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E. J. Langer's paper, 'The illusion of control' (1975), showed that people act in ways that suggest they hold illusory beliefs in their ability to control the outcome of chance-determined games. This highly cited paper influenced the emerging field of gambling studies, and became a building block for cognitive approaches to problem gambling. Over time, this work has inspired therapeutic approaches based on cognitive restructuring, preventative programmes focused upon gambling myths and regulatory scrutiny of skill mechanics in modern gambling products. However, the psychological mechanisms underlying the 'illusion of control' remain elusive.

Supplementary Information The online version contains supplementary material available at https://doi.org/10.1038/s41598-022-26963-9, The structural addictive characteristics of gambling products are important targets for prevention, but can be unintuitive to laypeople. In the PictoGRRed (Pictograms for Gambling Risk Reduction) study, we aimed to develop pictograms that illustrate the main addictive characteristics of gambling products and to assess their impact on identifying the addictiveness of gambling products by laypeople. We conducted a three-step study: (1) use of a Delphi consensus method among 56 experts from 13 countries to reach a consensus on the 10 structural addictive characteristics of gambling products to be illustrated by pictograms and their associated definitions, (2) development of 10 pictograms and their definitions, and (3) study in the general population to assess the impact of exposure to the pictograms and their definitions (n = 900). French-speaking experts from the panel assessed the addictiveness of gambling products (n = 25), in which the mean of expert's ratings was considered as the true value. Participants were randomly provided with the pictograms and their definitions, or with a standard slogan, or with neither (control group). We considered the control group as representing the baseline ability of laypeople to assess the addictiveness of gambling products. Each group and the French-speaking experts rated the addictiveness of 14 gambling products. The judgment criterion was the intraclass coefficients (ICCs) between the mean ratings of each group and the experts, reflecting the level of agreement between each group and the experts. Exposure to the pictograms and their definition doubled the ability of laypeople to assess the addictiveness of gambling products compared with that of the group that read a slogan or the control group (ICC = 0.28 vs. 0.14 (Slogan) and 0.14 (Control)). Laypeople have limited awareness of the addictive characteristics of gambling products. The pictograms developed herein represent an innovative tool for universally empowering prevention and for selective prevention., Santé Publique France

Background and aimsThe Conceptual Framework of Harmful Gambling moves beyond a symptoms-based view of harm and addresses a broad set of factors related to the risks and effects of gambling harmfully at the individual, family, and community levels. Coauthored by international research experts and informed by multiple stakeholders, Gambling Research Exchange (GREO) facilitated the framework development in 2013 and retains responsibility for regular updates and mobilization. This review article presents information about the revised version of the Conceptual Framework of Harmful Gambling completed in late 2018.MethodsWe describe eight interrelated factors depicted in the framework that represent major themes in gambling ranging from the specific (gambling environment, exposure, gambling types, and treatment resources) to the general (cultural, social, psychological, and biological influences). After outlining the framework development and collaborative process, we highlight new topics for the recent update that reflect changes in the gambling landscape and prominent discourses in the scientific community. Some of these topics include social and economic impacts of gambling, and a new model of understanding gambling related harm.Discussion and conclusionsWe address the relevance of the CFHG to the gambling and behavioral addictions research community. Harm-based frameworks have been undertaken in other areas of addiction that can both inform and be informed by a model dedicated to harmful gambling. Further, the framework brings a multi-disciplinary perspective to bear on antecedents and factors that co-occur with harmful gambling.

Modern slot machines are among the more harmful forms of gambling. Psychophysiological measures may provide a window into mental processes that underpin these harms. Here we investigated pupil dilation derived from eye tracking as a means of capturing changes in sympathetic nervous system arousal following outcomes on a real slot machine. We hypothesized that positively reinforcing slot machine outcomes would be associated with increases in arousal, reflected in larger pupil diameter. We further examined the contribution of game luminance fluctuations on pupil diameter. In Experiment 1A, experienced slot machine gamblers (N = 53) played a commercially-available slot machine in a laboratory for 20 minutes while wearing mobile eye tracking glasses. Analyses differentiated loss outcomes, wins, losses-disguised-as-wins, and (free-spin) bonus features. Bonus features were associated with rapid increases in pupil diameter following the onset of outcome-related audiovisual feedback, relative to losses. In Experiment 1B, luminance data were extracted from captured screen videos (derived from Experiment 1A) to characterize on-screen luminance changes that could modulate pupil diameter. Bonus features and wins were associated with pronounced and complex fluctuations in screen luminance (≈50 L and ≈25L, respectively). However, the pupil dilation that was observed to bonus features in Experiment 1A coincided temporally with only negligible changes in screen luminance, providing partial evidence that the pupil dilation to bonus features may be due to arousal. In Experiment 2, 12 participants viewed pairs of stimuli (scrambled slot machine images) at luminance difference thresholds of ≈25L, ≈50L, and ≈100L. Scrambled images presented at luminance differences of ≈25L and greater were sufficient to cause pupillary responses. Overall, pupillometry may detect event-related changes in sympathetic nervous system arousal following gambling outcomes, but researchers must pay careful attention to substantial in-game luminance changes that may confound arousal-based interpretations.

Funder: Gates Cambridge Trust; doi: https://doi.org/10.13039/501100005370, Funder: DH | National Institute for Health Research (NIHR); doi: https://doi.org/10.13039/501100000272, Serotonin is involved in updating responses to changing environmental circumstances. Optimising behaviour to maximise reward and minimise punishment may require shifting strategies upon encountering new situations. Likewise, autonomic responses to threats are critical for survival yet must be modified as danger shifts from one source to another. Whilst numerous psychiatric disorders are characterised by behavioural and autonomic inflexibility, few studies have examined the contribution of serotonin in humans. We modelled both processes, respectively, in two independent experiments (N = 97). Experiment 1 assessed instrumental (stimulus-response-outcome) reversal learning whereby individuals learned through trial and error which action was most optimal for obtaining reward or avoiding punishment initially, and the contingencies subsequently reversed serially. Experiment 2 examined Pavlovian (stimulus-outcome) reversal learning assessed by the skin conductance response: one innately threatening stimulus predicted receipt of an uncomfortable electric shock and another did not; these contingencies swapped in a reversal phase. Upon depleting the serotonin precursor tryptophan-in a double-blind randomised placebo-controlled design-healthy volunteers showed impairments in updating both actions and autonomic responses to reflect changing contingencies. Reversal deficits in each domain, furthermore, were correlated with the extent of tryptophan depletion. Initial Pavlovian conditioning, moreover, which involved innately threatening stimuli, was potentiated by depletion. These results translate findings in experimental animals to humans and have implications for the neurochemical basis of cognitive inflexibility.

