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High social status reduces stress responses in numerous species, but the stress-buffering effect of status may dissipate or even reverse during times of hierarchical instability. In an experimental test of this hypothesis, 118 participants (57.3% female) were randomly assigned to a high- or low-status position in a stable or unstable hierarchy and were then exposed to a social-evaluative stressor (a mock job interview). High status in a stable hierarchy buffered stress responses and improved interview performance, but high status in an unstable hierarchy boosted stress responses and did not lead to better performance. This general pattern of effects was observed across endocrine (cortisol and testosterone), psychological (feeling in control), and behavioral (competence, dominance, and warmth) responses to the stressor. The joint influence of status and hierarchy stability on interview performance was explained by feelings of control and testosterone reactivity. Greater feelings of control predicted enhanced interview performance, whereas increased testosterone reactivity predicted worse performance. These results provide direct causal evidence that high status confers adaptive benefits for stress reduction and performance only when the social hierarchy is stable. When the hierarchy is unstable, high status actually exacerbates stress responses.

The capacity to infer others' mental states (known as ‘mind reading’ and ‘cognitive empathy’) is essential for social interactions across species, and its impairment characterizes psychopathological conditions such as autism spectrum disorder and schizophrenia. Previous studies reported that testosterone administration impaired cognitive empathy in healthy humans, and that a putative biomarker of prenatal testosterone exposure (finger digit ratios) moderated the effect. However, empirical support for the relationship has relied on small sample studies with mixed evidence. We investigate the reliability and generalizability of the relationship in two large-scale double-blind placebo-controlled experiments in young men ( n = 243 and n = 400), using two different testosterone administration protocols. We find no evidence that cognitive empathy is impaired by testosterone administration or associated with digit ratios. With an unprecedented combined sample size, these results counter current theories and previous high-profile reports, and demonstrate that previous investigations of this topic have been statistically underpowered.

This study was to determine the effects of five-week high-intensity interval training (HIIT) on cardiorespiratory fitness, body composition, blood glucose, and relevant systemic hormones when compared to moderate-intensity continuous training (MICT) in overweight and obese young women. Methods. Eighteen subjects completed 20 sessions of HIIT or MICT for five weeks. HIIT involved 60 × 8 s cycling at ~90% of peak oxygen consumption ( V ˙ O 2 p e a k ) interspersed with 12 s recovery, whereas MICT involved 40-minute continuous cycling at 65% of V ˙ O 2 p e a k . V ˙ O 2 p e a k , body composition, blood glucose, and fasting serum hormones, including leptin, growth hormone, testosterone, cortisol, and fibroblast growth factor 21, were measured before and after training. Results. Both exercise groups achieved significant improvements in V ˙ O 2 p e a k (+7.9% in HIIT versus +11.7% in MICT) and peak power output (+13.8% in HIIT versus +21.9% in MICT) despite no training effects on body composition or the relevant systemic hormones. Blood glucose tended to be decreased after the intervention ( p = 0.062 ). The rating of perceived exertion in MICT was higher than that in HIIT ( p = 0.042 ). Conclusion. Compared with MICT, short-term HIIT is more time-efficient and is perceived as being easier for improving cardiorespiratory fitness and fasting blood glucose for overweight and obese young women.

Recently, we demonstrated that the steroid-hormone testosterone reduces interpersonal trust in humans. The neural mechanism which underlies this effect is however unknown. It has been proposed that testosterone increases social vigilance via neuropeptide systems in the amygdala, augmenting communication between the amygdala and the brain stem. However, testosterone also affects connectivity between the orbitofrontal cortex (OFC) and the amygdala, which could subsequently lead to increased vigilance by reduced top-down control over the amygdala. Here, in a placebo-controlled testosterone administration study with 16 young women, we use functional magnetic resonance imaging to get more insights into neural mechanisms whereby testosterone acts on trust. Several cortical systems, among others the OFC, are involved in the evaluation of facial trustworthiness. Testosterone administration decreased functional connectivity between amygdala and the OFC during judgments of unfamiliar faces, and also increased amygdala responses specifically to the faces that were rated as untrustworthy. Finally, connectivity between the amygdala and the brain stem was not affected by testosterone administration. Although speculative, a neurobiological explanation for these findings is that in uncertain social situations, testosterone induces sustained decoupling between OFC and amygdala by a prefrontal-dopaminergic mechanism, subsequently resulting in more vigilant responses of the amygdala to signals of untrustworthiness. ► Testosterone reduces amygdala–orbitofrontal cortex coupling in response to faces. ► Testosterone increases amygdala responses towards untrustworthy faces. ► By this mechanism testosterone can decrease interpersonal trust.

