Context: Melatonin may have a preventive effect on atherosclerosis by regulating sleep quality and circadian biological rhythmicity. However, whether endogenous melatonin is associated with arterial stiffness, a marker reflecting atherosclerosis, is unclear.
Objective: The objective of the study was to determine the association between endogenous melatonin and arterial stiffness.
Design And Participants: A total of 641 community-based elderly individuals were enrolled in this cross-sectional study (mean age 71.4 y).
Measures: We measured overnight urinary 6-sulfatoxymelatonin excretion (UME) and cardioankle vascular index (CAVI) as indices of melatonin secretion and arterial stiffness, respectively.
Results: The median UME was 6.8 μg (interquartile range 4.1-10.5) and the mean value of CAVI was 9.1 ± 1.1. High CAVI (ie, ≥ 9.0) was observed in 334 participants (52.1%). Univariate logistic regression models revealed marginal to significant associations between high CAVI and age, gender, body mass index, hypertension, diabetes, estimated glomerular filtration rate, log-transformed UME, bedtime, duration in bed, daytime physical activity, and log-transformed nighttime physical activity. In the multivariate logistic regression model, simultaneously adjusted for the former independent variables, higher log-transformed UME was significantly associated with a lower odds ratio (OR) for high CAVI (adjusted OR 0.708; 95% confidence interval 0.536-0.935; P = .015). This inverse association between log-transformed UME and high CAVI indicated that an increase in log-transformed UME by 1 SD was associated with an 18.1% (95% confidence interval 1.4-31.9) decrease in high CAVI prevalence.
Conclusions: UME is significantly and inversely associated with arterial stiffness in the general elderly population. The association was independent of several major causes of atherosclerosis.
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