Background and aims Immersion during slot machine gambling has been linked to disordered gambling. Current conceptualizations of immersion (namely dissociation, flow and the machine zone) make contrasting predictions as to whether gamblers are captivated by the game per se ('zoned in') or motivated by the escape that immersion provides ('zoned out'). We examined whether selected eye-movement metrics can distinguish between these predictions. Design and setting Pre-registered, correlational analysis in a laboratory setting. Participants gambled on a genuine slot machine for 20 minutes while wearing eye-tracking glasses. Participants Fifty-three adult slot machine gamblers who were not high-risk problem gamblers. Measurements We examined self-reported immersion during the gambling session and eye movements at different areas of the slot machine screen (the reels, the credit window, etc.). We further explored these variables' relationships with saccade count and amplitude. Findings The ratio of dwell time on the game's credit window relative to the game's reels was positively associated with immersion (t(51) = 1.68, P = 0.049 one-tailed, R2 = 0.05). Follow-up analyses described event-related changes in these patterns following different spin outcomes. Conclusions Immersion while gambling on a slot machine appears to be associated with active scanning of the game and a focus on the game's credit window. These results are more consistent with a 'zoned in' account of immersion aligned with flow theory than a 'zoned out' account based on escape.

Rationale: \ud Gambling and alcohol use are recreational behaviours that share substantial commonalities at a phenomenological, clinical, and neurobiological level. Past studies have shown that alcohol can have a disinhibiting effect on gambling behaviour, in terms of bet size and persistence. \ud Objectives: \ud To characterize how alcohol affects biases in judgment and decision-making that occur during gambling, with a focus on sequential decision-making including the gambler’s fallacy. \ud Methods: \ud Sequential biases were elicited via a roulette-based gambling task. Using a standard between-groups alcohol challenge procedure, male participants played the roulette task 20 minutes after receiving an alcoholic (0.8g/kg; n = 22) or placebo (n = 16) beverage. The task measured colour choice decisions (red/black) and bet size, in response to varying lengths of colour runs and winning/losing feedback streaks.\ud Results: \ud Across both groups, a number of established sequential biases were observed. On colour choice, there was an effect of run length in line with the gambler’s fallacy, which further varied by previous feedback (wins vs losses). Bet size increased with feedback streaks, especially for losing streaks. Compared to placebo, the alcohol group placed higher bets following losses compared to wins. \ud Conclusions: \ud Increased bet size after losses following alcohol consumption may reflect increased loss chasing that may amplify gambling harms. Our results do not fit a simple pattern of enhanced gambling distortions or reward sensitivity, but help contextualize the effects of alcohol on gambling to research on decision-making biases.

Loot boxes are virtual goods in video games that produce randomly-generated in-game rewards, and have attracted scrutiny because of a resemblance to gambling. This study tests relationships between gaming involvement, engagement with loot boxes, and their associations with disordered gambling and gambling-related cognitions. Online questionnaires were completed by 144 adults via MTurk (Study 1) and 113 undergraduates (Study 2). Gaming and loot box-related variables included estimated time spent gaming and monthly expenditure, the Internet Gaming Disorder Scale (IGDS), and questions that assessed perceptions and behaviours related to loot boxes. Most participants thought loot boxes were a form of gambling (68.1% & 86.2%). A subset of items were condensed into a unidimensional "Risky Loot-box Index" (RLI) via exploratory factor analysis. In Study 1, the RLI showed significant associations with the Problem Gambling Severity Index (r = .491, p < .001) and the Gambling Related Cognitions Scale (r = .518, p < .001). Overall, gambling-related variables predicted 37.1% (p < .001) of the variance in RLI scores. Findings were replicated, though attenuated, in Study 2. These results demonstrate that besides the surface similarity of loot boxes to gambling, loot box engagement is correlated with gambling beliefs and problematic gambling behaviour in adult gamers.

Background The prefrontal cortex regulates behavioural adaptation in response to feedback. However, the causal role of different prefrontal regions remains unclear, based on indirect evidence derived from functional neuroimaging. Neuroimaging studies show dorsomedial prefrontal activation during feedback monitoring, whereas the ventrolateral prefrontal cortex engages during behavioural adaptation (shifting). Objective We used high-definition transcranial direct current stimulation (HD-tDCS) to elucidate the roles of the ventrolateral prefrontal cortex (vlPFC) and the dorsomedial prefrontal cortex (dmPFC) in behaviour change, using a probabilistic reversal learning task (PRLT). Method Fifty-two healthy adults were randomly assigned to receive cathodal HD-tDCS to inhibit the vlPFC or the dmPFC versus sham stimulation, prior to completing the PRLT. The outcome measures were the number of perseverative errors and the electroencephalography (EEG) signals of feedback-related negativity (FRN) in the PRLT. We hypothesised that inhibition of the vlPFC would be specifically associated with more perseverative errors and weaker FRNs. Results We found that vlPFC inhibition was associated with higher perseverative errors compared to sham and dmPFC stimulation conditions. Although there were no statistically significant differences in FRN amplitudes, the effect sizes indicate an association between inhibition of the vlPFC and lower FRN amplitudes. Conclusion Our findings support a causal role of the vlPFC on feedback-based behavioural adaptation, which is critical for adaptive goal-driven behaviour.

Concerns regarding the similarities between video game 'loot boxes' and gambling have been supported by correlations in survey studies between loot box engagement and problem gambling scores. It is generally noted that this correlation could reflect loot box users migrating to conventional gambling, and/or people with gambling problems being attracted to loot boxes when they play video games. We describe a third possibility, that when gamers complete problem gambling screens they may be referring to harms incurred from their loot box use. Using three secondary datasets from cross-sectional online surveys, we explore this account in two ways. First, in participants who do not endorse any participation in conventional forms of gambling, we compare rates of positive (i.e. non-zero) scores on the Problem Gambling Severity Index (PGSI) in participants with and without loot box use. Second, noting that some PGSI items have less relevance to loot box use versus gambling, we compare endorsement rates of individual PGSI items, in gamers versus gamblers, and loot box users vs non-loot box users (focusing on item 3 "going back another day to win back the money you lost"). In analysis 1, positive PGSI scorers among non-gamblers were significantly elevated in loot box users vs non-loot box users, although absolute numbers were low overall. In analysis 2, there were no reliable differences (gamers vs gamblers, loot box users vs non-loot box users) in PGSI item 3 endorsement rates. We conclude that these results provide partial support for this third option, and highlight a need for future studies to consider this possibility more directly.

Background and aims Money is central to psychological definitions of gambling, but contemporary accounts are ambiguous regarding the role of financial motives in disordered gambling. The aims of the current research were to obtain meta-analytic weighted effect sizes for zero-order associations of financial motives against gambling frequency and level of problem gambling, as well as partial associations after controlling for other motives (e.g. coping). Methods A meta-analysis of the literature through February 2021 was undertaken. Studies were identified from multiple sources (e.g. database search, other researchers). PRISMA standards were followed when screening identified records and extracting relevant data. The data analytic plan was pre-registered. We included 44 cross-sectional studies that involved student, community and clinical samples of people who gamble (sample sizes ranged from 22-5666), using validated self-report measures of financial gambling motives alongside measures of either gambling frequency and/or problem gambling. Results Financial gambling motives were positively associated with gambling frequency, r = 0.29, 95% CI = [0.21, 0.37], n = 22 738, and level of problem gambling, r = 0.35, 95% CI = [0.31, 0.38], n = 38 204, with moderate effect sizes. Partial associations after controlling for overlapping variance with other gambling motives were also positive (gambling frequency: β = 0.14, 95% CI = [0.05, 0.22], n = 13 844; level of problem gambling: β = 0.18, 95% CI = [0.13, 0.22], n = 28 146), with small-to-moderate effect sizes. Effect sizes were heterogeneous and the extent of heterogeneity was high. Analyses of the zero-order association involving gambling frequency indicated that gambling motives measure (greater for Gambling Motives Questionnaire-Financial) and sample mean age (greater for younger samples) were moderators. No other moderators were statistically significant. Conclusions Financial gambling motives appear to be reliably and positively associated with both gambling frequency and level of problem gambling.

