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Mounting evidence supports an association between eating behaviour (EB) and obesity. However, poor characterisation of the nature of this relationship limits its application to obesity prevention. This thesis aims to advance understanding of the association between EB and the aetiology of obesity. Across 5 studies, a combination of approaches was used to interrogate: (1) the role of EB in genetic predisposition to obesity, (2) the interaction between infant EB and maternal attitudes in the determination of infant milk intake and weight and (3) the genetic basis of EB traits and risk-taking. First, the effect of body mass index (BMI)-related genetic variants on adult body composition was investigated using a genetic risk score (GRS) approach in the Fenland study (n=9667). The BMI-GRS primarily influenced fat mass, confirming its utility in modelling the effects of adiposity and BMI, as well as in exploring the mechanisms of genetic predisposition to obesity. Emotional eating (EE), uncontrolled eating (UE) and cognitive restraint (CR) were then modelled as potential mediators and modifiers of the BMI-GRS to BMI association amongst adults in the Fenland (n=3515) and EDEN (n=2154) studies. The association was partially mediated by EE and UE, and modified by CR. These results indicate that whilst appetitive EB traits (EE and UE) lie on the causal pathway between genetics and weight status in adulthood, restraint may protect genetically vulnerable individuals from obesity. Having demonstrated that interactions between obesity determinants can impact adult weight, I described the association of infant EB to both infant milk intake and weight in the Baby Milk Trial (n=669). I then investigated whether this could be modified by maternal factors. Positive maternal attitudes towards following healthy infant feeding guidelines attenuated the association between infant EB and both outcomes. Finally, I performed GWAS to explore the genetic basis of risk-taking and adult EB, behavioural phenotypes with a hypothesised role in the aetiology of obesity. A total of 26 genetic variants were identified in association with risk-taking (n=436,236). In aggregate, these were linked to higher BMI but heterogeneity in the impact of individual variants suggested the involvement of multiple pathways. No variants were identified for EE, UE or CR. This analysis was likely under-powered due to low sample size (n≤11,843) but indicated a genetic basis for UE that partially overlaps with that of BMI. Using a combination of approaches, this work demonstrates the role of EB pathways in the aetiology of obesity. The findings contribute to a deeper understanding of their likely causal role and the implications of their relationships with other behavioural traits, highlighting a range of behaviours as potential targets for obesity prevention amongst both infants and adults.