Role of Alcohol Consumption in Escalation to Violence

Abstract

No other drug has been associated with aggressive and violent behavior more than alcohol has. A major characteristic of the link between alcohol and social interactions is the very large variation in who becomes more aggressive while drinking and who does not. Tracing the origins of these individual differences has led to a focus on predispositions, such as the antisocial behavior of Type 2 alcoholics. Successful development of an experimental procedure to model heightened aggressive behavior after voluntary consumption of alcohol has facilitated the neurobiologic analysis of the link between alcohol and aggression. From a pharmacologic perspective, consumption of low to moderate doses of alcohol engenders heightened aggressive behavior in a significant minority of individuals before the circulation of appreciable amounts of the aldehyde metabolite. Ionophoric receptors such as NMDA, 5-HT(3) and GABA(A) have been identified in the brain as major sites of action for alcohol in the dose range that is relevant for engendering heightened aggression. Actions at the GABA(A) receptor complex that depend on particular GABA(A) subunits appear to be necessary for alcohol-heightened aggression. Genes that encode the synthesis of these alpha and gamma subunits are potentially significant markers for those individuals that are prone to engage in heightened aggressive behavior after the consumption of alcohol. Of particular importance are the reciprocal interactions between GABA and serotonin. Activating specific serotonin receptor subtypes such as 5-HT(1B) receptors reduces alcohol-heightened aggressive behavior. How these GABAergic and serotonergic corticolimbic mechanisms for alcohol-heightened aggression develop during the adolescent period remains an area of urgent study.

Prevention of Alcohol-Heightened Aggression by CRF-R1 Antagonists in Mice: Critical Role for DRN-PFC Serotonin Pathway

“…These results suggest that CRF-R1 in areas other than the DRN probably modulate species-typical levels of aggressive behavior, whereas DRN CRF-R1 are particularly important when aggression is performed under the influence of alcohol. In all but one of the several experiments of this study (MTIP systemic CRF-R1 and 5-HT on alcohol-heightened aggression IM Quadros et al experiment), alcohol-heightened aggression was significantly observed in the overall group of animals, despite the known individual differences in this phenomenon (see Miczek et al, 2004). Such differences may have contributed to the absence of alcohol-escalated aggression in that particular cohort of mice.…”

“…Evidence for alcohol as a promoter of escalated levels of aggressive behavior has been established in laboratory settings, particularly in susceptible subgroups of individuals (Cloninger, 1987;Miczek et al, 2004). In mice, low to moderate doses of alcohol can escalate aggressive behaviors to levels that are significantly higher and more injurious than species-typical aggression (Miczek et al, 1998;Miczek and de Almeida, 2001), modeling critical features of alcoholescalated aggression.…”

Associations between diurnal preference, sleep quality and externalizing behaviours: a behavioural genetic analysis

“…For example, individuals who prefer the night hours have more opportunities to engage in ASB. Activities such as consuming alcohol may be more likely in ' eveningtypes ' and alcohol consumption is an activity that is known to predispose to ASB (Miczek et al 2004).…”

Escalated Aggression after Alcohol Drinking in Male Mice: Dorsal Raphé and Prefrontal Cortex Serotonin and 5-HT1B Receptors

“…Importantly, in certain situations, Alc has the ability to facilitate aggressive actions. It has been repeatedly demonstrated, in multiple species, that some individuals are sensitive to the aggression-heightening effects of moderate doses of Alc, while most are not (Chance et al, 1973;Peeke et al, 1973;Miczek and O'Donnell, 1980;Lister and Hilakivi, 1988;Miczek et al, 1993Miczek et al, , 2004b. Although the neurobiological basis for the differential response to Alc is not yet known, there is compelling evidence for a significant role of the serotonin (5-HT) system in the modulation of impulsive aggressive behavior (Olivier et al, 1989;Olivier and Mos, 1992;Miczek et al, 2004a).…”