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Commentary on: Yuan C, Gaskins AJ, Blaine AI, et al. Association between cesarean birth and risk of obesity in offspring in childhood, adolescence, and early adulthood. JAMA Pediatr 2016;170:e162385.
Since 2008, several observational studies have reported an association between caesarean section (CS) and offspring obesity. The underlying biological mechanism hypothesised to explain this association is that children born via CS lack exposure to the maternal vaginal flora, resulting in colonisation of the gut with flora that increase energy harvesting from food, thereby contributing to the development of obesity. Maternal pre-pregnancy weight confounds this association, as obesity in the mother is associated with CS and offspring obesity. Not all previous studies were able to adjust for maternal pre-pregnancy weight, but a recent systematic review showed that in studies that were able to adjust for this confounder, there remained a statistically significant association of CS with obesity in the offspring.1 The large prospective cohort study by Yuan et al aimed to examine the association between CS and offspring obesity adjusting for all potential confounders.
The Growing Up Today Study (GUTS) included 22 068 children of women participating in the Nurses' Health Study-II. Children aged 9–14 years were enrolled starting in 1996 with a second wave of enrolment in 2004 and followed to the end of 2012 with annual or biennial self-administered and proxy-administered questionnaires. Information on mode of delivery was based on maternal recall in 2009, and offspring body mass index (BMI) was calculated from self-reported weight and height at each follow-up. The association between CS and offspring obesity was examined using log-binomial regression models adjusted for a range of confounders.
Twenty-two per cent of offspring were born by CS, and 13% were obese at the end of the study period. Women who underwent CS had a higher pre-pregnancy BMI and were more likely to have had gestational diabetes, hypertensive disorders of pregnancy and a previous CS. The RR for obesity in offspring born by CS versus vaginal delivery was 1.30 (95% CI 1.21 to 1.41); after adjustment for potential confounders, the RR was 1.15 (95% CI 1.06 to 1.26) with the most pronounced attenuation coming from the adjustment for pre-pregnancy BMI. This association remained fairly stable across strata of age at BMI assessment. The findings persisted in ancillary analyses performed to investigate the influence of residual confounding, such as adjusting for maternal BMI as a continuous variable and conducting a within-family analysis.
The study adds to the now ∼80 studies and several systematic reviews that examined the association between CS and offspring obesity.1 ,2 The study by Yuan and colleagues is one of the largest and stands out in its ability to thoroughly adjust for potential confounders. Although this study has a selected sample of families with socioeconomic status above the average, many previous population-based studies have had similar findings. Taking into consideration all of the available evidence, a true effect of CS on offspring obesity seems likely, but our understanding of the underlying biological mechanism remains incomplete. Differences in the microbiome of infants born via CS compared those born vaginally have been documented as have differences in the gut flora between persons of normal weight and those with obesity. The gut flora in the first years of life, however, will vary greatly and is influenced by factors such as diet and antibiotic therapy. To the best of our knowledge, no longitudinal study has investigated the persistence of differences in the gut flora from the neonatal period into childhood although some studies are currently underway (eg, http://www.canadianchildstudy.ca).
Implications for practice
The study provides further evidence for CS as a risk factor for obesity in the offspring. The finding reinforces the need to limit performing CS without a clear medical indication. For pregnancies, where delivery by CS is indicated, a greater understanding of the biological mechanism is needed to develop interventions to modify the effect that CS has on obesity. Assuming a causal relationship between CS and obesity (RR 1.20), the number needed to harm in a population with a prevalence of childhood obesity of 10% would be 50; that is, for every 50 CS performed, one additional child will become obese.
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