Medical Research Wiki

Medical TODOs

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tagsmedical-research, todos, clinician-questions, ulcerative-colitis, constipation, pelvic-floor, dairy, lactose, sibo

6 min read

Medical TODOs

Purpose: this is Paul’s lightweight action/research checklist for medical topics that should not get lost inside the larger research wiki. It is not medical advice; it is a clinician-prep and personal-research tracking page.

Active TODOs

UC/proctitis — dairy, milk allergy, and food-trigger rule-out

  • Build a milk/dairy trigger rule-out plan that separates lactose/SIBO from milk-protein, A1/A2, fat/bile, histamine, and additive mechanisms.

    • Why: Paul has a strong personal dairy → blood signal, but lactose intolerance alone usually explains gas/bloating/urgency/diarrhea rather than rectal bleeding. Dairy should be treated as a possible UC trigger/amplifier node crossing a low-reserve rectal barrier threshold, not assumed to be a single uniform cause.
    • Rule-out branches to compare:
      • lactose specifically: lactose-free or lactase-treated dairy comparison, or clinician-guided lactose hydrogen/methane breath testing;
      • SIBO separately: SIBO can mimic/confound lactose intolerance and breath-test interpretation;
      • if lactose-free still triggers symptoms: casein/whey, A1 vs A2 beta-casein, fat/bile load, fermented/histamine effects, protein powders, emulsifiers/additives;
      • celiac/gluten context: clarify whether celiac testing was done while eating gluten.
    • Track if ever tested: exact dairy form, dose, timing, flare/remission baseline, stool form, incomplete evacuation/contact time, mucus, blood, rectal pain, sleep/stress, and ideally fecal calprotectin before/after.
    • Safety note: avoid casual dairy rechallenge during active bleeding/flare; any intentional test should be conservative and clinician-aware.
    • Related pages: Wheat Food-Trigger Mechanisms in UC, Proctitis, Proctitis.

  • Ask GI/allergist to frame dairy as a differential: allergy vs intolerance vs UC flare trigger.

    • Key distinction: “milk allergy caused UC” is too strong; better working hypothesis is milk-triggered loss-of-tolerance / barrier-threshold amplification in a vulnerable distal gut.
    • Make the clinician distinguish these buckets:
      • IgE-mediated milk allergy: classic immediate allergy pathway; often fast symptoms such as hives, swelling, wheeze, vomiting, throat symptoms, or anaphylaxis risk. Possible tests: milk/casein/whey specific IgE blood tests and skin-prick testing. A positive test does not automatically prove it drives UC, but it changes safety/rechallenge planning.
      • Non-IgE milk-protein hypersensitivity: delayed immune reaction to milk proteins, often GI-predominant; skin-prick/specific-IgE tests can be negative. This is the bucket that best fits “food protein causes gut inflammation without classic hives/anaphylaxis,” but it is harder to prove in adults.
      • Eosinophilic GI overlap: eosinophils are allergy-associated immune cells that can infiltrate GI tissue in eosinophilic esophagitis/gastroenteritis/colitis or overlap states. Ask whether old/future biopsies show unusual eosinophils, mast cells, or an “eosinophilic pattern,” especially if symptoms are strongly food-linked.
      • Lactose intolerance / malabsorption: non-immune carbohydrate issue; can cause urgent BM, gas, bloating, cramps, diarrhea. It usually does not directly explain rectal bleeding but could amplify an already inflamed distal gut through urgency/fermentation/contact-time changes. Possible test: lactose hydrogen/methane breath test.
      • Milk-triggered UC flare without true allergy: dairy could reproducibly worsen UC via fat/bile, microbiome, histamine/mast-cell activation, additives/sweeteners, osmotic load, or low-barrier timing even if allergy testing is negative.
    • Clinician questions to preserve:
      • which of the above buckets best fits Paul’s history of milk protein shakes causing urgent bowel movements and later dairy → blood?
      • would testing be useful: milk/casein/whey specific IgE, skin-prick testing, lactose hydrogen/methane breath test, biopsy review for eosinophils/mast-cell/eosinophilic pattern, or calprotectin during dairy-free vs exposed periods?
      • are there red flags that would make any oral challenge/reintroduction unsafe outside medical supervision?
    • Why: non-IgE milk reactions can be GI-predominant and testing can be negative; lactose intolerance is non-immune; UC flare triggering may happen even without classic allergy.

