Abstract
Intermittent fasting describes dietary strategies in which the pattern of energy restriction (intermittent energy restriction, IER) or timing of food intake (time-restricted feeding, TRF) are altered such that individuals undergo repeated periods of “fasting”. The overarching aim of this PhD project was to investigate the metabolic health impacts of these intermittent fasting variants. Intermittent energy restriction: Study one assessed the acute metabolic effects of substantial energy restriction (ER) in healthy, overweight/obese participants using a cross-over design. Six-hour postprandial responses were assessed the morning following one day of total 100% ER, partial 75% ER and isoenergetic intake (0% ER) via serial blood sampling and indirect calorimetry. Postprandial substrate oxidation was shifted towards fat oxidation (p=0.080) and ketogenesis (p<0.001) in an apparent dose response manner following 75-100% ER, translating to a reduction in postprandial lipaemia (p<0.001). Conversely, glucose tolerance was impaired (p=0.002). Study two utilised similar methods to investigate the chronic effect of IER (75% ER for two days/week) on postprandial metabolism following 5% weight-loss. This was compared to matched weight-loss achieved via a “standard treatment” control of continuous ER (2510kJ/day deficit). Rates of weight-loss were similar between groups (p=0.446), despite greater reported reductions in energy intake during IER (p=0.012), which might be explained in part by an adaptive decline in resting energy expenditure (p=0.067). Both interventions comparatively (p=0.903) improved postprandial insulinaemia, whereas the relative reduction in postprandial lipaemia was greater following IER (p=0.042). Time-restricted feeding: Study three examined the effects of a 10-week, three-hour daily shortening of the eating window on fasting metabolism and adiposity utilising a parallel-armed controlled design. In a small group of lean and overweight/obese participants, TRF led to modest reductions in adiposity (p=0.047) and fasting glycaemia (p=0.073), possibly explained by the spontaneous reduction in energy intake observed. Combined, these data provide novel insights into the metabolic effects of intermittent fasting. Replication and mechanistic evaluation in diverse population groups, including those with established metabolic disorders, is warranted.