Characterization of the circadian system in binge eating disorder and the effects of morning bright light and individually timed exogenous melatonin administration: A 4-week feasibility double-blind randomized controlled mechanistic clinical trial
Aug 2026· Research Square· 0 citations· 97 references
Medicine
TL;DR
A later circadian phase correlated with greater BED severity, and dampened actigraphy rhythms, both support circadian disruption in BED.
Abstract
Introduction: Binge eating disorder (BED) exhibits features consistent with circadian system dysregulation. This two-phase study mechanistically examined BED chronobiology. We hypothesized that dim light melatonin onset (DLMO; circadian phase) is delayed in BED and associated with illness characteristics, and be modifiable via a chronobiotic intervention. Methods: Phase 1 (P1) was a 2-week observational study comparing adults with obesity with BED (n = 43) and without BED (controls, n = 41). Phase 2 (P2) was a 4-week double-blind, randomized, controlled pilot trial in BED (NCT04724668). Participants received morning bright light (BLT; 10,000 lx) plus individually timed exogenous melatonin (3 mg) administration (BLT+ITEMA, n = 13) or sham red light (50 lx) plus placebo (n = 10). Primary outcomes were baseline DLMO differences (P1) and DLMO change (P2). Secondary/exploratory measures included wrist actigraphy and clinical features. ANCOVA, correlation, and Bayesian methods were used for statistical analysis. Results: In P1, DLMO did not differ between groups, but later DLMO correlated with greater BED severity. BED participants showed lower 24-hour locomotor amplitude and MESOR (both, posterior probability [pp] = 1), poorer diet quality, higher night eating and leptin levels (all p < 0.05). In P2, DLMO change did not differ between groups. Compared to sham+placebo, BLT+ITEMA participants had smaller reductions in peak activity (pp = 0.97) and amplitude (pp = 0.87), plus increased dietary restraint and LcN-3 fatty acids (both p < 0.05). Later baseline DLMO correlated with greater phase advance and binge eating reduction (both p < 0.05). The intervention was well tolerated. Conclusions: A later circadian phase correlated with greater BED severity, and dampened actigraphy rhythms, both support circadian disruption in BED. The mechanistic intervention is feasible and warrants refinement.
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