Metabolic Effects of Late Dinner in Healthy Volunteers

A Randomized Crossover Clinical Trial

Chenjuan Gu; Nga Brereton; Amy Schweitzer; Matthew Cotter; Daisy Duan; Elisabet Børsheim; Robert R. Wolfe; Luu V. Pham; Vsevolod Y. Polotsky; Jonathan C. Jun

Disclosures

J Clin Endocrinol Metab. 2020;105(8) 

In This Article

Abstract and Introduction

Abstract

Context: 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.

Objective: The objective of this work is to examine the impact of late dinner on nocturnal metabolism in healthy volunteers.

Design and Setting: This is a randomized crossover trial of late dinner (LD, 22:00) vs routine dinner (RD, 18:00), with a fixed sleep period (23:00–07:00) in a laboratory setting.

Participants: Participants comprised 20 healthy volunteers (10 male, 10 female), age 26.0 ± 0.6 years, body mass index 23.2 ± 0.7 kg/m2, accustomed to a bedtime between 22:00 and 01:00.

Interventions: 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 with RD and 22:00 with LD.

Main Outcome Measures: Measurements included nocturnal and next-morning hourly plasma glucose, insulin, triglycerides, free fatty acids (FFAs), cortisol, dietary fatty acid oxidation, and overnight polysomnography.

Results: 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.

Conclusion: 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.

Introduction

Obesity is rapidly increasing in prevalence throughout the world. Evidence is accumulating that meal timing can influence the development of obesity and metabolic syndrome.[1] In cross-sectional studies, obese individuals reported consuming more meals later in the day compared to randomly selected controls.[2] Similarly, obesity was associated with the habit of omitting breakfast and eating at night, but not with total daily energy intake.[3] In an observational cohort, longitudinal increases in body mass were attenuated by regularly consuming breakfast, or by eating the largest meal in the morning.[4] Furthermore, participants enrolled in a 20-week weight loss program who reported late eating (based on timing of the midday meal) lost less weight than early eaters.[5] Another weight loss study randomly assigned women with metabolic syndrome into 2 isocaloric groups, one for which breakfast was the largest meal of the day, and the other for which dinner was the largest. Over 12 weeks, the large breakfast group exhibited greater improvements in weight loss and metabolic outcomes than the large dinner group.[6] However, most studies to date have not controlled for factors such as sleep time, nor have they examined detailed metabolic responses to meal timing. Such studies are needed to provide mechanistic insights into the harms of delayed eating, and to inform the design of clinical trials to discover the ideal timing and composition of meals to combat obesity, metabolic syndrome, and diabetes.

Late eating can predispose to obesity and metabolic syndrome through several potential mechanisms. Because sleep decreases metabolic rate,[7,8] eating close to bedtime may reduce the rate of oxidation of ingested nutrients. Meal digestion, absorption, and oxidation can also be influenced by circadian rhythm.[9] Circadian control of metabolism may therefore result in reductions in metabolic rate and shifts in substrate preference.[10] We hypothesized that consuming a late dinner shortly before sleep, as opposed to earlier in the evening, impairs the handling of ingested glucose and lipids, leading to postprandial hyperglycemia and lower dietary fat oxidation. We tested our hypothesis in this randomized crossover study comparing effects of routine dinner (RD) at 18:00 vs late dinner (LD) at 22:00 on the nocturnal and next-morning metabolic profile of healthy volunteers who had a fixed time period for sleep (23:00–07:00). Specifically, we examined the 20-hour level and rate of change of plasma glucose, insulin, triglycerides (TGs), free fatty acids (FFAs), and cortisol under each condition. We quantified serial oxidation of ingested fat at dinner time using an oral stable isotope tracer, [2H31] palmitate. In addition, we performed in-laboratory polysomnography (PSG) and ambulatory actigraphy, and provided questionnaires to investigate interactions between eating time, sleep, and circadian rhythm.

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