Individual Differences In Risk Research Articles

Factors Associated With Support for COVID-19 Travel Bans: The Role of Health Beliefs and Multilevel Institutional Trust

This study examined whether the Health Belief Model and the heuristic of multilevel institutional trust would help explain U.S. residents’ support for travel bans on foreigners during the COVID-19 pandemic. Analysis of data collected from two nationwide online surveys conducted in 2020 ( n = 511 fielded between March 19 and March 27; n = 472 fielded between April 30 and May 13) suggested that support for this policy was associated with individual differences in risk and benefit perceptions, the presence of interpersonal cues, and trust in domestic and foreign institutions. Efforts to promote or resist international travel restrictions during a pandemic may benefit from accounting for these differences.

Characterizing stress processes by linking big five personality states, traits, and day-to-day stressors

The accumulation of day-to-day stressors can impact mental and physical health. How people respond to stressful events is a key mechanism responsible for the effects of stress, and individual differences in stress responses can either perpetuate or prevent negative consequences. Most research on daily stress processes has focused on affective responses to stressors, but stress responses can involve more than just affect (e.g., behavior, cognitions). Additionally, most research has studied the role of neuroticism in shaping those responses, but many other individual differences are associated with stress. In this study, we more broadly characterized daily stress processes by expanding the nomological networks of stress responses to include Big Five personality states. We also linked those stress responses to all Big Five traits, as well as individual differences in stress variety, severity, and controllability. We studied a sample of participants (N = 1,090) who reported on stressful events, their appraisal of events in terms of severity and controllability, and their Big Five personality states daily for 8–10 days (N = 8,870 observations). Multi-level structural equation models were used to separate how characteristics of the perceived stressful situation and characteristics of the person play into daily stress processes. Results showed that (1) all Big Five personality states shift in response to perceived stress, (2) all Big Five personality traits relate to average levels of perceived stress variety, severity, and controllability, (3) individual differences in personality and average perceived stress variety and perceived severity relate to the strength of personality state responses to daily stress, albeit in a more limited fashion. Our results point to new pathways by which stressors affect people in everyday life and begin to clarify processes that may explain individual differences in risk or resilience to the harmful effects of stress.

Individual Differences in Risk and Protective Factors: The Role of Self-Compassion Components among Emergency Responders.

This study investigates individual differences in protective and risk factors among rescue workers (RWs), particularly Red Cross members, to optimize well-being and job performance under high-stress conditions. Employing a person-centered approach, two psychological profiles were identified: an adaptively resilient profile and a maladaptively vulnerable profile, characterized by distinct personality traits, coping methods, life events, and social support networks. A notable external criterion, self-compassion, discerned the profiles with maladaptively vulnerable individuals who exhibited higher self-judgment, social isolation, and emotional over-identification. The study also examined the impact of job roles on these profiles, discovering a prevalence of adaptive resilience among drivers, contrasting with team members who displayed maladaptive resilience and lower self-compassion scores. These insights suggest a nuanced method for identifying RWs who require specialized support, proposing tailored interventions, especially those enhancing self-compassion. The study, through an extensive psychological metric analysis, provides a deeper comprehension of resilience and vulnerability among RWs. This research highlights the importance of recognizing individual differences in protective and risk factors, thereby contributing to the enhancement of mental health and resilience in high-stress professions.

Are individual differences in loss aversion related to ADHD symptomatology?

Loss aversion, or the greater sensitivity to losses than equivalent gains, has been shown to vary across individuals, but has yet to be thoroughly examined in relation to Attention-Deficit/Hyperactivity Disorder (ADHD) symptomatology. Examining factors related to decision-making in ADHD has important implications for interventions as well as understanding engagement in risky behavior. Undergraduates (N = 98; 73% women) completed questionnaires measuring ADHD symptomatology, loss aversion, and gambling preference as well as the Balloon Analog Risk Task. Individuals with high ADHD symptomatology (n = 50) were less loss averse than those low in symptomatology, even after controlling for individual differences in risk taking and gambling preference. Inattention symptoms were not related to loss aversion after controlling for hyperactivity/impulsivity, risk taking, and gambling preference. Greater hyperactivity/impulsivity was related to less loss aversion, even after covariates were controlled. It is unclear if group differences were the result of reduced sensitivity to losses, increased attraction to gains, or both. Future research should examine if reduced loss aversion in those with high ADHD symptomatology replicates using other decision-making paradigms and whether or not loss aversion mediates the relationship between ADHD and risk-taking behavior.

