OSA in the aging population: Diagnostic and therapeutic considerations

Abstract

The extremely high prevalence of obstructive sleep apnea (OSA) in the elderly population approaches 50 % and is even higher among individuals older than 80 years, posing substantial challenges in defining an appropriate risk–benefit balance for OSA treatment in this age group. A major barrier to the formulation of coherent, evidence-based recommendations lies in the marked limitations of the available evidence, which is often derived from observational or post hoc analyses, affected by substantial heterogeneity, or based on small samples that lack adequate statistical power to detect clinically meaningful outcomes. Moreover, older adults—particularly the very old and those with multimorbidity or frailty—are systematically underrepresented in randomized controlled trials, further limiting the generalizability of existing findings. In this review, we synthesize the scarce and methodologically heterogeneous evidence on the impact of OSA in older adults, highlight conflicting results supporting either treatment or non-treatment in this population, and delineate the key unresolved clinical and research questions that must be addressed before robust consensus guidelines and informed healthcare policies can be developed.

1. Sleep in older adults

Globally, the number of people aged 65 and older worldwide will more than double in the next 30 years as 1.5 billion people will be 65 years and older by 2050. This trend is particularly evident and rapid in developing regions. This aging of the population will continue to have a massive negative impact on the strained healthcare systems worldwide [1]. Beyond its direct implications for healthcare utilization, population aging is accompanied by profound physiological changes including a marked disruption of an older adult’s daily sleep cycle, which is typically associated with poor quality of life, and increased morbidity and mortality [2,3].

Sleep in older adults differs from that of younger individuals due to age-related changes in several core regulatory systems that govern sleep timing, depth, and stability: 1) circadian rhythm regulation weakens with aging as the amplitude and precision of the central circadian pacemaker decline 2) Sleep homeostasis is also altered, with a reduced accumulation of sleep pressure and diminished slow-wave activity, resulting in lighter, less consolidated sleep and increased nocturnal awakenings 3) arousal thresholds decline, making older adults more susceptible to awakenings triggered by internal or external stimuli, including respiratory events, pain, and environmental noise and 4) sensory processing during sleep becomes less effectively gated, increasing cortical responsiveness to sensory inputs and further compromising sleep continuity and depth. Consequently, epidemiological studies have consistently reported that the prevalence of significant sleep complaints grows steadily with advancing age [4,5].

Sleep is composed of two different physiological states, rapid eye movement (REM) sleep and non-rapid eye movement (NREM) sleep, with NREM divided into three stages; N1 being the lightest and N2 and N3 being progressively deeper, that is, increasingly difficult to be awakened from. Sleep is typically organized into 90-min NREM/REM cycles. N3 sleep, also called deep sleep or slow wave sleep (SWS) because of its low-frequency electroencephalogram (EEG) profile, predominantly occurs in the first half of the night while most REM sleep occurs in the last half of the night [6]. This cyclic pattern can be interrupted by wakefulness, which may be infrequent and brief or frequent and of long duration (4). The most striking change in sleep in older adults is the frequent interruption of sleep by periods of wakefulness, possibly the result of age-dependent changes in homeostatic and/or wake-maintenance processes [7,8]. Older adults are also more easily aroused from nighttime sleep by environmental stimuli. These changes are indicative of impaired sleep maintenance and depth and characterize the sleep of older adults as lighter or more fragile than that of younger adults. Other age-dependent changes in sleep include decreases in total sleep time, sleep efficiency (percent of time in bed asleep), SWS and REM sleep, and increases in stages N1 and N2 sleep [7]. These age-dependent changes are mirrored by increased likelihood of napping or falling asleep during the day. Aging is also associated with a tendency to both fall asleep and awaken earlier and to be less tolerant of phase shifts in time of the sleep/wake schedule, such as those produced by jet lag, seasonal clock changes and shift work. All these changes suggest an age-related breakdown of the normal young-adult sleep/wake cycle [8]. Clearly sleep changes significantly with advancing age, but the questions remain: when do these changes occur, what is their cause, and are they treatable and perhaps partially reversible?

