Later eating timing in relation to an individual internal clock is associated with lower insulin sensitivity and affected by genetic factors.

backgroundAlthough the contribution of the circadian clock to metabolic regulation is widely recognized, the role of eating timing in glucose metabolism and diabetes risk remains insufficiently studied. This study aimed (i) to investigate the link between the eating timing pattern relative to individual clock and glucose homoeostasis and (ii) to explore the contribution of genetic and environmental factors to eating timing parameters.

methodsIn 92 adult twins (NCT01631123), glycaemic traits were assessed using the oral glucose tolerance test. Parameters of eating timing pattern (eating timing itself, daily calorie distribution, and eating frequency) were extracted from five-day food records. Caloric midpoint defined as the time point at which 50% of daily calories are consumed. Circadian timing of eating was determined as a time interval between the clock time of eating and a corrected midpoint of sleep, a chronotype marker. Heritability of eating timing components was estimated by comparing correlations within monozygotic and dizygotic twin pairs and fitting genetic structural equation models.

findingsAmong components of eating timing, the most associations were found for the circadian time of caloric midpoint (CCM). Later CCM was significantly associated with poorer insulin sensitivity, i.e. with lower ISI Stumvoll (β = 0.304, p = 5.9 × 10

interpretationLater eating timing in relation to an individual internal clock is associated with lower insulin sensitivity. Shifting the main calorie intake to earlier circadian times may improve glucose metabolism, but genetic factors could influence the feasibility and effectiveness of eating-timing based interventions. The findings should be investigated in a larger cohort.

fundingThis work was supported by the German Research Foundation (DFG RA 3340/4-1 to OP-R, project number 530918029), by the European Association for the Study of Diabetes (Morgagni Prize 2020 to OP-R), and by the German Federal Ministry of Education and Research (BMBF NUGAT 0315424 to AFHP). The DZD is funded by the German Federal Ministry for Education and Research (01GI0925).