Background: Many genetic variants show highly robust associations with BMI. However, the mechanisms through which genetic susceptibility to obesity operate are not well understood. Potentially modifiable mechanisms, including... [ view full abstract ]
Background: Many genetic variants show highly robust associations with BMI. However, the mechanisms through which genetic susceptibility to obesity operate are not well understood. Potentially modifiable mechanisms, including eating behaviours, are of particular interest to public health. Here we explore whether eating behaviours mediate or modify genetic susceptibility to obesity.
Methods: Genetic risk scores for BMI (BMI-GRS) were calculated for 3515 and 2154 adults in the Fenland and EDEN population-based cohort studies, respectively. The eating behaviours: emotional eating, uncontrolled eating and cognitive restraint, were measured using a validated questionnaire in both cohorts. The mediating effect of each eating behaviour on the association between the BMI-GRS and measured BMI was assessed using the Sobel test. Additionally, we tested for interactions between each eating behaviour and the BMI-GRS on BMI.
Results: The association between the BMI-GRS and BMI was mediated by both emotional eating (EDEN: P-Sobel=0.01; Fenland: P-Sobel=0.02) and uncontrolled eating (EDEN: P-Sobel=0.04; Fenland: P-Sobel=0.0006) in both sexes combined. Cognitive restraint did not to mediate this association (P-Sobel>0.10), except amongst women in EDEN (P-Sobel=0.0009). Cognitive restraint modified the relationship between the BMI-GRS and BMI amongst men (EDEN P-interaction=0.0001; Fenland: P-interaction=0.04) and women in Fenland (P-interaction=0.0004). By tertiles of cognitive restraint, the association between the BMI-GRS and BMI was strongest in the lowest tertile of cognitive restraint, and weakest in the highest tertile of cognitive restraint.
Conclusions: Genetic susceptibility to obesity was partially mediated by the ‘appetitive’ eating behaviour traits (uncontrolled and emotional eating) and, in 3 of the 4 population groups studied, was modified by cognitive restraint. High levels of cognitive control over eating appear to attenuate the genetic susceptibility to obesity. Future research into interventions designed to support cognitive restraint might help to protect genetically susceptible individuals from weight gain.
