Location: Arkansas Children's Nutrition CenterTitle: Metabolic effects of late dinner in healthy volunteers – A randomized crossover clinical trial
|GU, CHENJUAN - Johns Hopkins University|
|BRERETON, NGA - Johns Hopkins University|
|SCHWEITZER, AMY - Johns Hopkins University|
|COTTER, MATTHEW - Arkansas Children'S Nutrition Research Center (ACNC)|
|DUAN, DAISY - Johns Hopkins University|
|BORSHEIM, ELISABET - University Arkansas For Medical Sciences (UAMS)|
|WOLFE, ROBERT - University Arkansas For Medical Sciences (UAMS)|
|PHAM, LUU - Johns Hopkins University|
|POLOTSKY, VSEVOLOD - Johns Hopkins University|
|JUN, JONATHAN - Johns Hopkins University|
Submitted to: Journal of Clinical Endocrinology and Metabolism
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 6/2/2020
Publication Date: 6/11/2020
Citation: Gu, C., Brereton, N., Schweitzer, A., Cotter, M., Duan, D., Borsheim, E., Wolfe, R.R., Pham, L.V., Polotsky, V.Y., Jun, J.C. 2020. Metabolic effects of late dinner in healthy volunteers – A randomized crossover clinical trial. Journal of Clinical Endocrinology and Metabolism. https://doi.org/10.1210/clinem/dgaa354.
Interpretive Summary: Late night feeding has been associated with obesity in epidemiological studies of adults and children, but the underlying causes for this are not clear. The current study recruited adults to begin to understand if the timing of the dinner relative to sleep affects how the body is using carbohydrates and fat for energy overnight. We did a randomized crossover study in healthy young adult volunteers comparing effects of a routine dinner (RD) at 6 pm compared to a late dinner (LD) at 10 pm on the overnight and morning metabolic response. All volunteers had a fixed time period for sleep (11:00 pm - 7:00 am). Specifically, we examined 20-hour level and rate of change of plasma concentrations of glucose, insulin, triglycerides, free fatty acids (FFA), and cortisol under each condition. We also estimated oxidation (burning) of ingested fat at dinner time using an oral stable isotope tracer of palmitate. In addition, we used questionnaires combined with sophisticated technology (measurement of brain waves, physical activity etc.) to investigate interactions between eating time, sleep, and circadian rhythm. LD caused a shift in the response to the meal which was overlapping with the sleep period. Independent of this shift, the period following LD was characterized by higher blood glucose concentration, a delay in the triglyceride peak, and lower FFA concentrations and dietary fatty acid oxidation compared to RD. LD did not affect sleep pattern, but increased plasma cortisol. These changes were most pronounced in those that regularly (outside of the study) went to bed earlier in the evenings. The results indicate that LD leads to less effective handling of glucose and reduction in the usage of fat for energy. These effects might promote obesity if they recur on a chronic basis. Future studies can apply similar methods used in this study to other age groups, including children, to determine how meal patterns influence how the body adapts by changing the type of fuel it is using.
Technical Abstract: Consuming calories later in the day is associated with obesity and metabolic syndrome. We hypothesized that eating a late dinner alters substrate metabolism during sleep in a manner that promotes obesity. To examine the impact of late dinner on nocturnal metabolism in healthy volunteers. This is a randomized crossover trial of late dinner (LD, 22:00) versus routine dinner (RD, 18:00), with a fixed sleep period (23:00-07:00) in a laboratory setting. 20 healthy volunteers (10 males, 10 females), aged 26.0 +/- 0.6 years, BMI 23.2 +/- 0.7 kg/m2, accustomed to a bedtime between 22:00-01:00. An isocaloric macronutrient diet was administered on both visits. Dinner (35% daily kcal, 50% carbohydrate, 35% fat) with an oral lipid tracer ([2H31] palmitate, 15 mg/kg) was given at 18:00 on RD and 22:00 on LD. Nocturnal and next-morning hourly plasma glucose, insulin, triglycerides, free fatty acids (FFAs), cortisol, dietary fatty acid oxidation, and overnight polysomnography. LD caused a 4-hour shift in the postprandial period, overlapping with the sleep phase. Independent of this shift, the postprandial period following LD was characterized by higher glucose, a triglyceride peak delay, and lower FFA and dietary fatty acid oxidation. LD did not affect sleep architecture, but increased plasma cortisol. These metabolic changes were most pronounced in habitual earlier sleepers determined by actigraphy monitoring. LD induces nocturnal glucose intolerance, and reduces fatty acid oxidation and mobilization, particularly in earlier sleepers. These effects might promote obesity if they recur chronically.