Butyrate-promoting diet
What this marker measures
Thedegree to which the patient's diet likely promotes butyrate production by the gut microbiome.
Health categories/Interpretations informed by this marker
Gut environment
● Pro-inflammatory microbiome: A diet that does not sufficiently promote butyrate production may contribute to low levels of butyrate. Butyrate may reduce inflammation via multiple mechanisms.1–3
Gut barrier
● Reduced colonic butyrate availability: a diet that does not sufficiently promote butyrate production may contribute to reduced availability of butyrate for the colon cells.4–7
● Intestinal permeability link: butyrateis the primary energy source for colon cells. A diet that does not sufficiently promote butyrate production may contribute to impaired gut barrier integrity.4–7
Microbiome balance
● Putrefactive microbiome: a diet that does not sufficiently promote butyrate production may contribute to the accumulation of harmful products of protein putrefaction.
● Unbalanced SCFA-producers: a diet that does not sufficiently promote butyrate production may alter the balance of short-chain fatty acids and limit the anti-inflammatory impact of butyrate.8
Clinical features
● Dietary gaps: butyrate-promoting diet is a dietary feature that can affect nutritional adequacy.
Interpreting the result
Dietary support for butyrate production may be lower than optimal.
Patient management insights
Grade: PP
Tips for patients discussion
"Your questionnaire responses suggest your diet may not be giving your gut microbes enough of the foods they use to make butyrate. Butyrate is the main fuel for the cells lining your colon and may help support your gut barrier. Let's look at ways to include more fibre, especially from wholegrains and a wide variety of plant foods."
Source references for all clinical associations, interpretation definitions, and patient management insights on this card.
1. Arpaia, N. et al. Metabolites produced by commensal bacteria promote peripheral regulatory T-cellgeneration. Nature 504, 451–455 (2013).
2. Rosser, E. C. et al. Microbiota-derived metabolites suppress arthritis by amplifying aryl-hydrocarbon receptor activation in regulatory B cells. Cell Metab 31,837–851 (2020).
3. Singh, N. et al. Activation of Gpr109a, receptor for niacin and the commensal metabolite butyrate, suppresses colonic inflammation and carcinogenesis. Immunity 40,128–139 (2014).
4. Wang, R. X., Lee, J. S.,Campbell, E. L. & Colgan, S. P. Microbiota-derived butyrate dynamically regulates intestinal homeostasis through regulation of actin-associated proteinsynaptopodin. Proc Natl Acad Sci USA 117, 11648–11657 (2020).
5. Peng, L. et al. Butyrate enhances the intestinal barrier by facilitating tight junctionassembly via activation of AMP-activated protein kinase in Caco-2 cellmonolayers. J Nutr 139, 1619–1625 (2009).
6. Kelly, C. J. et al. Crosstalk between microbiota-derived short-chain fatty acids and intestinalepithelial HIF augments tissue barrier function. Cell Host Microbe 17,662–671 (2015).
7. Roediger, W. E. W. Role ofanaerobic bacteria in the metabolic welfare of the colonic mucosa in man. Gut21, 793–798 (1980).
8. Gomez-Arango, L. F. et al. Increased systolic and diastolic blood pressure is associated with altered gutmicrobiota composition and butyrate production in early pregnancy. Hypertension68, 974–981 (2016).
9. Stanford, J. et al.High-diversity plant-based diet and gut microbiome, plasma metabolome, andsymptoms in adults with CKD. Clin J Am Soc Nephrol 20, 619–631(2025).
10. Iversen, K. N. et al. The effects of high fiber rye, compared to refined wheat, on gut microbiotacomposition, plasma short chain fatty acids, and implications for weight lossand metabolic risk factors (the RyeWeight study). Nutrients 14,1669 (2022).
11. Zhao, L. et al. Gut bacteria selectively promoted by dietary fibers alleviate type 2 diabetes. Science 359, 1151–1156 (2018).
12. Ohashi, Y. et al. Consumption of partially hydrolysed guar gum stimulates Bifidobacteria andbutyrate-producing bacteria in the human large intestine. Benef Microbes6, 451–455 (2015).