eficiencies of vitamin B6 are known to increase the risk of developing cardiovascular disease. The mechanisms for this was first described by Kilmer McCully in his seminal paper in the 1960’s, in which he investigated cardiovascular disease risk in young subjects with homocysteinuria. Vitamin B6 is required for the metabolism of the amino acid homocysteine to cystathionine in the methionine pathway, and a lack of vitamin B6 decreases the activity of the converting enzyme cystathionine β-synthase. This in turn increases cellular levels of homocysteine, and as concentrations rise, the homocysteine spills out of cell causing plasma levels to rise. Because homocysteine is able to damage the endothelial lining of the arteries, possibly through free radical induced inhibition of nitric oxide synthase, rises in plasma homocysteine increase the risk of cardiovascular disease through detrimental changes to endothelial function.
However, recently research has highlighted that reductions in plasma levels of vitamin B6 may cause decreases in plasma levels of omega-3 (n-3) fatty acids. This may explain in part some of the detrimental effects of vitamin B6 with respect to cardiovascular disease. Animal experiments suggest that low plasma vitamin B6 status increases linoleic acid (LA, C18:2 (n-6)) concentrations in tissues. In a study published in the Journal of Nutrition1, researchers investigated the effects of following a vitamin B6 deficient diet for 28 days on plasma fatty acid concentrations in human subjects. The results showed that during the deficiency period, plasma levels of eicosapentanoic acid (EPA, C20:5 (n-3)) and docosahexanoic acid (DHA, C22:6 (n-3)) decreased significantly (from 548 to 490 µmol/L and from 37 to 32 µmol/L, respectively). This was reflected in an increased n-6 to n-3 fatty acid ratio in plasma (from 15.4 to 16.0 µmol/L).
These results suggest that a short-term deficiency of vitamin B6 can cause a detrimental change to the n-6 to n-3 fatty acid ratio and this in turn may explain part of the reason for the increased cardiovascular risk associated with low vitamin B6 status. This supports findings previously published from animal studies with respect to increases in LA in tissues with vitamin B6 deficiency. Although clinical deficiencies of vitamin B6 are considered rare in Western populations, marginal vitamin B6 deficiencies (insufficiencies) have been reported to be more common, particularly amongst female users of the contraceptive pill, male smokers and the elderly. These groups are at increased risk of cardiovascular disease and the vitamin B6 deficiencies may partially explain this increase risk. Although it was previously considered that this may be due to elevated homocysteine levels, detrimental changes to fatty acid metabolism may also play a role.
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