Vitamin B₆: a challenging link between nutrition and inflammation in CVD

Abstract

The objective of the present review is to highlight the relationship between low vitamin B 6 status and CVD through its link with inflammation. While overt vitamin B 6 deficiency is uncommon in clinical practice, increasing evidence suggests that marginal vitamin B 6 deficiency is rather frequent in a consistent proportion of the population and is related to an increased risk of inflammation-related diseases. Ample evidence substantiates the theory of atherosclerosis as an inflammatory disease, and low plasma vitamin B 6 concentrations have been related to increased CVD risk. Several studies have also shown that low vitamin B 6 status is associated with rheumatoid arthritis and chronic inflammatory bowel diseases, both of which hold an underlying chronic inflammatory condition. Furthermore, the inverse association observed between inflammation markers and vitamin B 6 supports the notion that inflammation may represent the common link between low vitamin B 6 status and CVD risk. In addition to the epidemiological evidence, there are a number of cell culture and animal studies that have suggested several possible mechanisms relating impaired vitamin B 6 status with chronic inflammation. A mild vitamin B 6 deficiency characterises, in most cases, a subclinical at-risk condition in inflammatory-linked diseases which should be addressed by an appropriate individually tailored nutritional preventive or therapeutic strategy.

Oral exposure to the anti-pyridoxine compound 1-amino d-proline further perturbs homocysteine metabolism through the transsulfuration pathway in moderately vitamin B6 deficient rats

“…Epidemiological studies have shown that, while overt deficiency is rare, the prevalence of moderate vitamin B 6 deficiency in the general population is more pronounced, ranging from approximately 18% in North America and reaching up to 50% in Europe [25,34]. Marginal B 6 deficiency has been linked to the development of chronic inflammation in rheumatoid arthritis, colorectal cancer and cardiovascular diseases [35,36]. Additionally, several factors including the consumption of B 6 antagonists may further perturb the biochemical availability of endogenous PLP [11].…”

Opposite associations between alanine aminotransferase and γ-glutamyl transferase levels and all-cause mortality in type 2 diabetes: Analysis of the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study

“…Alternative causes for the relationship between low ALT and mortality could include associations of low ALT with pyridoxine deficiency [9,42], low levels of sex hormones [32,43], higher Nterminal pro-Brain natriuretic peptide (BNP, secreted by ventricular myocytes in response to…”

Effect of Omega-3 and Vitamins E + C Supplements on the Concentration of Serum B-Vitamins and Plasma Redox Aminothiol Antioxidant Status in Elderly Men after Strength Training for Three Months

“…Furthermore, bioavailability of intracellular folate, vitamin B12 and vitamin B2 modulates the concentration of p-tHcy. It has been reported that 5-PLP acts as an antioxidant, and decreased concentrations of 5-PLP may be associated with inflammation and CVD [47][48][49] . A decrease in the concentration of plasma 5-PLP in individuals who consumed vitamins E + C may suggest that an interaction between 5-PLP and vitamins E + C may have caused increased secretion or utilization of 5-PLP in the elderly on strength training.…”