Pål Surén1, Nina Gunnes2, Christine Roth2, Michaeline Bresnahan3, Mady Hornig4, Deborah Hirtz5, Kari Kveim Lie6, W Ian Lipkin4, Per Magnus6, Ted Reichborn-Kjennerud7, Synnve Schjølberg6, Ezra Susser3, Anne-Siri Oyen8, George Davey Smith9, Camilla Stoltenberg10. 1. Norwegian Institute of Public Health, Oslo, Norway; Centre for Paediatric Epidemiology and Biostatistics, UCL Institute of Child Health, London, United Kingdom; pal.suren@fhi.no. 2. Norwegian Institute of Public Health, Oslo, Norway; Mailman School of Public Health, Columbia University, New York, New York; 3. Mailman School of Public Health, Columbia University, New York, New York; New York State Psychiatric Institute, New York, New York; 4. Mailman School of Public Health, Columbia University, New York, New York; 5. National Institute of Neurologic Disorders and Stroke, Bethesda, Maryland; 6. Norwegian Institute of Public Health, Oslo, Norway; 7. Norwegian Institute of Public Health, Oslo, Norway; Institute of Psychiatry, University of Oslo, Oslo, Norway; 8. Norwegian Institute of Public Health, Oslo, Norway; Nic Waals Institute, Lovisenberg Hospital, Oslo, Norway; 9. MRC Centre for Causal Analysis in Translational Epidemiology, University of Bristol, Bristol, United Kingdom; and. 10. Norwegian Institute of Public Health, Oslo, Norway; Department of Public Health and Primary Health Care, University of Bergen, Bergen, Norway.
Abstract
OBJECTIVES: The objective of the study was to investigate the associations among maternal prepregnancy BMI, paternal BMI, and the risk of autism spectrum disorders (ASDs) in children. METHODS: The study sample of 92 909 children was derived from the population-based, prospective Norwegian Mother and Child Cohort Study. The age range was 4.0 through 13.1 (mean 7.4) years. Relative risks of ASDs were estimated by odds ratios (ORs) and 95% confidence intervals (CIs) from logistic regression models. RESULTS: At the end of follow-up on December 31, 2012, 419 children in the study sample had been diagnosed with ASDs: 162 with autistic disorder, 103 with Asperger disorder, and 154 with pervasive developmental disorder not otherwise specified. Maternal obesity (BMI ≥30) was only weakly associated with ASD risk, whereas paternal obesity was associated with an increased risk of autistic disorder and Asperger disorder. The risk of autistic disorder was 0.27% (25 of 9267) in children of obese fathers and 0.14% (59 of 41 603) in children of fathers with normal weight (BMI <25), generating an adjusted OR of 1.73 (95% CI: 1.07-2.82). For Asperger disorder, analyses were limited to children aged ≥7 years (n = 50 116). The risk was 0.38% (18 of 4761) in children of obese fathers and 0.18% (42 of 22 736) in children of normal-weight fathers, and the adjusted OR was 2.01 (95% CI: 1.13-3.57). No associations were found for pervasive developmental disorder not otherwise specified. CONCLUSIONS: Paternal obesity is an independent risk factor for ASDs in children. The associations should be investigated further in genetic and epigenetic studies.
OBJECTIVES: The objective of the study was to investigate the associations among maternal prepregnancy BMI, paternal BMI, and the risk of autism spectrum disorders (ASDs) in children. METHODS: The study sample of 92 909 children was derived from the population-based, prospective Norwegian Mother and Child Cohort Study. The age range was 4.0 through 13.1 (mean 7.4) years. Relative risks of ASDs were estimated by odds ratios (ORs) and 95% confidence intervals (CIs) from logistic regression models. RESULTS: At the end of follow-up on December 31, 2012, 419 children in the study sample had been diagnosed with ASDs: 162 with autistic disorder, 103 with Asperger disorder, and 154 with pervasive developmental disorder not otherwise specified. Maternal obesity (BMI ≥30) was only weakly associated with ASD risk, whereas paternal obesity was associated with an increased risk of autistic disorder and Asperger disorder. The risk of autistic disorder was 0.27% (25 of 9267) in children of obese fathers and 0.14% (59 of 41 603) in children of fathers with normal weight (BMI <25), generating an adjusted OR of 1.73 (95% CI: 1.07-2.82). For Asperger disorder, analyses were limited to children aged ≥7 years (n = 50 116). The risk was 0.38% (18 of 4761) in children of obese fathers and 0.18% (42 of 22 736) in children of normal-weight fathers, and the adjusted OR was 2.01 (95% CI: 1.13-3.57). No associations were found for pervasive developmental disorder not otherwise specified. CONCLUSIONS: Paternal obesity is an independent risk factor for ASDs in children. The associations should be investigated further in genetic and epigenetic studies.
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