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- Class, Quetzal A., et al.
(författare)
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Fetal growth and psychiatric and socioeconomic problems : population-based sibling comparison
- 2014
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Ingår i: British Journal of Psychiatry. - London, United Kingdom : Royal College od Psychiatrists. - 0007-1250 .- 1472-1465. ; 205:5, s. 355-361
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Tidskriftsartikel (refereegranskat)abstract
- Background: It is unclear whether associations between fetal growth and psychiatric and socioeconomic problems are consistent with causal mechanisms.Aims: To estimate the extent to which associations are a result of unmeasured confounding factors using a sibling-comparison approach.Method: We predicted outcomes from continuously measured birth weight in a Swedish population cohort (n = 3 291 773), while controlling for measured and unmeasured confounding.Results: In the population, lower birth weight (⩽ 2500 g) increased the risk of all outcomes. Sibling-comparison models indicated that lower birth weight independently predicted increased risk for autism spectrum disorder (hazard ratio for low birth weight = 2.44, 95% CI 1.99-2.97) and attention-deficit hyperactivity disorder. Although attenuated, associations remained for psychotic or bipolar disorder and educational problems. Associations with suicide attempt, substance use problems and social welfare receipt, however, were fully attenuated in sibling comparisons.Conclusions: Results suggest that fetal growth, and factors that influence it, contribute to psychiatric and socioeconomic problems.
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| 2. |
- D'Onofrio, Brian M., et al.
(författare)
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Testing the Developmental Origins of Health and Disease Hypothesis for Psychopathology Using Family-Based Quasi-Experimental Designs
- 2014
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Ingår i: Child Development Perspectives. - Hoboken, USA : Wiley-Blackwell. - 1750-8592 .- 1750-8606. ; 8:3, s. 151-157
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Tidskriftsartikel (refereegranskat)abstract
- The Developmental Origin of Health and Disease (DOHaD) hypothesis is a broad theoretical framework that emphasizes how early risk factors have a causal influence on psychopathology. Researchers have raised concerns about the causal interpretation of statistical associations between early risk factors and later psychopathology because most existing studies have been unable to rule out the possibility of environmental and genetic confounding. In this paper we illustrate how family-based quasi-experimental designs can test the DOHaD hypothesis by ruling out alternative hypotheses. We review the logic underlying sibling-comparison, co-twin control, offspring of siblings/twins, adoption, and in vitro fertilization designs. We then present results from studies using these designs focused on broad indices of fetal development (low birth weight and gestational age) and a particular teratogen, smoking during pregnancy. The results provide mixed support for the DOHaD hypothesis for psychopathology, illustrating the critical need to use design features that rule out unmeasured confounding.
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| 3. |
- McCoy, Brittany M., et al.
(författare)
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Mediators of the association between parental severe mental illness and offspring neurodevelopmental problems
- 2014
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Ingår i: Annals of Epidemiology. - New York, USA : Elsevier. - 1047-2797 .- 1873-2585. ; 24:9, s. 629-634.e1
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Tidskriftsartikel (refereegranskat)abstract
- Purpose: Parental severe mental illness (SMI) is associated with an increased risk of offspring autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD). We conducted a study to examine the extent to which risk of preterm birth, low birth weight, and small for gestational age mediated this association.Methods: We obtained data on offspring born 1992-2001 in Sweden (n = 870,017) through the linkage of multiple population-based registers. We used logistic and Cox regression to assess the associations between parental SMI, adverse pregnancy outcomes, and offspring ASD and ADHD, as well as tested whether adverse pregnancy outcomes served as mediators.Results: After controlling for measured covariates, maternal and paternal SMI were associated with an increased risk for preterm birth, low birth weight, and gestational age, and for offspring ASD and ADHD. These pregnancy outcomes were also associated with an increased risk of ASD and ADHD. We found that pregnancy outcomes did not mediate the association between parental SMI and offspring ASD and ADHD, as there was no substantial change in magnitude of the risk estimates after controlling for pregnancy outcomes.Conclusions: Parental SMI and adverse pregnancy outcomes appear to be independent risk factors for offspring ASD and ADHD.
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