While interesting from a basic science perspective because of the information it provides about reward valuation processes, interest in delay discounting has been augmented recently due to an apparent relationship between discounting and substance dependence disorders, including alcohol dependence. Numerous studies have reported that individuals who are dependent on alcohol devalue delayed monetary rewards to a larger degree than people who are not, that is, they have steeper delay discounting functions (see recent reviews by Lejuez et al., 2010
; Perry & Carroll, 2008
; Reynolds, 2006
; Yi et al., 2010
). One explanation for this higher level of discounting in dependent individuals is that substance dependence in general, and alcohol use in particular, can be conceptualized as a choice between an immediate or rapid-onset pleasurable experience (including removal of withdrawal symptoms) versus the later benefits of increased health due to abstinence. Because discounting studies have focused on delayed monetary rewards, rather than immediate pleasure and later health, this explanation of the steep discounting functions relies on there being a commodity-independent delay-related component to delay discounting, such as that suggested by the data provided earlier. Commodity-independent discounting also suggests that procedures that alter discounting of one commodity might carry over to discounting of other commodities. This, in turn, implies that identifying procedures that reduce delay discounting for monetary rewards might be useful to reduce discounting of the delayed health benefits of alcohol abstinence and, thereby, be useful for treating alcohol dependence, or other forms of substance dependence. However, research is currently unavailable to examine whether this is indeed the case.
The conceptualization of drug use as a choice between immediate alcohol-associated pleasure versus delayed health benefits is not perfect for several reasons. First, the later health benefits are not assured, in that the individual might not be healthy later due to contracting an disease unrelated to alcohol consumption, which introduces a probabilistic element to the delay discounting scenario. Second, the choice of abstinence might be associated with an unpleasant detoxification experience before health can be enjoyed later. Third, choosing to drink alcohol may be associated with unpleasant consequences as well as positive ones, including somewhat delayed consequences such as hangover. Research examining delay discounting and alcohol dependence does not ordinarily utilize such complex models. However, incorporating negative features of the choice situation may reveal important individual differences due to the lack of a strong relationship between discounting positive and negative outcomes within individuals (Mitchell & Wilson, 2010
). Additional research is needed to determine whether the use of more complex discounting scenarios strengthens the observed relationship between discounting measures and measures of alcohol dependence and recovery.
Although a well-established relationship, the physiological mechanisms underlying the relationship between delay discounting and alcohol dependence are unclear. Further, it is unknown what the relationship of delay discounting is to other features of alcohol use known to be related to the development of dependence: initiation of alcohol use, maintenance of regular use and escalation to problematic levels of use (see Carroll et al., 2010
for a review of animal literature relating discounting to these features of cocaine use). Existing research indicates that these features of alcohol use involve distinct genetic, neurobiological and environmental factors (e.g., Kendler, et al., 2008
; also see Witt, 2010
for recent review). It is plausible, but as yet unexplored, that delay discounting has different genetic relationships to different stages of alcohol use predating alcohol dependence. However, researchers have focused on simpler models linking discounting and substance abuse (e.g., Mitchell, 2004
; Perry & Carroll, 2008
). Two models are depicted in . In Model 1, heightened discounting is associated with some mechanism that results in heightened alcohol drinking and the development of dependence (). At a neural level, the mechanism may involve slight differences in the structure or functioning of neural structures implicated in reward valuation, but the mechanism can be conceptualized at different levels. For example, discounting of delayed rewards might be altered by a difference in activity of receptor systems in the nucleus accumbens (Acheson et al., 2006
; Cardinal et al., 2001
; also see Basar et al., 2010
for review), which is an area known to be critical in the reinforcing effects of alcohol (e.g., Doyon et al., 2003
; Koob, 2000
). In Model 2, higher levels of alcohol exposure in alcohol dependent individuals are associated in some way with heightened discounting (). Again this could be a direct neural effect in which alcohol alters the brain in some way, for example, reducing gray matter volume in frontal areas (Chanraud et al., 2007
), which are implicated in choosing between different rewards. Alternatively, the mechanism might be conceptualized as altering cognitive processes like working memory, which is implicated in delay discounting (e.g., Bobova et al., 2009
; Hinson et al., 2003
Three models to describe the relationship between delay discounting and alcohol dependence
The directionality of Models 1 and 2 becomes less important if delay discounting and alcohol dependence are instead viewed as products of some underlying event () that alters activity in the brain in a way that alters the value of rewards (relative value of immediate vs delayed rewards but also the relative value of alcohol consumption vs abstinence). This event might be environmentally-driven, e.g., initiation of a stressful situation like job loss. Alternatively, the event might be an effect of the immediate reward experience on the brain, for example, winning a prize for some sporting behavior. Other types of events are also possible, but all are assumed by the model to affect choices in a delay discounting task or alcohol drinking though changes in neural processing. Further, effects of these environmentally-driven or behaviorally-initiated events on the brain at a molecular level are generated by mechanisms related to the individual’s genotype. This may involve differences in the way that the genes within specific neural structures are expressed thereby generating proteins or differences in the action of pre-existing proteins that regulate neurotransmission and composition (e.g., Clarke et al., 2008
; also see review by Hariri, 2009
for examples and expansion of this argument).
Because of the underlying importance of an individual’s genotype on brain function, including its potential impact on delay discounting and alcohol dependence, the remainder of this review focuses on the data indicating that genotype plays a role in delay discounting, and that there is a genetic relationship between delay discounting and alcohol dependence.