When obese individuals follow a low-calorie diet and then eat more again, their bodies burn fewer calories at rest than expected, and this is linked to stronger feelings of hunger and desire to eat,...

Caloric restriction during an 8-week low-energy diet creates a sustained energy deficit, triggering a homeostatic response to reduce energy expenditure beyond what is predicted by weight loss alone, a phenomenon termed metabolic adaptation, as directly measured by disproportionate reductions in resting metabolic rate (RMR) at week 9.

Metabolic adaptation is associated with increased plasma concentrations of the orexigenic hormone ghrelin and decreased concentrations of the anorexigenic hormones PYY and GLP-1, indicating a shift in gut hormone signaling that promotes hunger and reduces satiety, as directly measured in the same cohort undergoing the identical intervention.

Altered gut hormone levels act on hypothalamic appetite centers, particularly the arcuate nucleus, to increase neural drive for food intake and decrease satiety signaling, which is inferred from the strong correlation between hormonal changes and elevated subjective hunger, desire to eat, and composite appetite scores after adjusting for weight loss and respiratory quotient.

The combined effect of reduced energy expenditure and heightened appetite signaling creates a physiological drive to increase energy intake, which may promote weight regain by counteracting the initial energy deficit, as demonstrated by the association between the magnitude of metabolic adaptation and the magnitude of appetite score increases.