Acute stress does not affect risky monetary decision-making.
Ontology highlight
ABSTRACT:
SUBMITTER: Sokol-Hessner P
PROVIDER: S-EPMC5145911 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Affective experience has an important role in decision-making with recent theories suggesting a modulatory role of affect in ongoing subjective value computations. However, it is unclear how varying expectations and uncertainty dynamically influence affective experience and how dynamic representation of affect modulates risky choices. Using hierarchical Bayesian modeling on data from a risky choice task (N = 101), we find that the temporal integration of recently encountered choice parameters (expected value, uncertainty, and prediction errors) shapes affective experience and impacts subsequent choice behavior. Specifically, self-reported arousal prior to choice was associated with increased loss aversion, risk aversion, and choice consistency. Taken together, these findings provide clear behavioral evidence for continuous affective modulation of subjective value computations during risky decision-making.
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Project description:Some people love taking risks, while others avoid gambles at all costs. The neural mechanisms underlying individual variation in preference for risky or certain outcomes, however, remain poorly understood. Although behavioral pathologies associated with compulsive gambling, addiction and other psychiatric disorders implicate deficient serotonin signaling in pathological decision making, there is little experimental evidence demonstrating a link between serotonin and risky decision making, in part due to the lack of a good animal model. We used dietary rapid tryptophan depletion (RTD) to acutely lower brain serotonin in three macaques performing a simple gambling task for fluid rewards. To confirm the efficacy of RTD experiments, we measured total plasma tryptophan using high-performance liquid chromatography (HPLC) with electrochemical detection. Reducing brain serotonin synthesis decreased preference for the safe option in a gambling task. Moreover, lowering brain serotonin function significantly decreased the premium required for monkeys to switch their preference to the risky option, suggesting that diminished serotonin signaling enhances the relative subjective value of the risky option. These results implicate serotonin in risk-sensitive decision making and, further, suggest pharmacological therapies for treating pathological risk preferences in disorders such as problem gambling and addiction.
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Project description:Pubertal development is a potential trigger for increases in risk-taking behaviours during adolescence. Here, we sought to investigate the relationship between puberty and neural activation during risky decision-making in males using functional magnetic resonance imaging (fMRI). Forty-seven males aged 12.5-14.5 years completed an fMRI risk-taking task (BART) and reported their tendencies for risky decision-making using a self-report questionnaire. Puberty was assessed through self-reported pubertal status and salivary testosterone levels. Testosterone concentration, but not physical pubertal status, was positively correlated with self-reported risk-taking behaviour, while neither was correlated with BART performance. Across the whole sample, participants had greater activation of the bilateral nucleus accumbens and right caudate on trials when they made a successful risky decision compared to trials when they made a safe choice or when their risky decision was unsuccessful. There was a negative correlation between pubertal stage and brain activation during unsuccessful risky decision-making trials compared within unsuccessful control trials. Males at a lower stage of pubertal development showed increased activation in the left insula, right cingulate cortex, dorsomedial prefrontal cortex (dmPFC), right putamen and right orbitofrontal cortex (OFC) relative to more pubertally mature males during trials when they chose to take a risk and the balloon popped compared to when they watched the computer make an unsuccessful risky decision. Less pubertally mature males also showed greater activation in brain regions including the dmPFC, right temporal and frontal cortices, right OFC, right hippocampus and occipital cortex in unsuccessful risky trials compared to successful risky trials. These results suggest a puberty-related shift in neural activation within key brain regions when processing outcomes of risky decisions, which may reduce their sensitivity to negative feedback, and in turn contribute to increases in adolescent risk-taking behaviours.
| S-EPMC10073643 | biostudies-literature
Project description:Gambling disorder is a behavioral addiction associated with impairments in value-based decision-making and cognitive control. These functions are thought to be regulated by dopamine within fronto-striatal circuits, but the role of altered dopamine neurotransmission in the etiology of gambling disorder remains controversial. Preliminary evidence suggests that increasing frontal dopamine tone might improve cognitive functioning in gambling disorder. We therefore examined whether increasing frontal dopamine tone via a single dose of the catechol-O-methyltransferase (COMT) inhibitor tolcapone would reduce risky choice in human gamblers (n = 14) in a randomized double-blind placebo-controlled crossover study. Data were analyzed using hierarchical Bayesian parameter estimation and a combined risky choice drift diffusion model (DDM). Model comparison revealed a nonlinear mapping from value differences to trial-wise drift rates, confirming recent findings. An increase in risk-taking under tolcapone versus placebo was about five times more likely, given the data, than a decrease [Bayes factor (BF) = 0.2]. Examination of drug effects on diffusion model parameters revealed that an increase in the value dependency of the drift rate under tolcapone was about thirteen times more likely than a decrease (BF = 0.073). In contrast, a reduction in the maximum drift rate under tolcapone was about seven times more likely than an increase (BF = 7.51). Results add to previous work on COMT inhibitors in behavioral addictions and to mounting evidence for the applicability of diffusion models in value-based decision-making. Future work should focus on individual genetic, clinical and cognitive factors that might account for heterogeneity in the effects of COMT inhibition.
