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results are presented as the constants of correlation equations and almost always the degree of correlation is very poor (low correlation coefficient).

HOW ABOUT FAMILIAL HYPERCHOLESTEROLEMIA (FH)? Individuals with FH have very high TC and LDL due, it is thought, to what is called an LDL-receptor deficiency which results from a mutation. An argument for the Cholesterol Hypothesis involves claiming that members of

such families run a great risk of dying form CHD atherosclerosis and CHD. To use individuals with this

at an early age. mutation as “proof”

Ergo, elevated TC and LDL cause of the Cholesterol Hypothesis requires

that the only difference between the FH people and the rest of thus LDL. But it is not that simple. Individuals who inherit from

us is that they produce huge excesses of TC and both parents not only have highly abnormal levels

of or

cholesterol in their atherosclerotic deposits, but also in other organs. Cholesterol higher. And lowering their cholesterol levels drastically does not reverse their

levels can go to atherosclerosis.

1000 mg/dL Also, these

individuals have blood-clotting abnormalities which may responsible for the also argued by some that the nature of the atherosclerosis is different in FH

elevated rate as compared

of to

heart attacks. It is non-FH individuals

[19]. This does atherosclerosis or

not seem to be an ideal group to use in justifying a hypothesis regarding the CHD. Nevertheless it is one of the major pillars upon which the hypothesis rests.



An interesting and perhaps unique study from the Netherlands relates to this question. A large pedigree was traced back to a single pair of ancestors in the 19th century and a family tree mortality study conducted which started in the early 1800s. All members had a 50-50 chance of carrying the mutation for familial hypercholesterolemia. Mortality data over the full time span up to modern times was available for this large group as well as for the corresponding general population. Overall mortality was not increased in carriers of the mutation during the 19th and early 20th century. The mortality then rose reaching a maximum between 1935 and 1964. The authors comment that the risk of death varied significantly among patients with FH and that this was, in their opinion an indication of strong interaction with environmental factors. One can of course ask why for over more than a century no excess mortality showed up because of the elevated TC and LDL levels if in fact these

lipoproteins cause atherosclerosis and CHD.

Kendrick [3] suggests that perhaps lipoprotein (a) is involved since there seems little doubt that this protein is elevated in those with the FH mutation and that this protein is regarded as a strong independent risk factor for CHD. However, he finds the strongest argument against FH causing CHD is that most people who die with heart disease do not have highly elevated LDL levels and most who have these LDL levels do not die of heart disease, even people with FH.

THE MONICA STUDY This is an acronym for a huge World Health Organization study of cardiovascular disease. Among other things, the association of CHD deaths and TC was examined for a large number of countries. In one looks at a plot that displays the results from this set of countries, two things jump out at you [8]. First the data, which clusters between TC of about 210 and 250 mg/dL and covers a CHD death rate from some very low number to over 450 events per 100,000, shows that no matter what the cholesterol level is in this range, both very high and very low rates of CHD mortality are found. At a level of about 225 mg/dL the mortality for a number of countries ranges from 70 to 427 deaths per 100,000. Also, when data from several sites within a country are provided, there is a large variation in mortality at a given TC level. Overall, there is no apparent correlation between CHD deaths and TC, contrary to what would be expected on the basis of the Cholesterol Hypothesis. Just two countries are outside the main scatter, China and Japan, and both have both low TC and low rates.

Japan merits a bit of discussion. The Japanese living in Japan in general had both low cholesterol levels and low rates CHD mortality, but immigrants to the U.S. had high cholesterol levels and had CHD mortality comparable to Americans. Convincing proof of the Cholesterol Hypothesis. But let’s dig deeper and look at what a British physician found during his Ph.D. research. He looked at the relationship between TC levels and social factors, eating habits and lifestyle among the immigrant Japanese. He found conclusive evidence that it was not the food that raised the cholesterol of the Japanese immigrants, or that elevated cholesterol values increased their risk of CHD death. Rather, he found that those who maintained their cultural traditions were protected against heart attacks, even though their cholesterol increased as much as in the immigrants who adopted the Western lifestyle and diet and who died from CHD at a rate comparable to the Americans. In fact, the Japanese who preferred lean Japanese food but adopted other aspects of the American way of life had CHD

International Health News

November 2007

Page 14

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