Dehydroepiandrosterone (DHEA) is an endogenous steroid hormone. It is the most abundant circulating steroid hormone in humans, in whom it is produced in the adrenal glands, the gonads, and the brain.
DHEA is present in the blood serum as DHEA- Sulfate (DHEA-S). The level of DHEA-S declines dramatically with age.
A study conducted by the American College of Cardiology Foundation in October 2014, tested the hypothesis that serum DHEA and DHEA-S are predictors of major coronary heart disease (CHD) and/or cerebrovascular disease (CBD) events in a large cohort of elderly men. 1
The study used data from Osteoporotic Fractures in Men study in Sweden (2,416 men, ages 69 to 81 years).
The study period lasted 5 years. In that time, 302 participants experienced a CHD event, and 225 had a CBD event.
The 302 CHD participants showed low levels of both DHEA and DHEA-S, whereas, the DHEA/-S showed no statistically significant association with the risk of CBD events. The study also took into consideration and adjusted for traditional cardiovascular risk factors, serum total testosterone and estradiol, C-reactive protein, and renal function. Even after these considerations, the association between DHEA and CHD risk remained significant.
The authors of the study concluded:
“Low serum levels of DHEA and its sulfate predict an increased risk of CHD, but not CBD, events in elderly men.” 2
In another study from 1995, published in the Annals of the New York Academy of Sciences, the Department of Family and Preventive Medicine, University of California, San Diego found that:
“In 1986 the authors reported that high levels of plasma dehydroepiandrosterone sulfate (DHEAS) reduced the risk of fatal cardiovascular disease (CVD) in 242 men and increased the risk in 289 women from the Rancho Bernardo cohort who were followed up for 12 years. The authors report here an update on the epidemiology of DHEAS and CVD based on a 19-year follow-up of 1,029 men and 942 women aged 30-88 years from the same cohort. In cross-sectional analyses, DHEAS levels decreased with age in both sexes and were lower in women than men.
Men who were overweight were more likely to have low DHEAS levels; women who had hypercholesterolemia or hypertension or were nonusers of estrogen therapy had higher DHEAS levels.
Alcohol intake and cigarette smoking were associated with higher DHEAS levels in both sexes. All differences were no longer statistically significant after adjusting for alcohol intake. All participants were followed for vital status.
After 19 years there were 254 CVD deaths in men and 199 CVD deaths in women. DHEAS was not associated with CVD or ischemic heart disease (IHD) deaths in age-adjusted analyses where the comparison group was individuals without CVD or IHD death. In contrast, when the comparison group was survivors, multiply adjusted models showed a statistically significant, modestly reduced risk of fatal CVD (RR = 0.85) in men and a nonsignificant increased risk of fatal CVD (RR = 1.11) in women.
This epidemiological study found that a 100 ug/dL increase in blood DHEAS is associated with a 48% reduction in cardiovascular disease mortality.” 3
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