An extensive meta-analysis of objective sleep measures across the human life span by Ohayon et al. [7] indicates that the bulk of the changes seen in adult sleep patterns occur between early and middle adulthood, between ages 19 to 60, and that after age 60 such sleep-pattern changes effectively asymptote, declining only minimally with further advancing age (see Fig. 1) [7]. It is important to remember that Ohayon and colleagues used very rigorous selection criteria in choosing the study subjects for their meta-analyses. The approximately 2400 subjects were not representative of the entire older population but rather represent individuals who are “optimally” or “successfully” aging. What these findings also demonstrated is that when the comorbidities that typically accompany the aging process are controlled for and optimal aging examined, then the bulk of age-related sleep changes are found to occur by middle adulthood and that, after age 60, assuming one remains in good health, further age-related sleep changes are, at most, modest. Conversely, if comorbidities, such as physical or mental illnesses or primary sleep disorders such as obstructive sleep apnea, insomnia or restless legs syndrome are present, then age-related sleep changes will be exacerbated [7,8].

Fig. 1.

Schematic diagram illustrating the potential pathways that promote the emergence or worsening of frailty in the elderly.

2. Aging and upper airway function

The prevalence of sleep apnea increases with age. In young women, the prevalence is 1.4 %. In both men and women 70 years or older, it reaches 90 % and more [9,10] (Table 1). Of important relevance is the fact that the presence of OSA in the aged adults is associated with increased mortality [11,12]. This remarkable increase in prevalence is explainable, at least in part, by escalating body weight with age. However, aging alone irrespective of changes in BMI can increase [13]: 1. OSA severity; 2. Higher Pcrit, indicating higher upper airway collapsibility; 3. Neck and waist circumference; 4. Upper airway and visceral fat volumes; 5. Tongue and abdominal muscle fat infiltration. These findings suggest that aging-associated upper airway and visceral fat infiltration may help to explain the association between OSA and increasing age.

Table 1.

Potential factors contributing to the increasing prevalence of OSA with aging.

In a detailed cross-sectional physiological study, Edwards and colleagues [14] compared the effects of aging on four known pathophysiologic traits of OSA; upper airway collapsibility, upper airway dilator muscle activity/responsiveness, respiratory arousal threshold, and stability of ventilatory control as measured by sensitivity (loop gain) and minute ventilation, in 10 young adult and in 10 older adult patients (mean age of 32 years and 65 years, respectively) with treated OSA, matched by body mass index(mean body mass index, 34.9 and 31.3 kg/m², respectively) and sex. There was no significant difference in continuous positive airway pressure therapeutic requirement in the younger compared with the older patients (11.4 vs.11.9 cm H₂O), continuous positive airway pressure adherence (6.5 vs. 6.6 h/night), major sleep characteristics, or respiratory event frequency (apnea–hypopnea index of 48.8 vs. 43.0 events/hr). In the older patients however, upper airway collapsibility tended to be higher (P value = 0.05), whereas the sensitivity of the ventilatory control system and minute ventilation were significantly lower (P value < 0.05). The upper airway dilator muscle responsiveness and arousal threshold did not differ significantly between the groups, although the small sample size may have had inadequate power to detect a difference. Taken together this suggests that severe OSA in older obese patients is caused primarily by worsening of upper airway collapsibility, which is offset by reduced ventilatory demand and feedback control sensitivity. In comparison, OSA in younger patients is driven primarily by increased ventilatory sensitivity and demand, and less by airway collapsibility. The study identified ventilatory demand as a potential fifth physiologic trait because lowering of the ventilatory demand, through either metabolic demand or ventilatory controller characteristics (i.e., reducing the slope of the ventilatory response to carbon dioxide or shifting the curve to the right) demonstrated the potential to achieve stable breathing [14]. In a study focused on the hypoxic response during exposure to high altitude hypoxia, the ventilatory response to hypoxia increased while desaturation was less pronounced with ageing in men. Cardiac responses to hypoxia were blunted with ageing in both sexes in the cross-sectional arm encompassing 4675 subjects, similar results were found in the 10-year longitudinal study with decreases in cardiac and increases in ventilatory response to hypoxia with ageing [15].

Aging is also associated with reduced circadian amplitude, phase-advance and increased fragmentation of sleep-wake rhythms. A recent study in over 1000 older adults followed annually for up to 16 years found that decreased rhythm strength, reduced stability, or increased variation were associated with a higher risk of incident frailty and faster progress of frailty over time [16]. This circadian dysregulation can exacerbate nocturnal sleep fragmentation, alter ventilatory stability and metabolic/inflammatory profiles, worsen daytime symptoms, and reduce tolerance or adherence to therapies—suggesting that circadian stabilization (light therapy, sleep-schedule regularization, timed melatonin) may complement conventional OSA management in older adults.

