Effects of 7.5% carbon dioxide (CO2) inhalation and ethnicity on face memory

AbstractThe ability to accurately verify facial identity has important forensic implications, but this ability is fallible. Research suggests that anxiety at the time of encoding can impair subsequent recall, but no studies have investigated the effects of anxiety at the time of recall in an experimental paradigm. This study addresses this gap using the carbon dioxide (CO2) model of anxiety induction. Thirty participants completed two inhalations: one of 7.5% CO2-enriched air and one of medical air (i.e., placebo). Prior to each inhalation, participants were presented with 16 facial images (50% own-ethnicity, 50% other-ethnicity). During the inhalation they were required to identify which faces had been seen before from a set of 32 images (16 seen-before and 16 novel images). Identification accuracy was lower during CO2 inhalation compared to air (F[1,29]=5.5, p=.026, ηp2=.16), and false alarm rate was higher for other-ethnicity faces compared to own-ethnicity faces (F[1,29]=11.3, p=.002, ηp2=.28). There was no evidence of gas by ethnicity interactions for accuracy or false alarms (ps>.34). Ratings of decision confidence did not differ by gas condition, suggesting that participants were unaware of differences in performance. These findings suggest that anxiety, at the point of recognition, impairs facial identification accuracy. This has substantial implications for eyewitness memory situations, and suggests that efforts should be made to attenuate the anxiety in these situations in order to improve the validity of identification

Genome-by-Trauma Exposure Interactions in Adults With Depression in the UK Biobank

IMPORTANCE: Self-reported trauma exposure has consistently been found to be a risk factor for major depressive disorder (MDD), and several studies have reported interactions with genetic liability. To date, most studies have examined gene-environment interactions with trauma exposure using genome-wide variants (single-nucleotide variations [SNVs]) or polygenic scores, both typically capturing less than 3% of phenotypic risk variance. OBJECTIVE: To reexamine genome-by-trauma interaction associations using genetic measures using all available genotyped data and thus, maximizing accounted variance. DESIGN, SETTING, AND PARTICIPANTS: The UK Biobank study was conducted from April 2007 to May 1, 2016 (follow-up mental health questionnaire). The current study used available cross-sectional genomic and trauma exposure data from UK Biobank. Participants who completed the mental health questionnaire and had available genetic, trauma experience, depressive symptoms, and/or neuroticism information were included. Data were analyzed from April 1 to August 30, 2021. EXPOSURES: Trauma and genome-by-trauma exposure interactions. MAIN OUTCOMES AND MEASURES: Measures of self-reported depression, neuroticism, and trauma exposure with whole-genome SNV data are available from the UK Biobank study. Here, a mixed-model statistical approach using genetic, trauma exposure, and genome-by-trauma exposure interaction similarity matrices was used to explore sources of variation in depression and neuroticism. RESULTS: Analyses were conducted on 148 129 participants (mean [SD] age, 56 [7] years) of which 76 995 were female (52.0%). The study approach estimated the heritability (SE) of MDD to be approximately 0.160 (0.016). Subtypes of self-reported trauma exposure (catastrophic, adult, childhood, and full trauma) accounted for a significant proportion of the variance of MDD, with heritability (SE) ranging from 0.056 (0.013) to 0.176 (0.025). The proportion of MDD risk variance accounted for by significant genome-by-trauma interaction revealed estimates (SD) ranging from 0.074 (0.006) to 0.201 (0.009). Results from sex-specific analyses found genome-by-trauma interaction variance estimates approximately 5-fold greater for MDD in male participants (0.441 [0.018]) than in female participants (0.086 [0.009]). CONCLUSIONS AND RELEVANCE: This cross-sectional study used an approach combining all genome-wide SNV data when exploring genome-by-trauma interactions in individuals with MDD; findings suggest that such interactions were associated with depression manifestation. Genome-by-trauma interaction accounts for greater trait variance in male individuals, which points to potential differences in depression etiology between the sexes. The methodology used in this study can be extrapolated to other environmental factors to identify modifiable risk environments and at-risk groups to target with interventions

Disordered eating and self-harm as risk factors for poorer mental health during the COVID-19 pandemic: a UK-based birth cohort study