The link between cognitive abilities and risk preference depends on measurement

Risk preference is an important construct for understanding individual differences in risk taking throughout the behavioral sciences. An active stream of research has focused on better understanding risk preference through its connection to other psychological constructs, in particular, cognitive abilities. Here, we examine two large-scale multimethod data sets and demonstrate that the method used to measure risk preference is an important moderator. In self-report measures, we found small but consistent positive correlations between working memory capacity/numeracy, facets of cognitive abilities, and risk tolerance. In behavioral measures, we found, on average, no correlation and large intermethod heterogeneity. This heterogeneity can be explained by the choice architecture that is created in behavioral methods—in particular, the relation between risk and reward and the impact of decision error in a task. Consequently, investigating how risk preference relates to psychological constructs such as cognitive abilities require a profound understanding of the choice architecture in measurements of risk preference and in the real world.

How can genetic factors be best leveraged to explain individual differences in risk to onset, course of illness and response to treatment in depression and other mood disorders?

The clinical field of depression and other mood disorders is characterised by the vast heterogeneity between those who present for care, and the highly variable degree of response to the range of psychological, pharmacological and physical treatments currently provided. These individual differences likely have a genetic component, and leveraging genetic risk is appealing because genetic risk factors point to causality. The possibility that individual genotyping at entry to health care may be a key way forward is worthy of discussion (Torkamani et al., 2018).

Ovarian Hormones and Binge Eating in Adulthood: Summary of Findings and Implications for Individual Differences in Risk in Women

Ovarian hormone influences on general food intake have been studied in animals for 60+ years. Yet, extensions of these data to key eating disorder symptoms in humans (e.g., binge eating [BE]) have only recently occurred. In this article, we summarize findings from studies examining the effects of ovarian hormones on BE. Findings suggest ovarian hormones contribute to BE in animals and humans, although studies are few in number and effects are not present in all women or all animals exposed to high-risk hormonal milieus. Differences in susceptibility may be due to gene × hormone interactions that can explain why some, but not all, women develop BE in the presence of risky hormonal environments.

The role of brain white matter in depression resilience and response to sleep interventions.

Insomnia poses a high risk for depression. Brain mechanisms of sleep and mood improvement following cognitive behavioural therapy for insomnia remain elusive. This longitudinal study evaluated whether (i) individual differences in baseline brain white matter microstructure predict improvements and (ii) intervention affects brain white matter microstructure. People meeting the Diagnostic and Statistical Manual of Mental Disorders-5 criteria for Insomnia Disorder (n = 117) participated in a randomized controlled trial comparing 6 weeks of no treatment with therapist-guided digital cognitive behavioural therapy for insomnia, circadian rhythm support or their combination (cognitive behavioural therapy for insomnia + circadian rhythm support). Insomnia Severity Index and Inventory of Depressive Symptomatology-Self Report were assessed at baseline and followed up at Weeks 7, 26, 39 and 52. Diffusion-weighted magnetic resonance images were acquired at baseline and Week 7. Skeletonized white matter tracts, fractional anisotropy and mean diffusivity were quantified both tract-wise and voxel-wise using tract-based spatial statistics. Analyses used linear and mixed effect models while correcting for multiple testing using false discovery rate and Bonferroni for correlated endpoint measures. Our results show the following: (i) tract-wise lower fractional anisotropy in the left retrolenticular part of the internal capsule at baseline predicted both worse progression of depressive symptoms in untreated participants and more improvement in treated participants (fractional anisotropy × any intervention, PFDR = 0.053, Pcorr = 0.045). (ii) Only the cognitive behavioural therapy for insomnia + circadian rhythm support intervention induced a trend-level mean diffusivity decrease in the right superior corona radiata (PFDR = 0.128, Pcorr = 0.108), and individuals with a stronger mean diffusivity decrease showed a stronger alleviation of insomnia (R = 0.20, P = 0.035). In summary, individual differences in risk and treatment-supported resilience of depression involve white matter microstructure. Future studies could target the role of the left retrolenticular part of the internal capsule and right superior corona radiata and the brain areas they connect.