Likewise, the post-menopausal decline in estrogen and progesterone reduces upper-airway muscle tone and central ventilatory drive and is accompanied by changes in fat distribution, all of which increase airway collapsibility and OSA prevalence/severity in older women [17]; these hormonal effects can modify the magnitude of benefit from CPAP, oral appliances or positional therapy and imply that menopausal status and, where appropriate, hormone-modulating strategies should be considered when individualizing diagnostic thresholds and therapeutic plans for late-life OSA.

3. Frailty and age-related vulnerability in OSA

Along with the physiological consequences of the aging upper airway function, aging will progressively be accompanied by features of frailty. Aging-associated frailty is traditionally defined as a multisystem aging syndrome characterized by decreased physiological and functional reserve in physical, mental, and physiological functions that cumulatively enhance the vulnerability to adverse health outcomes [18]. This term can be extrapolated to 3 major categories, namely Frailty Syndrome (age-related declines in muscle strength, stamina, endurance, and overall fitness), Clinical Frailty (based on criteria such as weakness, slowness, low physical activity, exhaustion, and unintentional weight loss), and Biological Frailty (reflected by chronic inflammation and hormonal changes that reduce muscle function and overall resilience). A substantial body of research has focused on preventive strategies and interventions to help prevent or mitigate frailty. In this context, behaviors that can increase physical activity and fitness or alternatively improve sleep are routinely incorporated into such approaches considering the strong associations between inadequate sleep quantity and quality and frailty [19–23]. It is therefore not surprising that OSA and frailty are closely intertwined in aging individuals through several bidirectional physiological and systemic mechanisms encompassing intermittent hypoxia and sleep fragmentation induced systemic inflammation and oxidative stress, and their consequences manifesting as neurocognitive impairments and depression, reduced physical activity and muscle wasting, metabolic dysfunction, hypertension and cardiovascular disease [24–29] (see Fig. 1).

Emerging evidence indicates that OSA may contribute to the hormonal dysregulation that characterizes biological frailty: intermittent hypoxia and sleep fragmentation can perturb the hypothalamic–pituitary–adrenal and somatotropic axes (with relative reductions in GH/IGF-1 and sex steroids), promote hypercortisolemia and proinflammatory cytokine release, and alter metabolic hormones (insulin, leptin, ghrelin), thereby favoring sarcopenia, insulin resistance and loss of physiological reserve—although causal pathways are incompletely defined and some hormonal abnormalities may be at least partly reversible with effective OSA treatment [30–32].

To address the question regarding whether treatment of OSA may reduce the incidence of frailty, a study by Xue et al. [33] in 70 subjects (mean age 68.7 years at enrollment) with OSA and adherent to continuous positive airway pressure (CPAP) reported that after a median follow-up period of 4.5 years, a significant reduction in incident frailty was observed even after adjustments for potential confounders (11.26 % in CPAP-treated subjects vs. 21.83 % in untreated OSA, P = 0.045). We are unaware of any additional studies to date that have specifically explored the impact of treatment on mitigation of frailty in OSA patients and whether increased frailty actually enhances the severity of OSA. However, initial guidelines have been formulated to address these important issues [34].

4. Definition of OSA syndrome (OSAS) in the elderly patient

The International Classification of Sleep Disorders (ICSD-3) defines OSAS broadly, applicable across all ages, as: 1) clinical symptoms such as diurnal sleepiness, witnessed apnea, or cardiometabolic abnormalities with an apnea-hypopnea index (AHI) ≥5 events per hour; or 2) ≥15 predominantly obstructive events per hour without specific symptoms or comorbidities. In elderly patients, this definition may be less appropriate considering that: (1) daytime sleepiness and symptoms of OSAS are often absent, 2) clinical presentations include atypical symptoms like fatigue, insomnia, or cognitive impairment which are not mentioned in the ICSD-3 definition, 3) cardiometabolic abnormalities are often already present as related more to aging rather than to OSA. Regarding sleepiness, considering that sleepiness assessed with questionnaire in the elderly might result in underestimating of sleepiness, many different reasons can explain why such symptom can be less frequent in the elderly: altered sleep–wake regulation, compensatory daytime napping that might result in less perceived daytime sleepiness, multimorbidity overlap and psychomotor slowing [35].

