Individual Differences In Risk Research Articles

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.

The Individual and Combined Effects of Multiple Factors on the Risk of Soft Tissue Non-contact Injuries in Elite Team Sport Athletes.

Aim: Relationships between athlete monitoring-derived variables and injury risk have been investigated predominantly in isolation. The aim of this study was to evaluate the individual and combined effects of multiple factors on the risk of soft-tissue non-contact injuries in elite team sport athletes.Methods: Fifty-five elite Australian footballers were prospectively monitored over two consecutive seasons. Internal and external training load was quantified using the session rating of perceived exertion and GPS/accelerometry, respectively. Cumulative load and acute-to-chronic workload ratios were derived using rolling averages and exponentially weighted moving averages. History of injuries in the current and previous seasons was recorded along with professional experience, weekly musculoskeletal screening, and subjective wellness scores for individual athletes. Individual and combined effects of these variables on injury risk were evaluated with generalized linear mixed models.Results: High cumulative loads and acute-to-chronic workload ratios were associated with increased risk of injuries. The effects for measures derived using exponentially weighted moving averages were greater than those for rolling averages. History of a recent injury, long-term experience at professional level, and substantial reductions in a selection of musculoskeletal screening and subjective wellness scores were associated with increased risk. The effects of high cumulative loads were underestimated by ~20% before adjusting for previous injuries, whereas the effects of high acute-to-chronic workload ratios were overestimated by 10–15%. Injury-prone players, identified via player identity in the mixed model, were at > 5 times higher risk of injuries compared to robust players (hazard ratio 5.4, 90% confidence limits 3.6–12) despite adjusting for training load and previous injuries. Combinations of multiple risk factors were associated with extremely large increases in risk; for example, a hazard ratio of 22 (9.7–52) was observed for the combination of high acute load, recent history of a leg injury, and a substantial reduction in the adductor squeeze test score.Conclusion: On the basis of our findings with an elite team of Australian footballers, the information from athlete monitoring practices in team sports should be interpreted collectively and used as a part of the injury prevention decision-making process along with consideration of individual differences in risk.

Linking testosterone and antisocial behavior in at-risk transitional aged youth: Contextual effects of parentification

Parentification refers to parents bestowing adult-like roles on children within families, and studies have linked parentification to individual differences in risk and resilience. The depth of our understanding of the pathways that translate parentification into risk for negative developmental outcomes remains shallow. This study examined whether parentification has a contextual effect moderating the expression of links between testosterone and antisocial behavior. Eighty-three participants (M age = 21.37 years, SD = 1.87; 48% Black; 60% female) were interviewed initially and one year later. Audio Computer Assisted Self-Interview methods were used to measure parentification and antisocial behavior. Saliva was sampled on multiple occasions and later assayed for testosterone. Results revealed, for both sexes, testosterone was positively associated with antisocial behavior at baseline and at follow-up when participants scored low on perceived benefits of parentification. This relationship became weaker as levels of perceived benefits of parentification increased. At the highest levels of perceived benefits of parentification, testosterone and antisocial behavior were inversely related. The findings suggest a potentially important role for perceptions of parentification as a moderator for the expression of hormone-behavior relationships and are discussed in terms of implications for the biosocial model of the family.

Impaired fear extinction in serotonin transporter knockout rats is associated with increased 5-hydroxymethylcytosine in the amygdala.

