Common perinatal mental disorders and post-infancy child development in rural Ethiopia:a population-based cohort study

Objective: To investigate whether maternal common mental disorders (CMD) in the postnatal period are prospectively associated with child development at 2.5 and 3.5 years in a rural low-income African setting. Methods: This study was nested within the C-MaMiE (Child outcomes in relation to Maternal Mental health in Ethiopia) population-based cohort in Butajira, Ethiopia, and conducted from 2005 to 2006. The sample comprised of 496 women who had recently given birth to living, singleton babies with recorded birth weight measurements, who were 15 to 44 years of age, and residing in six rural sub-districts. Postnatal CMD measurements were ascertained 2 months after delivery. Language, cognitive, and motor development were obtained from the child 2.5 and 3.5 years after birth using a locally adapted version of the Bayley Scales of Infant Development (3rd Ed). Maternal CMD symptoms were measured using a locally validated WHO Self-Reporting Questionnaire. A linear mixed-effects regression model was used to analyze the relationship between postnatal CMD and child development. Results: After adjusting for confounders, there was no evidence for an association between postnatal CMD and overall child development or the cognitive sub-domain in the preschool period. There was no evidence of effect modification by levels of social support, socioeconomic status, stunting, or sex of the child. Conclusions: Previous studies from predominantly urban and peri-urban settings in middle-income countries have established a relationship between maternal CMD and child development, which contrasts with the findings from this study. The risk and protective factors for child development may differ in areas characterized by high social adversity and food insecurity. More studies are needed to investigate maternal CMD’s impact on child development in low-resource and rural areas

The role of genetic liability in the association of urbanicity at birth and during upbringing with schizophrenia in Denmark

Background: Studies have indicated that the association of urbanicity at birth and during upbringing with schizophrenia may be driven by familial factors such as genetic liability. We used a population-based nested case–control study to assess whether polygenic risk score (PRS) for schizophrenia was associated with urbanicity at birth and at age 15, and to assess whether PRS and parental history of mental disorder together explained the association between urbanicity and schizophrenia. Methods: Data were drawn from Danish population registries. Cases born since 1981 and diagnosed with schizophrenia between 1994 and 2009 were matched to controls with the same sex and birthdate (1549 pairs). Genome-wide data were obtained from the Danish Neonatal Screening Biobank and PRSs were calculated based on results of a separate, large meta-analysis. Results: Those with higher PRS were more likely reside in the capital compared with rural areas at age 15 [odds ratio (OR) 1.19, 95% confidence interval (CI) 1.01–1.40], but not at birth (OR 1.09, 95% CI 0.95–1.26). Adjustment for PRS produced almost no change in relative risks of schizophrenia associated with urbanicity at birth, but slightly attenuated those for urban residence at age 15. Additional adjustment for parental history led to slight attenuation of relative risks for urbanicity at birth [incidence rate ratio (IRR) for birth in capital = 1.54, 95% CI 1.18–2.02; overall p = 0.016] and further attenuation of relative risks for urbanicity at age 15 (IRR for residence in capital = 1.32, 95% CI 0.97–1.78; overall p = 0.148). Conclusions: While results regarding urbanicity during upbringing were somewhat equivocal, genetic liability as measured here does not appear to explain the association between urbanicity at birth and schizophrenia

Treating the “E” in “G × E”: Trauma-Informed Approaches and Psychological Therapy Interventions in Psychosis

Despite advances in genetic research, causal variants affecting risk for schizophrenia remain poorly characterized, and the top 108 loci identified through genome-wide association studies (GWAS) explain only 3.4% of variance in risk profiles. Such work is defining the highly complex nature of this condition, with omnigenic models of schizophrenia suggesting that gene regulatory networks are sufficiently interconnected such that altered expression of any “peripheral” gene in a relevant cell type has the capacity to indirectly modulate the expression of “core” schizophrenia-associated genes. This wealth of associated genes with small effect sizes makes identifying new druggable targets difficult, and current pharmacological treatments for schizophrenia can involve serious side effects. However, the fact that the majority of schizophrenia genome-wide associated variants fall within non-coding DNA is suggestive of their potential to modulate gene regulation. This would be consistent with risks that can be mediated in a “gene × environment” (G × E) manner. Stress and trauma can alter the regulation of key brain-related pathways over the lifetime of an individual, including modulation of brain development, and neurochemistry in the adult. Recent studies demonstrate a significant overlap between psychotic symptoms and trauma, ranging from prior trauma contributing to psychosis, as well as trauma in response to the experience of psychosis itself or in response to treatment. Given the known effects of trauma on both CNS gene expression and severity of psychosis symptoms, it may be that pharmacological treatment alone risks leaving individuals with a highly stressful and unresolved environmental component that continues to act in a “G × E” manner, with the likelihood that this would negatively impact recovery and relapse risk. This review aims to cover the recent advances elucidating the complex genetic architecture of schizophrenia, as well as the long-term effects of early life trauma on brain function and future mental health risk. Further, the evidence demonstrating the role of ongoing responses to trauma or heightened stress sensitivity, and their impact on the course of illness and recovery, is presented. Finally, the need for trauma-informed approaches and psychological therapy-based interventions is discussed, and a brief overview of the evidence to determine their utility is presented

