OBJECTIVES: To examine in an older population all‐cause and cause‐specific mortality associated with underweight (body mass index (BMI)<18.5), normal weight (BMI 18.5–24.9), overweight (BMI 25.0–29.9), and obesity (BMI≥30.0). DESIGN: Cohort study. SETTING: The Health in Men Study and the Australian Longitudinal Study of Women's Health. PARTICIPANTS: Adults aged 70 to 75, 4,677 men and 4,563 women recruited in 1996 and followed for up to 10 years. MEASUReMENTS: Relative risk of all‐cause mortality and cause‐specific (cardiovascular disease, cancer, and chronic respiratory disease) mortality. RESULTS: Mortality risk was lowest for overweight participants. The risk of death for overweight participants was 13% less than for normal‐weight participants (hazard ratio (HR)=0.87, 95% CI=0.78–0.94). The risk of death was similar for obese and normal‐weight participants (HR=0.98, 95% CI=0.85–1.11). Being sedentary doubled the mortality risk for women across all levels of BMI (HR=2.08, 95% CI=1.79–2.41) but resulted in only a 28% greater risk for men (HR=1.28 (95% CI=1.14–1.44). CONCLUSION: These results lend further credence to claims that the BMI thresholds for overweight and obese are overly restrictive for older people. Overweight older people are not at greater mortality risk than those who are normal weight. Being sedentary was associated with a greater risk of mortality in women than in men.

Background: Dementia is a growing problem, causing substantial burden for patients, their families, and society. General practitioners (GPs) play an important role in diagnosing and managing dementia; however, there are gaps between recommended and current practice. The aim of this study was to explore GPs’ reported practice in diagnosing and managing dementia and to describe, in theoretical terms, the proposed explanations for practice that was and was not consistent with evidence-based guidelines. Methods: Semi-structured interviews were conducted with GPs in Victoria, Australia. The Theoretical Domains Framework (TDF) guided data collection and analysis. Interviews explored the factors hindering and enabling achievement of 13 recommended behaviours. Data were analysed using content and thematic analysis. This paper presents an in-depth description of the factors influencing two behaviours, assessing co-morbid depression using a validated tool, and conducting a formal cognitive assessment using a validated scale. Results: A total of 30 GPs were interviewed. Most GPs reported that they did not assess for co-morbid depression using a validated tool as per recommended guidance. Barriers included the belief that depression can be adequately assessed using general clinical indicators and that validated tools provide little additional information (theoretical domain of ‘Beliefs about consequences’); discomfort in using validated tools (‘Emotion’), possibly due to limited training and confidence (‘Skills’; ‘Beliefs about capabilities’); limited awareness of the need for, and forgetting to conduct, a depression assessment (‘Knowledge’; ‘Memory, attention and decision processes’). Most reported practising in a manner consistent with the recommendation that a formal cognitive assessment using a validated scale be undertaken. Key factors enabling this were having an awareness of the need to conduct a cognitive assessment (‘Knowledge’); possessing the necessary skills and confidence (‘Skills’; ‘Beliefs about capabilities’); and having adequate time and resources (‘Environmental context and resources’). Conclusions: This is the first study to our knowledge to use a theoretical approach to investigate the barriers and enablers to guideline-recommended diagnosis and management of dementia in general practice. It has identified key factors likely to explain GPs’ uptake of the guidelines. The results have informed the design of an intervention aimed at supporting practice change in line with dementia guidelines, which is currently being evaluated in a cluster randomised trial.

Severe mental illnesses are leading causes of disability worldwide. Their prevalence declines with age, possibly due to premature death. It is unclear, however, if people with severe mental disorders who reach older age still have lower life expectancy compared with their peers and if their causes of death differ. Cohort study of a community-representative sample of 37892 Australian men aged 65–85 years in 1996–1998. Follow up was censored on the 31st December 2010. Lifetime prevalence of schizophrenia spectrum, bipolar, depressive and alcohol-induced disorder was established through record linkage. A subsample of 12136 consented to a face-to-face assessment of sociodemographic, lifestyle and clinical variables. Information about causes of death was retrieved from the Australian Death Registry. The prevalence of schizophrenia spectrum, bipolar, depressive and alcohol-induced disorders was 1.2%, 0.3%, 2.5% and 1.8%. The mortality hazard for men with a severe mental disorder was 2.3 and their life expectancy was reduced by 3 years. Mortality rates increased with age, but the gap between men with and without severe mental disorders was not attenuated by age. Cardiovascular diseases and cancer were the most frequent causes of death. The excess mortality associated with severe mental disorders could not be explained by measured sociodemographic, lifestyle or clinical variables. The excess mortality associated with severe mental disorders persists in later life, and the causes of death of younger and older people with severe mental disorders are similar. Hazardous lifestyle choices, suboptimal access to health care, poor compliance with treatments, and greater severity of medical comorbidities may all contribute to this increased mortality. Unlike young adults, most older people will visit their primary care physician at least once a year, offering health professionals an opportunity to intervene in order to minimise the harms associated with severe mental disorders.

