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)

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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Abstract and Introduction
Materials and Methods
Results
Discussion
References

Table 1. Clinical characteristics of study participants (n = 20)
Variable	Mean ± SEM (%)
Age, y	26.0 ± 0.6
Sex
Male, n (%)	10 (50)
Female, n (%)	10 (50)
Race
African American, n (%)	1(5)
Asian, n (%)	11 (55)
White, n (%)	8 (40)
Hispanic, n (%)	1 (5)
Body composition
Body mass index, kg/m²	23.2 ± 0.7
Waist: hip ratio	0.84 ± 0.01
Fat mass, %
Male	23.2 ± 3.3
Female	33.9 ± 1.7
Lean mass, %
Male	72.6 ± 3.3
Female	62.2 ± 1.6
MEQ score	44.5 ± 2.1
Chronotype
Definite evening, n (%)	1 (5)
Moderate evening, n (%)	6 (30)
Intermediate, n (%)	10 (50)
Moderate morning, n (%)	1 (5)
Definite morning, n (%)	0
Unknown, n (%)	2 (10)

Abbreviation: MEQ. Morningness-eveningness questionnaire.

Table 2. Nutrient composition of the meals consumed during routine dinner and late dinner visits (n = 20)
Variable	Day 2—All meals			Day 3—Breakfast only
Variable	Routine dinner	Late dinner	P	Routine dinner	Late dinner	P
Total caloric intake, kcal	2150.2 ± 87.0	2094.2 ± 91.5	.28	519.8 ± 21.5	514.7 ± 23.3	.39
% calories from carbohydrates	48.2 ± 0.4	47.7 ± 0.4	.28	49.3 ± 0.6	49.4 ± 0.5	.77
% calories from fat	35.9 ± 0.5	36.4 ± 0.4	.22	35.0 ± 0.6	34.7 ± 0.6	.87
% calories from protein	15.8 ± 0.2	15.8 ± 0.2	.49	15.7 ± 0.2	15.9 ± 0.2	.62
Total carbohydrates	264.4 ± 10.8	255.4 ± 11.7	.19	66.2 ± 2.6	65.7 ± 2.8	.63
Meal glycemic index	57.8 ± 0.7	58.0 ± 0.6	.28	57.6 ± 0.5	58.0 ± 0.4	.14
Dietary fiber, g	24.4 ± 2.7	23.9 ± 2.7	.78	7.2 ± 0.6	7.2 ± 0.6	.46
Soluble fiber	8.7 ± 0.5	8.7 ± 0.5	.56	3.4 ± 0.3	3.5 ± 0.3	.54
Insoluble fiber	15.7 ± 2.4	15.1 ± 2.3	.33	3.7 ± 0.3	3.7 ± 0.3	.41
Total grains, ounce equivalents	7.8 ± 0.4	7.6 ± 0.4	.26	2.3 ± 0.1	2.2 ± 0.1	.77
Whole grains	1.1 ± 0.2	1.1 ± 0.2	.26	1.7 ± 0.2	1.6 ± 0.2	.25
Refined grains	6.7 ± 0.4	6.5 ± 0.4	.54	0.6 ± 0.2	0.7 ± 0.2	.19
Total fat, g	87.6 ± 4.0	86.3 ± 3.9	.97	21.2 ± 1.1	20.9 ± 1.2	.53
Cholesterol, mg	255.5 ± 18.5	251.4 ± 17.8	.33	140.1 ± 15.2	146.8 ± 12.6	.35
Fatty acids
% calories from SFAs	9.9 ± 0.4	10.0 ± 0.4	.53	9.7 ± 1.0	10.2 ± 0.9	.44
% calories from MUFAs	12.4 ± 0.4	12.6 ± 0.3	.55	9.7 ± 0.6	9.6 ± 0.6	.89
% calories from PUFAs	11.2 ± 0.5	11.4 ± 0.5	.15	12.3 ± 1.2	11.6 ± 1.2	.31
Total protein (g)	85.7 ± 3.3	83.4 ± 3.6	.20	20.7 ± 0.9	20.7 ± 1.0	.35
Animal protein	54.4 ± 3.9	53.0 ± 3.7	.24	10.3 ± 0.8	9.9 ± 0.8	.2
Vegetable protein	31.3 ± 4.0	30.3 ± 3.8	.28	10.4 ± 1.1	10.8 ± 1.1	.11

Values are shown as mean ± SEM. Two-sided paired t test was performed for the comparison of each variable between 2 visits.
Abbreviations: Meal glycemic index, glucose was used as reference food; MUFA, monounsaturated fatty acids; PUFA, polyunsaturated fatty acids; SFA, saturated fatty acids.

