JMIR Publications

ABSTRACT

Background:

Maintaining stable glucose levels is important for metabolic health. Glucose excursions (GEs), which are marked increases in glucose following food intake, have been associated with higher risk for cardiovascular disease and metabolic dysfunction. Individuals with overweight or obesity who do not have diabetes may still show impaired glucose regulation, as reflected in increased glucose variability. Hunger, as a real-time physiological cue, may serve as a predictor of imminent glucose excursions and represents a potential target for just-in-time adaptive interventions (JITAIs).

Objective:

This study aimed to investigate the temporal relationship between self-reported hunger and subsequent glucose dynamics, including the likelihood of GE occurring, in adults with overweight or obesity using continuous glucose monitoring and ecological momentary assessment.

Methods:

Data from 84 non-diabetic adults with overweight or obesity (mean age = 47.7 years, SD = 11.5) were analyzed over a 14-day period. Ecological momentary assessment reports of hunger were collected and interstitial glucose levels were captured via continuous glucose monitoring. Three linear mixed-effects models were applied to examine (1) the association between hunger and immediate glucose level, (2) glucose level 30 minutes after hunger, and (3) glucose trajectories from 30 to 180 minutes post-hunger. In addition, a logistic mixed-effects model was used to estimate the likelihood of a GE occurring within 30 to 180 minutes following a hunger report.

Results:

Hunger reports were associated with significantly lower glucose levels both at the time of reporting (mean difference [MD] = –13.6 mg/dL, 95% CI –15.9 to –11.3; P < .001) and 30 minutes afterward (MD = –11.0 mg/dL, 95% CI –13.4 to –8.6; P < .001). A significant time-by-hunger interaction revealed a progressive increase in glucose levels over 180 minutes post-hunger (MD = +6.7 mg/dL at 180 minutes, 95% CI +5.1 to +8.3; P < .001). Hunger increased the odds of experiencing a GE by 23.7% at 30–60 minutes (P = .022), 36.1% at 60–90 minutes (P < .001), and 13.0% at 90–120 minutes (P = .01). No significant GE risk was observed beyond 120 minutes.

Conclusions:

Hunger is associated with an initial drop in glucose followed by a delayed rise and heightened risk of glucose excursions within 30 to 120 minutes. These findings support hunger as a real-time behavioral marker for impending GEs and highlight its potential utility in triggering JITAIs aimed at improving glycemic stability among non-diabetic adults with overweight or obesity. Moreover, hunger may serve as a practical proxy for eating behavior in real-world contexts, offering a dynamic target for behavioral and digital health interventions. Clinical Trial: Not applicable