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Normal progression in science involves falsifying hypotheses rather than proving associated with a hypothesis a number of inconsistencies, observations that appear

them. When to contradict or

there are falsify the

hypothesis, then there should be cause for concern that it is flawed or false and might in fact be leading down a dead-end road. The Bohr atom studied by every high school chemistry student is an example where a beautiful hypothesis (theory) was eventually falsified and replaced by quantum theory. But Einstein spent much time trying to find a so-called thought experiment to demonstrate that one of the essential pillars of the quantum theory was false. Incidentally, he failed but this is how progress is made. But today, anyone who questions the hypothesis that cholesterol in general or LDL cholesterol in particular causes or is a risk factor for atherosclerosis is ignored, branded a nut, or ostracized by professional colleagues, or perhaps told not to worry because it is really oxidized LDL that is important—just wait until this revision becomes a genuine truth that no one can question. Cholesterol is really LDL is really oxidized LDL, no problem. In the literature it is repeatedly stated that

















publications where this statement is made, it More about this later. And there indeed are validity both the causality and association

turns out to be impossible to find this overwhelming evidence. deniers within the medical profession, i.e. those who deny the aspects of the Cholesterol Hypothesis, and their voices are

occasionally heard, mostly in one of several peer-reviewed British medical journals Amazon.com. The quotation given above represents the strong opinion of one high will attempt to critically evaluate the merits of the position taken by the deniers,

or in books one can buy at profile denier. This Review in particular with regard to


The cholesterol hypothesis goes back a long way, in fact to the mid-19th Virchow found plaques in arteries of cadavers and observed that they

century in Berlin where Rudolf Von contained cholesterol—an amazing

observation given the development of medical science at the time. He made no connection with heart disease or heart attacks since these problems did not exist or were not recognized then. In fact the first medical description of a myocardial infarct (heart attack) as a clinical pathologic entity did not appear in the medical literature until 1915. Fifty years after Virchow’s observation for some reason or other a Russian named Anitschkov fed rabbits a diet high in cholesterol and observed that their arteries thickened and filled up with cholesterol. But rabbits are not carnivores and cholesterol is totally foreign to their natural diet. Rabbits do not normally eat meat, eggs or milk products. It is doubtful that such studies are at all relevant to humans. After the WWII more cases of heart disease were being identified and there was growing interest as to both the cause and possible therapies. The breakthrough for the Cholesterol Hypothesis came with the study of Ancel Keys from the University of Minnesota, the instigator of the famous “Seven Countries” study of the relationship between heart disease, serum cholesterol levels and fat intake. As was eventually pointed out, Professor Keyes actually selected seven countries from a larger set in order to support his hypothesis. As Dr. Malcolm Kendrick, M.D., in his book The Great Cholesterol Con points out, by selecting a different set of seven countries using data available to Keys, one can get exactly the opposite correlation. Also, if one uses all the data the correlation disappears. Keys’ work was followed by the famous Framingham Study which provided evidence, albeit rather weak, for a connection between cholesterol and coronary heart disease (CHD), particularly in young men, and by additional studies where rabbits were fed a diet containing cholesterol and fat, and the Hypothesis was well on its way to becoming enshrined. The final pillar was added when it was shown that lowering cholesterol in patients who had suffered a heart attack reduced the risk of a second heart attack (secondary prevention). Add to this the high rate of coronary heart disease among those with a familial predisposition to very high cholesterol levels even at a young age, and the story was complete. Circulating cholesterol caused heart disease and since heart disease involved atherosclerosis, cholesterol must be involved in the development and progression of atherosclerosis as well. Case closed. The evidence was compelling. No reasonable person could conclude otherwise. The end result has been a 55 billion dollar (U.S.) worldwide business in cholesterol lowering drugs, numerous successful careers in academic medicine, and a Nobel Prize for two researchers. Perhaps more importantly, there arose a widespread fear among many individuals of high blood levels of cholesterol as well as dietary cholesterol and fat and the result was psychological stress and in some cases an adherence to diets that may in fact be unhealthy. In addition, a hostile environment now exists for anyone who even suggests that there may be serious problems with what are almost universally viewed as the evidence-based foundations of the Cholesterol Hypothesis.

Today LDL cholesterol or its oxidized form largely replaces total cholesterol (TC) as the agent viewed as responsible for causing coronary heart disease (CHD). But TC and LDL go hand in hand. LDL levels are generally not directly measured but calculated from measurements of triglycerides (TG), HDL and TC. The calculation assumes that the TC can be regarded as the following:

International Health News

November 2007

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