  • Design one small objective dairy-free tracking block before any reintroduction decision.

    • Keep it lightweight: define the dairy-free window, baseline symptom state, and success markers before changing multiple variables. Goal is not “prove dairy is evil”; goal is to learn whether removing milk exposure lowers the distal inflammatory threshold.
    • Baseline to record before starting: current mucus/blood level, urgency, stool form, straining/incomplete evacuation, rectal pain, sleep quality, stress, recent infection/stomach bug, meds/supplements, and whether disease feels active or quiet.
    • Minimum markers during the block: mucus, blood, urgency, stool form, straining/incomplete evacuation, rectal pain, sleep/stress, infections, and ideally fecal calprotectin if practical.
    • Define what would count as a meaningful signal: e.g., less mucus/blood, less urgency after breakfast, improved stool consistency, less rectal pain, lower calprotectin, or fewer “threshold crossing” days when sleep/stress is bad.
    • Reintroduction distinction to preserve if ever attempted: test only one axis at a time — lactose-only vs whey vs casein vs A1/A2 vs additives/sweeteners/fat load. Do not bundle these together, because “dairy” could mean several different biological exposures.
    • Safety note: no challenge during active bleeding, severe symptoms, or poor baseline control; use clinician guidance if allergy is plausible, especially if any immediate allergy symptoms ever occurred.

UC/proctitis — constipation, evacuation, pelvic floor

  • Look into pelvic-floor physical therapy / biofeedback for constipation and incomplete evacuation management.

    • Why: Digest 008 found a small IBD-remission cohort where gut-directed behavioral/pelvic-floor treatment led to “much better” or “very much better” outcomes in 83% of constipation patients.
    • Discuss with: GI, colorectal specialist, or pelvic-floor PT referral source.
    • Related pages: Pelvic Floor Mechanics in UC Proctitis, Proctitis.
    • Safety note: distinguish active inflammation/bleeding from pelvic-floor dysfunction; urgent symptoms such as severe pain, distension, vomiting, fever, inability to pass gas/stool, or heavy bleeding need clinician evaluation.

  • Look into other foods, routines, or methods for reducing constipation and ensuring more complete evacuation.

    • Why: Paul’s personal pattern often includes mucus → constipation/incomplete evacuation → blood/rectal pain, so contact-time reduction may be an important flare-amplifier lever.
    • Research branches to compare: hydration/electrolytes, soluble fiber vs insoluble fiber, psyllium, resistant starch, magnesium/osmotic options, meal timing, toileting posture, motility routines, stress/autonomic downshift, and clinician-guided constipation strategies safe for UC/proctitis.
    • Related pages: Proctitis, Proctitis Methods, Pelvic Floor Mechanics in UC Proctitis.
    • Safety note: avoid aggressive laxative/enema protocols during active bleeding or severe symptoms without clinician guidance.
    • Completed first pass: Digest 011 and Full-Evacuation Strategy in UC Proctitis. Next: discuss/track candidate ladder with clinician context rather than trying high-dose fiber blindly.

  • Build a clinician-safe tracking ladder for constipation candidates.

    • Candidate order to compare: footstool/posture + breathing, kiwi, psyllium/Plantago, PHGG, resistant starch/4-SURE-style diet, PEG/non-fermentative clinician-guided options, pelvic-floor PT/testing if soft stool still feels stuck.
    • Track: stool form, straining, incomplete evacuation, tenesmus, mucus, blood, rectal pain, bloating/gas, sleep/stress, and calprotectin if available.
    • Related page: Full-Evacuation Strategy in UC Proctitis.

  • Research Faecalibacterium prausnitzii / Roseburia / butyrate-producing beneficial commensals in UC.

    • Why: Paul caught that Digest 009 emphasized pathobionts but under-called the beneficial butyrate-producing side of the ecology model.
    • Research branches to compare: whether F. prausnitzii is reduced in UC vs Crohn’s, whether stool abundance reflects mucosal function, what foods/prebiotics may support it, fiber tolerance during UCAC/constipation, and whether any direct next-generation probiotic evidence exists.
    • Related pages: Proctitis, Microbial Positioning in UC.
    • Completed first pass: Digest 010 and Butyrate Ecology in UC. Next: compare constipation-safe prebiotic/fiber/food methods.

Completed TODOs

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