How does the First Drink really get you Drunk?

In treatment circles, I have constantly heard the refrain “one is not enough and two is too many!” and “the first drink gets you drunk” which points to a difficulty certain people have with stopping once they start drinking; a “loss of control” over drinking.

It is as if drinking gives you a thirst rather than taking it away. Many thousands of recovering alcoholics will tell you about this phenomenon – how they had only intended to have a couple but then lost a weekend to drinking instead.

It is an essential question to get to the bottom of, why do certain people not have the ability  or have a reduced ability to stop once they start.

I came across an article from a few years back which addressed this issue (1) .

In those with a family history of alcoholism,  drinking alcohol affects how the brain responds to an alcohol cue – in other words these individuals appear to want more compared to controls when they see alcohol cues. So drinking alcohol heightens a wanting for alcohol  rather than causing a  feeling of having had enough (not wanting). 

Although a family history of alcoholism is the strongest risk factor for developing alcohol dependence, there are few studies of the association between familial alcoholism and the human brain’s reward system activity. This study used a functional magnetic resonance imaging (fMRI) to determine how family history affects the brain’s response to subjects’ preferred alcoholic drink odors (AO).

A family history of alcoholism doubles the odds of developing alcoholism (Hasin et al., 1997; Nurnberger et al., 2004). While environmental influences exert considerable influence in early adolescence, twin studies show an increasingly larger genetic influence by age 18 (Dick, Rose, & Kaprio, 2006), with a family history of alcoholism being a significant factor in the transition from abusive to dependent drinking (Hasin, Paykin, & Endicott, 2001).

While a number of studies have examined the human cerebral response to alcohol-related cues, particularly in alcoholics (e.g., Bragulat et al., 2008; Filbey et al., 2008b;Kareken et al., 2004; Myrick et al., 2008; Tapert et al., 2004;Wrase et al., 2007), very little research shows how familial alcoholism affects the brain response to alcohol-related cues— particularly in at-risk individuals who have yet to become dependent.

 

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Animal research suggests that selective breeding for alcohol preference might affect the heavily dopaminergic mesocorticolimbic reward system. For example, rodents selectively bred to prefer alcohol have reduced dopamine in the striatum (see Murphy et al., 2002; Strother et al., 2005) and medial prefrontal cortex (Engleman et al., 2006), but greater striatal dopaminergic responses to alcohol itself (Bustamante et al., 2008; also see Smith & Weiss, 1999;Weiss et al., 1993). In at least one case, alcohol-preferring rats (compared to Wistar rats) showed a greater dopaminergic response in the ventral striatum during alcohol anticipation (Katner, Kerr, & Weiss, 1996). In non-abusive drinkers without a family history of alcoholism there is greater striatal dopamine receptor availability (Volkow et al., 2006), suggesting a potential protective factor.

Family history affects the brain’s response to alcohol’s olfactory (smell) cues in non-dependent, at-risk heavy drinkers and this study  sought to determine how acute alcohol exposure affects the reward system’s response to alcohol’s conditioned cues by using intravenous (IV) alcohol infusion— a method that prescribes a constant level of brain alcohol throughout functional imaging and avoids the highly variable time courses of breath alcohol concentrations that accompany oral consumption (O’Connor et al., 1998; Plawecki et al., 2007;Ramachandi et al., 2004; Ramchandani et al., 1999).

So in effect alcohol was infused rather than simply drunk.

The researchers hypothesized that a family history of alcoholism would be associated with stronger responses to alcoholic drink aromas in the mesocorticolimbic reward system, and that a low-level of steady-state brain exposure to alcohol would potentiate these stimulus-induced responses (Bragulat et al., 2008). Such a potentiation could reflect a possible substrate for priming, when alcohol exposure increases desire to drink (De WitDe Wit, 2000).

In this study (1) fourteen non-dependent heavy drinkers (HD) who were family history positive (FHP) participated, as did 12 HD who were family history negative (FHN). Subjects were imaged under both alcohol intoxication and placebo.

In this study alcohol intoxication dampened this “cued” response in the HD-FHP but potentiated (heightened)  it in the HD-FHN.

This suggests that a family history of alcoholism and brain exposure to alcohol interact in heavy drinkers to differentially affect how the brain responds to alcohol cues.

In conclusion, frontal regions thought to process reward value may respond differently to alcohol’s classically conditioned cues in subjects with a family history of alcoholism. While alcohol appears to dampen medial frontal responses to alcohol cues in HD-FHP, it may enhance it in HD-FHN. Genetic background may therefore determine when, and under what circumstances, cues activate the reward network

References

Kareken, D. A., Bragulat, V., Dzemidzic, M., Cox, C., Talavage, T., Davidson, D., & O’Connor, S. J. (2010). Family history of alcoholism mediates the frontal response to alcoholic drink odors and alcohol in at-risk drinkers. Neuroimage,50(1), 267-276.

 

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