Effects of Alcohol on Human Aggression.
Ontology highlight
ABSTRACT:
SUBMITTER: Parrott DJ
PROVIDER: S-EPMC5480964 | biostudies-literature | 2018 Feb
REPOSITORIES: biostudies-literature
Publications
Effects of Alcohol on Human Aggression.
Parrott Dominic J DJ Eckhardt Christopher I CI
Current opinion in psychology 20180201
There is little debate that alcohol is a contributing cause of aggressive behavior. The extreme complexity of this relation, however, has been the focus of extensive theory and research. And, likely due to this complexity, evidence-based programs to prevent or reduce alcohol-facilitated aggression are quite limited. We integrate I<sup>3</sup> Theory and Alcohol Myopia Theory to provide a framework that (1) organizes the myriad instigatory and inhibitory factors that moderate the effect of alcoho ...[more]
Similar Datasets
Project description:RationaleAlcohol and cannabis use have been implicated in aggression. Alcohol consumption is known to facilitate aggression, whereas a causal link between cannabis and aggression has not been clearly demonstrated.ObjectivesThis study investigated the acute effects of alcohol and cannabis on subjective aggression in alcohol and cannabis users, respectively, following aggression exposure. Drug-free controls served as a reference. It was hypothesized that aggression exposure would increase subjective aggression in alcohol users during alcohol intoxication, whereas it was expected to decrease subjective aggression in cannabis users during cannabis intoxication.MethodsHeavy alcohol (n = 20) and regular cannabis users (n = 21), and controls (n = 20) were included in a mixed factorial study. Alcohol and cannabis users received single doses of alcohol and placebo or cannabis and placebo, respectively. Subjective aggression was assessed before and after aggression exposure consisting of administrations of the point-subtraction aggression paradigm (PSAP) and the single category implicit association test (SC-IAT). Testosterone and cortisol levels in response to alcohol/cannabis treatment and aggression exposure were recorded as secondary outcome measures.ResultsSubjective aggression significantly increased following aggression exposure in all groups while being sober. Alcohol intoxication increased subjective aggression whereas cannabis decreased the subjective aggression following aggression exposure. Aggressive responses during the PSAP increased following alcohol and decreased following cannabis relative to placebo. Changes in aggressive feeling or response were not correlated to the neuroendocrine response to treatments.ConclusionsIt is concluded that alcohol facilitates feelings of aggression whereas cannabis diminishes aggressive feelings in heavy alcohol and regular cannabis users, respectively.
| S-EPMC4988999 | biostudies-literature
Project description:Although alcohol consumption is linked to increased aggression, its neural correlates have not directly been studied in humans so far. Based on a comprehensive neurobiological model of alcohol-induced aggression, we hypothesized that alcohol-induced aggression would go along with increased amygdala and ventral striatum reactivity and impaired functioning of the prefrontal cortex (PFC) under alcohol. We measured neural and behavioral correlates of alcohol-induced aggression in a provoking vs non-provoking condition with a variant of the Taylor aggression paradigm (TAP) allowing to differentiate between reactive (provoked) and proactive (unprovoked) aggression. In a placebo-controlled cross-over design with moderate alcohol intoxication (~0.6 g/kg), 35 young healthy adults performed the TAP during functional magnetic resonance imaging (fMRI). Analyses revealed that provoking vs non-provoking conditions and alcohol vs placebo increased aggression and decreased brain responses in the anterior cingulate cortex/dorso-medial PFC (provoking<non-provoking) and the ventral striatum (alcohol<placebo) across our healthy sample. Interestingly, alcohol specifically increased proactive (unprovoked) but not reactive (provoked) aggression (alcohol × provocation interaction). However, investigation of inter-individual differences revealed (1) that pronounced alcohol-induced proactive aggression was linked to higher levels of aggression under placebo, and (2) that pronounced alcohol-induced reactive aggression was related to increased amygdala and ventral striatum reactivity under alcohol, providing evidence for their role in human alcohol-induced reactive aggression. Our findings suggest that in healthy young adults a liability for alcohol-induced aggression in a non-provoking context might depend on overall high levels of aggression, but on alcohol-induced increased striatal and amygdala reactivity when triggered by provocation.
