Introduction and Objective: While late eating has been linked with an increased risk for obesity and diabetes, its impact on glycemia in relation to endogenous circadian rhythm, rather than clock hour, remains unclear. Methods: We are conducting a randomized, crossover trial comparing the metabolic effects of early vs late meal timing relative to individualized circadian phase (dim light melatonin onset; DLMO) in persons without diabetes, with and without obesity. Participants undergo 2 controlled inpatient isocaloric feeding visits: (1) Early Dinner (ED): dinner (DLMO-3h) then snack (DLMO+1h); (2) Late Dinner (LD): snack (DLMO-3h) then dinner (DLMO+1h), with an identical 8h sleep period (DLMO+2h to DLMO+10h). All meals consist of 50% carbohydrates, 35% fat, and 15% protein, with dinner having 3.5 times the calories of the snack. Main outcomes include differences in 4h post-dinner, 4h post-snack, and 13h combined postprandial and sleep period (DLMO-3h to DLMO+10h) incremental area under the curve (iAUC) glucose levels measured by blinded continuous glucose sensors. ED and LD values were compared using Wilcoxon signed-rank tests. Results: Interim data from 11 participants are analyzed (10 females; mean (SD) age 29.2 (8.6) yrs, BMI 26.1 (10.1) kg/m²). Post-dinner 4h iAUC glucose did not differ between ED and LD (P0.05). In contrast, post-snack 4h iAUC glucose was higher in LD compared to ED by a median (IQR) of 23.5 (19.1) mg/dL·h (P=0.01). LD also induced higher iAUC glucose during the postprandial and sleep period by a median of 50.8 (38.3) mg/dL·h (P=0.02). Conclusion: Preliminary data suggest that a late circadian-based eating pattern characterized by a smaller meal followed by a larger one, leads to greater postprandial and overnight glycemia compared to the reverse order, even in the context of controlled caloric intake and sleep. These findings highlight the interplay between meal timing and size in dietary strategies for diabetes prevention, which need to be confirmed with the full dataset. Disclosure S.L. Cantor: None. S.B. Glaros: None. I.N. Kacker: None. N.A. Macheret: None. M.M. Gaydos: None. N. Sala: None. L. Mabundo: None. A. Ishihara: None. R. Brychta: None. A.B. Courville: None. N. Maruthur: None. K.Y. Chen: None. J. Jun: Research Support; Current; Ketone IQ. Advisory Panel; Ended; ApniMed. S. Chung: None. D. Duan: Research Support; Current; Endogenex Inc. Funding NIH (K23DK133690; NIH ZIADK075176)
CANTOR et al. (Fri,) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: