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Objective: The fetal programming model hypothesizes that developmental programming in utero and in early life induces adaptations that predetermine the adult phenotype. This study investigated whether prenatal/perinatal complications are associated with lifetime eating disorders in women. Method: Participants included 46,373 adult women enrolled in the Norwegian Mother and Child Cohort Study (den norske Mor & barn‐undersøkelsen [MoBa]). MoBa mothers and their mothers (MoBa grandmothers) were the focus of the current study. MoBa mothers with lifetime eating disorders were compared to a referent group. Results: MoBa mothers who weighed more at birth (birth weight, adjusted odds ratio [OR] = 1.14; 95% confidence interval [CI]: 1.10–1.19) or were born large‐for‐gestational‐age (adjusted OR = 1.39; 95% CI: 1.27–1.52) were more likely to develop binge‐eating disorder in later life. MoBa mothers who weighed less at birth were more likely to develop anorexia nervosa (birth weight, adjusted OR = 0.88; 95% CI: 0.81–0.95). Bulimia nervosa and purging disorder (PD) were not significantly predicted by the prenatal and perinatal factors examined. Discussion: Results of this study, which include the first known investigation of prenatal and perinatal factors in binge‐eating disorder and PD, suggest that fetal programming may be relevant to the development of anorexia nervosa and binge‐eating disorder. Future genetically informative research is needed to help disentangle whether these associations are a function of genetic influences or a true environmental fetal programming effect. [ABSTRACT FROM AUTHOR]

Previous studies of the relationship between maternal eating disorders and adverse perinatal outcomes have failed to control for familial transmission of perinatal phenotypes, which may confound the reported association. In a unique design afforded by the Norwegian Mother and Child Cohort Study and Medical Birth Registry of Norway, we linked three generations through birth register records and maternal-reported survey data to investigate whether maternal eating disorders increase risk after parsing out the contribution of familial transmission of perinatal phenotypes. The samples were 70,881 pregnancies in grandmother-mother-child triads for analyses concerning eating disorder exposure during pregnancy and 52,348 for analyses concerning lifetime maternal eating disorder exposure. As hypothesized, eating disorders predicted a higher incidence of perinatal complications even after adjusting for grandmaternal perinatal phenotypes. For example, anorexia nervosa immediately prior to pregnancy was associated with smaller birth length (relative risk = 1.62; 95% CI [1.20, 2.14]), bulimia nervosa with induced labor (relative risk = 1.21; 95% CI [1.07, 1.36]), and binge-eating disorder with several delivery complications, larger birth length (relative risk = 1.25; 95% CI [1.17, 1.34]), and large-for-gestational-age (relative risk = 1.04; 95% CI [1.01, 1.06]). Maternal pregravid body mass index and gestational weight mediated most associations. Our results support that exposure to eating disorders increases the risk for negative health outcomes in pregnant women and their babies. (PsycINFO Database Record [ABSTRACT FROM AUTHOR]

ABSTRACT Objective The aim of this paper was to internally validate previously reported relations (Knoph Berg et al., Aust N Z J Psychiatry, 42, 396-404, 2008) between psychosocial factors and bulimia nervosa (BN) outcomes during pregnancy. Method This study is based on the Norwegian Mother and Child Cohort Study (MoBa) conducted by the Norwegian Institute of Public Health. Participants were women enrolled during pregnancy ( N = 69,030). Internal validity was evaluated by way of bootstrapped parameter estimates using the overall sample and a split sample calibration approach. Results Bootstrap bias estimates were below the problematic threshold, and extend earlier findings (Knoph Berg et al., Aust N Z J Psychiatry, 42, 396-404, 2008) by providing support for the validity of the models at the population level of all pregnant women in Norway. Bootstrap risk ratios indicated that prevalence, incidence, and remission of BN during pregnancy were significantly associated with psychosocial factors. The split sample procedure showed that the models developed on the training sample did not predict risks in the validation sample. Discussion This study characterizes associations between psychosocial exposures and BN outcomes among pregnant women in Norway. Women with lifetime and current self-reported psychosocial adversities were at a much higher risk for BN during pregnancy. Psychosocial factors were associated with BN remission during pregnancy, inviting the prospect of enhancing therapeutic interventions. We consider the findings in the context of reproducibility in science. © 2014 Wiley Periodicals, Inc. (Int J Eat Disord 2015; 48:654-662) [ABSTRACT FROM AUTHOR]