Cholesterol and Cardiovascular Disease
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The Scene | The Players | The Problems | Why We Need Cholesterol | References | Print this page

This article is a continuation of the article "Cholesterol, How Low is Too Low?" from my Winter 2010 newsletter...

Setting the Scene

“When the U.S. Surgeon General’s Office set off in 1988 to write the definitive report on the dangers of dietary fat, the scientific task appeared straightforward. Four years earlier, the National Institute of Health (NIH) had begun advising every American old enough to walk to restrict fat intake, and the president of the American Heart Association (AHA) had told Time magazine that if everyone went along, "we will have [atherosclerosis] conquered" by the year 2000. The Surgeon General’s Office itself had just published its 700-page landmark "Report on Nutrition and Health," declaring fat the single most unwholesome component of the American diet.

All of this was apparently based on sound science. So the task before the project officer was merely to gather that science together in one volume, have it reviewed by a committee of experts, which had been promptly established, and publish it. The project did not go smoothly, however. Four project officers came and went over the next decade. "It consumed project officers," says Marion Nestle, who helped launch the project and now runs the nutrition and food studies department at New York University (NYU). Members of the oversight committee saw drafts of an early chapter or two, criticized them vigorously, and then saw little else.

Finally, in June 1999, 11 years after the project began, the Surgeon General’s Office circulated a letter, authored by the last of the project officers, explaining that the report would be killed. There was no other public announcement and no press release. The letter explained that the relevant administrators "did not anticipate fully the magnitude of the additional external expertise and staff resources that would be needed." In other words, says Nestle, the subject matter "was too complicated."

For most of the last 50 years, the links between cardiovascular disease, dietary fat, and cholesterol have been taken as gospel. The proposition that dietary fat is a bane to health is based chiefly on the assumption that fat, specifically the hard, saturated fat found primarily in meat and dairy products, elevates blood cholesterol levels. This in turn raises the likelihood that cholesterol will clog arteries, a condition known as atherosclerosis, which then increases risk of coronary artery disease, heart attack, and early death.

Cholesterol levels in the blood are tested regularly, and we feel like we’ve passed some big important test if the numbers come back looking good. We feel like a naughty child if the numbers look bad, as if something as simple as foregoing one more chocolate chip cookie would profoundly reduce our risk factors of dying from heart disease. Medical journals and news media proclaim the evils of saturated fat and dietary cholesterol. They claim foods such as nuts, coconut, and avocados are "unhealthy" and bad for your heart. Food science created thousands of "heart healthy" products with lowered saturated fat and cholesterol. Many of these products carry an endorsement by the American Heart Association.

We have “good” cholesterol (HDL), “bad” cholesterol (LDL), “total” cholesterol (HDL + LDL), triglycerides, saturated fat, unsaturated fat, trans fat, and others, and hundreds of companies hungry for our business proclaiming the goods and evils of each.

How did we get to this place where functional, necessary molecules within our bodies have become the object of such vilification?? back to top

The Players

The low fat movement was started by biochemist Ancel Keys in the 1950s. He noted a dramatic increase in cardiac conditions following World War II, and determined that dietary fat and cholesterol were at fault. By 1952, Keys was arguing that Americans should reduce their fat intake to less than 30% of total calories, although he simultaneously recognized that "direct evidence on the effect of the diet on human arteriosclerosis is very little and likely to remain so for some time."

Around the same time E.H. Pete Ahrens, the chair of the Diet-Heart Review Panel of the National Heart Institute (now the National Heart, Lung, and Blood Institute, or NHLBI) and his panel — ten experts in clinical medicine, epidemiology, biostatistics, human nutrition, and metabolism — were equally concerned that eating less fat could have profound effects throughout the body, many of which could be harmful. The brain is actually 70% fat, most of which is there to provide insulation to neurons. Fat and cholesterol are integral components of cell membranes, neurotransmitters (such as serotonin and dopamine), and hormones (such as estrogen and progesterone). Fat serves a variety of necessary functions in the body, and Ahrens was concerned about how altering the amount of fat and the percentages of saturated versus unsaturated fat would impact normal physiology of everything from glucose metabolism to hormone production. (Taubs)

To proponents of the anti-fat message, the heart disease epidemic noted by Ancel Keys has always been an indisputable reality. Yet, to the statisticians at the mortality branch of the National Center for Health Statistics (NCHS), the source of all the relevant statistics, the epidemic was illusory. In their view, heart disease deaths had been steadily declining since the late 1940s. The actual risk of dying from a heart attack at any particular age remained unchanged: rather, the rising number of 50-year-olds dropping dead of heart attacks was primarily due to the rising number of 50-year-olds.

