Obstructive sleep apnea (OSA) is a dangerous condition that can potentially harm individuals. When people with OSA sleep, their throat muscles relax and block airflow into the lungs, causing them to repeatedly stop breathing. Common symptoms of OSA include restless sleep, loud snoring, daytime sleepiness, and prolonged morning headaches, which can significantly affect both the patient and their partner.

Despite its severity, OSA is underdiagnosed, with estimates suggesting that it may affect 15 to 30% of men and 10 to 15% of women, approximately 1 billion adults worldwide, of which 80% are unaware of their condition. Major risk factors for OSA include middle or old age, obesity, smoking, chronic nasal blockage, high blood pressure, and being male.

A recent study published in Frontiers in Sleep has shown that obstructive sleep apnea (OSA) can lead to early cognitive decline in middle-aged men, regardless of their overall health and weight. The research was conducted by scientists from the UK, Germany, and Australia, and represents the first evidence of such a link.

The findings reveal “poorer executive functioning and visuospatial memory and deficits in vigilance, sustained attention, and psychomotor and impulse control in men with OSA. Most of these deficits had previously been ascribed to co-morbidities,” remarks lead author Dr. Ivana Rosenzweig.

They “also demonstrated for the first time that OSA can cause significant deficits in social cognition.”

A unique cohort with no co-morbidities

Rosenzweig and the research team investigated 27 male participants aged between 35 and 70 years old who were diagnosed with mild to severe OSA but did not have any co-morbidities, which is a rare case. Most individuals with OSA tend to have additional health conditions such as cardiovascular and metabolic disease, diabetes, depression, chronic systemic inflammation, or stroke.

The men did not have a current history of smoking or alcohol abuse, and had a body mass index (BMI) below 30, indicating that they were not obese. A control group of seven men matched for age, BMI, and education but without OSA was also studied. The OSA diagnosis was confirmed through a WatchPAT test of their respiratory function during sleep at home, as well as video-polysomnography at King’s College sleep center. The latter method involved measuring the brain waves of sleeping subjects with electroencephalography (EEG), while tracking their blood oxygen levels, heart rate, breathing, eye, and leg movements.

The researchers additionally evaluated the participants’ cognitive abilities using a battery of tests called CANTAB, which stands for “Cambridge Neuropsychological Test Automated Battery.”

Early cognitive decline

The findings indicated that individuals with severe OSA had lower scores in vigilance, executive function, short-term visual recognition memory, and social and emotional recognition than the control group, who were matched in terms of age, BMI, and education. Meanwhile, those with mild OSA performed better in these domains than those with severe OSA, but worse than the control group.

“The most significant deficits…were demonstrated in the tests that assess both simultaneous visual matching ability and short-term visual recognition memory for non-verbalizable patterns, tests of executive functioning and cued attentional set shifting, in vigilance and psychomotor functioning, and lastly, in social cognition and emotion recognition,” adds the authors.

According to the authors, the cognitive deficits observed in middle-aged men with OSA can be attributed solely to the condition itself, rather than the common co-morbidities associated with OSA such as systemic hypertension, cardiovascular and metabolic diseases, and type 2 diabetes, as previous studies had suggested.

Not clear how it works

The underlying mechanism of how OSA causes premature cognitive decline remains unclear. However, the authors suggest that intermittent hypoxia and hypercapnia, changes in cerebral blood flow, sleep fragmentation, and neuroinflammation could contribute to cognitive deficits in OSA patients.

“This complex interplay is still poorly understood, but it’s likely that these lead to widespread neuroanatomical and structural changes in the brain and associated functional cognitive and emotional deficits,” points out Rosenzweig.

It is still unclear whether co-existing medical conditions have similar adverse effects on cognitive function that go beyond the direct impact of OSA.

This work “is a proof of concept. However, our findings suggest that co-morbidities likely worsen and perpetuate any cognitive deficits caused directly by OSA itself,” adds Rosenzweig.

“What remains to be clarified in future studies is whether co-morbidities have an additive or synergistic effect on the latter deficits, and whether there is a difference in brain circuitry in OSA patients with or without co-morbidities.”

Source: 10.3389/frsle.2023.1097946

Image Credit: Jeenah Moon/Bloomberg via Getty Images

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