Aging, physical activity, insulin-like growth factor I, and body composition in Guatemalan women.

Aging is associated with diminished secretion of growth hormone and the major endogenous mediator of growth hormone action, insulin-like growth factor I (IGF-I). Aging is also associated with decreased physical activity. Alterations in body composition characteristic of the aging process (increased fat mass and decreased lean body mass) may be related to the decline in anabolic effects of IGF-I with aging, decreased physical activity, or both. Guatemalan women often maintain a high level of physical activity during aging. The purpose of this study was to determine whether IGF-I concentrations correlated with physical activity level (determined by standardized scoring of a self-report questionnaire) and body composition (determined by bioelectrical impedance analysis) in elderly Guatemalan women. In 112 women aged 20-87 y, we found a progressively lower serum IGF-I with age (r = -0.732). In subjects > 60 y of age, the self-reported activity level was associated with a lower percentage body fat (P < 0.001) but there was no significant relation between physical activity level and either lean body mass or IGF-I. We conclude that there is a significant age-related decline in serum IGF-I concentrations in Guatemalan women, similar to that observed in both men and women in the United States. An increased level of physical activity in the elderly Guatemalan population was associated with reduced body fat but did not modify the expected reduction in circulating IGF-I concentrations that occurs with aging.

Prevalence of medium-chain acyl-coenzyme A dehydrogenase deficiency in the sudden infant death syndrome.

Disorders of fatty acid beta-oxidation have been suggested as playing a significant role in the sudden infant death syndrome (SIDS). To elucidate the role of medium-chain acyl-coenzyme A dehydrogenase (MCAD) deficiency in SIDS, we identified all cases of SIDS occurring in Los Angeles County between January 1986 through December 1991. A total of 1304 SIDS deaths were identified; tissue samples were collected in 1236 cases (94.8%). Extraction of DNA was successful in 1224 tissue samples (93.9%), which were examined for the presence of the G985 mutation, identified as occurring in more than 88% of affected cases of MCAD deficiency. Three heterozygotes and no homozygotes were identified; this incidence does not differ from that reported in the general population. Review of the pathologic specimens from the identified heterozygotes and from 18 ethnic-, age-, and sex-matched control subjects revealed significant fatty infiltration of all organs examined in one of the three heterozygotes and in none of the control subjects. We conclude that MCAD deficiency does not play a significant role in the causation of SIDS.