News Release

High maternal BMI during pregnancy unlikely to cause fatness in childhood and adolescence

Peer-Reviewed Publication

PLOS

There is little evidence to support any long-term impact of maternal body mass index (BMI) in pregnancy on a child's risk of fatness in childhood and adolescence, according to a new study published in PLOS Medicine by Rebecca Richmond of the University of Bristol, UK, and colleagues.

Research has shown that a mother's BMI during pregnancy is associated with greater birth size of her offspring. However, whether this association continues through childhood and is mediated by processes that occur during gestation--such as effects of circulating glucose and lipids levels--had been unclear. In the new study, the researchers used body mass and genetic information on 6,057 mother-offspring pairs from two prospective birth cohort studies. In one cohort, the offspring's BMI was measured around age 6; in the other it was taken multiple times between ages 7 and 18.

While the researchers found associations between maternal BMI before pregnancy and offspring BMI at all ages, these associations were largely explained by transmission of genes associated with fatness. When a weighted genetic risk score was integrated into the analysis, the remaining association between pre-pregnancy BMI of a mother and her offspring's childhood BMI was nearly null. The study had limited power for some sensitivity tests, relied on self-reported pre-pregnancy BMI, and did not include any study of weight gain during pregnancy.

"These findings suggest that public health interventions directed at all family members and at different stages of the life course are likely to be important and are potentially more likely to halt the obesity epidemic than a focus on maternal overweight and obesity status in pregnancy," the authors say.

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Research Article

Funding:

This work was supported by grants from the European Research Council (ObesityDevelop; 669545), the US National Institute of Health (R01 DK10324), and the Wellcome Trust (WT094529MA). RCR, NJT, GDS, and DAL work in a unit that receives funds from the University of Bristol and the UK Medical Research Council (MC_UU_12013/1, MC_UU_12013/3, and MC_UU_12013/5). RCR is supported by Cancer Research UK (C18281/A19169). DAL is a UK National Institute of Health Research Senior Investigator (NF-SI-0611-10196). The UK Medical Research Council and Wellcome Trust (102215/2/13/2) and the University of Bristol provide core support for Avon Longitudinal Study of Parents and Children (ALSPAC). A grant from the Wellcome Trust funded genotyping in the ALSPAC mothers (WT088806). ALSPAC offspring genome-wide association studies data were generated by Sample Logistics and Genotyping Facilities at the Wellcome Trust Sanger Institute and Laboratory Corporation of America (LabCorp) using support from 23andMe. The general design of Generation R Study is made possible by financial support from the Erasmus Medical Center, Rotterdam; the Erasmus University, Rotterdam; the Netherlands Organisation for Health Research and Development (ZonMw); the Netherlands Organisation for Scientific Research (NWO); the Ministry of Health, Welfare, and Sport; and the Ministry of Youth and Families. VWJ received an additional grant from the Netherlands Organization for Health Research and Development (VIDI 016.136.361) and a European Research Council Consolidator Grant (ERC-2014-CoG-648916). JFF has received funding from the European Union's Horizon 2020 research and innovation programme under grant agreement No. 633595 (DynaHEALTH). The Generation R Study received funding from the European Union's Horizon 2020 research and innovation programme (733206, LIFECYCLE). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing Interests:

I have read the journal's policy and the authors of this manuscript have the following competing interests: GDS is a member of the Editorial Board of PLOS Medicine. In addition to grant funding that is acknowledged in the paper and that was relevant to the conduct of the study reported in the paper, the University of Bristol has received funds from public, charity, and industry funders from grants on which DAL is the Principal applicant (UK Medical Research Council, UK Economic and Social Research Council, UK National Institute of Health Research, Wellcome Trust, British Heart Foundation, Roche Diagnostics, Ferring Pharmaceuticals, and Medtronic PLC). These funders had no impact on any aspect of the work presented in this paper.

Citation:

Richmond RC, Timpson NJ, Felix JF, Palmer T, Gaillard R, McMahon G, et al. (2017) Using Genetic Variation to Explore the Causal Effect of Maternal Pregnancy Adiposity on Future Offspring Adiposity: A Mendelian Randomisation Study. PLoS Med 14(1): e1002221. doi:10.1371/journal.pmed.1002221

Author Affiliations:

MRC Integrative Epidemiology Unit, University of Bristol, Bristol, United Kingdom
School of Social and Community Medicine, University of Bristol, Bristol, United Kingdom
The Generation R Study Group, Erasmus MC, University Medical Center Rotterdam, Rotterdam, the Netherlands
Department of Epidemiology, Erasmus MC, University Medical Center Rotterdam, Rotterdam, the Netherlands
Department of Pediatrics, Erasmus MC, University Medical Center Rotterdam, Rotterdam, the Netherlands
Department of Mathematics and Statistics, Lancaster University, Lancaster, United Kingdom

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