Table 3. Sleep and physical activity for routine dinner and late dinner visits
Variable	Routine dinner	Late dinner	P
Actigraphy data, n = 17
Preadmission mean sleep onset, h after midnight	0.41 ± 0.28	0.49 ± 0.28	.81
Preadmission mean total sleep time, min	365.1 ± 20.8	367.8 ± 14.6	.99
Preadmission mean daily active energy expenditure, kcal	1379.9 ± 170.16	1423.5 ± 134.4	.66
In-lab daily active energy expenditure, kcal	657.4 ± 78.1	703.6 ± 72.7	.31
Preadmission mean daily total activity counts	1 281 574.4 ± 96 765.0	1 371 510.8 ± 85 684.2	.31
In-lab daily total activity counts	612 657.1 ± 45 366.7	664 553.6 ± 52 307.1	.30
Polysomnography data, n = 20
Total sleep time, min	413.1 ± 8.1	421.0 ± 6.3	.37
Sleep efficiency, %	86.5 ± 1.8	88.4 ± 1.4	.31
Sleep latency, min	22.0 ± 5.9	14.6 ± 3.2	.29
REM latency, min	109.9 ± 10.7	90.9 ± 9.2	.15
Wake after sleep onset, min	43.2 ± 5.1	41.3 ± 5.8	.79
Stage NREM 1, %	7.5 ± 0.7	7.5 ± 0.7	.96
Stage NREM 2, %	47.9 ± 1.6	49.2 ± 1.2	.47
Stage NREM 3, %	24.0 ± 1.9	22.9 ± 1.8	.55
Stage REM, %	20.8 ± 1.2	20.6 ± 1.2	.87
Apnea hypopnea index, events/h	1.8 ± 0.5	1.2 ± 0.3	.14

Values are shown as mean ± SEM. Two-sided paired t test was performed for the comparison of each variable between 2 visits. The actigraphy data are shown as the average of the values of at least 7 days before each clinical research unit admission.
Abbreviations: NREM, non–rapid eye movement sleep; REM, rapid eye movement sleep; Sleep efficiency, minutes asleep per time in bed.

Table 4. Mixed-effects regression models of metabolic outcomes
Model 1: outcome—4-h postdinner AUC-glucose (mg/dL*h)
Fixed effects	β coefficient	95% CI	P
Late dinner	88.8	70.3 to 107.3	< .001
Habitual sleep onset	17.7	–5.0 to 40.3	.127
Late dinner × habitual sleep onset	–28.4	–40.4 to –16.5	< .001
Model 2: outcome—postdinner FAO rate (%/h)
Fixed effects	β coefficient	95% CI	P
Late dinner	–1.1	–1.6 to –0.6	< .001
Habitual sleep onset	–.5	–1.5 to 0.6	.375
Late dinner × habitual sleep onset	.6	–0.04 to 1.21	.067

β coefficients are obtained from the fixed part of mixed effects models, in which each metabolic outcome was regressed against the listed fixed factors and the random factor subject number. Bold P values mean statistically significant.
Abbreviations: AUC, area under the curve; FAO, fatty acid oxidation; Late dinner, 0 = routine dinner visit; 1 = late dinner visit; Habitual sleep onset, average of 2 preadmission mean sleep onset measurements by actigraphy watch, expressed as hour postmidnight; Late dinner × habitual sleep onset, interaction term of late dinner and habitual sleep onset; postdinner FAO rate, cumulative FAO at 14 hours after dinner divided by 14 hours.

Table 5. Mixed-effects regression models of metabolic outcomes in male and female participants
Male participants
Outcome	Fixed factor	β coefficient	95% CI	P
4-h postdinner AUC-glucose (mg/dL*h)	Late dinner	84.1	42.3 to 125.9	< .001
Postdinner FAO rate (%/h)	Late dinner	–.6	–1.18 to 0.01	0.05
Female participants
Outcome	Fixed factor	β coefficient	95% CI	P
4-h postdinner AUC-glucose (mg/dL*h)	Late dinner	73.9	45.7 to 102.0	< .001
Post-dinner FAO rate (%/h)	Late dinner	–.8	–1.74 to 0.07	0.07

This is a subgroup analysis performed in male and female participants, respectively. β coefficients are obtained from the fixed part of mixed-effects models, in which each metabolic outcome was regressed against the fixed factor and the random factor subject number. Bold P values mean statistically significant.
Abbreviations: AUC, area under the curve; FAO, fatty acid oxidation; Late dinner, 0 = routine dinner visit, 1 = late dinner visit; postdinner FAO rate, cumulative FAO at 14 hours after dinner divided by 14 hours.

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Metabolic Effects of Late Dinner in Healthy Volunteers

A Randomized Crossover Clinical Trial

Abstract and Introduction

Abstract

Introduction

Tables

Tables

Tables

Tables

Tables

References

Authors and Disclosures

Authors and Disclosures

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