Foraging is a fundamental behavior, and many types of animals appear to have solved foraging problems using a shared set of mechanisms. Perhaps the most common foraging problem is the choice between exploiting a familiar option for a known reward and exploring unfamiliar options for unknown rewards-the so-called explore/exploit trade-off. This trade-off has been studied extensively in behavioral ecology and computational neuroscience, but is relatively new to the field of psychiatry. Explore/exploit paradigms can offer psychiatry research a new approach to studying motivation, outcome valuation, and effort-related processes, which are disrupted in many mental and emotional disorders. In addition, the explore/exploit trade-off encompasses elements of risk-taking and impulsivity-common behaviors in psychiatric disorders-and provides a novel framework for understanding these behaviors within an ecological context. Here we explain relevant concepts and some common paradigms used to measure explore/exploit decisions in the laboratory, review clinically relevant research on the neurobiology and neuroanatomy of explore/exploit decision making, and discuss how computational psychiatry can benefit from foraging theory.
Delay discounting (DD) has been shown to be related to smoking status and-less consistently-frequency of cigarette use, but its independent relationship with dependence has not been examined. In this study, we evaluated the relationship between smoking and DD as a function of both smoking quantity and level of dependence controlling for use. A sample of 710 adults completed a DD task using hypothetical monetary rewards, and participants were classified according to smoking status. Current smokers were further characterized as light, moderate, or heavy smokers on the basis of number of cigarettes smoked per day (CPD). Dependence was assessed using the Fagerström Test of Nicotine Dependence (FTND), with the CPD item removed. Current smokers discounted delayed rewards more than never, occasional, or ex-smokers; the latter three groups did not differ. DD was not related to CPD, analyzed continuously or categorically. FTND scores independently predicted DD, controlling for CPD. Analysis of individual FTND items revealed a relationship between DD and morning smoking. When analyzed categorically based on a median split, individuals high in dependence discounted delayed rewards more steeply than low dependence, never, tried-it, and ex-smokers, while these groups did not differ from each other. These results suggest that DD among smokers is not simply the result of nicotine exposure, but may be an important marker for dependence, especially urgency to smoke in the morning.
BackgroundAttention-deficit/hyperactivity disorder (ADHD) is a risk factor for problematic cannabis use. However, clinical and anecdotal evidence suggest an increasingly popular perception that cannabis is therapeutic for ADHD, including via online resources. Given that the Internet is increasingly utilized as a source of healthcare information and may influence perceptions, we conducted a qualitative analysis of online forum discussions, also referred to as threads, on the effects of cannabis on ADHD to systematically characterize the content patients and caregivers may encounter about ADHD and cannabis.MethodsA total of 268 separate forum threads were identified. Twenty percent (20%) were randomly selected, which yielded 55 separate forum threads (mean number of individual posts per forum thread = 17.53) scored by three raters (Cohen’s kappa = 0.74). A final sample of 401 posts in these forum threads received at least one endorsement on predetermined topics following qualitative coding procedures.ResultsTwenty-five (25%) percent of individual posts indicated that cannabis is therapeutic for ADHD, as opposed to 8% that it is harmful, 5% that it is both therapeutic and harmful, and 2% that it has no effect on ADHD. This pattern was generally consistent when the year of each post was considered. The greater endorsement of therapeutic versus harmful effects of cannabis did not generalize to mood, other (non-ADHD) psychiatric conditions, or overall domains of daily life. Additional themes emerged (e.g., cannabis being considered sanctioned by healthcare providers).ConclusionsDespite that there are no clinical recommendations or systematic research supporting the beneficial effects of cannabis use for ADHD, online discussions indicate that cannabis is considered therapeutic for ADHD—this is the first study to identify such a trend. This type of online information could shape ADHD patient and caregiver perceptions, and influence cannabis use and clinical care.
Background Theories of addiction suggest that chronic smoking may be associated with both hypersensitivity to smoking and related cues and hyposensitivity to alternative reinforcers. However, neural responses to smoking and non-smoking rewards are rarely evaluated within the same paradigm, leaving the extent to which both processes operate simultaneously uncertain. Furthermore, behavioral evidence and theoretical models suggests that dysregulated reward processing may be more pronounced during deprivation from nicotine, but neuroimaging evidence on the effects of deprivation on reward processing is limited. The current study examined the impact of deprivation from smoking on neural processing of both smoking and monetary rewards. Methods Thirty-eight daily smokers participated in two separate fMRI scans, one after smoking without restriction and one following 24 hours of abstinence. A rewarded guessing task was conducted during each scan to evaluate striatal BOLD response during anticipation of both smoking and monetary rewards. Results A significant reward type X abstinence interaction was observed in the bilateral caudate and medial prefrontal cortex during reward anticipation. BOLD response to anticipation of smoking reward was significantly higher, and anticipation of monetary rewards significantly lower, during abstinence compared with non-abstinence. Furthermore, attenuation of monetary reward-related activation during abstinence was significantly correlated with abstinence-induced increases in craving and withdrawal. Conclusions These results provide the first direct evidence of dissociated effects of smoking versus monetary rewards as a function of abstinence. The findings suggest an important neural pathway that may underlie the choice to smoke in lieu of alternate reinforcement during a quit attempt.