The increase was due to new diagnostic technologies - the wider use of electrocardiograms, for instance - and the changing terminology of death certificates. In 1949, the International Classification of Diseases (ICD) added a new category, "arteriosclerotic heart disease," under the more general "diseases of the heart." The result, as a 1958 report to the American Heart Association noted, was dramatic: "In one year, 1948 to 1949, the effect of this revision was to raise coronary disease death rates by about 20% for white males and about 35% for white females." In 1965, the ICD added a category for coronary heart disease, which added yet more deaths and capped off the apparent epidemic. (Taubs) back to top

The Problems

Since the 1970s, dozens of studies have demonstrated a link between elevated cholesterol and heart disease. What they have been unable to do is demonstrate that cholesterol CAUSES heart disease. In fact, dozens of studies have shown that reducing dietary fat and cholesterol INCREASES the risk of death from causes other than heart disease, and numerous studies have shown that limiting dietary cholesterol has no significant impact on serum cholesterol, and that lower serum cholesterol has no significant causal relationship to death from cardiovascular disease.

If cholesterol caused heart disease, it should be a risk factor in 1) all ages, 2) both sexes, and 3) all populations around the world (barring any protective factor). Also, if cholesterol caused heart disease we would expect that lowering cholesterol would reduce heart disease. But none of these assumptions turn out to be true.

Another consistent thorn in the side of supporters of the “lipid hypothesis” is that women suffer 300% less heart disease than men, in spite of having higher average cholesterol levels. At the recent Conference on Low Blood Cholesterol, which reviewed 11 major studies including 125,000 women, it was determined that there was absolutely no relationship between total cholesterol levels and mortality from cardiovascular or any other causes. (Kressner)

It appears that the “healthiest” people have cholesterol levels in the 200-250 range, despite a slightly elevated risk of heart diseases. For example, The Honolulu Heart Program study, with 8,000 participants, published in 2001 found: “Long-term persistence of low cholesterol concentration actually increases the risk of death. Thus, the earlier the patients start to have lower cholesterol concentrations, the greater the risk of death.” (Schatz) The huge Japanese Lipid Intervention Trial with over 47,000 participants found: “The highest death rate observed was among those with lowest cholesterol (under 160mg/dl); lowest death rate observed was with those whose cholesterol was between 200-259mg/dl.” (Okayama)

Additionally, The Framingham study, the longest lasting, most respected study into the causes of heart disease (started in 1948) reported in 1992 that "In Framingham, Massachusetts, the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower people's serum cholesterol." (Dr William Castelli, director of the Framingham study at the time.) This study further finds “There is a direct association between falling cholesterol levels over the first 14 years of the study and mortality over the following 18 years. 11% overall and 14% CVD death rate increase per 1mg/dl per year drop in cholesterol levels”. (Kendrick) In other words, the more cholesterol levels dropped, the more likely it was that a subject would die.

More recently, a major eight year long interventional study on fifty thousand women (the Woman's Health Initiative) found that a 25% reduction in saturated fat intake had no effect on LDL ‘bad cholesterol' levels, or heart disease rates. (Howard)

In short, once your cholesterol level starts to fall, you are much more likely to die from heart disease or other causes: approximately a 150% increase in relative risk for every 10% fall. Add this to another very big study of the elderly, published in the Lancet: "Our data accord with previous findings of increased mortality in elderly people with low serum cholesterol levels, and show that long term persistence of low cholesterol concentration actually increases the risk of death." Thus, the earlier that patients start to have lower cholesterol concentrations the greater the risk of death. (Schatz, et al)

It is undisputed that elevated levels of cholesterol, especially LDL and triglycerides, in the blood are associated with increases in atherosclerosis, heart attack, and stroke. The question is, does elevated cholesterol CAUSE heart disease, or is it an early warning sign of heart disease? What if, by forcing cholesterol levels lower and lower we are short circuiting our bodies’ abilities to protect themselves from factors which do cause heart disease, while profoundly affecting our bodies’ abilities to maintain normal hormone and neurotransmitter function? Cholesterol levels below 160 have been associated with increased risk for depression, anxiety, and violent behavior. (Golomb) Perhaps at levels that low we are unable to produce enough dopamine, serotonin, testosterone, estrogen, and other substances we need for normal function! back to top

Why Do We Need Cholesterol, Anyway?