Stage 2 Registered Report: Epigenetic Intergenerational Transmission: Mothers’ Adverse Childhood Experiences and DNA Methylation

Individual differences in risk for mental disorders over the lifespan are shaped by forces acting before the individual is born-in utero, but likely even earlier, during the mother's own childhood. The environmental epigenetics hypothesis proposes that sustained effects of environmental conditions on gene expression are mediated by epigenetic mechanisms. Recent human studies have shown that adversities in childhood are correlated with DNA methylation (DNAm) in adulthood. In the current study, we tested the following pre-registered hypotheses: Mothers' adverse childhood experiences (ACEs) are correlated with DNAm in peripheral blood during pregnancy (hypothesis 1) and in cord blood samples from newborn infants (hypothesis 2), and women's depression and anxiety symptoms during pregnancy mediate the association between mothers' ACE exposure and prenatal/neonatal DNA methylation (hypothesis 3). Data were from the Avon Longitudinal Study of Parents and Children Accessible Resource for Integrated Epigenomic Studies substudy. Women provided retrospective self-reports during pregnancy of ACE exposure. We conducted an epigenome-wide association study testing whether mothers' ACE exposure, cumulative score (0-10), was associated with DNAm in maternal antenatal blood and infant cord blood in more than 450,000 CpG (point on DNA sequence where cytosine and guanine base pairs are linked by a phosphate, where methylation usually occurs) sites on the Illumina 450K BeadChip. Analyses for cord blood were separated by infant sex, a pre-registered analysis. Hypothesis 1: In 896 mother-infant pairs with available methylation and ACE exposure data, there were no significant associations between mothers' ACE score and DNAm from antenatal peripheral blood, after controlling for covariates. Hypothesis 2: In infant cord blood, there were 5 CpG sites significantly differentially methylated in relation to mothers' ACEs (false discovery rate [FDR]< .05), but only in male offspring. Effect sizes were medium, with partial eta squared values ranging from 0.060 to 0.078. CpG sites were in genes related to mitochondrial function and neuronal development in the cerebellum. Hypothesis 3: There was no mediation by maternal anxiety/depression symptoms found between mothers' ACEs score and DNAm in the significant CpG sites in male cord blood. Mediation was not tested in antenatal peripheral blood, because no direct association between mothers' ACE score and antenatal peripheral blood was found. Our results show that mothers' ACE exposure is associated with DNAm in male offspring, supporting the notion that DNAm could be a marker of intergenerational biological embedding of mothers' childhood adversity. Epigenetic Intergenerational Transmission: Mothers' Adverse Childhood Experiences and DNA Methylation; https://doi.org/10.1016/j.jaac.2020.03.008.

Putative risk and resiliency factors among Royal Canadian Mounted Police cadets.

Mental health disorders are prevalent among active-duty Royal Canadian Mounted Police (RCMP) officers. The current study was designed to assess whether RCMP cadets commencing the Cadet Training Program are inherently at greater risk of developing mental health challenges by statistically comparing cadet putative risk and resiliency scores to scores from young adult populations. The study was also designed to assess for sociodemographic differences in putative risk and resiliency variables among RCMP cadets in order to facilitate future comparisons. Cadets (n = 772; 72.2% men) completed self-report measures of several putative risk variables (i.e., anxiety sensitivity, fear of negative evaluation, pain anxiety, illness and injury sensitivity, intolerance of uncertainty, and state anger) and resiliency. Scores were statistically compared to samples from Canadian, American, Australian, and European young adult populations. Cadets had statistically significantly lower scores on all putative risk variables and statistically significantly higher resiliency scores compared to the young adult populations. In the cadet sample, there were statistically significant differences in putative risk and resiliency variables across gender and sex. Cadets' significantly lower scores on putative risk variables and higher scores on resiliency suggest that they may be psychologically strong; as such, it may be that the nature of police work, as opposed to inherent individual differences in risk and resiliency, accounts for active-duty RCMP officers' comparatively higher prevalence of mental health disorders over time.Clinical Trial Registration: ClinicalTrials.gov, Identifier NCT05527509.

Cognitive mechanisms underlying decision making involving risk of explicit punishment in male and female rats.

