We cite and quote directly from a very interesting article on how a family history of alcoholism contributes to impulsivity, the one psychological domain that turns up repeatedly and is supported in studies of alcoholics, addicts and those at risk genetically from these addictive disorders. Impulsivity from an early age is one variable that appears central to later addictive disorders.
“Impulsive behavior is associated with both alcohol use disorders and a family history of alcoholism (FHA). One operational definition of impulsive behavior is the stop signal task (SST), which measures the time needed to stop a ballistic hand movement.
Twenty two family history positive (FHP; age = 22.7 years, SD= 1.9) and 18 family history negative (FHN; age = 23.7, SD= 1.8) subjects performed the SST in fMRI in two randomized visits: once during intravenous infusion of alcohol. The results showed FHP being less sensitive to alcohol’s effects.
A family history of alcoholism (FHA) doubles the risk of alcohol dependence (Nurnberger et al., 2004). Beyond the risk for alcohol use disorders, familial alcoholism is also significantly associated with impulsive and externalizing behaviors (Marmorstein et al., 2009)–behaviors thought to be relevant to drinking initiation, escalation, and treatment relapse (Perry & Carroll, 2008).
Stop signal reaction time (SSRT) is distinct from delay discounting, which measures impulsive devaluing of reward as a function of time, the motor impulsiveness assessed by SSRT represents the speed (or slowness) with which an individual can accommodate an environmental demand to halt a behavior. Using the stop signal task (SST) to quantify SSRT, Nigg et al. (2004) found that alcohol-naïve adolescent offspring of alcoholic fathers had slower SSRTs than children from control families, and that SSRT predicted aggregate future alcohol and drug problems (Nigg et al., 2006).
Beyond its potential as a reflection of baseline behavioral impulsiveness, SSRT and inhibition success (but not choice reaction time) are worsened by alcohol intoxication (e.g., De Wit et al., 2000; Fillmore & Vogel-Sprott, 1999). In turn, this aggravated motor impulsiveness (lengthened SSRT) has been found to correlate with increasingly maladaptive reward-seeking behaviors (Loeber & Duka, 2009). Thus, as inhibitory control worsens during intoxication, so does ad lib alcohol consumption (Weafer & Fillmore, 2008), speaking to a potential mechanism in the loss of control of drinking.
The principal finding from this experiment (1) was a significant interaction between alcohol exposure and those with family history of alcoholism (FHA) in right prefrontal BOLD activation during motor inhibition. During clamped alcohol infusion, however, this right frontal activation in FHN was significantly reduced, while in FHP activation remained essentially unchanged. Those subjects with a smaller right prefrontal BOLD response during behavioral inhibition (FHN) also tended to need more time (had a longer SSRT) to successfully inhibit their behavioral responses so SSRT may have been lengthened by alcohol infusion.
While we found only an insignificantly smaller difference in frontal responses to correct stop signal responses in FHP subjects, which is consistent with data on another task measuring impulsivity, the Go/No-Go, of Schweinsburg, et al. (2004), which showed only FHN subjects’ activation frontal activation was significantly reduced by alcohol.
Schuckit et al. (1980) first proposed that individuals with FHA are less sensitive to alcohol’s effects. A recent meta-analysis (Quinn & Fromme, 2011) found that, when compared to lower drinkers, heavier drinkers are more sensitive to alcohol’s stimulant effects, and less sensitive to alcohol’s sedative effects.
The data form this study (1) the data are generally consistent with the concept that FHP subjects are less susceptible to (in this case, the adverse cognitive) effects of alcohol exposure in a brain region that plays an important role in behavioral inhibition.
…a resistance to the cognitively impairing effects of intoxication may carry its own risks, as subjects may perceive a reduced vulnerability to alcohol’s punishing consequences— or in this case the adverse effects in brain systems regulating behavioral control. Thus, the combination of an increased sensitivity to reward and a tolerance to alcohol’s cognitively impairing effects could represent a mechanism of increased risk of progression to heavier drinking, in particular by creating expectancies in drinkers that they can increase their consumption without adverse consequences to their behavior (Vogel-Sprott & Sdao-Jarvie, 1989).”
So to summarise, solely from our own perspective, it may not be the effect of alcohol that prompts impulsive, loss of control drinking observed in alcohol dependent individuals but impulsivity that prompts drinking behaviour initially and with an apparent lack of cognitive impairment as the result of drinking then leading some individuals to thinking they can “handle the drink” and it negative psychological effects and consequences when, over time and chronic use, it may be progressively contributing to an increased impulsive behaviour to the point where this impulsivity becomes compulsivity.
It may be that in thinking they are “in control” of drinking and it’s consequences that this paradoxically gives rise to loss of control in drinking via an increased compulsivity but much more on this another time!
1. Kareken, D. A., Dzemidzic, M., Wetherill, L., Eiler II, W., Oberlin, B. G., Harezlak, J., … & O’Connor, S. J. (2013). Family history of alcoholism interacts with alcohol to affect brain regions involved in behavioral inhibition.Psychopharmacology, 228(2), 335-345.
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