Summary: New research argues that obstructive sleep apnea functions as a persistent, low-grade inflammatory disease that contributes to organ dysfunction and accelerated biological aging.
Source: University of Missouri Columbia.
Researchers pursuing longer, healthier lives are increasingly focused on how sleep and inflammation influence aging and disease.
“Aging has become the next frontier in medicine,” said sleep specialist David Gozal, MD, chair of the Department of Child Health at the University of Missouri School of Medicine.
Gozal explains the difference between chronological age — the number of years lived — and biological age, which reflects physiological condition compared with peers. While chronological age cannot be reversed, biological age can be improved through healthier habits. Sleep quality, he emphasizes, plays a central role in how well a person ages.
In the paper “Obstructive Sleep Apnea and Inflammation: Proof of Concept Based on Two Illustrative Cytokines,” published in the International Journal of Molecular Sciences, the authors reviewed evidence linking obstructive sleep apnea syndrome (OSAS) to systemic inflammation and related organ damage. Their analysis supports the view that OSAS promotes a persistent, low-intensity inflammatory state that can harm multiple body systems.
Leila Kheirandish-Gozal, MD, director of the MU School of Medicine’s Child Health Research Institute, and David Gozal argue that sleep-disordered breathing such as OSAS should be regarded as a chronic inflammatory condition. Repeated airway obstruction in OSAS alters ventilation and lowers blood oxygen levels, events that can trigger and sustain inflammatory responses throughout the body.
Chronic inflammation linked to OSAS is associated with changes in cognition, mood and behavior, along with disturbances in cardiovascular function and metabolism. The authors note connections between OSAS-related inflammation and a range of conditions, including chronic kidney disease, erectile dysfunction, eye disease and cancer, all of which may reflect long-term organ injury driven by inflammatory mechanisms.
To clarify these processes, Kheirandish-Gozal and Gozal carried out an intensive literature review with special attention to two well-studied pro-inflammatory cytokines, tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6). These cytokines serve as representative examples of the broader inflammatory milieu observed in OSAS patients. By contrasting how TNF-α and IL-6 act on tissues and cells, the authors draw a clearer picture of how intermittent hypoxia and disrupted sleep can produce persistent immune activation and downstream organ dysfunction.
Understanding specific inflammatory pathways could enable more targeted therapeutic strategies. At present, common treatments remain surgical removal of enlarged tonsils and adenoids in children and continuous positive airway pressure (CPAP) therapy for many adults. The review suggests that complementary treatments tailored to the inflammatory profile — for example, selective antioxidant therapy such as vitamin C or plant-derived compounds — might help limit or reverse inflammation-driven damage if chosen based on the underlying molecular signals.
Gozal highlights the promise of identifying biomarkers that reveal individual vulnerability to certain inflammatory pathways. Such markers could guide personalized interventions aimed at preventing cellular injury and restoring healthier biological aging.
He envisions that therapies directed at the inflammatory drivers of OSAS could not only reduce symptoms and disease risk but also slow or reverse aspects of biological aging, leading to longer, healthier lives.
Funding: This research was primarily supported by the National Institutes of Health (HL130984 and HL140548) and the Office of Medical Research at the University of Missouri School of Medicine. The authors report no conflicts of interest; the content reflects the authors’ views and not necessarily those of the funding agencies.
Source: Caroline Dohack, University of Missouri Columbia.
Publisher: Organized by NeuroscienceNews.com.
Image source: Public domain.
Original research: Open access article “Obstructive Sleep Apnea and Inflammation: Proof of Concept Based on Two Illustrative Cytokines” by Leila Kheirandish-Gozal and David Gozal, International Journal of Molecular Sciences. Published February 2019.
DOI: 10.3390/ijms20030459
University of Missouri Columbia. “Obstructive Sleep Apnea Linked to Inflammation and Organ Dysfunction.” NeuroscienceNews. Published February 12, 2019.
Abstract
Obstructive Sleep Apnea and Inflammation: Proof of Concept Based on Two Illustrative Cytokines
Obstructive sleep apnea syndrome (OSAS) is common across all ages and especially prevalent in overweight and obese populations. It has been independently linked to neurocognitive, behavioral, and mood disorders as well as cardiovascular and metabolic diseases, contributing to increased mortality risk. In adults, excessive daytime sleepiness often prompts clinical evaluation; children may present differently, sometimes without obvious sleepiness, especially when body mass index is normal. A growing body of evidence supports the conceptual framework that sleep-disordered breathing, and OSAS in particular, functions as a chronic, low-grade inflammatory disease. Under this model, some of the disease manifestations arise from inflammation-driven end-organ dysfunction. This review critically examines published links between OSAS and systemic inflammation, with emphasis on TNF-α and IL-6 as representative pro-inflammatory cytokines within the broader spectrum of inflammatory mediators studied in OSAS patients.