Background and aimsIndividuals with gambling disorder display increased levels of risk-taking, but it is not known if it is associated with an altered subjective valuation of gains and/or losses, perception of their probabilities, or integration of these sources of information into expected value.MethodsParticipants with gambling disorder (n = 48) were compared with a healthy comparison group (n = 35) on a two-choice lottery task that involved either gains-only or losses-only gambles. On each trial, two lotteries were displayed, showing the associated probability and magnitude of the possible outcome for each. On each trial, participants chose one of the two lotteries, and the outcome was revealed.ResultsChoice behaviour was highly sensitive to the expected value of the two gambles in both the gain and loss domains. This sensitivity to expected value was attenuated in the group with gambling disorder. The group with gambling disorder used both probability and magnitude information less, and this impairment was greater for probability information. By contrast, they used prior feedback (win vs loss) to inform their next choice, despite the independence of each trial. Within the gambling disorder group, problem gambling severity and trait gambling-related cognitions independently predicted reduced sensitivity to expected value. The majority of observed effects were consistent across both gain and loss domains.Discussion and ConclusionsOur results provide a thorough characterization of decision processes in gain and loss domains in gambling disorder, and place these problems in the context of theoretical constructs from behavioural economics.

Counterfactual thinking is a component of human decision-making that entails “if only” thinking about unselected choices and outcomes. It is associated with strong emotional responses of regret (when the obtained outcome is inferior to the counterfactual) and relief (vice versa). Counterfactual thinking may play a role in various cognitive phenomena in disordered gambling, such as the effects of near-misses. This study compared individuals with gambling disorder (n = 46) and healthy controls (n = 25) on a behavioural economic choice task that entailed choosing between two gambles, designed to measure counterfactual thinking. Participants provided affect ratings following both the obtained and the non-obtained outcomes. Choices were analyzed using a computational model that derived parameters reflecting sensitivity to expected value, risk variance, and anticipated regret. In the computational choice model, the group with gambling disorder showed increased sensitivity to anticipated regret, reduced sensitivity to expected value, and increased preference for high risk-variance gambles. On the affect ratings, the group with gambling disorder displayed blunted emotional sensitivity to obtained and counterfactual outcomes. Effect sizes of the group differences were modest. Participants with gambling disorder show wide-ranging alterations in decision-making processes and emotional reactivity to choice outcomes. Altered sensitivity to anticipatory regret in gambling disorder may contribute to the development of gambling-related cognitive distortions, and the influences of gambling marketing.

Electronic Gaming Machines (EGMs) are regarded as a relatively harmful gambling product, and are associated with psychological immersion (the ‘machine zone’) and physiological arousal. Specifically, immersion is a phenomenon of attention manifesting as an intense focus on the game at the expense of peripheral stimuli and goals. Past research has indicated significant levels of immersion in response to modern multi-line EGMs when the overall bet is increased, which further scales with risk for problem gambling ( Dixon et al., 2014 ). The present study sought to separate the effects of multi-line play and bet size, on measures of immersion and cardiac activity. Seventy-six male undergraduate students played an authentic EGM on each of 4 pre-defined play strategies while providing electrocardiogram data. The strategies varied the number of paylines and the bet multiplier. From the physiological data, we extracted Respiratory Sinus Arrhythmia (RSA), a marker of task attention derived from heart rate variability. We found that immersion ratings were significantly greater when both paylines and bet-size were high. Importantly, selectively increasing the paylines, but not bet multiplier, produced significant increases in immersion. RSA change indicated parasympathetic withdrawal, consistent with increases in attention during EGM use, but did not differentiate game settings. These results suggest that multi-line EGMs capture attention across a range of play-styles, and that immersion may be effectively amplified by multi-line play.

Serotonin is involved in updating responses to changing environmental circumstances. Optimising behaviour to maximise reward and minimise punishment may require shifting strategies upon encountering new situations. Likewise, autonomic responses to threats are critical for survival yet must be modified as danger shifts from one source to another. Whilst numerous psychiatric disorders are characterised by behavioural and autonomic inflexibility, few studies have examined the contribution of serotonin in humans. We modelled both processes, respectively, in two independent experiments (N = 97). Experiment 1 assessed instrumental (stimulus-response-outcome) reversal learning whereby individuals learned through trial and error which action was most optimal for obtaining reward or avoiding punishment initially, and the contingencies subsequently reversed serially. Experiment 2 examined Pavlovian (stimulus-outcome) reversal learning assessed by the skin conductance response: one innately threatening stimulus predicted receipt of an uncomfortable electric shock and another did not; these contingencies swapped in a reversal phase. Upon depleting the serotonin precursor tryptophan—in a double-blind randomised placebo-controlled design—healthy volunteers showed impairments in updating both actions and autonomic responses to reflect changing contingencies. Reversal deficits in each domain, furthermore, were correlated with the extent of tryptophan depletion. Initial Pavlovian conditioning, moreover, which involved innately threatening stimuli, was potentiated by depletion. These results translate findings in experimental animals to humans and have implications for the neurochemical basis of cognitive inflexibility.

Reward-related stimuli can potently influence behavior; for example, exposure to drug-paired cues can trigger drug use and relapse in people with addictions. Psychological mechanisms that generate such outcomes likely include cue-induced cravings and attentional biases. Recent animal data suggest another candidate mechanism: reward-paired cues can enhance risky decision making, yet whether this translates to humans is unknown. Here, we examined whether sensory reward-paired cues alter decision making under uncertainty and risk, as measured respectively by the Iowa Gambling Task and a two-choice lottery task. In the cued versions of both tasks, gain feedback was augmented with reward-concurrent audiovisual stimuli. Healthy human volunteers (53 males, 78 females) performed each task once, one with and the other without cues (cued Iowa Gambling Task/uncued Vancouver Gambling Task:n= 63; uncued Iowa Gambling Task/cued Vancouver Gambling Task:n= 68), with concurrent eye-tracking. Reward-paired cues did not affect choice on the Iowa Gambling Task. On the two-choice lottery task, the cued group displayed riskier choice and reduced sensitivity to probability information. The cued condition was associated with reduced eye fixations on probability information shown on the screen and greater pupil dilation related to decision and reward anticipation. This pupil effect was unrelated to the risk-promoting effects of cues: the degree of pupil dilation for risky versus risk-averse choices did not differ as a function of cues. Together, our data show that sensory reward cues can promote riskier decisions and have additional and distinct effects on arousal.SIGNIFICANCE STATEMENTAnimal data suggest that reward-paired cues can promote maladaptive reward-seeking by biasing cost-benefit decision making. Whether this finding translates to humans is unknown. We examined the effects of salient reward-paired audiovisual cues on decision making under risk and uncertainty in human volunteers. Cues had risk-promoting effects on a risky choice task and independently increased task-related arousal as measured by pupil dilation. By demonstrating risk-promoting effects of cues in human participants, our data identify a mechanism whereby cue reactivity could translate into maladaptive behavioral outcomes in people with addictions.

