Vitamin B6 is an essential nutrient in humans. This means it cannot be synthesised endogenously, but instead must be present in the diet. Once absorbed vitamin B6 is converted to its active form through addition of a phosphate molecule, forming pyridoxal 5’-phosphate (PLP). In this form, vitamin B6 acts as a coenzyme to a number of reactions important to human metabolism. As well as energy production, pyridoxal 5’-phosphate is involved in one carbon metabolism because it acts as a cofactor in the enzymes glycine decarboxylase, serine hydroxymethyltransferase, cystathionine γ-lyase and cystathionine β-synthase. Pyridoxal 5’-phosphate is also required as a cofactor in the catabolism of L-tryptophan and in this role vitamin B6 regulates tryptophan turnover rates. Because tryptophan is a precursor niacin, which in turn forms nicotinamide adenine dinucleotide (NAD), vitamin B6 is also involved in the synthesis of NAD through its role in the degradation of tryptophan.
Normal plasma levels of pyridoxal 5’-phosphate range from 20 to 30 nmol/L and evidence suggests that one-carbon metabolism can be maintained over a wide range of plasma levels including moderate deficiency. However, poor vitamin B6 status is associated with detrimental effects on amino acid metabolism, and this likely reflect the role of vitamin B6 in one carbon metabolism and the degradation pathway involving tryptophan. Because vitamin B6 is water soluble it is not stored in the body and a daily intake is required to maintain proper metabolic regulation. The speed at which detrimental changes can occur following restriction of vitamin B6 have been assessed in research studies and it appears that within 28 days metabolic deterioration can be detected. For example, in one study1, researchers fed healthy men and women a controlled diet that restricted their vitamin B6 intake to 0.04 mg per day for 26 days. Then the researchers measured their enzymes levels to assess the effects of the restriction.
Analysis of the compounds relevant to one-carbon metabolism showed that vitamin B6 restriction resulted in increases in levels of cystathionine and serine and lower levels of creatine, creatinine and dimethylglycine compared to the vitamin B6 replete state. Restriction of vitamin B6 also caused a reduction in the amount of kynurenic acid and increases in 3-hydroxykynurenine compared to the vitamin B6 replete state. These results suggest that restriction of vitamin B6 for 28 days is able to cause aberrations to normal amino acid metabolism. The association of a poor vitamin B6 status with vascular disease suggests that these changes to amino acid metabolism may be contributory factors in the development of serious illness. It is known for example that elevated levels of homocysteine are a risk factor for cardiovascular disease, and that as its role as a cofactor in cystathionine β-synthase vitamin B6 is able to help maintain normal plasma levels of homocysteine.
Dr Robert Barrington’s Comments: Maintaining adequate levels of water soluble vitamins requires a daily intake. Even short periods of time with low intakes of water soluble vitamins is enough to lower plasma levels and cause metabolic dysfunction. Eating a high quality diet that contains all of the essential micronutrients is therefore necessary in order to prevent serious illness. Chronic low intakes of the water soluble vitamins likely leads to vitamin insufficiencies and these can cause subclinical symptoms and idiosyncratic illness that maintains the individual in a perpetual unhealthy state. The best insurance policy to ensure adequate vitamin status is to take a high potency multivitamin and mineral tablet daily as a supplement to a high quality plant based diet.
RdB
