Nutrition and Coronary Heart Disease
There exists biochemical and experimental evidence that supports the hypothesis that
oxidative modification of LDL causes atherosclerosis (Steinberg, 1992). This is now
supported by epidemiological evidence (Gey et al, 1991; Riemersma et al, 1991 and
Stampferetal, 1993).
Oxidisation is caused by the presence of free radicals in the body. Free radicals are
produced through the normal metabolic process. The free radicals can produce lipid
radicals, which in turn produce peroxyl radicals. This process is highly unstable and
will continue to consume valuable polyunsaturated fatty acids (Parthasarathy and
Rankin, 1992). This process ceases when two peroxyl radicals combine to form an
inactive by-product. LDL is particularly susceptible to an oxidative modification.
The presence of perioxid modified components of LDL can cause the development of
atherosclerosis (Silagy and Mant, 1996 & Steinberg, 1992). Antioxidants can inhibit
the modification of LDL by bonding with the free radicals and perioxyl radicals forming
stable compounds.
A number of early studies failed to find an association between antioxidant vitamins and
the rates of CHD (Salonen et al, 1985; Salonen et al, 1988; Gey et al, 1987 and Kok et
al, 1987). Following the publication of the biomedical evidence mentioned above, a
number of more recent studies have found evidence of an association between
antioxidants and CHD.
Riemesma et al (1991) found an inverse relationship between plasma concentrations of
vitamin C and E and carotene and the risk CHD. Stampfer et al (1993) performed a
prospective study that also supported the hypothesis that vitamin E and beta-carotene
intakes were inversely correlated with CHD.
Gey et al (1991) supply strong evidence that antioxidants protect against CHD. In their
cross country study, they found that vitamin E levels were a very strong predictor of
CHD. Most recently Rimm et al (1996) have shown that there are lower rates of CHD
among people eating higher amounts of fruit and vegetables. This is also supported by
further studies that have focused on the consumption of foods high in carotenoids
(Street et al, 1994 and Kardinaal et al, 1993).
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