Suchergebnisse

Aims: To examine if divorce is associated with an increased risk of psychiatric disorder. Methods: A register-based cohort study of all married or divorced individuals aged 45–54 in Sweden in 2006. After exclusion of 129,669 individuals with a history of psychiatric care in 1987–2005, we followed 703,960 persons for psychiatric disorder during 2007, measured as psychiatric inpatient care, outpatient care and use of psychotropic medication. Marital trajectories were taken into consideration. Data were analysed using Poisson regression. Results: Divorced women and men had a higher risk for psychiatric inpatient care compared to married (ORwomen = 3.2, 95%CI = 1.6–6.3, ORmen = 3.3, 95%CI = 2.0–5.4). The longer the marriage, the lower the risk for psychiatric disorders. Lower educational level increased the risk for psychiatric inpatient care. Conclusions: In conclusion, our study supports both the selection hypothesis, linking healthy individuals to long and stable marriages, and the social causation hypothesis, linking the stress of recent divorce to increased psychiatric disorder for both women and men.

OBJECTIVE: Original case descriptions of autism noted that parents of the affected children tended to be highly educated and intelligent, a characterization that has endured publicly. Recent genetic studies indicate that risk for autism spectrum disorders (ASD) is associated with high intelligence. We examined the association between paternal intelligence and ASD, considering co-occurring intellectual disability (ID) and attention-deficit hyper-activity disorder (ADHD). METHOD: We used a register-based cohort study design including 360151 individuals with fathers conscripted to the Swedish military, resident in Stockholm, Sweden, born 1984-2008, and followed until December 31, 2011 for diagnosis of ASD, ADHD, and/or ID. Risk of neurodevelopmental disorders relative to paternal IQ (rated on a nine-point scale) was assessed using a score of 5 (average intelligence) as the referent in models accounting for potentially non-linear relationships and clustering of siblings. RESULTS: We observed an association between high paternal IQ and offspring risk of ASD without ID/ADHD in models adjusted for individual and family characteristics [ORIQ=9 1.32 (95% CI 1.15-1.52)], an association that appeared to be driven largely by the fathers' score on the technical comprehension portion of the test [ORTechnical IQ=9 1.53 (1.31-1.78)]. Conversely, low paternal IQ was associated with ASD+ID [ORIQ=11.78 (1.27-2.49)] and ASD+ADHD [ORIQ=11.40 (1.16-1.70)]; low paternal IQ was strongly associated with ID [ORIQ=1 4.46 (3.62-5.49)] and present also for ADHD [ORIQ=11.56 (1.42-1.72)] without co-occurring ASD or ID. CONCLUSION: The relationship between paternal IQ and offspring risk of ASD was non-monotonic and varied by the presence of co-occurring disorders, probably reflecting phenotypic diversity among affected individuals.

Importance: Being born or raised in more densely populated or deprived areas is associated with increased risk of nonaffective psychosis in adulthood, but few studies to date have examined the role of general cognitive ability in these associations. Objective: To investigate whether lower IQ contributed to the association between population density or deprivation and nonaffective psychosis (mediation) and whether these associations were stronger in people with lower IQ (effect modification). Design, Setting, and Participants: This prospective cohort study evaluated a population-based sample of men born in Sweden from January 1, 1982, to December 31, 1988, and conscripted into military service at 18 years of age. Data were collected from January 1, 1982, to December 31, 2016, and analyzed from May 1 to December 31, 2018. Exposures: Continuous measures of small area-level population density (persons per square kilometer) and socioeconomic deprivation at birth. Deprivation was based on area-level social, criminal, and unemployment data. IQ was assessed during conscription at 18 years of age (mean [SD] IQ, 100 [15]). Main Outcomes and Measures: First diagnosis of International Statistical Classification of Diseases and Related Health Problems, Tenth Revision, nonaffective psychosis from 18 years of age until December 31, 2016, recorded in the National Patient Register. Results: The study sample included a total of 227 429 men who were classified as at risk of psychosis from 18 years of age until the end of follow-up. Of these, 1596 men (0.7%) were diagnosed with nonaffective psychosis. After adjustments for confounders, odds of nonaffective psychosis increased per 1-SD increase in population density (odds ratio [OR], 1.07; 95% CI, 1.04-1.14) and deprivation (OR, 1.09; 95% CI, 1.02-1.13) at birth. IQ was negatively associated with deprivation after adjustments (effect estimate per 1-SD increase in deprivation: -0.70 points; 95% CI, -0.78 to -0.62 points) but not with population density. In mediation analyses, based ...

Importance: Associations between childhood infection, IQ and adult non-affective psychosis (NAP) are well established. However, examination of sensitive periods for exposure, effect of familial confounding, and whether IQ provides a link between childhood infection and adult NAP may elucidate pathogenesis of psychosis further. Objective: To test (1) association of childhood infection with IQ and adult NAP; (2) whether shared familial confounding explains the infection-NAP and IQ-NAP relationships; (3) whether IQ mediates and/or moderates the childhood infection-NAP relationship. Design, Setting and Participants: Longitudinal design using linkage of Swedish national registers. The risk set included all Swedish men born 1973–1992 and conscripted into military until end of 2010 (N=771,698). We included 647,515 participants in the analysis. Measurement of exposure: Hospitalisation with any infection from age 0–13 years. Main outcomes and measures: Hospitalisation with an ICD diagnosis of NAP until end of 2011. IQ was assessed at conscription around age 18 years. Results: Exposure to infections particularly in early-childhood was associated with lower IQ (adjusted mean difference for infection at 0-1y: -1.61; 95% CI, -1.74, -1.47), and with increased risk of adult NAP (adjusted hazard ratio for infection at 0-1y: 1.19; 95% CI, 1.06-1.33). There was a linear association between lower premorbid IQ and adult NAP, which persisted after excluding prodromal cases (adjusted hazard ratio per 1-point increase in IQ: 0.976; 95% CI, 0.974-0.978). The infection-NAP and IQ-NAP associations were similar in the general population and in full-sibling pairs discordant for exposure. IQ both moderated (P=0.02 and P=0.001) and mediated (P<0.001) the association between infection and NAP. Childhood infection had a greater impact on NAP risk in the lower, compared with higher, IQ range. Conclusions and Relevance: Early-childhood is a sensitive period for the effects of infection on IQ and NAP. The associations of adult NAP with early-childhood infection and adolescent IQ are not fully explained by shared familial factors, so may be causal. Lower premorbid IQ in psychosis arises from unique environmental factors, such as early-childhood infection. Early-childhood infections may increase risk of NAP by affecting neurodevelopment and by exaggerating the effects of cognitive vulnerability to psychosis.

