ArticleAnnals of medicine2026
Lower 24-hour urinary 6-sulfatoxymelatonin and exploratory bile-acid and microbiome associations in adults with dyslipidemia: a prospectively enrolled cross-sectional study.
Article in Annals of medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundWe tested the primary hypothesis that lower continuous 24-hour urinary 6-sulfatoxymelatonin (6-SMT) is associated with an adverse lipid and inflammatory profile in adults with dyslipidemia. Associations with FGF19, bile-acid composition, and gut microbiome features were secondary and exploratory.
methodsThis prospectively enrolled, single-center cross-sectional study included 577 consecutive adults evaluated at the Institute for Personalized Medicine, Tbilisi, Georgia, during 2020-2025. Each participant completed three non-consecutive 24-hour urine collections. Validity required a measured-to-predicted creatinine-excretion ratio of 0.80-1.20, and the participant-level 6-SMT value was the arithmetic mean of three valid collections. Fasting lipids, hs-CRP, FGF19, bile-acid profiles, and 16S rRNA taxonomic composition were assessed. An internal method-matched but unmatched normolipidemic reference comparator (
resultsMedian 6-SMT was 8.4 μg/24 h (IQR 5.2-12.1). Lower 6-SMT was associated with higher LDL-C (Spearman ρ = -0.38; approximate 95% CI -0.45 to -0.31), triglycerides (ρ = -0.31; -0.38 to -0.23), and hs-CRP (ρ = -0.35; -0.42 to -0.28), and with lower HDL-C (ρ = 0.29; 0.21 to 0.36). FGF19 was above the stated fasting reference range in 489/577 participants (85%; median 312 pg/mL) and correlated inversely with 6-SMT (ρ=-0.42; -0.48 to -0.35). The emphasized microbial taxa correlated positively with 6-SMT. In a post hoc unadjusted statin-stratified sensitivity analysis, the mean difference in 6-SMT for statin users versus non-users was -0.30 μg/24 h (95% CI -0.83 to 0.23;
conclusionsLower 24-hour urinary 6-SMT clustered with adverse lipid and inflammatory measures and with exploratory enterohepatic and taxonomic microbiome features. The findings are hypothesis-generating and do not establish a coordinated biological axis, directionality, diagnostic utility, incremental predictive value, or treatment effect.
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