| S-EPMC4864624 | biostudies-literature
Project description:Decades of research has identified alcohol use as a contributing cause of intimate partner aggression (IPA) perpetration; however, there have been fewer studies that seek to identify mediators of the relation between alcohol use and IPA perpetration. Building on research showing a positive association between problematic drinking and relationship dissatisfaction and relationship dissatisfaction and IPA, we examined whether relationship dissatisfaction accounted for the relation between problematic drinking and IPA perpetration in couples using statistical modeling that accounted for the interdependence between partners. Our results showed that (a) actor problematic drinking was related to actor psychological and physical IPA perpetration and that this relation was partially explained by actor relationship dissatisfaction, (b) partner problematic drinking was related to actor physical and psychological IPA perpetration and that this relation was partially explained by actor relationship dissatisfaction, and (c) partner problematic drinking was related to actor psychological IPA perpetration and that this relation was partially explained by partner relationship dissatisfaction. Together, our results highlight that when partner interdependence is considered, relationship dissatisfaction could be a potential mechanism of the alcohol-IPA association and provide some evidence for different pathways for psychological and physical aggression. (PsycInfo Database Record (c) 2020 APA, all rights reserved).
| S-EPMC7609462 | biostudies-literature
Project description:Dating aggression has been identified as a priority public health concern. Although alcohol use is a known robust risk factor for dating aggression involvement, such usage is neither necessary nor sufficient for dating aggression involvement. As such, a growing topic of interest is a better understanding of when, and for whom, alcohol use increases risk. A theoretical moderator model posits that associations between alcohol use and dating aggression involvement vary depending on both background (e.g., psychopathology) and situational (e.g., relationship characteristics) risk factors. Alcohol use is thought to be more strongly associated with dating aggression in the context of these other risk factors. Using an intensive longitudinal design, we collected six waves of data spanning 6 months from 120 participants (60 females; M age W1?=?22.44). Alcohol use and relationship risk were both associated with increases in dating aggression involvement. Consistent with a moderator model, interactions emerged between alcohol use and relationship risk for subsequent dating aggression involvement. The findings underscore the importance of alcohol use and relationship risk for the development of intervention and prevention programs.
| S-EPMC5822426 | biostudies-literature
Project description:Diagnosis of mental illness (MI) inconsistently predicts aggressive behavior although co-occurrence of substance use appears to increase the frequency of aggression in MI populations. We propose that alcohol use should moderate the relationship between mental disorders marked by deficits in self-control and aggression and victimization. In the present study, alcohol use, physical aggression perpetration, physical aggression victimization, injury and psychiatric symptoms were assessed in a sample of 297 substance use disorder patients (102 women; Mage = 38.9, SD = 20.2) recruited from a residential treatment facility. Negative binomial regression analyses examined the relationship of physical aggression, victimization, and injury over the previous 12 months to symptoms of bipolar mania, psychosis, posttraumatic stress disorder, antisocial personality disorder (ASPD), and daily volume of alcohol consumed. Consistent with past research relating MI to aggression, rates of victimization were higher than rates of perpetration. Results demonstrated that alcohol use moderated the relationship of manic symptoms of bipolar disorder to perpetration of aggression and causing injury to others. Three way-interactions between gender, alcohol use, and both psychotic and ASPD symptoms were related to victimization. The combination of heavy alcohol use and increased psychotic or ASPD symptoms was related to greater victimization for women but not for men. Women with more psychotic symptoms who were heavy drinkers were also more likely to report causing injury to another person. Results were generally consistent with the multiple-thresholds model of alcohol-related aggression; however, the moderating effects of alcohol use were dependent on gender and type MI. (PsycINFO Database Record (c) 2018 APA, all rights reserved).
