Subjective and objective experiences of childhood adversity: a meta-analysis of their agreement and relationships with psychopathology

Background: Researchers use both subjective self-report and objective measures, such as official records, to investigate the impact of childhood adversity on psychopathology. However, it is unclear whether subjective and objective measures of childhood adversity (a) show agreement, and (b) differentially predict psychopathology. Method: To address this, we conducted a pre-registered meta-analysis to examine the agreement between subjective and objective measures of childhood adversity, and their prediction of psychopathology. We searched in PubMed, PsycINFO and Embase for articles with both subjective measures (self-reports) and objective measures of childhood adversity (comprising official records, or reports from multiple informants unrelated to the target individual), and measures of psychopathology. Results: We identified 22 studies (n = 18,163) with data on agreement between subjective and objective measures of childhood adversities, and 17 studies (n = 14,789) with data on the associations between subjective and objective measures with psychopathology. First, we found that subjective and objective measures of childhood adversities were only moderately correlated (e.g. for maltreatment, r =.32, 95% CI = 0.23–0.41). Second, subjective measures of childhood adversities were associated with psychopathology, independent of objective measures (e.g. for maltreatment, r =.16, 95% CI = 0.09–0.22). In contrast, objective measures of childhood adversities had null or minimal associations with psychopathology, independent of subjective measures (e.g. r for maltreatment =.06, 95% CI = −0.02–0.13). Conclusions: Our findings suggest that the effects of childhood adversity on psychopathology are primarily driven by a person's subjective experience. If this is the case, clinical interventions targeting memories and cognitive processes surrounding childhood adversity may reduce the risk of psychopathology in exposed individuals

Identifying risk factors involved in the common versus specific liabilities to substance use: A genetically informed approach

Individuals most often use several rather than one substance among alcohol, cigarettes or cannabis. This widespread co‐occurring use of multiple substances is thought to stem from a common liability that is partly genetic in origin. Genetic risk may indirectly contribute to a common liability to substance use through genetically influenced mental health vulnerabilities and individual traits. To test this possibility, we used polygenic scores indexing mental health and individual traits and examined their association with the common versus specific liabilities to substance use

Longitudinal and Sex Measurement Invariance of the Affective Neuroscience Personality Scales

The Affective Neuroscience Personality Scales (ANPS) is a personality instrument based on six evolutionary-related brain systems that are at the foundation of human emotions and behaviors: SEEKING, CARING, PLAYFULNESS, FEAR, ANGER, and SADNESS. We sought to assess for the short and long versions of the ANPS: (a) the longitudinal measurement invariance and long-term (4-year) stability and (b) the sex measurement invariance. Using data from a Canadian cohort (N = 518), we used single-group confirmatory factor analysis to assess longitudinal invariance and multiple-group confirmatory factor analysis to assess sex invariance, according to a five-step approach evaluating five invariance levels (configural, metric, scalar, residual, and complete). Results supported full longitudinal invariance for both versions for all invariance levels. Partial residual invariance was supported for sex invariance. The long-term stability of both versions was good to excellent. Implications for personality assessment and ANPS development are discussed

Causal inference methods for intergenerational research using observational data

Identifying early causal factors leading to the development of poor mental health and behavioral outcomes is essential to design efficient preventive interventions. The substantial associations observed between parental risk factors (e.g., maternal stress in pregnancy, parental education, parental psychopathology, parent-child relationship) and child outcomes point toward the importance of parents in shaping child outcomes. However, such associations may also reflect confounding, including genetic transmission-that is, the child inherits genetic risk common to the parental risk factor and the child outcome. This can generate associations in the absence of a causal effect. As randomized trials and experiments are often not feasible or ethical, observational studies can help to infer causality under specific assumptions. This review aims to provide a comprehensive summary of current causal inference methods using observational data in intergenerational settings. We present the rich causal inference toolbox currently available to researchers, including genetically informed and analytical methods, and discuss their application to child mental health and related outcomes. We outline promising research areas and discuss how existing approaches can be combined or extended to probe the causal nature of intergenerational effects. (PsycInfo Database Record (c) 2023 APA, all rights reserved)

Combining multivariate genomic approaches to elucidate the comorbidity between autism spectrum disorder and attention deficit hyperactivity disorder

