RESUMO
Family emotional climate is often assessed as expressed emotion (EE) using the five-minute speech sample (FMSS). Parent EE is related to child externalizing behavior, but the relationship with ADHD apart from externalizing is unclear. We report the largest ADHD-non-ADHD study of EE to date, introduce computational scoring of the FMSS to assay parent negative sentiment, and use this to evaluate reciprocal parent-child effects over time in ADHD while considering comorbid ODD. Parents of 810 children (nADHD = 509), aged 7-13 years old, completed the FMSS at three points. The FMSS was expert-coded for EE-Criticism at Time 1 and Time 2, negative sentiment was scored at all three time points. Sentiment and EE-Criticism were moderately correlated (r =.39, p <.001, 95% CI [0.32, 0.46]), and each was similarly correlated with baseline ADHD symptoms (r's range 0.31-0.33, p <.001) and ODD symptoms (r(ODD-EE) = 0.35, p <.001; r(ODD-sentiment = 0.28, p <.001). A longitudinal, cross-lagged panel model revealed that increases over time in parental negative sentiment scores led to increased ODD symptoms. Parent sex (namely fathers, but not mothers) showed an interaction effect of sentiment with ADHD. ADHD and ODD are independently and jointly associated with parental EE-Criticism and negative sentiment assessed by the FMSS cross-sectionally. A recursive effects model is supported for ODD, but for ADHD effects depend on which parent is assessed. For fathers, ADHD was related to negative sentiment in complex manners but for mothers, negative sentiment was related primarily to ODD.
RESUMO
Background: attention-deficit/hyperactivity disorder (ADHD) is associated with both polygenic liability and environmental exposures, both intrinsic to the family, such as family conflict, and extrinsic, such as air pollution. However, much less is known about the interplay between environmental and genetic risks relevant to ADHD-a better understanding of which could inform both mechanistic models and clinical prediction algorithms. Methods: Two independent data sets, the population-based Adolescent Brain Cognitive Development Study (ABCD) (N = 11,876) and the case-control Oregon-ADHD-1000 (N = 1449), were used to examine additive (G + E) and interactive (GxE) effects of selected polygenic risk scores (PRS) and environmental factors in a cross-sectional design. Genetic risk was measured using PRS for nine mental health disorders/traits. Exposures included family income, family conflict/negative sentiment, and geocoded measures of area deprivation, lead exposure risk, and air pollution exposure (nitrogen dioxide and fine particulate matter). Results: ADHD PRS and family conflict jointly predicted concurrent ADHD symptoms in both cohorts. Additive-effects models, including both genetic and environmental factors, explained significantly more variation in symptoms than any individual factor alone (joint R 2 = .091 for total symptoms in ABCD; joint R 2 = .173 in Oregon-ADHD-1000; all delta-R 2 p-values <2e-7). Significant effect size heterogeneity across ancestry groups was observed for genetic and environmental factors (e.g., Q = 9.01, p = .011 for major depressive disorder PRS; Q = 13.34, p = .001 for area deprivation). GxE interactions observed in the full ABCD cohort suggested stronger environmental effects when genetic risk is low, though they did not replicate. Conclusions: Reproducible additive effects of PRS and family environment on ADHD symptoms were found, but GxE interaction effects were not replicated and appeared confounded by ancestry. Results highlight the potential value of combining exposures and PRS in clinical prediction algorithms. The observed differences in risks across ancestry groups warrant further study to avoid health care disparities.