SummaryAimsOne potential risk factor for posttraumatic stress disorder (PTSD) involves the low activity (short; s) allelic variant of the serotonin transporter‐linked polymorphic region (5‐HTTLPR), possibly due to reduced prefrontal control over the amygdala. Evidence shows that DNA methylation/demethylation is crucial for fear extinction in these brain areas and is associated with neuronal activation marker c‐Fos expression. We hypothesized that impaired fear extinction in serotonin transporter knockout (5‐HTT −/−) rats is related to changes in DNA (de) methylation and c‐Fos expression in the prefrontal cortex (PFC) and/or amygdala.Methods5‐HTT −/− and 5‐HTT +/+ rats were subjected to fear extinction. 2 hours after the extinction session, the overall levels of DNA methylation (5‐mC), demethylation (5‐hmC), and c‐Fos in fear extinction and nonfear extinction rats were measured by immunohistochemistry.Results5‐HTT −/− rats displayed decreased fear extinction. This was associated with reduced c‐Fos activity in the infralimbic PFC. In the central nucleus of the amygdala, c‐Fos immunoreactivity was increased in the fear extinction group compared to the no‐fear extinction group, regardless of genotype. 5‐hmC levels were unaltered in the PFC, but reduced in the amygdala of nonextinction 5‐HTT −/− rats compared to nonextinction wild‐type rats, which caught up to wild‐type levels during fear extinction. 5‐mC levels were stable in central amygdala in both wild‐type and 5‐HTT −/− extinction rats. Finally, c‐Fos and 5‐mC levels were correlated with the prelimbic PFC, but not amygdala.ConclusionsIn the amygdala, DNA demethylation, independent from c‐Fos activation, may contribute to individual differences in risk for PTSD, as conferred by the 5‐HTTLPR s‐allele.

Individual differences in risk-taking tendencies modulate the neural processing of risky and ambiguous decision-making in adolescence

Although many neuroimaging studies have investigated adolescent risk taking, few studies have dissociated between decision-making under risk (known probabilities) and ambiguity (unknown probabilities). Furthermore, which brain regions are sensitive to individual differences in task-related and self-reported risk taking remains elusive. We presented 198 adolescents (11–24 years, an age-range in which individual differences in risk taking are prominent) with an fMRI paradigm that separated decision-making (choosing to gamble or not) and reward outcome processing (gains, no gains) under risky and ambiguous conditions, and related this to task-related and self-reported risk taking. We observed distinct neural mechanisms underlying risky and ambiguous gambling, with risk more prominently associated with activation in parietal cortex, and ambiguity more prominently with dorsolateral prefrontal cortex (PFC), as well as medial PFC during outcome processing. Individual differences in task-related risk taking were positively associated with ventral striatum activation in the decision phase, specifically for risk, and negatively associated with insula and dorsomedial PFC activation, specifically for ambiguity. Moreover, dorsolateral PFC activation in the outcome phase seemed a prominent marker for individual differences in task-related risk taking under ambiguity as well as self-reported daily-life risk taking, in which greater risk taking was associated with reduced activation in dorsolateral PFC. Together, this study demonstrates the importance of considering multiple risk-taking measures, and contextual moderators, in understanding the neural mechanisms underlying adolescent risk taking.

Identification of a novel gene regulating amygdala-mediated fear extinction

Recent years have seen advances in our understanding of the neural circuits associated with trauma-related disorders, and the development of relevant assays for these behaviors in rodents. Although inherited factors are known to influence individual differences in risk for these disorders, it has been difficult to identify specific genes that moderate circuit functions to affect trauma-related behaviors. Here, we exploited robust inbred mouse strain differences in Pavlovian fear extinction to uncover quantitative trait loci (QTL) associated with this trait. We found these strain differences to be resistant to developmental cross-fostering and associated with anatomical variation in basolateral amygdala (BLA) perineuronal nets, which are developmentally implicated in extinction. Next, by profiling extinction-driven BLA expression of QTL-linked genes, we nominated Ppid (peptidylprolyl isomerase D, a member of the tetratricopeptide repeat (TPR) protein family) as an extinction-related candidate gene. We then showed that Ppid was enriched in excitatory and inhibitory BLA neuronal populations, but at lower levels in the extinction-impaired mouse strain. Using a virus-based approach to directly regulate Ppid function, we demonstrated that downregulating BLA-Ppid impaired extinction, while upregulating BLA-Ppid facilitated extinction and altered in vivo neuronal extinction encoding. Next, we showed that Ppid colocalized with the glucocorticoid receptor (GR) in BLA neurons and found that the extinction-facilitating effects of Ppid upregulation were blocked by a GR antagonist. Collectively, our results identify Ppid as a novel gene involved in regulating extinction via functional actions in the BLA, with possible implications for understanding genetic and pathophysiological mechanisms underlying risk for trauma-related disorders.

