despite apparently lower B6 status, as indicated by plasma PLP levels, the black subjects were more efficient than the whites in catalyzing the transsulfuration of homocysteine to cysteine.
The increase in plasma homocysteine concentration after a methionine load or a meal is responsive to and primarily affected by B6 status, but data are not sufficient to support using this as the criterion on which to base the EAR. Because the fasting homocysteine concentration is primarily responsive to folate status (Ubbink et al., 1996), it is not a good candidate for use in setting the EAR. Results from population-based studies using data adjusted for folate and B12 status and for age indicate that B6 status as measured by PLP is inversely correlated with nonfasting plasma homocysteine concentration (Selhub et al., 1993). At least part of the increase in plasma homocysteine concentration that occurs with aging may be due to decreased renal function (Hultberg et al., 1993) rather than B6 status.
Moderate hyperhomocysteinemia was identified recently as a possible risk factor for vascular disease (Selhub et al., 1995; see also Chapter 8), and vitamin intervention can be used to reduce plasma homocysteine values. A recent prospective observational study has examined the effect of self-selection for intake of folate and B6 on the incidence of myocardial infarction (MI) and fatal coronary heart disease (CHD) (Rimm et al., 1998). After other risk factors for CHD were controlled for and vitamin intake was adjusted for energy intake, about a twofold reduction in MI and CHD was found for individuals in the quintile with the highest folate and B6 intakes compared with those with the lowest intakes. When intakes of each of the vitamins were considered separately, the multivariate analyses suggested about a 30 percent reduction in disease incidence between individuals in the highest and lowest quintiles of intake for each of the vitamins. For B6 the data are compatible with the Framingham study (Selhub et al., 1993), in which the lowest deciles of B6 intake were associated with higher circulating homocysteine. However, in the current study although multivariate analysis indicated a trend in risk reduction across the quintiles of intake, the major reduction appeared to occur between the fourth and fifth quintiles of intake (median intakes 2.7 and 4.6 mg). At these high B6 intakes, there is little effect of B6 intake on homocysteine levels, which are mainly affected by changes in intake at much lower intakes. Although these data are intriguing and suggest that self-