Jul 2026· Journal of Affective Disorders· Vol 414, pp.
122317
· 0 citations· 53 references
Medicine
Abstract
Background
Prior twin studies have shown genetic and environmental overlap between autistic traits and internalising symptoms. However, it remains unknown whether this overlap reflects a common latent liability or similar aetiological influences operating through independent pathways. We investigated the genetic and environmental origins of the co-occurrence of autistic traits and internalising symptoms with a meta-analysis and an empirical twin study.
Methods
Study 1 meta-analysed six twin studies examining autistic traits and internalising symptoms, predominantly in Western child and adolescent samples. Study 2 applied multivariate genetic modelling to a Chinese community sample of 178 twin pairs (109 monozygotic and 69 dizygotic, aged 24-35).
Results
Study 1 showed genetic (rA = 0.42) and non-shared environmental (rE = 0.15) overlap between autistic traits and internalising symptoms, although substantial heterogeneity was observed across estimates. Study 2 was broadly consistent with the findings of Study 1. It further suggested that the co-occurrence of autistic traits, anxiety and depressive symptoms may be partly explained by a common latent factor shaped by genetic and non-shared environmental influences, although the common pathway model was only tentatively favoured over the independent pathway model.
Conclusion
Across meta-analytic and empirical twin studies, the co-occurrence of autistic traits, anxiety and depressive symptoms appears to be shaped in part by shared genetic and non-shared environmental influences across these three traits. This generally aligns with the transdiagnostic framework of psychopathology. It also highlights that individuals presenting autistic traits may benefit from screening for internalising symptoms, and vice versa.
Evidence is found for additive effects of other genetic factors in contributing to some latent co-occurring neurodevelopmental and mental health conditions in autism.
Adeniran Okewole, Vincent-Raphaël Bourque, M. Koko et al.· Molecular Psychiatry· 1 citation
Externalizing and internalizing behaviours capture heritable, transdiagnostic dimensions of psychopathology, but their genetic architecture and links to societal outcomes remain incompletely understood. This study applied a multivariate framework to population-based, non-clinical traits to explore simultaneous genetic...
B. Šakić, M. Klein, N. Roth Mota et al.· European Neuropsychopharmaco...· 0 citations
Genetic factors influence vulnerability to common mental health conditions, but their role in early-life mental health remains understudied. We analysed genotype array (n = 4709-6687) and exome sequence data (n = 4500-5424) from the Millennium Cohort Study (MCS) and Avon Longitudinal Study of Parents and Children (ALSP...
O. Wootton, E. Wade, D. Malawsky et al.· Molecular Psychiatry· 0 citations
The conceptual and symptom overlap between depression and loneliness is so strong that depressive symptom rating scales often include measures of loneliness, and their linear association ranges between .40 and .68. Despite these findings, few genetically informed studies have investigated the genetic and environmental...
Morgan E. Lynch, Molly Gonenne, Colin D. Freilich et al.· Behavior Genetics· 0 citations
Cross-disorder AN and PD research identified shared risk variants at chr3p21.31, genes and mechanisms linked to a shared endophenotype linked to a shared endophenotype.
Andrew W. Bergen, Carolina Makowski, Michael Garvin et al.· European eating disorders re...· 0 citations
Comorbidity—the co-occurrence of multiple conditions within
the same individual—is a defining feature of both psychiatric and
physical illness, yet the biological mechanisms driving comorbidity
remain poorly understood. This thesis investigates shared genetic lia-
bility underlying comorbid traits and disorders using g...
Cato Romero· 0 citations
We use cookies to run the site and, with your consent, for analytics and to show ads.
See our Cookie Policy.