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      Tendencies toward Internet-pornography-use disorder: Differences in men and women regarding attentional biases to pornographic stimuli

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          Abstract

          Background and aims

          Several authors consider Internet-pornography-use disorder (IPD) as addictive disorder. One of the mechanisms that has been intensively studied in substance- and non-substance-use disorders is an enhanced attentional bias toward addiction-related cues. Attentional biases are described as cognitive processes of individual’s perception affected by the addiction-related cues caused by the conditioned incentive salience of the cue itself. It is assumed in the I-PACE model that in individuals prone to develop IPD symptoms implicit cognitions as well as cue-reactivity and craving arise and increase within the addiction process.

          Methods

          To investigate the role of attentional biases in the development of IPD, we investigated a sample of 174 male and female participants. Attentional bias was measured with the Visual Probe Task, in which participants had to react on arrows appearing after pornographic or neutral pictures. In addition, participants had to indicate their sexual arousal induced by pornographic pictures. Furthermore, tendencies toward IPD were measured using the short-Internetsex Addiction Test.

          Results

          The results of this study showed a relationship between attentional bias and symptom severity of IPD partially mediated by indicators for cue-reactivity and craving. While men and women generally differ in reaction times due to pornographic pictures, a moderated regression analysis revealed that attentional biases occur independently of sex in the context of IPD symptoms.

          Discussion

          The results support theoretical assumptions of the I-PACE model regarding the incentive salience of addiction-related cues and are consistent with studies addressing cue-reactivity and craving in substance-use disorders.

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          Most cited references 61

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

          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.
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            Review. The incentive sensitization theory of addiction: some current issues.

            We present a brief overview of the incentive sensitization theory of addiction. This posits that addiction is caused primarily by drug-induced sensitization in the brain mesocorticolimbic systems that attribute incentive salience to reward-associated stimuli. If rendered hypersensitive, these systems cause pathological incentive motivation ('wanting') for drugs. We address some current questions including: what is the role of learning in incentive sensitization and addiction? Does incentive sensitization occur in human addicts? Is the development of addiction-like behaviour in animals associated with sensitization? What is the best way to model addiction symptoms using animal models? And, finally, what are the roles of affective pleasure or withdrawal in addiction?
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              Attentional bias in addictive behaviors: a review of its development, causes, and consequences.

               M. Field,  W. Cox (2008)
              A wealth of research from the past two decades shows that addictive behaviors are characterized by attentional biases for substance-related stimuli. We review the relevant evidence and present an integration of existing theoretical models to explain the development, causes, and consequences of addiction-related attentional biases. We suggest that through classical conditioning, substance-related stimuli elicit the expectancy of substance availability, and this expectancy causes both attentional bias for substance-related stimuli and subjective craving. Furthermore, attentional bias and craving have a mutual excitatory relationship such that increases in one lead to increases in the other, a process that is likely to result in substance self-administration. Cognitive avoidance strategies, impulsivity, and impaired inhibitory control appear to influence the strength of attentional biases and subjective craving. However, some measures of attentional bias, particularly the addiction Stroop, might reflect multiple underlying processes, so results need to be interpreted cautiously. We make several predictions that require testing in future research, and we discuss implications for the treatment of addictive behaviors.
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                Author and article information

                Journal
                jba
                JBA
                Journal of Behavioral Addictions
                J Behav Addict
                Akadémiai Kiadó (Budapest )
                2062-5871
                2063-5303
                10 September 2018
                September 2018
                : 7
                : 3
                : 574-583
                Affiliations
                [ 1 ]Department of General Psychology: Cognition and Center for Behavioral Addiction Research (CeBAR), University of Duisburg-Essen , Duisburg, Germany
                [ 2 ]Department of Psychology and Systems Neuroscience, Justus Liebig University Giessen , Giessen, Germany
                [ 3 ]Bender Institute of Neuroimaging, Justus Liebig University Giessen , Giessen, Germany
                [ 4 ] Erwin L. Hahn Institute for Magnetic Resonance Imaging , Essen, Germany
                Author notes
                [* ]Corresponding author: Matthias Brand; Department of General Psychology: Cognition and Center for Behavioral Addiction Research (CeBAR), University of Duisburg-Essen, Forsthausweg 2, 47057 Duisburg, Germany; Phone: +49 203 379 2541; Fax: +49 203 379 1846; E-mail: jaroslaw.pekal@ 123456uni-due.de
                Article
                10.1556/2006.7.2018.70
                6426393
                30203692
                © 2018 The Author(s)

                This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License, which permits unrestricted use, distribution, and reproduction in any medium for non-commercial purposes, provided the original author and source are credited, a link to the CC License is provided, and changes – if any – are indicated.

                Page count
                Figures: 5, Tables: 4, Equations: 0, References: 61, Pages: 10
                Funding
                Funding sources: No financial support was received for this study.
                Categories
                FULL-LENGTH REPORT

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