Sex bias in pain management decisions.

In the pursuit of mental and physical health, effective pain management stands as a cornerstone. Here, we examine a potential sex bias in pain management. Leveraging insights from psychological research showing that females' pain is stereotypically judged as less intense than males' pain, we hypothesize that there may be tangible differences in pain management decisions based on patients' sex. Our investigation spans emergency department (ED) datasets from two countries, including discharge notes of patients arriving with pain complaints (N = 21,851). Across these datasets, a consistent sex disparity emerges. Female patients are less likely to be prescribed pain-relief medications compared to males, and this disparity persists even after adjusting for patients' reported pain scores and numerous patient, physician, and ED variables. This disparity extends across medical practitioners, with both male and female physicians prescribing less pain-relief medications to females than to males. Additional analyses reveal that female patients' pain scores are 10% less likely to be recorded by nurses, and female patients spend an additional 30 min in the ED compared to male patients. A controlled experiment employing clinical vignettes reinforces our hypothesis, showing that nurses (N = 109) judge pain of female patients to be less intense than that of males. We argue that the findings reflect an undertreatment of female patients' pain. We discuss the troubling societal and medical implications of females' pain being overlooked and call for policy interventions to ensure equal pain treatment.

Physicians prescribe fewer analgesics during night shifts than day shifts.

Adequate pain management is one of the biggest challenges of the modern healthcare system. Physician perception of patient subjective pain, which is crucial to pain management, is susceptible to a host of potential biases. Here we explore the timing of physicians' work as a previously unrecognized source of systematic bias in pain management. We hypothesized that during night shifts, sleep deprivation, fatigue, and stress would reduce physicians' empathy for others' pain, leading to underprescription of analgesics for patient pain relief. In study 1, 67 resident physicians, either following a night shift or not, performed empathy for pain assessment tasks and simulated patient scenarios in laboratory conditions. As predicted, following a night shift, physicians showed reduced empathy for pain. In study 2, we explored this phenomenon in medical decisions in the field. We analyzed three emergency department datasets from Israel and the United States that included discharge notes of patients arriving with pain complaints during 2013 to 2020 (n = 13,482). Across all datasets, physicians were less likely to prescribe an analgesic during night shifts (compared to daytime shifts) and prescribed fewer analgesics than generally recommended by the World Health Organization. This effect remained significant after adjusting for patient, physician, type of complaint, and emergency department characteristics. Underprescription for pain during night shifts was particularly prominent for opioids. We conclude that night shift work is an important and previously unrecognized source of bias in pain management, likely stemming from impaired perception of pain. We consider the implications for hospitals and other organizations employing night shifts.

The Long-Term Associations of Perinatal Obesogenic Environment with Offspring Biological Aging.

Biological age (BA), reflecting aging-related health decline beyond chronological age, varies among individuals. While previous research explored associations of maternal pregnancy-related body size with offspring health outcomes, its implications for BA in young adults remain unclear. Utilizing longitudinal data of 1,148 mother-offspring pairs from the Jerusalem Perinatal Study, we analyzed associations of maternal pre-pregnancy BMI and gestational weight gain (GWG) with offspring Klemera-Doubal method (KDM)-based BA at age 32, and potential familial life-course underlying mechanisms. Maternal pregnancy-related body size, adjusted for sociodemographic/lifestyle factors was associated with offspring BA (ßmaternal pre-pregnancy BMI=0.183,95%CI:0.098,0.267;ßGWG=0.093,95%CI:0.021,0.165). Association of GWG with BA was largely direct (90%,95%CI,44%,100%), while association with maternal pre-pregnancy BMI was partially mediated through adolescent BMI (36%,95%CI=18%,75%), with both associations eliminated after adjustment for offspring adult BMI. Associations persisted after adjusting for offspring polygenic risk score for BMI (ßmaternal pre-pregnancy BMI=0.128;95%CI=0.023,0.234; ßGWG=0.102;95%CI=0.006,0.198), and somewhat altered after adjustment for maternal cardiometabolic conditions (ßmaternal pre-pregnancy BMI=0.144,95%CI=0.059, 0.230). Impact on GWG associations was negligible. Thus, perinatal obesogenic environment contributes to offspring BA beyond sociodemographic factors and maternal cardiometabolic history, yet intergenerational transmission of obesity seems to underlie these associations. Nonetheless, the period between adolescence and young adulthood could be targeted for weight-reducing interventions, ultimately promoting healthy aging.

