These include positive moderating effects of craving inductions by minor alleles of the OPRM1, DRD2 TaqI A, and SLC6A3 genes [[ 77, 78]; cf. [ 37]], although at this point these represent isolated reports.
Specifically, the visceral theory proposes that it is not simply the experience of craving that precipitates substance use, but rather it is the effects of craving, including increased relative value of the substance, increased discounting of delayed rewards, and narrowed temporal perception, among others.
Here we show in cocaine abusers exposed to Cocaine-cues an unexpected decrease in metabolic activity in limbic brain regions (neutral > cocaine cues) and a blunting of these regional brain responses to Cocaine-cues when oral MP was administered but showed no effect on the subjective experience of craving.
Factorial analyses revealed a significant effect of the craving induction on craving, but not on the relative value of alcohol and no interaction with DRD4 VNTR genotype.
Verheul et al [ 3] proposed three types of craving – reward craving, relief craving and obsessive craving.
Both polymorphisms of interest were associated with greater craving, and exhibited an additive effect such that possession of neither polymorphism was associated with the least amount of craving, possession of either was associated with greater craving, and possession of both was associated with the greatest amount of craving.
Hence, single-item rating of subjective craving may not well manifest the nature of craving.
Possibly, the overall reduced inhibitory capacity of smokers, which was observed in the present study, reflects a general effect of nicotine craving.
In terms of the effect of the craving induction on the relative value of alcohol, no significant effect was evident (R2 =.01, F (1, 33) =.02, p >.80).
In addition, some additional methodological considerations may be relevant to no significant effect of the craving induction on the relative value of alcohol.
