ObjectiveReports of rising prevalence of autism spectrum disorders (ASD), along with their profound personal and societal burden, emphasize the need of methodologically sound studies to explore their causes and consequences. We here present the design of a large intergenerational resource for ASD research, along with population-based prevalence estimates of ASD and their diagnostic validity.MethodThe Stockholm Youth Cohort is a record-linkage study comprising all individuals aged 0–17 years, ever resident in Stockholm County in 2001–2007 (N = 589,114). ASD cases (N = 5,100) were identified using a multisource approach, involving registers covering all pathways to ASD diagnosis and care, and categorized according to co-morbid intellectual disability. Prospectively recorded information on potential determinants and consequences of ASD were retrieved from national and regional health and administrative registers. Case ascertainment was validated through case-note review, and cross validation with co-existing cases in a national twin study.ResultsThe 2007 year prevalence of ASD in all children and young people was 11.5 per 1,000 (95% confidence interval 11.2–11.8), with a co-morbid intellectual disability recorded in 42.6% (41.0–44.2) of cases. We found 96.0% (92.0–98.4) of reviewed case-notes being consistent with a diagnosis of ASD, and confirmed ASD in 85.2% (66.2–95.8) of affected twins.ConclusionsFindings from this contemporary study accords with recently reported prevalence estimates from Western countries at around 1%, based on valid case ascertainment. The Stockholm Youth Cohort, in light of the availability of extensive information from Sweden's registers, constitutes an important resource for ASD research. On-going work, including collection of biological samples, will enrich the study further.

In a record-linkage study in Stockholm, Sweden, the year 2011 prevalence of diagnosed autism spectrum disorders (ASD) was found to be 0.40, 1.74, 2.46, and 1.76% among 0-5, 6-12, 13-17, and 18-27 year olds, respectively. The corresponding proportion of cases with a recorded diagnosis of intellectual disability was 17.4, 22.1, 26.1 and 29.4%. Between 2001 and 2011, ASD prevalence increased almost 3.5 fold among children aged 2-17 years. The increase was mainly accounted for by an eightfold increase of ASD without intellectual disability (from 0.14 to 1.10 %), while the prevalence of ASD with intellectual disability increased only slightly (from 0.28 to 0.34%). The increase in ASD prevalence is likely contributed to by extrinsic factors such as increased awareness and diagnostics.

BackgroundMigration has been implicated as a risk factor for autism, but evidence is limited and inconsistent.AimsTo investigate the relationship between parental migration status and risk of autism spectrum disorder, taking into consideration the importance of region of origin, timing of migration and possible discrepancies in associations between autism subtypes.MethodRecord-linkage study within the total child population of Stockholm County between 2001 and 2007. Individuals with high- and low-functioning autism were defined as having autism spectrum disorder with and without comorbid intellectual disability, and ascertained via health and habilitation service registers.ResultsIn total, 4952 individuals with autism spectrum disorder were identified, comprising 2855 children with high-functioning autism and 2097 children with low-functioning autism. Children of migrant parents were at increased risk of low-functioning autism (odds ratio (OR) = 1.5, 95% CI 1.3–1.7); this risk was highest when parents migrated from regions with a low human development index, and peaked when migration occurred around pregnancy (OR = 2.3, 95% CI 1.7–3.0). A decreased risk of high-functioning autism was observed in children of migrant parents, regardless of area of origin or timing of migration. Parental age, income or obstetric complications did not fully explain any of these associations.ConclusionsEnvironmental factors associated with migration may contribute to the development of autism presenting with comorbid intellectual disability, especially when actingin utero.High- and low-functioning autism may have partly different aetiologies, and should be studied separately.

Background: Prenatal environmental factors such as maternal adiposity may influence the risk of offspring autism spectrum disorders (ASD), though current evidence is inconsistent. The objective of this study was to assess the relationship of parental BMI and gestational weight gain (GWG) with risk of offspring ASD in a population-based cohort study using family-based study designs.Methods: The cohort was based in Stockholm County, Sweden, including 333 057 individuals born 1984–2007, of whom 6420 were diagnosed with an ASD. We evaluated maternal body mass index (BMI) at first antenatal visit, GWG and paternal BMI at the time of conscription into the Swedish military as exposures using general estimating equation (GEE) models with logit link.Results: At the population level, maternal overweight/obesity was associated with increased risk of offspring ASD [odds ratio (OR)25 ≤ BMI < 30 1.31, 95% confidence interval = 1.21–1.41; ORBMI ≥ 30 1.94, 1.72–2.17], as was paternal underweight (ORBMI < 18.5, 1.19, 1.06–1.33) and obesity (ORBMI ≥ 30 1.47, 1.12–1.92) in mutually adjusted models. However, in matched sibling analyses, the relationship between elevated maternal BMI and ASD risk was not apparent. GWG had a U-shaped association with offspring ASD at the population level (ORinsufficient 1.22, 1.07–1.40; ORexcessive 1.23, 1.08–1.40). Matched sibling analyses were suggestive of elevated risk with excessive GWG (ORinsufficient 1.12, 0.68–1.84; ORexcessive 1.48, 0.93–2.38).Conclusions: Whereas population-level results suggested that maternal BMI was associated with ASD, sibling analyses and paternal BMI analyses indicate that maternal BMI may also be a proxy marker for other familial risk factors. Evidence is stronger for a direct link between GWG and ASD risk.