Is Prepregnancy Obesity Associated With Risk of Cerebral Palsy and Epilepsy in Children?

Pan, Chun; Deroche, Chelsea B; Mann, Joshua R.; McDermott, Suzanne; Hardin, James W.

doi:10.1177/0883073813510971

Cited by 27 publications

(58 citation statements)

References 46 publications

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“…by guest on April 29, 2019 www.aappublications.org/news Downloaded from Our findings are in agreement with recently published studies on maternal obesity and risk of CP, 23,24 but demonstrate an association across the entire BMI scale less explored in previous studies. In a Swedish case-control study, Ahlin et al 25 found a 7% increased odds of CP for every 1 unit increase in maternal BMI (odds ratio, 1.07; 95% CI, 1.03-1.12) for babies born at term, but the authors did not state when BMI was measured.…”

Section: Figuresupporting

confidence: 83%

Maternal Prepregnancy BMI and Risk of Cerebral Palsy in Offspring

et al. 2016

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OBJECTIVES: To investigate the association between maternal pre-pregnancy BMI and risk of cerebral palsy (CP) in offspring. METHODS:The study population consisted of 188 788 children in the Mothers and Babies in Norway and Denmark CP study, using data from 2 population-based, prospective birth cohorts: the Norwegian Mother and Child Cohort Study and the Danish National Birth Cohort. Prepregnancy BMI was classified as underweight (BMI <18.5), lower normal weight , upper normal weight ), overweight , and obese (BMI ≥30). CP diagnoses were obtained from the national CP registries. Associations between maternal prepregnancy BMI and CP in offspring were investigated by using logbinomial regression models. RESULTS:The 2 cohorts had 390 eligible cases of CP (2.1 per 1000 live-born children). Compared with mothers in the lower normal weight group, mothers in the upper normal group had a 40% excess risk of having a child with CP (relative risk [RR], 1.35; 95% confidence interval [CI], 1.03-1.78). Excess risk was 60% (RR, 1.56; 95% CI, 1.21-2.01) for overweight mothers and 60% (RR, 1.55; 95% CI 1.11-2.18) for obese mothers. The risk of CP increased ∼4% for each unit increase in BMI (RR, 1.04; 95% CI, 1.02-1.06). Estimates changed little with adjustment for mother's occupational status, age, and smoking habits. CONCLUSIONS:Higher prepregnancy maternal BMI was associated with increased risk of CP in offspring.a Department of Global Public Health and Primary Care, University of Bergen, Bergen, Norway; b Department of Pediatrics, Haukeland University Hospital, Bergen, Norway; c Epidemiology Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Durham, North Carolina; d Ms Forthun was responsible for the analysis and interpretation of data, and the drafting of the manuscript; Dr Wilcox participated in the analysis and interpretation of data and reviewed and revised the manuscript; Drs Lie and Moster provided advice regarding study design, participated in the interpretation of data, and reviewed and revised the manuscript; Drs Strandberg-Larsen, Nohr, and Surén participated in the interpretation of data and reviewed and revised the manuscript; Dr Tollånes proposed the study, participated in the analysis and interpretation of data, and reviewed and revised the manuscript; and all authors approved the fi nal manuscript as submitted. The prevalence of overweight and obesity among pregnant women is increasing worldwide with adverse effects on maternal and child health. 6 Obese pregnant women (BMI >29.9) have increased risk of gestational diabetes, hypertension, and preeclampsia, and their offspring are at increased risk of preterm birth, macrosomia, complications during delivery, and perinatal death. 6 -9 Maternal obesity is also associated with birth defects, in particular neural tube defects. 10 We used pooled data from 2 large prospective Nordic birth cohorts to investigate the association between BMI before pregnancy and risk of CP in offspring, both overall and for variou...

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Section: Figuresupporting

confidence: 83%

Maternal Prepregnancy BMI and Risk of Cerebral Palsy in Offspring

et al. 2016

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“…A dose-dependent increase in relative risk of cerebral palsy in offspring has been noted as maternal BMI increased from overweight to morbidlyobese (Ahlin et al 2013; Crisham Janik et al 2013; Mehta et al 2014; Pan et al 2014). …”

Section: Maternal Obesity and Offspring Neurodevelopmentmentioning

confidence: 99%

“…Although paternal obesity may contribute to deleterious fetal programming, an obesogenic in utero environment seems to be the most impactful, with maternal body mass index (BMI) being more significantly associated with offspring risk than paternal BMI (Lawlor et al 2007). Recent evidence also indicates that maternal obesity is associated with adverse neurodevelopmental outcomes in children, including lower overall cognitive capabilities (Van Lieshout et al 2011; Tanda et al 2012); increased incidence of autism spectrum disorders and developmental delay (Hinkle et al 2012; Krakowiak et al 2012); increased incidence of attention deficit hyperactivity disorder (ADHD), anxiety, and other psychiatric disorders (Rodriguez et al 2008); and increased incidence of cerebral palsy (Ahlin et al 2013; Crisham Janik et al 2013; Mehta et al 2014; Pan et al 2014). Although such studies can show an association between maternal obesity and these adverse outcomes, they cannot prove causality and do not provide information about the underlying mechanisms.…”

