Environmental risk factors for autism spectrum disorders

Aims: Two overarching hypotheses were tested in this thesis- first, that the environmental factors studied during pregnancy or the time preceding birth would be associated with a higher risk of autism spectrum disorders (ASD) in the offspring; and second, that these risk factors and/or their magnitude of associations may be different for autism spectrum disorders with and without intellectual disability (ID). Methods: Studies I-IV were case-control studies nested within a population-based cohort of all children 0 to 17 years old, living in Stockholm County between the years 2001 to 2007 (n=589,114). ASD cases, identified using multisource case-ascertainment, were matched by age and sex to 10 living non-ASD controls. Prospectively collected information on exposures and potential confounders was ascertained by record linkage with relevant registers, and timed to the prenatal period. Exposures included measures of parental socioeconomic status (Study I), migration (Study II), life events (Study III) and parental depression and maternal antidepressant use during pregnancy (Study IV). For Study III, an additional cohort in England (maximum n = 11554) was used to study the risk of offspring ASD in relation to a combined maternal exposure to up to 42 common and rare life events, as well as their perceived impact upon the mother during pregnancy and early life. Results: In Study I, measures of a lower parental socioeconomic status – specifically, lower household income, and unskilled, manual or unclassified occupations were associated with a higher risk of ASD. The associations were similar in ASD with or without ID. In Study II, maternal migration had divergent relationships with ASD with and without ID- showing heightened risks for ASD with ID and reduced ones for ASD without ID. This study found that associations of migration with autism varied by the geographical region of origin of the mother, by the human development of the region of origin, and the timing of migration in relation to pregnancy. In Study III, no evidence for a relationship between stressful life events during pregnancy and a heightened risk of ASD was found, using data from the two population-based studies in Sweden and England respectively. In Study IV, a higher risk of ASD was associated with a prenatal history of maternal depression, but did not appear to be associated with paternal depression. In a smaller sample, when maternal antidepressant use was simultaneously studied, the associations of maternal depression with ASD appeared to be confined to the group of women who reported taking antidepressants during pregnancy. The associations were higher for ASD without ID, and were not observed for ASD with ID. Conclusion: In three of the four studies there was evidence of a relationship between the prenatal factors studied and a higher risk of autism spectrum disorders. In two studies, the timing of the event (migration, antidepressant use or severe depression during pregnancy) was indicative of pregnancy related exposures, highlighting the importance of considering environmental factors acting in utero in the pathways to autism. The marked differences in risks for autism with and without intellectual disability with exposures in two studies highlight the value of studying these categories separately, since they may have different determinants

“It was like walking without knowing where I was going”:A Qualitative Study of Autism in a UK Somali Migrant Community

Increasing recognition of autism in Somali migrant communities means that appropriate support services are needed. Attitudes to autism and barriers related to help-seeking in these communities are poorly understood. We aimed to assess what families affected by autism need, and how health, education and social care services can support them. In partnership with the local Somali community the research team conducted 15 in-depth interviews with parents affected by autism. Two themes are reported; ‘Perceptions of Autism’ and ‘Navigating the System’. Our research shows the importance of understanding cultural views of autism and the need to raise awareness, reduce stigma and provide support to encourage families not to delay seeking help for their children

Gendered play behaviours in autistic and non-autistic children:a population-based cohort study

Lay abstractNon-autistic children tend to show gendered patterns of play behaviours - boys are more likely to play with 'masculine' toys, and girls are more likely to play with 'feminine' toys. However, little is known about whether autistic children follow these patterns as well. We looked at the masculinity and femininity of autistic and non-autistic children's play behaviours at multiple time points. Parents reported their children's play behaviours at ages 30, 42 and 57 months, and children reported their own play behaviours at 8 years old. We found no difference between autistic and non-autistic girls, who both showed more feminine play behaviours as they got older. Autistic boys' play behaviours were reported as less masculine than non-autistic boys at 42 and 57 months, and at 8 years old. We also found that non-autistic boys' play tended to become more masculine as they got older, but this was not the case for autistic boys. Our findings suggest that differences in autistic and non-autistic boys' play behaviours may develop at around 42 months old

Complete Issue 45(4)

Complete digitized issue (volume 45, issue 4, May 1963) of The Gavel of Delta Sigma Rho

The population impact of common mental disorders and long-term physical conditions on disability and hospital admission