Postpartum women's attitudes to disclosure of adult-onset conditions in pregnancy.

BACKGROUND: Advanced prenatal genomic technologies can identify risks for adult-onset (AO) conditions in the fetus, challenging the traditional purpose of prenatal testing. Professional guidelines commonly support disclosure of high-penetrance AO actionable conditions, yet attitudes of women/parents to these findings and factors affecting their attitudes are understudied. METHODS: We explored 941 (77% response rate) postpartum women's attitudes towards receiving prenatal genetic information, and associations of sociodemographic, medical and psychological characteristics with their choices, focusing on AO conditions. RESULTS: Women largely support the disclosure of actionable AO findings (58.4%), in line with professional guidelines. A third of the women also supported the disclosure of non-actionable AO conditions. Stronger religious observance (p < 0.001) and higher psychological distress (p = 0.024) were associated with decreased interest in receiving actionable AO conditions, whereas higher concern for fetal health yielded increased interest (p = 0.032). Attitudes towards disclosure were strongly associated with women's perceived benefit of such information for their own, partner's, and future child's health. Termination of pregnancy based on such information received very little support. CONCLUSION: In-light of the demonstrated understanding of nuanced genetic information and the observed diversity in attitudes, a culturally competent opt-in/out policy could be considered. If full-disclosure is practiced, support should be provided to those expressing higher levels of distress.

Little evidence for associations between the Big Five personality traits and variability in brain gray or white matter.

Attempts to link the Big Five personality traits of Openness-to-Experience, Conscientiousness, Extraversion, Agreeableness, and Neuroticism with variability in trait-like features of brain structure have produced inconsistent results. Small sample sizes and heterogeneous methodology have been suspected in driving these inconsistencies. Here, using data collected from 1,107 university students (636 women, mean age 19.69 â€‹± â€‹1.24 years), representing the largest sample to date of unrelated individuals, we tested for associations between the Big Five personality traits and measures of cortical thickness and surface area, subcortical volume, and white matter microstructural integrity. In addition to replication analyses based on a prior study, we conducted exploratory whole-brain analyses. Four supplementary analyses were also conducted to examine 1) possible associations with lower-order facets of personality; 2) modulatory effects of sex; 3) effect of controlling for non-target personality traits; and 4) parcellation scheme effects. Our analyses failed to identify significant associations between the Big Five personality traits and brain morphometry, except for a weak association between greater surface area of the superior temporal gyrus and lower conscientiousness scores. As the latter association is not supported by previous studies, it should be treated with caution. Our supplementary analyses mirrored these predominantly null findings, suggesting they were not substantively biased by our analytic choices. Collectively, these results indicate that if there are associations between the Big Five personality traits and brain structure, they are likely of very small effect size and will require very large samples for reliable detection.

Quantification of biological aging in young adults.

Antiaging therapies show promise in model organism research. Translation to humans is needed to address the challenges of an aging global population. Interventions to slow human aging will need to be applied to still-young individuals. However, most human aging research examines older adults, many with chronic disease. As a result, little is known about aging in young humans. We studied aging in 954 young humans, the Dunedin Study birth cohort, tracking multiple biomarkers across three time points spanning their third and fourth decades of life. We developed and validated two methods by which aging can be measured in young adults, one cross-sectional and one longitudinal. Our longitudinal measure allows quantification of the pace of coordinated physiological deterioration across multiple organ systems (e.g., pulmonary, periodontal, cardiovascular, renal, hepatic, and immune function). We applied these methods to assess biological aging in young humans who had not yet developed age-related diseases. Young individuals of the same chronological age varied in their "biological aging" (declining integrity of multiple organ systems). Already, before midlife, individuals who were aging more rapidly were less physically able, showed cognitive decline and brain aging, self-reported worse health, and looked older. Measured biological aging in young adults can be used to identify causes of aging and evaluate rejuvenation therapies.