Importance: Associations between childhood infection, IQ, and adult nonaffective psychosis (NAP) are well established. However, examination of sensitive periods for exposure, effect of familial confounding, and whether IQ provides a link between childhood infection and adult NAP may elucidate pathogenesis of psychosis further. Objectives: To test the association of childhood infection with IQ and adult NAP, to find whether shared familial confounding explains the infection-NAP and IQ-NAP associations, and to examine whether IQ mediates and/or moderates the childhood infection-NAP association. Design, Setting, and Participants: Population-based longitudinal cohort study using linkage of Swedish national registers. The risk set included all Swedish men born between 1973 and 1992 and conscripted into the military until the end of 2010 (n = 771 698). We included 647 515 participants in the analysis. Measurement of Exposures: Hospitalization with any infection from birth to age 13 years. Main Outcomes and Measures: Hospitalization with an International Classification of Diseases diagnosis of NAP until the end of 2011. At conscription around age 18 years, IQ was assessed for all participants. Results: At the end of follow-up, the mean (SD) age of participants was 30.73 (5.3) years. Exposure to infections, particularly in early childhood, was associated with lower IQ (adjusted mean difference for infection at birth to age 1 year: -1.61; 95% CI, -1.74 to -1.47) and with increased risk of adult NAP (adjusted hazard ratio for infection at birth to age 1 year: 1.19; 95% CI, 1.06 to 1.33). There was a linear association between lower premorbid IQ and adult NAP, which persisted after excluding prodromal cases (adjusted hazard ratio per 1-point increase in IQ: 0.976; 95% CI, 0.974 to 0.978). The infection-NAP and IQ-NAP associations were similar in the general population and in full-sibling pairs discordant for exposure. The association between infection and NAP was both moderated (multiplicative, β = .006; SE = 0.002; P = .02 and additive, β = .008; SE = 0.002; P = .001) and mediated (β = .028; SE = 0.002; P < .001) by IQ. Childhood infection had a greater association with NAP risk in the lower, compared with higher, IQ range. Conclusions and Relevance: Early childhood is a sensitive period for the effects of infection on IQ and NAP. The associations of adult NAP with early-childhood infection and adolescent IQ are not fully explained by shared familial factors and may be causal. Lower premorbid IQ in individuals with psychosis arises from unique environmental factors, such as early-childhood infection. Early-childhood infections may increase the risk of NAP by affecting neurodevelopment and by exaggerating the association of cognitive vulnerability with psychosis. ; Dr Khandaker is supported by an Intermediate Clinical Fellowship from the Wellcome Trust (201486/Z/16/Z) and a Clinical Lecturer Starter Grant from the Academy of Medical Sciences, UK (80354). Dr Jones reports having grant support from the Wellcome Trust (095844/Z/11/Z and 088869/Z/09/Z) and from the National Institute for Health Research: RP-PG-0616-20003, Cambridge Biomedical Research Centre and Collaboration for Leadership in Applied Health Research and Care East of England. Dr Dalman reports grant support from the Swedish Research Council. Dr Karlsson reports grant support from the Stanley Medical Research Institute.

Neurodevelopmental disorders affect a substantial minority of the general population. Their origins are still largely unknown, but a complex interplay of genetic and environmental factors causing disturbances of the central nervous system's maturation and a variety of higher cognitive skills is presumed. Only limited research of rather small sample size and narrow scope has been conducted in neurodevelopmental disorders using a twin-differences design. The Roots of Autism and ADHD Twin Study in Sweden (RATSS) is an ongoing project targeting monozygotic twins discordant for categorical or dimensional autistic and inattentive/hyperactive-impulsive phenotypes as well as other neurodevelopmental disorders, and typically developing twin controls. Included pairs are 9 years of age or older, and comprehensively assessed for psychopathology, medical history, neuropsychology, and dysmorphology, as well as structural, functional, and molecular brain imaging. Specimens are collected for induced pluripotent (iPS) and neuroepithelial stem cells, genetic, gut bacteria, protein-/monoamine, and electron microscopy analyses. RATSS's objective is to generate a launch pad for novel surveys to understand the complexity of genotype-environment-phenotype interactions in autism spectrum disorder and attention-deficit hyperactivity disorder (ADHD). By October 2013, RATSS had collected data from 55 twin pairs, among them 10 monozygotic pairs discordant for autism spectrum disorder, seven for ADHD, and four for other neurodevelopmental disorders. This article describes the design, recruitment, data collection, measures, collected pairs' characteristics, as well as ongoing and planned analyses in RATSS. Potential gains of the study comprise the identification of environmentally mediated biomarkers, the emergence of candidates for drug development, translational modeling, and new leads for prevention of incapacitating outcomes.