In older adults, the clinical relevance of OSA should therefore be interpreted through a broader, age-specific lens that extends beyond traditional symptoms and cardiometabolic endpoints. Emerging evidence suggests that OSA may contribute to geriatric-relevant outcomes such as sarcopenia [36], impaired balance, and falls [37], nocturia, and neuropsychiatric manifestations including depression, anxiety, and cognitive vulnerability. These outcomes, which directly affect independence, functional status, and quality of life, are often of greater clinical importance to older individuals than excessive daytime sleepiness or long-term cardiovascular risk. Incorporating such symptom domains and functional outcomes into both clinical assessment and research frameworks may allow for a more meaningful identification of older patients who stand to benefit from targeted OSA interventions.

Overview of diagnostic tools and treatment options in elderly patients with OSAS Tools for OSAS diagnosis and symptoms evaluation might also be of limited value in the elderly population: the Epworth Sleepiness Scale remains unvalidated in the elderly who are often unable to answer all the ESS items [38]. The lack of appropriate screening tools in this population adds to the magnitude of underdiagnosis even in elderly patients with OSAS features: in a sample of 1052 community-dwelling Medicare beneficiaries (>65 years old), 56 % were classified through questionnaires as high-OSA-risk patients, but only 8 % were tested for OSA [39]. Similarly, use of a widely used tool such as STOP-BANG failed to identify a considerable proportion of OSA older adult patients (32). Notwithstanding, a moderate association between frailty and sleep problems and OSA emerged in a cohort of aging adults [40].

From an instrumental standpoint, in-laboratory polysomnography (PSG) remains the diagnostic gold standard, as it provides comprehensive information on sleep architecture, respiratory events, arousals, and comorbid sleep disorders such as central sleep apnea or Cheyne–Stokes respiration. This is particularly relevant in elderly patients, who frequently present with insomnia, fragmented sleep, and multiple comorbidities. While in-lab polysomnography (PSG) remains the gold standard, home polygraphy (PG) is widely used for suspected moderate-to-severe OSA due to its accessibility. However, PG can lead to misestimation of AHI due to insomnia, which is highly prevalent in the elderly, difficulty with self-application, particularly when the hook up procedure is not performed by a sleep technician and increased artifact risk. Furthermore, PG lacks EEG, precluding adequate assessment of sleep duration and arousals. This is critical in elderly patients, who often suffer from insomnia and other comorbidity related-sleep conditions such as central sleep apnea (CSA)/Cheyne-Stokes respiration (CSR). Conversely, PSG allows a more thorough definition of OSA, but is often cumbersome, not widely available, and less well tolerated among older adults. It should however be prioritized in complex cases with multiple comorbidities or sleep-related symptoms. Finally, the AHI criteria currently used in clinical practice may not necessarily be accurate to define disease severity in elderly populations considering the increased collapsibility of the upper airway with chronological age [41], [42].

Treatment options for OSAS in elderly patients include continuous positive airway pressure (CPAP), oral appliances, and positional therapy. CPAP remains the first-line treatment for moderate-to-severe OSAS and is effective in improving respiratory events and symptoms, although adherence may be reduced by cognitive impairment. Oral appliances represent a valid alternative in patients with mild-to-moderate OSAS or in those intolerant to CPAP, but their efficacy may be limited by dental status, temporomandibular joint disorders, and reduced mandibular protrusion capacity, which are more prevalent with aging. Positional therapy may be beneficial in selected patients with position-dependent OSAS, although long-term adherence and effectiveness in frail or mobility-limited elderly individuals remain uncertain. Overall, diagnostic and therapeutic strategies in older adults should be individualized, balancing accuracy, feasibility, tolerance, and expected clinical benefit.