Experimental studies examining the relationship between alcohol use and gambling have focused predominantly on alcohol's influence on gambling behavior. There has been little consideration of the reverse pathway: whether gambling influences subsequent alcohol use. Two experiments examined whether gambling and gambling outcomes (i.e. profits during a gambling session) influenced subsequent alcohol consumption. Experiment 1 (n = 53) used an ad libitum consumption test, in which participants could request beverages during a 30 min window. Experiment 2 (n = 29) used a beer taste test procedure, in which participants were asked to rate a series of beers. In both studies, male regular gamblers were assigned to watch a television show or play a modern slot machine for 30 min, before being provided with access to alcohol. On the ad libitum procedure, gambling significantly increased the number of alcoholic drinks ordered, the volume of alcohol consumed, the participants' speed of drinking, and their intention to drink alcohol. These effects were not corroborated using the taste test procedure. Across both studies, gambling outcomes were not associated with alcohol consumption. In conjunction with prior findings, the observation that gambling can promote alcohol consumption under certain conditions highlights a possible feedback loop whereby gambling and alcohol reinforce one another. However, the divergent results between the ad libitum and taste test experiments point to boundary conditions for the effect and raise methodological considerations for future work measuring alcohol consumption in gambling environments.

Testosterone has been implicated in the regulation of emotional responses and risky decision-making. However, the causal effect of testosterone upon emotional decision-making, especially in non-social settings, is still unclear. The present study investigated the role of testosterone in counterfactual thinking: regret is an intense negative emotion that arises from comparison of an obtained outcome from a decision against a better, non-obtained (i.e. counterfactual) alternative. Healthy male participants (n = 64) received a single-dose of 150 mg testosterone Androgel in a double-blind, placebo-controlled, between-participants design. At 180 min post-administration, participants performed the counterfactual thinking task. We applied a computational model derived from behavioral economic principles to uncover latent decision-making mechanisms that may be invisible in simple choice analyses. Our data showed that testosterone increased the ability to use anticipated regret to guide choice behavior, while reducing choice based on expected value. On affective ratings, testosterone increased sensitivity to both obtained and counterfactual outcomes. These findings provide evidence that testosterone causally modulates emotional decision-making, and highlight the role of testosterone in affective sensitivity.

© 2017, The Author(s). Altered decision making processes and excessive risk-seeking behaviours are key features of conduct disorder (CD). Previous studies have provided compelling evidence of abnormally increased preference for risky options, higher sensitivity to rewards, as well as blunted responsiveness to aversive outcomes in adolescents with CD. However, most studies published to date have focused on males only; thus, it is not known whether females with CD show similar alterations in decision making. The current study investigated potential sex differences in decision making and risk-seeking behaviours in adolescents with CD. Forty-nine adolescents with CD (23 females) and 51 control subjects (27 females), aged 11-18 years, performed a computerised task assessing decision making under risk—the Risky Choice Task. Participants made a series of decisions between two gamble options that varied in terms of their expected values and probability of gains and losses. This enabled the participants’ risk preferences to be determined. Taking the sample as a whole, adolescents with CD exhibited increased risk-seeking behaviours compared to healthy controls. However, we found a trend towards a sex-by-group interaction, suggesting that these effects may vary by sex. Follow-up analyses showed that males with CD made significantly more risky choices than their typically developing counterparts, while females with CD did not differ from typically developing females in their risk-seeking behaviours. Our results provide preliminary evidence that sex may moderate the relationship between CD and alterations in risk attitudes and reward processing, indicating that there may be sex differences in the developmental pathways and neuropsychological deficits that lead to CD. European Commission’s Seventh Framework Programme for research, technological development and demonstration (FP7/2007-2013) under Grant Agreement no. 602407 (FemNAT-CD).

Humans seek admiration to boost their social rank and engage in rivalry to protect it when fearing defeat. These social behaviors are shaped by traits and affective states, such as narcissism and depression, that influence perception of status and motivation for dominance. Narcissistic traits and depressive states are thought to prompt opposite coping mechanisms: highly narcissistic persons are compelled to protect and enhance their social rank at any cost, whereas depressed individuals may accept their inferior position to avoid further damage. Experimental data supporting these theories are however lacking. We investigated the effects of dimensionally-assessed narcissism, trait dominance and depression in a rigged video game tournament, designed to elicit rivalry (stealing points from opponents) and admiration-seeking (paying for rank). The experiment was performed by an undergraduate sample (N = 70, mean age = 21.5 years) and a clinical sample of predominantly depressed elderly (N = 85, mean age = 62.6 years). Both rivalry and admiration-seeking increased with time and were particularly enhanced in individuals high in trait dominance or narcissism. Additionally, participants engaged in more rivalry against high-ranked opponents and this tendency was accentuated by trait dominance but suppressed by depression. Our findings suggest that narcissism and social dominance manifest in increased rivalry and admiration-seeking during social contests. Depression does not generally suppress competitiveness but selectively inhibits upward-focused rivalry.

BACKGROUND AND AIMS: The Pathways Model (Blaszczynski & Nower, 2002) posits that problem gambling is a heterogeneous disorder with distinct subgroups (behaviorally conditioned gamblers, emotionally vulnerable gamblers, and antisocial-impulsivist gamblers). Impulsivity traits and gambling-related cognitions are recognized as two key psychological factors in the onset and maintenance of problem gambling. To date, these constructs have been explored separately, and their joint role in determining problem gambling subtypes has received little attention. The goal of our study was to identify subgroups of gamblers based on impulsivity traits and gambling-related cognitions, and to determine whether this approach is consistent with the Pathways model. METHODS: Gamblers from the community (N = 709) and treatment-seeking pathological gamblers (N = 122) completed questionnaires measuring gambling habits, disordered gambling symptoms, gambling-related cognitions, and impulsivity traits. RESULTS: Cluster analyses revealed that three clusters globally aligned with the pathways proposed by Blaszczynski & Nower (2002). Two other clusters emerged: (1) impulsive gamblers without cognitive-related cognitions; and (2) gamblers without impulsivity or gambling-related cognitions. Gamblers with both heightened impulsive traits and gambling-related cognitions had more severe problem gambling symptoms. CONCLUSION: We successfully identified, based on an a priori theoretical framework, different subtypes of gamblers that varied in terms of problem gambling symptoms and clinical status. The diversity of the cluster profiles supports the development of personalized prevention strategies and psychological interventions. ispartof: JOURNAL OF AFFECTIVE DISORDERS vol:260 pages:473-482 ispartof: location:Netherlands status: published

Although there is increasing clinical recognition of behavioral addictions, of which gambling disorder is the prototype example, there is a limited understanding of the psychological properties of (non-substance-related) behaviors that enable them to become 'addictive' in a way that is comparable to drugs of abuse. According to an influential application of reinforcement learning to substance addictions, the direct effects of drugs to release dopamine can create a perpetual escalation of incentive salience. This article focusses on reward uncertainty, which is proposed to be the core feature of gambling that creates the capacity for addiction. We describe the neuro-dynamics of the dopamine response to uncertainty that may allow a similar escalation of incentive salience, and its relevance to behavioral addictions. We review translational evidence from both preclinical animal models and human clinical research, including studies in people with gambling disorder. Further, we describe the evidence for 1) the effects of the omission of expected reward as a stressor and to promote sensitization, 2) the effect of the resolution of reward uncertainty as a source of value, 3) structural characteristics of modern Electronic Gaming Machines (EGMs) in leveraging these mechanisms, 4) analogies to the aberrant salience hypothesis of psychosis for creating and maintaining gambling-related cognitive distortions. This neurobiologically-inspired model has implications for harm profiling of other putative behavioral addictions, as well as offering avenues for enhancing neurological, pharmacological and psychological treatments for gambling disorder, and harm reduction strategies for EGM design.