This study examined hormonal responses to competition in relation to gender, social context, and implicit motives. Participants (N = 326) were randomly assigned to win or lose in a 10-round, virtual face-to-face competition, in same-sex individual- and team-competition contexts. Saliva samples, taken before and twice after the competition, were assayed for testosterone (T), estradiol (E), progesterone (P), and cortisol (C). Implicit needs for power (nPower) and affiliation (nAffiliation) were assessed with a picture-story exercise before the competition. Aggression was measured via the volume at which participants set noise blasts for their opponents. Men competing individually and women competing as teams showed similar T increases after winning. C was differentially associated with outcome in the team matches, with higher post-match cortisol for winning women, and an opposite effect for male teams. Analyses including implicit motives indicated that situational variables interacted with motivational needs in shaping hormonal responses to competition: in naturally cycling women, nPower predicted T increases after winning and T and E decreases after losing. In men, nPower predicted T increases after losing and decreases after winning. In male teams, nPower predicted C increases after losing, but not after winning, whereas in individual competitions, nPower was a general negative predictor of C changes in women. nAffiliation predicted P increases for women competing as teams, and P decreases for women competing individually. Aggression was higher in men, losers, and teams than in women, winners, and individuals. High aggression was associated with high baseline C in women competing individually and with low baseline C and C decreases in women competing as teams and in men generally. Our findings suggest that while situational and gender factors play a role in hormonal responses to competition, they also depend on their interplay with motivational factors. They also suggest that while aggression is strongly affected by situational factors in the context of a competition, it has no direct association with motivational and hormonal correlates of dominance (nPower, T, E) and instead is associated with (mostly) low levels of C.

Abstract Context Glucagon increases energy expenditure; consequently, glucagon receptor agonists are in development for the treatment of obesity. Obesity negatively affects the reproductive axis, and hypogonadism itself can exacerbate weight gain. Therefore, knowledge of the effects of glucagon receptor agonism on reproductive hormones is important for developing therapeutics for obesity; but reports in the literature about the effects of glucagon receptor agonism on the reproductive axis are conflicting. Objective The objective of this work is to investigate the effect of glucagon administration on reproductive hormone secretion in healthy young men. Design A single-blinded, randomized, placebo-controlled crossover study was conducted. Setting The setting of this study was the Clinical Research Facility, Imperial College Healthcare NHS Trust. Participants Eighteen healthy eugonadal men (mean ± SEM: age 25.1 ± 1.0 years; body mass index 22.5 ± 0.4 kg/m2; testosterone 21.2 ± 1.2 nmol/L) participated in this study. Intervention An 8-hour intravenous infusion of 2 pmol/kg/min glucagon or rate-matched vehicle infusion was administered. Main Outcome Measures Luteinizing hormone (LH) pulsatility; LH, follicle-stimulating hormone (FSH), and testosterone levels were measured. Results Although glucagon administration induced metabolic effects (insulin area under the curve: vehicle 1065 ± 292 min.µU/mL vs glucagon 2098 ± 358 min.µU/mL, P < .001), it did not affect LH pulsatility (number of LH pulses/500 min: vehicle 4.7 ± 0.4, glucagon 4.2 ± 0.4, P = .22). Additionally, there were no significant differences in circulating LH, FSH, or testosterone levels during glucagon administration compared with vehicle administration. Conclusions Acute administration of a metabolically active dose of glucagon does not alter reproductive hormone secretion in healthy men. These data are important for the continued development of glucagon-based treatments for obesity.

Prior research has shown that an individual’s hormonal profile can influence the individual’s social standing within a group. We introduce a different construct—a collective hormonal profile—which describes a group’s hormonal make-up. We test whether a group’s collective hormonal profile is related to its performance. Analysis of 370 individuals randomly assigned to work in 74 groups of three to six individuals revealed that group-level concentrations of testosterone and cortisol interact to predict a group’s standing across groups. Groups with a collective hormonal profile characterized by high testosterone and low cortisol exhibited the highest performance. These collective hormonal level results remained reliable when controlling for personality traits and group-level variability in hormones. These findings support the hypothesis that groups with a biological propensity toward status pursuit (high testosterone) coupled with reduced stress-axis activity (low cortisol) engage in profit-maximizing decision-making. The current work extends the dual-hormone hypothesis to the collective level and provides a neurobiological perspective on the factors that determine who rises to the top across, not just within, social hierarchies.

