# Time-Restricted Eating, Cardiometabolic Health in Obesity and The Optimal Length of the Eating Window

**Authors:** Bianca Monteiro Silva, Gabriela Geraldo Benzoni, Marcela Coffacci de Lima Viliod, Caroline Fogagnolo, Gabriela Ferreira Abud, Gabriela Ueta Ortiz, Ivo Vieira de Sousa Neto, Ana Cláudia Rossini-Venturini, Sofia Germano Travieso, Ellen Cristini de Freitas

PMC · DOI: 10.1007/s13668-026-00742-8 · Current Nutrition Reports · 2026-03-09

## TL;DR

This review examines how different eating window lengths in time-restricted eating affect cardiometabolic health in people with obesity.

## Contribution

The study identifies 8–10 hour eating windows as the most sustainable and effective for cardiometabolic benefits in TRE.

## Key findings

- Short eating windows (4–6h) show metabolic benefits but poor adherence due to hunger and fatigue.
- Moderate eating windows (8–10h) balance metabolic benefits and adherence effectively.
- Long eating windows (12–14h) are easier to follow but offer limited metabolic benefits and may disrupt circadian rhythms.

## Abstract

This narrative review aims to evaluate how the duration of eating windows influences the cardiometabolic effects of Time-Restricted Eating (TRE) protocols among individuals with obesity. In the context of the global obesity epidemic, TRE has emerged as a promising dietary approach, alternative to conventional energy restriction, capable of improving cardiometabolic health by aligning food intake with circadian rhythms. However, due to the heterogeneity across TRE protocols, the impact of eating windows length on these outcomes remains uncertain. Therefore, this review comprehensively analyzes clinical trials assessing cardiometabolic responses across various durations of eating windows to identify which protocol may provide the greatest benefits.

Short eating windows (4–6 h), although associated with promising metabolic outcomes, often exhibit poor adherence due to increased hunger, fatigue and social constraints, limiting their long-term viability. Moderate eating windows (8–10 h) appear to offer the optimal balance between metabolic benefits, minimal adverse effects and adherence. Long eating windows (12–14 h), despite higher adherence, provide limited metabolic outcomes and are frequently associated with circadian misalignment, potentially increasing the risk of obesity and related metabolic disorders. All the data mentioned were obtained from clinical trials.

TRE has evolved as a promising strategy to enhance cardiometabolic health, especially in individuals with obesity. Eating windows of 8-10h appear to represent the most sustainable TRE protocol, balancing metabolic efficacy with adherence. Nevertheless, further well-designed, long-term randomized controlled trials incorporating chrononutritional assessments are required to establish the optimal eating window for maximizing health outcomes in obesity.

## Linked entities

- **Diseases:** obesity (MONDO:0011122)

