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Background: Polygenic risk scores (PRSs) capture genetic vulnerability to psychiatric conditions. However, PRSs are often associated with multiple mental health problems in children, complicating their use in research and clinical practice. The current study is the first to systematically test which PRSs associate broadly with all forms of childhood psychopathology, and which PRSs are more specific to one or a handful of forms of psychopathology. Methods: The sample consisted of 4717 unrelated children (mean age = 9.92, s.d. = 0.62; 47.1% female; all European ancestry). Psychopathology was conceptualized hierarchically as empirically derived general factor (p -factor) and five specific factors: externalizing, internalizing, neurodevelopmental, somatoform, and detachment. Partial correlations explored associations between psychopathology factors and 22 psychopathology-related PRSs. Regressions tested which level of the psychopathology hierarchy was most strongly associated with each PRS. Results: Thirteen PRSs were significantly associated with the general factor, most prominently Chronic Multisite Pain-PRS (r = 0.098), ADHD-PRS (r = 0.079), and Depression-PRS (r = 0.078). After adjusting for the general factor, Depression-PRS, Neuroticism-PRS, PTSD-PRS, Insomnia-PRS, Chronic Back Pain-PRS, and Autism-PRS were not associated with lower order factors. Conversely, several externalizing PRSs, including Adventurousness-PRS and Disinhibition-PRS, remained associated with the externalizing factor (| r | = 0.040–0.058). The ADHD-PRS remained uniquely associated with the neurodevelopmental factor (r = 062). Conclusions: PRSs developed to predict vulnerability to emotional difficulties and chronic pain generally captured genetic risk for all forms of childhood psychopathology. PRSs developed to predict vulnerability to externalizing difficulties, e.g. disinhibition, tended to be more specific in predicting behavioral problems. The results may inform translation of existing PRSs to pediatric research and future clinical practice. [ABSTRACT FROM AUTHOR]

Depression, conduct, and hyperactivity symptoms are chronic and frequently co-occur in adolescence. Common genetic and environmental vulnerability to these conditions have previously been demonstrated, however, the manner in which common versus disorder-specific etiological influences operate across development and maintain symptom co-occurrence is unclear. Thus, the current study investigated the role of common genetic and environmental influences in the comorbidity of depression, conduct, and hyperactivity across adolescence. Over 10,000 twins and their parents reported adolescents' symptoms at mean ages 11 and 16 years. Biometric independent pathway models were fitted to estimate genetic and environmental contributions to the continuity of symptom co-occurrence over time, as well as time‐ and symptom‐specific influences. Results found that a common stable genetic factor accounted for the concurrent and longitudinal co-occurrence of depression, conduct, and hyperactivity symptoms. New genetic influences common to these three symptom scales emerged at 16 years, and further contributed to symptom co-occurrence. Conversely, environmental influences largely contributed to the time-specific associations. The findings were generally consistent for self- and parent-reported symptoms. Overall, the results suggest that stable, overlapping genetic influences contribute to the co-occurrence of depression, conduct, and hyperactivity symptoms across adolescence. The results are in line with hierarchical causal models of psychopathology, which posit that much of the developmental co-occurrence between different symptoms is due to common liability. Specifically, current findings indicate that only genetic influences constitute common liability over time. Future studies should identify genetically influenced transdiagnostic risk and maintenance factors to inform prevention and treatment of comorbid internalizing and externalizing symptoms in adolescence. [ABSTRACT FROM AUTHOR]

Increased anxiety and depression symptoms have been reported in individuals with neurodevelopmental disorders, and have been found to be associated with motor coordination difficulties, but little is known about the etiology of these associations. This study aimed to assess genetic, shared (making twins/siblings alike) and non-shared (individual-specific) environmental influences on the association between poor coordination and symptoms of anxiety and depressed mood using a sample of adult twin and sibling pairs. Participants were asked about their coordination skill and anxiety and depression symptoms. About half of the variance in coordination difficulty was explained by familial (combined genetic and shared environmental) influences, with the remaining variance explained by non-shared environmental influences. Phenotypic associations between coordination and anxiety (r=.46) and depression symptoms (r=.44) were largely underpinned by shared familial liability for the three traits. Non-shared environment accounted for about a third of the phenotypic association. Results suggest that both familial and non-shared environmental influences play a role in the etiology of coordination difficulty and its association with internalizing symptoms. The current study highlights that both biological and environmental pathways shared between these symptoms should be examined in future research to inform prevention and treatment approaches in clinical settings. [ABSTRACT FROM AUTHOR]

