Age, Disease, and Changing Sex Hormone Levels in Middle-Aged Men: Results of the Massachusetts Male Aging Study*

Abstract

To evaluate the hypothesis that endocrine profiles change with aging independently of specific disease states, we examined the age trends of 17 major sex hormones, metabolites, and related serum proteins in 2 large groups of adult males drawn from the Massachusetts Male Aging Study, a population-based cross-sectional survey of men aged 39-70 yr conducted in 1986-89. Group 1 consisted of 415 men who were free of obesity, alcoholism, all prescription medication, prostate problems, and chronic illness (cancer, coronary heart disease, hypertension, diabetes, and ulcer). Group 2 consisted of 1294 men who reported 1 or more of the above conditions. Each age trend was satisfactorily described by a constant percent change per yr between ages 39-70 yr. Free testosterone declined by 1.2%/yr, and albumin-bound testosterone by 1.0%/yr. Sex hormone-binding globulin (SHBG), the major serum carrier of testosterone, increased by 1.2%/yr, with the net effect that total serum testosterone declined more slowly (0.4%/yr) than the free or albumin-bound pools alone. Among the major androgens and metabolites, androstane-3 alpha,17 beta-diol (androstanediol; 0.8%/yr) and androstanediol glucuronide (0.6%/yr) declined less rapidly than free testosterone, while 5 alpha-dihydrotestosterone remained essentially constant between ages 39-70 yr. Androstenedione declined at 1.3%/yr, a rate comparable to that of free testosterone, while the adrenal androgen dehydroepiandrosterone (3.1%/yr) and its sulfate (2.2%/yr) declined 2-3 times more rapidly. The levels of testosterone, SHBG, and several androgen metabolites followed a parallel course in groups 1 and 2, remaining consistently 10-15% lower in group 2 across the age range of the study. Subgroup analyses suggested that obese subjects might be responsible for much of the group difference in androgen level. Serum concentrations of estrogens and cortisol did not change significantly with age or differ between groups. Of the pituitary gonadotropins, FSH increased at 1.9%/yr, LH increased at 1.3%/yr, and PRL declined at 0.4%/yr, with no significant difference between groups 1 and 2.(ABSTRACT TRUNCATED AT 400 WORDS)

Changes in BMI modulate age-associated changes in sex hormone binding globulin and total testosterone, but not bioavailable testosterone in young adult men: the CARDIA Male Hormone Study

“…[1][2][3][4][5][6][7] Additionally, there is an age-related increase in sex hormone binding globulin (SHBG), which binds about 44% of testosterone with high affinity. The non-SHBG-bound fraction of testosterone, the bioavailable testosterone fraction, appears to decrease with age.…”

“…2,5,7,[10][11][12][13][14][15] Because total testosterone decreases and SHBG increases with age, it is possible that the age-related decline in total testosterone and/or bioavailable testosterone might differ among men whose body mass index (BMI) remains stable, decreases or increases as they age. If the amount of weight change differentially affects the relationship of age with hormone and SHBG levels in men, then efforts at preventing or reducing weight gain could have important implications for the use of testosterone replacement therapy.…”

Modelling the influence of age, body size and sex on maximum oxygen uptake in older humans

“…Human growth hormone secretion declines after the age of 40, especially in men (Isaksson et al 1985). Testosterone levels in the men also decline with advancing age (Gray et al 1991;Proctor et al 1998) and this decline has been shown to be mirrored by a loss of LBM and muscular strength (Larsson & Karlsson 1978;Balagopal et al 1997). Older women do not experience such a rapid change in anabolic steroids and growth hormones with increasing age (Isaksson et al 1985), and thus they would tend not to experience such a decline in BM and FFM.…”

18F-FDG Uptake of Human Testis on PET/CT: Correlation with Age, Sex Hormones, and Vasectomy

“…The ability to assess glucose metabolism in a variety of tissues makes 18 F-fluoro-2-deoxyglucose ( 18 F-FDG) positron emission tomography (PET) a powerful diagnostic tool in the management of many cancers. 18 F-FDG accumulates in almost all cancer cells due to enhanced glycolysis, however it may also accumulate due to infection, inflammation, or physical activity, and it may be influenced by chemotherapy or high serum glucose level.…”

“…18 F-FDG accumulates in almost all cancer cells due to enhanced glycolysis, however it may also accumulate due to infection, inflammation, or physical activity, and it may be influenced by chemotherapy or high serum glucose level. 18 F-FDG also accumulates preferentially in the spleen, kidneys, liver, and brain.…”