Objectives: To compare birth weight, gestational age and weight for gestational age (WGA) with the outcome of childhood autism in the Finnish population 1987 - 2007.
Methods: A nested case-control study. Cases were identified from the Finnish Hospital Discharge Register (FHDR) and controls (1:4) were defined from the Finnish Medical Birth Register (FMBR). Data on birth weight and gestational age was obtained from the FMBR. Birth weight categories were: ≤ 1500, 1501 to 2500, 2501 to 4000, 4001 to 4500 and ≥ 4501 g. Gestational age was categorized into four categories: ≤ 31, 32 to 37, 38 to 41 and ≥ 42 weeks. WGA was estimated according to Finnish birth weight standards and it was categorized into three groups: small for gestational age (SGA, < -2 SD), appropriate for gestational age (AGA, -2 SD - + 2 SD) and large for gestational age (LGA, > +2 SD). Sociodemographic confounders (maternal age and maternal socioeconomic status, SES) and potential markers for genetic susceptibility (parental psychiatric history) were included in adjusted analyses.
Results: A total of 1132 cases and 4538 controls were identified from the FHDR. In unadjusted analyses, all three neonatal factors were associated with the outcome of childhood autism (very low birth weight, <1500g: OR 1.89; CI 1.1, 3.4; p=.034, very short gestational age, <31 weeks: OR 2.13; CI 1.1, 4.1; p=.025 and being SGA: OR 1.68; CI 1.2, 2.5; p=.008). However, none of the associations remained statistically significant in adjusted analyses, although SGA status approached significance (OR 1.52; CI 0.98, 2.4; p=.062).
Conclusions: We found no evidence that low birth weight, abnormal gestational age or SGA/LGA would increase the risk of childhood autism. No independent effects were found for birth weight characteristics after adjusting for maternal sociodemographic factors (age and SES) and for both maternal and paternal psychiatric history, which represented markers for genetic susceptibility. It has been suggested that obstetric and neonatal factors may play a role in autism etiology especially among those with low genetic susceptibility, but have a lesser role in individuals with genetic predisposition. We believe that our sample is representative of the severe end of the autism spectrum and other diagnostic/milder subtypes of ASD need to be studied in the future.
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