We provide current, normative data on the prevalence of impotence, and its physiological and psychosocial correlates in a general population using results from the Massachusetts Male Aging Study. The Massachusetts Male Aging Study was a community based, random sample observational survey of noninstitutionalized men 40 to 70 years old conducted from 1987 to 1989 in cities and towns near Boston, Massachusetts. Blood samples, physiological measures, socio-demographic variables, psychological indexes, and information on health status, medications, smoking and lifestyle were collected by trained interviewers in the subject's home. A self-administered sexual activity questionnaire was used to characterize erectile potency. The combined prevalence of minimal, moderate and complete impotence was 52%. The prevalence of complete impotence tripled from 5 to 15% between subject ages 40 and 70 years. Subject age was the variable most strongly associated with impotence. After adjustment for age, a higher probability of impotence was directly correlated with heart disease, hypertension, diabetes, associated medications, and indexes of anger and depression, and inversely correlated with serum dehydroepiandrosterone, high density lipoprotein cholesterol and an index of dominant personality. Cigarette smoking was associated with a greater probability of complete impotence in men with heart disease and hypertension. We conclude that impotence is a major health concern in light of the high prevalence, is strongly associated with age, has multiple determinants, including some risk factors for vascular disease, and may be due partly to modifiable para-aging phenomena.

Although prevalence estimates and cross-sectional correlates of erectile dysfunction have recently been established, incidence estimates were lacking. Incidence is necessary to assess risk, and plan treatment and prevention strategies. The risk of erectile dysfunction was about 26 cases per 1,000 men annually, and increased with age, lower education, diabetes, heart disease and hypertension.

We used longitudinal data from the Massachusetts Male Aging Study, a large population-based random-sample cohort of men aged 40 -70 yr at baseline, to establish normative age trends for serum level of T and related hormones in middle-aged men and to test whether general health status affected the age trends. Of 1,709 men enrolled in 1987-1989, 1,156 were followed up 7-10 yr afterward. By repeated-measures statistical analysis, we estimated simultaneously the cross-sectional age trend of each hormone between subjects within the baseline data, the cross-sectional trend between subjects within the follow-up data, and the longitudinal trend within subjects between baseline and follow-up.Total T declined cross-sectionally at 0.8%/yr of age within the follow-up data, whereas both free and albumin-bound T declined at about 2%/yr, all significantly more steeply than within the baseline data. Sex hormone-binding globulin increased cross-sectionally at 1.6%/yr in the follow-up data, similarly to baseline. The longitudinal decline within subjects between baseline and follow-up was considerably steeper than the cross-sectional trend within measurement times for total T (1.6%/yr) and bioavailable T (2-3%/yr). Dehydroepiandrosterone, dehydroepiandrosterone sulfate, cortisol, and estrone showed significant longitudinal declines, whereas dihydrotestosterone, pituitary gonadotropins, and PRL rose longitudinally.Apparent good health, defined as absence of chronic illness, prescription medication, obesity, or excessive drinking, added 10 -15% to the level of several androgens and attenuated the cross-sectional trends in T and LH but did not otherwise affect longitudinal or cross-sectional trends.The paradoxical finding that longitudinal age trends were steeper than cross-sectional trends suggests that incident poor health may accelerate the age-related decline in androgen levels. (J Clin Endocrinol Metab 87: 589 -598, 2002)

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)

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OBJECTIVE -Short-term partial sleep restriction results in glucose intolerance and insulin resistance. The purpose of this study was to assess the long-term relationship between sleep duration and the incidence of clinical diabetes. RESEARCH DESIGN AND METHODS -A cohort of men from the MassachusettsMale Aging Study without diabetes at baseline (1987)(1988)(1989) were followed until 2004 for the development of diabetes. Average number of hours of sleep per night was grouped into the following categories: Յ5, 6, 7, 8, and Ͼ8 h. Incidence rates and relative risks (RRs) were calculated for the development of diabetes in each sleep duration category. Those reporting 7 h of sleep per night served as the reference group. Multivariate analysis was performed using Poisson regression.RESULTS -Men reporting short sleep duration (Յ5 and 6 h of sleep per night) were twice as likely to develop diabetes, and men reporting long sleep duration (Ͼ8 h of sleep per night) were more than three times as likely to develop diabetes over the period of follow-up. Elevated risks remained essentially unchanged after adjustment for age, hypertension, smoking status, self-rated health status, education, and waist circumference .01] for Յ5 h and 3.12 [1.53-6.37] for Ͼ8 h). RRs were altered considerably for the two extreme sleep groups when adjusted for testosterone (1.51 [0.71-3.19] for Յ5 h and 2.81 [1. 34 -5.90] for Ͼ8 h), suggesting that the effects of sleep on diabetes could be mediated via changes in endogenous testosterone levels.CONCLUSIONS -Short and long sleep durations increase the risk of developing diabetes, independent of confounding factors. Sleep duration may represent a novel risk factor for diabetes. Diabetes Care 29:657-661, 2006D iabetes remains a critical public health challenge. The prevalence of diabetes continues to increase, and it affects an estimated 18 million people in the U.S. (1-3). Patients with diabetes require frequent contact with the health care system for effective management and prevention of complications, and they are at increased risk for premature mortality and hospitalization for conditions such as cardiovascular and kidney disease. Although lifestyle changes such as weight loss and increasing physical activity are the cornerstone of diabetes prevention, efforts are needed to better understand other determinants of the disease and to develop additional prevention strategies. Understanding the link between diabetes and sleep may represent one important part of that effort.Sleep loss is a common condition in modern society, with evidence showing that we are sleeping on average only 6.8 h per night, which is 1.5 h less than we did a century ago (4,5). Nearly one-third of adults report sleeping Ͻ6 h per night, leading some to suggest we live in a sleepdeprived society (6). Factors responsible for this change include increases in environmental light, longer work days/ commuting time, an increase in shift and night work, and the advent of television, radio, and the Internet (7).We are only beginning to reco...

Prevalence of symptomatic androgen deficiency in men 30 and 79 yr of age is 5.6% and increases substantially with age. The aging of the U.S. male population will cause a large increase in the burden of symptomatic androgen deficiency. Future work should address the clinical significance of low testosterone levels in asymptomatic men.

RESEARCH DESIGN AND METHODS -Analyses were conducted on the cohort of the Massachusetts Male Aging Study, a population-based random sample of men aged 40-70. Of the 1,709 men enrolled in 1987-1989 (T 1 ), 1,156 were followed up 7-10 years later (T 2 ). Te s t o st e rone and SHBG levels at T 1 w e re used to predict new cases of diabetes between T 1 and T 2 . R E S U LT S -After controlling for potential confounders, diabetes at follow-up was pre d i c t e d jointly and independently by lower baseline levels of free testosterone and SHBG. The odds ratio for future diabetes was 1.58 for a decrease of 1SD in free testosterone (4 ng/dl) and 1.89 for a 1SD decrease in SHBG (16 nmol/l), both significant at P 0 . 0 2 .C O N C L U S I O N S -Our prospective findings are consistent with previous, mainly cro s ssectional re p o rts, suggesting that low levels of testosterone and SHBG play some role in the development of insulin resistance and subsequent type 2 diabetes. Diabetes Care 2 3 :4 9 0-494, 2000