When sleep disrupts nerves: obstructive sleep apnoea linked to neuropathy in type 2 diabetes

Aims: To examine the association between obstructive sleep apnoea (OSA) severity and diabetic peripheral neuropathy (DPN), including small fibre pathology, in individuals with type 2 diabetes (T2D).

Methods: In this cross-sectional study, 228 inpatients with T2D underwent overnight polysomnography to assess OSA, standard evaluations for DPN (signs, symptoms, and nerve conduction studies), and corneal confocal microscopy (CCM) to quantify small fibre morphology. Additional anthropometric (e.g., waist circumference, BMI) and biochemical (e.g., HbA1c, lipids) measurements were collected.

Results: OSA was common, present in 67.5% of participants, and its severity correlated with higher DPN prevalence: 40.5% (no OSA), 52.9% (mild OSA, defined as apnoea-hypopnoea index [AHI] of 5-14 events/hour), and 67.9% (moderate to severe OSA, defined as AHI ≥15). Moderate-to-severe OSA was independently associated with over twice the odds of DPN (AOR = 2.18, p = 0.037) after adjustment for smoking, diabetes duration, HbA1c, dyslipidaemia, abnormal obesity, and other factors. Increasing apnea–hypopnea index was significantly correlated with reduced corneal nerve fibre length and higher nerve fibre tortuosity, indicating small fibre damage.

Conclusions: OSA is not only highly prevalent in T2D but is independently linked to both clinical DPN and small fibre neuropathy. These findings highlight sleep apnoea as a potential contributor to diabetes-related nerve injury.

Comments. A major strength is the comprehensive assessment of both large and small fibres: nerve conduction studies (NCS), 10 g monofilament, and vibration perception for large fibres; and corneal confocal microscopy (CCM), pinprick, and warm/cold thermal discrimination for small fibres. Though the study applies a robust examination across multiple domains of neuropathy, the clinical evaluation of signs and symptoms appears less structured.

The independent association of moderate-to-severe OSA with more than twice the odds of DPN is clinically relevant. The correlation between AHI and corneal nerve fibre loss highlights a link with small fibre pathology; although the explained variance was modest, suggesting that OSA is one of multiple contributors.

This work reinforces the concept that OSA may contribute to diabetes-related complications beyond its metabolic effects, potentially through mechanisms such as intermittent hypoxia, oxidative stress, and inflammation—all of which are known to impair nerve health. Nonetheless, the cross-sectional design precludes causal inference, and residual confounding remains possible. In addition, several relevant aspects of the relationship were not evaluated, including inflammatory biomarkers.

It also remains unclear whether treatment of OSA, for example, with CPAP, can mitigate neuropathy risk in this population. Excluding participants on CPAP reduces confounding and clarifies the association between untreated OSA and neuropathy, but limits generalisability and prevents assessment of whether therapy can prevent or slow DPN, highlighting the need for future longitudinal and interventional studies.

In conclusion, this study provides compelling evidence of an association between OSA and both large- and small-fibre neuropathy in T2D. The findings position OSA as a potential contributor to diabetes complications beyond metabolic control.

Mette Krabsmark Borbjerg

Reference. Lu N, Cheng G, Qian Y, An D, Yin F, Hou Y, Liu X, Lu Q, Ma C, Wang R. The association between obstructive sleep apnoea and diabetic peripheral neuropathy in subjects with type 2 diabetes. Front Endocrinol (Lausanne). 2025 Aug 29;16:1643826. doi: 10.3389/fendo.2025.1643826. PMID: 40951416; PMCID: PMC12425751.

🔗 https://www.frontiersin.org/journals/endocrinology/articles/10.3389/fendo.2025.1643826/full