Background Mindfulness-based therapies have been shown to be effective in treating depression and reducing cognitive biases. Anxiety sensitivity is one cognitive bias that may play a role in the association between mindfulness and depressive symptoms. It refers to an enhanced sensitivity toward symptoms of anxiety, with a belief that these are harmful. Currently, little is known about the mechanisms underpinning the association between mindfulness, depression, and anxiety sensitivity. The aim of this study was to examine the role of genetic and environmental factors in trait mindfulness, and its genetic and environmental overlap with depressive symptoms and anxiety sensitivity. Methods Over 2,100 16-year-old twins from a population-based study rated their mindfulness, depressive symptoms, and anxiety sensitivity. Results Twin modeling analyses revealed that mindfulness is 32% heritable and 66% due to nonshared environmental factors, with no significant influence of shared environment. Genetic influences explained over half of the moderate phenotypic associations between low mindfulness, depressive symptoms, and anxiety sensitivity. About two-thirds of genetic influences and almost all nonshared environmental influences on mindfulness were independent of depression and anxiety sensitivity. Conclusions This is the first study to show that both genes and environment play an important role in the etiology of mindfulness in adolescence. Future research should identify the specific environmental factors that influence trait mindfulness during development to inform targeted treatment and resilience interventions. Shared genetic liability underpinning the co-occurrence of low mindfulness, depression, and anxiety sensitivity suggests that the biological pathways shared between these traits should also be examined. [ABSTRACT FROM AUTHOR]

Offspring of depressed mothers have elevated risk of developing depression because they are exposed to greater stress. While generally assumed that youth's increased exposure to stress is due to the environmental effects of living with a depressed parent, youth's genes may influence stress exposure through gene-environment correlations (rGEs). To understand the relationship between risk for depression and stress, we examined the effects of polygenic risk for depression on youth stress exposure. We examined the relations of a polygenic risk score (PRS) for depression (DEP-PRS), as well as PRSs for 5 other disorders, with youth stress exposure. Data were from a longitudinal study of a community sample of youth and their parents (n = 377) focusing on data collected at youth's aged 12 and 15 assessments. Elevated youth DEP-PRS was robustly associated with increased dependent stress, particularly interpersonal events. Exploratory analyses indicated that findings were driven by major stress and were not moderated by maternal nor paternal history of depression, and of the 5 additional PRSs tested, only elevated genetic liability for bipolar I was associated with increased dependent stress—particularly non-interpersonal events. Like other PRS studies, we focused on those of European ancestry thus, generalizability of findings is limited. Polygenic risk contributes to youth experiencing stressful life events which are dependent on their behavior. This rGE appears to be specific to genetic risk for mood disorders. • Youth elevated polygenic risk for depression is robustly associated with elevated youth stress exposure, supporting a stress generation model. • Of the 5 additional PRSs tested, only bipolar I disorder was associated with elevated youth stress exposure. • Findings suggest that there are gene-environment correlations that are specific to mood disorders--depression and bipolar 1. [ABSTRACT FROM AUTHOR]

Recent research on artificial intelligence has demonstrated that natural language can be used to provide valid indicators of psychopathology. The present study examined artificial intelligence-based language predictors (ALPs) of seven trauma-related mental and physical health outcomes in responders to the World Trade Center disaster. The responders (N = 174, M age = 55.4 years) provided daily voicemail updates over 14 days. Algorithms developed using machine learning in large social media discovery samples were applied to the voicemail transcriptions to derive ALP scores for several risk factors (depressivity, anxiousness, anger proneness, stress, and personality). Responders also completed self-report assessments of these risk factors at baseline and trauma-related mental and physical health outcomes at two-year follow-up (including symptoms of depression, posttraumatic stress disorder, sleep disturbance, respiratory problems, and GERD). Voicemail ALPs were significantly associated with a majority of the trauma-related outcomes at two-year follow-up, over and above corresponding baseline self-reports. ALPs showed significant convergence with corresponding self-report scales, but also considerable uniqueness from each other and from self-report scales. The study has a relatively short follow-up period relative to trauma occurrence and a limited sample size. This study shows evidence that ALPs may provide a novel, objective, and clinically useful approach to forecasting, and may in the future help to identify individuals at risk for negative health outcomes. [ABSTRACT FROM AUTHOR]