To investigate whether a population-level decline in serum testosterone exists in Finnish men. In comparison with other European populations, Finnish men have compared well in the studies of reproductive health (i.e. semen quality, incidence of cryptorchidism and testicular cancer); thus, we expected no significant cohort-dependent decrease in serum testosterone.
We analysed serum levels of testosterone, gonadotrophin and sex hormone binding globulin (SHBG) in 3271 men representing different ages (25-74 years) and birth cohorts within three large Finnish population surveys conducted in 1972, 1977 and 2002.
Serum testosterone levels decreased (from 25.3 nmol/l in 25- to 29-year-old men gradually to 16.9 nmol/l in 70- to 74-year-old men), whereas SHBG and gonadotrophin levels increased with increasing age. In addition, a significant secular trend in testosterone (total and free), SHBG and gonadotrophin levels was observed with lower levels in more recently born age-matched men. Serum testosterone level decreased in men aged 60-69 years from 21.9 nmol/l (men born 1913-1922) to 13.8 nmol/l (men born 1942-1951). These decreases remained significant following adjustment for BMI. An age-independent birth cohort effect existed on reproductive hormones measured in the Finnish men. In concert with the lower free testosterone levels, we observed lower gonadotrophin levels, suggesting that while there may be detrimental changes at the gonad level, the hypothalamus-pituitary-axis is not responding appropriately to this change.
The more recently born Finnish men have lower testosterone levels than their earlier born peers. This study offers no explanation for this substantial recent adverse development.
"Cross-sectional studies have associated low testosterone levels with increased cardiovascular risk factors (diabetes mellitus, the metabolic syndrome, abnormal lipid profile) and increased cardiovascular risk in men.2–5 This is particularly important given the progressive population-level decline in serum testosterone concentrations in men from developed countries6–8 which has resulted in a dramatic increase in the use of androgen replacement therapy (ART). Indeed, there has been a 10-fold increase in prescribed ART in the USA9 and nearly a 3-fold increase in the UK10 in the past decade. "
[Show abstract][Hide abstract] ABSTRACT: Aims
Low androgen levels have been linked with an increased risk of cardiovascular disease in men. Previous studies have suggested that androgens directly inhibit atherosclerotic lesion formation although the underlying mechanisms for this remain unclear. This study addressed the hypothesis that endogenous androgens inhibit arterial remodelling by a direct action on the androgen receptor (AR) in the vascular wall.
Methods and results
We studied a series of novel mouse lines with cell-specific deletion of the AR in either the endothelium or in smooth muscle cells or both cell types. Findings were compared with a model of global androgen deficiency in wild-type mice (castrated). We characterized the cardiovascular phenotype, vascular pharmacology and histology, and assessed neointimal lesion formation following vascular injury to the femoral artery. Cell-specific AR deletion did not alter body weight, circulating testosterone levels or seminal vesicle weight, but caused limited alterations in arterial contractility and blood pressure. Neointimal lesion formation was unaltered by selective deletion of AR from the vascular endothelium, smooth muscle, or both cell types. Castration in wild-type mice increased neointimal lesion volume (Sham vs. Castration: 2.4 × 107 ± 4.5 × 106 vs. 3.9 × 107 ± 4.9 × 106 µm3, P = 0.04, n = 9–10).
Vascular cell-specific AR deletion had no effect on neointimal lesion formation, while low systemic androgen levels adversely affect neointimal lesion size. These findings suggest that the cardio-protective effects of androgens are mediated either by AR outside the vasculature or by AR-independent mechanisms.
Cardiovascular Research 06/2014; 103(2). DOI:10.1093/cvr/cvu142 · 5.94 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The testosterone of men in industrial societies peaks in their twenties and tends to decline with increasing age. Apart from this individual-level decline, there have been reports of a secular (age-independent population-level) decline in testosterone among American and Scandinavian men during the past few decades, possibly an indication of declining male reproductive health. It has been suggested that both declines in testosterone (individual-level and population-level) are due to increasing male obesity because men in industrial society tend to add body fat as they age, and overall rates of obesity are increasing. Using an unusually large and lengthy longitudinal dataset (991 US Air Force veterans examined in six cycles over 20 years), we investigate the relationship of obesity to individual and population-level declines in testosterone. Over twenty years of study, longitudinal decline in mean testosterone was at least twice what would be expected from cross-sectional estimates of the aging decline. Men who put on weight intensified their testosterone decline, some greatly so, but even among those who held their weight constant or lost weight during the study, mean testosterone declined 117 ng/dl (19%) over 20 years. We have not identified the reason for secular decline in testosterone, but we exclude increasing obesity as a sufficient or primary explanation, and we deny the supposition that men who avoid excessive weight will maintain their youthful levels of testosterone.
PLoS ONE 10/2013; 8(10):e76178. DOI:10.1371/journal.pone.0076178 · 3.23 Impact Factor
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