Psychological and neurobiological markers in individuals with gambling disorder (GD) could reflect transdiagnostic vulnerability to addiction or neuroadaptive consequences of long-term gambling. Using an endophenotypic approach to identify vulnerability markers, we tested the biological relatives of cases with GD. Male participants seeking treatment for GD (n = 20) were compared with a male control group (n = 18). Biological siblings of cases with GD (n = 17, unrelated to the current GD group) were compared with a separate control group (n = 19) that overlapped partially with the GD control group. Participants completed a comprehensive assessment of clinical scales, neurocognitive functioning, and fMRI of unexpected financial reward. The GD group displayed elevated levels of self-report impulsivity and delay discounting, and increased risk-taking on the Cambridge Gamble Task. We did not observe impaired motor impulsivity on the stop-signal task. Siblings of GD showed some overlapping effects; namely, elevated impulsivity (negative urgency) and increased risk-taking on the Cambridge Gamble Task. We did not observe any differences in the neural response to win outcomes, either in the GD or sibling analysis compared with their control group. Within the GD group, activity in the thalamus and caudate correlated negatively with gambling severity. Increased impulsivity and risk-taking in GD are present in biological relatives of cases with GD, suggesting these markers may represent pre-existing vulnerability to GD.

Testosterone has been linked to modulation of impulsivity and risky choice, potentially mediated by changes in reward or punishment sensitivity. This study investigated the effect of testosterone on risk-taking and the adjustment of risk-taking on trials following a gain or a loss. Loss chasing is operationalized herein as the propensity to recover losses by increasing risky choice. Healthy female participants (n = 26) received a single-dose of 0.5 mg sublingual testosterone in a double-blind, placebo-controlled crossover design. At 240 min post-administration, participants performed a gambling task with a high and a low risk option. In the placebo condition, participants were more likely to choose the high risk option following losses compared to wins. This effect was abolished on the testosterone session. Ignoring prior outcomes, no overall changes in risk-taking were observed. Our data indicate that testosterone affects human decision-making via diminishing sensitivity to punishment.

As a popular form of recreational risk taking, gambling games offer a paradigm for decision neuroscience research. As an individual behavior, gambling becomes dysfunctional in a subset of the population, with debilitating consequences. Gambling disorder has been recently reconceptualized as a “behavioral addiction” in the DSM-5, based on emerging parallels with substance use disorders. Why do some individuals undergo this transition from recreational to disordered gambling? The biomedical model of problem gambling is a “brain disorder” account that posits an underlying neurobiological abnormality. This article first delineates the neural circuitry that underpins gambling-related decision making, comprising ventral striatum, ventromedial prefrontal cortex, dopaminergic midbrain, and insula, and presents evidence for pathophysiology in this circuitry in gambling disorder. These biological dispositions become translated into clinical disorder through the effects of gambling games. This influence is better articulated in a public health approach that describes the interplay between the player and the (gambling) product. Certain forms of gambling, including electronic gambling machines, appear to be overrepresented in problem gamblers. These games harness psychological features, including variable ratio schedules, near-misses, “losses disguised as wins,” and the illusion of control, which modulate the core decision-making circuitry that is perturbed in gambling disorder.

The "winner-loser effect" refers to a phenomenon in testosterone research where the outcome of a social competition induces increases (wins) and/or decreases (losses) in testosterone levels. Here, we sought to test to what extent changes in testosterone occur in response to gambling behavior. More specifically, we hypothesized that the winner-loser effect would extend to slot machine gambling as a solitary (noncompetitive) gambling activity in players who "anthropomorphized" the slot machine, thus treating the machine as a human opponent. Male participants (n = 113) were recruited into a quasi-experimental design involving 15 min of authentic slot machine gambling, incentivized by a $10 cash bonus for participants who finished in profit. In addition to salivary measures of testosterone, salivary cortisol and self-reported anthropomorphization of the slot machine were tested as potential moderators. Contrary to predictions, winning and losing slot machine sessions did not exert significant differential effects on testosterone, and this pattern was not moderated by cortisol levels or slot machine anthropomorphization. Exploratory analyses tested relationships between subjective gambling experiences in the sessions and testosterone change. Higher positive affect and flow predicted greater testosterone declines from pre- to postgambling. The testosterone results add to a growing literature on the boundary conditions of the winner-loser effect and inform future studies on testosterone reactivity in relation to gambling and disordered gambling. The tendency to anthropomorphize slot machines is a neglected cognitive distortion in gambling that merits further study. (PsycINFO Database Record (c) 2018 APA, all rights reserved).

Gambling has longstanding links with excitement and physiological arousal, but prior research has not considered (a) gamblers' ability to detect internal physiological signals, or (b) markers of parasympathetic functioning. The present study measured interoception in individuals with gambling disorder, using self-report measures and a heartbeat counting task administered at rest. Resting state respiratory sinus arrhythmia (RSA), an index of heart rate variability, was measured as a proxy for parasympathetic control and emotional regulation capacity. In a case-control design, 50 individuals with gambling disorder were compared against 35 controls without gambling problems. Participants completed two self-report measures of bodily awareness and a behavioral test of heartbeat counting. A resting state electrocardiogram (5 min) was used to calculate RSA. There were no significant differences on the self-report or behavioral interoception probes. The group with gambling disorder displayed significantly reduced RSA, which at face value is consistent with reduced parasympathetic control. However, the group difference in RSA did not survive controlling for age and smoking status, as established predictors of heart rate variability. Our findings do not support any changes in interoceptive processing in people with gambling disorder, at least under resting conditions. Our observation that group differences in RSA are partly explained by smoking behavior highlights the importance of controlling for nicotine use in future research characterizing physiological functioning and emotional regulation in disordered gambling.

