Addiction is driven by excessive goal-directed drug choice under negative affect: translational critique of habit and compulsion theory

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

Drug addiction may be a goal-directed choice driven by excessive drug value in negative affective states, a habit driven by strong stimulus−response associations, or a compulsion driven by insensitivity to costs imposed on drug seeking. Laboratory animal and human evidence for these three theories is evaluated. Excessive goal theory is supported by dependence severity being associated with greater drug choice/economic demand. Drug choice is demonstrably goal-directed (driven by the expected value of the drug) and can be augmented by stress/negative mood induction and withdrawal—effects amplified in those with psychiatric symptoms and drug use coping motives. Furthermore, psychiatric symptoms confer risk of dependence, and coping motives mediate this risk. Habit theory of addiction has weaker support. Habitual behaviour seen in drug-exposed animals often does not occur in complex decision scenarios, or where responding is rewarded, so habit is unlikely to explain most human addictive behaviour where these conditions apply. Furthermore, most human studies have not found greater propensity to habitual behaviour in drug users or as a function of dependence severity, and the minority that have can be explained by task disengagement producing impaired explicit contingency knowledge. Compulsion theory of addiction also has weak support. The persistence of punished drug seeking in animals is better explained by greater drug value (evinced by the association with economic demand) than by insensitivity to costs. Furthermore, human studies have provided weak evidence that propensity to discount cost imposed on drug seeking is associated with dependence severity. These data suggest that human addiction is primarily driven by excessive goal-directed drug choice under negative affect, and less by habit or compulsion. Addiction is pathological because negative states powerfully increase expected drug value acutely outweighing abstinence goals.

Related collections

Most cited references 283

Record: found
Abstract: found
Article: not found

The neural basis of drug craving: an incentive-sensitization theory of addiction.

T E Robinson, K C Berridge (1993)

This paper presents a biopsychological theory of drug addiction, the 'Incentive-Sensitization Theory'. The theory addresses three fundamental questions. The first is: why do addicts crave drugs? That is, what is the psychological and neurobiological basis of drug craving? The second is: why does drug craving persist even after long periods of abstinence? The third is whether 'wanting' drugs (drug craving) is attributable to 'liking' drugs (to the subjective pleasurable effects of drugs)? The theory posits the following. (1) Addictive drugs share the ability to enhance mesotelencephalic dopamine neurotransmission. (2) One psychological function of this neural system is to attribute 'incentive salience' to the perception and mental representation of events associated with activation of the system. Incentive salience is a psychological process that transforms the perception of stimuli, imbuing them with salience, making them attractive, 'wanted', incentive stimuli. (3) In some individuals the repeated use of addictive drugs produces incremental neuroadaptations in this neural system, rendering it increasingly and perhaps permanently, hypersensitive ('sensitized') to drugs and drug-associated stimuli. The sensitization of dopamine systems is gated by associative learning, which causes excessive incentive salience to be attributed to the act of drug taking and to stimuli associated with drug taking. It is specifically the sensitization of incentive salience, therefore, that transforms ordinary 'wanting' into excessive drug craving. (4) It is further proposed that sensitization of the neural systems responsible for incentive salience ('for wanting') can occur independently of changes in neural systems that mediate the subjective pleasurable effects of drugs (drug 'liking') and of neural systems that mediate withdrawal. Thus, sensitization of incentive salience can produce addictive behavior (compulsive drug seeking and drug taking) even if the expectation of drug pleasure or the aversive properties of withdrawal are diminished and even in the face of strong disincentives, including the loss of reputation, job, home and family. We review evidence for this view of addiction and discuss its implications for understanding the psychology and neurobiology of addiction.

0 comments Cited 601 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Human and rodent homologies in action control: corticostriatal determinants of goal-directed and habitual action.

Bernard W. Balleine, John O'Doherty (2010)

Recent behavioral studies in both humans and rodents have found evidence that performance in decision-making tasks depends on two different learning processes; one encoding the relationship between actions and their consequences and a second involving the formation of stimulus-response associations. These learning processes are thought to govern goal-directed and habitual actions, respectively, and have been found to depend on homologous corticostriatal networks in these species. Thus, recent research using comparable behavioral tasks in both humans and rats has implicated homologous regions of cortex (medial prefrontal cortex/medial orbital cortex in humans and prelimbic cortex in rats) and of dorsal striatum (anterior caudate in humans and dorsomedial striatum in rats) in goal-directed action and in the control of habitual actions (posterior lateral putamen in humans and dorsolateral striatum in rats). These learning processes have been argued to be antagonistic or competing because their control over performance appears to be all or none. Nevertheless, evidence has started to accumulate suggesting that they may at times compete and at others cooperate in the selection and subsequent evaluation of actions necessary for normal choice performance. It appears likely that cooperation or competition between these sources of action control depends not only on local interactions in dorsal striatum but also on the cortico-basal ganglia network within which the striatum is embedded and that mediates the integration of learning with basic motivational and emotional processes. The neural basis of the integration of learning and motivation in choice and decision-making is still controversial and we review some recent hypotheses relating to this issue.

0 comments Cited 508 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Drug Addiction: Updating Actions to Habits to Compulsions Ten Years On.

Barry Everitt, Trevor W. Robbins (2016)

A decade ago, we hypothesized that drug addiction can be viewed as a transition from voluntary, recreational drug use to compulsive drug-seeking habits, neurally underpinned by a transition from prefrontal cortical to striatal control over drug seeking and taking as well as a progression from the ventral to the dorsal striatum. Here, in the light of burgeoning, supportive evidence, we reconsider and elaborate this hypothesis, in particular the refinements in our understanding of ventral and dorsal striatal mechanisms underlying goal-directed and habitual drug seeking, the influence of drug-associated Pavlovian-conditioned stimuli on drug seeking and relapse, and evidence for impairments in top-down prefrontal cortical inhibitory control over this behavior. We further review animal and human studies that have begun to define etiological factors and individual differences in the propensity to become addicted to drugs, leading to the description of addiction endophenotypes, especially for cocaine addiction. We consider the prospect of novel treatments for addiction that promote abstinence from and relapse to drug use.

0 comments Cited 372 times – based on 0 reviews      Review now

Bookmark

All references

Author and article information

Contributors

Lee Hogarth:

ORCID: http://orcid.org/0000-0002-0299-5748

L.hogarth@exeter.ac.uk

Journal

Journal ID (nlm-ta): Neuropsychopharmacology

Journal ID (iso-abbrev): Neuropsychopharmacology

Title: Neuropsychopharmacology

Publisher: Springer International Publishing (Cham )

ISSN (Print): 0893-133X

ISSN (Electronic): 1740-634X

Publication date (Electronic): 6 January 2020

Publication date PMC-release: 6 January 2020

Publication date (Print): April 2020

Volume: 45

Issue: 5

Pages: 720-735

Affiliations

ISNI 0000 0004 1936 8024, GRID grid.8391.3, School of Psychology, , University of Exeter, ; Washington Singer Building, Perry Road, Exeter, EX4 4QG UK

Author information

Lee Hogarth http://orcid.org/0000-0002-0299-5748

Article

Publisher ID: 600

DOI: 10.1038/s41386-020-0600-8

PMC ID: 7265389

PubMed ID: 31905368

SO-VID: 989f658d-41cc-4f79-a71b-fda108dd2455

License:

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.