Delaying mealtimes reduces fat oxidation: A randomized, crossover, controlled feeding study.

OBJECTIVE: This study investigated the effects of circadian misalignment (CM), induced by delaying mealtimes, independent of sleep timing and duration and eating window duration, on energy expenditure (EE), respiratory quotient (RQ), and substrate oxidation. METHODS: Healthy adults, aged 20 to 49 years, participated in this randomized crossover study under controlled feeding conditions. Eating window duration was identical in both conditions (circadian alignment [CA]: 9:00 am-7:00 pm; CM: 1:00 pm-11:00 pm), and bedtimes were constant (11:30 pm-8:00 am). EE, RQ, and substrate oxidation were obtained over 23 hours in a metabolic chamber on days 3 and 4 and days 14 and 15 in each condition. Twenty-four-hour and post-meal outcomes were analyzed using a linear mixed-effects model including condition, day, and day-by-condition interaction as main predictors and sex as a covariate. RESULTS: Three men and four women (age 37.4 ± 8.8 years, BMI 30.4 ± 3.3 kg/m2 ) completed the study. Twenty-four-hour EE did not differ between conditions. Post-meal RQ for dinner and snack was higher in CM versus CA (both p < 0.001) with correspondingly higher glucose oxidation (both p < 0.01) and lower fat oxidation (dinner only p = 0.0001). CONCLUSIONS: CM, induced by delaying mealtimes by 4 hours relative to CA, independently shifts nutrient metabolism toward greater carbohydrate and lower fat oxidation.

Sleep exerts lasting effects on hematopoietic stem cell function and diversity.

A sleepless night may feel awful in its aftermath, but sleep's revitalizing powers are substantial, perpetuating the idea that convalescent sleep is a consequence-free physiological reset. Although recent studies have shown that catch-up sleep insufficiently neutralizes the negative effects of sleep debt, the mechanisms that control prolonged effects of sleep disruption are not understood. Here, we show that sleep interruption restructures the epigenome of hematopoietic stem and progenitor cells (HSPCs) and increases their proliferation, thus reducing hematopoietic clonal diversity through accelerated genetic drift. Sleep fragmentation exerts a lasting influence on the HSPC epigenome, skewing commitment toward a myeloid fate and priming cells for exaggerated inflammatory bursts. Combining hematopoietic clonal tracking with mathematical modeling, we infer that sleep preserves clonal diversity by limiting neutral drift. In humans, sleep restriction alters the HSPC epigenome and activates hematopoiesis. These findings show that sleep slows decay of the hematopoietic system by calibrating the hematopoietic epigenome, constraining inflammatory output, and maintaining clonal diversity.

Circadian rhythms and meal timing: impact on energy balance and body weight.

Energy metabolism and appetite regulating hormones follow circadian rhythms which, when disrupted, could lead to adverse metabolic consequences. Such circadian misalignment, a mismatch between endogenous circadian rhythms and behavior, is most severely experienced by shift workers, due to nighttime wake, daytime sleep, and eating at night. However, circadian misalignment is not restricted to shift workers; milder shifts in sleep and mealtimes, termed social and eating jetlag, are highly prevalent in the general population. Social and eating jetlag result in later mealtimes, which may promote positive energy balance and weight gain. Earlier meal timing, specific to individual endogenous circadian patterns, could serve to reduce cardiometabolic disease burden and aid in weight loss and interventions should be done to test this.