Personalizing and Optimizing Preventive Intervention Models via a Translational Neuroscience Framework.

A new generation of research, building upon developmental psychopathology (Luthar et al. 1997; Luthar et al. (Child Development, 71, 543-562, 2000)), provides evidence that individual differences in risk for behavioral health problems result from intrapersonal and environmental modulation of neurophysiologic and genetic substrates. This transdisciplinary model suggests that, in any given individual, the number of genetic variants implicated in high-risk behavior and the way in which they are assorted and ultimately suppressed or activated in the brain by experiential and contextual factors help to explain behavioral orientations. Implications are that behavioral health problems can be amplified or reduced based on characteristics of an individual and socio-contextual influences on those characteristics. This emerging research has extraordinary implications for the design of prevention programs that more precisely target the malleable mechanisms that underlie behavioral health problems and, hence, more effectively prevent behavioral problems and promote resilience. A detailed, theory-driven examination of all evidence-based interventions is called for to identify the active ingredients that specifically impact these underlying mechanisms. Such an approach will enhance the ability of preventive interventions to achieve effect sizes indicative of beneficial impacts for a greater number of recipients. This paper presents the significant implications of this collective knowledge base for the next generation of precision-based, prevention-focused personalized interventions.

Neural Mechanisms Underlying Risk and Ambiguity Attitudes.

Individual differences in attitudes to risk (a taste for risk, known probabilities) and ambiguity (a tolerance for uncertainty, unknown probabilities) differentially influence risky decision-making. However, it is not well understood whether risk and ambiguity are coded differently within individuals. Here, we tested whether individual differences in risk and ambiguity attitudes were reflected in distinct neural correlates during choice and outcome processing of risky and ambiguous gambles. To these ends, we developed a neuroimaging task in which participants ( n = 50) chose between a sure gain and a gamble, which was either risky or ambiguous, and presented decision outcomes (gains, no gains). From a separate task in which the amount, probability, and ambiguity level were varied, we estimated individuals' risk and ambiguity attitudes. Although there was pronounced neural overlap between risky and ambiguous gambling in a network typically related to decision-making under uncertainty, relatively more risk-seeking attitudes were associated with increased activation in valuation regions of the brain (medial and lateral OFC), whereas relatively more ambiguity-seeking attitudes were related to temporal cortex activation. In addition, although striatum activation was observed during reward processing irrespective of a prior risky or ambiguous gamble, reward processing after an ambiguous gamble resulted in enhanced dorsomedial PFC activation, possibly functioning as a general signal of uncertainty coding. These findings suggest that different neural mechanisms reflect individual differences in risk and ambiguity attitudes and that risk and ambiguity may impact overt risk-taking behavior in different ways.

A Review of Developmental Considerations in Human Laboratory Alcohol Research.

Human laboratory studies involving alcohol administration have generated critical knowledge about individual differences in risk for alcohol use disorder (AUD), but have primarily involved adult populations and cross-sectional research designs. Ethical constraints have largely precluded human laboratory alcohol research in adolescence, and prospective studies have been rare. This paper provides an overview of developmental considerations in human laboratory alcohol research, with a focus on studies conducted with youth. Recent human laboratory studies from Europe and Canada have examined aspects of alcohol response during late adolescence, while recent survey studies from the United States have highlighted methods for circumventing alcohol administration in studies of adolescents. Across several decades of research, exceedingly few laboratory studies have examined developmental differences in alcohol responses or utilized prospective designs. Efforts to prioritize prospective research would further clarify the role of alcohol sensitivity traits as predictors or markers of AUD onset and progression.

Personality, Affectivity, and Alexithymia in Scuba Diving: Two Types of Risk Taking

Objectives for this study were, first, to describe individual differences in risk taking among scuba divers. Differences were examined on personality dimensions and psycho-affective variables, including positive and negative affect, as well as alexithymia. In addition, the study examined contributors to two types of behavior associated with scuba diving—deliberate risk taking and controlled participation in a high-risk sport (non-risk-taking). A cross-sectional design was used, and 131 participants were assessed on extraversion-neuroticism, affectivity, and alexithymia. The broad dimensions of personality and affectivity explained risk taking among divers. Alexithymia differentially predicted two types of risktaking behavior (direct or short-term and indirect or long-term) and was associated significantly with short-term risk-taking behavior.

