Abstract:Objective: Although associations between testosterone and cardiovascular (CV) morbidity in women have been proposed, no large prospective study has evaluated potential associations between testosterone and mortality in women. The objective was to determine whether baseline testosterone levels in women are associated with future overall or CV morbidity and mortality. Design: Prospective cohort study with a 4.5-year follow-up period. Methods: From a representative sample of German primary care practices, 2914 fe… Show more
“…Sievers et al (2010) reported that low baseline testosterone in relatively older women is associated with increased all-cause mortality and cardiovascular events, which is largely independent of traditional risk factors. Low-dose testosterone supplementation improved functional capacity, insulin sensitivity and muscle strength in elderly female patients with chronic heart failure, and no androgenic side effects were detected (Iellamo et al 2010).…”
After menopause, the development of cardiovascular disease (CVD) is due not only to estrogen decline but also to androgen decline. This study examined the effects of either estradiol (E 2 ) or testosterone replacement alone or E 2 -testosterone combination on isolated myocytes in ovariectomized (Ovx) rats subjected to ischemia/reperfusion (I/R). Furthermore, we determined whether the effects are associated with b 2 -adrenoceptor (b 2 -AR). Five groups of adult female Sprague-Dawley rats were used: Sham operation (Sham) rats, bilateral Ovx rats, Ovx rats with E 2 40 mg/kg per day (OvxCE), Ovx rats with testosterone 150 mg/kg per day (OvxCT), and Ovx rats with E 2 40 mg/kg per dayC testosterone 150 mg/kg per day (OvxCE/T). We determined the lactate dehydrogenase (LDH) release, percentage of rod-shaped cells and apoptosis of ventricular myocytes from rats of all groups subjected to I/R. Then, we determined the above indices and contractile function with or without a selective b 2 -AR antagonist ICI 118 551. We also determined the expression of b 2 -AR. Our data show that either E 2 or testosterone replacement alone or E 2 and testosterone in combination decreased the LDH release, increased the percentage of rod-shaped cells, reduced apoptotic cells (%), and combination treatment appeared to be more effective than either E 2 or testosterone replacement alone. ICI 118 551 abolished the effects of the three. Combination supplementation also enhanced the expression of b 2 -AR. We concluded that in Ovx rats, testosterone enhances E 2 's cardioprotection, while E 2 and testosterone in combination was more effective and the protective effects may be associated with b 2 -AR. The study highlights the potential therapeutic application for CVD in postmenopausal women.
“…Sievers et al (2010) reported that low baseline testosterone in relatively older women is associated with increased all-cause mortality and cardiovascular events, which is largely independent of traditional risk factors. Low-dose testosterone supplementation improved functional capacity, insulin sensitivity and muscle strength in elderly female patients with chronic heart failure, and no androgenic side effects were detected (Iellamo et al 2010).…”
After menopause, the development of cardiovascular disease (CVD) is due not only to estrogen decline but also to androgen decline. This study examined the effects of either estradiol (E 2 ) or testosterone replacement alone or E 2 -testosterone combination on isolated myocytes in ovariectomized (Ovx) rats subjected to ischemia/reperfusion (I/R). Furthermore, we determined whether the effects are associated with b 2 -adrenoceptor (b 2 -AR). Five groups of adult female Sprague-Dawley rats were used: Sham operation (Sham) rats, bilateral Ovx rats, Ovx rats with E 2 40 mg/kg per day (OvxCE), Ovx rats with testosterone 150 mg/kg per day (OvxCT), and Ovx rats with E 2 40 mg/kg per dayC testosterone 150 mg/kg per day (OvxCE/T). We determined the lactate dehydrogenase (LDH) release, percentage of rod-shaped cells and apoptosis of ventricular myocytes from rats of all groups subjected to I/R. Then, we determined the above indices and contractile function with or without a selective b 2 -AR antagonist ICI 118 551. We also determined the expression of b 2 -AR. Our data show that either E 2 or testosterone replacement alone or E 2 and testosterone in combination decreased the LDH release, increased the percentage of rod-shaped cells, reduced apoptotic cells (%), and combination treatment appeared to be more effective than either E 2 or testosterone replacement alone. ICI 118 551 abolished the effects of the three. Combination supplementation also enhanced the expression of b 2 -AR. We concluded that in Ovx rats, testosterone enhances E 2 's cardioprotection, while E 2 and testosterone in combination was more effective and the protective effects may be associated with b 2 -AR. The study highlights the potential therapeutic application for CVD in postmenopausal women.
“…It is therefore possible that more recent studies may have greater power to detect an association between sex steroid levels and ischemic CVD risk. In support of this possibility, more recent prospective cohort studies [5,6,17,19,21,24,28] have tended to report the presence of significant relationships between endogenous sex steroids and ischemic CVD risk.…”
For decades, it has been recognized that men have a higher age-adjusted risk of ischemic cardiovascular (CVD) events compared to women, thus generating hypotheses that sex steroids contribute to CVD risk. Potential mechanisms include genomic and non-genomic effects of sex steroids as well as mediation through classic CVD risk factors and obesity. However, results from randomized studies suggest that sex steroid supplementation in men and women do not result in improved CVD outcomes and may increase CVD risk. In contrast, prospective observations from endogenous sex steroid studies, i.e. among participants not using sex steroids, have suggested the opposite relationship. We reviewed the findings of prospective observational studies in men (17 studies) and women (8 studies) that examined endogenous sex steroids and CVD risk. These studies suggested a lack of association or that lower levels of testosterone or dihydrotestosterone are associated with higher CVD risk in both men and women. Higher, rather than lower, estradiol levels were associated with higher CVD risk in women. There were several significant gaps in the literature. First, it is unclear whether more sensitive measures of sex steroid levels might detect significant differences. Second, there are few prospective studies in women. Similarly, no studies report outcomes for high-risk groups such as African-Americans and Hispanics. Finally, few studies report upon ischemic coronary disease as opposed to ischemic stroke separately, although relationships between sex steroids and CVD may vary by vascular bed. Future investigations need to examine high risk groups and to distinguish between subtypes of CVD.
“…Elevated testosterone levels and low levels of sex hormone-binding globulin have been found to be positively associated with CV risk factors and the metabolic syndrome in postmenopausal women [3,4]. However, others have reported an increased CV morbidity and mortality in postmenopausal women with low testosterone levels [5,6]. …”
Section: Introductionmentioning
confidence: 99%
“…In premenopausal women, hyperandrogenism, such as is present in polycystic ovary syndrome, is associated with adverse metabolic effects. In postmenopausal women, however, various studies have reported conflicting results in CV outcomes in association with high- as well as low-circulating testosterone levels [3,4,5,6]. …”
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