Raw scite source audit — UC functional distal microenvironment

This file preserves the source set used for the scite-heavy pass on the distal UC microenvironment: H₂S/sulfur, indole/protein fermentation, SCFA/butyrate ecology, 4-SURE/reduced-sulfur diet studies, and contact-time/UC-associated constipation (UCAC). It intentionally stores DOIs and extracted evidence summaries only, not scite access URLs containing account identifiers.

Scite search branches run

1. "4-SURE" "ulcerative colitis" sulfide reducing diet SCFA
2. "ulcerative colitis" "hydrogen sulfide" "sulfate-reducing bacteria" Desulfovibrio
3. "ulcerative colitis" indole "tryptophan" microbial metabolites barrier
4. "ulcerative colitis" "protein fermentation" sulfur amino acids diet microbiome
5. "ulcerative colitis" "Faecalibacterium prausnitzii" Roseburia butyrate mucosa
6. DOI bundle: 10.1093/ibd/izaf177, 10.1093/jn/nxac093, 10.1097/MCO.0000000000000881, 10.3390/nu11040931, 10.3390/ijms26104596
7. DOI bundle: 10.1136/gutjnl-2013-304833, 10.1002/ibd.20903, 10.1038/ismej.2016.176, 10.1080/19490976.2016.1216748
8. "ulcerative colitis" "low-fat" "high-fiber" diet randomized trial microbiome SCFA
9. "hydrogen sulfide" butyrate oxidation colonocytes ulcerative colitis sulfide nitric oxide
10. "ulcerative colitis associated constipation" fecal stasis contact time microbiome metabolites

