Elevated levels of plasma homocysteine are an independent risk factor for cardiovascular disease because homocysteine can cause damage to the endothelial linings of arteries. Homocysteine in humans can be metabolised to a number of different compounds and these metabolic steps control the plasma levels of homocysteine. In particular, methionine synthase can convert homocysteine to methionine and cystathionine β-synthase can convert homocysteine to cystathionine. These enzyme require a number of B vitamins as co-factors and deficiency of these vitamins in the diet can cause elevations in plasma levels of homocysteine. Folate and vitamin B12 are required for activity of methionine synthase and vitamin B6 is required for activity of cystathionine β-synthase. Because of the importance of these three B vitamin in the control of homocysteine, research has attempted to gain a clear understanding of the association of vitamin B12, vitamin B6 and folate with the risk of developing hyperhomocysteinaemia.
For example researchers1 investigated the B vitamin status of 44 men with hyperhomocysteinaemia. The subjects, who had homocysteine plasma concentrations above 16.3 µmol/L, were compared with 274 control subjects with plasma homocysteine levels below 16.3 µmol/L. Low levels of pyridoxal 5-phosphate (PLP; the activated form of vitamin B6), cobalamin and folate were present in the hyperhomocysteinaemic men. Within the hyperhomocysteinaemic men, 25.0 % had suboptimal vitamin B6 status (<5 nmol/L), 56.8 % had suboptimal vitamin B12 (<200 pmol/L) status and 59.1 % had suboptimal folate status (<5 nmol/L). Plasma folate levels were negatively associated with homocysteine concentrations, but no significant association was found for cobalamin or PLP. Supplementation of the hyperhomocysteinaemic men with 12.2 mg pyridoxal hydrochloride, 1 mg folic acid and 0.4 mg cyanocobalamin normalised the homocysteine concentrations within 6 weeks.
These results support other research by suggesting a role for suboptimal pyridoxal (B6), folate and cobalamin (B12) intakes in the development of elevated homocysteine plasma levels. They also support previous findings in that supplementation of these vitamins was successful at reducing plasma levels of homocysteine. These finding are particularly relevant when considering the losses of these vitamins during the processing of whole cereal grains to refined flour, losses which can be substantial. Because additional losses may then be encountered during cooking, it is important to consider that diets based on the consumption of refined cereal grains may contain suboptimal levels of the B vitamins necessary to control homocysteine levels. Interestingly, doubling the vitamin intake of the subjects had no further effect on the reductions in plasma homocysteine, despite further increases in plasma levels of the vitamins, suggesting that the doses mentioned previously were the maximum needed to control homocysteine.
Dr Robert Barrington’s Nutritional Recommendation: the best way to obtain adequate vitamin B6, vitamin B12 and folate is through a high quality diet containing unrefined sources of grains. However, even a high quality diet might not be able to provide enough B vitamins to certain individuals, particularly those with increased exposure to stress. In such cases, supplements of brewer’s yeast or synthetic B vitamins in the form of a B complex are the best insurance to ensure optimal metabolic function of the homocysteine pathway.
RdB