5. Consequences of OSA in older adults

5.1. Cognitive and behavioral

OSAS in aging patients appears to adversely impact cognitive and behavioral functions thereby accelerating the rate of cognitive decline [43]. The major mechanisms include intermittent hypoxemia and disrupted sleep and sleep architecture changes, leading to central nervous system, inflammation, oxidative stress, endothelial dysfunction including blood brain barrier and altered glymphatic clearance, all of which contribute to brain dysfunction. These processes also underlie the progression of small-vessel disease, strokes, reduced neurogenesis, potentially creating a vicious cycle that worsens sleep and brain health, increasing senile dementia risk [44]. Current evidence highlights the associations between OSA and deficits in attention, vigilance, episodic memory, working memory, and executive function, with less consistent effects on psychomotor, language, and visuospatial abilities [45]. A meta-analysis of fourteen studies covering a total of 4 288 419 elderly patients showed that those with OSA were 26 % (risk ratio, 1.26; 95 % CI, 1.05–1.50) more likely to develop cognitive impairments with a less pronounced worsening of executive function [46].

Behaviorally, cognitive deficits manifest as forgetfulness, poor decision-making, and difficulty with daily tasks, all of which are often more likely with advanced age, even if OSAS is not present. Such symptoms can be exacerbated by excessive daytime sleepiness, which contributes to depressive symptoms, impaired social interactions, and reduced work effectiveness [47]. Personality changes and automatic behaviors are also noted, particularly in aged adults.

OSAS is linked to increased Alzheimer’s disease (AD) biomarkers, including amyloid-β and tau deposition, with EEG changes reflected as slow oscillations and spindles mirroring AD patterns, suggesting shared mechanisms [48]. CPAP therapy may improve attention, particularly in severe cases, but its long-term efficacy remains a matter of concern, with 30 % of patients refusing treatment and over 33 % discontinuing use [49]. A recent pilot randomised controlled trial (RCT) showed that CPAP treatment was associated with modest improvements in verbal learning and memory retention compared with no treatment [50]. However, no improvements in processing speed or executive functioning were seen in the CPAP arm (primary endpoint). A systematic review and meta-analysis of RCTs confirmed the role of CPAP on some domains of the cognitive functions such as the trail making test with no significant improvements on other cognitive domains (information processing speed, executive functions, working memory [51]. Therefore, further longitudinal studies are needed to clarify the potential benefits of CPAP and the specific components of OSAS (e.g., hypoxic burden; respiratory arousal index) that drive impairments in cognitive and behavioral outcomes. Studies in animal models have indicated that aging animals exposed to intermittent hypoxia mimicking OSA results in more severe reductions in proteasome activity and cognitive performance, likely due to increased neuronal cell apoptosis within specific brain regions [52]. In a more recent study involving mice exposed to intermittent hypoxia [53], older mice exhibited evidence of increased inflammation, fibrosis, and oxidative stress long with concomitant reductions in neuromuscular control. Thus, increased vulnerability of older patients to OSA may specifically manifest functional brain aspects that may vary across subjects while the recovery form such insults may or may not occur even with ideal treatment.

5.2. Cardiovascular

In elderly patients OSAS is strongly associated with an increased risk of cardiovascular events, including stroke, heart failure, and hypertension [54]. Several large observational studies have confirmed that the severity of OSA, as measured by the AHI, correlates with higher cardiovascular risk and mortality in those aged 65 and older [55]. Untreated severe OSA is linked to significantly higher rates of stroke and heart failure, while treatment with CPAP appears to reduce this risk [56]. However, evidence on coronary heart disease (CHD) is less consistent: while OSA elevates CHD risk in younger populations, this association appears weaker or absent in older adults [57,58]. Similarly, the relationship between OSA and atrial fibrillation in the elderly remains poorly defined, even if CPAP reduces recurrence rates [59]. Observational data support a modest link between OSAS and hypertension in older individuals, but increasing age seems to attenuate this association [60] Furthermore, although data from observational studies seems to suggest that CPAP treatment might be associated with a longer survival in very elderly persons with moderate to severe OSA [61], data from randomised controlled studies showed that CPAP treatment was not associated with improvements in blood pressure [62] or new cardiovascular events [63] in elderly (≥70 years) and very elderly (≥80 years) patients.

A recent post hoc analysis of pooled randomized controlled trials confirmed that continuous positive airway pressure preferentially improves cardiovascular outcomes in high-risk OSA in the setting of secondary prevention [63]. Although a specific sub-analysis on elderly patients was not performed, given the median age of 61 (55–68) years, it can be speculated that this effect may also, at least in part, extend to elderly patients.

