Sleep duration is recognized as a modifiable factor influencing cardiometabolic health. However, its association with apolipoproteins—sensitive biomarkers of atherogenic dyslipidemia—remains inadequately examined in community and primary care populations.To investigate the relationship between habitual sleep duration and apolipoprotein profiles, focusing on ApoB, ApoA1, and the ApoB/A1 ratio, and to compare these associations with traditional lipid markers.We analyzed 4,677 adults from the 2007 Taiwanese Survey on Hypertension, Hyperglycemia, and Hyperlipidemia. Sleep duration was categorized as short (<7 hours), normal (7–9 hours), or long (>9 hours). Linear and logistic regression models were applied with sequential adjustments for age, sex, smoking, alcohol use, and physical activity. Outcomes included ApoB, ApoA1, ApoB/A1 ratio, and conventional lipid parameters.Of all participants, 57.6% reported short sleep, 39.1% normal sleep, and 3.4% long sleep. After full adjustment, long sleep was associated with higher ApoB (β=+3.59 mg/dL; 95% CI: 0.07–7.11), lower ApoA1 (β=–4.71 mg/dL; 95% CI: –7.89 to –1.52), and an increased ApoB/A1 ratio (β=+0.056; 95% CI: 0.025–0.088). Long sleep also increased the odds of high ApoB (OR 2.00; 95% CI: 1.00–3.68) and high ApoB/A1 ratio (OR 1.93; 95% CI: 1.34–2.81). Short sleep showed no significant deviations from normal sleep. Traditional lipid measures demonstrated minimal variation across sleep categories.Findings suggest a U-shaped relationship between sleep duration and apolipoproteins, driven predominantly by adverse profiles in long sleepers rather than short sleepers. Apolipoproteins appeared more sensitive than conventional lipid markers in detecting sleep-related metabolic risk.Long sleep duration (>9 hours) is independently associated with a more atherogenic apolipoprotein profile, while short sleep shows no meaningful differences. Incorporating sleep assessment and apolipoprotein testing may enhance cardiometabolic risk detection in primary care.