Gambling may constitute a strategy for coping with depressive mood, but a direct influence of depressive mood on gambling behaviors has never been tested via realistic experimental designs in gamblers. The current study tested whether experimentally induced sadness increases persistence on a simulated slot machine task using real monetary reinforcement in recreational gamblers. Sixty participants were randomly assigned to an experimental (sadness induction) or control (no emotional induction) condition, and then performed a slot machine task consisting of a mandatory phase followed by a persistence phase. Potential confounding variables (problem gambling symptoms, impulsivity traits, gambling cognitions) were measured to ensure that the experimental and control groups were comparable. The study showed that participants in the sadness condition displayed greater gambling persistence than control participants (p = .011). These data support the causal role of negative affect in decisions to gamble and persistence, which bears important theoretical and clinical implications. (PsycINFO Database Record

Contains fulltext : 165874.pdf (Publisher’s version ) (Closed access) Near-misses in gambling games are losing events that come close to a win. Near-misses were previously shown to recruit reward-related brain regions including the ventral striatum, and to invigorate gambling behavior, supposedly by fostering an illusion of control. Given that pathological gamblers are particularly vulnerable to such cognitive illusions, their persistent gambling behavior might result from an amplified striatal sensitivity to near-misses. In addition, animal studies have shown that behavioral responses to near-miss-like events are sensitive to dopamine, but this dopaminergic influence has not been tested in humans. To investigate these hypotheses, we recruited 22 pathological gamblers and 22 healthy controls who played a slot machine task delivering wins, near-misses and full-misses, inside an fMRI scanner. Each participant played the task twice, once under placebo and once under a dopamine D2 receptor antagonist (sulpiride 400 mg), in a double-blind, counter-balanced design. Participants were asked about their motivation to continue gambling throughout the task. Across all participants, near-misses elicited higher motivation to continue gambling and increased striatal responses compared with full-misses. Crucially, pathological gamblers showed amplified striatal responses to near-misses compared with controls. These group differences were not observed following win outcomes. In contrast to our hypothesis, sulpiride did not induce any reliable modulation of brain responses to near-misses. Together, our results demonstrate that pathological gamblers have amplified brain responses to near-misses, which likely contribute to their persistent gambling behavior. However, there is no evidence that these responses are influenced by dopamine. These results have implications for treatment and gambling regulation. 10 p.

Near-misses occur across many forms of gambling and are rated as unpleasant while simultaneously increasing the motivation to continue playing. On slot machines, the icon position relative to the payline moderates the effects of near-misses, with near-misses before the payline increasing motivation, and near-misses after the payline being rated as aversive. Near-misses are also known to increase physiological arousal compared to full-misses, but physiological measures to date have not been able to dissociate positive and negative emotional responses. The present study measured facial electromyography at the corrugator (brow) and zygomaticus (cheek) sites, as well as electrodermal activity (EDA), following gambling outcomes on a two-reel slot machine simulation in 77 novice gamblers. Behavioral data was collected using trial-by-trial ratings of motivation and valence. Wins were rated as more pleasant and increased motivation to continue playing, compared to non-win outcomes. Wins were also accompanied by increased EDA and zygomaticus activity. Near-misses after the payline were rated as more aversive than other non-wins, and this was accompanied by increased EDA and zygomaticus activity. Near-misses before the payline increased motivation to continue playing, and were accompanied by increased EDA. Thus, both subjective and physiological responses to near-misses differ for events falling either side of the payline. The 'near-miss effect' is not a unitary phenomenon. Facial EMG has differential sensitivity to positive and negative valence and may be a useful measure for future studies of gambling behavior.

International audience; Bipolar disorder is associated with impaired decision-making. Little is known about how treatment, especially lithium, influences decision-making abilities in bipolar patients when euthymic. We aimed at testing for an association between lithium medication and decision-making performance in remitted bipolar patients. Decision-making was measured using the Iowa Gambling Task in 3 groups of subjects: 34 and 56 euthymic outpatients with bipolar disorder, treated with lithium (monotherapy and lithium combined with anticonvulsant or antipsychotic) and without lithium (anticonvulsant, antipsychotic and combination treatment), respectively, and 152 matched healthy controls. Performance was compared between the 3 groups. In the 90 euthymic patients, the relationship between different sociodemographic and clinical variables and decision-making was assessed by stepwise multivariate regression analysis. Euthymic patients with lithium (p=0.007) and healthy controls (p=0.001) selected significantly more cards from the safe decks than euthymic patients without lithium, with no significant difference between euthymic patients with lithium and healthy controls (p=0.9). In the 90 euthymic patients, the stepwise linear multivariate regression revealed that decision-making was significantly predicted (p

Behavioral addictions are slowly becoming recognized as a valid category of psychiatric disorder as shown by the recent allocation of pathological gambling to this category in DSM-5. However, several other types of psychiatric disorder proposed to be examples of behavioral addictions have yet to be accorded this formal acknowledgment and are dispersed across other sections of the DSM-5. This brief review marks this important point in the evolution of this concept and looks to future investigation of behavioral addictions with the theoretical frameworks currently being used successfully to investigate substance addiction and obsessive-compulsive disorder, in a potentially new spectrum of impulsive-compulsive disorders.

Serotoninergic transmission is reliably implicated in inhibitory control processes. The aim of this study was to test the hypothesis if serotonin transporter polymorphisms mediate inhibitory control in healthy people. 141 healthy subjects, carefully screened for previous and current psychopathology, were genotyped for the 5-HTTLPR and rs25531 polymorphisms. Inhibitory control was ascertained with the Stop Signal Task (SST) from the Cambridge Neuropsychological Test Automated Battery (CANTAB). The triallelic gene model, reclassified and presented in a biallelic functional model, revealed a dose-dependent gene effect on SST performance with Individuals carrying the low expressive allele had inferior inhibitory control compared to high expressive carriers. This directly implicates serotonin transporter polymorphisms (5-HTTLPR plus rs25531) in response inhibition in healthy subjects.

Gambling disorder (GD) was reclassified as a behavioral addiction in the DSM-5 and shares clinical and behavioral features with substance use disorders (SUDs). Neuroimaging studies of GD hold promise in isolating core features of the addiction syndrome, avoiding confounding effects of drug neurotoxicity. At the same time, a neurobiologically-grounded theory of how behaviors like gambling can become addictive remains lacking, posing a significant hurdle for ongoing decisions in addiction nosology. This article integrates research on reward-related brain activity (functional MRI) and neurotransmitter function (PET) in GD, alongside the consideration of structural MRI data as to whether these signals more likely reflect pre-existing vulnerability or neuroadaptive change. Where possible, we point to qualitative similarities and differences with established markers for SUDs. Structural MRI studies indicate modest changes in regional gray matter volume and diffuse reductions in white matter integrity in GD, contrasting with clear structural deterioration in SUDs. Functional MRI studies consistently identify dysregulation in reward-related circuitry (primarily ventral striatum and medial prefrontal cortex), but evidence is mixed as to the direction of these effects. The need for further parsing of reward sub-processes is emphasized, including anticipation vs outcome, gains vs. losses, and disorder-relevant cues vs natural rewards. Neurotransmitter PET studies indicate amplified dopamine (DA) release in GD, in the context of minimal differences in baseline DA D2 receptor binding, highlighting a distinct profile from SUDs. Preliminary work has investigated further contributions of opioids, GABA and serotonin. Neuroimaging data increasingly highlight divergent profiles in GD vs. SUDs. The ability of gambling to perpetually activate DA (via maximal uncertainty) may contribute to neuroimaging similarities between GD and SUDs, whereas the supra-physiological DA effects of drugs may partly explain differences in the neuroimaging profile of the two syndromes. Coupled with consistent observations of correlations with gambling severity and related clinical variables within GD samples, the overall pattern of effects is interpreted as a likely combination of shared vulnerability markers across GD and SUDs, but with further experience-dependent neuroadaptive processes in GD.

