Vitamin Be and Hyperhomocysteinemia

The identification of hyperhomocysteinemia as an independent risk factor in atherosclerosis and coronary heart disease (Section 10.3.4.2) has led to suggestions that intakes of vitamin B6 higher than are currently considered adequate to meet requirements may be desirable. Homocysteine is an intermediate in methionine metabolism and may undergo one of two metabolic fates, as shown in Figure 9.5: remethylation to methionine (a reaction that is dependent on vitamin B12 and folic acid) or onward metabolism leading to the synthesis of cysteine (trans-sulfuration). Therefore, intakes of folate, vitamin B12, and/or vitamin B6 may affect homocysteine metabolism.

Epidemiological studies suggest that hyperhomocysteinemia is most significantly correlated withlow folate status, but there is also a significant association with low vitamin B6 status (Selhub etal., 1993). Trials of supplementation have shown that whereas folate supplements lower fasting homocysteine in moderately hyperhomocysteinemic subjects, supplements of 10 mgper day of vitamin B6 have no effect, although supplements do reduce the peak plasma concentration of homocysteine after a test dose of methionine (Ubbink et al., 1994; Ubbink, 1997; Dierkes et al., 1998). This can probably be explained on the basis of the kinetics of the enzymes involved; the Km of cystathionine synthetase is 10-fold higher than that of methionine synthetase. Under basal conditions, little homocysteine is metabolized by way of the transsulfuration pathway; it is only alter a loading dose of methionine, when homocysteine rises to high levels, that the activity of cystathionine synthetase, rather than the concentration of its substrate, is limiting.

It thus seems unlikely that intakes of vitamin B6 above amounts that are adequate to prevent metabolic signs of deficiency will be beneficial in lowering plasma concentrations of homocysteine (Homocysteine Lowering Trialists' Collaboration, 1998).

Your Heart and Nutrition

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