According to the Centers for Disease Control and Prevention, 13.7 million children and adolescents struggle with obesity, including 18.4% of children aged six to 11 years and 13.9% of children aged two to five years.
Childhood obesity is potentially influenced by a large number of factors. One that has been understudied until recently is the prenatal environment. As researchers have begun exploring the role that this might play, compelling evidence has emerged indicating that there is a meaningful correlation between maternal consumption of sugar-sweetened beverages (SSBs) (e.g. soda and sweetened fruit drinks) and childhood obesity and overweight (i.e. high BMI) status. In a new study, my colleagues and I attempted to disentangle the contributors to childhood obesity, including prenatal factors, in hopes of improving the quality of data that policymakers need to address this complex health crisis.
Whether and to what extent maternal consumption of SSBs during pregnancy itself drives child obesity and high BMI is an important, multi-faceted question. On the one hand, this consumption may just be a proxy for parental food preferences and their household’s overall consumption patterns, which can both affect children’s BMI. In other words, this might simply be a case of correlation but not causation.
Alternatively, biological pathways might account for some of the observed relationship. For example, during the second trimester, the fetus begins to ingest amniotic fluid in addition to receiving glucose through direct blood transfer, and chronically high glucose levels driven by maternal consumption of SSBs may be matched by chronically high levels of fetal insulin production that can trigger increased lipogenesis (the metabolic formation of fat) as well as altered expression of genes and proteins related to metabolic functioning in the offspring. That is, maternal consumption of SSBs might have a direct, causal impact on children’s physiology in ways that affect their BMI.
These two explanations have different implications for future research as well as policy and practice. In our study exploring the impact of SSB consumption during pregnancy, my colleagues and I used a rich set of longitudinal data from a high-quality, long-duration cohort study of children, and a lab-validated microsimulation model of childhood consumption, growth, and physiology from infancy through adolescence to infer caloric intake throughout childhood; this process removes some known, major influences on BMI, such as those related to physical activity.
We then estimated the association between maternal consumption of SSBs during pregnancy and later caloric intake by the child. Our results suggest that, as expected, much of the observed correlation between prenatal exposure to SSBs and later childhood predisposition to high BMI reflects other social and environmental influences (e.g. the food parents feed their children). However, the results leave open the possibility that there may be biological effects of prenatal SSB exposure that operate either independently of or in concert with these other factors.
This work should motivate additional research to more definitively characterize the biological effects of prenatal SSB exposure. Such research might employ data that are collected with this purpose in mind. Even as that research proceeds, given the overwhelming evidence of other negative health outcomes associated with SSB consumption, policymakers might still wish to consider actions that would reduce maternal consumption of them pregnancy.
One approach that policymakers might consider, which would mirror many past policy efforts, would seek to change health behaviors at the individual level. Policy efforts in this vein might include such things as advocating that physicians strongly highlight SSB recommendations during prenatal consultations or public messaging campaigns.