Whether circulating sex hormones modulate mortality and cardiovascular disease (CVD) risk in aging men is controversial. To clarify associations of sex hormones with these outcomes. Systematic literature review to July 2019, with bridge searches to March 2024. Prospective cohort studies of community-dwelling men with sex steroids measured using mass spectrometry and at least 5 years of follow-up. Independent variables were testosterone, sex hormone-binding globulin (SHBG), luteinizing hormone (LH), dihydrotestosterone (DHT), and estradiol concentrations. Primary outcomes were all-cause mortality, CVD death, and incident CVD events. Covariates included age, body mass index, marital status, alcohol consumption, smoking, physical activity, hypertension, diabetes, creatinine concentration, ratio of total to high-density lipoprotein cholesterol, and lipid medication use. Nine studies provided individual participant data (IPD) (255 830 participant-years). Eleven studies provided summary estimates (n = 24 109). Two-stage random-effects IPD meta-analyses found that men with baseline testosterone concentrations below 7.4 nmol/L (<213 ng/dL), LH concentrations above 10 IU/L, or estradiol concentrations below 5.1 pmol/L had higher all-cause mortality, and those with testosterone concentrations below 5.3 nmol/L (<153 ng/dL) had higher CVD mortality risk. Lower SHBG concentration was associated with lower all-cause mortality (median for quintile 1 [Q1] vs. Q5, 20.6 vs. 68.3 nmol/L; adjusted hazard ratio [HR], 0.85 [95% CI, 0.77 to 0.95]) and lower CVD mortality (adjusted HR, 0.81 [CI, 0.65 to 1.00]). Men with lower baseline DHT concentrations had higher risk for all-cause mortality (median for Q1 vs. Q5, 0.69 vs. 2.45 nmol/L; adjusted HR, 1.19 [CI, 1.08 to 1.30]) and CVD mortality (adjusted HR, 1.29 [CI, 1.03 to 1.61]), and risk also increased with DHT concentrations above 2.45 nmol/L. Men with DHT concentrations below 0.59 nmol/L had increased risk for incident CVD events. Observational study design, heterogeneity among studies, and imputation of missing data. Men with low testosterone, high LH, or very low estradiol concentrations had increased all-cause mortality. SHBG concentration was positively associated and DHT concentration was nonlinearly associated with all-cause and CVD mortality. Medical Research Future Fund, Government of Western Australia, and Lawley Pharmaceuticals. (PROSPERO: CRD42019139668).

There is increasing evidence that some lifestyle factors are linked to the development of Alzheimer's disease. Many of these are potentially modifiable and include smoking, physical activity, education, social engagement, cognitive stimulation, and d

Depression in older men has been associated with low circulating testosterone concentration but data from prospective studies are limited. We conducted a prospective longitudinal study in a community representative cohort of 3179 older men free of clinically significant depressive symptoms at baseline. The main objective of this study was to determine if low serum testosterone, dihydrotestosterone and estradiol concentrations are associated with the development of depressive symptoms. Incident depression was assessed with the Patient Health Questionnaire and via an electronic health record database (The West Australian Data Linkage System). The main exposures of interest were serum testosterone, dihydrotestosterone and estradiol measured by liquid chromatography-mass spectrometry and calculated free testosterone in baseline blood samples (collected between 2001 and 2004). One hundred and thirty five men (4.2%) developed depression over a median follow up time of 9.4 years (range 8.4-10.9). Men with incident depression were older (median age 77.7 vs 76.1 years, z=-3.82, p=0<0.001) and were more likely to have cardiovascular disease (43.0% vs 32.6%, χ(2)=6.32, p=0.012) and diabetes (22.2% vs 13.2%, χ(2)=8.95, p=0.003). Low serum total testosterone (<6.4 nmol/L) was associated with incident depression (HR 2.07, 95%CI 1.17-3.68) and this remained significant after adjustment for relevant potential confounding factors (HR 1.86, 95%CI 1.05-3.31). Low serum dihydrotestosterone, estradiol and calculated free testosterone were not associated with risk of depression. Low serum total testosterone, but not calculated free testosterone, was associated with incident depression in this sample of older men.