Objectives: To determine if levels of neighbourhood poverty and neighbourhood antisocial behaviour modify associations between household poverty and child and youth mental health problems.
Methods: Data come from the 2014 Ontario Child Health Study-a provincially representative survey of 6537 families with 10,802 four- to 17-year-olds. Multivariate multilevel modelling was used to test if neighbourhood poverty and antisocial behaviour interact with household poverty to modify associations with children's externalizing and internalizing problems based on parent assessments of children (4- to 17-year-olds) and self-assessments of youth (12- to 17-year-olds).
Results: Based on parent assessments, neighbourhood poverty, and antisocial behaviour modified associations between household poverty and children's mental health problems. Among children living in households below the poverty line, levels of mental health problems were 1) lower when living in neighbourhoods with higher concentrations of poverty and 2) higher when living in neighbourhoods with more antisocial behaviour. These associations were stronger for externalizing versus internalizing problems when conditional on antisocial behaviour and generalized only to youth-assessed externalizing problems.
Conclusion: The lower levels of externalizing problems reported among children living in poor households in low-income neighbourhoods identify potential challenges with integrating poorer households into more affluent neighbourhoods. More important, children living in poor households located in neighbourhoods exhibiting more antisocial behaviour are at dramatically higher risk for mental health problems. Reducing levels of neighbourhood antisocial behaviour could have large mental health benefits, particularly among poor children.
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http://dx.doi.org/10.1177/0706743719830027 | DOI Listing |
Sci Rep
January 2025
Donders Institute for Brain, Cognition and Behavior, Radboud University, Thomas Van Aquinostraat 4, 6525, Nijmegen, The Netherlands.
Psychopathic traits and antisocial behavior show a well-documented relationship with decreased empathic processing. It has been proposed that a reduced own experience of pain leads to perceiving others' pain as less severe, which potentially facilitates exploitative, aggressive behavior towards others. We evaluated the link between psychopathic traits, experimental pain sensitivity and empathy for pain in a community sample (n = 74).
View Article and Find Full Text PDFTransl Psychiatry
January 2025
Radboud University, Donders Institute for Brain, Cognition and Behavior, Thomas van Aquinostraat 4, 6525 GD, Nijmegen, The Netherlands.
Impairments in reinforcement learning (RL) might underlie the tendency of individuals with elevated psychopathic traits to behave exploitatively, as they fail to learn from their mistakes. Most studies on the topic have focused on binary choices, while everyday functioning requires us to learn the value of multiple options. In this study, we evaluated the cognitive correlates of naturalistic foraging-type decision-making and their electrophysiological signatures in a community sample (n = 108) with varying degrees of psychopathic traits.
View Article and Find Full Text PDFSoc Sci Comput Rev
February 2025
Dalhousie University, Canada.
Many forms of online political incivility threaten democratic norms, contribute to polarization, and are often directed at women and racial minorities. Recent research shows that online political incivility may come from a minority of users that are just as hostile offline as they are online, meaning that individual differences in personality traits may be an important predictor of online political incivility. Drawing upon a large sample of adults living in Canada = 1725), we examined the association between personality traits and online political incivility using robust measures of psychopathy, narcissism, Machiavellianism, and the general traits of the HEXACO.
View Article and Find Full Text PDFNeuropharmacology
January 2025
School of Pharmacy and Biomedical Sciences, The University of Central Lancashire, Preston UK. Electronic address:
Personality disorders (PDs) are psychiatric conditions characterized by enduring patterns of cognition, emotion, and behaviour that deviate significantly from cultural norms, causing distress or impairment. The aetiology of PDs is complex, involving both genetic and environmental factors. Genetic studies estimate the heritability of PDs at 30% to 60%, implicating genes involved in neurotransmitter regulation, such as those for serotonin transporters and dopamine receptors.
View Article and Find Full Text PDFNeuropharmacology
January 2025
Division of Molecular Psychiatry, Center of Mental Health, University Hospital Würzburg, Würzburg, Germany; Department of Psychiatry, Psychosomatics and Psychotherapy, Center of Mental Health, University Hospital Würzburg, Würzburg, Germany.
While healthy brain function relies on a dynamic but tightly regulated interaction between excitation (E) and inhibition (I), a spectrum of social cognition disorders, including antisocial behavior and antisocial personality disorder (ASPD), frequently ensuing from irregular neurodevelopment, may be associated with E/I imbalance and concomitant alterations in neural connectivity. Technological advances in the evaluation of structural and functional E/I balance proxies in clinical settings and in human cell culture models provide a general basis for identification of biomarkers providing a powerful concept for prevention and intervention across different dimensions of mental health and disease. In this perspective we outline a framework for research to characterize neurodevelopmental pathways to antisocial behavior and ASPD driven by (epi)genetic factors across life, and to identify molecular targets for preventing the detrimental effects of cognitive dysfunction and maladaptive social behavior, considering psychosocial experience; to validate signatures of E/I imbalance and altered myelination proxies as biomarkers of pathogenic neural circuitry mechanisms to determine etiological processes in the transition from mental health to antisocial behavior and ASPD and in the switch from prevention to treatment; to develop a neurobiologically-grounded integrative model of antisocial behavior and ASPD resultant of disrupted E/I balance, allowing to establish objective diagnoses and monitoring tools, to personalize prevention and therapeutic decisions, to predict treatment response, and thus counteract relapse; and finally, to promote transformation of dimensional disorder taxonomy and to enhance societal awareness and reception of the neurobiological basis of antisocial behavior and ASPD.
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