## 4 Discussion  
In our community-based sample of Colombian adults, higher SCFA levels in the stool were associated with indicators of lower gut microbiota diversity, and higher gut permeability (measured by LPS binding protein), systemic inflammation (measured by hs-CRP), glycemia, dyslipidemia, obesity, central obesity, and hypertension. All associations remained after adjustment for possible confounders, including dietary fiber, total calories and physical activity, and the findings were not explained by medication use. As such, our results appear to favor the hypothesis that greater excretion of SCFAs in stool is a marker of poor gut health and cardiometabolic dysregulation. Previous cross-sectional studies have reported higher fecal SCFA concentrations in overweight or obese individuals compared to lean individuals [13; 15; 32; 33; 34]. Moreover, [PERSON] et al. demonstrated that genetically obese mice (i.e., homozygous for a mutation in the leptin gene (\(ob/ob\)) that produces a stereotyped, fully penetrant obesity phenotype) compared to their lean siblings (\(ob/+\) and \(+/+\)) have a gut microbiome composition that promotes obesity through excess SCFA production and increased energy availability [14]. Our study extends these findings by showing that higher fecal SCFAs are also associated with central obesity, hypertension, subclinical measures of cardiometabolic disease (e.g., inflammation, glycemia and dyslipidemia), as well as a measure of gut permeability (LPS binding protein). Our findings on fecal excretion of SCFAs may not be generalizable to SCFAs measured in circulation, which may better represent SCFA production and absorption. [PERSON] and [PERSON] [35] eloquently \begin{table}
\begin{tabular}{c c c c c c c} \hline \hline  & \multicolumn{3}{c}{**Fecal Budyrate**} & \multicolumn{3}{c}{**OTU Richness**} \\ \cline{2-7}  & **Tertile 1** & **Tertile 2** & **Tertile 3** & **Tertile 1** & **Tertile 2** & **Tertile 3** \\ \hline
**Obesity1** & \(N=80\) & \(N=93\) & \(N=90\) & \(N=80\) & \(N=86\) & \(N=97\) \\ Undayusted model & Referent & 1.12 (0.91, 1.33) & 1.72 (1.51, 1.93) & Referent & 0.91 (0.69, 1.12) & 0.75 (0.55, 0.95) \\ Confounder-adjusted & Referent & 1.22 (1.02, 1.43) & 1.95 (1.74, 2.16) & Referent & 0.98 (0.77, 1.20) & 0.72 (0.52, 0.93) \\ Confounder-adjusted & Referent & 1.08 (0.88, 1.29) & 1.73 (1.52, 1.94) & Referent & 1.05 (0.84, 1.27) & 0.78 (0.58, 0.98) \\ + LBP model & Referent & 1.07 (1.06, 1.29) & 1.73 (1.52, 1.94) & Referent & 1.05 (0.84, 1.27) & 0.78 (0.58, 0.98) \\ \hline
**Central obesity2** & \(N=144\) & \(N=143\) & \(N=144\) & \(N=144\) & \(N=144\) & \(N=143\) \\ Undayusted model & Referent & 1.22 (1.06, 1.39) & 1.56 (1.40, 1.73) & Referent & 0.95 (0.78, 1.12) & 0.96 (0.79, 1.12) \\ Confounder-adjusted & Referent & 1.22 (1.06, 1.39) & 1.54 (1.37, 1.71) & Referent & 0.97 (0.80, 1.13) & 0.92 (0.75, 1.09) \\ Confounder-adjusted & Referent & 1.10 (0.93, 1.27) & 1.39 (1.22, 1.58) & Referent & 0.99 (0.82, 1.15) & 0.97 (0.80, 1.14) \\ \hline
**Hypreteness3** & \(N=144\) & \(N=143\) & \(N=144\) & \(N=144\) & \(N=144\) & \(N=143\) \\ Unadjusted model & Referent & 1.16 (0.39, 1.32) & 1.33 (1.16, 1.49) & Referent & 0.91 (0.74, 1.07) & 0.98 (0.82, 1.15) \\ Confounder-adjusted & Referent & 1.12 (0.96, 1.29) & 1.31 (1.14, 1.47) & Referent & 0.92 (0.76, 1.09) & 0.89 (0.73, 1.06) \\ Confounder-adjusted & Referent & 1.08 (0.91, 1.24) & 1.25 (1.08, 1.42) & Referent & 0.92 (0.76, 1.09) & 0.90 (0.73, 1.06) \\ + LBP model & Referent & 1.08 (0.91, 1.24) & 1.25 (1.08, 1.42) & Referent & 0.92 (0.76, 1.09) & 0.90 (0.73, 1.06) \\ \hline \hline \end{tabular}  
* Defined as BMI \(\geq 30\) kg/m\({}^{2}\); 2 defined as waist circumference \(\geq\)102 cm (men) and \(\geq\)88 cm (women); 3 defined as SBP \(\geq 130\) mm Hg or DBP \(\geq 80\) mm Hg or previous diagnosis of hypertension or use of antihypertensive medications; 4 Model adjusted for participant age, city of residence, physical activity, fiber intake, and total caloric intake.  
\end{table}