Individuals engage in the process of risk-based decision making on a daily basis to navigate various aspects of life. There are, however, individual differences in this form of decision making, with some individuals exhibiting preference for riskier choices (risk taking) and others exhibiting preference for safer choices (risk aversion). Recent work has shown that extremes in risk taking (e.g., excessive risk taking or risk aversion) are not only cognitive features of neuropsychiatric diseases, but may in fact predispose individuals to the development of such diseases. To better understand individual differences in risk taking, and thus the mechanisms by which they confer disease vulnerability, the current study investigated the cognitive contributions to risk taking in both males and females. Rats were first behaviorally characterized in a decision-making task involving risk of footshock punishment and then tested on a battery of cognitive behavioral assays. Individual variability in risk taking was compared with performance on these tasks. Consistent with prior work, females were more risk averse than males. With the exception of the Set-shifting Task, there were no sex differences in performance on other cognitive assays. There were, however, sex-dependent associations between risk taking and specific cognitive measures. Greater risk taking was associated with better cognitive flexibility in males whereas greater risk aversion was associated with better working memory in females. Collectively, these findings reveal that distinct cognitive mechanisms are associated with risk taking in males and females, which may account for sex differences in this form of decision making.

P424. Epigenetic Intergenerational Transmission: Mothers’ Adverse Childhood Experiences and DNA Methylation

Individual differences in risk for mental disorders over the lifespan are shaped by forces acting before the individual is born— in utero, but likely even earlier, during the mother’s own childhood. In the current study, we tested whether mothers’ adverse childhood experiences (ACEs) are correlated with DNA methylation (DNAm) in peripheral blood during pregnancy and in cord blood samples from newborn infants.

Context matters: Neighborhood disadvantage is associated with increased disordered eating and earlier activation of genetic influences in girls.

Emerging evidence suggests socioeconomic disadvantage may increase risk for eating disorders (EDs). However, there are very few studies on the association between disadvantage and EDs, and all have focused on individual-level risk factors (e.g., family income). Neighborhood disadvantage (i.e., elevated poverty and reduced resources in one's neighborhood) is associated with increased risk for anxiety/depression and poor physical health. To date, no studies have examined phenotypic associations between neighborhood disadvantage and disordered eating, or how any form of disadvantage may interact with genetic individual differences in risk for EDs. We examined phenotypic and etiologic associations between neighborhood disadvantage and disordered eating in 2,922 girls ages 8-17 from same-sex twin pairs recruited through the Michigan State University Twin Registry. Parents rated the twins on nine items assessing core disordered eating symptoms (e.g., weight preoccupation, binge eating), and neighborhood disadvantage was calculated from 17 indicators of contextual disadvantage (e.g., median home value, neighborhood unemployment). Puberty was measured using the Pubertal Development Scale to examine whether associations were consistent across development. At a phenotypic level, greater neighborhood disadvantage was associated with significantly greater disordered eating symptoms in girls at all stages of puberty (β = .07). Moreover, Genotype × Environment models showed that girls living in more disadvantaged neighborhoods exhibited stronger and earlier (i.e., during pre/early puberty) activation of genetic influences on disordered eating. Results highlight the critical importance of considering contextual disadvantage in research on etiology and risk for disordered eating, and the need for increased screening and treatment for EDs in disadvantaged youth. (PsycInfo Database Record (c) 2021 APA, all rights reserved).

The roles of attachment and emotion dysregulation in the association between childhood maltreatment and PTSD in an inner-city sample

BackgroundMost people will experience a traumatic event in their lifetime, but only a subset (<10%) will develop posttraumatic stress disorder (PTSD). ObjectiveTo facilitate prevention and intervention of PTSD, it is important to understand how risk and resilience factors interact with one another to explain individual differences in risk for PTSD, especially in underprivileged groups, who often experience greater burden of trauma and PTSD. MethodThe current study utilized multiple and moderated regression to examine the relation between childhood maltreatment and adulthood PTSD risk in the context of various attachment patterns and emotion dysregulation in a sample (n = 856) of mostly low-income, African American participants. ResultsModeration analysis indicated that the strongest association between self-reported childhood maltreatment and PTSD symptoms was manifest in participants reporting the highest levels of both attachment anxiety and attachment avoidance (b = 0.22, 95% CI [0.15, 0.29], p < .001), whereas, among those low on both these dimensions (i.e., more securely attached participants), there was no significant association between childhood maltreatment and current PTSD (b = 0.07, 95% CI [−0.01, 0.14], p = .07). Separately, multiple regression predicting current PTSD symptoms revealed an effect size for the two attachment dimensions similar to that of emotion dysregulation, while controlling for childhood maltreatment. ConclusionsThese findings suggest more secure attachment may buffer against the deleterious effects of childhood maltreatment, and both attachment difficulties and emotion dysregulation serve as robust correlates of adulthood PTSD.

