Vitamin B6 (here) is a group of vitamers made up of pyridoxine, pyridoxal and pyridoxamine, which are required in human metabolism for amino acid metabolism. Food sources of vitamin B6 include meat and whole grain foods, but supplements containing the vitamin are widely available. Research suggests that the high intakes present in supplements may reverse inhibition of the homocysteine to cystathionine reaction of the methionine pathway, caused by low intakes of dietary vitamin B6. Supplements of vitamin B6 may therefore be protective of cardiovascular disease. While the liver has an ability to store a small amount of vitamin B6 despite its water soluble nature, generally a daily intake of the vitamin is required to maintain plasma levels. However, controversy surround the exact amount of vitamin B6 required for optimal metabolic function of the methionine pathway. Because of its water soluble nature, higher doses are safe and excessive intakes are effectively excreted. Therefore researchers have analysed plasma and urine levels following high dose supplementation.
For example, in one study1, researchers administered 10, 25, 50 or 100 mg of pyridoxine to healthy female human volunteers. Plasma level of pyridoxal and the the active form of vitamin B6, pyridoxal-5′-phosphate, both increased as doses rose from 10 to 25 mg, and then again when doses rose from from 25 to 50 mg. However, increasing the dose from 50 to 100 mg per day did not increase plasma levels of pyridoxal-5′-phosphate further, but did increase levels of pyridoxal by a factor of around 3.85 times. However, this high levels of pyridoxal was eliminated from circulation within 24 hours. When renal clearance of pyridoxal was measured, it remained at less than 2% for each supplemental dosage, irrespective of the high circulating plasma levels. Because tissue levels of pyridoxal-5′-phosphate rise with increasing plasma levels of pyridoxal, this study suggest that tissue levels would have increased in the subjects. Pyridoxal and pyridoxal-5′-phosphate levels increasing throughout the study period also the subject may have had sub-optimal levels at baseline.
During the study, urinary levels of 4-pyridoxic acid, a product of pyridoxal metabolism increased significantly, as would be expected. Evidence from other studies shows that 4-pyridoxic acid levels increase and decrease with supplementation and cessation of supplementation, respectively. Therefore fact that pyridoxal excretion did not increase above 2% of the plasma levels, in combination with the rise in 4-pyridoxic acid excretion, is suggestive of an efficient metabolism of pyridoxal in the study subjects. The low excretion of pyridoxal could be a result of its effective binding to albumin, which maintains plasma levels more favourably that might be expected for a water soluble vitamin. However, renal reabsorption of pyridoxal may have occurred, thus maintaining plasma levels for longer, and the authors concluded that this could not be excluded. Taken as a whole these results suggest that 50 mg may be enough to raise plasma levels of pyridoxal and pyridoxal-5′-phosphate high enough to allow tissue saturation of pyridoxal-5′-phosphate.
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