on neo-natal intensive care, but less on the upstream solutions of prenatal care and preconception care, that would decrease the epidemic we have of low-birth-weight babies in relationship to the rest of the industrial world. That's the real problem.

And the New England journal of Medicine editorial that went along with Elliott Fisher's article describing the variation of neonatologists by a factor of four, pointed out that one of the problems is that the neonatologists are supplied by a for-profit company that's traded on the New York Stock Exchange, that hires neonatologists, and they turn a profit of $50,000 per doctor that they hire! So, it's economically driven.

Question: From their standpoint. ...

And from the hospital's standpoint—the hospital makes money on neo-natal beds. And what new mother is going say "no" to the doctor, when they say, "we think your baby would be safer if we transfer him to the intensive care unit." Who's going to turn that down, and what HMO would dare turn that down?

There's a chapter in the book, "Follow the Money," that's about medical care being pushed into use by the financial incentives to the providers, rather than the health needs of the patients. The pressure comes from the business consequences to the suppliers of care.

Question: Let me get back to cholesterol: Why is the NIH, NHLBI so afraid to have an independent review of the cholesterol issues you raised?

Beats me. If I were head of the National Institutes of Health, I would say, "The question's been raised, there were financial conflicts, we believe in our data, therefore it's in everybody's interest to have guidelines that don't have a commercial shadow over them, so let's reevaluate them." That was not their response.

Question: Their response was really just to reiterate what they said to begin with. ...

And to misinterpret what our argument was.

Question: Do you think that most physicians go along with the Guidelines because they have never seen anything else, they've never seen the criticism of the Guidelines?

Yes. And they have to, because they're at risk of getting sued if they don't. In other words: You come to me. Say you're a woman who has two risk factors for heart disease. Say you're over 55 and you have a low HDL. And I do the risk score, and the risk score comes out that there's a 10 to 20 percent risk of your developing heart disease over the next 10 years, and your LDL level is 105. According to the new guidelines, I should offer you the "therapeutic option"—that's their language; the new guidelines say that I should offer you the therapeutic option of a statin drug, right then at baseline, no longer tell you to go out and eat a good diet, etc.—right then, that I should offer you the therapeutic option of a statin. Now among women in that category, maybe there's going to be one heart attack out of—I'm going to make up a number—out of 1 ,000 women over the next few years. And if I have not offered that one out of a thousand women the therapeutic option of a statin, I can get sued. And the Guidelines are admissible in court as evidence.

Here's the important point: We were talking before about the challenge of physicians working in 15-minute time blocks to re-frame health for their patients as mostly determined by how they live their lives and the environment they are in, rather than prescribing medicines, and that is a challenge, that's true. But think how great the challenge if I'm a physician, and you come in, and I'm trying to explain to you that the Guidelines are over-reading the data—as I believe, and others believe—and that I'm going to explain to you the Guidelines, and explain to you the counter-argument, so that you can make an informed decision about whether or not you want to take a statin drug. That's a time burden. That's an obstacle that I think is sinful, and a distraction to good medical care and to doctor-patient relationships. That's why the subtitle of my book is "The Broken Promise of American Medicine."

Question: It's a big problem; I understand that because many of my colleagues and friends are taking statin drugs, and they've been upset by what I have told them about cholesterol, because it challenges what they have been told by medical authorities. I think that the way the Ottobonis wrote their article is a good approach: They urge people to get more informed, and look at the evidence themselves.

I wrote an op-ed piece that was published in the Los Angeles Times, after the Guidelines came out in July, summarizing my criticism. A hospital in the Los Angeles area invited me to speak on the issue. Most of the people in the room were following me, but there was a mini-rebellion, from one or two guys, researchers, who couldn't stand it. And a professor from UCLA got up and said, "Look, I'm a guest here, but I've published hundreds of papers, and I know a lot about research, and what Dr. Abramson is telling you is so vanilla, in the middle of the road, just presenting the numbers that are in the studies that the Guidelines people are using. If I were presenting this information, I would be presenting a very different picture, which would be far more critical of the research upon which these guidelines are based."

So if we can somehow communicate this idea, that what I am telling you is totally middle-of-the-road. It is not biased, it is not overstated, it is just the studies that were used by the National Cholesterol Education Program. We're not even questioning the legitimacy of the studies (most of which were sponsored by drug companies) that were included in the Cholesterol Guidelines. I know a lot about the problems with the way that the Vioxx and Celebrex research data were misrepresented in JAMA and the New England journal of Medicine. I haven't done that with the cholesterol studies. I'm just saying: "I'll take your studies at face value. You've misinterpreted them. You've misrepresented them."

Question: Well, it's a very political issue, and an important issue, especially as people get older.

Absolutely. It goes to the heart of a functioning democracy. Have you seen Philip Kitcher's book, Science, Truth, and Democracy? It's a philosophical book, but his argument is that at bottom, these are political issues. It's not science, but it's the political context in which science occurs. It's just like corporate behavior is politics.