Serotonin has been implicated in promoting self-control, regulation of hunger and physiological homeostasis, and regulation of caloric intake. However, it remains unclear whether the effects of serotonin on caloric intake reflect purely homeostatic mechanisms, or whether serotonin also modulates cognitive processes involved in dietary decision making. We investigated the effects of an acute dose of the serotonin reuptake inhibitor citalopram on choices between food items that differed along taste and health attributes, compared with placebo and the noradrenaline reuptake inhibitor atomoxetine. Twenty-seven participants attended three sessions and received single doses of atomoxetine, citalopram, and placebo in a double-blind randomised cross-over design. Relative to placebo, citalopram increased choices of more healthy foods over less healthy foods. Citalopram also increased the emphasis on health considerations in decisions. Atomoxetine did not affect decision making relative to placebo. The results support the hypothesis that serotonin may influence food choice by enhancing a focus on long-term goals. The findings are relevant for understanding decisions about food consumption and also for treating health conditions such as eating disorders and obesity.

Psychopharmacological studies in humans suggest important roles for dopamine (DA) D2 receptors in human executive functions, such as cognitive planning and spatial working memory (SWM). However, studies that investigate an impairment of such functions using the selective DA D2/3 receptor antagonist sulpiride have yielded inconsistent results, perhaps because relatively low doses were used. We believe we report for the first time, the effects of a higher (800 mg p.o.) single dose of sulpiride as well as of genetic variation in the DA receptor D2 gene (DA receptor D2 Taq1A polymorphism), on planning and working memory. With 78 healthy male volunteers, we apply a between-groups, placebo-controlled design. We measure outcomes in the difficult versions of the Cambridge Neuropsychological Test Automated Battery One-Touch Stockings of Cambridge and the self-ordered SWM task. Volunteers in the sulpiride group showed significant impairments in planning accuracy and, for the more difficult problems, in SWM. Sulpiride administration speeded response latencies in the planning task on the most difficult problems. Volunteers with at least one copy of the minor allele (A1+) of the DA receptor D2 Taq1A polymorphism showed better SWM capacity, regardless of whether they received sulpiride or placebo. There were no effects on blood pressure, heart rate or subjective sedation. In sum, a higher single dose of sulpiride impairs SWM and executive planning functions, in a manner independent of the DA receptor D2 Taq1A polymorphism.

Competition is prevalent. People often resort to unethical means to win (e.g., the recent Volkswagen scandal). Not surprisingly, competition is central to the study of economics, psychology, sociology, political science, and more. Although we know much about contestants’ behavior before and during competitions, we know little about contestants’ behavior after the competition has ended. Connecting postcompetition behaviors with preceding competition experience, we find that after a competition is over winners behave more dishonestly than losers in an unrelated subsequent task. Furthermore, the subsequent unethical behavior effect seems to depend on winning, rather than on mere success. Providing insight into the issue is important in gaining understanding of how unethical behavior may cascade from exposure to competitive settings.

Recent accounts of problematic electronic gaming machine (EGM) gambling have suggested attentional pathology among at-risk players. A putative slot machine zone is characterized by an intense immersion during game play, causing a neglect of outside events and competing goals. Prior studies of EGM immersion have relied heavily upon retrospective self-report scales. Here, the authors attempt to identify behavioral and psychophysiological correlates of the immersion experience. In samples of undergraduate students and experienced EGM users from the community, they tested 2 potential behavioral measures of immersion during EGM use: peripheral target detection and probe-caught mind wandering. During the EGM play sessions, electrocardiogram data were collected for analysis of respiratory sinus arrhythmia (RSA), a measure of calming self-regulation governed by the parasympathetic nervous system. Subjective measures of immersion during the EGM play session were consistently related to risk of problem gambling. Problem gambling score, in turn, significantly predicted decrements in peripheral target detection among experienced EGM users. Both samples showed robust RSA decreases during EGM play, indicating parasympathetic withdrawal, but neither immersion nor gambling risk were related to this change. This study identifies peripheral attention as a candidate for quantifying game immersion and its links with risk of problem gambling, with implications for responsible gambling interventions at both the game and venue levels. (PsycINFO Database Record

BackgroundAltered corticostriatothalamic encoding of reinforcement is a core feature of depression. Here we examine reinforcement learning in late-life depression in the theoretical framework of the vascular depression hypothesis. This hypothesis attributes the co-occurrence of late-life depression and poor executive control to prefrontal/cingulate disconnection by vascular lesions.MethodOur fMRI study compared 31 patients aged ⩾60 years with major depression to 16 controls. Using a computational model, we estimated neural and behavioral responses to reinforcement in an uncertain, changing environment (probabilistic reversal learning).ResultsPoor executive control and depression each explained distinct variance in corticostriatothalamic response to unexpected rewards. Depression, but not poor executive control, predicted disrupted functional connectivity between the striatum and prefrontal cortex. White-matter hyperintensities predicted diminished corticostriatothalamic responses to reinforcement, but did not mediate effects of depression or executive control. In two independent samples, poor executive control predicted a failure to persist with rewarded actions, an effect distinct from depressive oversensitivity to punishment. The findings were unchanged in a subsample of participants with vascular disease. Results were robust to effects of confounders including psychiatric comorbidities, physical illness, depressive severity, and psychotropic exposure.ConclusionsContrary to the predictions of the vascular depression hypothesis, altered encoding of rewards in late-life depression is dissociable from impaired contingency learning associated with poor executive control. Functional connectivity and behavioral analyses point to a disruption of ascending mesostriatocortical reward signals in late-life depression and a failure of cortical contingency encoding in elderly with poor executive control.

Gambling is a naturalistic example of risky decision-making. During gambling, players typically display an array of cognitive biases that create a distorted expectancy of winning. This study investigated brain regions underpinning gambling-related cognitive distortions, contrasting patients with focal brain lesions to the ventromedial prefrontal cortex (vmPFC), insula, or amygdala ("target patients") against healthy comparison participants and lesion comparison patients (i.e., with lesions that spare the target regions). A slot machine task was used to deliver near-miss outcomes (i.e., nonwins that fall spatially close to a jackpot), and a roulette game was used to examine the gambler's fallacy (color decisions following outcome runs). Comparison groups displayed a heightened motivation to play following near misses (compared with full misses), and manifested a classic gambler's fallacy effect. Both effects were also observed in patients with vmPFC and amygdala damage, but were absent in patients with insula damage. Our findings indicate that the distorted cognitive processing of near-miss outcomes and event sequences may be ordinarily supported by the recruitment of the insula. Interventions to reduce insula reactivity could show promise in the treatment of disordered gambling.

