During protein digestion, amino acids including ‘methionine’, and homocysteine, an intermediate in the methionine metabolism, are released. Healthy individuals utilize two different pathways to metabolize homocysteine: the conversion of homocysteine back to methionine is dependent on vitamin B9 (folic acid) and vitamin B12, while the conversion of homocysteine to the amino acid ‘cysteine’ requires two vitamin B6 (PLP)-dependent enzymes. Thus, the amount of homocysteine in the blood is regulated by at least three vitamins: vitamin B9, B12, and B6. Deficiencies of one of these vitamins can lead to high blood homocysteine level (43).
Several large observational studies have demonstrated an association between low vitamin B6 intake or status combined with increased blood homocysteine levels and increased risk of cardiovascular diseases. A large prospective study found the risk of heart disease in women who consumed, on average, 4.6 mg vitamin B6 daily was only 67% of the risk in women who consumed an average of 1.1 mg daily (7). Another large prospective study found higher plasma levels of PLP were associated with a decreased risk of cardiovascular disease independent of homocysteine levels (8). Furthermore, several studies have reported that low plasma PLP status is a risk factor for coronary artery disease (9, 10, 11).
Presently it is not clear whether lowering levels of homocysteine by increasing vitamin B6 intake will reduce the risk of heart disease.
Low vitamin B6 intake and nutritional status have been associated with impaired immune function, especially in the elderly. Decreased production of immune system cells known as ‘lymphocytes’, as well as decreased production of an important immune system protein called ‘interleukin-2’, have been reported in vitamin B6 deficient individuals (12). Restoration of vitamin B6 status has resulted in normalization of lymphocyte cell division (‘proliferation’) and interleukin-2 production, suggesting that adequate vitamin B6 intake is important for optimal immune system function in older individuals (12, 13).
One study found that the amount of vitamin B6 required to reverse these immune system impairments in the elderly was 2.9 mg/day for men and 1.9 mg/day for women; these vitamin B6 requirements are higher than the current recommended dietary allowance (RDA) (12).
A few studies have associated cognitive decline in the elderly or Alzheimer's disease with inadequate nutritional status of vitamin B9(folic acid), vitamin B12, and vitamin B6 and thus, elevated levels of homocysteine (14).
A review of randomized controlled trials concluded that there is insufficient evidence that supplementation with vitamin B6, vitamin B12, or vitamin B9 improves cognition in those with normal or impaired cognitive function (17).
Because of mixed findings, it is presently unclear whether supplementation with B vitamins might blunt cognitive decline in the elderly. Furthermore, it is not known if marginal B vitamin deficiencies, which are relatively common in the elderly, even contribute to age-associated declines in cognitive function, or whether both result from processes associated with aging and/or disease.
In a large prospective study in more than 85,000 women without a prior history of kidney stones were followed over 14 years. Those who consumed at least 40 mg/day vitamin B6 had only two thirds the risk of developing kidney stones compared with those who consumed 3 mg or less (18).
However, in a group of more than 45,000 men followed over six years, no association was found between vitamin B6 intake and the occurrence of kidney stones (19).
Presently, the relationship between vitamin B6 intake and the risk of developing kidney stones requires further study before any recommendations can be made.
Authored by Dr Peter Engel in 2010, reviewed and revised by Angelika Friedel on 14.06.2017