Credit scores, cardiovascular disease risk, and human capital.

Credit scores are the most widely used instruments to assess whether or not a person is a financial risk. Credit scoring has been so successful that it has expanded beyond lending and into our everyday lives, even to inform how insurers evaluate our health. The pervasive application of credit scoring has outpaced knowledge about why credit scores are such useful indicators of individual behavior. Here we test if the same factors that lead to poor credit scores also lead to poor health. Following the Dunedin (New Zealand) Longitudinal Study cohort of 1,037 study members, we examined the association between credit scores and cardiovascular disease risk and the underlying factors that account for this association. We find that credit scores are negatively correlated with cardiovascular disease risk. Variation in household income was not sufficient to account for this association. Rather, individual differences in human capital factors­educational attainment, cognitive ability, and self-control­predicted both credit scores and cardiovascular disease risk and accounted for ∼45% of the correlation between credit scores and cardiovascular disease risk. Tracing human capital factors back to their childhood antecedents revealed that the characteristic attitudes, behaviors, and competencies children develop in their first decade of life account for a significant portion (∼22%) of the link between credit scores and cardiovascular disease risk at midlife. We discuss the implications of these findings for policy debates about data privacy, financial literacy, and early childhood interventions.

Cardiorespiratory fitness and cognitive function in midlife: neuroprotection or neuroselection?

OBJECTIVE: A study was undertaken to determine whether better cognitive functioning at midlife among more physically fit individuals reflects neuroprotection, by which fitness protects against age-related cognitive decline, or neuroselection, by which children with higher cognitive functioning select more active lifestyles. METHODS: Children in the Dunedin Longitudinal Study (N = 1,037) completed the Wechsler Intelligence Scales and the Trail Making, Rey Delayed Recall, and Grooved Pegboard tasks as children and again at midlife (age = 38 years). Adult cardiorespiratory fitness was assessed using a submaximal exercise test to estimate maximum oxygen consumption adjusted for body weight in milliliters/minute/kilogram. We tested whether more fit individuals had better cognitive functioning than their less fit counterparts (which could be consistent with neuroprotection), and whether better childhood cognitive functioning predisposed to better adult cardiorespiratory fitness (neuroselection). Finally, we examined possible mechanisms of neuroselection. RESULTS: Participants with better cardiorespiratory fitness had higher cognitive test scores at midlife. However, fitness-associated advantages in cognitive functioning were already present in childhood. After accounting for childhood baseline performance on the same cognitive tests, there was no association between cardiorespiratory fitness and midlife cognitive functioning. Socioeconomic and health advantages in childhood and healthier lifestyles during young adulthood explained most of the association between childhood cognitive functioning and adult cardiorespiratory fitness. INTERPRETATION: We found no evidence for a neuroprotective effect of cardiorespiratory fitness as of midlife. Instead, children with better cognitive functioning are selecting healthier lives. Fitness interventions may enhance cognitive functioning. However, observational and experimental studies testing neuroprotective effects of physical fitness should consider confounding by neuroselection.

Intranasal oxytocin interacts with testosterone reactivity to modulate parochial altruism.

The neuropeptide hormone oxytocin and the steroid hormone testosterone have received attention as modulators of behavior in the context of intergroup conflict. However, to date, their interactive effect has yet to be tested. Here, in a double-blind placebo-control design, 204 participants (102 female participants) self-administrated oxytocin or placebo and completed an experimental economic game modeling intergroup conflict. Salivary testosterone (n = 192) was measured throughout the task to assess endogenous reactivity. As a caveat, even at this sample size, our derived power to detect small effects for 2- and 3-way interactions was relatively low. For male participants, changes in testosterone predicted willingness to sacrifice investments for the betterment of the group. Intranasal administration of oxytocin strongly diminished this effect. In female participants, we found no credible evidence for association between changes in testosterone and investments, rather, oxytocin effects were independent of testosterone. This 3-way interaction was of medium to large effect size (Odds Ratio 5.11). Behavior was also affected by social cues such as signaling of ingroup and outgroup members. Our findings provide insights as to the biological processes underpinning parochial altruism and suggest an additional path for the dual influence of oxytocin and testosterone on human social behavior.