Low testosterone (T) levels in men have been shown to predict development of the metabolic syndrome, but the effects of T on lipid metabolism are incompletely understood. In a randomized, double-blind, placebo-controlled, crossover study, 12 healthy, young males received gonadotropin-releasing hormone agonist treatment 1 month prior to 3 of 4 trial days to induce castrate levels of T. On trial days, T gel was applied to the body containing either high or low physiological T dose or placebo. On the 4th trial day, participants constituted their own eugonadal controls. Each study comprised a 5-h basal period and a 3-h hyperinsulinemic-euglycemic clamp. Short-term hypogonadism did not affect VLDL triglyceride (TG) secretion, nor did it affect VLDL-TG concentrations. It was, however, characterized by lower total lipid oxidation. In addition, acute rescue with high physiological T increased VLDL-TG secretion during both basal and clamp conditions. These data show that T can act through fast nongenomic pathways in the liver. In addition, the early hypogonadal state is characterized by decreased total lipid oxidation, but whether these changes represent early hypogonadal metabolic dysfunction warrants further investigations. T is not a major determinant of resting VLDL-TG kinetics in men.

The purpose of this study was (1) to determine the effect of single bouts of volume- and intensity-equated low- (LL) and high-load (HL) full-body resistance exercise (RE) on AR-DNA binding, serum/muscle testosterone and dihydrotestosterone, muscle androgen receptor (AR), and AR-DNA binding; and, (2) to determine the effect of RE on sarcoplasmic and nucleoplasmic β-catenin concentrations in order to determine their impact on mediating AR-DNA binding in the absence/presence of serum/muscle androgen and AR protein. In a cross-over design, 10 resistance-trained males completed volume- and intensity-equated LL and HL full-body RE. Blood and muscle samples were collected at pre-, 3 h-, and 24 h post-exercise. Separate 2 × 3 factorial analyses of variance (ANOVAs) with repeated measures and pairwise comparisons with a Bonferroni adjustment were used to analyze the main effects. No significant differences were observed in muscle AR, testosterone, dihydrotestosterone, or serum total testosterone in either condition (p > 0.05). Serum-free testosterone was significantly decreased 3 h post-exercise and remained significantly less than baseline 24 h post-exercise in both conditions (p < 0.05). In response to HL, AR-DNA binding significantly increased at 3 h post-exercise (p < 0.05), whereas no significant differences were observed at any time in response to LL (p > 0.05). Moreover, sarcoplasmic β-catenin was significantly greater in HL (p < 0.05) without significant changes in nucleoplasmic β-catenin (p > 0.05). In conclusion, increases in AR-DNA binding in response to HL RE indicate AR signaling may be load-dependent. Furthermore, despite the lack of increase in serum and muscle androgens or AR content following HL RE, elevations in AR-DNA binding with elevated sarcoplasmic β-catenin suggests β-catenin may be facilitating this response.

Life expectancy in the developed West is currently stagnated and remains shorter in men than women. Well-established evolutionary biology theory suggests lifespan trades-off against reproductive success, possibly sex-specifically. We examined whether a key driver of reproductive success, testosterone, affected survival using a Mendelian randomization longevity study in the UK Biobank to obtain unbiased estimates, along with control exposures. We applied published genetic instruments for testosterone to obtain inverse variance weighted estimates of associations with survival to (i.e., age at) recruitment, in 167,020 men and 194,174 women. We similarly obtained estimates for a positive control (smoking initiation), and a negative control (absorbate), a marker of vitamin C metabolism. Testosterone was associated with poorer survival (0.10 years younger at recruitment per effect size of testosterone, 95% confidence interval (CI) 0.004 to 0.20). As expected, smoking initiation was also associated with poorer survival (0.37 years younger, 95% CI 0.25 to 0.50), but not absorbate (0.01 years younger, 95% CI − 0.09 to 0.11). Several aspects of a healthy lifestyle (low animal fat diet) and several widely used medications (statins, metformin, dexamethasone and possibly aspirin) may modulate testosterone. Explicitly designing interventions sex-specifically based on these insights might help address stagnating life expectancy and sexual disparities.