High-signal sources retained

Source	DOI	Study/source class	Why retained	Main extracted takeaway	Novelty status
Day et al. 2022, 4-SURE feasibility study	10.1093/jn/nxac093	Open-label clinical feasibility study, n=28 adults with mild-moderately active UC	Direct UC diet intervention targeting sulfide/protein fermentation	4-SURE was tolerated; prescribed targets were achieved; clinical response 13/28 (46%), endoscopic improvement 10/28 (36%), 2/28 worsened; fecal SCFA increased 69%; branched-chain-to-SCFA ratio suppressed 27%; FRQoL improved.	Strengthens existing 4-SURE branch; adds specific endpoints and caution.
Day et al. 2025, functional profiling of 4-SURE	10.1093/ibd/izaf177	Metagenomic/metabolomic follow-up in same intervention framework	Most direct evidence that a diet can hit intended microenvironmental targets	8-week 4-SURE significantly increased alpha diversity; reduced taxa containing H₂S-producing genera such as Odoribacter and Peptostreptococcaceae; altered 12/67 sulfur-metabolizing genes; decreased H₂S production and indole, a protein-fermentation marker.	New/high-value; core digest anchor.
Teigen et al. 2019, sulfur metabolism in UC	10.3390/nu11040931	Mechanistic review/hypothesis synthesis	Best conceptual frame for distal toxin/benefit gradient	UC distal severity may reflect dilution of beneficial factors, concentration of toxic factors, and changing host detox capacity tied to nutrient flow; protein/sulfur, fiber, pH, SCFAs, H₂S, and detox enzymes interact.	Reinforces central theory; adds biogeography language.
Teigen et al. 2022, diet and H₂S	10.1097/mco.0000000000000881	Clinical nutrition review with scite citation-context	Clarifies protein-vs-fiber nuance	Protein intake may increase H₂S, but fiber can reduce H₂S even with high protein; 4-SURE and low-fat/high-fiber UC diet studies both imply the protein/fiber/fat matrix matters more than protein alone.	Strategy-changing nuance; protects against oversimplified sulfur restriction.
Fritsch et al. 2021, low-fat high-fiber UC diet	10.1016/j.cgh.2020.05.026	Randomized crossover diet trial in UC remission	Independent diet evidence supporting high-fiber/lower-fat microenvironment improvement	Low-fat/high-fiber diet reduced markers of inflammation/dysbiosis and improved quality of life; scite context notes protein increased on LFD, but benefit still occurred with higher fiber/lower fat.	Useful comparator to 4-SURE; suggests fiber/fat context matters.
Ye/Raman et al. 2025, reduced sulfur diet	10.3390/ijms26104596	Small pilot/post-hoc microbiome/metabolome study	Independent recent reduced-sulfur human UC signal	Reduced sulfur intake shifted microbiome/metabolome, increased alpha diversity, decreased LBP, decreased pathobionts including Eggerthella lenta, and reported expansion of SCFA-producing bacteria including F. prausnitzii and Blautia wexlerae.	New/high-value but small/open-label; hypothesis-generating.
Machiels et al. 2013, Roseburia/F. prausnitzii in UC	10.1136/gutjnl-2013-304833	Human microbiome study, heavily cited	Canonical beneficial-butyrate dysbiosis source	UC patients showed reduced Roseburia hominis and F. prausnitzii, both butyrate producers; scite tally: 1313 total, 80 supporting, 6 contrasting, 1887 citing publications.	Strongly reinforces beneficial side.
Sokol et al. 2009, low F. prausnitzii in colitis microbiota	10.1002/ibd.20903	Human IBD microbiota study, heavily cited	Broad IBD/F. prausnitzii anchor	F. prausnitzii underrepresented in active IBD and indeterminate colitis; low counts associated with reduced mucosal protection; scite tally: 890 total, 49 supporting, 11 contrasting.	Reinforces but not UC-specific enough alone.
López-Siles et al. 2017, F. prausnitzii review	10.1038/ismej.2016.176	Review with citation context	Adds ecology/modulation nuance	F. prausnitzii is a major butyrate producer; pH, bile salts, substrate availability, phylogroups, and mucosal-vs-fecal sampling complicate interpretation; some strains respond to inulin/pectin-like substrates.	Prevents oversimplifying stool-test interpretation.
Lavelle et al. 2016, colonic biogeography	10.1080/19490976.2016.1216748	Review/addendum	Supports functional location model	UC has no simple universal “core microbiota”; fecal vs mucosal sampling and luminal vs mucus niches matter; F. prausnitzii/Roseburia reductions and Desulfovibrio/Enterobacteriaceae increases are recurrent but context-dependent.	Reinforces “position/function > stool labels.”
Jørgensen 2001, H₂S and epithelial metabolism	10.1023/a:1010661706385	Experimental colonocyte/metabolism study	Important contradiction/caution	Fecal H₂S did not differ in health vs quiescent/active UC and bound/fecal H₂S had limited effect on butyrate oxidation; other fecal agents may be more potent metabolic inhibitors.	Counterweight: H₂S alone is not proven universal cause.
Picton et al. 2007, H₂S detoxication	10.1007/s10620-006-9529-y	Human enzymatic detox study	Important contradiction/caution	No evidence of defective enzymatic sulfide detoxication by rhodanese or thiol methyltransferase in UC/CD mucosa; UC erythrocyte activity was higher, not lower.	Counterweight against simplistic detox-defect story.
Blachier et al. 2021, microbiota/epithelial H₂S	10.1152/ajpgi.00261.2020	Mechanistic review	Dose/context model	Low/endogenous H₂S can be physiological or anti-inflammatory; excessive luminal H₂S can impair mucus integrity, inflammation, and mitochondrial respiration when oxidation capacity is overwhelmed.	Supports “dose/context, not all sulfur bad.”
Stummer et al. 2023, H₂S in IBD	10.3390/antiox12081570	Review	Balanced H₂S/IBD overview	Both too little and too much H₂S may drive inflammation; diet, microbiota, and endogenous metabolism all matter.	Reinforces balance model.
James et al. 2018, UCAC	10.1002/jgh3.12076	Cross-sectional UC cohort	Contact-time/retention anchor	58/125 (46%) UC patients met proximal constipation definition; active disease OR 5.56, left-sided OR 2.84; symptoms included reduced stool frequency, hard stools, pain, flatus, straining, incomplete emptying.	Existing branch, essential integration.
Bassotti et al. 2025, constipation in UC	10.3390/jcm14155428	Review	Adds motility/stasis nuance	UC can feature fecal stasis/constipation due to inflammation-related motility changes, enteric nerve/muscle injury, fibrosis over time, and pelvic floor dyssynergia; stasis may occur proximal to inflamed segments.	Newer review reinforces UCAC.
Touw et al. 2017, intestinal stasis models	10.14814/phy2.13182	Animal/humanized-mouse constipation microbiome model	Mechanistic bridge between transit and microbiome function	Slow transit promoted dysbiosis and reduced cecal butyrate; constipation-associated microbiota transferred delayed transit to germ-free mice.	Indirect but useful for contact-time feedback loop.

Reviewed but not promoted as core anchors

• Quercetin/tryptophan metabolism mouse studies surfaced in the indole search. These may matter later for tryptophan/AhR/barrier research, but were not promoted because this pass focused on UC human diet/metabolite targets rather than supplement-specific animal models.
• General H₂S biochemistry papers (e.g., SQOR reviews) were used for background on H₂S toxicity/oxidation but not promoted as UC-specific anchors.
• Old Roediger-style “curative therapy” claims and FMT+diet case reports were retained as hypothesis-generating only. They were not promoted as cure evidence because they are uncontrolled/case-level and can encourage unsafe overreach.