Commentary: Assessing the impact of breastfeeding on child health: where conventional methods alone fall short for reliably establishing causal inference

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Given the strong social patterning of both breastfeeding and child health in high-income countries (HICs), there is a high probability of observing associations that are confounded by broader socio-economic factors rather than being due to any biological effects of breastfeeding. Even where extensive adjustments for confounders are made, residual confounding remains a persistant problem. As the exact nature of the relationship between socio-economic position (SEP) and health-related characteristics and disease are complex and not entirely understood, it is difficult to fully capture this in analyses and comprehensively control for confounding by SEP. As such, conventional observational methods, relying on the adjustment of associations for measured confounders, will likely be, on their own, insufficient for reliably establishing causal inference. This is evident, for example, from recent antioxidant trials failing to replicate the results of large-scale observational studies reporting protective effects that were independent of a wide range of confounders. This is the most likely attributable to the presence of residual confounding in the observational studies. With respect to the association between breastfeeding and child obesity, various observational studies have reported decreased risk on child obesity associated with breastfeeding in infancy; however, a meta-analysis indicated that this may be largely due to publication bias and confounding. In contrast, family studies using siblings discordant for breastfeeding duration to control for social, familial and environmental confounding, suggest that associations may not in fact be completely confounded by these factors. Thus, the picture in terms of causal effects of breastfeeding on child obesity is unclear. Ideally, a randomized trial would provide the gold standard for causal inference. However, a trial randomizing mothers to breastfeed or not breastfeed would clearly be unfeasible and unethical. A recent trial of breastfeeding promotion in Belarus has been carried out. This trial resulted in a large increase in exclusive breastfeeding in the intervention group (43.3 vs 6.4%) and a higher prevalence of any breastfeeding at all ages 412 months, but mean adiposity and levels of obesity were similar by randomized group, suggesting that breastfeeding is not causally related to child obesity. It is thus becoming increasingly apparent that combining conventional approaches with additional methods of testing causal inference are required to establish the long-term effects of breastfeeding and other developmental exposures on later life outcomes. Various new methods for improving causal inference in observational studies in general have been advanced, including new statistical approaches, maternal–paternal comparisons, sibling comparisons, Mendelian randomization and other genetically informed studies. However, not all of these will be applicable to breastfeeding, being, for example, specific to prenatal exposures or, where genetic variants are used, it is not clear if an appropriate genetic variant relating to breastfeeding will be available. The study by Kwok et al. using the children of 1997 cohort in this issue of the IJE takes advantage of differences in the confounding structure of breastfeeding and child obesity in Hong Kong compared with Western/European countries (where the majority of existing studies reporting associations on breastfeeding have been carried out) to explore causal inference. As the authors discuss, in high-income populations, individuals of higher SEP are more likely to breastfeed and less likely to have obese children. In contrast, in non-Westernized countries child obesity tends to be less clearly socially patterned and, in Hong Kong in particular, sustained exclusive breastfeeding is more common in less-educated women. This means that if the inverse associations of breastfeeding with adiposity, reported in studies of Western populations, are largely explained by Published by Oxford University Press on behalf of the International Epidemiological Association