Does obesity pharmacotherapy change eating behaviour in humans? Evaluation of the literature using learnings from bariatric surgery

Abstract

Obesity is characterised by the dysregulation of the neurobiological systems governing hunger, satiety and food reward. Dysfunction in signalling across the gut-brain axis impairs both homeostatic and hedonic control of eating, ultimately resulting in excessive energy intake. The weight loss achieved through pharmacological and surgical interventions is not primarily the result of cognitive behavioural restraint; it instead reflects the direct biological modification of the neuroendocrine circuits involved in regulation of eating behaviour. This review applies a conceptual framework structured around two axes; homeostatic versus hedonic eating and the appetitive versus consummatory phases of feeding to interpret how these interventions change eating behaviour. Bariatric surgery has a substantially more mature evidence base. The Roux-en-Y gastric bypass in particular, produces sustained modification in consummatory homeostatic behaviour – with earlier satiation and meal termination, in conjunction with short-term changes in food preferences. Evidence for GLP-1 receptor agonists and dual GIP/GLP-1 receptor agonists demonstrates a parallel profile of reduced hunger, increased satiety, attenuated food-cue reactivity and subduing of the hedonic drive. Whether the effects of pharmacotherapy and surgery engage in the same biological processes and whether their effects follow a similar time course remains an unresolved question. We consider the implications of this framework for nutrition and dietetic practice.