Understanding how eating behaviours mediate genetic susceptibility to obesity

Tackling the obesity epidemic is one of our most urgent global health challenges. In the UK, the majority of adults (64%) are overweight or obese (NHS Digital, 2020). Previous studies show that those with strong implicit preferences for energy-dense palatable foods, combined with poor inhibitory control over food intake, are most likely to gain weight (Nederkoorn et al., 2010). It is hypothesised that these preferences mainly stem from BMI-genes involved in brain physiology which are particularly vulnerable to maladaptation in the obesogenic environment (Locke et al., 2015, Willer et al., 2009, Bogdan et al., 2017, Kentistou et al., 2019). My PhD aims to tease apart how, and to what extent, eating behaviours (and their possible cognitive and neural correlates) mediate genetic susceptibility to obesity - the behavioural susceptibility theory. In particular, our first study utilised the local EXETER 10,000 cohort data and structural equation modelling to examine the role of disinhibited eating – a loss of control over food intake due to emotional and everyday/habitual triggers – in mediating genetic risk for obesity. Furthermore, we explored whether flexible versus rigid restraint (self-control) attenuated the genetic risk of obesity expressed via disinhibition and susceptibility to hunger. The results of my work so far and future studies will be discussed.