After the inactive forms of vitamin B6—pyridoxine, pyridoxal, pyridoxamine, and their derivatives—have been absorbed, the body converts them in the liver and small intestine into the biologically active forms pyridoxal phosphate (PLP) and pyridoxamine phosphate (PMP).
The coenzyme forms PLP and PMP participate in numerous enzymatic reactions involved in amino acid metabolism, homocysteine metabolism, and nucleotide synthesis. These coenzymes are essential for the proper functioning of the nervous system, immune system, and blood formation. Within the nervous system, for example, PLP is involved in both the synthesis and function of neurotransmitters. The conversion of L-DOPA into active dopamine depends on PLP, as does the function of serotonin receptors in the brain.
What Are the Benefits of Vitamin B6 Supplementation?
To date, the European Food Safety Authority (EFSA) has authorized ten health claims for vitamin B6, reflecting a solid body of scientific evidence. For example, vitamin B6 contributes to the normal functioning of the immune system. Accordingly, a vitamin B6 deficiency may lead to impaired immune function. Whether vitamin B6 supplementation beyond normal nutritional requirements further enhances immune function is not covered by the approved EFSA health claims.
Because vitamin B6 plays a crucial role in amino acid metabolism, the body's vitamin B6 requirements depend on protein turnover. The German Nutrition Society recommends a daily intake of 1.4–1.6 mg for men and 1.2 mg for women. On average, men consume approximately 1.8 mg and women approximately 1.5 mg of vitamin B6 per day—around 130% of the recommended intake.
Groups at increased risk of vitamin B6 deficiency include people with chronic excessive alcohol consumption, underweight individuals, smokers, and older adults with low food intake. Individuals with kidney disease are also at increased risk. In addition, certain medications such as L-DOPA may increase vitamin B6 requirements. For these groups in particular, controlled supplementation with B vitamins may help prevent hypovitaminosis (vitamin deficiency).
Current research is investigating the effects of vitamin B6 supplementation on obesity and diseases such as cancer, depression, and cardiovascular disease. In cancer research, an adequate dietary intake of vitamin B6 has shown benefits; however, these benefits have not been observed for vitamin B6 obtained from supplements. In fact, observational studies suggest that excessive vitamin B6 intake (hypervitaminosis B6) may even increase cancer risk. Similarly, research findings regarding dementia, autism, and depression have so far been rather disappointing.
When combined with 2.25 g of leucine, supplementation with 30 mg of vitamin B6 increased fat loss in overweight participants by approximately 34 g per day. The supplement reduced calcium concentrations within fat cells, leading researchers to hypothesize that this inhibited calcium's positive influence on fat cell formation.
Vitamin B6 has relatively low toxicity. However, hypervitaminosis has been associated with neurotoxic effects in both animal and human studies and has occurred after long-term supplementation over several months with daily doses ranging from 50 mg to 500 mg. Consequently, the German Federal Institute for Risk Assessment (BfR) has established 25 mg as the tolerable upper intake level (UL) and recommends a maximum content of 3.5 mg vitamin B6 in dietary supplements. Overall, there is still insufficient evidence regarding the safety of daily vitamin B6 intakes between 10 mg and 200 mg.
References
Further information and scientific studies on the active ingredient vitamin B6 can be found here.
The Intestine Plays a Substantial Role in Human Vitamin B6 Metabolism: A Caco-2 Cell Model
www.pubmed.ncbi.nlm.nih.gov/23342087
Effects of Pyridoxine on Dreaming: A Preliminary Study
www.pubmed.ncbi.nlm.nih.gov/11883552
Effects of a Leucine- and Pyridoxine-Containing Nutraceutical on Fat Oxidation, and Oxidative and Inflammatory Stress in Overweight and Obese Subjects
www.pubmed.ncbi.nlm.nih.gov/22822451
Adipogenic Effect of Calcium-Sensing Receptor Activation
www.pubmed.ncbi.nlm.nih.gov/24005534
The Calcium-Sensing Receptor Promotes Adipocyte Differentiation and Adipogenesis Through the PPARγ Pathway
www.pubmed.ncbi.nlm.nih.gov/22038624