Vitamins in the prevention or delay of cognitive disability of aging.Curr Aging Sci. 2014; 7(3):187-213.CA
During the 20th century, the average lifespan in the industrialized societies has enormously increased and it is still rising. With the increase in the number of old people, a parallel increase in the number of the disabled elderly is postulated. Thus, the whole society might suffer from an imbalance between the productive segment of the society and a huge segment of helpless people. Moderation of the physiological processes, which enhance disability in aging, turns out to be a major concern in health research and clinical practice. Preservation of brain integrity, which is partly influenced by nutrition, presumably is the main target in the attempt to delay the development of disability of aging. Optimal micronutrient status would moderate the deterioration in brain integrity. The human brain is probably the most vulnerable tissue affected by a long-term unbalanced nutrition and is particularly vulnerable to reactive oxygen species and to oxidative stress, because of its high oxygen requirement, its iron storage capacity and its elevated polyunsaturated fatty acid content, and because of its low synthesis capacity of endogenous antioxidants. The capability of central nervous system (CNS) cells to regenerate is most limited, because their repair is inhibited by anti-apoptotic molecules. Efficient autophagy is the major mechanism that moderates accumulation of aggregating compounds. Autophagy is probably a crucial and a major process in the preservation of brain integrity. Micronutrients (vitamins, trace-elements and also antioxidants) most likely affect brain integrity by normalizing efficient autophagy. Brain sensitivity to metabolic disorders is demonstrated by the effect of homocysteine on metabolic pathways, on brain integrity and on the cognitive capacity. Brain imaging might be used as a surrogate for detecting long-lasting low status of micronutrients. Comprehensive evaluation of brain scans concomitantly with blood micronutrient examinations may provide reliable criteria for the estimation of the optimal micronutrient intakes or blood concentrations. Recommended dietary intakes for micronutrients are based on a list of biomarkers, but have not been suggested a safe range for their intake or blood concentration. According to many studies, a U-shaped curve prevails for the effect of serum calcidiol concentration on the relative risk of morbidity and mortality. An increased relative risk of morbidity and mortality with lower serum calcidiol has been shown in almost all the studies. A safe range of 20-40 ng/mL was identified for serum calcidiol. A significant detrimental effect of serum calcidiol on the hazard ratio for the combined data of all-cause mortality and acute coronary syndrome morbidity was shown at a concentration higher than 36 ng/ml. Most of the tolerable upper intake levels for the micronutrients, published by authorized institutions, were set without considering the long-term effects of overdosing. Excessive intake of almost all the micromutrients, particularly for a long period of time, produces adverse effects. In most of the elderly people prevail an insufficient intake of one or more micronutruients. Therefore, until an efficient laboratory system for evaluating blood levels is established, a moderate 'multivitamin' supplementation at an amount of about half the American RDA for most of the micronutrients is suggested.