Background: Long-term physical conditions (LTCs) consume the largest share of healthcare budgets. Although common mental disorders (CMDs) and LTCs often co-occur, the potential impact of improved mental health treatment on severe disability and hospital admissions for physical health problems remains unknown. Method: A cross-sectional study of 7403 adults aged 16–95 years living in private households in England was performed. LTCs were ascertained by prompted self-report. CMDs were ascertained by structured clinical interview. Disability was assessed using questions about problems with activities of daily living. Population impact and potential preventive gain were estimated using population-attributable fraction (PAF), and conservative estimates were obtained using ‘treated non-cases’ as the reference group. Results: Of the respondents, 20.7% reported at least one LTC. The prevalence of CMDs increased with the number of LTCs, but over two-thirds (71.2%) of CMD cases in people with LTCs were untreated. Statistically significant PAFs were found for CMDs and recent hospital admission [13.5%, 95% confidence intervals (CI) 6.6–20.0] and severe disability (31.3%, 95% CI 27.1–35.2) after adjusting for LTCs and other confounders. Only the latter remained significant when using the most conservative estimate of PAF (21.8%, 95% CI 14.0–28.9), and this was reduced only slightly when considering only participants with LTCs (18.5%, 95% CI 7.9–27.9). Conclusions: Better treatments for CMDs in people with LTCs could achieve almost the same population health gain in terms of reducing severe disability as those targeted at the entire population. Interventions to reduce the prevalence of CMDs among people with LTCs should be part of routine medical care

Prenatal and Early Life Exposure to Stressful Life Events and Risk of Autism Spectrum Disorders: Population-Based Studies in Sweden and England

Background and Aim Exposure to stressful life events during pregnancy has been suggested as a potential risk factor for offspring Autism Spectrum Disorders (ASD), but the literature is limited and inconsistent. We tested the hypothesis that maternal exposure to stressful life events would be associated with increased risks of offspring ASD, and that these risks would be highest for exposures during the prenatal period. Methods and Results We used prospectively collected data from two large population based studies in Sweden and England. In the Swedish study of 4429 ASD cases and 43277 controls, our exposure comprised the occurrence of any severe life event before and during pregnancy and the child's early life. In the English study (maximum n = 11554, ASD n = 72), we studied the risk of offspring ASD in relation to a combined maternal exposure to multiple (up to 42) common and rare life events, as well as their perceived impact upon the mother during pregnancy and early life. In crude and adjusted regression analyses in both studies, we found no evidence of an association between prenatal life events, or their number and perceived impact and the risk of offspring ASD. Sub-group analysis of ASD with and without intellectual disability in the Swedish study yielded similar results. Conclusion We found no evidence to support the hypotheses that exposure to stressful life events during the prenatal period is associated with an increased risk of offspring ASD

Genetic liability to rheumatoid arthritis on autism and autistic traits:polygenic risk score and mendelian randomization analyses

Higher prevalence of autism in offspring born to mothers with rheumatoid arthritis has been reported in observational studies. We investigated (a) the associations between maternal and offspring’s own genetic liability for rheumatoid arthritis and autism-related outcomes in the offspring using polygenic risk scores (PRS) and (b) whether the effects were causal using Mendelian randomization (MR). Using the latest genome-wide association (GWAS) summary data on rheumatoid arthritis and individual-level data from the Avon Longitudinal Study of Parents and Children, United Kingdom, we constructed PRSs for maternal and offspring genetic liability for rheumatoid arthritis (single-nucleotide polymorphism [SNP] p-value threshold 0.05). We investigated associations with autism, and autistic traits: social and communication difficulties, coherence, repetitive behaviours and sociability. We used modified Poisson regression with robust standard errors. In two-sample MR analyses, we used 40 genome-wide significant SNPs for rheumatoid arthritis and investigated the causal effects on risk for autism, in 18,381 cases and 27,969 controls of the Psychiatric Genetics Consortium and iPSYCH. Sample size ranged from 4992 to 7849 in PRS analyses. We found little evidence of associations between rheumatoid arthritis PRSs and autism-related phenotypes in the offspring (maternal PRS on autism: RR 0.89, 95%CI 0.73–1.07, p = 0.21; offspring’s own PRS on autism: RR 1.11, 95%CI 0.88–1.39, p = 0.39). MR results provided little evidence for a causal effect (IVW OR 1.01, 95%CI 0.98–1.04, p = 0.56). There was little evidence for associations between genetic liability for rheumatoid arthritis on autism-related outcomes in offspring. Lifetime risk for rheumatoid arthritis has no causal effects on autism