The introduction is also posted on Spotify as a podcast by “Gerry at The Health Equation”

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Gerry Gajadharsingh writes:

“Obstructive sleep apnoea (OSA) continues to emerge as one of the most clinically important—yet highly modifiable—risk factors influencing long-term brain health. A new study, published in JAMA Neurology and presented at the 2025 American Academy of Neurology meeting, has reinforced what many of us working at the interface of respiratory physiology, autonomic regulation, and metabolic health have long suspected: untreated OSA does not simply disrupt sleep; it disrupts the brain. In this very large cohort of over 11 million US veterans, OSA was associated with almost double the risk of developing Parkinson’s disease, a neurodegenerative condition medicine typically considers to be largely non-modifiable. Crucially, early treatment with CPAP reduced this risk by 31%, suggesting that the way we breathe at night may meaningfully influence the trajectory of our neurological ageing.

From a physiological standpoint, this makes intuitive sense. Repeated episodes of apnoea create cycles of intermittent hypoxia, hypercapnia instability, sympathetic activation, and sleep fragmentation. This chronic pattern erodes autonomic balance, increases systemic inflammation, and places ongoing metabolic stress on neurons. Over time, such oscillations in oxygen and CO₂ homeostasis are likely to reduce the resilience of dopaminergic pathways that are already vulnerable in individuals predisposed to Parkinsonian disorders.

This is where the tools I routinely use in clinic—capnometry and heart-rate variability (HRV)—become essential. Capnometry allows us to assess the patient’s CO₂ regulation in real time, offering objective insight into chronic hyperventilation tendencies or unstable breathing patterns that often accompany OSA, even during wakefulness. HRV, meanwhile, reflects the health of the autonomic nervous system, which is profoundly affected by nocturnal breathing disturbances. When HRV is chronically low and ETCO₂ patterns are erratic, it is a strong clue that sleep-disordered breathing may be undermining neurological, cardiovascular, and psychological resilience long before overt disease appears.

It is also important to highlight the role of nasal breathing. Nasal airflow supports nitric oxide production, optimises CO₂tolerance, stabilises the diaphragm, and maintains upper airway tone. Mouth breathing, by contrast, increases airway collapsibility and worsens OSA severity. Encouraging patients to restore nasal breathing during both day and night—sometimes incorporating simple functional interventions such as myofunctional therapy or supportive taping techniques—can meaningfully improve nocturnal respiratory stability and autonomic balance. For some individuals, these foundational strategies help reduce CPAP pressures or increase CPAP tolerance; for others, they may reduce apnoea burden independently.

Taken together, this new research adds compelling weight to the argument that OSA should be viewed as a treatable neurological risk factor. Early screening—especially in patients with autonomic dysregulation, low HRV, chronic hyperventilation patterns, or metabolic stress—allows us to intervene before irreversible neurodegenerative processes become established.”

https://www.thehealthequation.co.uk/heart-rate-variability-hrv-and-capnometry/

https://www.thehealthequation.co.uk/breathwork-breathing-re-training/

Medscape

Dawn Attride

Obstructive sleep apnoea (OSA) has been linked to a significantly increased risk for Parkinson’s disease (PD). However, early treatment of OSA with continuous positive airway pressure (CPAP) significantly lowered the risk for PD.

“If you stop breathing and oxygen is not at a normal level, your neurons are probably not functioning at a normal level either. Add that up night after night, year after year, and it may explain why fixing the problem by using CPAP may build in some resilience against neurodegenerative conditions, including Parkinson’s,” lead author Lee Neilson, MD, neurologist and assistant professor of neurology at Oregon Health & Science University in Portland, Oregon, said in a news release.

The findings were initially presented at the American Academy of Neurology (AAN) 2025 Annual Meeting and were published online on November 24 in JAMA Neurology.

A Modifiable Risk Factor

While previous studies have suggested a link between the OSA and PD, Neilson and colleagues are the first to investigate whether CPAP can modify the risk for PD incidence.

Using data from the US Department of Veterans Affairs Corporate Data Warehouse, the investigators analysed data from 11,310,411 veterans (9.8% female; mean age, 60.5 years). Those with incomplete records and those younger than 40 were excluded from the analysis.

OSA and PD were identified based on International Classification of Diseases-10th Revision (ICD-10) codes. In addition, PD was defined by a minimum of 5 years of medical records before the first ICD code and two filled PD medication prescriptions.

Veteran’s use of CPAP was pulled from medical interview data. Age, sex, race, ethnicity, and smoking history were balanced between OSA and non-OSA groups using inverse probability of treatment weighting.

Fewer Falls, Fractures, and Deaths

After accounting for age, sex, race, ethnicity, smoking status, and competing risk for death, the researchers found that OSA was associated with nearly a twofold increased risk for PD (hazard ratio [HR], 1.92, P < .001) compared to no OSA.

At 6 years of follow-up, OSA was associated with 1.61 additional PD cases per 1000 individuals (95% CI, 1.13-2.09). The association was stronger in women than in men.

Both mild and severe OSA were associated with a higher risk for incident PD (mild: HR, 3.17; 95% CI, 2.45-4.11; severe: HR, 3.42; 95% CI, 2.87-4.09; P < .001).

However, this elevated risk was modifiable: CPAP use within 2 years of OSA diagnosis was linked to a 31% lower risk for PD (HR, 0.69; 95% CI, 0.56-0.85) compared with no CPAP.

The association held after adjustment for BMI, vascular comorbidities, rapid eye movement sleep behaviour disorder, hypersomnia, psychiatric conditions, hypertension, traumatic brain injury, and relevant medication exposures.

Early CPAP use was also associated with reduced rates of falls, fractures, and death.

A key limitation of the study was the reliance on electronic health records, which prevented investigators from assessing CPAP adherence beyond the identification of relevant administrative codes.

These data not only suggest that OSA is a modifiable risk factor for PD, they also “establish additional clinical rationale for early screening and intervention of sleep-disordered breathing as a key strategy in supporting brain health,” the investigators noted.