Randomized controlled trial for time-restricted eating in overweight and obese young adults

Abstract

Time-restricted eating (TRE) is known to improve metabolic health, whereas very few studies have compared the effects of early and late TRE (eTRE and lTRE) on metabolic health. Overweight and obese young adults were randomized to 6-h eTRE (eating from 7 a.m. to 1 p.m.) (n = 21), 6-h lTRE (eating from 12 p.m. to 6 p.m.) (n = 20), or a control group (ad libitum intake in a day) (n = 19). After 8 weeks, 6-h eTRE and lTRE produced comparable body weight loss compared with controls. Compared with control, 6-h eTRE reduced systolic blood pressure, mean glucose, fasting insulin, insulin resistance, leptin, and thyroid axis activity, whereas lTRE only reduced leptin. These findings shed light on the promise of 6-h eTRE and lTRE for weight loss. Larger studies are needed to assess the promise of eTRE to yield better thyroid axis modulation and overall cardiometabolic health improvement.

Keywords: Health sciences; Human metabolism; Obesity medicine.

Conflict of interest statement

The authors declare no competing interests.

© 2022 The Author(s).

Figures

Graphical abstract

Figure 1

Time-restricted eating (TRE) interventions and CONSORT flow diagram (A) TRE interventions. Participants were randomized to a control group (ad libitum intake), 6-h eTRE group (ad libitum intake from 7:00 a.m. to 13:00 p.m.), or 6-h lTRE group (ad libitum intake from 12:00 p.m. to 18:00 p.m.). (B) CONSORT flow diagram describing the process of participant enrollment, intervention, and data analysis.

Figure 2

Weight and body composition (A–D) Changes in percentage weight loss (A), fat mass (B), percent body fat (C), and lean mass (D) after 4 and 8 weeks of intervention. Data are presented as least squares mean ± SEM; ∗p < 0.05 versus control group, ∗∗p < 0.01 versus control group, ∗∗∗p < 0.001 versus control group, ##p < 0.01 versus eTRE group. See also Figure S1 and Tables S2 and S4.

Figure 3

Cardiometabolic risk markers (A) Glucose regulation. C-P, C-peptide; HOMA-IR, homeostasis model assessment insulin resistance. (B) Blood pressure. BP, blood pressure. (C) Lipid profile. TC, total cholesterol; TG, triglyceride; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol. (D) Hormones. TSH, thyroid-stimulating hormone; TT3, triiodothyronine. Data are presented as least squares mean ± SEM; ∗p < 0.05 versus control group, ∗∗p < 0.01 versus control group, ∗∗∗p < 0.001 versus control group, ###p < 0.001 versus eTRE group. See also Figure S2 and Tables S1, S2, S4, and S5.

Figure 4

Oxidative stress markers and inflammatory (A–G) Changes in superoxide dismutase (SOD) (A), malondialdehyde (MDA) (B), 8-isoprostane (C), high-sensitivity C-reactive protein (hs-CRP) (D), tumor necrosis factor alpha (TNF-α) (E), interleukin-6 (IL-6) (F), and cortisol (G) levels after 4 and 8 weeks of intervention. Data are presented as least squares mean ± SEM; ∗∗∗p < 0.001 versus control group, #p < 0.05 versus eTRE group, ##p < 0.01 versus eTRE group. See also Table S2.

Figure 5

Subjective appetite Participants rated their appetite on a 0–100 mm visual analog scale, ranging from “Not at All” (0 mm) to “Extremely” (100 mm). (A–E) Hunger (A), capacity to eat (B), desire to eat (C), fullness (D), and stomach fullness (E) in the morning, midday, and evening in 8 weeks. Data are presented as mean ± SEM; ∗p < 0.05 versus control group, #p < 0.05 versus eTRE group.

Figure 6

Change in eating window and compliance (A and B) Mean time and SD for the participant started and stopped eating at baseline (red) and intervention (blue) in the 6-h eTRE (A) and 6-h lTRE group (B) y axis: each blue/red combination represents an individual participant. x axis: clock hour for eating event. (C) Daily compliance of the dietary regimen for the 6-h eTRE and lTRE groups during the 8-week intervention period. See also Figure S3.