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Karami, Esmail, Mohammadi, Mohammad Taghi, Shirvani, Hossein, Bazgir, Behzad. (1405). The Gut–Brain Axis in Sleep Deprivation: Mechanisms, Dysbiosis, and Potential Therapeutic Avenues. سامانه مدیریت نشریات علمی, 51(8), 533-542. doi: 10.30476/ijms.2025.108475.4351
Esmail Karami; Mohammad Taghi Mohammadi; Hossein Shirvani; Behzad Bazgir. "The Gut–Brain Axis in Sleep Deprivation: Mechanisms, Dysbiosis, and Potential Therapeutic Avenues". سامانه مدیریت نشریات علمی, 51, 8, 1405, 533-542. doi: 10.30476/ijms.2025.108475.4351
Karami, Esmail, Mohammadi, Mohammad Taghi, Shirvani, Hossein, Bazgir, Behzad. (1405). 'The Gut–Brain Axis in Sleep Deprivation: Mechanisms, Dysbiosis, and Potential Therapeutic Avenues', سامانه مدیریت نشریات علمی, 51(8), pp. 533-542. doi: 10.30476/ijms.2025.108475.4351
Karami, Esmail, Mohammadi, Mohammad Taghi, Shirvani, Hossein, Bazgir, Behzad. The Gut–Brain Axis in Sleep Deprivation: Mechanisms, Dysbiosis, and Potential Therapeutic Avenues. سامانه مدیریت نشریات علمی, 1405; 51(8): 533-542. doi: 10.30476/ijms.2025.108475.4351

The Gut–Brain Axis in Sleep Deprivation: Mechanisms, Dysbiosis, and Potential Therapeutic Avenues

Iranian Journal of Medical Sciences
مقاله 1، دوره 51، شماره 8، آبان 2026، صفحه 533-542    اصل مقاله (341.67 K)
نوع مقاله: Review Article
شناسه دیجیتال (DOI): 10.30476/ijms.2025.108475.4351
نویسندگان
Esmail Karami1؛ Mohammad Taghi Mohammadi2؛ Hossein Shirvani1؛ Behzad Bazgir* 1
1Exercise Physiology Research Center, Life Style Institute, Baqiyatallah University of Medical Sciences, Tehran, Iran
2Department of Physiology and Medical Physics, Faculty of Medicine, Baqiyatallah University of Medical Sciences, Tehran, Iran
چکیده
Sleep is fundamental to metabolic regulation, cardiovascular health, immune balance, and cognitive performance. Emerging evidence indicates that sleep deprivation alters gut microbial communities and immune signaling, thereby influencing the gut-brain axis. This narrative review synthesized current findings on how sleep loss engages gut–brain pathways and evaluated therapeutic avenues linked to specific mechanisms, drawing on peer-reviewed human and animal studies and prioritizing sleep- and brain-relevant outcomes. Evidence converged on three mechanistic pillars: (1) circadian and microbial misalignment, which disrupts diurnal microbiome dynamics; (2) inflammatory and barrier dysfunction loops that increase permeability and immune activation; and (3) altered neurotransmitter and metabolite signaling, including shifts in tryptophan pathways and reduced short-chain fatty acid production, with downstream effects on neuroinflammation and plasticity. Human data supported associations between sleep loss, poor sleep quality, and impaired cognition. However, causal inference was limited by small sample sizes, study heterogeneity, and mixed endpoints. Interventions such as probiotics, prebiotics, postbiotics, synbiotics, diet-based short-chain fatty acid strategies, and chronobiotics are biologically plausible, yet they are supported mainly by small trials or preclinical models. Fecal microbiota transplantation shows exploratory, yet faces significant safety, standardization, and regulatory challenges. Collectively, the evidence indicated that sleep deprivation disrupts gut microbiota composition and gut-brain signaling, with consequences for neuroinflammation, neurotransmitter balance, and cognition. This review highlighted the consequent need for standardized endpoints, strain-resolved microbiome analyses, and well-powered randomized controlled trials.

تازه های تحقیق

Esmail Karami (Google Scholar) 
Behzad Bazgir (Google Scholar) 

کلیدواژه‌ها
Sleep deprivation؛ Gut–brain axis (GBA)؛ Microbiota؛ Neuroinflammation؛ Probiotics
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