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Primary Submission Category: Chronic disease
Sleep Duration and Cardiometabolic Risk in U.S. Adults: Does Educational Attainment Modify the Association?
Authors: Ummat Safwat Sristy, Muntasir Masum PhD,
Presenting Author: Ummat Safwat Sristy*
Introduction: Whether sleep-health disparities reflect effect modification by socioeconomic position or shared upstream pathways is a central question for population health equity. We tested whether educational attainment modifies the association between sleep duration and hypertension in U.S. adults.
Methods: Cross-sectional analysis using NHANES 2021–2023 (N = 5,561 adults 18+). Hypertension: systolic BP ≥130 mmHg, diastolic BP ≥80 mmHg, or antihypertensive use. Sleep: short (<7 h), normal (7–9 h, reference), or long (>9 h). Educational attainment (<HS, HS/GED, some college, college+) was the potential effect modifier. Logistic regression estimated adjusted odds ratios (adjusted ORs) controlling for age, sex, race/ethnicity, BMI, smoking, and diabetes, with a sleep × education interaction term; all analyses used NHANES complex survey design.
Results: In crude models, both short sleep (OR = 1.28, 95% CI: 1.12–1.47) and long sleep (OR = 1.34, 95% CI: 1.15–1.57) were associated with higher odds of hypertension. After adjustment, short sleep attenuated to non-significance (adjusted OR = 1.07, 95% CI: 0.92–1.25), while long sleep remained independently significant (adjusted OR = 1.22, 95% CI: 1.02–1.47), suggesting residual cardiometabolic risk not fully explained by measured confounders. Lower educational attainment was independently associated with hypertension (HS/GED: adjusted OR = 1.34; Some College: adjusted OR = 1.17). No sleep × education interaction was detected, indicating the sleep–hypertension association did not vary across educational levels.
Conclusion: Although short sleep duration was associated with hypertension in unadjusted analyses, this relationship was attenuated by adjustment for sociodemographic and metabolic confounders. Educational attainment was independently associated with hypertension risk but did not modify the sleep–hypertension link. Critically, the null interaction itself is a substantive finding: sleep-related cardiometabolic risk appears to operate through pathways shared with SES rather than via effect modification. This underscores the value of upstream structural interventions targeting housing, work conditions, and neighborhood safety that simultaneously address sleep health and socioeconomic inequities.