Justin M. Carré

In your face: facial metrics predict aggressive behaviour in the laboratory and in varsity and professional hockey players

Facial characteristics are an important basis for judgements about gender, emotion, personality, motivational states and behavioural dispositions. Based on a recent finding of a sexual dimorphism in facial metrics that is independent of body size, we conducted three studies to examine the extent to which individual differences in the facial width-to-height ratio were associated with trait dominance (using a questionnaire) and aggression during a behavioural task and in a naturalistic setting (varsity and professional ice hockey). In study 1, men had a larger facial width-to-height ratio, higher scores of trait dominance, and were more reactively aggressive compared with women. Individual differences in the facial width-to-height ratio predicted reactive aggression in men, but not in women (predicted 15% of variance). In studies 2 (male varsity hockey players) and 3 (male professional hockey players), individual differences in the facial width-to-height ratio were positively related to aggressive behaviour as measured by the number of penalty minutes per game obtained over a season (predicted 29 and 9% of the variance, respectively). Together, these findings suggest that the sexually dimorphic facial width-to-height ratio may be an ‘honest signal’ of propensity for aggressive behaviour.

Testosterone responses to competition predict future aggressive behaviour at a cost to reward in men

The extent to which trait factors (baseline testosterone concentrations, trait dominance) and state factors (change in social status, change in testosterone concentrations) would predict reactive aggression in a subsequent task that involved provocation was examined in 99 participants (39 men and 60 women). Participants first competed in same-sex dyads on a Number Tracing Task for which the outcome (win or loss) was rigged. After the competition, participants performed the Point Subtraction Aggression Paradigm (PSAP), a behavioural measure of reactive aggression against an opponent (actually a computer program). Trait dominance predicted baseline testosterone in men, but not women, and men made more aggressive responses than did women. Baseline testosterone concentrations did not predict aggressive behaviour in either men or women. Winners and losers did not differ in competition-induced change in testosterone. However, change in testosterone concentrations predicted aggressive responses in the PSAP for men in the loss condition, and aggressive responses were made at a cost to obtaining reward points. For men in the win condition, aggressive responses were predicted by an interaction between trait dominance and change in testosterone concentrations. These findings suggest that situational changes in testosterone concentrations modulate future aggressive behaviour in men.

Aggressive behavior and change in salivary testosterone concentrations predict willingness to engage in a competitive task

The current study investigated relationships among aggressive behavior, change in salivary testosterone concentrations, and willingness to engage in a competitive task. Thirty-eight male participants provided saliva samples before and after performing the Point Subtraction Aggression Paradigm (a laboratory measure that provides opportunity for aggressive and defensive behavior while working for reward; all three involve pressing specific response keys). Baseline testosterone concentrations were not associated with aggressive responding. However, aggressive responding (but not point reward or point protection responding) predicted the pre- to post-PSAP change in testosterone: Those with the highest aggressive responding had the largest percent increase in testosterone concentrations. Together, aggressive responding and change in testosterone predicted willingness to compete following the PSAP. Controlling for aggression, men who showed a rise in testosterone were more likely to choose to compete again (p=0.03) and controlling for testosterone change, men who showed the highest level of aggressive responding were more likely to choose the non-competitive task (p=0.02). These results indicate that situation-specific aggressive behavior and testosterone responsiveness are functionally relevant predictors of future social behavior.

The neural signatures of distinct psychopathic traits.

Recent studies suggest that psychopathy may be associated with dysfunction in the neural circuitry supporting both threat- and reward-related processes. However, these studies have involved small samples and often focused on extreme groups. Thus, it is unclear to what extent current findings may generalize to psychopathic traits in the general population. Furthermore, no studies have systematically and simultaneously assessed associations between distinct psychopathy facets and both threat- and reward-related brain function in the same sample of participants. Here, we examined the relationship between threat-related amygdala reactivity and reward-related ventral striatum (VS) reactivity and variation in four facets of self-reported psychopathy in a sample of 200 young adults. Path models indicated that amygdala reactivity to fearful facial expressions is negatively associated with the interpersonal facet of psychopathy, whereas amygdala reactivity to angry facial expressions is positively associated with the lifestyle facet. Furthermore, these models revealed that differential VS reactivity to positive versus negative feedback is negatively associated with the lifestyle facet. There was suggestive evidence for gender-specific patterns of association between brain function and psychopathy facets. Our findings are the first to document differential associations between both threat- and reward-related neural processes and distinct facets of psychopathy and thus provide a more comprehensive picture of the pattern of neural vulnerabilities that may predispose to maladaptive outcomes associated with psychopathy.

The social neuroendocrinology of human aggression

Testosterone concentrations fluctuate rapidly in response to competitive and aggressive interactions, suggesting that changes in testosterone rather than baseline differences shape ongoing and/or future competitive and aggressive behaviors. Although recent experiments in animal models provide compelling empirical support for this idea, studies in humans have focused largely on how competitive interactions drive changes in testosterone concentrations and not how these changes influence subsequent behavior. In this paper, we provide a review of the literature on testosterone and human aggression with a main focus on the role of testosterone dynamics in modulating reactive aggression. We also speculate on one putative neural mechanism through which testosterone may bias human aggressive behavior. Finally, we conclude by highlighting important questions that should be addressed in future research.