Little is known regarding the underlying neurobiology of smoking cessation. Neuroimaging studies indicate a role for the insula in connecting the interoceptive awareness of tobacco craving with a larger brain network that motivates smoking. We investigated differences in insula-based functional connectivity between smokers who did not relapse during a quit attempt vs those who relapsed. Smokers (n=85) underwent a resting-state functional connectivity scan and were then randomized into two groups (either smoking usual brand cigarettes or smoking very low nicotine cigarettes plus nicotine replacement therapy) for 30 days before their target quit date. Following the quit date, all participants received nicotine replacement therapy and their smoking behavior was observed for 10 weeks. Participants were subsequently classified as nonrelapsed (n=44) or relapsed (i.e., seven consecutive days of smoking ⩾1 cigarette/day; n=41). The right and left insula, as well as insula subdivisions (posterior, ventroanterior, and dorsoanterior) were used as seed regions of interest in the connectivity analysis. Using the right and left whole-insula seed regions, the nonrelapsed group had greater functional connectivity than the relapsed group with the bilateral pre- and postcentral gyri. This effect was isolated to the right and left posterior insula seed regions. Our results suggest that relapse vulnerability is associated with weaker connectivity between the posterior insula and primary sensorimotor cortices. Perhaps greater connectivity in this network improves the ability to inhibit a motor response to cigarette cravings when those cravings conflict with a goal to remain abstinent. These results are consistent with recent studies demonstrating a positive relationship between insula-related functional connectivity and cessation likelihood among neurologically intact smokers.
Inconsistent or null findings among studies associating behaviors on the externalizing spectrum--addictions, impulsivity, risk-taking, novelty-seeking traits--with presence of the 7-repeat allele of a common length polymorphism in the gene encoding the dopamine D4 receptor (DRD4) may stem from individuals' variable exposures to prominent environmental moderators (gene × environment interaction). Here, we report that relative preference for immediate, smaller rewards over larger rewards delayed in time (delay discounting), a behavioral endophenotype of impulsive decision-making, varied by interaction of DRD4 genotype with childhood socioeconomic status (SES) among 546 mid-life community volunteers. Independent of age, sex, adulthood SES and IQ, participants who were both raised in families of distinctly low SES (low parental education and occupational grade) and carried the DRD4 7-repeat allele discounted future rewards more steeply than like-reared counterparts of alternate DRD4 genotype. In the absence of childhood socioeconomic disadvantage, however, participants carrying the 7-repeat allele discounted future rewards less steeply. This bidirectional association of DRD4 genotype with temporal discounting, conditioned by participants' early life circumstances, accords with a recently proposed developmental model of gene × environment interaction ('differential susceptibility') that posits genetically modulated sensitivity to both adverse and salubrious environmental influences.
The ventral and dorsal striatum are critical substrates of reward processing and motivation and have been repeatedly linked to addictive disorders, including nicotine dependence. However, little is known about how functional connectivity between these and other brain regions is modulated by smoking withdrawal and may contribute to relapse vulnerability. In the present study, 37 smokers completed resting state fMRI scans during both satiated and 24-h abstinent conditions, prior to engaging in a 3-week quit attempt supported by contingency management. We examined the effects of abstinence condition and smoking outcome (lapse vs non-lapse) on whole-brain connectivity with ventral and dorsal striatum seed regions. Results indicated a significant condition by lapse outcome interaction for both right and left ventral striatum seeds. Robust abstinence-induced increases in connectivity with bilateral ventral striatum were observed across a network of regions implicated in addictive disorders, including insula, superior temporal gyrus, and anterior/mid-cingulate cortex among non-lapsers; the opposite pattern was observed for those who later lapsed. For dorsal striatum seeds, 24-h abstinence decreased connectivity across both groups with several regions, including medial prefrontal cortex, posterior cingulate cortex, hippocampus, and supplemental motor area. These findings suggest that modulation of striatal connectivity with the cingulo-insular network during early withdrawal may be associated with smoking cessation outcomes.
Introduction: Understanding factors that render some individuals more vulnerable to smoking relapse during the early stages of a quit attempt is critical to tailoring treatment efforts. Development of laboratory models of relapse can provide a framework for identifying underlying mechanisms that may contribute to vulnerability. Here, we explored predictors of abstinence in a novel incentive-based model of relapse.Methods: Fifty-six nontreatment seeking daily smokers completed several nicotine dependence measures prior to participating in a 1-week abstinence incentive test. During the abstinence procedure, participants earned monetary reinforcement for each biochemically verifi ed day of abstinence according to a descending schedule of reinforcement. Results:Compliance with the procedure was excellent. All but 3 participants were able to initiate abstinence; nearly 70% lapsed as incentives were reduced. Scores on the Fagerström Test for Nicotine Dependence (FTND), number of cigarettes smoked per day, and self-reported craving on the first day of abstinence each independently predicted time to lapse. The single item of time to fi rst cigarette in the morning on the FTND signifi cantly predicted time to lapse, even when controlling for other signifi cant predictors just listed. The Nicotine Dependence Syndrome Scale (NDSS) and Wisconsin Inventory of Smoking Dependence Motives did not predict lapse, but the NDSS did predict reinitiation of abstinence among those experiencing an initial lapse. Conclusions:These fi ndings partially replicate those of previous full-scale clinical trials and support the feasibility and validity of an incentive-based model of relapse. The time-limited and laboratory-based nature of this model has the potential to further investigations of underlying mechanisms contributing to relapse.
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