Despite the promising findings, most studies are observational, with few randomized controlled trials in elderly populations. Most importantly, none of the available studies targets frail elderly patients. Considering that adherence to CPAP is a major challenge in the elderly, future research is needed to clarify potential specific benefits, optimize management strategies, and develop personalized approaches for elderly patients with OSAS.

5.3. Cancer

As is often the case, current scientific evidence regarding the pathogenesis, proliferation, or metastatic spread of cancer in the very elderly population with OSA is extremely limited, primarily due to the underrepresentation of individuals at the extremes of age in clinical studies. For example, among the 443 patients with melanoma included in a prospective study assessing the effectiveness of CPAP therapy on tumor aggressiveness, only 12.5 % were older than 75 years, and a mere 5.1 % were aged 80 or above, despite a mean age in this cohort exceeding 56 years. Similar patterns of age underrepresentation are observed in studies of other cancer types with comparable objectives [64].

In general, cancer incidence is higher in older adults than in younger individuals, due to several age-related factors such as the accumulation of mutations with impaired DNA repair capacity, immunosenescence, prolonged exposure to carcinogens, hormonal changes, cellular aging, and chronic low-grade inflammation. Some of these mechanisms—such as inflammation, oxidative stress, and immune dysfunction—may be exacerbated by chronic intermittent hypoxia induced by OSA, particularly in frail older adults or those with accumulated risk factors [65]. However, paradoxical findings have emerged from studies in aged animal models, whereby intermittent hypoxia appeared to be less effective and even ineffective in fostering the progression of lung adenocarcinoma compared to younger mice [66].

To date, these pathophysiological pathways have not been systematically investigated in clinical studies focused exclusively on elderly populations (≥75 years) yielding inconsistent results. For instance, Martínez-García et al., in a study of 5427 patients with suspected OSA followed over a median of 4.5 years, reported increased cancer mortality only among individuals younger than 65 years [67]. In contrast, Wei et al., in a meta-analysis involving nearly 1.4 million women, found a more pronounced association between OSA and breast cancer risk in older women [68]. Most studies examining the relationship between OSA severity and cancer risk treat age primarily as a confounding variable rather than a principal focus of investigation [69]. Moreover, the presence of several other coexisting risk factors such as obesity and inflammation which are themselves associated with increased cancer risk make it difficult to disentangle causality.

In summary, based on the limited currently available evidence, it cannot be definitively stated that the presence of OSA increases the incidence or aggressiveness of cancer in elderly patients.

5.4. Metabolic

As with other OSA-related processes and CPAP interventions, there is a paucity of literature specifically addressing the metabolic consequences of OSA and their treatment in older patients. The three principal metabolic changes typically observed in the elderly include: a general reduction in basal metabolic rate, increased physical inactivity often resulting in weight or body fat gain, and alterations in carbohydrate metabolism—such as heightened risk of glucose intolerance, type 2 diabetes, and increased insulin resistance. Additionally, elderly individuals tend to show elevated total cholesterol levels, primarily driven by increased low-density lipoprotein (LDL) concentrations [70].

All these metabolic changes are also associated with OSA and seem to be at least partially responsive to CPAP therapy. However, what remains unclear is how these mechanisms interact with advanced chronological age in OSA patients. Logically, one might expect OSA to potentiate age-related metabolic dysfunction and CPAP to exert a protective effect. Nevertheless, a significant confounding factor is the high prevalence of obesity, which is common to both OSA and age-related metabolic disturbances. In a recent study of 134 patients with a mean age of 71.1 years, it was not possible to rule out that the observed associations between OSA, CPAP treatment, and metabolic changes were primarily, if not overwhelmingly, influenced by obesity. Furthermore, even when beneficial effects are observed, they may not be sustained over time. McMillan et al., in a randomized controlled trial involving 278 patients aged ≥65 years, found that CPAP reduced total and LDL cholesterol levels during the first three months of treatment. However, these improvements were not sustained after six months [71].

In summary, the impact of OSA on metabolic function is at best very subtle among aged individuals and as such, the likelihood of benefits derived from treatment is marginal at best.