Imagine your mood: Study design and protocol of a randomized controlled micro-trial using app-based experience sampling methodology to explore processes of change during relapse prevention interventions for recurrent depression.

BackgroundRelapse prevention strategies include continuation of antidepressant medication and preventive psychological interventions. This study aims to gain understanding that may inform tailoring of relapse prevention to individual differences, to improve their effects. Such treatment personalization may be based on repeated assessments within one individual, using experience sampling methodology. As a first step towards informing decisions based on this methodology, insight is needed in individual differences in risk of relapse and response to treatment, and how relapse prevention strategies may differentially target vulnerability for relapse.MethodsThe smartphone application ‘Imagine your mood’ has been developed specifically for this study to assess emotions, imagery, cognitions, and behaviors in daily life. Parallel to the randomized controlled trial ‘Disrupting the rhythm of depression’, 45 remitted recurrently depressed individuals taking continuation antidepressant medication will be randomly assigned to either continuing antidepressant medication (n = 15), continuing antidepressant medication combined with an eight-session preventive cognitive therapy (n = 15), or tapering of antidepressant medication in combination with preventive cognitive therapy (n = 15). Relapse and return of depressive symptomatology over a 24-month follow-up will be assessed. Additionally, matched never depressed individuals (n = 15) will be recruited as controls.DiscussionThis innovative study combines the strengths of a randomized controlled trial and experience sampling methodology in a micro-trial to explore individual differences in risk of relapse and what works for whom to prevent relapse. Results may ultimately pave the way for therapists to tailor relapse prevention strategies to individual (affective) vulnerability.Trial registrationISRCTN15472145, retrospectively registered.

The Youth Mental Health Risk and Resilience Study (YouR-Study)

BackgroundThe transition from adolescence to adulthood is associated with the emergence of psychosis and other mental health problems, highlighting the importance of this developmental period for the understanding of developing psychopathology and individual differences in risk and resilience. The Youth Mental Health Risk and Resilience Study (YouR-Study) aims to identify neurobiological mechanisms and predictors of psychosis-risk with a state-of-the-art neuroimaging approach (Magnetoencephalography, Magnetic Resonance Spectroscopy, Magnetic Resonance Imaging) in combination with core psychological processes, such as affect regulation and attachment, that have been implicated in the development and maintenance of severe mental health problems.Methods/DesignOne hundred participants meeting clinical high-risk criteria (CHR) for psychosis through the Comprehensive Assessment of At-Risk Mental State and Schizophrenia Proneness Instrument, Adult Version, in the age range from 16 to 35 years of age will be recruited. Mental-state monitoring up to a total of 2 years will be implemented to detect transition to psychosis. In addition, a sample of n = 40 help-seeking participants will be recruited who do not meet CHR-criteria, a group of n = 50 healthy control participants and a sample of n = 25 patients with first-episode psychosis. MEG-activity will be obtained during auditory and visual tasks to examine neural oscillations and event-related fields. In addition, we will obtain estimates of GABA and Glutamate levels through Magnetic Resonance Spectroscopy (MRS) to examine relationships between neural synchrony and excitatory-inhibition (E/I) balance parameters. Neuroimaging will be complemented by detailed neuropsychological assessments as well as psychological measures investigating the impact of childhood abuse, attachment experiences and affect regulation.DiscussionThe YouR-study could potentially provide important insights into the neurobiological mechanisms that confer risk for psychosis as well as biomarkers for early diagnosis of severe mental health problems. Moreover, we expect novel data related to the contribution of affect regulation and attachment-processes in the development of mental health problems, leading to an integrative model of early stage psychosis and the factors underlying risk and resilience of emerging psychopathology.

