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Objective: Several clinical and population-based studies suggest that dehydroepiandrosterone (DHEA) and its sulphate (DHEA-S) play a protective role against atherosclerosis and coronary artery disease in human. However, the mechanisms underlying this action are still unknown. It has recently been suggested that DHEA-S could delay atheroma formation through an increase in nitric oxide (NO) production.

Study design and methods: Twenty-four aged male subjects [age (mean /- SEM): 65[middle dot]4 /- 0[middle dot]7 year; range: 58[middle dot]2-67[middle dot]6 years] underwent a blinded placebo controlled study receiving DHEA (50 mg p.o. daily at bedtime) or placebo for 2 months. Platelet cyclic guanosine-monophosphate (cGMP) concentration (as marker of NO production) and serum levels of DHEA-S, DHEA, IGF-I, insulin, glucose, oestradiol (E2), testosterone, plasminogen activator inhibitor (PAI)-1 antigen (PAI-1 Ag), homocysteine and lipid profile were evaluated before and after the 2-month treatment with DHEA or placebo.

Results: At the baseline, all variables in the two groups were overlapping. All parameters were unchanged after treatment with placebo. Conversely, treatment with DHEA (a) increased (P < 0[middle dot]001 vs. baseline) platelet cGMP (111[middle dot]9 /- 7[middle dot]1 vs. 50[middle dot]1 /- 4[middle dot]1 fmol/106 plts), DHEA-S (13[middle dot]6 /- 0[middle dot]8 vs. 3[middle dot]0 /- 0[middle dot]3 [mu]mol/l), DHEA (23[middle dot]6 /- 1[middle dot]7 vs. 15[middle dot]3 /- 1[middle dot]4 nmol/l), testosterone (23[middle dot]6 /- 1[middle dot]0 vs. 17[middle dot]7 /- 1[middle dot]0 nmol/l) and E2 (72[middle dot]0 /- 5[middle dot]0 vs. 60[middle dot]0 /- 4[middle dot]0 pmol/l); and (b) decreased (P < 0[middle dot]05 vs. baseline) PAI-1 Ag (27[middle dot]4 /- 3[middle dot]8 vs. 21[middle dot]5 /- 2[middle dot]5 ng/ml) and low-density lipoprotein (LDL) cholesterol (3[middle dot]4 /- 0[middle dot]2 vs. 3[middle dot]0 /- 0[middle dot]2 mmol/l). IGF-I, insulin, glucose, triglycerides, total cholesterol, HDL cholesterol, HDL2 cholesterol, HDL3 cholesterol, apolipoprotein A1 (ApoA1), apolipoprotein B (ApoB) and homocysteine levels were not modified by DHEA treatment.

Conclusions: This study shows that short-term treatment with DHEA increased platelet cGMP production, a marker of NO production, in healthy elderly subjects. This effect is coupled with a decrease in PAI-1 and LDL cholesterol levels as well as an increase in testosterone and E2 levels. These findings, therefore, suggest that chronic DHEA supplementation would exert antiatherogenic effects, particularly in elderly subjects who display low circulating levels of this hormone.

Copyright (C) 2006 Blackwell Publishing Ltd.