## Full-text entities

- **Genes:** NPAS2 (neuronal PAS domain protein 2) [NCBI Gene 4862] {aka MOP4, PASD4, bHLHe9}, TRE-TTC3-1 (tRNA-Glu (anticodon TTC) 3-1) [NCBI Gene 7193] {aka TRE, TRNAE1, TRNE}, RORA (RAR related orphan receptor A) [NCBI Gene 6095] {aka IDDECA, NR1F1, ROR1, ROR2, ROR3, RORa1}, MLST8 (MTOR associated protein MLST8) [NCBI Gene 64223] {aka GBL, GbetaL, LST8, POP3, WAT1}, CRY2 (cryptochrome circadian regulator 2) [NCBI Gene 1408] {aka HCRY2, PHLL2}, CRY1 (cryptochrome circadian regulator 1) [NCBI Gene 1407] {aka DSPD, PHLL1}, POMC (proopiomelanocortin) [NCBI Gene 5443] {aka ACTH, CLIP, LPH, MSH, NPP, OBAIRH}, RORB (RAR related orphan receptor B) [NCBI Gene 6096] {aka EIG15, NR1F2, ROR-BETA, RORbeta, RZR-BETA, RZRB}, MTOR (mechanistic target of rapamycin kinase) [NCBI Gene 2475] {aka FRAP, FRAP1, FRAP2, RAFT1, RAPT1, SKS}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, LINC-ROR (long intergenic non-protein coding RNA, regulator of reprogramming) [NCBI Gene 100885779] {aka ROR, lincRNA-RoR, lincRNA-ST8SIA3}, BMAL1 (basic helix-loop-helix ARNT like 1) [NCBI Gene 406] {aka ARNTL, ARNTL1, BMAL1c, JAP3, MOP3, PASD3}, NR1D1 (nuclear receptor subfamily 1 group D member 1) [NCBI Gene 9572] {aka EAR1, REVERBA, REVERBalpha, THRA1, THRAL, ear-1}, PER2 (period circadian regulator 2) [NCBI Gene 8864] {aka FASPS, FASPS1}, DEPTOR (DEP domain containing MTOR interacting protein) [NCBI Gene 64798] {aka DEP.6, DEPDC6, hDEPTOR}, PRKAB1 (protein kinase AMP-activated non-catalytic subunit beta 1) [NCBI Gene 5564] {aka AMPK, HAMPKb}, PPARGC1A (PPARG coactivator 1 alpha) [NCBI Gene 10891] {aka LEM6, PGC-1(alpha), PGC-1alpha, PGC-1v, PGC1, PGC1A}, NR1D2 (nuclear receptor subfamily 1 group D member 2) [NCBI Gene 9975] {aka BD73, EAR-1R, REVERBB, REVERBbeta, RVR}, SIRT1 (sirtuin 1) [NCBI Gene 23411] {aka SIR2, SIR2L1, SIR2alpha}, PER1 (period circadian regulator 1) [NCBI Gene 5187] {aka PER, RIGUI, hPER}, AKT1S1 (AKT1 substrate 1) [NCBI Gene 84335] {aka Lobe, PRAS40}, RPTOR (regulatory associated protein of MTOR complex 1) [NCBI Gene 57521] {aka KOG1, Mip1}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, EREG (epiregulin) [NCBI Gene 2069] {aka EPR, ER, Ep}, TERF1 (telomeric repeat binding factor 1) [NCBI Gene 7013] {aka PIN2, TRBF1, TRF, TRF1, hTRF1-AS, t-TRF1}, CLOCK (clock circadian regulator) [NCBI Gene 9575] {aka KAT13D, bHLHe8}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}
- **Diseases:** disordered eating behaviors (MESH:D001068), EI (MESH:D000080146), T2DM (MESH:D003924), Disrupted or insufficient sleep (MESH:D012892), adipose tissue (MESH:D018205), impaired glycemic control (MESH:D007174), glucose (MESH:D018149), RHT (MESH:D014570), time-restricted eating (MESH:D002313), nutritional inadequacy (MESH:D044342), hypertension (MESH:D006973), weight loss (MESH:D015431), Insulin resistance (MESH:D007333), cardiovascular disease (MESH:D002318), ADF (MESH:D007003), fatigue (MESH:D005221), overweight (MESH:D050177), weight gain (MESH:D015430), hepatic steatosis (MESH:D005234), Obesity (MESH:D009765), Metabolic Diseases (MESH:D008659), metabolic dysregulation (MESH:D021081), dyslipidemia (MESH:D050171), sleep disturbances (MESH:D012893), inflammation (MESH:D007249), MetS (MESH:D024821), IR (MESH:C537629), prediabetes (MESH:D011236), irritability (MESH:D001523), cancer (MESH:D009369), diabetes (MESH:D003920)
- **Chemicals:** lipid (MESH:D008055), ATP (MESH:D000255), AMP (MESH:D000249), glucose (MESH:D005947), ROS (MESH:D017382), TG (MESH:D013866), 8-IP (-), fatty acid (MESH:D005227), appetite-regulating hormones (MESH:D054439), 8-isoprostane (MESH:C075750), glycogen (MESH:D006003), cholesterol (MESH:D002784), ketone body (MESH:D007657), blood glucose (MESH:D001786), NE (MESH:D009356), fat (MESH:D005223), Triglycerides (MESH:D014280)
- **Species:** Homo sapiens (human, species) [taxon 9606], Mus musculus (house mouse, species) [taxon 10090]

## Full text

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## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12971787/full.md

## References

6 references — full list in the complete paper: https://tomesphere.com/paper/PMC12971787/full.md

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Source: https://tomesphere.com/paper/PMC12971787