| S-EPMC6242760 | biostudies-literature
Project description:Alcohol is associated with nearly half of all violent crimes committed in the United States; yet, a potential neural basis for this type of pathological aggression remains elusive. Alcohol may act on N-methyl-d-aspartate receptors (NMDARs) within cortical circuits to impede processing and to promote aggression. Here, male mice were characterized as alcohol-heightened (AHAs) or alcohol non-heightened aggressors (ANAs) during resident-intruder confrontations after self-administering 1.0 g/kg alcohol (6% w/v) or water. Alcohol produced a pathological-like pattern of aggression in AHAs; these mice shifted their bites to more vulnerable locations on the body of a submissive animal, including the anterior back and ventrum after consuming alcohol. In addition, through immunoblotting, we found that AHAs overexpressed the NMDAR GluN2D subunit in the prefrontal cortex (PFC) as compared to ANAs while the two phenotypes expressed similar levels of GluN1, GluN2A and GluN2B. After identifying several behavioral and molecular characteristics that distinguish AHAs from ANAs, we tested additional mice for their aggression following preferential antagonism of GluN2D-containing NMDARs. In these experiments, groups of AHAs and ANAs self-administered 1.0 g/kg alcohol (6% w/v) or water before receiving intraperitoneal (i.p.) doses of ketamine or memantine, or infusions of memantine directly into the prelimbic (PLmPFC) or infralimbic medial PFC (ILmPFC). Moderate doses of IP ketamine, IP memantine, or intra-PLmPFC memantine increased aggression in AHAs, but only in the absence of alcohol. Prior alcohol intake blocked the pro-aggressive effects of ketamine or memantine. In contrast, only memantine, administered systemically or intra-PLmPFC, interacted with prior alcohol intake to escalate aggression in ANAs. Intra-ILmPFC memantine had no effect on aggression in either AHAs or ANAs. In sum, this work illustrates a potential role of GluN2D-containing NMDARs in the PLmPFC in alcohol-heightened aggression. GluN2D-containing NMDARs are highly expressed on cortical parvalbumin-containing interneurons, suggesting that, in a subset of individuals, alcohol may functionally alter signal integration within cortical microcircuits to dysregulate threat reactivity and promote aggression. This work suggests that targeting GluN2D-NMDARs may be of use in reducing the impact of alcohol-related violence in the human population.
| S-EPMC5916347 | biostudies-literature
Project description:BackgroundFamily members resemble each other in their propensity for aggression. In twin studies, approximately 50% of the variance in aggression can be explained by genetic influences. However, if there are genotype-environment correlation mechanisms, such as environmental manifestations of parental and sibling genotypes, genetic influences may partly reflect environmental influences. In this study, we investigated the importance of indirect polygenic score (PGS) effects on aggression.MethodsWe modeled the effect of PGSs based on 3 genome-wide association studies: early-life aggression, educational attainment, and attention-deficit/hyperactivity disorder (ADHD). The associations with aggression were tested in a within- and between-family design (37,796 measures from 7740 individuals, ages 3-86 years [mean = 14.20 years, SE = 12.03], from 3107 families, 55% female) and in a transmitted/nontransmitted PGS design (42,649 measures from 6653 individuals, ages 3-61 years [mean = 11.81 years, SE = 8.68], from 3024 families, 55% female). All participants are enrolled in the Netherlands Twin Register.ResultsWe found no evidence for contributions of indirect PGS effects on aggression in either a within- and between-family design or a transmitted/nontransmitted PGS design. Results indicate significant direct effects on aggression for the PGSs based on early-life aggression, educational attainment, and ADHD, although explained variance was low (within- and between-family: early-life aggression R2 = 0.3%, early-life ADHD R2 = 0.6%, educational attainment R2 = 0.7%; transmitted/nontransmitted PGSs: early-life aggression R2 = 0.2%, early-life ADHD R2 = 0.9%, educational attainment R2 = 0.5%).ConclusionsPGSs included in the current study had a direct (but no indirect) effect on aggression, consistent with results of previous twin and family studies. Further research involving other PGSs for aggression and related phenotypes is needed to determine whether this conclusion generalizes to overall genetic influences on aggression.