Background and aims: Precommitment refers to the ability to prospectively restrict the access to temptations. This study examined whether risk-taking during gambling is decreased when an individual has the opportunity to precommit to his forthcoming bet. Methods: Sixty individuals participated in a gambling task that consisted of direct choice (simply chose one monetary option among four available ones, ranging from low-risk to high-risk options) or precommitment trials (before choosing an amount, participants had the opportunity to make a binding choice that made high-risk options unavailable). Results: We found that participants utilized the precommitment option, such that risk-taking was decreased on precommitment trials compared to direct choices. Within the precommitment trials, there was no significant difference in risk-taking following decisions to restrict versus non-restrict. Discussion: These findings suggest that the opportunity to precommit may be sufficient to reduce the attractiveness of risk. Conclusions: Present results might be exploited to create interventions aiming at enhancing one's ability to anticipate self-control failures while gambling., SCOPUS: ar.j, info:eu-repo/semantics/published

Summary Humans can resist temptations by exerting willpower, the effortful inhibition of impulses. But willpower can be disrupted by emotions and depleted over time. Luckily, humans can deploy alternative self-control strategies like precommitment, the voluntary restriction of access to temptations. Here, we examined the neural mechanisms of willpower and precommitment using fMRI. Behaviorally, precommitment facilitated choices for large delayed rewards, relative to willpower, especially in more impulsive individuals. While willpower was associated with activation in dorsolateral prefrontal cortex (DLPFC), posterior parietal cortex (PPC), and inferior frontal gyrus, precommitment engaged lateral frontopolar cortex (LFPC). During precommitment, LFPC showed increased functional connectivity with DLPFC and PPC, especially in more impulsive individuals, and the relationship between impulsivity and LFPC connectivity was mediated by value-related activation in ventromedial PFC. Our findings support a hierarchical model of self-control in which LFPC orchestrates precommitment by controlling action plans in more caudal prefrontal regions as a function of expected value., Highlights • Precommitment is the voluntary restriction of access to temptations • Precommitment is a more effective self-control strategy than willpower • Precommitment engages LFPC; willpower engages DLPFC and PPC • During precommitment, LFPC increases connectivity with DLPFC and PPC, Crocket et al. show that during precommitment, which involves voluntarily restricting access to temptations, lateral frontopolar cortex is activated and increases functional connectivity with dorsolateral prefrontal and posterior parietal cortex—the same regions associated with actively resisting temptations.

Neuroscientific explanations of gambling disorder can help people make sense of their experiences and guide the development of psychosocial interventions. However, the societal perceptions and implications of these explanations are not always clear or helpful. Two workshops in 2013 and 2014 brought together multidisciplinary researchers aiming to improve the clinical and policy-related effects of neuroscience research on gambling. The workshops revealed that neuroscience can be used to improve identification of the dangers of products used in gambling. Additionally, there was optimism associated with the diagnostic and prognostic uses of neuroscience in problem gambling and the provision of novel tools (eg, virtual reality) to assess the effectiveness of new policy interventions before their implementation. Other messages from these workshops were that neuroscientific models of decision making could provide a strong rationale for precommitment strategies and that interdisciplinary collaborations are needed to reduce the harms of gambling. This research was supported by funding from Monash University and the Victorian Responsible Gambling Foundation.

OBJECTIVE: The authors’ goal was to characterize cognitive flexibility and verbal learning in relatives of patients with bipolar disorder and in euthymic patients with recurrent major depression. METHOD: The intradimensional/extradimensional shift task and California Verbal Learning Test were administered to 27 first-degree relatives of probands with bipolar I disorder, 15 euthymic outpatients with recurrent unipolar depression, and 47 healthy comparison subjects. RESULTS: The relatives of patients with bipolar I disorder and the euthymic patients with unipolar depression were more likely to fail the intradimensional/extradimensional shift task than the healthy comparison subjects. The impairments at the extradimensional shift stage were pronounced. Verbal learning, delayed recall, and recognition were unimpaired in all groups. CONCLUSIONS: Attentional set shifting may represent an endophenotype in mood disorder, related to underlying vulnerability rather than the actual disease phenotype.

Humans are willing to incur personal costs to punish others who violate social norms. Such “costly punishment” is an important force for sustaining human cooperation, but the causal neurobiological determinants of punishment decisions remain unclear. Using a combination of behavioral, pharmacological, and neuroimaging techniques, we show that manipulating the serotonin system in humans alters costly punishment decisions by modulating responses to fairness and retaliation in the striatum. Following dietary depletion of the serotonin precursor tryptophan, participants were more likely to punish those who treated them unfairly, and were slower to accept fair exchanges. Neuroimaging data revealed activations in the ventral and dorsal striatum that were associated with fairness and punishment, respectively. Depletion simultaneously reduced ventral striatal responses to fairness and increased dorsal striatal responses during punishment, an effect that predicted its influence on punishment behavior. Finally, we provide behavioral evidence that serotonin modulates specific retaliation, rather than general norm enforcement: depleted participants were more likely to punish unfair behavior directed toward themselves, but not unfair behavior directed toward others. Our findings demonstrate that serotonin modulates social value processing in the striatum, producing context-dependent effects on social behavior.

Euthymic patients with bipolar disorder have been reported to show persistent deficits in sustained attention. However, the sustained attention task which was used also placed demands on working memory. Bipolar disorder patients in the euthymic state were therefore compared with healthy controls on two measures of sustained attention with and without a working memory component. Signal detection methodology was applied to the results. Euthymic patients with bipolar disorder were particularly impaired at detecting targets in the sustained attention task without a working memory component. This deficit was still apparent in a sub-group of patients who were not currently receiving lithium medication. By contrast, performance in the sustained attention task involving working memory task was not significantly different in the two groups. Sustained attention deficits apparent during the euthymic period of bipolar disorder cannot be explained in terms of working memory impairment and represents a reduced inherent capacity rather than a change in response bias. Deficits in sustaining attention may help explain the difficulties in psychological and occupational functioning in bipolar disorder patients during remission.

Human cooperation may partly depend on the presence of individuals willing to incur personal costs to punish noncooperators. The psychological factors that motivate such 'altruistic punishment' are not fully understood; some have argued that altruistic punishment is a deliberate act of norm enforcement that requires self-control, while others claim that it is an impulsive act driven primarily by emotion. In the current study, we addressed this question by examining the relationship between impulsive choice and altruistic punishment in the ultimatum game. As the neurotransmitter serotonin has been implicated in both impulsive choice and altruistic punishment, we investigated the effects of manipulating serotonin on both measures. Across individuals, impulsive choice and altruistic punishment were correlated and increased following serotonin depletion. These findings imply that altruistic punishment reflects the absence rather than the presence of self control, and suggest that impulsive choice and altruistic punishment share common neural mechanisms.

The neuromodulator serotonin has been implicated in a large number of affective and executive functions, but its precise contribution to motivation remains unclear. One influential hypothesis has implicated serotonin in aversive processing; another has proposed a more general role for serotonin in behavioral inhibition. Because behavioral inhibition is a prepotent reaction to aversive outcomes, it has been a challenge to reconcile these two accounts. Here, we show that serotonin is critical for punishment-induced inhibition but not overall motor response inhibition or reporting aversive outcomes. We used acute tryptophan depletion to temporarily lower brain serotonin in healthy human volunteers as they completed a novel task designed to obtain separate measures of motor response inhibition, punishment-induced inhibition, and sensitivity to aversive outcomes. After a placebo treatment, participants were slower to respond under punishment conditions compared with reward conditions. Tryptophan depletion abolished this punishment-induced inhibition without affecting overall motor response inhibition or the ability to adjust response bias in line with punishment contingencies. The magnitude of reduction in punishment-induced inhibition depended on the degree to which tryptophan depletion reduced plasma tryptophan levels. These findings extend and clarify previous research on the role of serotonin in aversive processing and behavioral inhibition and fit with current theorizing on the involvement of serotonin in predicting aversive outcomes.