Influence Of Meal Timing On Glycemic Variability In Mid-life Adults On A Controlled Diet

Advancing age is associated with increased risk of type 2 diabetes (T2D). Habitual diet and physical activity are key modulators of 24-hour glucose control and glycemic variability (GV), which are associated with insulin resistance and T2D development. Later meal times are associated with increased blood glucose concentrations and T2D risk, yet this has not been studied in mid-life adults within the context of a controlled diet. Determining optimal meal timing may be an effective strategy to control GV and prevent T2D development in at-risk individuals. PURPOSE: To explore the effect of meal timing on 24-hour glucose control and GV in mid-life adults. METHODS: Sedentary-to-recreationally active adults (n = 6, 4F/2M; age = 54 + 8 years; BMI = 25 + 5 kg/m2) were provided with a eucaloric controlled diet (50% carbohydrate, 35% fat, 15% protein) with a consistent added sugar and fiber content for 14 days. Participants were instructed to consume their meals consistently at their usual meal times. During days 8-14, participants wore a continuous glucose monitor (CGM) and recorded meal times using daily logs. Mean 24-hour glucose and Mean Amplitude of Glycemic Excursions (MAGE) were assessed with CGM. Participants were classified as early eaters (EE, last meal prior to 8 pm, n = 3) or late eaters (LE, last meal after 8 pm, n = 3). Mann Whitney U tests were used to evaluate group differences in CGM outcomes. RESULTS: There were no group differences in 24-hr glucose (EE = 94.0 + 10.6 mg/dL; LE = 99.4 + 3.0 mg/dL) between EE and LE (U = 5.00, p = 1.00). Further, there were no group differences in MAGE (EE = 38.1 + 5.4 mg/dL; LE = 51.6 + 16.6 mg/dL) between EE and LE (U = 7.00, p = 0.40). However, the effect size (Cohen’s d) was d = 1.1, indicating a large effect. CONCLUSION: These preliminary findings could be used to determine sample sizes needed for larger-scale studies designed to evaluate the impact of meal timing on glucose control and GV in mid-life adults. Supported by NIH R21AG077143 & R21AG075930