6. Should be treat elderly people with OSA and IF SO, WHOM?

Despite the central role of CPAP in OSA management, the current evidence base has largely been developed without a geriatric sleep medicine framework. Most studies inadequately account for age-related heterogeneity in physiological reserve, multimorbidity, frailty, functional status, and patient-centered goals of care. As a result, therapeutic decision-making in older adults has been disproportionately device-centered rather than syndrome- or function-oriented. Importantly, several biological and clinical considerations support the rationale for multimodal, non-CPAP interventions as first-line therapy in selected older individuals, particularly those with mild-to-moderate OSA or limited symptom burden. These approaches may include lifestyle interventions (dietary [72] modification and combined aerobic and resistance exercise [73]), oropharyngeal exercises, positional therapy, and mandibular advancement devices—many of which can be adapted even in the presence of edentulism. Such strategies may better align with the complex needs of older patients, improve tolerability and adherence, and target pathophysiological mechanisms of OSA that are particularly relevant in aging, including reduced muscle tone, altered ventilatory control, and increased sleep fragmentation.

Nevertheless, CPAP remains the treatment of choice for moderate-to-severe symptomatic OSA however most randomized controlled trials (RCTs) have been conducted in middle-aged male populations. Although most international guidelines do not currently consider age a determining factor for initiating CPAP, only four RCTs have exclusively evaluated individuals over 70 years of age (63, [74–77].

Data from meta-analyses of observational and interventional studies suggest that CPAP therapy may be just as effective in patients aged ≥65–70 years as it is in younger cohorts. However, a more nuanced analysis of these RCTs reveals that the benefits of CPAP may be attenuated in elderly patients with moderate OSA, particularly as it relates to neurocognitive and cardiovascular morbidities. In a pooled analysis of two multicenter RCTs involving 369 patients with moderate-to-severe OSA, the subset of individuals aged ≥80 years (n = 97; 26.3 %; mean age: 81 years, SD: 2.4), who used CPAP for an average of 4.3 h per night (53.5 % met the ≥4 h/night adherence threshold), showed no evidence of significant improvements in neurocognitive, cardiovascular, metabolic, or symptomatic outcomes, despite a substantial reduction in AHI from 42 to 5 events/hour. The only significant benefit observed was a reduction in snoring and associated witnessed apneas [61]. Similarly, a large study in France in >3000 subjects compared the beneficial effects of CPAP over 6 months among younger and older patients with OSA and concluded that the latter were less likely to derive improvements in their quality of life and symptomatic relief [78].

These findings are, however, challenged by other large-scale studies that have relied on databases or that have not followed RCT designs. For example, Mazzotti et al. [79] reported substantial cardiovascular benefits and reduced overall mortality among 888 835 Medicare beneficiaries with OSA aged 65 years and older. In this large cohort, CPAP improved both all-cause mortality) and MACE (major adverse cardiovascular events) particularly among those ages 80 years or older. A prospective cohort study reported their findings on survival rate and incidence of cardiovascular events in elderly patients with moderate to severe OSA who either did or did not receive CPAP treatment [80]. Over a mean follow-up period of 5 years 130 patients (104 male, 26 female; mean age: 77.8 ± 6.2 years), 36 patients received CPAP and 88 either refused or were not offered CPAP. In the untreated group, mortality (21.6 %) was significantly higher than in the CPAP-treated group (5.6 %).

Regarding adherence, limited evidence indicates that it remains relatively stable up to age 75 years, and thereafter markedly declines. In a cohort of 939 patients aged ≥65 years treated with CPAP and followed for a median of 69 months (IQR: 48–87), nightly usage declined progressively from 5.2 h (SD: 2.6) in those aged 65–69 (78 % good adherence) to just 2.9 h (SD: 1.7) in those aged ≥80 (23.8 % good adherence) [81] (Fig. 2). These values fall below the internationally accepted minimum of 4 h per night.

Fig. 2.

CPAP adherence in OSA patients ages 65–69; 70–74; 75–79 and ≥80 years old (With Permission. European Respiratory Journal Open Research).

Several factors may contribute to the poor adherence documented in this age group, and may include living alone, edentulism, neurosensory and neurocognitive impairments, multiple comorbidities, frailty, and reduced manual dexterity. Moreover, it remains unclear what constitutes pathological OSA in individuals of extreme age, given the physiological increase in sleep-disordered breathing events with aging.

Notwithstanding, demographic changes are undeniable: life expectancy now exceeds 80 years in many countries, and a substantial proportion of elderly individuals maintain a good quality of life into advanced age. However, health care systems are facing several issues in terms of sustainability therefore understanding whether CPAP treatment remains cost effective not only in the short term as shown in the PREDICT trial [63] but also in the long term for the elderly population is of paramount importance.

