The Incentive Salience of Alcohol

Hutchison, Kent E.; Haughey, Heather M.; Niculescu, Michelle; Schacht, Joseph P.; Kaiser, A. B.; Stitzel, Jerry A.; Horton, W. J.; Filbey, Francesca M.

doi:10.1001/archpsyc.65.7.841

Cited by 94 publications

(50 citation statements)

References 49 publications

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“…Accordingly, individuals also differ considerably in their susceptibility to mesolimbic sensitization, even when exposed to the same drugs and doses (Becker, Perry, & Westenbroek, 2012; Robinson & Berridge, 2008). Genetic factors are important determinants of susceptibility to sensitization in rodents, and genes also contribute strongly to addiction vulnerability in humans (Franklin et al, 2011; Hoft, Stitzel, Hutchison, & Ehringer, 2011; Hutchison et al, 2008; Moeller et al, 2013). Other determinants of sensitization vulnerability include gender and the presence of sex hormones, and whether the individual has had major stresses in life before taking drugs (Becker, Perry, & Westenbroek, 2012; T.…”

Section: Addiction Distorts ‘Wanting’ Versus ‘Liking’mentioning

confidence: 99%

Liking, wanting, and the incentive-sensitization theory of addiction.

Berridge¹,

Robinson²

2016

American Psychologist

968

618

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Rewards are both ‘liked’ and ‘wanted’, and those two words seem almost interchangeable. However, the brain circuitry that mediates the psychological process of ‘wanting’ a particular reward is dissociable from circuitry that mediates the degree to which it is ‘liked’. Incentive salience or ‘wanting’, a form of motivation, is generated by large and robust neural systems that include mesolimbic dopamine. By comparison, ‘liking’, or the actual pleasurable impact of reward consumption, is mediated by smaller and fragile neural systems, and is not dependent on dopamine. The incentive-sensitization theory posits the essence of drug addiction to be excessive amplification specifically of psychological ‘wanting’, especially triggered by cues, without necessarily an amplification of ‘liking’. This is due to long-lasting changes in dopamine-related motivation systems of susceptible individuals, called neural sensitization. A quarter-century after its proposal, evidence has continued to grow in support the incentive-sensitization theory. Further, its scope is now expanding to include diverse behavioral addictions and other psychopathologies.

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Section: Addiction Distorts ‘Wanting’ Versus ‘Liking’mentioning

confidence: 99%

Liking, wanting, and the incentive-sensitization theory of addiction.

Berridge¹,

Robinson²

2016

American Psychologist

968

618

View full text Add to dashboard Cite

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“…Candidate gene studies are very often undertaken from this perspective. For example, a recent study suggested that the effects of the cannabinoid 1 receptor gene (CNR1) on the risk for an alcohol use disorder is mediated by the effect of CNR1 on both the effect of alcohol on the brain and sensitivity to the rewarding effects of alcohol [23]. Similarly, others have shown that the FTO gene appears to influence obesity partially through its effects on energy intake and reduced perceptions of satiety [1].…”

Section: Indirect Influences Of Genomics On Health Behaviormentioning

confidence: 99%

The Role of Genomics in Health Behavior Change: Challenges and Opportunities

Bryan

Hutchison

2012

Public Health Genomics

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The most common causes of morbidity and mortality in the western world can be accounted for by unhealthy patterns of behavior (e.g. smoking, sedentary lifestyle, unhealthy diet, and alcohol consumption). Interventions to improve health behavior are sorely needed. To fully realize the potential of health behavior change interventions, be they individual level, community level, social structural, or policy-based, a greater understanding of the extent to which genomics can inform efforts at health behavior change is warranted. In this commentary, we explore three relatively novel possible routes to the integration of genomics and health behavior: (1) genomics may influence health behavior indirectly through intermediate phenotypes, requiring well-defined theory-based and mechanistic models of health behavior, (2) genomics may moderate response to interventions to change health behavior, and (3) genomics, specifically epigenetic variation, may be influenced by health behavior. The integration of genomics into research on interventions to change health behavior is not without challenges and will certainly require transdisciplinary collaborative science to succeed. We provide specific action points for moving the science forward to explore the extent to which genomic information can be harnessed to ultimately decrease morbidity and mortality associated with unhealthy behavior.

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“…This SNP located in exon three encodes an A–G substitution resulting in an alternative splice variant [Zhang et al, 2004]. The rs2023239 G allele has been demonstrated to be associated with greater CB1 expression in postmortem prefrontal cortex [Hutchison et al, 2008] and greater withdrawal and craving in recently abstinent cannabis users [Haughey et al, 2008]. Variation in rs2023239 also appears to influence brain response to cannabis cues with greater activation in reward circuitry including the orbitofrontal cortex, anterior cingulate gyrus, and nucleus accumbens [Filbey et al, 2010].…”

Section: Discussionmentioning

confidence: 99%

Longitudinal predictors of cannabis use and dependence in offspring from families at ultra high risk for alcohol dependence and in control families

Hill¹,

Jones²,

Steinhauer

et al. 2016

American J of Med Genetics Pt B

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Cannabis use is common among adolescents. Identification of the factors associated with continued heavy use into young adulthood and development of cannabis abuse and dependence is of considerable importance. The role of familial risk for addiction and an associated endophenotype, P300 amplitude, has not previously been related to cannabis use and dependence. A prospective longitudinal study spanning childhood and young adulthood provided the opportunity for exploring these factors, along with genetic variation, in the cannabis use behaviors of 338 young adult offspring from high and low familial risk for alcohol dependence families (ages 19–30). P300 data were collected multiple times in childhood. The association between young adult patterns of cannabis use or cannabis abuse/dependence was tested with genetic variation in the cannabinoid gene, CNR1, the ANKK1-DRD2 gene, and childhood developmental trajectories of P300. Young adult patterns of cannabis use was characterized by three patterns: (i) no use throughout; (ii) declining use from adolescence through young adulthood; and (iii) frequent use throughout. Following the low P300 trajectory in childhood predicted cannabis abuse and dependence by young adulthood. A four SNP ANKK1-DRD2 haplotype (G-G-G-C) was found to be significantly associated with the frequency of use patterns (P= 0.0008). Although CNR1 variation overall was not significantly associated with these patterns, among individuals with cannabis abuse/dependence the presence of one or both copies of the rs806368 A > G minor allele conferred a 5.4-fold increase (P= 0.003) in the likelihood that they would be in the frequent and persistent use group rather than the declining use group.

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The Incentive Salience of Alcohol

Cited by 94 publications

References 49 publications

Liking, wanting, and the incentive-sensitization theory of addiction.

Liking, wanting, and the incentive-sensitization theory of addiction.

The Role of Genomics in Health Behavior Change: Challenges and Opportunities

Longitudinal predictors of cannabis use and dependence in offspring from families at ultra high risk for alcohol dependence and in control families

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