Genetic predisposition to high anxiety- and depression-like behavior coincides with diminished DNA methylation in the adult rat amygdala

Understanding biological mechanisms that shape vulnerability to emotional dysfunction is critical for elucidating the neurobiology of psychiatric illnesses like anxiety and depression. To elucidate molecular and epigenetic alterations in the brain that contribute to individual differences in emotionality, our laboratory utilized a rodent model of temperamental differences. Rats bred for low response to novelty (Low Responders, LRs) are inhibited in novel situations and display high anxiety, helplessness, and diminished sociability compared to High Novelty Responder (HR) rats. Our current transcriptome profiling experiment identified widespread gene expression differences in the amygdala of adult HR/LR rats; we hypothesize that HR/LR gene expression and downstream behavioral differences stem from distinct epigenetic (specifically DNA methylation) patterning in the HR/LR brain. Although we found similar levels of DNA methyltransferase proteins in the adult HR/LR amygdala, next-generation sequencing analysis of the methylome revealed 793 differentially methylated genomic sites between the groups. Most of the differentially methylated sites were hypermethylated in HR versus LR, so we next tested the hypothesis that enhancing DNA methylation in LRs would improve their anxiety/depression-like phenotype. We found that increasing DNA methylation in LRs (via increased dietary methyl donor content) improved their anxiety-like behavior and decreased their typically high levels of Forced Swim Test (FST) immobility; however, dietary methyl donor depletion exacerbated LRs’ high FST immobility. These data are generally consistent with findings in depressed patients showing that treatment with DNA methylation-promoting agents improves depressive symptoms, and highlight epigenetic mechanisms that may contribute to individual differences in risk for emotional dysfunction.

Genetic divergence in the transcriptional engram of chronic alcohol abuse: A laser-capture RNA-seq study of the mouse mesocorticolimbic system.

Genetic factors that influence the transition from initial drinking to dependence remain enigmatic. Recent studies have leveraged chronic intermittent ethanol (CIE) paradigms to measure changes in brain gene expression in a single strain at 0, 8, 72h, and even 7 days following CIE. We extend these findings using LCM RNA-seq to profile expression in 11 brain regions in two inbred strains - C57BL/6J (B6) and DBA/2J (D2) - 72h following multiple cycles of ethanol self-administration and CIE. Linear models identified differential expression based on treatment, region, strain, or interactions with treatment. Nearly 40% of genes showed a robust effect (FDR<0.01) of region, and hippocampus CA1, cortex, bed nucleus stria terminalis, and nucleus accumbens core had the highest number of differentially expressed genes after treatment. Another 8% of differentially expressed genes demonstrated a robust effect of strain. As expected, based on similar studies in B6, treatment had a much smaller impact on expression; only 72 genes (p<0.01) are modulated by treatment (independent of region or strain). Strikingly, many more genes (415) show a strain-specific and largely opposite response to treatment and are enriched in processes related to RNA metabolism, transcription factor activity, and mitochondrial function. Over 3 times as many changes in gene expression were detected in D2 compared to B6, and weighted gene co-expression network analysis (WGCNA) module comparison identified more modules enriched for treatment effects in D2. Substantial strain differences exist in the temporal pattern of transcriptional neuroadaptation to CIE, and these may drive individual differences in risk of addiction following excessive alcohol consumption.

The full translational spectrum of prevention science.

A new generation of research now demonstrates that individual differences in risk for psychopathology result from intrapersonal and environmental modulation of neurophysiologic and genetic substrates. This transdisciplinary model suggests that, in any given individual, the number of genetic variants implicated in high-risk behaviors and the way in which they are assorted and ultimately suppressed or activated by experiential and contextual factors will help to explain propensity and ultimate outcomes. Thus, risk can be amplified or reduced based on characteristics of an individual and his/her environment. This emerging research generated by multiple disciplines has extraordinary potential for preventing behavioral problems and promoting resilience. Unfortunately, however, the relevant sciences continue to be overly silo’ed, for example, with researchers focusing on socio-emotional and contextual influences working independently from those studying neurobiologic and genetic processes. Recent trends, however, are responding to a burgeoning body of research on the brain and behavior, promising to increase integration of basic science into a holistic model of prevention research. And, near-futuristically, an end-goal is to guide development of new and innovative interventions and inform policy change. In essence, the state-of-the-science highlights the need for a transdisciplinary and translational model of prevention.

