Men's help-seeking in the first year after diagnosis of localised prostate cancer.

This study describes sources of support utilised by men with localised prostate cancer in the first year after diagnosis and examines characteristics associated with help-seeking for men with unmet needs. A cross-sectional survey of 331 patients from a population-based sample who were in the first year after diagnosis (M = 9.6, SD = 1.9) was conducted to assess sources of support, unmet supportive care needs, domain-specific quality of life and psychological distress. Overall, 82% of men reported unmet supportive care needs. The top five needs were sexuality (58%); prostate cancer-specific (57%); psychological (47%); physical and daily living (41%); and health system and information (31%). Professional support was most often sought from doctors (51%). Across most domains, men who were older (Ps ≤ 0.03), less well educated (Ps ≤ 0.04) and more depressed (Ps ≤ 0.05) were less likely to seek help for unmet needs. Greater sexual help-seeking was related to better sexual function (P = 0.03), higher education (P ≤ 0.03) and less depression (P = 0.05). Unmet supportive care needs are highly prevalent after localised prostate cancer diagnosis with older age, lower education and higher depression apparent barriers to help-seeking. Interventions that link across medicine, nursing and community based peer support may be an accessible approach to meeting these needs. Clinical Trial Registry: Trial Registration: ACTRN12611000392965

Sex Differences in the Association between Serum Levels of Testosterone and Frailty in an Elderly Population: The Toledo Study for Healthy Aging

BACKGROUND: Age-associated decline in testosterone levels represent one of the potential mechanisms involved in the development of frailty. Although this association has been widely reported in older men, very few data are available in women. We studied the association between testosterone and frailty in women and assessed sex differences in this relationship. METHODS: We used cross-sectional data from the Toledo Study for Healthy Aging, a population-based cohort study of Spanish elderly. Frailty was defined according to Fried's approach. Multivariate odds-ratios (OR) and 95% confidence intervals (CI) associated with total (TT) and free testosterone (FT) levels were estimated using polytomous logistic regression. RESULTS: In women, there was a U-shaped relationship between FT levels and frailty (p for FT(2) = 0.03). In addition, very low levels of FT were observed in women with ≥ 4 frailty criteria (age-adjusted geometric means = 0.13 versus 0.37 in subjects with <4 components, p = 0.010). The association of FT with frailty appeared confined to obese women (p-value for interaction = 0.05).In men, the risk of frailty levels linearly decreased with testosterone (adjusted OR for frailty = 2.9 (95%CI, 1.6-5.1) and 1.6 (95%CI, 1.0-2.5), for 1 SD decrease in TT and FT, respectively). TT and FT showed association with most of frailty criteria. No interaction was found with BMI. CONCLUSION: There is a relationship between circulating levels of FT and frailty in older women. This relation seems to be modulated by BMI. The relevance and the nature of the association of FT levels and frailty are sex-specific, suggesting that different biological mechanisms may be involved

Sarcopenia: etiology, clinical consequences, intervention, and assessment

The aging process is associated with loss of muscle mass and strength and decline in physical functioning. The term sarcopenia is primarily defined as low level of muscle mass resulting from age-related muscle loss, but its definition is often broadened to include the underlying cellular processes involved in skeletal muscle loss as well as their clinical manifestations. The underlying cellular changes involve weakening of factors promoting muscle anabolism and increased expression of inflammatory factors and other agents which contribute to skeletal muscle catabolism. At the cellular level, these molecular processes are manifested in a loss of muscle fiber cross-sectional area, loss of innervation, and adaptive changes in the proportions of slow and fast motor units in muscle tissue. Ultimately, these alterations translate to bulk changes in muscle mass, strength, and function which lead to reduced physical performance, disability, increased risk of fall-related injury, and, often, frailty. In this review, we summarize current understanding of the mechanisms underlying sarcopenia and age-related changes in muscle tissue morphology and function. We also discuss the resulting long-term outcomes in terms of loss of function, which causes increased risk of musculoskeletal injuries and other morbidities, leading to frailty and loss of independence

