Linking sleep apnea and arthritis in the National Alzheimer Coordinating Center Cohort: A cross-sectional analysis

Sleep apnea-related intermittent hypoxia and the chronic inflammation of arthritis share oxidative-stress pathways, yet their epidemiologic overlap remains under-described. The prevalence of both conditions increases with age and presents unique challenges for patient management. To quantify the association between clinician-suspected arthritis and self-reported sleep apnea and to explore whether demographic or cognitive factors modify that link. We analyzed 17,013 adults enrolled in the referral-based National Alzheimer Coordinating Center Uniform Data Set, version 3. Complete-case binary logistic regression modeled obstructive sleep apnea (OSA) (yes/no) on arthritis (yes/no) with adjustment for age, sex, race (White vs non-White), years of education, cognitive status (normal, mild cognitive impairment, Alzheimer disease), body mass index, and cardiometabolic comorbidities. A pre-specified interaction term tested whether cognition modified the arthritis–OSA association. Multiple imputation was used to address missing data. Arthritis was associated with 60% higher odds of OSA (adjusted odds ratio = 1.60, 95% confidence interval: 1.46–1.76, P < .001). The effect was attenuated in Alzheimer disease. Male sex, atrial fibrillation, stroke, diabetes, and higher body mass index were additional correlates (all P < .001); age was not independently significant. Imputation yielded similar estimates. Clinician-suspected arthritis was robustly associated with self-reported OSA even after extensive adjustment, although unmeasured confounding and exposure misclassification cannot be excluded. Both OSA and arthritis were ascertained by self-report or single-clinician designation without polysomnography, actigraphy, imaging, or serology, raising non-differential misclassification potential. The cross-sectional design prevents causal interpretation, and the predominantly White, highly educated volunteer cohort limits generalizability. Prospective, objectively phenotyped studies, ideally with arthritis sub-typing, are needed to verify directionality and clarify mechanisms. We used records from more than 17,000 volunteers at U.S. Alzheimer Disease Research Centers to ask whether people who say they have arthritis are also more likely to report OSA. After controlling for age, sex, education, cognitive status, weight, and common medical conditions, arthritis still raised the odds of OSA by about 60%. Joint pain and poor sleep can feed off 1 another, so recognizing both problems may help doctors treat them earlier. Neither arthritis nor OSA was confirmed with X-rays, lab tests, or sleep studies, we relied on what participants or clinicians reported. Furthermore, the study looked at 1 point in time, so we cannot tell which problem came 1st; and most volunteers were White and highly educated, so the findings may not reflect every community. Future research that tracks patients over time and uses overnight sleep tests and detailed arthritis subtypes will be crucial.