Is testosterone linked to human aggression? A meta-analytic examination of the relationship between baseline, dynamic, and manipulated testosterone on human aggression.

Testosterone is often considered a critical regulator of aggressive behaviour. There is castration/replacement evidence that testosterone indeed drives aggression in some species, but causal evidence in humans is generally lacking and/or-for the few studies that have pharmacologically manipulated testosterone concentrations-inconsistent. More often researchers have examined differences in baseline testosterone concentrations between groups known to differ in aggressiveness (e.g., violent vs non-violent criminals) or within a given sample using a correlational approach. Nevertheless, testosterone is not static but instead fluctuates in response to cues of challenge in the environment, and these challenge-induced fluctuations may more strongly regulate situation-specific aggressive behaviour. Here, we quantitatively summarize literature from all three approaches (baseline, change, and manipulation), providing the most comprehensive meta-analysis of these testosterone-aggression associations/effects in humans to date. Baseline testosterone shared a weak but significant association with aggression (r = 0.054, 95% CIs [0.028, 0.080]), an effect that was stronger and significant in men (r = 0.071, 95% CIs [0.041, 0.101]), but not women (r = 0.002, 95% CIs [-0.041, 0.044]). Changes in T were positively correlated with aggression (r = 0.108, 95% CIs [0.041, 0.174]), an effect that was also stronger and significant in men (r = 0.162, 95% CIs [0.076, 0.246]), but not women (r = 0.010, 95% CIs [-0.090, 0.109]). The causal effects of testosterone on human aggression were weaker yet, and not statistically significant (r = 0.046, 95% CIs [-0.015, 0.108]). We discuss the multiple moderators identified here (e.g., offender status of samples, sex) and elsewhere that may explain these generally weak effects. We also offer suggestions regarding methodology and sample sizes to best capture these associations in future work.

Sex hormones play a role in vulnerability to sleep loss on emotion processing tasks.

The central aim of this study was to investigate hormones as a predictor of individual vulnerability or resiliency on emotion processing tasks following one night of sleep restriction. The restriction group was instructed to sleep 3 a.m.-7 a.m. (13 men, 13 women in follicular phase, 10 women in luteal phase of menstrual cycle), and a control group slept 11 p.m.-7 a.m. (12 men, 12 follicular women, 12 luteal women). Sleep from home was verified with actigraphy. Saliva samples were collected on the evening prior to restriction, and in the morning and afternoon following restriction, to measure testosterone, estradiol, and progesterone. In the laboratory, event-related potentials (ERPs) were recorded during presentation of images and faces to index neural processing of emotional stimuli. Compared to controls, sleep-restricted participants had a larger amplitude Late Positive Potential (LPP) ERP to positive vs neutral images, reflecting greater motivated attention towards positive stimuli. Sleep-restricted participants were also less accurate categorizing sad faces and exhibited a larger N170 to sad faces, reflecting greater neural reactivity. Sleep-restricted luteal women were less accurate categorizing all images compared to control luteal women, and progesterone was related to several outcomes. Morning testosterone in men was lower in the sleep-restricted group compared to controls; lower testosterone was associated with lower accuracy to positive images, a greater difference between positive vs neutral LPP amplitude, and lower accuracy to sad and fearful faces. In summary, women higher in progesterone and men lower in testosterone were more vulnerable to the effects of sleep restriction on emotion processing tasks. This study highlights a role for sex and sex hormones in understanding individual differences in vulnerability to sleep loss.