Question: Science is politics…and science should be truth. We aim for printing the truth, not what's popular opinion.

Well, I think there's a philosophical problem with that, and here I'll paraphrase the doctor appointed by President Bush to be the head of his bioethics commission, Leon Kass, who I think makes a very important point, and I don't say this at all facetiously. He says that the kinds of truths that science can discover are different from the kinds of truths that emanate from our values. And that we need to be clear about what our values are, if we are going to be able to use scientific truths in the service of humanity.

Question: What is he talking about? People's religious values?

In the context that we're talking, the moral question is, what do we think ought to be the function of the health care system? Ought it to be, to improve Americans' health most effectively and efficiently, or ought it to be to support a marketplace, whose product is health care?

Question: I certainly go with the former. ...

I do too, but our current Administration seems more interested in the latter.

Question: That's a real problem, with this Administration, but that is a whole other issue.

I think that this question of values, of defining your values and knowing what your target is, is important. I think that one of the biggest health care emergencies in the United States is the lack of universal health insurance. Eighteen thousand Americans die each year because they don't have health insurance. That's like a 9/11 every two months. I've got a paper coming out with a health policy colleague, called "When Health Policy Is the Problem." And what we are saying is that health policy is in the way of solving this problem. If you believe that there should be universal health insurance, stop doing pilot projects, stop doing studies that show this and that, and implement universal health care.

That’s our problem. We're not implementing universal health care. Seventy-nine percent of Americans think we should have universal health care, and they are willing to pay higher taxes to get it. These are the moral issues In the United States, not whether there should be gay marriage or not.

Question: I agree. The economic issues are far more important, and the others were a diversion. ...One final question on cholesterol: How did you get involved with this issue?

I was very fortunate to have the opportunity to do a two-year Robert Wood Johnson Fellowship, after finishing my residency in family medicine. During that time I studied epidemiology, research design, and health care delivery. I thought I was headed for a career in academic medicine—teaching in a family practice department in a university hospital. But watching my mentor work, I realized that family physicians in academic medical centers remain low doctors on the totem pole. Watching the difficulties he encountered on a daily basis, I decided that I could be most helpful by becoming a full-time clinician. So, I went into private practice. Toward the end of my 20 years in practice, I saw the commercial intrusion into the medical care that I was practicing, and that was being practiced on my patients by other doctors, growing exponentially.

I started to use the skills I had learned as a Robert Wood Johnson fellow, to research the research. The first major issue I sank my teeth into was Celebrex and Vioxx, and when I realized—this is in September 2001—how misleading the two articles about Vioxx in the New England Journal of Medicine were, and an article in the American Medical Association Journal about Celebrex, how they had misrepresented the data from the companies' own studies, I realized that we had crossed a line, where our most respected medical journals could no longer be trusted. I felt compelled to figure out how our medical knowledge was being corrupted by commercial influence and to tell the story to patients and doctors.

So, I started to write a book documenting the extent and consequences of the Celebrex® and Vioxx® data. The next thing I got into was the 2001 Cholesterol Guidelines, and the deceptions in that. For example, they say that there's evidence that statins help women for primary prevention (without heart disease or diabetes), and they quote six studies. But none of the six studies provides significant evidence.

They say that there's evidence—they quote nine studies— that statins help people over 65 for primary prevention, but none of the nine studies provides evidence to support their comment. About 200 pages after the claim about women, they say, evidence for women is "generally lacking"—that's in the eighth section—and that their recommendations for women are based on the extrapolation of data from men.

Question: Well, that's a big red flag.

That's when I sunk my teeth into this issue, when I realized that the Guidelines were a partisan argument for using more drugs, instead of a dispassionate analysis of the science. You'll see in my book, which went to bed in March, after two and a half years of writing, that I anticipated the July update of the Guidelines, because I talk about the studies—the ALLHAT study, the PROSPER study, the ASCOT study—and I bring them into the book as evidence that the 2001 Guidelines were wrong, and these studies show how wrong they were. And then the National Cholesterol Education Program uses the same studies to add millions more Americans to those already taking statins.


1. "Prevention of Coronary Heart Disease with Pravastin in Men with Hypercholesterolemia," New England Journal of Medicine, Vol. 333, pp. 1301-7 {1995).

2. LDL-cholesterol, commonly called "bad cholesterol," enters artery walls, causing plaque to build up that can block blood flow. HDL-cholesterol, commonly called "good cholesterol," can remove cholesterol from arterial walls, minimizing plaque formation.

3. "Primary Prevention of Acute Coronary Events with lovastatin in Men and Women with Average Cholesterol levels: Results of AFCAPS/TexCAPS," Journal of the American Medical Association, Vol. 279, pp. 1615-22 {1998).

4. HERS -- The Heart and Estrogen/Progesterone Replacement Study.

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Copyright © 2012 Elmer M. Cranton, M.D., all rights reserved

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