Micronutrients prevent cancer and delay aging

Approximately 40 micronutrients are required in the human diet. Deficiency of vitamins B-12, folic acid, B-6, niacin, C, or E, or iron, or zinc, appea rs to mimic radiation in damaging DNA by causing single- and double-strand breaks, oxidative lesions, or both. The percentage of the US population tha t has a low intake (< 50% of the RDA) for each of these eight micronutrient s ranges from 2% to greater than or equal to 20%; half of the population ma y be deficient in at least one of these micronutrients. Folate deficiency o ccurs in approximately 10% of the US population, and in a much higher perce ntage of the poor. Folate deficiency causes extensive incorporation of urac il into human DNA (4 million/cell), leading to chromosomal breaks. This mec hanism is the likely cause of the increased cancer risk, and perhaps the co gnitive defects associated with low folate intake. Same evidence, and mecha nistic considerations, suggest that vitamin B-12 and B-6 deficiencies also cause high uracil and chromosome breaks. Micronutrient deficiency may expla in, in good part, why the quarter of the population that eats the fewest fr uits and vegetables (five portions a day is advised) has approximately doub le the cancer rate for most types of cancer when compared to the quarter wi th the highest intake. Eighty percent of American children and adolescents and 68% of adults do not eat five portions a day. Common micronutrient defi ciencies are likely to damage DNA by the same mechanism as radiation and ma ny chemicals, appear to be orders of magnitude more important, and should b e compared for perspective. Remedying micronutrient deficiencies is likely to lead to a major improvement in health and an increase in longevity at lo w cost. Aging appears to be due, in good part, to the oxidants produced by mitochon dria as by-products of normal metabolism. In old rats mitochondrial membran e potential, cardiolipin levels, respiratory control ratio, and overall cel lular O-2 consumption are lower than in young rats, and the level of oxidan ts (per unit O-2) is higher. The level of mutagenic aldehydes from lipid pe roxidation is also increased. Ambulatory activity declines markedly in old rats. Feeding old rats the normal mitochondrial metabolites acetyl carnitin e and lipoic acid for a few weeks, restores mitochondrial function, lowers oxidants to the level of a young rat, and increases ambulatory activity. Th us,these two metabolites can be considered necessary for health in old age and are therefore conditional micronutrients. This restoration suggests a p lausible mechanism: with age-increased oxidative damage to proteins and lip id membranes causes a deformation of structure of key enzymes, with a conse quent lessening of affinity (K-m) for the enzyme substrate; an increased le vel of the substrate restores the velocity of the reaction, and thus restor es function. (C) 1998 Elsevier Science Ireland Ltd. All rights reserved.