'Apnea and the biological clock': Heavy snorers have shorter telomeres - especially after age 50

A paper by Taiwanese researchers was published in Scientific Reports: they compared telomere length (TL) in people without obstructive sleep apnea (OSA) and with OSA of varying severity. The main finding: the more severe the nocturnal apnea, the shorter the telomeres, especially in participants over 50 years old. This fits in with the idea that nocturnal hypoxia and inflammation in OSA accelerate cellular aging.

Study Background

Obstructive sleep apnea (OSA) is a common condition in which multiple pauses in breathing and oxygen desaturation occur during sleep due to narrowing of the upper airways. These episodes lead to hypoxia-reoxygenation alternation, sleep fragmentation, and chronic activation of the sympathetic nervous system. This results in a "bundle" of systemic effects: oxidative stress, low-level inflammation, endothelial dysfunction, and metabolic shifts that increase the risk of cardiovascular and metabolic diseases.

Telomeres, the protective regions at the ends of chromosomes, naturally shorten with age, but this process is accelerated by oxidative stress and inflammation. Therefore, telomere length is considered a marker of "biological" aging, not just calendar aging. Hypoxia and repeated "flares" of reactive oxygen species in OSA should theoretically increase telomere wear, especially in blood cells, which are most often used to measure this indicator.

A number of observational studies have already found a link between OSA and telomere shortening, but the results were heterogeneous due to differences in age composition, methods for assessing the severity of apnea (AHI, minimum SpO₂, time below 90%), and methods for measuring telomere length. In addition, in younger patients, compensatory mechanisms (telomerase activity, general "resource" for recovery) can smooth out the differences, while at older ages they are more pronounced.

Against this background, it is important to clarify how exactly the severity of OSA correlates with telomere length and whether there is an age dependence of this effect. Such data are important not only for understanding the biology of the disease, but also for practice: if severe OSA is associated with accelerated "biological aging", then timely diagnosis and treatment (for example, CPAP and body weight control) can be considered as potential measures to slow down age-associated risks.

How the study was conducted

The study included 103 visitors to a sleep clinic, all of whom underwent overnight polysomnography; the final analysis included 99 people (46 men and 53 women) with a full set of data. Participants were divided into four groups based on the apnea-hypopnea index: no apnea, mild, moderate, and severe. DNA was extracted from blood, telomere length was measured by absolute qPCR and expressed as kilobases per chromosome "end". The models took into account age, gender, body mass index, minimum nocturnal saturation, hypoxemia time, and comorbidities. Important: Those who consistently used CPAP therapy for more than 4 hours per night for at least three months were classified as the “no apnea” group, since the treatment removes the pathophysiological triggers of the disease.

What was found

In the overall sample, telomere length was highest in people without apnea and decreased stepwise with increasing severity: about 8.4±5.1 kb in the no apnea group versus ~6.0±3.2 kb for mild, ~5.8±2.2 kb for moderate, and ~4.8±2.7 kb for severe apnea; the differences are statistically significant. In the subanalysis by age, the picture diverged: no significant difference was found for those under 50 years old, and after 50 years, patients without apnea had significantly longer telomeres than patients with moderate and severe apnea (approximately 9.4 ± 6.7 kb versus 4.9 ± 1.5 and 3.8 ± 1.8 kb, respectively). In multivariate models, where the authors "clamped" age, gender, BMI, and concomitant diagnoses, the severity of apnea remained an independent predictor of telomere shortening.

Why might this be so

Obstructive apnea is recurring episodes of partial or complete occlusion of the upper airways during sleep, accompanied by a drop in oxygen and sleep fragmentation. This hypoxia-reperfusion "swing" triggers oxidative stress, proinflammatory cascades, and sympathetic activation - factors that accelerate telomere wear and push cells to stop dividing or undergo apoptosis. The authors also discuss the age aspect: in younger people, protective mechanisms (including possible activation of telomerase and immune compensatory responses) can still offset the impact of apnea on telomeres, whereas after 50 years, accumulated damage and comorbidities make the contribution of apnea more noticeable.

What does this mean in practice

The association of apnea with telomere shortening does not prove causality, but adds another argument in favor of early diagnosis and treatment of sleep-disordered breathing - not only to protect the heart and blood vessels, but also potentially to slow down biological aging. Classical therapy (CPAP) eliminates nocturnal hypoxia and is theoretically capable of relieving some of the "telomere" stress, although this needs to be confirmed prospectively. For middle-aged and elderly patients with snoring, daytime sleepiness, obesity and high blood pressure, the idea is simple: undergo sleep diagnostics and, if apnea is confirmed, achieve good adherence to therapy.

Limitations of the study

This is a cross-sectional study from one clinic with a small sample, so we are observing associations, not causes and effects. Telomere length was measured in peripheral blood leukocytes - this is a convenient but indirect marker of systemic tissue aging. There may be residual confounding from unaccounted lifestyle factors, diet, and low-grade inflammation. In addition, classifying CPAP users as "no apnea" reduces the pathological burden in the control group and may have enhanced the contrast. Finally, longitudinal studies before and after therapy are needed to discuss the modifiability of telomeres in apnea treatment.

Conclusion

Severe obstructive sleep apnea in middle and old age is associated with significantly shorter telomeres, a biomarker of accelerated aging. The results support the concept of apnea as a systemic disease in which nocturnal hypoxia and inflammation are reflected even at the levels of chromosomal protection. The next step is to monitor whether effective apnea therapy slows telomere wear and reduces the "speed" of biological aging in real patients.