A randomized, controlled trial of 3.0 mg of liraglutide in weight management

BACKGROUND Obesity is a chronic disease with serious health consequences, but weight loss is difficult to maintain through lifestyle intervention alone. Liraglutide, a glucagonlike peptide-1 analogue, has been shown to have potential benefit for weight management at a once-daily dose of 3.0 mg, injected subcutaneously. METHODS We conducted a 56-week, double-blind trial involving 3731 patients who did not have type 2 diabetes and who had a body-mass index (BMI; the weight in kilograms divided by the square of the height in meters) of at least 30 or a BMI of at least 27 if they had treated or untreated dyslipidemia or hypertension. We randomly assigned patients in a 2:1 ratio to receive once-daily subcutaneous injections of liraglutide at a dose of 3.0 mg (2487 patients) or placebo (1244 patients); both groups received counseling on lifestyle modification. The coprimary end points were the change in body weight and the proportions of patients losing at least 5% and more than 10% of their initial body weight. RESULTS At baseline, the mean (±SD) age of the patients was 45.1±12.0 years, the mean weight was 106.2±21.4 kg, and the mean BMI was 38.3±6.4; a total of 78.5% of the patients were women and 61.2% had prediabetes. At week 56, patients in the liraglutide group had lost a mean of 8.4±7.3 kg of body weight, and those in the placebo group had lost a mean of 2.8±6.5 kg (a difference of -5.6 kg; 95% confidence interval, -6.0 to -5.1; P&lt;0.001, with last-observation-carried-forward imputation). A total of 63.2% of the patients in the liraglutide group as compared with 27.1% in the placebo group lost at least 5% of their body weight (P&lt;0.001), and 33.1% and 10.6%, respectively, lost more than 10% of their body weight (P&lt;0.001). The most frequently reported adverse events with liraglutide were mild or moderate nausea and diarrhea. Serious events occurred in 6.2% of the patients in the liraglutide group and in 5.0% of the patients in the placebo group. CONCLUSIONS In this study, 3.0 mg of liraglutide, as an adjunct to diet and exercise, was associated with reduced body weight and improved metabolic control. (Funded by Novo Nordisk; SCALE Obesity and Prediabetes NN8022-1839 ClinicalTrials.gov number, NCT01272219.)

The effect of testosterone and a nutritional supplement on hospital admissions in under-nourished, older people

Extent: 8p.Background: Weight loss and under-nutrition are relatively common in older people, and are associated with poor outcomes including increased rates of hospital admissions and death. In a pilot study of 49 undernourished older, community dwelling people we found that daily treatment for one year with a combination of testosterone tablets and a nutritional supplement produced a significant reduction in hospitalizations. We propose a larger, multicentre study to explore and hopefully confirm this exciting, potentially important finding (NHMRC project grant number 627178). Methods/Design: One year randomized control trial where subjects are allocated to either oral testosterone undecanoate and high calorie oral nutritional supplement or placebo medication and low calorie oral nutritional supplementation. 200 older community-dwelling, undernourished people [Mini Nutritional Assessment score 7.5% over 3 months)]. Hospital admissions, quality-adjusted life years, functional status, nutritional health, muscle strength, body composition and other variables will be assessed. Discussion: The pilot study showed that combined treatment with an oral testosterone and a supplement drink was well tolerated and safe, and reduced the number of people hospitalised and duration of hospital admissions in undernourished, community dwelling older people. This is an exciting finding, as it identifies a treatment which may be of substantial benefit to many older people in our community. We now propose to conduct a multi-centre study to test these findings in a substantially larger subject group, and to determine the cost effectiveness of this treatment. Trial registration: Australian Clinical Trial Registry: ACTRN 12610000356066Cynthia Piantadosi, Renuka Visvanathan, Vasi Naganathan, Peter Hunter, Ian D. Cameron, Kylie Lange, Jonathan Karnon and Ian M. Chapma

Cross-sectional and longitudinal determinants of serum sex hormone binding globulin (SHBG) in a cohort of community-dwelling men.