Background: Young adults and especially those with pre-existing mental health conditions, such as disordered eating and self-harm, appear to be at greater risk of developing metal health problems during the COVID-19 pandemic. However, it is unclear whether this increased risk is affected by any changes in lockdown restrictions, and whether any lifestyle changes could moderate this increased risk. Methods: In a longitudinal UK-based birth cohort (The Avon Longitudinal Study of Parents and Children, ALSPAC) we assessed the relationship between pre-pandemic measures of disordered eating and self-harm and mental health during the COVID-19 pandemic in 2657 young adults. Regression models examined the relationship between self-reported disordered eating, self-harm, and both disordered eating and self-harm at age 25 years and depressive symptoms, anxiety symptoms and mental wellbeing during a period of eased restrictions in the COVID-19 pandemic (May–July 2020) when participants were aged 27–29 years. Analyses were adjusted for sex, questionnaire completion date, pre-pandemic socioeconomic disadvantage and pre-pandemic mental health and wellbeing. We also examined whether lifestyle changes (sleep, exercise, alcohol, visiting green space, eating, talking with family/friends, hobbies, relaxation) in the initial UK lockdown (April–May 2020) moderated these associations. Results: Pre-existing disordered eating, self-harm and comorbid disordered eating and self-harm were all associated with the reporting of a higher frequency of depressive symptoms and anxiety symptoms, and poorer mental wellbeing during the pandemic compared to individuals without disordered eating and self-harm. Associations remained when adjusting for pre-pandemic mental health measures. There was little evidence that interactions between disordered eating and self-harm exposures and lifestyle change moderators affected pandemic mental health and wellbeing. Conclusions: Young adults with pre-pandemic disordered eating, self-harm and comorbid disordered eating and self-harm were at increased risk for developing symptoms of depression, anxiety and poor mental wellbeing during the COVID-19 pandemic, even when accounting for pre-pandemic mental health. Lifestyle changes during the pandemic do not appear to alter this risk. A greater focus on rapid and responsive service provision is essential to reduce the impact of the pandemic on the mental health of these already vulnerable individuals. Plain English summary: The aim of this project was to explore the mental health of young adults with disordered eating behaviours (such as fasting, vomiting/taking laxatives, binge-eating and excessive exercise) and self-harm during the COVID-19 pandemic. We analysed data from an established study that has followed children from birth (in 1991 and 1992) up to present day, including during the pandemic when participants were 28 years old. We looked at the relationship between disordered eating and/or self-harm behaviours from before the pandemic and mental health problems (symptoms of depression and anxiety) and mental wellbeing during the pandemic. We also explored whether there were any lifestyle changes (such as changes in sleep, exercise, visiting green space) that might be linked to better mental health and wellbeing in young adults with disordered eating and self-harm. We found that young adults with prior disordered eating and/or self-harm had more symptoms of depression and anxiety, and worse mental wellbeing than individuals without prior disordered eating or self-harm. However, lifestyle changes did not appear to affect mental health and wellbeing in these young adults. Our findings suggest that people with a history of disordered eating and/or self-harm were at high risk for developing mental health problems during the pandemic, and they will need help from mental health services

Father absence and trajectories of offspring mental health across adolescence and young adulthood: findings from a UK-birth cohort

Background: High prevalence of parental separation and resulting biological father absence raises important questions regarding its impact on offspring mental health across the life course. We specifically examined whether these relationships vary by sex and the timing of exposure to father absence (early or middle childhood). Methods: This study is based on up to 8409 children from the Avon Longitudinal Study of Parents and Children (ALSPAC). Participants provided self-reports of depression (Clinical Interview Schedule-Revised) at age 24 years and depressive symptoms (Short Mood and Feelings Questionnaire) between the ages of 10 and 24 years. Biological father absence in childhood was assessed through maternal questionnaires at regular intervals from birth to 10 years. We estimated the association between biological father absence and trajectories of depressive symptoms using multilevel growth-curve modelling. Results: Early but not middle childhood father absence was strongly associated with increased odds of offspring depression and greater depressive symptoms at age 24 years. Early childhood father absence was associated with higher trajectories of depressive symptoms during adolescence and early adulthood compared with father presence. Differences in the level of depressive symptoms between middle childhood father absent and father present groups narrowed into adulthood. Limitations: This study could be biased by attrition and residual confounding. Conclusions: We found evidence that father absence in childhood is persistently associated with offspring depression in adolescence and early adulthood. This relationship varies by sex and timing of father's departure, with early childhood father absence emerging as the strongest risk factor for adverse offspring mental health trajectories Further research is needed to identify mechanisms that could inform preventative interventions to reduce the risk of depression in children who experience father absence

Polygenic risk for depression, anxiety and neuroticism are associated with the severity and rate of change in depressive symptoms across adolescence

Background Adolescence marks a period where depression will commonly onset. Twin studies show that genetic influences play a role in how depression develops and changes across adolescence. Recent genome‐wide association studies highlight that common genetic variants – which can be combined into polygenic risk scores (PRS) – are also implicated in depression. However, the role of PRS in adolescent depression and changes in adolescent depression is not yet understood. We aimed to examine associations between PRS for five psychiatric traits and depressive symptoms measured across adolescence using cross‐sectional and growth‐curve models. The five PRS were as follows: depression (DEP), major depressive disorder (MDD), anxiety (ANX), neuroticism (NEU) and schizophrenia (SCZ). Methods We used data from over 6,000 participants of the Avon Longitudinal Study of Parents and Children (ALSPAC) to examine associations between the five PRS and self‐reported depressive symptoms (Short Mood and Feelings Questionnaire) over 9 occasions from 10 to 24 years. The PRS were created from well‐powered genome‐wide association studies conducted in adult populations. We examined cross‐sectional associations between the PRS at each age and then again with longitudinal trajectories of depressive symptoms in a repeated measures framework using multilevel growth‐curve analysis to examine the severity and the rate of change. Results There was strong evidence that higher PRS for DEP, MDD and NEU were associated with worse depressive symptoms throughout adolescence and into young adulthood in our cross‐sectional analysis, with consistent associations observed across all nine occasions. Growth‐curve analyses provided stronger associations (as measured by effect sizes) and additional insights, demonstrating that individuals with higher PRS for DEP, MDD and NEU had steeper trajectories of depressive symptoms across development, all with a greater increasing rate of change during adolescence. Evidence was less consistent for the ANX and SCZ PRS in the cross‐sectional analysis, yet there was some evidence for an increasing rate of change in adolescence in the growth‐curve analyses with the ANX PRS. Conclusions These results show that common genetic variants as indexed by varying psychiatric PRS show patterns of specificity that influence both the severity and rate of change in depressive symptoms throughout adolescence and then into young adulthood. Longitudinal data that make use of repeated measures designs have the potential to provide greater insights how genetic factors influence the onset and persistence of adolescent depression