Source: Chung Y.-P., Chung W.-S. Telomere shortening in middle-aged and elderly individuals with varying severities of obstructive sleep apnea. Scientific Reports 15, 30277 (published August 19, 2025). https://doi.org/10.1038/s41598-025-15895-9

">Scientific Reports published a paper by Taiwanese researchers: they compared telomere length (TL) in people without obstructive sleep apnea (OSA) and with OSA of varying severity. The main finding: the more severe the nocturnal apnea, the shorter the telomeres, especially in participants over 50 years old. This fits in with the idea that nocturnal hypoxia and inflammation in OSA accelerate cellular aging.

Background of the study

Obstructive sleep apnea (OSA) is a common condition in which multiple pauses in breathing and oxygen desaturation occur during sleep due to narrowing of the upper airways. These episodes lead to hypoxia-reoxygenation alternations, sleep fragmentation, and chronic activation of the sympathetic nervous system. The result is a “bundle” of systemic effects: oxidative stress, low-level inflammation, endothelial dysfunction, and metabolic shifts that increase the risks of cardiovascular and metabolic diseases.

Telomeres, the protective regions at the ends of chromosomes, naturally shorten with age, but this process is accelerated by oxidative stress and inflammation. Telomere length is therefore considered a marker of “biological” aging, not just chronological aging. Hypoxia and repeated “flares” of reactive oxygen species in OSA should theoretically increase telomere wear, especially in blood cells, which are most often used to measure this indicator.

A number of observational studies have already found a link between OSA and telomere shortening, but the results were heterogeneous due to differences in age groups, methods of assessing the severity of apnea (AHI, minimum SpO₂, time below 90%) and methods of measuring telomere length. In addition, in younger patients, compensatory mechanisms (telomerase activity, general "resource" of recovery) can smooth out the differences, while at older ages they are more pronounced.

Against this background, it is important to clarify how exactly the severity of OSA correlates with telomere length and whether there is an age dependence of this effect. Such data are important not only for understanding the biology of the disease, but also for practice: if severe OSA is associated with accelerated "biological aging", then timely diagnosis and treatment (for example, CPAP and body weight control) can be considered as potential measures to slow down age-associated risks.

How the study was conducted

The study included 103 visitors to a sleep clinic, all of whom underwent nocturnal polysomnography; the final analysis included 99 people (46 men and 53 women) with a complete set of data. Participants were divided into four groups based on the apnea-hypopnea index: no apnea, mild, moderate, and severe. DNA was isolated from blood, telomere length was measured by absolute qPCR and expressed as kilobases per chromosome “end”. The models took into account age, gender, body mass index, minimum nocturnal saturation, hypoxemia time, and comorbidities. Important: those who consistently used CPAP therapy for more than 4 hours per night for at least three months were classified as “no apnea” group, since the treatment removes pathophysiological triggers of the disease.

What was discovered

In the overall sample, telomere length was greatest in people without apnea and decreased stepwise with increasing severity: about 8.4±5.1 kb in the no-apnea group versus ~6.0±3.2 kb with mild, ~5.8±2.2 kb with moderate, and ~4.8±2.7 kb with severe apnea; the differences are statistically significant. The picture diverged in the age subanalysis: no significant difference was found for those under 50 years, while after 50 years, patients without apnea had significantly longer telomeres than patients with moderate and severe apnea (approximately 9.4±6.7 kb versus 4.9±1.5 and 3.8±1.8 kb, respectively). In multivariate models where the authors controlled for age, gender, BMI, and comorbid diagnoses, apnea severity remained an independent predictor of telomere shortening.

Why might this be?

Obstructive sleep apnea is recurring episodes of partial or complete upper airway occlusion during sleep, accompanied by a drop in oxygen and sleep fragmentation. This hypoxia-reperfusion "swing" triggers oxidative stress, proinflammatory cascades, and sympathetic activation - factors that accelerate telomere wear and push cells to stop dividing or undergo apoptosis. The authors also discuss the age aspect: in younger people, protective mechanisms (including possible activation of telomerase and immune compensatory responses) can still offset the impact of apnea on telomeres, whereas after 50 years, accumulated damage and comorbidities make the contribution of apnea more noticeable.

What does this mean in practice?

The association of apnea with telomere shortening does not prove causality, but adds another argument in favor of early diagnosis and treatment of sleep-disordered breathing - not only to protect the heart and blood vessels, but also potentially to slow down biological aging. Classical therapy (CPAP) eliminates nocturnal hypoxia and is theoretically capable of relieving some of the "telomere" stress, although this needs to be confirmed prospectively. For middle-aged and elderly patients with snoring, daytime sleepiness, obesity and high blood pressure, the idea is simple: undergo sleep diagnostics and, if apnea is confirmed, achieve good adherence to therapy.

Limitations of the study

This is a cross-sectional study from a single clinic with a small sample size, so we are looking at associations rather than causes and effects. Telomere length was measured in peripheral blood leukocytes, a convenient but indirect marker of systemic tissue aging. There may be residual confounding from unaccounted lifestyle factors, diet, and low-grade inflammation. In addition, classifying CPAP users as “no apnea” reduces the pathological burden in the control group and may have enhanced the contrast. Finally, to talk about telomere modifiability in apnea treatment, longitudinal studies before and after therapy are needed.

Conclusion

Severe obstructive sleep apnea in middle and old age is associated with significantly shorter telomeres, a biomarker of accelerated aging. The results support the idea of apnea as a systemic disease in which nocturnal hypoxia and inflammation are reflected even at the levels of chromosomal protection. The next step is to see whether effective apnea therapy slows telomere wear and reduces the “speed” of biological aging in real patients.

Source: Chung Y.-P., Chung W.-S. Telomere shortening in middle-aged and elderly individuals with varying severities of obstructive sleep apnea. Scientific Reports 15, 30277 (published August 19, 2025). https://doi.org/10.1038/s41598-025-15895-9