Endogenous hormones and carotid atherosclerosis in elderly men

AW Van den Beld, ML Bots, J Janssen… - American journal of …, 2003 - academic.oup.com
AW Van den Beld, ML Bots, J Janssen, HAP Pols, SWJ Lamberts, DE Grobbee
American journal of epidemiology, 2003academic.oup.com
The aging process is characterized by a number of gradual changes in circulating hormone
concentrations as well as a gradual increase in the degree of atherosclerosis. The authors
studied whether serum hormone levels are related to atherosclerosis of the carotid artery in
independently living, elderly men. In 1996, 403 men (aged 73–94 years) were randomly
selected from the general population of Zoetermeer, the Netherlands. Carotid artery intima-
media thickness was determined. Serum concentrations of testosterone; estrone; estradiol; …
Abstract
The aging process is characterized by a number of gradual changes in circulating hormone concentrations as well as a gradual increase in the degree of atherosclerosis. The authors studied whether serum hormone levels are related to atherosclerosis of the carotid artery in independently living, elderly men. In 1996, 403 men (aged 73–94 years) were randomly selected from the general population of Zoetermeer, the Netherlands. Carotid artery intima-media thickness was determined. Serum concentrations of testosterone; estrone; estradiol; dehydroepiandrosterone and dehydroepiandrosterone sulfate; insulin-like growth factor I (IGF-I) (total and free) and its binding proteins IGFBP-1, IGFBP-2, and IGFBP-3; and leptin were measured. After the authors adjusted for age, serum testosterone, estrone, and free IGF-I were inversely related to intima-media thickness. The strength of these relations was as powerful in subjects with as in those without prevalent cardiovascular disease. Serum estradiol; dehydroepiandrosterone sulfate; total IGF-I, IGFBP-1, IGFBP-2, and IGFBP-3; and leptin showed no association. These findings suggest that endogenous testosterone, estrone, and free IGF-I levels may play a protective role in the development of atherosclerosis in aging men.
Oxford University Press