Mood and anxiety profiles differentially associate with physical conditions in US adolescents.

Mood and anxiety are widely associated with physical conditions, but research and treatment are complicated by their overlap, clinical heterogeneity, and manifestation on a spectrum rather than as discrete disorders. In contrast to previous work relying on threshold-level disorders, we examined the association between empirically-derived profiles of mood and anxiety syndromes with physical conditions in a nationally-representative sample of US adolescents. Participants were 2,911 adolescents (aged 13-18) from the National Comorbidity Survey-Adolescent Supplement who provided information on physical conditions and reported at least one lifetime mood-anxiety 'syndrome' based on direct interviews with the Composite International Diagnostic Interview Version 3.0. Mood-anxiety syndromes reflected 3-level ratings from subthreshold to severe distress/impairment, and subtyped mood episodes. Stepwise latent profile analysis identified mood-anxiety profiles and tested associations with physical conditions. Three mood-anxiety profiles were identified: "Mood-GAD" (25.6%)-non-atypical depression, mania, generalized anxiety; "Atypical-Panic" (11.3%)-atypical depression, panic; and "Reference" (63.1%)-lower mood and anxiety except specific phobia. Headaches were more prevalent in Mood-GAD and Atypical-Panic than Reference (47.9%, 50.1%, and 37.7%, respectively; p=0.011). Heart problems were more common in Mood-GAD than Atypical-Panic (7.4% v 2.2%, p=0.004) and Reference, with back/neck pain more prevalent in Mood-GAD than Reference (22.5% v 15.3%, p=0.016). Broad categories of physical conditions without information on specific diagnoses; replication regarding specificity is recommended. Heart problems and pain-related conditions were differentially associated with specific mood-anxiety profiles. Subtyping depression and anxiety-inclusive of subthreshold syndromes-and their patterns of clustering may facilitate etiologic and intervention work in multimorbidity

Stability and change in reported age of onset of depression, back pain, and smoking over 29 years in a prospective cohort study

Accurate age of onset (AOO) measurement is vital to etiologic and preventive research. While AOO reports are known to be subject to recall error, few population-based studies have been used to investigate agreement in AOO reports over more than a decade. We examined AOO reports for depression, back/neck pain, and daily smoking, in a population-based cohort spanning 29 years. A stratified sample of participants from Zurich, Switzerland (n = 591) completed a psychiatric and physical health interview 7 times between 1979, at ages 20 (males) and 21 (females), and 2008. We used one-way ANOVA to estimate intraclass correlations (ICCs) and weighted mixed models to estimate mean change over time and test for interactions with sex and clinical characteristics. Stratum-specific ICCs among those with 2 + reports were 0.19 and 0.29 for depression, 0.46 and 0.35 for back pain, and 0.66 and 0.75 for smoking. The average yearly increases in AOO report from the wave of first 12-month diagnosis or reported smoking, estimated in mixed models, were 0.57 years (95% confidence interval: 0.35, 0.79) for depression, 0.44 (95%CI: 0.28, 0.59) years for back pain, and 0.08 (95%CI: 0.03, 0.14) years for smoking. Initial impairment and frequency of treatment were associated with differences in average yearly change for depression. There is substantial variability in AOO reports over time and systematic increase with age. The degree of increase may differ by outcome, and for some outcomes, by participant clinical characteristics. Future studies should identify predictors of AOO report stability to ultimately benefit etiologic and preventive research