Jul 2026· European Journal of Psychotraumatology· Vol 17 1, pp.
2692768
· 0 citations· 40 references
Medicine
TL;DR
Genetic evidence linking composite CM liability with selected sleep-related phenotypes, particularly self-reported DS, insomnia symptoms, and DN is provided, providing suggestive genetic evidence linking composite CM liability with selected sleep-related phenotypes.
Abstract
Background: Childhood maltreatment (CM) is associated with sleep disturbance, but observational findings may be affected by confounding, shared familial liability, and reverse-direction explanations. We conducted bidirectional two-sample Mendelian randomization (MR) to examine genetic evidence linking composite CM liability with six sleep-related phenotypes.Methods: Genetic instruments for CM were obtained from a large European-ancestry multi-cohort GWAS meta-analysis. CM was defined as a composite phenotype encompassing multiple abuse and neglect subtypes and ascertainment modes. Summary statistics for chronotype, daytime sleepiness (DS), insomnia symptoms, sleep apnea (SA), daytime napping (DN), and sleep duration (SD) were derived from large European-ancestry GWASs. Inverse-variance weighted MR was the primary method, with weighted median and MR-Egger sensitivity analyses. Benjamini-Hochberg correction was applied and reported as P(BH).Results: In forward MR, genetically proxied CM was associated with higher DS (OR = 1.04, 95% CI 1.01-1.07; P(BH) = 0.030), insomnia symptoms (OR = 1.08, 95% CI 1.01-1.15; P(BH) = 0.030), and DN (β = 0.07, 95% CI 0.03-0.09; P(BH) = 0.002). Little evidence was observed for chronotype, SA, or SD. In exploratory reverse-direction MR, genetic liability to DN (β = 0.16, 95% CI 0.05-0.27; P(BH) = 0.012) and insomnia symptoms (β = 0.21, 95% CI 0.07-0.35; P(BH) = 0.012) was associated with CM liability.Conclusions: This study provides suggestive genetic evidence linking composite CM liability with selected sleep-related phenotypes, particularly self-reported DS, insomnia symptoms, and DN. Reverse-direction findings may reflect shared genetic liability, gene-environment correlation, reporting-related mechanisms, or broader familial pathways rather than temporal effects of adult sleep traits on CM. Given modest effects and uneven sensitivity support, findings should be interpreted cautiously.
Which sleep PRS performed well across diverse populations and which sleep definitions better captured genetic underpinnings was highlighted by evaluating several types of sleep PRSs and sleep phenotypes.
A. Wyss, Michael Brown, Xiang Li et al.· Sleep· 0 citations
Findings indicate that genetically determined short sleep duration and insomnia symptoms are associated with mental and neurological problems, cardiovascular disease and musculoskeletal disorders, suggesting a potentially preventive, causal role of healthy sleeping patterns on chronic disease.
Marta H Hernandez, Camille Lassale, A. Camps-Vilaró et al.· Journal of Sleep Research· 0 citations
Background Premenstrual disorder (PMD) and postpartum depression (PPD) have a strong phenotypic link and echo women’s hormone fluctuations. Yet, the extent to which they may be cross-inherited remains poorly understood. Methods Using the nationwide cohort of 907,841 women who born 1950-2007 and gave birth during 2001-2021 in Sweden, we estimated the cumulative incidence functions-based heritability and genetic correlation for PMD and PPD. We also analyzed genome-wide association study (GWAS) summary statistics from the largest European-ancestry cohorts for PMD (17,511 cases and 54,786 controls) and PPD (16,145 cases and 46,609 controls) using linkage disequilibrium score regression (LDSC). Fixed-effect cross-trait meta-analysis and imputed transcriptome-wide association analyses (TWAS) were conducted to identify shared loci and gene-tissue associations. Results The register-based heritability was 0.35 (95% CI: 0.29-0.41) for PMD and 0.31 (95% CI: 0.23-0.37) for PPD, with a positive genetic correlation between these disorders (rg = 0.47, 95% CI: 0.25–0.69). LDSC also showed a positive genetic correlation between PMD and PPD (rg = 0.66, SE = 0.10, P = 1.014×10−10), indicating sizable shared heritable influences. Cross-trait meta-analysis identified two novel genome-wide significant loci jointly associated with PMD and PPD, mapping to an intronic region of PCDH9 and the 3’ untranslated region of KCTD16. The KCTD16 locus implicates GABAB–mediated inhibitory signaling in both disorders. Consistent with this, TWAS revealed a hippocampus regulatory signal for KCTD16, with no detectable trend effects in other brain regions or peripheral tissues. Beyond the lead loci, TWAS suggested that the shared risk variants may partially act through genetically regulated gene expression across brain, endocrine and immune-related tissues. Conclusions Together, these findings provide the first evidence for sizable genetic overlap between PMD and PPD and highlight novel and convergent biological mechanisms underlying the abnormal brain response of some women to gonadal hormone fluctuations.
Susu Qu, Kejia Hu, J. Guintivano et al.· Research Square· 0 citations
Evidence is provided of a potential causal relationship between other cataract and anxiety, though findings were method-dependent and no significant associations were observed for senile cataract or most psychiatric disorders.
Postpartum depression (PPD) is a common mental health disorder after childbirth. Although microbiome research in PPD has mainly focused on the gut, the role of skin microbiota remains unclear. We used Mendelian randomization (MR) to assess potential causal associations between skin microbiota and PPD. A bidirectional 2-sample MR analysis used genome-wide association study (GWAS) summary statistics. Genetic instruments for skin microbial features were obtained from a published skin microbiota GWAS, and PPD data were derived from 67,205 mothers (7604 cases, 59,601 controls). Instruments were selected at P <1 × 10−5, linkage disequilibrium-clumped, harmonized, and filtered for weak instruments (F statistic <10). Because this microbiome threshold is exploratory, Benjamini-Hochberg false discovery rate correction was applied within taxonomic levels. The inverse-variance weighted method was primary, complemented by weighted median and mode-based methods. Heterogeneity, pleiotropy, and outliers were assessed using Cochran Q, MR-Egger intercept, and MR-PRESSO. Three skin microbial taxa showed nominal associations with PPD. Higher genetically predicted Acinetobacter on the dorsal forearm (dry skin; 9 single nucleotide polymorphisms [SNPs]; mean F = 22.12) and Proteobacteria in the antecubital fossa (moist skin; 6 SNPs; mean F = 23.44) were associated with increased PPD risk, whereas Betaproteobacteria in the antecubital fossa (11 SNPs; mean F = 21.54) was associated with decreased risk. Associations were directionally consistent, with no substantial heterogeneity or horizontal pleiotropy. After multiple-testing assessment, the findings were exploratory rather than definitive. Reverse MR did not support an effect of PPD on the identified skin microbiota. This MR study provides exploratory genetic evidence linking specific skin microbial features to PPD risk. The findings extend microbiota-related hypotheses beyond the gut microbiome but require validation in larger microbiome GWAS datasets, longitudinal cohorts, and mechanistic studies before clinical or causal conclusions are drawn.
