Study Reveals Distinct Cognitive Changes in Men with Untreated Obstructive Sleep Apnea and No Co-Morbidities - medtigo



Study Reveals Distinct Cognitive Changes in Men with Untreated Obstructive Sleep Apnea and No Co-Morbidities

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Obstructive sleep apnea (OSA) is a sleep disorder affecting millions worldwide. It is characterized by repeated episodes of partial or complete obstruction of the upper airway during sleep, which can cause loud snoring, choking, or gasping for air and disrupted sleep. OSA has been linked to numerous health problems, including cardiovascular disease, metabolic disorders, and cognitive impairment. 

Cognitive decline refers to a gradual decline in mental abilities, such as memory, attention, language, and problem-solving. It is a common problem in aging populations and associated with certain medical conditions, such as Alzheimer’s disease and stroke. Recent studies have shown that OSA may also contribute to cognitive decline in older adults.

According to researchers, obstructive sleep apnoea (OSA) is a persistent breathing condition that happens during sleeping and can cause a range of mental deficits. According to research, people with OSA have difficulty paying attention, making judgments, and recalling recent experiences (episodic memory). Numerous studies have found that people with OSA have much greater rates of depression, anxiety, and other mental illnesses than the general population.  

As per Frontiers in Sleep, cognitive talents are traditionally defined as the more fundamental ability to pay attention and remember information, but also more complicated abilities such as planning, problem-solving, and mental flexibility. OSA impairs long-term verbal and visual memory, expressive and receptive language, and visuospatial and constructional ability. Cognitive domains are not unitary constructs; only a careful deconstruction of their sub-capabilities and susceptibility to various OSA-specific risks and protective factors can provide a more accurate assessment of a patient’s deficits, even though evidence for short-term memory impairments is more dispersed.  

There are also one-way correlations between OSA and neurodegenerative illnesses such as Alzheimer’s. It is unclear how the severity of OSA links to the level of reported cognitive deficits. Establishing a link between OSA, cognitive impairment, and old age has also been difficult. Aging-related physiological changes may increase vulnerability to obstructive sleep apnea. It has been proposed that this is because, regardless of BMI, people become more prone to upper airway collapse in reaction to negative pressure as they age. This is due, in part, to changes in upper airway morphology, which can result in decreased upper airway dilator muscle activity at sleep onset.  

Despite their disparate look, it has been expected that only middle-aged OSA patients will have a typical pattern of cognitive impairments. Some researchers have hypothesized that underlying OSA processes have less impact on the development of impairments than more common cardiovascular and metabolic comorbidities. Patients with OSA typically have preexisting diseases such as systemic hypertension, type 2 diabetes, and dyslipidemia, supporting the idea that these variables contribute to the development of OSA.  

A recent study has found a distinct pattern of cognitive deficits in middle-aged male patients with severe obstructive sleep apnea (OSA), even without other neuropsychiatric, cardiovascular, or metabolic conditions. The study by Bubu et al. in 2020 shows that OSA-related processes may be sufficient for cognitive changes to occur in otherwise healthy male individuals as early as middle age. The findings are consistent with previous studies showing aberrant executive functioning, visuospatial short-term memory, deficits in vigilance, and psychomotor control in OSA patients with multiple comorbidities. 

The study also reports, for the first time, diminished social cognition in this group of middle-aged severe OSA patients. Social and emotional cognition is a crucial ability to interpret and identify socially relevant information, known to be impaired in several psychiatric conditions, including major depressive disorder. The study suggests that disrupting normal sleep processes, particularly REM-related fragmentation, may impair discrete affective neural systems, disrupting the identification of salient affective and social cues.  

Moreover, sleep loss and sleep’s diminished quality and quantity, which are essential features of OSA, have been linked to diminished altruism. One night of sleep loss was shown to trigger the withdrawal of help from one individual to another, with associated fMRI findings showing the deactivation of critical nodes within the social cognition brain network that facilitate prosociality. 

Even without associated co-morbidities, the clinical and societal impact of OSA’s effects on cognition dictates urgent attention and a joint multidisciplinary effort. Approximately one-seventh of the world’s adult population, or approximately one billion people, are estimated to have OSA. The functional neuropsychiatric impact of OSA may go well beyond OSA’s currently best-recognized role in increasing driving and occupational accident risks.  


The study’s limitations include its small size, small control group, multiple comparisons, and cross-sectional design. Including male participants only prevents generalization to female patients, despite the study’s ability to control for possible effects of the estrous cycle.

Future multi-center multi-modal longitudinal studies should confirm these findings and decipher how these cognitive deficits may interplay in men and women with other comorbidity-driven impairments over time. The study supports early treatment for male patients with severe OSA to prevent the widespread intricate physiologic central nervous changes that may already exist. 


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