In our opinion, CPAP treatment in this population should be personalized and driven primarily by symptom burden—especially excessive daytime sleepiness—and an AHI ≥30 events/hour. Under such circumstances, a limited trial of CPAP may be warranted, with support through education and home assistance to ensure adequate adherence (≥4 h/night). In this context, the validation and adoption of frameworks for clinicians targeting elderly and frail OSA patients, as proposed in patients in primary cardiovascular prevention, might be useful [82]. If no subjective or objective benefit is observed during a follow-up period of 3–6 months, discontinuation of therapy may be contemplated. In parallel, there is little doubt that we have reached a point where conclusive evidence is urgently needed to warrant optimal decision-making regarding treatment of OSA in older individuals. Ultimately, addressing these uncertainties will require well-designed, pragmatic randomized controlled trials specifically enrolling adults aged ≥65 years, with adequate representation of the very old and frail. Such trials should prioritize patient-centered and functional outcomes, incorporate multimodal and individualized intervention strategies, and move beyond apnea–hypopnea index–based definitions by integrating refined OSA severity metrics, such as hypoxic burden and measures of sleep fragmentation. Generating this level of evidence is essential to inform sustainable, value-based care pathways and to guide treatment decisions that are both clinically meaningful and economically justified in an aging population.

7. Practice points for the evaluation and management of OSA in older adults

7.1. Use age-adapted diagnostic approaches

Clinicians should interpret OSA symptoms and diagnostic thresholds through an age-specific lens. Because older adults often present with atypical symptoms (fatigue, insomnia, cognitive decline, falls) and minimal sleepiness, diagnostic evaluation should emphasize functional status, cognitive changes, nocturia, and frailty indicators, not just the Epworth Sleepiness Scale or classic daytime sleepiness.

7.2. Prioritize polysomnography in complex or frail older adults

In-laboratory polysomnography (PSG) should be the preferred diagnostic modality in older adults with multimorbidity, insomnia, suspected central sleep apnea, or fragmented sleep, as home polygraphy frequently misestimates AHI and fails to capture arousals or sleep architecture—features particularly relevant in this age group.

7.3. Individualize treatment based on symptom burden, functional outcomes, and frailty

Initiation of CPAP should be guided by excessive daytime sleepiness, AHI ≥30 events/hour, functional impairment(s), or high hypoxic burden, rather than AHI alone. Treatment decisions should incorporate frailty status, cognitive capacity, comorbidities, manual dexterity, and patient-centered goals of care.

7.4. Implement multimodal, Non-CPAP strategies when appropriate

For older adults with mild-to-moderate OSA, limited symptoms, or reduced CPAP tolerance, clinicians should consider exercise programs (aerobic + resistance), weight management, oropharyngeal exercises, positional therapy, or mandibular advancement devices, adapted as needed for dental limitations or frailty.

7.5. Address circadian and sleep-maintenance dysregulation

Because aging is associated with circadian rhythm weakening and increased sleep fragmentation, management plans should include regular sleep–wake schedules, morning bright light exposure, environmental noise reduction, and optional timed melatonin, as these complementary measures may improve sleep continuity and therapy adherence.

7.6. Monitor and target geriatric-relevant outcomes

Evaluation and follow-up should emphasize outcomes with the highest impact on independence and quality of life in aging adults—falls risk, cognitive function, mood, muscle strength, frailty progression, and functional capacity—as these domains may be more sensitive to OSA’s impact than traditional cardiometabolic endpoints.

8. Research agenda

Based on current evidence, several critical (and unanswered) questions emerge.

• Beyond lifestyle interventions and management of cardiovascular, metabolic, and cognitive risk factors, is it worthwhile to initiate CPAP or alternative treatments in patients over 75–80 years with OSA, considering the low incidence of adverse events, poor adherence, and the absence of an established pathological AHI threshold for this population?

• Could treatment be counterproductive, particularly in long-term survivors of intermittent hypoxia who may have developed adaptive cerebrovascular or coronary collateral circulation?

• What treatment guidelines should be implemented even before the conclusive clinical trials address the aforementioned questions?

• What is the role of caregivers in elderly OSA patients? Can caregivers help improve adherence through CPAP programs and home-based support strategies particularly in elderly institutionalized patients?