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confidence: 99%

Effects of Maternal Obesity on Fetal Programming: Molecular Approaches

Neri

Edlow

2015

Cold Spring Harb Perspect Med

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Maternal obesity has become a worldwide epidemic. Obesity and a high-fat diet have been shown to have deleterious effects on fetal programming, predisposing offspring to adverse cardiometabolic and neurodevelopmental outcomes. Although large epidemiological studies have shown an association between maternal obesity and adverse outcomes for offspring, the underlying mechanisms remain unclear. Molecular approaches have played a key role in elucidating the mechanistic underpinnings of fetal malprogramming in the setting of maternal obesity. These approaches include, among others, characterization of epigenetic modifications, microRNA expression, the gut microbiome, the transcriptome, and evaluation of specific mRNA expression via quantitative reverse transcription polmerase chain reaction (RT-qPCR) in fetuses and offspring of obese females. This work will review the data from animal models and human fluids/cells regarding the effects of maternal obesity on fetal and offspring neurodevelopment and cardiometabolic outcomes, with a particular focus on molecular approaches.

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“…8,9 Recent epidemiologic studies suggest associations between prepregnancy obesity and various neurodevelopmental outcomes. [10][11][12][13][14][15][16][17][18][19][20][21] However, these studies were limited by small sample sizes, insufficient information on confounders and mediators, and imprecise neurodevelopment measures. Additionally, 1 study reported no association.…”

Section: What This Study Addsmentioning

confidence: 99%

Maternal Prepregnancy Body Mass Index and Child Psychosocial Development at 6 Years of Age

et al. 2015

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BACKGROUND: Both obesity and developmental disabilities have increased in recent decades. Limited studies suggest associations between maternal prepregnancy obesity and child neurodevelopment. METHODS:The Infant Feeding Practices Study II, a US nationally distributed longitudinal study of maternal health and infant health and feeding practices, was conducted from 2005 to 2007. In 2012, mothers were recontacted for information on their children's health and development. We examined associations between maternal prepregnancy BMI and child psychosocial development in 1311 mother-child pairs included in this follow-up study. Children's development was assessed by maternal report of child psychosocial difficulties from the Strengths and Difficulties Questionnaire, past developmental diagnoses, and receipt of special needs services.RESULTS: Adjusting for sociodemographic factors, children of obese class II/III mothers (BMI .35.0) had increased odds of emotional symptoms (adjusted odds ratio [aOR] 2.24; 95% confidence interval [CI], 1.27-3.98), peer problems (aOR 2.07; 95% CI, 1.26-3.40), total psychosocial difficulties (aOR 2.17; 95% CI, 1.24-3.77), attention-deficit/hyperactivity disorder diagnosis (aOR 4.55; 95% CI, 1.80-11.46), autism or developmental delay diagnosis (aOR 3.13; 95% CI, 1.10-8.94), receipt of speech language therapy (aOR 1.93; 95% CI, 1.18-3.15), receipt of psychological services (aOR 2.27; 95% CI, 1.09-4.73), and receipt of any special needs service (aOR 1.99; 95% CI, 1.33-2.97) compared with children of normal weight mothers ). Adjustment for potential causal pathway factors including pregnancy weight gain, gestational diabetes, breastfeeding duration, postpartum depression, and child's birth weight did not substantially affect most estimates.CONCLUSIONS: Children whose mothers were severely obese before pregnancy had increased risk for adverse developmental outcomes.WHAT'S KNOWN ON THIS SUBJECT: Both obesity and developmental disabilities have increased in recent decades; however, the full long-term effects of prepregnancy obesity on a child' s psychosocial development remain unknown. Limited studies suggest associations between maternal prepregnancy obesity and child psychosocial development. WHAT THIS STUDY ADDS:This study in 6-year-old children provides evidence that severe prepregnancy obesity is associated with adverse child psychosocial outcomes, including attentiondeficit/hyperactivity disorder. These findings were not explained by many pregnancy and postpartum factors related to maternal obesity or child development.

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Is Prepregnancy Obesity Associated With Risk of Cerebral Palsy and Epilepsy in Children?

Cited by 27 publications

References 46 publications

Maternal Prepregnancy BMI and Risk of Cerebral Palsy in Offspring

Maternal Prepregnancy BMI and Risk of Cerebral Palsy in Offspring

Effects of Maternal Obesity on Fetal Programming: Molecular Approaches

Maternal Prepregnancy Body Mass Index and Child Psychosocial Development at 6 Years of Age

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