BACKGROUND: Attention deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD) are two highly heritable neurodevelopmental disorders. Several lines of evidence point towards the presence of shared genetic factors underlying ASD and ADHD. We conducted genomic analyses of common risk variants (i.e. single nucleotide polymorphisms, SNPs) shared by ASD and ADHD, and those specific to each disorder. METHODS: With the summary data from two GWAS, one on ASD (N = 46,350) and another on ADHD (N = 55,374) individuals, we used genomic structural equation modelling and colocalization analysis to identify SNPs shared by ASD and ADHD and SNPs specific to each disorder. Functional genomic analyses were then conducted on shared and specific common genetic variants. Finally, we performed a bidirectional Mendelian randomization analysis to test whether the shared genetic risk between ASD and ADHD was interpretable in terms of reciprocal relationships between ASD and ADHD. RESULTS: We found that 37.5% of the SNPs associated with ASD (at p < 1e-6) colocalized with ADHD SNPs and that 19.6% of the SNPs associated with ADHD colocalized with ASD SNPs. We identified genes mapped to SNPs that are specific to ASD or ADHD and that are shared by ASD and ADHD, including two novel genes INSM1 and PAX1. Our bidirectional Mendelian randomization analyses indicated that the risk of ASD was associated with an increased risk of ADHD and vice versa. CONCLUSIONS: Using multivariate genomic analyses, the present study uncovers shared and specific genetic variants associated with ASD and ADHD. Further functional investigation of genes mapped to those shared variants may help identify pathophysiological pathways and new targets for treatment

Nernst and Seebeck Coefficients of the Cuprate SuperconductorYBa2_2Cu3_3O6.67_{6.67}: A Study of Fermi Surface Reconstruction

The Seebeck and Nernst coefficients $S$ and $\nu$ of the cuprate superconductor YBa$_2$Cu$_3$O$_y$ (YBCO) were measured in a single crystal with doping $p = 0.12$ in magnetic fields up to H = 28 T. Down to T=9 K, $\nu$ becomes independent of field by $H \simeq 30$ T, showing that superconducting fluctuations have become negligible. In this field-induced normal state, $S/T$ and $\nu/T$ are both large and negative in the $T \to 0$ limit, with the magnitude and sign of $S/T$ consistent with the small electron-like Fermi surface pocket detected previously by quantum oscillations and the Hall effect. The change of sign in $S(T)$ at $T \simeq 50$ K is remarkably similar to that observed in La$_{2-x}$Ba$_x$CuO$_4$, La$_{2-x-y}$Nd$_y$Sr$_x$CuO$_4$ and La$_{2-x-y}$Eu$_y$Sr$_x$CuO$_4$, where it is clearly associated with the onset of stripe order. We propose that a similar density-wave mechanism causes the Fermi surface reconstruction in YBCO.Comment: Final version accepted for publication in Phys. Rev. Lett. New title, shorter abstract, minor revision of text and added reference

Contribution of birth weight to mental health, cognitive and socioeconomic outcomes: two-sample Mendelian randomisation

BACKGROUND: Low birth weight is associated with adult mental health, cognitive and socioeconomic problems. However, the causal nature of these associations remains difficult to establish owing to confounding. AIMS: To estimate the contribution of birth weight to adult mental health, cognitive and socioeconomic outcomes using two-sample Mendelian randomisation, an instrumental variable approach strengthening causal inference. METHOD: We used 48 independent single-nucleotide polymorphisms as genetic instruments for birth weight (genome-wide association studies' total sample: n = 264 498) and considered mental health (attention-deficit hyperactivity disorder (ADHD), autism spectrum disorder, bipolar disorder, major depressive disorder, obsessive-compulsive disorder, post-traumatic stress disorder (PTSD), schizophrenia, suicide attempt), cognitive (intelligence) and socioeconomic (educational attainment, income, social deprivation) outcomes. RESULTS: We found evidence for a contribution of birth weight to ADHD (OR for 1 s.d. unit decrease (~464 g) in birth weight, 1.29; 95% CI 1.03-1.62), PTSD (OR = 1.69; 95% CI 1.06-2.71) and suicide attempt (OR = 1.39; 95% CI 1.05-1.84), as well as for intelligence (β = -0.07; 95% CI -0.13 to -0.02) and socioeconomic outcomes, i.e. educational attainment (β = -0.05; 95% CI -0.09 to -0.01), income (β = -0.08; 95% CI -0.15 to -0.02) and social deprivation (β = 0.08; 95% CI 0.03-0.13). However, no evidence was found for a contribution of birth weight to the other examined mental health outcomes. Results were consistent across a wide range of sensitivity analyses. CONCLUSIONS: These findings support the hypothesis that birth weight could be an important element on the causal pathway to mental health, cognitive and socioeconomic outcomes

Genetics of co-developing conduct and emotional problems during childhood and adolescence

