FACTORS CONTRIBUTING TO THE ESCALATION OF ALCOHOL CONSUMPTION

Abstract

Understanding factors that contribute to the escalation of alcohol consumption is key to understanding how an individual transitions from non/social drinking to AUD and to providing better treatment. In this review, we discuss how the way ethanol is consumed as well as individual and environmental factors contribute to the escalation of ethanol consumption from intermittent low levels to consistently high levels. Moreover, we discuss how these factors are modelled in animals. It is clear a vast array of complex, interacting factors influence changes in alcohol consumption. Some of these factors act early in the acquisition of ethanol consumption and initial escalation, while others contribute to escalation of ethanol consumption at a later stage and are involved in the development of alcohol dependence. There is considerable need for more studies examining escalation associated with the formation of dependence and other hallmark features of AUD, especially studies examining mechanisms, as it is of considerable relevance to understanding and treating AUD.

Keywords: alcohol; alcohol dependence; alcohol deprivation effect; alcohol use disorder; alcohol withdrawal; alcoholic; alcoholism; continuous ethanol access; drinking in the dark; ethanol; incubation of craving; intermittent ethanol access; social anxiety; social isolation; sucrose fading.

Figure 1.

Factors contributing to escalation of alcohol consumption throughout the lifespan and at different stages of drinking, and animal models.

Figure 2.. Theories of brain regions that are involved in the neurobiology of alcohol use disorder.

A. Brain regions of the mesolimbic dopamine system. B. Brain regions consisting of cortico-striatal loops. C. Extended amygdala brain regions. D. Three-stage theory. Reprinted from Kimbrough et al. (2020).

Figure 3.. Exploring the interactions between alcohol and social anxiety using murine models.

A. When adult male C57BL/6 mice were administered 0.25 g/kg ethanol i.p. prior to an extinction session after undergoing social fear conditioning (SFC+) or no fear conditioning (SFC-), it had no impact on social investigation time in either the conditioned or unconditioned mice. B. In contrast, in adolescent mice, the same dose of ethanol significantly inhibited social avoidance in the conditioned mice, while having no impact on social investigation time in unconditioned mice. A and B are adapted from Raymond et al. (2016). C. N = 10 male C57BL/6 mice underwent daily (Monday – Friday) 2 h DID sessions two hours into the dark cycle with 20% ethanol available and an empty wire mesh stimulus cage (7 × 7 × 6 cm) in the back corner of their home cage. After two weeks, mice underwent the social fear conditioning procedure, with half receiving conditioning (SFC+) and half not (SFC-). DID resumed as normal the following day. The next day (~42 h after social fear conditioning), mice underwent DID with a social stimulus (novel mouse inside a cage) for the duration of the drinking session. Cage in the graph is the average consumption on the three days when only the cage was present in the home cage during the drinking session. Consumption was measured 30 min into each session and 2 h into each session. Only data for the first 30 min is shown as the manipulation only impacted consumption in the first 30 min. Conditioned mice showed no difference in ethanol consumption during the first 30 min of their drinking session whether a social stimulus or stimulus cage was present. In contrast, unconditioned mice reduced their consumption of ethanol in the first 30 min of the drinking session when a social stimulus was present (SFC- cage vs social p < 0.05). This indicates that induction of social anxiety-like behaviour in mice removes the social buffering effect of social interactions on alcohol consumption in the first 30 min of DID.