An early demonstration of the link between hy-percholesterolaemia and atherosclerosis took place in 1913 when Anitschkow in Russia observed that feeding pure cholesterol to rabbits produced elevated blood cholesterol levels as well as atherosclerosis in the aorta and coronary arteries.
The causal relationship between high blood cholesterol levels and atherosclerosis is demonstrated unequivocally by the genetic disorder familial hypercholesterolaemia (FH). This disorder is an example of an inborn error of metabolism and is due to impaired production of the LDL receptor. There are two forms of FH: a heterozygous form and a more severe homozygous form. FH heterozygotes inherit one mutant gene and number about one in 500 people in most ethnic groups. The cells of these individuals produce approximately half the normal number of LDL receptors. As a result, LDL is removed from the circulation at half the normal rate, the lipoprotein accumulates in blood to levels twofold above normal, and heart attacks occur typically in the fourth and fifth decades of life. If two heterozygotes of the opposite sex have a child, that child has a one in four chance of inheriting two copies of the mutant gene, one from each parent. Such FH homozygotes (about one in a million people) have plasma LDL levels 6-10-fold above normal. Heart attacks can occur at the age of two and are almost inevitable by the age of 20 (Goldstein & Brown, 1987).
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