Department of Psychology, Nipissing University, 100 College Dr. North Bay, ON P1B8L7, Canada; Department of Psychology, University of the Fraser Valley, 33844 King Rd, Abbotsford, BC V2S 7M8, Canada; Department of Basic Psychological Research and Research Methods, Faculty of Psychology, University of Vienna, Liebiggasse 5, 1160, Vienna, Austria.
Department of Psychology, Simon Fraser University, 8888 University Dr, Burnaby, British Columbia, V5A 1S6, Canada.
Horm Behav. 2020 Jul;123:104644. doi: 10.1016/j.yhbeh.2019.104644. Epub 2019 Dec 28.
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.
睾酮通常被认为是攻击性行为的关键调节者。有去势/替代的证据表明，睾酮确实会促使某些物种产生攻击性，但在人类中，因果证据通常缺乏，或者——对于少数通过药理学手段改变睾酮浓度的研究——不一致。更多时候，研究人员研究了已知在攻击性上存在差异的群体（例如，暴力罪犯与非暴力罪犯）或在特定样本中使用相关方法的基础睾酮浓度差异。然而，睾酮并不是静态的，而是会根据环境中挑战的线索而波动，这些挑战引起的波动可能更强烈地调节特定情境下的攻击行为。在这里，我们定量总结了来自所有三种方法（基础、变化和操作）的文献，提供了迄今为止对人类中这些睾酮-攻击关联/效应的最全面的荟萃分析。基础睾酮与攻击性呈微弱但显著的正相关（r=0.054，95%置信区间 [0.028, 0.080]），这种效应在男性中更强且显著（r=0.071，95%置信区间 [0.041, 0.101]），但在女性中不显著（r=0.002，95%置信区间 [-0.041, 0.044]）。T 的变化与攻击性呈正相关（r=0.108，95%置信区间 [0.041, 0.174]），这种效应在男性中也更强且显著（r=0.162，95%置信区间 [0.076, 0.246]），但在女性中不显著（r=0.010，95%置信区间 [-0.090, 0.109]）。睾酮对人类攻击性的因果效应更弱，且不具有统计学意义（r=0.046，95%置信区间 [-0.015, 0.108]）。我们讨论了这里（例如，样本的罪犯身份、性别）和其他地方确定的多个调节因素，这些因素可能解释了这些普遍较弱的效应。我们还就未来工作中最佳捕获这些关联的方法和样本量提出了建议。