Brain-Behavior Associations for Risk Taking Depend on the Measures Used to Capture Individual Differences.

Maladaptive risk taking can have severe individual and societal consequences; thus, individual differences are prominent targets for intervention and prevention. Although brain activation has been shown to be associated with individual differences in risk taking, the directionality of the reported brain–behavior associations is less clear. Here, we argue that one aspect contributing to the mixed results is the low convergence between risk-taking measures, especially between the behavioral tasks used to elicit neural functional markers. To address this question, we analyzed within-participant neuroimaging data for two widely used risk-taking tasks collected from the imaging subsample of the Basel–Berlin Risk Study (N = 116 young human adults). Focusing on core brain regions implicated in risk taking (nucleus accumbens, anterior insula, and anterior cingulate cortex), for the two tasks, we examined group-level activation for risky versus safe choices, as well as associations between local functional markers and various risk-related outcomes, including psychometrically derived risk preference factors. While we observed common group-level activation in the two tasks (notably increased nucleus accumbens activation), individual differences analyses support the idea that the presence and directionality of associations between brain activation and risk taking varies as a function of the risk-taking measures used to capture individual differences. Our results have methodological implications for the use of brain markers for intervention or prevention.

Comparison of Food Cue-Evoked and Resting-State Functional Connectivity in Obesity.

Obesity is associated with differences in task-evoked and resting-state functional brain connectivity (FC). However, no studies have compared obesity-related differences in FC evoked by high-calorie food cues from that observed at rest. Such a comparison could improve our understanding of the neural mechanisms of reward valuation and decision making in the context of obesity. The sample included 122 adults (78% female; mean age = 44.43 [8.67] years) with body mass index (BMI) in the overweight or obese range (mean = 31.28 [3.92] kg/m). Participants completed a functional magnetic resonance imaging scan that included a resting period followed by a visual food cue task. Whole-brain FC analyses examined seed-to-voxel signal covariation during the presentation of high-calorie food and at rest using seeds located in the left and right orbitofrontal cortex, left hippocampus, and left dorsomedial prefrontal cortex. For all seeds examined, BMI was associated with stronger FC during the presentation of high-calorie food, but weaker FC at rest. Regions exhibiting BMI-related modulation of signal coherence in the presence of palatable food cues were largely located within the default mode network (z range = 2.34-4.91), whereas regions exhibiting BMI-related modulation of signal coherence at rest were located within the frontostriatal and default mode networks (z range = 3.05-4.11). All FC results exceeded a voxelwise threshold of p < .01 and cluster-defining familywise error threshold of p < .05. These dissociable patterns of FC may suggest separate neural mechanisms contributing to variation in distinct cognitive, psychological, or behavioral domains that may be related to individual differences in risk for obesity.

The Effect of Tobacco Smoking Differs across Indices of DNA Methylation-Based Aging in an African American Sample: DNA Methylation-Based Indices of Smoking Capture These Effects

Smoking is one of the leading preventable causes of morbidity and mortality worldwide, prompting interest in its association with DNA methylation-based measures of biological aging. Considerable progress has been made in developing DNA methylation-based measures that correspond to self-reported smoking status. In addition, assessment of DNA methylation-based aging has been expanded to better capture individual differences in risk for morbidity and mortality. Untested to date, however, is whether smoking is similarly related to older and newer indices of DNA methylation-based aging, and whether DNA methylation-based indices of smoking can be used in lieu of self-reported smoking to examine effects on DNA methylation-based aging measures. In the current investigation we examine mediation of the impact of self-reported cigarette consumption on accelerated, intrinsic DNA methylation-based aging using indices designed to predict chronological aging, phenotypic aging, and mortality risk, as well as a newly developed DNA methylation-based measure of telomere length. Using a sample of 500 African American middle aged smokers and non-smokers, we found that a) self-reported cigarette consumption was associated with accelerated intrinsic DNA methylation-based aging on some but not all DNA methylation-based aging indices, b) for those aging outcomes associated with self-reported cigarette consumption, DNA methylation-based indicators of smoking typically accounted for greater variance than did self-reported cigarette consumption, and c) self-reported cigarette consumption effects on DNA methylation-based aging indices typically were fully mediated by DNA methylation-based indicators of smoking (e.g., PACKYRS from GrimAge; or cg05575921 CpG site). Results suggest that when DNA methylation-based indices of smoking are substituted for self-reported assessments of smoking, they will typically fully reflect the varied impact of cigarette smoking on intrinsic, accelerated DNA methylation-based aging.