| S-EPMC10593934 | biostudies-literature
Project description:Aggression can be conceptualized as any behavior, physical or verbal, that involves attacking another person or animal with the intent of causing harm, pain or injury. Because of its high prevalence worldwide, aggression has remained a central clinical and public safety issue. Aggression can be caused by several risk factors, including biological and psychological, such as genetics and mental health disorders, and socioeconomic such as education, employment, financial status, and neighborhood. Research over the past few decades has also proposed a link between alcohol consumption and aggressive behaviors. Alcohol consumption can escalate aggressive behavior in humans, often leading to domestic violence or serious crimes. Converging lines of evidence have also shown that trauma and posttraumatic stress disorder (PTSD) could have a tremendous impact on behavior associated with both alcohol use problems and violence. However, although the link between trauma, alcohol, and aggression is well documented, the underlying neurobiological mechanisms and their impact on behavior have not been properly discussed. This article provides an overview of recent advances in understanding the translational neurobiological basis of aggression and its intricate links to alcoholism and trauma, focusing on behavior. It does so by shedding light from several perspectives, including in vivo imaging, genes, receptors, and neurotransmitters and their influence on human and animal behavior.
| S-EPMC10044835 | biostudies-literature
Project description:In terrestrial mammals, body volatiles can effectively trigger or block conspecific aggression. Here, we tested whether hexadecanal (HEX), a human body volatile implicated as a mammalian-wide social chemosignal, affects human aggression. Using validated behavioral paradigms, we observed a marked dissociation: Sniffing HEX blocked aggression in men but triggered aggression in women. Next, using functional brain imaging, we uncovered a pattern of brain activity mirroring behavior: In both men and women, HEX increased activity in the left angular gyrus, an area implicated in perception of social cues. HEX then modulated functional connectivity between the angular gyrus and a brain network implicated in social appraisal (temporal pole) and aggressive execution (amygdala and orbitofrontal cortex) in a sex-dependent manner consistent with behavior: increasing connectivity in men but decreasing connectivity in women. These findings implicate sex-specific social chemosignaling at the mechanistic heart of human aggressive behavior.
| S-EPMC8604408 | biostudies-literature
Project description:Territorial aggression in birds is widely observed and is commonly linked to sex, age, body size, physiology, seasonal cues, food resource, urbanization, and a variety of social contexts including conspecific audience effects. However, little is known about the heterospecific audience effects on territorial aggression.Here, we address an emerging idea that heterospecific audience effects may be pervasive influences in the social lives of free-living birds. We tested the hypothesis that the composition, number, and relative body size of heterospecific audiences observing an aggressive contest will influence the response probability and intensity of aggression displayed.We subjected two Paridae species, tufted titmouse (TUTI, Baeolophus bicolor) and Carolina chickadee (CACH, Poecile carolinensis), to playbacks of aggressive calls during a breeding season in north-central Florida. At widely spaced playback sites (N = 134) in woodland habitats, we characterized the makeup of heterospecific audiences, aggression type (intra vs. interspecific territoriality), local population density, and various environmental factors (tree density, wind speed, and noise level) that are likely to influence territorial aggression.We found that the presence of heterospecific audiences increased TUTI aggression levels and that both parids were more likely to respond to playback stimuli when their audiences had higher heterospecific diversity (more heterospecific individuals and species). We also found TUTI were more likely to respond when CACH were present but not vice versa.In conclusion, we found evidence that heterospecific audiences significantly influenced the metrics of territorial aggression of free-living animals and we suggest that the definition of audience effects on the behavior of free-living animals be expanded to incorporate heterospecific audiences.
| S-EPMC8131767 | biostudies-literature