Vitamin E, Inflammatory/Immune Response, and the Elderly

Aging is a complex biological phenomenon in which the deficiency of the nutritional state combined with the presence of chronic inflammation and oxidative stress contribute to the development of many age-related diseases. Under this profile, the free radicals produced by the oxidative stress lead to the damage of DNA, lipids, and proteins with subsequent altered cellular homeostasis and integrity, in particular in cells of the immune system. Supplementation with vitamin E can protect against the deteriorating effects of oxidative stress, progression of degenerative diseases, altered inflammatory/immune response, and aging. Such a protective role has been well documented in immune cells from old animals describing how the vitamin E works both at cytoplasmaic and nuclear levels with an influence on many genes related to the inflammatory/immune response. All these findings have supported a lot of clinical trials in old humans and in inflammatory age-related diseases, which, however, have given contradictory and inconsistent results and even indicated a dangerous role of vitamin E in being able to affect mortality. Various factors can contribute to all the discrepancies, especially the doses and the various isoforms of vitamin E family (?, ?, ?, ?) tocopherols and the corresponding tocotrienols used in different trials. However, the more plausible gap is the poor consideration of the vitamin E-gene interactions that may open new roadmaps for a correct and personalized vitamin E supplementation in aging and age-related diseases with satisfactory results in order to reach healthy aging and longevity. This peculiar nutrigenomic and/or nutrigenetic aspect is herein reported and discussed in the light of specific polymorphisms affecting vitamin E bioactivity.