About 90% of the cholesterol in our bodies is made in the liver. LDL transports fat from the liver to tissues that need it, HDL transports fats back to the liver to be broken down and re-formed into other molecules. Cholesterol is the building block for source for testosterone, estrogen, and progesterone. These sex hormones have remarkable similarity with each other and with the original cholesterol parent from which they were derived. Cholesterol is also the parent of aldosterone and cortisol, hormones produced in the adrenal glands and responsible for regulating a variety of physiological functions.

Another offspring of cholesterol, calcitrol, maintains the proper level of calcium in our bodies. Calcium functions optimally within a very narrow range in the blood stream. Too much or too little has profound effects on physiological function, and we can not live without it.

Additionally, cholesterol is required for the production of bile acids. Secreted by the liver and stored in the gallbladder these chemicals make it possible for us to emulsify fats and other nutrients enabling them to be digested and absorbed as food. In the absence of sufficient bile acids we would produce voluminous stools of undigested material while slowly starving. (Graveline)

Cholesterol is also required for production of vitamin D which is necessary for normal immune system function. It is a vital component of all cell membranes, and it profoundly affects the way nutrients and waste are transported into and out of every cell in the body. Cholesterol, as an integral component of myelin, helps to insulate neurons and brain cells and allows normal nervous system function.

You can see that cholesterol is a vital substance which is necessary for our bodies to function normally, yet public policy continues to recommend amounts so low that it is impossible to achieve them without medication. Doctors continue to recommend cholesterol-lowering medications to everyone with cholesterol levels above 200 regardless of other risk factors. This is not to say there should be no upper limit – studies consistently show a U-shaped curve relating to blood cholesterol levels and increased risk of death, suggesting that levels which are too high (above 260) do indeed add to one’s risk of untimely demise.

I’ll conclude this article with a quote from Dr. Joseph Mercola: “A mistake that is rarely made in the hard-core sciences such as physics seems to be frequently made in medicine. This is confusing correlation with cause. There may be a weak correlation of elevated cholesterol with heart attacks, however this does not mean it is the cholesterol that caused the heart attack. Certainly gray hair is correlated with getting older; however one could hardly say that the gray hair caused one to get old. Using hair dye to reduce the gray hair would not really make you any younger. Neither it appears would just lowering your cholesterol.” (Mercola) back to top


Golomb, Beatrice A.; Evans, Marcella A. Statin Adverse Effects: A Review of the Literature and Evidence for a Mitochondrial Mechanism. Am J Cardiovasc Drugs. 2008;8(6):373-418. 

Graveline, Duane MD MPH Cholesterol - Friend or Foe?

Howard BV. Dietary Fat and Cardiovascular Disease: Putting the Women's Health Initiative in Perspective. Nutr Metab Cardiovasc Dis 2007 Mar;17(3):171-4. Epub 2007 Feb 21.

Jacobs D, et al. Report of the Conference on Low Blood Cholesterol: Mortality Associations. Circulation. 1992 Sep;86(3):1046-60.

Kendrick, Malcolm. Dr. Malcolm Kendrick M.D. looks at Cholesterol.

Kresser, Chris. Heart Disease, Myths & Truths: Cholesterol doesn’t cause heart disease. The Healthy Skeptic (blog). June 10, 2008.

Mercola, Jospeh. Cholesterol is NOT the Cause of Heart Disease. Posted By Dr. Mercola. May 28 2005

Okayama, A., et. al. Changes in Total Serum Cholesterol and Other Risk Factors for Cardiovascular Disease in Japan, 1980–1989. International Journal of Epidemiology Volume 22,(6), p.1038-1047

Schatz, I., Cholesterol and all-cause mortality in elderly people from the Honolulu Heart Program: a cohort study. The Lancet, Volume 358, Issue 9279, Pages 351 - 355, 4 August 2001.

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