Attenuation of visual exploration following stress.

When we explore our surroundings, we frequently move our gaze to collect visual information. Studies have extensively examined gaze behavior in response to different visual scenes. Here, we examined how differences in an individual's state may affect visual exploration, for example, following acute stress. In this study, participants were exposed to either a psychosocial stressor-performing a public speaking task in front of a two-person committee-or a control condition absent stress induction. Elicitation of stress responses was validated using cortisol levels and subjective reports. Stress also led to an extended increase in pupil diameter (a proxy of arousal responses), suggesting it may also affect eye movements. Gaze behavior measures were taken prior and following the stress or control tasks. Acute stress attenuated visual exploration, reflected by fewer saccades and a smaller scanned area. Stress did not have a significant effect on either the tendency to look at social features or at salient regions of the images. These findings diverge from theoretical predictions suggesting that acute stress may facilitate social affiliative behaviors (e.g., Tend-and-Befriend theory). Reduced saccades and a smaller scanned area may be a possible mechanism explaining previous reports showing stress-related effects on various cognitive processes (e.g., visual working memory) that rely on visual exploration.

Familial aggregation of the aging process: biological age measured in young adult offspring as a predictor of parental mortality.

Measures of biological age (BA) integrate information across organ systems to quantify "biological aging," i.e., inter-individual differences in aging-related health decline. While longevity and lifespan aggregate in families, reflecting transmission of genes and environments across generations, little is known about intergenerational continuity of biological aging or the extent to which this continuity may be modified by environmental factors. Using data from the Jerusalem Perinatal Study (JPS), we tested if differences in offspring BA were related to mortality in their parents. We measured BA using biomarker data collected from 1473 offspring during clinical exams in 2007-2009, at age 32 ± 1.1. Parental mortality was obtained from population registry data for the years 2004-2016. We fitted parametric survival models to investigate the associations between offspring BA and parental all-cause and cause-specific mortality. We explored potential differences in these relationships by socioeconomic position (SEP) and offspring sex. Participants' BAs widely varied (SD = 6.95). Among those measured to be biologically older, parents had increased all-cause mortality (HR = 1.10, 95% CI: 1.08, 1.13), diabetes mortality (HR = 1.19, 95% CI: 1.08, 1.30), and cancer mortality (HR = 1.07, 95% CI: 1.02, 1.13). The association with all-cause mortality was stronger for families with low compared with high SEP (Pinteraction = 0.04) and for daughters as compared to sons (Pinteraction < 0.001). Using a clinical-biomarker-based BA estimate, observable by young adulthood prior to the onset of aging-related diseases, we demonstrate intergenerational continuity of the aging process. Furthermore, variation in this familial aggregation according to household socioeconomic position (SEP) at offspring birth and between families of sons and daughters proposes that the environment alters individuals' aging trajectory set by their parents.

Empathy Modulates the Effect of Stress Reactivity on Generous Giving.

How does acute stress influence the degree to which we cooperate with others? Research on the effects of stress on social decision-making is guided by two seemingly contrasting theories. Acute stress may trigger a Fight-or-Flight response, manifested by increased anxiety, and more egocentric or selfish behavior. Alternatively, according to the Tend-and-Befriend model, acute stress may induce affiliative behaviors, marked by increased prosociality in an effort to seek and receive social support and protection. Extant studies on the topic do not provide consistent support for either pattern of behavior, with studies showing evidence for both Fight-or-Flight or Tend-and-Befriend like responses. One possibility, may be the nature of social responses to stressful situations differ as a function of the individual. In the current study, we demonstrate an example of such a person-by-situation interaction, showing that acute stress can cause either pro-social or selfish responses, contingent on individual differences in trait empathy. One hundred and twenty three participants (60 F) were assessed for trait empathy using the Interpersonal Reactivity Index; consequently, they underwent either the Trier Social Stress Test-a well-validated paradigm for eliciting acute psychosocial stress-or a non-stress inducing control condition. Following exposure to either the stress or control condition, participants played a one-shot Dictator Game to evaluate their generosity levels. Statistical analyses revealed that acute stress by itself did not affect the amount transferred in the Dictator Game. Rather, individual differences in trait empathy moderated the effects of stress on giving. Elevations in stress-induced cortisol resulted in more generous behavior, but only in individuals high in empathy. In contrast, in individuals low in empathy, a greater rise in stress-induced cortisol resulted in more selfish behavior. Effects were more pronounced in females than males. Our findings highlight the necessity of integrating personality traits as important moderators of the link between stress and sociality.