Associations between peer attachment and neural correlates of risk processing across adolescence

Adolescence is a period of increased risk-taking behavior where individual differences in risk taking may relate to both adverse and positive experiences with peers. Yet, knowledge on how risk processing develops in the adolescent brain and whether this development is related to peer attachment is limited. In this longitudinal functional magnetic resonance imaging (fMRI) study, we collected data from 167 adolescents (53% male) followed for four annual assessments across ages 13–17 years. At each assessment, participants completed a lottery choice task to assess neural risk processing and reported on their perceived attachment to peers and parents. Behaviorally, risk-preference on the lottery choice task decreased linearly with age. Neural activation during risk processing was consistently found in the insula and dACC across the four assessments and increased linearly from ages 13–17 years. Furthermore, higher peer attachment was related to greater right insula risk processing for males but not for females, even after controlling for parental attachment. The magnitudes of this association did not change with age. Findings demonstrate that neural risk processing shows maturation across adolescence and high peer attachment may be associated with low risk taking by heightening neural sensitivity to potential risks for male adolescents.

Genetic Burden for Late-Life Neurodegenerative Disease and Its Association With Early-Life Lipids, Brain, Behavior, and Cognition.

BackgroundGenetics play a significant role in the etiology of late-life neurodegenerative diseases like Alzheimer’s disease, Parkinson’s disease, and frontotemporal dementia. Part of the individual differences in risk for these diseases can be traced back decades before the onset of disease symptoms. Previous studies have shown evidence for plausible links of apolipoprotein E (APOE), the most important genetic marker for Alzheimer’s disease, with early-life cognition and neuroimaging markers. We aimed to assess whether genome-wide genetic burden for the aforementioned neurodegenerative diseases plays a role in early-life processes.MethodsWe studied children from the Generation R Study, a prospective birth cohort. APOE genotypes and polygenic genetic burdens for Alzheimer’s disease, Parkinson’s disease, and frontotemporal dementia were obtained through genome-wide genotyping. Non-verbal intelligence was assessed through cognitive tests at the research center around the age of 6 years, and educational attainment through a national school performance test around the age of 11 years. The Child Behavior Checklist was administered around the age of 10 years, and data from the anxious/depressed, withdrawn/depressed, and the internalizing behavior problems scales were used. Children participated in a neuroimaging study when they were 10 years old, in which structural brain metrics were obtained. Lipid serum profiles, which may be influenced by APOE genotype, were assessed from venal blood obtained around the age of 6 years. The sample size per analysis varied between 1,641 and 3,650 children due to completeness of data.ResultsWe did not find evidence that APOE genotype or the polygenic scores impact on childhood nonverbal intelligence, educational attainment, internalizing behavior, and global brain structural measures including total brain volume and whole brain fractional anisotropy (all p > 0.05). Carriership of the APOE ε2 allele was associated with lower and APOE ε4 with higher low-density lipoprotein cholesterol concentrations when compared to APOE ε3/ε3 carriers.ConclusionWe found no evidence that genetic burden for late-life neurodegenerative diseases associates with early-life cognition, internalizing behavior, or global brain structure.

Is the DOSPERT gender invariant? A psychometric test of measurement invariance

AbstractIt is well established in the risk literature that men tend to take more risks than women. This gender difference, however, is often qualified by its domain specificity. Considering recent research on the domain generality of risk taking as a disposition, there is a need to examine the degree to which men take more risks than women, in general. In order to make substantive conclusions about the gender differences in risk‐taking propensity, one must first establish measurement invariance, which is required for the meaningful interpretation of observed group differences. In this paper, we examined the measurement invariance of the Domain‐Specific Risk‐Taking scale (DOSPERT)—one of the most popular measures of individual differences in risk taking. We found that the DOSPERT violated configural invariance in a bifactor model, indicating that the underlying factor structure of the DOSPERT differs between men and women. Even after removing the social risk dimension, DOSPERT still failed to reach scalar invariance. Taken together, these findings suggest that score differences in the DOSPERT may be due to response artifacts rather than true differences in the latent construct. Therefore, gender differences in the DOSPERT must be interpreted with caution. Implications for the measurement of risk taking are discussed.