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Interpregnancy Interval and Risk of Autistic Disorder

Gunnes, Ninaa; Surén, Påla; Bresnahan, Michaelineb,c; Hornig, Madyb,d; Lie, Kari Kveima; Lipkin, W. Ianb,d; Magnus, Pera; Nilsen, Roy Miodinie,f; Reichborn-Kjennerud, Teda,g; Schjølberg, Synnvea; Susser, Ezra Saulb,c; Øyen, Anne-Siria,h; Stoltenberg, Camillaa,e

doi: 10.1097/01.ede.0000434435.52506.f5
Autism

Background: A recent California study reported increased risk of autistic disorder in children conceived within a year after the birth of a sibling.

Methods: We assessed the association between interpregnancy interval and risk of autistic disorder using nationwide registry data on pairs of singleton full siblings born in Norway. We defined interpregnancy interval as the time from birth of the first-born child to conception of the second-born child in a sibship. The outcome of interest was autistic disorder in the second-born child. Analyses were restricted to sibships in which the second-born child was born in 1990–2004. Odds ratios (ORs) were estimated by fitting ordinary logistic models and logistic generalized additive models.

Results: The study sample included 223,476 singleton full-sibling pairs. In sibships with interpregnancy intervals <9 months, 0.25% of the second-born children had autistic disorder, compared with 0.13% in the reference category (≥36 months). For interpregnancy intervals shorter than 9 months, the adjusted OR of autistic disorder in the second-born child was 2.18 (95% confidence interval 1.42–3.26). The risk of autistic disorder in the second-born child was also increased for interpregnancy intervals of 9–11 months in the adjusted analysis (OR = 1.71 [95% CI = 1.07–2.64]).

Conclusions: Consistent with a previous report from California, interpregnancy intervals shorter than 1 year were associated with increased risk of autistic disorder in the second-born child. A possible explanation is depletion of micronutrients in mothers with closely spaced pregnancies.

From the aNorwegian Institute of Public Health, Oslo, Norway; bDepartment of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY; cNew York State Psychiatric Institute, New York, NY; dCenter for Infection and Immunity, Mailman School of Public Health, Columbia University, New York, NY; eDepartment of Global Public Health and Primary Care, University of Bergen, Bergen, Norway; fCentre for Clinical Research, Haukeland University Hospital, Bergen, Norway; gInstitute of Psychiatry, University of Oslo, Oslo, Norway; and hNic Waals Institute, Lovisenberg Diakonale Hospital, Oslo, Norway.

The study was funded by grants from the Research Council of Norway (grant nos. 189457/V40 and 190694/V50). The authors reported no conflicts of interest.

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Correspondence: Nina Gunnes, Norwegian Institute of Public Health, P.O. Box 4404 Nydalen, N-0403 Oslo, Norway. E-mail: Nina.Gunnes@fhi.no.

Received January 14, 2013

Accepted July 9, 2013

© 2013 by Lippincott Williams & Wilkins, Inc