The general psychopathology factor from early to middle childhood: Longitudinal genetic and risk analyses.

Accumulating research suggests the structure of psychopathology is best represented by continuous higher-order dimensions, including a general dimension, "p," and more specific dimensions, for example, externalizing and internalizing factors. Here, we aimed to (a) replicate p in early childhood, (b) examine stability and change of genetic and environmental influences on the psychopathology factors from early to midchildhood, (c) externally validate the factors with key constructs of psychological functioning, and (d) test whether the factors can be predicted by early-life measures (e.g., neonatal complications). Data are based on the Longitudinal Israeli Study of Twins. Mothers reported on pregnancy and neonatal conditions and repeatedly filled in questionnaires on each twin's externalizing and internalizing symptoms from ages 3 to 9. Cognitive ability was assessed in the lab at age 6.5, and personality traits, self-esteem, and life satisfaction were self-reported by the twins at ages 11-13. A bifactor model that included p and externalizing and internalizing factors fit the data best, and associations between p, cognitive ability, and personality were replicated. Longitudinal twin analyses indicated that p is highly heritable (64-73%) with a substantial proportion of the genetic influences stable from age 3. The specific internalizing and externalizing factors (net of p) were also highly heritable. Higher p predicted lower self-esteem at age 11. Early-life measures were not strongly associated with psychopathology. Our results show that p is discernible in early childhood, highly heritable, and prospectively associated with negative outcomes. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

Independent associations of inter-spousal gaps in age and education with long-term mortality and cancer survival: The Jerusalem Perinatal Study 1964-2016.

PURPOSE: To identify factors responsible for variation in health among married individuals, we investigated the independent associations of gaps in spousal age and education (or "heterogamy") with all-cause and cause-specific mortality as well as with survival of cancer patients. METHODS: Using over four decades of follow-up data on 36,717 couples from Jerusalem (1964-2016), we compared heterogamous with homogamous couples. RESULTS: Having a less educated spouse was associated with an increased risk for several outcomes in both genders, such as all-cause mortality in males (hazard ratio [HR] = 1.18, 95% confidence interval [CI]: 1.12, 1.25) and in females (HR = 1.11, CI: 1.01, 1.22). Having a more educated spouse was associated with decreased all-cause mortality in males (HR = 0.93, CI: 0.87, 0.99), but not in females. Having an older spouse was detrimental for health of both genders. For example, increased all-cause mortality was seen in men (HR = 1.22, CI: 1.10, 1.34) and in women (HR = 1.10, CI: 1.02, 1.19). A younger spouse was beneficial for some of the outcomes in males, such as decreased cancer-specific mortality (HR = 0.88, CI: 0.78, 0.99), but not in females. CONCLUSIONS: Spousal gaps in education and age may be independently associated with health outcomes. The observed relationships may be driven by combined amounts of marital strain as well as shared spousal resources (such as knowledge or income) depending on gender.

All-trans retinoic acid upregulates reduced CD38 transcription in lymphoblastoid cell lines from Autism spectrum disorder.

