Fibre-focused diet
What this marker measures
The degree to which the patient's diet focuses on a pattern of eating fibre-rich foods, based on reported intake across five food groups that contribute to total fibre intake: vegetables, fruit, legumes, nuts and seeds, and wholegrains.1 It is not intended to estimate total fibre content.
Health categories/Interpretations informed by this marker
Microbiome balance
● Putrefactive microbiome: A diet with limited fibre could lead to unbalanced levels of short-chain fatty acids, which may contribute to the accumulation of harmful products of protein putrefaction.2–4
● Unbalanced SCFA-producers: A diet with limited fibre could limit production of short-chain fatty acids, which help to regulate gut inflammation and intestinal barrier integrity.5–14
Clinical features
● Dietary gaps: Fibre-focused diet is a dietary feature that can affect nutritional adequacy.
Interpreting the result
Tips for patients discussion
"Your questionnaire responses suggest that fibre-rich foods aren't yet a regular part of your diet across all the main food groups. Fibre feeds gut microbes that produce short-chain fatty acids, which may help to regulate gut inflammation and support your gut barrier. Let's look at simple ways to include more vegetables, fruit, legumes, nuts and seeds, and wholegrains."
Source references for all clinical associations, interpretation definitions, and patient management insights on this card.
1. Marlett, J. A. & Cheung, T. F. Database and quick methods of assessing typical dietary fiber intakes using data for 228 commonly consumed foods. J Am Diet Assoc 97, 1139–1148 (1997).
2. Stanford, J. et al. High-diversity plant-based diet and gut microbiome, plasma metabolome, and symptoms in adults with CKD. Clin J Am Soc Nephrol 20, 619–631 (2025).
3. Iversen, K. N. et al. The effects of high fiber rye, compared to refined wheat, on gut microbiota composition, plasma short chain fatty acids, and implications for weight loss and metabolic risk factors (the RyeWeight study). Nutrients 14, 1669 (2022).
4. Zhao, L. et al. Gut bacteria selectively promoted by dietary fibers alleviate type 2 diabetes. Science 359, 1151–1156 (2018).
5. Xu, M. et al. Acetate attenuates inflammasome activation through GPR43-mediated Ca²⁺-dependent NLRP3 ubiquitination. Exp Mol Med 51, 1–13 (2019).
6. Park, J. et al. Short-chain fatty acids induce both effector and regulatory T cells by suppression of histone deacetylases and regulation of the mTOR–S6K pathway. Mucosal Immunol 8, 80–93 (2015).
7. Deleu, S. et al. High acetate concentration protects intestinal barrier and exerts anti-inflammatory effects in organoid-derived epithelial monolayer cultures from patients with ulcerative colitis. Int J Mol Sci 24, 768 (2023).
8. Wang, R. X., Lee, J. S., Campbell, E. L. & Colgan, S. P. Microbiota-derived butyrate dynamically regulates intestinal homeostasis through regulation of actin-associated protein synaptopodin. Proc Natl Acad Sci USA 117, 11648–11657 (2020).
9. Peng, L. et al. Butyrate enhances the intestinal barrier by facilitating tight junction assembly via activation of AMP-activated protein kinase in Caco-2 cell monolayers. J Nutr 139, 1619–1625 (2009).
10. Kelly, C. J. et al. Crosstalk between microbiota-derived short-chain fatty acids and intestinal epithelial HIF augments tissue barrier function. Cell Host Microbe 17, 662–671 (2015).
11. Roediger, W. E. W. Role of anaerobic bacteria in the metabolic welfare of the colonic mucosa in man. Gut 21, 793–798 (1980).
12. Arpaia, N. et al. Metabolites produced by commensal bacteria promote peripheral regulatory T-cell generation. Nature 504, 451–455 (2013).
13. 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).
14. 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).