Despite its widespread clinical use, there is little data available from population-based studies on the determinants of serum sex hormone binding globulin (SHBG). We aimed to examine multifactorial determinants of circulating SHBG levels in community-dwelling men. Study participants comprised randomly selected 35-80 y.o. men (n = 2563) prospectively-followed for 5 years (n = 2038) in the Men Androgen Inflammation Lifestyle Environment and Stress (MAILES) study. After excluding men with illness or medications known to affect SHBG (n = 172), data from 1786 men were available at baseline, and 1476 at follow-up. The relationship between baseline body composition (DXA), serum glucose, insulin, triglycerides, thyroxine (fT4), sex steroids (total testosterone (TT), oestradiol (E2)), and pro-inflammatory cytokines and serum SHBG level at both baseline & follow-up was determined by linear and penalized logistic regression models adjusting for age, lifestyle & demographic, body composition, metabolic, and hormonal factors. Restricted cubic spline analyses was also conducted to capture possible non-linear relationships. At baseline there were positive cross-sectional associations between age (β = 0.409, p<0.001), TT (β = 0.560, p<0.001), fT4 (β = 0.067, p = 0.019) and SHBG, and negative associations between triglycerides (β = -0.112, p<0.001), abdominal fat mass (β = -0.068, p = 0.032) and E2 (β = -0.058, p = 0.050) and SHBG. In longitudinal analysis the positive determinants of SHBG at 4.9 years were age (β = 0.406, p = <0.001), TT (β = 0.461, p = <0.001), and fT4 (β = 0.040, p = 0.034) and negative determinants were triglycerides (β = -0.065, p = 0.027) and abdominal fat mass (β = -0.078, p = 0.032). Taken together these data suggest low SHBG is a marker of abdominal obesity and increased serum triglycerides, conditions which are known to have been associated with low testosterone and low T4

A pilot study on the relationship between sleep restriction, endogenous testosterone and cognitive performance

Reynolds, AC ORCiD: 0000-0001-9534-8699Aims: Both high endogenous testosterone and sleep restriction impact adversely on cognitive performance. The normal daily testosterone rhythm may also be disrupted by sleep restriction. As such, sleep restriction could degrade cognitive performance both directly and through its effect on testosterone. This study investigated the relationship between sleep restriction, testosterone levels and cognitive functioning. Methods: Fourteen healthy men (mean ± SD, age: 27.4 ± 3.8 yr; BMI: 23.5 ± 2.9 kg/m2) with normal plasma glucose and lipid levels and normal liver, renal and thyroid function participated in a live-­‐in, laboratory-­‐based sleep restriction protocol. Participants underwent two baseline nights (B1, B2; 10 h time in bed (TIB); 22:00 h -­‐ 08:00 h) followed by five nights of sleep restriction (SR1 5; 4 h TIB; 04:00 h -­‐ 08:00 h) and one recovery night (10 h TIB; 22:00 h -­‐ 08:00 h). The timing of meals and caloric intake were strictly controlled, and only non-­‐vigorous physical activity was allowed. Blood was sampled on B1 and SR5 via an indwelling catheter at 09:00 h, and then every 2 h from 10:00 h until 20:00 h. Lapses in sustained attention were assessed using the Psychomotor Vigilance Test (PVT) and subjective sleepiness was assessed using the Karolinska Sleepiness Scale (KSS) throughout scheduled waking periods. On B1 and SR5, the PVT and KSS were completed at 11:00 h, 12:30 h, 16:30 h and 19:30 h. The relationships between sleep restriction, endogenous testosterone and cognitive performance were assessed using mixed effects linear regression comprising effects of day, trial and day*trial interaction. Testosterone was entered as a covariate, and a day*testosterone interaction effect was examined to determine whether there was a modulatory influence of testosterone on PVT lapses and KSS subjective sleepiness. Results: There was a significant effect of sleep restriction on PVT lapses (F(1,83) = 41.4, p < .001) and KSS sleepiness (F(1,83) = 51.9, p < .001) but not on testosterone (F(1,90) = 4.1, p = .08). There was no main effect of testosterone on PVT lapses (F(1,82) = 0.92, p = .34) or subjective sleepiness (F(1,82) = 0.04, p = .85). However, higher endogenous testosterone levels were associated with greater changes after sleep restriction in PVT lapses (F(2,81) = 12.3, p < .001) and subjective sleepiness (F(2,81) = 12.7, p < .001). Conclusions: The findings suggest that young adult men with higher endogenous testosterone levels (within the normal range) experience greater degradation of cognitive functioning following 5 days of sleep restriction. This relationship may point to endogenous testosterone as a modulator of individual vulnerability to sleep restriction. Further investigation is needed to determine the mechanisms underpinning this relationship.Associated Grant:see Notes sectio

A pilot study on the relationship between sleep restriction, endogenous testosterone and cognitive performance

