Androgen levels show inverse correlation with coronary artery diseases


Androgen levels show inverse correlation with coronary artery diseases
by Anthony Roberts

Although the anti-steroid crowd likes to claim that testosterone is the cause for everything from prostate cancer to heart disease, a recent study has suggested that decreases in free testosterone and Androgen receptor levels can accelerate the progression of coronary atherosclerosis. It’s interesting to note that a decade or two ago, we were told that prostate disease was related to testosterone levels, that they caused Lyle Alzado’s cancer, and a bunch of other nonsense – while nearly all of the current research seems to swing towards the other end of the spectrum, showing modest health improvements for those with higher androgen levels and yes…even for those who use anabolic steroids.

Zhonghua Yi Xue Za Zhi. 2011 Apr;91(14):984-986.
[Correlation of endogenous androgen and androgen receptor level with coronary artery diseases in elderly males.]
[Article in Chinese]
Zhang XJ, Li XY, Cao TT, Ye L.
Source

Department of Geriatric Cardiology, Chinese PLA General Hospital, Beijing 100853, China.

Abstract
OBJECTIVE:

To investigate the correlation of endogenous androgen and androgen receptor (AR) level with coronary artery diseases (CAD) in elderly males and elucidate the potential mechanism of gender difference in the prevalence of CAD.
METHODS:

A total of 296 male patients from different centers were divided into the CAD group (n = 237) and the control group (n = 59) according to the results of coronary angiography. Their mean ages were 68.6 ± 6.8 and 66.2 ± 6.5 years old respectively. The serum levels of FT (free testosterone), TT (total testosterone), E2 (estradiol), LH (luteinizing hormone), FSH (follicle-stimulating hormone), SHBG (sex hormone-binding globulin) and DHEA (dehydroepiandrosterone) were measured in all participants. And the androgen receptors of peripheral lymphocytes were assessed by flow cytometry.
RESULTS:

The serum level of FT was lower in the CAD group than that in the control group [(24.1 ± 22.2) × 10(-9) mmol/L vs (34.1 ± 31.8) × 10(-9) mmol/L, P = 0.06]. But two groups showed no statistic differences in the levels of TT, E(2), LH, FSH, SHBG, DHEA and lymphocyte AR (56.3% ± 24.00 vs 57.1% ± 20.8%). As demonstrated by the logistic regression analysis, the level of FT was negatively correlated with the CAD risk (OR = 0.98, P = 0.0049) and positively correlated with the peripheral lymphocyte AR level. However age was negatively correlated with the levels of FT and AR.

CONCLUSION:
The deficiency of endogenous androgen contributes to a high prevalence of CAD in elderly males. The age-related decreases of FT and AR impair the physiological functions of androgen so as to accelerate the progression of coronary atherosclerosis.

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