Changes in testosterone mediate the effect of winning on subsequent aggressive behaviour

Testosterone concentrations rise rapidly in the context of competitive interactions and remain elevated in winners relative to losers. Theoretical models suggest that this divergent neuroendocrine response serves to mediate future dominance behaviours. Although research in animal models provides compelling support for this model, evidence for its applicability to human social behaviour is limited. In the current study, men and women were randomly assigned to experience a series of victories or defeats, after which aggressive behaviour was assessed using a well-validated behavioural measure. Winning produced elevated testosterone concentrations relative to losing in men, but not women. More importantly, testosterone reactivity to competition mediated the effect of winning on subsequent aggressive behaviour in men, but not women. We discuss limitations of the current study (e.g., the status manipulation may have affected other variables not measured in the study including competitiveness and physical activity expended), as well as discuss a potential neural mechanism underlying the effect of testosterone reactivity on aggressive behaviour.

Social neuroendocrinology of human aggression: Examining the role of competition-induced testosterone dynamics

A large body of evidence indicates that individual differences in baseline concentrations of testosterone (T) are only weakly correlated with human aggression. Importantly, T concentrations are not static, but rather fluctuate rapidly in the context of competitive interactions, suggesting that acute fluctuations in T may be more relevant for our understanding of the neuroendocrine mechanisms underlying variability in human aggression. In this paper, we provide an overview of the literature on T and human competition, with a primary focus on the role of competition-induced T dynamics in the modulation of human aggression. In addition, we discuss potential neural mechanisms underlying the effect of T dynamics on human aggression. Finally, we highlight several challenges for the field of social neuroendocrinology and discuss areas of research that may enhance our understanding of the complex bi-directional relationship between T and human social behavior.

Testosterone Rapidly Increases Neural Reactivity to Threat in Healthy Men: A Novel Two-Step Pharmacological Challenge Paradigm

BACKGROUND Previous research suggests that testosterone (T) plays a key role in shaping competitive and aggressive behavior in humans, possibly by modulating threat-related neural circuitry. However, this research has been limited by the use of T augmentation that fails to account for baseline differences and has been conducted exclusively in women. Thus, the extent to which normal physiologic concentrations of T affect threat-related brain function in men remains unknown. METHODS In the current study, we use a novel two-step pharmacologic challenge protocol to overcome these limitations and to evaluate causal modulation of threat- and aggression-related neural circuits by T in healthy young men (n = 16). First, we controlled for baseline differences in T through administration of a gonadotropin releasing hormone antagonist. Once a common baseline was established across participants, we then administered T to within the normal physiologic range. During this second step of the protocol we acquired functional neuroimaging data to examine the impact of T augmentation on neural circuitry supporting threat and aggression. RESULTS Gonadotropin releasing hormone antagonism successfully reduced circulating concentrations of T and brought subjects to a common baseline. Administration of T rapidly increased circulating T concentrations and was associated with heightened reactivity of the amygdala, hypothalamus, and periaqueductal grey to angry facial expressions. CONCLUSIONS These findings provide novel causal evidence that T rapidly potentiates the response of neural circuits mediating threat processing and aggressive behavior in men.

Interaction between trait anxiety and trait anger predict amygdala reactivity to angry facial expressions in men but not women

The amygdala is critically involved in mediating physiological and behavioral responses to threat. In particular, neuroimaging research indicates that the amygdala is highly responsive to facial signals of threat such as fearful and angry expressions. However, individuals differ substantially in both their relative sensitivity to threat and the magnitude of amygdala reactivity to facial signals of threat. Here, we report the novel finding that individual differences in trait anger are positively correlated with bilateral dorsal amygdala reactivity to angry facial expressions, but only among men with elevated trait anxiety scores. These findings add to the growing body of evidence indicating that variability in personality traits contribute to individual differences in threat-related amygdala reactivity and further suggest that heightened amygdala reactivity to angry faces may be uniquely involved in the expression of reactive aggression in men.

Testosterone and cortisol jointly modulate risk-taking

Recent theories propose that testosterone should be positively related to risk-taking, but empirical support is mixed. Building on the dual-hormone hypothesis, the present research tested whether testosterones role in risk-taking depends on cortisol. Study 1 (N=115) tested this hypothesis in a mixed-sex sample with self and informant reports of risk-taking. Study 2 (N=165) tested this hypothesis in a male-only sample with the Balloon Analog Risk Task, a behavioral measure of risk-taking. Across both studies, there was a positive association between basal testosterone and risk-taking among individuals low in basal cortisol but not individuals high in basal cortisol. This pattern emerged in both males and females and across multiple measures of risk-taking (self reports, informant reports, behavior). These studies provide novel empirical support for the claim that testosterone and cortisol jointly regulate risk-taking. Discussion focuses on putative mechanisms as well as implications for real-world risk-taking behaviors.