© 2000 American Heart Association, Inc.
Atherosclerosis and Lipoproteins |
No Association Between Dehydroepiandrosterone Sulfate and Development of Atherosclerosis in a Prospective Population Study (Bruneck Study)
From the Department of Neurology (S.K., J.W.) and the Institute of General and Experimental Pathology (S.S.), University of Innsbruck, Innsbruck, Austria; the Division of Endocrinology and Metabolism (E.B.), University of Verona, Verona, Italy; and the Institute for Biomedical Aging Research (Q.X.), Austrian Academy of Science, Innsbruck, Austria.
Correspondence to Dr S. Kiechl, Department of Neurology, Innsbruck University Hospital, Anichstr. 35, A-6020 Innsbruck, Austria.
Abstract—Antiatherogenic
properties of dehydroepiandrosterone (DHEA) have been postulated for
>40 years. Large-scale epidemiological studies on this important
issue, however, are still sparse, and those available have yielded
contradictory results. The Bruneck Study involved a large random sample
of men and women aged 40 to 79 years that were enrolled in 1990 and
reevaluated 5 years later. Baseline DHEA sulfate (DHEAS) levels were
measured in 867 subjects after an overnight fast. Development and
progression of carotid atherosclerosis was monitored by
high-resolution duplex ultrasound. DHEAS levels declined with advancing
age (29% and 44% per decade in men and women) and showed a complex
sex-specific association with various vascular risk attributes and
factors conferring protection against atherosclerosis.
Age- and sex-adjusted DHEAS baseline levels did not differ between
subjects with or without incident/progressive
atherosclerosis (geometric mean 1161 versus 1253
µg/L). After adjustment for vascular risk factors and potential
confounders, the odds ratio of incident/progressive
atherosclerosis comparing a 50% increase in DHEAS
levels was 0.99 (95% CI 0.89 to 1.11). Lack of an association between
DHEAS and atherogenesis was confirmed in sex-specific and a variety of
supplementary analyses. Statistical power would be high enough
to detect differences in DHEAS between outcome categories as low as
15% (
=0.05). This prospective community-based study does not
support a role for endogenous DHEA(S) in the development of
human atherosclerosis.
Key Words: dehydroepiandrosterone • atherosclerosis • aging • insulin resistance • risk factors
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