Have you ever wondered why we act aggressively? This type of behavior is generally defined as intentional infliction of damage or harm, and among our more “civilized” cultures of the modern world is also considered a serious problem. Yet, aggression played a central role in our evolution in the context of defending or obtaining resources, and virtually every other species does it. To better understand the basis for human aggression, Rosa Martins de Almeida and colleagues from Brazil synthesize the existing research on the topic and propose an integration of behavioral, hormonal, and neural routes through which aggression arises.

Aggression can take many forms, which has led to several classifications and dimensions. One example is the way in which it is expressed: directly and indirectly.While the first is characterized by physical or verbal behavior intended to cause harm to someone, the second one is characterized by a behavior intended to harm social relations of an individual or a group. This classification has a strong sexual dimorphism, with males tending to be more direct, especially physically, and externalize their problems onto others, and females tending to be more indirect, especially verbally, and internalize their issues. Another classification system is based on the function of the aggression. Impulsive aggression is defined as a hostile act in response to stimuli perceived as threatening or frustrating, and instrumental aggression is a deliberately planned behavioral pattern to attain a goal.

Regardless of the type of aggression, Martins de Almeida proposes that biological and environmental factors must be considered. The first is hormonal regulation, with testosterone being the poster-child of aggressive behavior. There has been a consistent association between the two in research, with testosterone being strongly related to dominance behavior and victory in both men and women. However, its role in aggression has not been fully established, which may be explained (at least in part) by cortisol. Chronically elevated levels of this hormone can suppress gonad function and synthesis of androgens such as testosterone, and the ratio of testosterone and cortisol can regulate social aggression. Additionally, high levels of DHEA are correlated with the severity of aggressive events and antisocial behavior, which may be explained by the fact that DHEA is an androgen precursor hormone.

Second are neurobiological mechanisms, neurotransmitters, and their connection with several genes and hormones. The Prefrontal Cortex (PFC), which plays a central role in the control of behavior and decision-making, is the region that is most extensively associated with impulsive aggression in humans. However, other regions such as the orbitofrontal cortex (OFC) and the Amygdala also play a role. For instance, the amygdala is involved in the processing of emotional reactions and is regulated by the OFC, and testosterone increases the neural activity in the amygdala through hindering its connectivity with the OFC. This may partly explain the role of testosterone in increasing impulsive aggression.On the other hand, cortisol works against the amygdala. In other words, the testosterone/cortisol ratio can increase the bottom-up reaction (i.e., emphasizing amygdala activation) and impair the top-down control (reducing the inhibitory action of the OFC and ACC) of impulsive aggression.

Aside from actual brain structure, human aggression is related to the inhibitory action of the GABA neurotransmitter and the dysfunction of the serotonergic system. Regarding the former, alcohol is a great example as it is a positive allosteric modulator of the GABA receptor, and its recreational intake or abuse often increases the occurrence of aggressive behaviors. Stress can be another decisive factor for the sensitivity of the GABA receptor, as cortisol can interfere with the endogenous positive modulators of the GABA receptors, and consequently, reduce impulsive aggression. Regarding the latter, it has been shown that the use of selective serotonin reuptake inhibitors (SSRI) has a significant clinical effect in reducing violent behavior and that psychiatric patients with a history of aggression usually have changes in serotonergic neurotransmission. Interestingly, in people with a high level of aggression, there is a greater density of serotonergic receptors in brain regions related to impulse control.

Lastly there is a genetic component (isn’t there always?). Monoamine Oxidase A (MAOA) is an enzyme involved in the degradation of monoamines, especially 5-HT, and the allele responsible for low expression of MAOA is epidemiologically correlated with a higher probability of the occurrence of aggression and impulsiveness. Similar findings have been reported when investigating the role of the functional polymorphism related to the 5-HT transporter, and the 5-HT transporter gene responsible for low transcriptional activity and decreased 5-HT reuptake, has been associated with the occurrence of violent acts.

OFC = Orbitofrontal Cortex; PFC = Prefrontal Cortex; GABA = γ-Aminobutyric Acid; 5-HT = serotonin; HPA = hypothalamic–pituitary–adrenal axis; vmPFC = Ventromedial Prefrontal Cortex; ACC = Anterior Cingulate Cortex.