Aims: Both high endogenous testosterone and sleep restriction impact adversely on cognitive performance. The normal daily testosterone rhythm may also be disrupted by sleep restriction. As such, sleep restriction could degrade cognitive performance both directly and through its effect on testosterone. This study investigated the relationship between sleep restriction, testosterone levels and cognitive functioning. Methods: Fourteen healthy men (mean ± SD, age: 27.4 ± 3.8 yr; BMI: 23.5 ± 2.9 kg/m2) with normal plasma glucose and lipid levels and normal liver, renal and thyroid function participated in a live-­‐in, laboratory-­‐based sleep restriction protocol. Participants underwent two baseline nights (B1, B2; 10 h time in bed (TIB); 22:00 h -­‐ 08:00 h) followed by five nights of sleep restriction (SR1 5; 4 h TIB; 04:00 h -­‐ 08:00 h) and one recovery night (10 h TIB; 22:00 h -­‐ 08:00 h). The timing of meals and caloric intake were strictly controlled, and only non-­‐vigorous physical activity was allowed. Blood was sampled on B1 and SR5 via an indwelling catheter at 09:00 h, and then every 2 h from 10:00 h until 20:00 h. Lapses in sustained attention were assessed using the Psychomotor Vigilance Test (PVT) and subjective sleepiness was assessed using the Karolinska Sleepiness Scale (KSS) throughout scheduled waking periods. On B1 and SR5, the PVT and KSS were completed at 11:00 h, 12:30 h, 16:30 h and 19:30 h. The relationships between sleep restriction, endogenous testosterone and cognitive performance were assessed using mixed effects linear regression comprising effects of day, trial and day*trial interaction. Testosterone was entered as a covariate, and a day*testosterone interaction effect was examined to determine whether there was a modulatory influence of testosterone on PVT lapses and KSS subjective sleepiness. Results: There was a significant effect of sleep restriction on PVT lapses (F(1,83) = 41.4, p < .001) and KSS sleepiness (F(1,83) = 51.9, p < .001) but not on testosterone (F(1,90) = 4.1, p = .08). There was no main effect of testosterone on PVT lapses (F(1,82) = 0.92, p = .34) or subjective sleepiness (F(1,82) = 0.04, p = .85). However, higher endogenous testosterone levels were associated with greater changes after sleep restriction in PVT lapses (F(2,81) = 12.3, p < .001) and subjective sleepiness (F(2,81) = 12.7, p < .001). Conclusions: The findings suggest that young adult men with higher endogenous testosterone levels (within the normal range) experience greater degradation of cognitive functioning following 5 days of sleep restriction. This relationship may point to endogenous testosterone as a modulator of individual vulnerability to sleep restriction. Further investigation is needed to determine the mechanisms underpinning this relationship

Timing of food intake during simulated night shift impacts glucose metabolism: A controlled study

Eating during the night may increase the risk for obesity and type 2 diabetes in shift workers. This study examined the impact of either eating or not eating a meal at night on glucose metabolism. Participants underwent four nights of simulated night work (SW1–4, 16:00–10:00 h, <50 lux) with a daytime sleep opportunity each day (10:00–16:00 h, <3 lux). Healthy males were assigned to an eating at night (NE; n = 4, meals; 07:00, 19:00 and 01:30 h) or not eating at night (NEN; n = 7, meals; 07:00 h, 09:30, 16:10 and 19:00 h) condition. Meal tolerance tests were conducted post breakfast on pre-night shift (PRE), SW4 and following return to day shift (RTDS), and glucose and insulin area under the curve (AUC) were calculated. Mixed-effects ANOVAs were used with fixed effects of condition and day, and their interactions, and a random effect of subject identifier on the intercept. Fasting glucose and insulin were not altered by day or condition. There were significant effects of day and condition × day (both p < 0.001) for glucose AUC, with increased glucose AUC observed solely in the NE condition from PRE to SW4 (p = 0.05) and PRE to RTDS (p < 0.001). There was also a significant effect of day (p = 0.007) but not condition × day (p = 0.825) for insulin AUC, with increased insulin from PRE to RTDS in both eating at night (p = 0.040) and not eating at night (p = 0.006) conditions. Results in this small, healthy sample suggest that not eating at night may limit the metabolic consequences of simulated night work. Further study is needed to explore whether matching food intake to the biological clock could reduce the burden of type 2 diabetes in shift workers. © 2017 Taylor & Francis Group, LLC