Institute of Psychiatry, Psychology & Neuroscience, Kings College, London, UK.
Department of Pediatrics Gynaecology and Obstetrics, Faculty of Medicine, University of Geneva, Geneva, Switzerland.
Int J Obes (Lond). 2022 Jul;46(7):1271-1279. doi: 10.1038/s41366-022-01106-2. Epub 2022 Mar 19.
Parental-feeding behaviors are common intervention targets for childhood obesity, but often only deliver small changes. Childhood BMI is partly driven by genetic effects, and the extent to which parental-feeding interventions can mediate child genetic liability is not known. Here we aim to examine how potential interventions on parental-feeding behaviors can mitigate some of the association between child genetic liability and BMI in early adolescence, using causal inference methods.
Data from the Avon Longitudinal Study of Parents and Children were used to estimate an interventional disparity measure for a child polygenic score for BMI (PGS-BMI) on BMI at 12 years. The approach compares counterfactual outcomes for different hypothetical interventions on parental-feeding styles applied when children are 10-11 years (n = 4248). Results are presented as adjusted total association (Adj-Ta) between genetic liability (PGS-BMI) and BMI at 12 years, versus the interventional disparity measure-direct effect (IDM-DE), which represents the association that would remain, had we intervened on parental-feeding under different scenarios.
For children in the top quintile of genetic liability, an intervention shifting parental feeding to the levels of children with lowest genetic risk, resulted in a difference of 0.81 kg/m in BMI at 12 years (Adj-Ta = 3.27, 95% CI: 3.04, 3.49; versus IDM-DE = 2.46, 95% CI: 2.24, 2.67).
Findings suggest that parental-feeding interventions have the potential to buffer some of the genetic liability for childhood obesity. Further, we highlight a novel way to analyze potential interventions for health conditions only using secondary data analyses, by combining methodology from statistical genetics and social epidemiology.
父母喂养行为是儿童肥胖的常见干预目标,但通常只能带来微小的变化。儿童 BMI 部分受遗传效应的影响,父母喂养干预可以在多大程度上调节儿童遗传易感性尚不清楚。在这里,我们旨在使用因果推理方法研究潜在的父母喂养行为干预措施如何减轻儿童遗传易感性与青少年早期 BMI 之间的一些关联。
利用阿冯纵向研究父母与子女的数据,估计儿童 BMI 多基因评分(PGS-BMI)对 12 岁时 BMI 的干预性差异度量。该方法比较了在儿童 10-11 岁时应用不同假设的父母喂养方式的干预情况下(n=4248),不同假设的干预情况下的 BMI 的反事实结果。结果表示为遗传易感性(PGS-BMI)与 12 岁时 BMI 之间的调整总关联(Adj-Ta),与干预性差异度量-直接效应(IDM-DE)相对,该效应代表如果我们在不同情景下干预父母喂养行为,仍会存在的关联。
对于遗传易感性最高五分位数的儿童,将父母喂养方式转变为遗传风险最低的儿童的水平,会导致 12 岁时 BMI 差异为 0.81kg/m(Adj-Ta=3.27,95%CI:3.04,3.49;IDM-DE=2.46,95%CI:2.24,2.67)。
研究结果表明,父母喂养干预有可能缓冲儿童肥胖的部分遗传易感性。此外,我们通过结合统计遗传学和社会流行病学的方法,突出了仅使用二次数据分析分析健康状况的潜在干预措施的一种新方法。