| Summary: | The aim of this thesis is to test one of the assumptions of the behavioural susceptibility model of weight that inherited differences in appetite are already present in infancy, and that shared genetic effects are contributing to associations with weight from very early on in life. Data from a British birth cohort of 2402 families with infant twins (Gemini) were used to explore associations between appetite and weight, assess genetic influences on appetite, and examine shared genetic pathways underlying appetite and weight. Study 1 describes the development of a parent-report psychometric measure of infant appetite during the period of exclusive milk-feeding. Four underlying dimensions were identified – ‘enjoyment of food’ (EF), ‘food responsiveness’ (FR), ‘slowness in eating’ (SE), ‘satiety responsiveness’ (SR), along with a single general item that correlated with all traits (‘appetite size’, AS). Study 2 established that all traits were significantly associated with higher weight at 3 months and greater increase in weight from birth to 3 months. Study 3 used the twin design to demonstrate moderate to high heritability for all traits (EF: 83%; FR: 59%; SE: 84%; SR: 72%; AS: 77%). Study 4 showed common genetic influence on EF, SE and SR, which explained 78% of the covariation between them, and Study 5 demonstrated common genetic influence between the two satiety-related traits (SE and SR) and weight. Finally, Study 6 was an in-depth exploration of a single case of an infant with extreme appetitive avidity whose parents were forced to exert drastic control measures to avoid severe overeating. This thesis provides evidence for a behavioural susceptibility model of weight because inherited individual differences in appetite are present from early infancy, are phenotypically associated with weight, and share common genetic pathways with weight. Inherited differential susceptibility to the obesogenic environment may be contributing to variability in childhood adiposity.
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