A population-based Swedish Twin and Sibling Study of cannabis, stimulant and sedative abuse in men

BackgroundPrior studies, utilizing interview-based assessments, suggest that most of the genetic risk factors for drug abuse (DA) are non-specific with a minority acting specifically on risk for abuse of particular psychoactive substance classes. We seek to replicate these findings using objective national registry data. MethodsWe examined abuse of cannabis, stimulants (including cocaine) and sedatives ascertained from national Swedish registers in male–male monozygotic (1720 pairs) and dizygotic twins (1219 pairs) combined with near-age full siblings (76,457 pairs) to provide sufficient power. Modeling was performed using Mx. ResultsA common pathway model fitted better than an independent pathway model. The latent liability to DA was highly heritable but also influenced by shared environment. Cannabis, stimulant and sedative abuse all loaded strongly on the common factor. Estimates for the total heritability for the three forms of substance abuse ranged from 64 to 70%. Between 75 and 90% of that genetic risk was non-specific, coming from the common factor with the remainder deriving from substance specific genetic risk factors. By contrast, all of the shared environmental effects, which accounted for 18–20% of the variance in liability, were non-specific. ConclusionsIn accord with prior studies based on personal interviews, the large preponderance of genetic risk factors for abuse of specific classes of psychoactive substance are non-specific. These results suggest that genetic variation in the primary sites of action of the psychoactive drugs, which differ widely across most drug classes, play a minor role in human individual differences in risk for DA.

Testosterone and Economic Risk Taking: A Review

Since precise forecasting of the future is not possible, most of life’s decisions are made with uncertain outcomes. One important facet of uncertainty that is of particular interest to decision scientists is risk—the choice between an option that is less rewarding but more certain and an option that is less certain, but potentially more rewarding. Recent developments in both neuroscience and behavioral endocrinology have helped to reveal the biological mechanisms that support decision-making involving economic risk, and consequently, potential factors associated with individual differences in risk taking. This review is dedicated to surveying recent developments that link the hormone testosterone to economic risk taking. Like neuroeconomics, endocrinological approaches may provide a potentially powerful framework from which to understand decision-making and may help to make sense of a number of well-documented behavioral anomalies involving economic risk. Specifically, we suggest that testosterone functions to modulate risky behaviors in ways that appear to be adaptive. Still, more work is needed to understand the nature of the relationship between testosterone and risk in both sexes.

Differential strain vulnerability to binge eating behaviors in rats

Binge eating is a significantly heritable phenotype, but efforts to detect specific risk genes have fallen short. Identification of animal strain differences in risk for binge eating could highlight genetic differences across individuals of the same species that can be exploited in future animal and molecular genetic research. The current study aimed to explore strain differences in risk for binge eating in Sprague–Dawley versus Wistar female rats using the Binge Eating Resistant/Binge Eating Prone model. A sample of male Sprague–Dawley rats, a known low-risk group for binge eating, was included as a comparison group. A total of 83 rats (23 Wistar females, 30 Sprague–Dawley females, 30 Sprague–Dawley males) completed a protocol of intermittently administered, palatable food. Binge eating prone (BEP) and binge eating resistant (BER) rats were identified using a tertile approach. Sprague–Dawley female rats consumed the highest amount of palatable food and were more likely to be classified as BEP compared to Wistar female and Sprague–Dawley male rats. Wistar female rats were not significantly different from Sprague–Dawley male rats in their palatable food intake and tendency to be classified as BER rather than BEP. Sprague–Dawley female rats appear to be a particularly vulnerable genotype for binge eating. Comparisons between this group and others could help identify specific genetic/biological factors that differentiate it from lower risk groups. The reward system, linked to binge eating in humans, is a possible candidate to explore. Strain differences in the reward system could help increase understanding of individual differences in risk for binge eating in humans.