Deficits in social behavior in mice lacking the CD38 gene have been attributed to impaired secretion of oxytocin. In humans, similar deficits in social behavior are associated with autistic spectrum disorder (ASD), for which genetic variants of CD38 have been pinpointed as provisional risk factors. We sought to explore, in an in vitro model, the feasibility of the theory that restoring the level of CD38 in ASD patients could be of potential clinical benefit. CD38 transcription is highly sensitive to several cytokines and vitamins. One of these, all-trans retinoic acid (ATRA), a known inducer of CD38, was added during cell culture and tested on a large sample of N = 120 lymphoblastoid cell (LBC) lines from ASD patients and their parents. Analysis of CD38 mRNA levels shows that ATRA has an upmodulatory potential on LBC derived from ASD patients as well as from their parents. The next crucial issue addressed in our study was the relationship between levels of CD38 expression and psychological parameters. The results obtained indicate a positive correlation between CD38 expression levels and patient scores on the Vineland Adaptive Behavior Scale. In addition, analysis of the role of genetic polymorphisms in the dynamics of the molecule revealed that the genotype of a single-nucleotide polymorphism (rs6449182; C>G variation) in the CpG island of intron 1, harboring the retinoic-acid response element, exerts differential roles in CD38 expression in ASD and in parental LBC. In conclusion, our results provide an empirical basis for the development of a pharmacological ASD treatment strategy based on retinoids.

Vasopressin needs an audience: neuropeptide elicited stress responses are contingent upon perceived social evaluative threats.

The nonapeptide arginine vasopressin (AVP) plays an important role in hypothalamus-pituitary-adrenal axis regulation and also functions as a social hormone in a wide variety of species, from voles to humans. In the current report we use a variety of stress inducing tasks, including the Trier Social Stress Test (TSST) and intranasal administration of AVP to show that intranasal administration of this neuropeptide leads to a significant increase in salivary cortisol and pulse rate, specifically in conditions where subjects perform tasks in the presence of a social evaluative threat (task performance could be negatively judged by others). In contrast, in conditions without a social evaluative threat (no task condition, modified TSST without audience and bike ergometry), subjects receiving AVP did not differ from subjects receiving placebo. Thus exogenous AVP's influence is contingent upon a circumscribed set of initial conditions that constitute a direct threat to the maintenance of our social selves. Stress evoked by social threat is an integral part of social life and is related to self-esteem and in extreme forms, to poor mental health (e.g., social phobia). Our findings suggest that AVP is a key component in the circuit that interlaces stress and social threat and findings offer inroads to our understanding of individual differences in sociability and in stress response elicited in threatening social situations.

Heritability of children's prosocial behavior and differential susceptibility to parenting by variation in the dopamine receptor D4 gene.

Theoretical considerations and new empirical evidence suggest that children's development cannot simply be explained by either genes or environment but that their interaction is important to understanding child behavior. In particular, a genetic polymorphism, the exon III repeat region of the dopamine receptor D4, has been the focus of interest regarding differential susceptibility to parental influence. To study environmental and genetic influences on children's prosocial behavior, 168 twin pairs (mean age = 44 months) participated in an experiment that assessed prosocial behavior via three measures: compliant prosocial behavior elicited in response to social requests, self-initiated prosocial behavior enacted voluntarily, and mothers' rating of children's behavior. Genetic effects accounted for 34% to 53% of the variance in prosocial behavior. The rest of the variance was accounted for by nonshared environment and error. Parenting measures of maternal positivity, negativity, and unexplained punishment did not correlate significantly with children's prosocial behavior. However, when parenting was stratified by presence or absence of the child's dopamine receptor D4 7-repeat allele in an overlapping sample of 167 children to model differential susceptibility to parental influence, a richer picture emerged. Positive parenting related meaningfully to mother-rated prosocial behavior, and unexplained punishment related positively to self-initiated prosocial behavior, but only among children carrying the 7-repeat allele. The findings demonstrate that a molecular genetic strategy, based on genotyping of common polymorphisms and combined with a classic twin approach, provides a richer description of how genes and environment interact to shape children's behavior, and allows for the identification of differential sensitivity to parental influence.

Intranasal oxytocin, testosterone reactivity, and human competitiveness.

