## 5 Conclusions  
We presented a comprehensive analysis demonstrating that fecal SCFA excretion, which cannot be equated to SCFA production or absorption, was positively associated with measures of gut microbiome dysbiosis, gut permeability, and cardiometabolic dysregulation, as well as higher prevalence of obesity, central obesity, and hypertension. Gut microbiota richness and the differential abundance of many microbial taxa were also associated with fecal SCFA excretion, as was the intake of dietary fiber, highlighting the potential for SCFA modification through diet, pre- and pro-biotic interventions. In light of the contradictory findings on SCFAs and health, controlled human feeding trials that assess both fecal and circulating SCFAs are needed to test the hypothesis that the association of higher fecal SCFA concentrations with obesity and cardiometabolic dysregulation is due to less efficient absorption and utilization of these metabolites. The following are available online at [[http://www.mdpi.com/2072-6643/11/1/51/s1](http://www.mdpi.com/2072-6643/11/1/51/s1)]([http://www.mdpi.com/2072-6643/11/1/51/s1](http://www.mdpi.com/2072-6643/11/1/51/s1)). Figure S1: Distribution of the gut microbiota diversity according to multivariable-adjusted fecal SCFA concentrations; Figure S2: Distribution of cardiometabolic health indicators according to multivariable-adjusted fecal butyrate concentration; Figure S3: Distribution of cardiometabolic health indicators according to multivariable-adjusted gut microbiota diversity; Figure S4: Principal coordinates analysis (PCoA) plot based on weighted UniFrac distances; Figure S5: Heatmap showing the correlations between rarefied OTU abundances and multivariable-adjusted fecal SCFA concentrations in the subset of participants who did not report smoking or use of pharmacological treatments; Table S1: Parameters of the single-ion monitoring (SIM) mode acquisition and performance of the SCFA quantification method using GC/MS; Table S2: Characteristics of the study population overall and according to tertiles of unadjusted fecal SCFA levels; Table S3: Multivariable-adjusted fecal SCFA concentrations according to stool consistency; Table S4: Procrustes analysis correlating the gut microbiota-beta diversity with SCFA concentrations and variables informing about the risk of cardiometabolic disease; Table S5: Prevalence ratios of total fecal SCFAs, acetate and propionate concentrations for obesity, central obesity, and hypertension with robust 95% confidence intervals; and Table S6: Prevalence ratios of fecal butyrate and total SCFA concentrations for obesity, central obesity, and hypertension with robust 95% confidence intervals in the subset of participants who did not report smoking or use of pharmacological treatments. [PERSON]-[PERSON] processed fecal samples and DNA sequences, performed analyses, and wrote the manuscript; [PERSON] discussed analyses and results, and wrote the manuscript; [PERSON]-Q. quantified fecal SCFAs; [PERSON]-M. processed fecal samples and DNA sequences; [PERSON] quantified plasma lipopolysaccharide-shorleading binding protein levels; [PERSON]-A. coordinated field work and performed diet and physical activity interviews; [PERSON] coordinated blood biochemistry measures, transport and treatment of samples; [PERSON] coordinated recruitment of participants and field work; [PERSON] designed and supervised the study, recruited participants, coordinated field work, performed analyses, and wrote the manuscript. All the authors read and approved the final version of the manuscript. This study was funded by Grupo Empresarial Nutresa, Dinamica IPS, EPS SURA and Universidad de Antioquia. NTM is supported by the National Heart, Lung, and Blood Institute of the National Institutes of Health under Award Number K01 HL141589, and by grants from the Mid-Atlantic Nutrition Obesity Research Center (P30 DK072488), and the Foundation for Gender Specific Medicine.