The risk of developing atherosclerosis and heart disease may be higher in people who have a low dietary Se intake. Endothelial dysfunction is a primary factor in the pathogenesis of atherosclerosis. Laboratory-based research has provided considerable evidence to suggest that Se may be beneficial to the endothelium and thus help to prevent atherosclerotic disease. Se supplementation of cell cultures protects the endothelium from oxidative damage and can alter platelet function, cytokine signalling and transcription of pro-atherogenic adhesion molecules (Fig. 12.4).
The contribution of Se deficiency to the pathogenesis of cardiovascular disease was originally suggested from epidemiological studies that correlated low Se content of forage crops, drinking water and blood with regional mortality rates from cardiovascular disease (Schamberger et al., 1979). Other studies have failed to confirm this link. Huttunen (1997) postulated that the conflicting data from these studies can be explained by a threshold effect of Se intake on the risk of cardiovascular disease; that is, in populations with low Se status, a correlation between serum Se and cardiovascular risk is observed, while populations with a high Se intake (serum Se levels > 45 ^g l-1) would show no such correlation (Korpela, 1993). There are data that support this 'threshold hypothesis' (Kardinaal et al., 1997): from the ten centres across nine European countries, only one (Germany, with the lowest measured Se concentrations) demonstrated a statistically significant inverse association between toenail Se levels and risk of myocardial infarction.
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