| S-EPMC7294471 | biostudies-literature
Project description:Psychology; Jumping to conclusions; Iowa gambling task; Risky decision making; Game of dice task; Delusion proneness
| S-EPMC6895726 | biostudies-literature
Project description:RationaleChronic alcohol misuse can escalate into alcohol use disorder (AUD). The causal mechanisms through which recreational social drinking develops into compulsive uncontrolled alcohol misuse are multifaceted. For example, stress is an important risk factor that influences alcohol craving in both healthy and addicted individuals. In addition, those that are high in impulsivity/risk taking drink more and are at greater risk of developing addiction. At present, however, it is not possible accurately to predict those at risk of escalation in alcohol use, or of developing AUD.ObjectivesThe aim of this study was to investigate how underlying physiological and personality traits affect stress-induced craving for, and consumption of, alcohol, in a sample of social drinkers. The primary hypothesis was that impulsivity/risk-taking would modulate stress-induced alcohol craving and consumption.MethodsThirty-nine participants (22 male and 17 female; mean age = 23.92 years [SD = 4.90]) were randomly allocated to 'stress' and 'no-stress' groups; in the stress group, participants took part in the Trier Social Stress Test (TSST). Participants completed several questionnaires and computer tasks in order to assess prior alcohol use, impulsivity/risk-taking, stress-reactivity, craving and physiological biomarkers of stress. Finally, participants completed a voluntary drinking task, in which increasing numbers of presses on a computer keyboard were reinforced with 5-ml shots of 37% ABV vodka (plus mixer).ResultsParticipants exposed to the TSST showed an increase in craving following the stressor. Several factors predicted voluntary drinking, including risky decision making, slow HR recovery from stress, poor vagal tone during recovery from stress and greater stress reactivity. Surprisingly, we found no correlation between craving and consumption.ConclusionsOur data suggest that variation in physiological stress parameters and poor decision-making abilities increase risk of stress-induced alcohol consumption. This may provide a useful translational framework through which we can further study early predictive markers for the shift between controlled recreational drinking to uncontrolled alcohol misuse, including AUD.
| S-EPMC6208948 | biostudies-literature
Project description:BackgroundThe effects of acute tryptophan depletion on human decision-making suggest that serotonin modulates the processing of rewards and punishments. However, few studies have assessed which of the many types of serotonin receptors are responsible.MethodsUsing a within-subject, double-blind, sham-controlled design in 26 subjects, we examined whether individual differences in serotonin system gene transcription, measured in peripheral blood, predicted the effect of acute tryptophan depletion on decision-making. Participants performed a task in which they chose between successive pairs of fixed, lower-stakes (control) and variable, higher-stakes (experimental) gambles, each involving wins or losses. In 21 participants, mRNA from 9 serotonin system genes was measured in whole blood prior to acute tryptophan depletion: 5-HT1B, 5-HT1F, 5-HT2A, 5-HT2B, 5-HT3A, 5-HT3E, 5-HT7 (serotonin receptors), 5-HTT (the serotonin transporter), and tryptophan hydroxylase 1.ResultsAcute tryptophan depletion did not significantly influence participants' sensitivity to probability, wins, or losses, although there was a trend for a lower tendency to choose experimental gambles overall following depletion. Significant positive correlations, which survived correction for multiple comparisons, were detected between baseline 5-HT1B mRNA levels and acute tryptophan depletion-induced increases in both the overall tendency to choose the experimental gamble and sensitivity to wins. No significant relationship was observed with any other peripheral serotonin system markers. Computational analyses of decision-making data provided results consistent with these findings.ConclusionsThese results suggest that the 5-HT1B receptor may modulate the effects of acute tryptophan depletion on risky decision-making. Peripheral levels of serotonin markers may predict response to treatments that act upon the serotonin system, such as selective serotonin reuptake inhibitors.
| S-EPMC5480594 | biostudies-literature