What are we doing wrong?

For decades, obstructive sleep apnea (OSA) has been framed as a predominantly male disease.¹ Early epidemiological studies linked OSA to central obesity, while women’s more peripheral fat distribution was associated with milder OSA than in men for similar levels of obesity.² Differences in upper airway anatomy and physiology reinforced the idea that women were less prone to airway collapse³. The prevailing belief was that women developed OSA only at extreme levels of obesity, and when they did, the disease was milder.

Over time, a broader understanding of OSA has emerged, driven by recognition that the disorder does not present as a single uniform entity. Different clinical and physiological phenotypes exist,⁴ with distinct symptom profiles, comorbidity patterns and treatment responses. Excessive daytime sleepiness, once considered the defining feature of OSA, is absent in more than half of affected individuals. Phenotypes characterized by minimal symptoms, disturbed sleep and insomnia are common, and they are more frequently occurring in women.⁵

When cultural assumptions shape diagnosis and treatment

Despite a growing literature on sex differences in OSA, the paradigm of OSA as a man’s disease remains difficult to dismantle. This reflects not only historical gaps in evidence, but also deeply ingrained cultural clinical habits. The male model of OSA has rigidly shaped how symptoms are interpreted, how risk is assessed and how urgency is assigned in clinical practice.

The consequences are not theoretical. Women remain underrepresented in randomized clinical trials⁶, and there is uncertainty around the effects of OSA on mortality and cardiovascular risk in women, with some studies showing worse outcomes in women even when they are treated with positive airway pressure (PAP) therapy.⁷ Overall, poor recognition of OSA in women leads to delayed diagnosis and delayed initiation of treatment.

These assumptions also extend into the therapeutic phase. Women are more likely than men to discontinue PAP therapy⁸, a finding that is often interpreted as PAP intolerance or, at times, as misdiagnosis of OSA. The prevailing belief that OSA in women is milder, less dangerous or less likely to respond to treatment continues to influence clinical decision-making, referral patterns and the level of support offered once therapy is initiated.

Recent large-scale registry data challenge this narrative. Healthcare costs related to OSA are substantial in women, both before and after diagnosis, and mortality is higher in women than in men⁷. This stands in clear contradiction to the notion that OSA in women is a benign or low-impact condition.

The cost of these assumptions is borne not only by patients, but also by health systems, through avoidable morbidity, fragmented care pathways and repeated cycles of missed or delayed intervention.

Menopause and the myth of “equalization”

Women’s transition into menopause also introduces an additional layer of complexity.^9,10 OSA prevalence increases after menopause and nears that observed in men, a finding often interpreted as evidence that sex differences disappear in later life. This interpretation is misleading.

While AHI values in postmenopausal women may resemble those seen in men, the broader clinical picture does not. Women often carry a higher burden of cardiometabolic and psychiatric comorbidities, which strongly influence prognosis.¹¹ Similar AHI values do not imply similar disease trajectories.

Equating postmenopausal OSA in women with male OSA risks oversimplification. It reinforces severity-based thinking while obscuring the importance of context, comorbidity and symptom burden, all of which are central to personalized care.

When symptoms do not fit the template

The consequences of applying male-centric symptom frameworks are especially evident in clinical practice. Several studies have shown that women report less snoring and witnessed apneas than men, and more fatigue, depression, poor sleep quality with frequent awakenings and/or insomnia, nocturia and morning headaches.^12-14

Taken together, these features describe a phenotype dominated by sleep fragmentation and subjective distress rather than overt sleepiness. If clinicians rely on classic symptom profiles derived from male populations, the likelihood of missing the OSA diagnosis in women is high.

Complicating matters further, women’s sleep complaints often overlap with other conditions such as restless legs syndrome. Sleep symptoms in women can be secondary to a variety of causes, alone or in combination with OSA.¹⁵ Not considering these possibilities may lead to incomplete symptom resolution on PAP therapy and contribute to early disengagement from therapy.

What phenotyping has taught us

Over the past decade, phenotype-based analyses have provided important diagnostic clues to detect OSA in women. Early cluster analyses from an Icelandic cohort demonstrated that disturbed sleep and insomnia-related phenotypes are as common as the classic sleepy phenotype, with a clear predominance in women.⁵ These findings were confirmed in larger international cohorts, including the Sleep Apnea Global Interdisciplinary Consortium and the Sleep Heart Health Study, with minor changes.^16,17

European registry data further refined this picture. Analyses from the European Sleep Apnea Database (ESADA) examining the relationship between subjective daytime sleepiness and nighttime complaints showed that women were more likely to present with insomnia-related phenotypes, marked by poor sleep quality, short sleep duration or use of hypnotics rather than overt sleepiness. These phenotypes were associated with higher cardiovascular and psychiatric comorbidity and poorer acceptance of PAP therapy.¹⁶ Similar patterns were reported across another cohort.¹⁷

Across multiple other analyses, men remained the majority of participants, leading most cluster findings to reflect male-dominant patterns. Still, some clusters, such as one described by Gagnadoux et al., showed a higher proportion of women, who again demonstrated the lowest PAP adherence.¹⁸ In a larger ESADA analysis of over 23,000 patients, eight clinical phenotypes were identified, including four gender-based clusters (two male-only and two female-only) and four additional largely male clusters differing in age, body mass index, OSA severity and comorbidities.¹⁹ Even when men and women presented similar OSA profiles, women tended to have more comorbidities and were less likely to continue PAP treatment.

For years, however, women have remained statistical minorities within male-dominated datasets. But that has begun to change. In 2024, two large cluster analyses conducted exclusively in women with OSA marked a turning point. These studies identified reproducible female-specific phenotypes, including clusters characterized by obesity and sleepiness, by mild OSA with low comorbidity, by advanced age with multimorbidity, and notably, by ischemic heart disease despite only moderate apnea-hypopnea index (AHI) values.^20,21

While more research is needed to confirm and further characterize the peculiar symptom and comorbidity profiles of women with OSA, the implications are clear. In women, symptom burden, comorbidity and cardiovascular risk are not reliably predicted by AHI alone. Phenotyping reveals clinically meaningful subgroups that would otherwise remain invisible.

Heterogeneity to action

The growing body of phenotyping research makes one point unmistakably clear. OSA in women is not simply a milder version of the disease seen in men. It is more heterogeneous, more context-dependent and often more tightly linked to comorbidity. When clinical frameworks fail to reflect this reality, women pay the price through delayed diagnosis, fragmented care and reduced treatment benefit.

Phenotyping offers a path forward, but only if its insights are translated into practice. This requires moving beyond one-size-fits-all models and embedding sex- and phenotype-aware thinking into diagnostic pathways, treatment decisions and female-specific guideline development.