Competitiveness is an essential feature of human social interactions. Despite an extensive body of research on the underlying psychological and cultural factors regulating competitive behavior, the role of biological factors remains poorly understood. Extant research has focused primarily on sex hormones, with equivocal findings. Here, we examined if intranasal administration of the neuropeptide oxytocin (OT) - a key regulator of human social behavior and cognition - interacts with changes in endogenous testosterone (T) levels in regulating the willingness to engage in competition. In a double-blind placebo-control design, 204 subjects (102 females) self-administrated OT or placebo and were assessed for their willingness to compete via an extensively-validated economic laboratory competition paradigm, in which, before completing a set of incentivized arithmetic tasks, subjects are asked to decide what percentage of their payoffs will be based on tournament paying-scheme. Salivary T concentrations (n = 197) were measured throughout the task to assess endogenous reactivity. Under both OT and placebo, T-reactivity during competition was not associated with competitiveness in females. However, in males, the association between T-reactivity and competitiveness was OT-dependent. That is, males under placebo demonstrated a positive correlation between T-reactivity and the willingness to engage in competition, while no association was observed in males receiving OT. The interaction between OT, T-reactivity, and sex on competitive preferences remained significant even after controlling for potential mediators such as performance, self-confidence, and risk-aversion, suggesting that this three-way interaction effect was specific to competitive motivation rather than to other generalized processes. These findings deepen our understanding of the biological processes underlying human preferences for competition and extend the evidence base for the interplay between hormones in affecting human social behavior.

Social evaluation under stress: Does acute stress affect social attributions and eye gaze?

Acute stress has been found to elicit pro-social, anti-social or null responses in humans. The causes for these contradicting findings are currently poorly understood, and may rise from subjects' characteristics, such as sex or hormonal status, as well as stimuli-based traits, such as group membership. In the current study, 120 subjects performed either the Trier Social Stress Test or a control (non-stress inducing) condition, followed by ranking displayed faces according to several attributes (e.g., trustworthiness, attractiveness, dominance). Participants' eye gaze was also tracked while viewing facial stimuli. We examined how acute stress interacts with participants' sex, female participants' hormonal status (hormonal contraceptives, early-follicular phase and mid-luteal phase), and the observed faces' social group (ethnicity-based in-group or out-groups). In general, frequentist and Bayesian analyses showed that acute stress exposure did not affect social attributions or gaze behavior, nor did it interact with subjects' sex or the group membership of the observed faces. Interestingly, sub-group analyses showed that in females, acute stress interacted with hormonal status to yield heterogenous anti-social effects, such as post-stress reductions in perceived trustworthiness in the early-follicular phase, and lower perceived attractiveness in the mid-luteal phase. Given the small sample sizes for the sub-groups, these results should be viewed as preliminary until further replicated. Our results highlight the necessity for large-scale studies, particularly in females, to further refine existing theories regarding the nature and contexts by which acute stress elicits changes in social cognition and behavior.

Vital personality scores and healthy aging: Life-course associations and familial transmission.

OBJECTIVES: Personality traits are linked with healthy aging, but it is not clear how these associations come to manifest across the life-course and across generations. To study this question, we tested a series of hypotheses about (a) personality-trait prediction of markers of healthy aging across the life-course, (b) developmental origins, stability and change of links between personality and healthy aging across time, and (c) intergenerational transmission of links between personality and healthy aging. For our analyses we used a measure that aggregates the contributions of Big 5 personality traits to healthy aging: a "vital personality" score. METHODS: Data came from two population-based longitudinal cohort studies, one based in New Zealand and the other in the UK, comprising over 6000 study members across two generations, and spanning an age range from birth to late life. RESULTS: Our analyses revealed three main findings: first, individuals with higher vital personality scores engaged in fewer health-risk behaviors, aged slower, and lived longer. Second, individuals' vital personality scores were preceded by differences in early-life temperament and were relatively stable across adulthood, but also increased from young adulthood to midlife. Third, individuals with higher vital personality scores had children with similarly vital partners, promoted healthier behaviors in their children, and had children who grew up to have more vital personality scores themselves, for genetic and environmental reasons. CONCLUSION: Our study shows how the health benefits associated with personality accrue throughout the life-course and across generations.