Common genetic influences offer a partial explanation for comorbidity between different psychiatric disorders1,2,3. However, the genetics underlying co-development—the cross-domain co-occurrence of patterns of change over time—of psychiatric symptoms during childhood and adolescence has not been well explored. Here, we show genetic influence on joint symptom trajectories of parent-reported conduct and emotional problems (overall N = 15,082) across development (4–16 years) using both twin- and genome-wide polygenic score analyses (genotyped N = 2,610). Specifically, we found seven joint symptom trajectories, including two characterized by jointly stable and jointly increasing symptoms of conduct and emotional problems, respectively (7.3% of the sample, collectively). Twin modelling analyses revealed substantial genetic influence on trajectories (heritability estimates range of 0.41–0.78). Furthermore, individuals’ risk of being classified in the most symptomatic trajectory classes was significantly predicted by polygenic scores for years-of-education-associated alleles and depressive symptoms-associated alleles. Complementary analyses of child self-reported symptoms across late childhood and early adolescence yielded broadly similar results. Taken together, our results indicate that genetic factors are involved in the co-development of conduct and emotional problems across childhood and adolescence, and that individuals with co-developing symptoms across multiple domains may represent a clinical subgroup characterized by increased levels of genetic risk

Association Between Continued Cannabis Use and Risk of Relapse in First-Episode Psychosis: A Quasi-Experimental Investigation Within an Observational Study

IMPORTANCE: Cannabis use after first-episode psychosis is associated with poor outcomes, but the causal nature of this association is unclear. OBJECTIVE: To examine the precise nature of the association between continued cannabis use after the onset of psychosis and risk of relapse of psychosis. DESIGN, SETTING, AND PARTICIPANTS: This prospective cohort study followed up for at least 2 years after the onset of psychosis 220 patients who presented to psychiatric services in South London, England, from April 12, 2002, to July 26, 2013, with first-episode psychosis. Longitudinal modeling (fixed-effects analysis, cross-lagged path analysis) was used to examine whether the association between changes in cannabis use and risk of relapse over time is the result of shared vulnerability between psychosis and cannabis use, psychosis increasing the risk of cannabis use (reverse causation), or a causal effect of cannabis use on psychosis relapse. INTERVENTIONS: Exposure to cannabis within the first and second years after onset of psychosis. MAIN OUTCOMES AND MEASURES: The main outcome measure was relapse of psychosis, defined as subsequent hospitalization for psychosis. Effect of cannabis use status in the first year (Ct1) and second year (Ct2) and pattern of cannabis use continuation in the first year and second year were modeled for risk of relapse in the first year (Rt1) and risk of relapse in the second year (Rt2) after psychosis onset. RESULTS: A total of 220 patients with first-episode psychosis were included in the analysis (mean [SD] age, 28.62 [8.58] years; age range, 18-65 years; 90 women [40.9%] and 130 men [59.1%]). Fixed-effects models that adjusted for time-variant (other illicit drug use, antipsychotic medication adherence) and time-invariant (eg, genetic or premorbid environment) unobserved confounders revealed that there was an increase in the odds of experiencing a relapse of psychosis during periods of cannabis use relative to periods of no use (odds ratio, 1.13; 95% CI, 1.03-1.24). Change in the pattern of continuation significantly increased the risk (odds ratio, 1.07; 95% CI, 1.02-1.13), suggesting a dose-dependent association. Cross-lagged analysis confirmed that this association reflected an effect of cannabis use on subsequent risk of relapse (Ct1→Rt2: β = 0.44, P = .04) rather than an effect of relapse on subsequent cannabis use (Rt1→Ct2: β = -0.29, P = .59). CONCLUSIONS AND RELEVANCE: These results reveal a dose-dependent association between change in cannabis use and relapse of psychosis that is unlikely to be a result of self-medication or genetic and environmental confounding

Social Withdrawal Behaviour at One Year of Age Is Associated with Delays in Reaching Language Milestones in the EDEN Mother-Child Cohort Study

OBJECTIVE: The aim of the study was to examine the relationship between social withdrawal behaviour at one year and motor and language milestones. MATERIALS AND METHODS: One-year old children from the EDEN French population-based birth cohort study (Study on the pre- and postnatal determinants of the child’s development and prospective health Birth Cohort Study) were included. Social withdrawal at one year was assessed by trained midwives using the Alarm Distress BaBy (ADBB) scale. Midwives concurrently examined infants’ motor and language milestones. Parents reported on child’s psychomotor and language milestones, during the interview with the midwife. RESULTS: After adjusting for potential confounding factors, social withdrawal behaviour was significantly associated with concurrent delays in motor and language milestones assessed by the midwife or the parents. DISCUSSION: Higher scores on social withdrawal behaviour as assessed with the ADBB were associated with delays in reaching language milestones, and to a lesser extent with lower motor ability scores. Taking the contribution of social withdrawal behaviour into account may help understand the unfolding of developmental difficulties in children