Currently following the
What regular test(s) should I be taking?
- Heavy metals test? - Stool - Viome Stool Test - Blood, stool, hormone - [ ] How to best measure microbiome diversity? - [ ] Ulta Health Panels - [ ] Labcorp Men’s panel - [ ] https://guthealth.org/How can I target dysbiosis in the rectum/distal colon where the proctitis is?
- Fiber reaches the distal colon. Some species of bacteria feed on the gut lining if unfed. Fiber is probably important to keep dysbiotic bacteria behaved. - Studies show that a fiber-free diet can inhibit colitis in certain genetic/microbial contexts by preventing a mucus-dwelling bacterium from triggering inflammation, primarily by limiting nutrient availability and altering microbial metabolism and localization. - This effectively starves out those mucosal dwelling bacteria over time.Which probiotics or prebiotics are best for colitis or proctitis? Mutaflor or Visbiome?
Stool markers to monitor for colitis?
Stool (Fecal) Markers:
- Calprotectin:
- Why it matters: A key marker of intestinal inflammation. Elevated levels strongly indicate active colitis or other inflammatory bowel disease.
- Secretory IgA:
- Why it matters: Reflects the gut’s immune barrier function. Low or high can be relevant in autoimmunity, infections, or unresolved inflammation.
- Occult Blood:
- Why it matters: Detects hidden blood in the stool—bleeding is a classic concern in active colitis.
- Short-chain fatty acids (acetate, propionate, butyrate):
- Why it matters: Levels reflect the health and metabolic activity of your gut microbiome. Butyrate is especially important for colon lining health and healing.
- Pancreatic elastase-1:
- Why it matters: Tests digestive enzyme function. Low levels can cause malabsorption (sometimes misdiagnosed as colitis).
- Commensal bacteria (via qPCR):
- Why it matters: Assesses beneficial vs. harmful bacteria, which is fundamental to gut health and colitis management.
- Aerobic/anaerobic bacterial & yeast cultures, parasite DNA:
- Why it matters: Identifies overgrowths or infections that mimic or worsen gut inflammation.
- Fecal fat, protein breakdown products:
- Why it matters: Help rule out malabsorption or pancreatic insufficiency, which can worsen gut symptoms.
Blood Markers (less specific, but sometimes ordered for colitis):
- CRP (not specifically mentioned here) and F2-isoprostane/Lipid peroxides:
- Why they matter: CRP is general for inflammation; F2-isoprostane & lipid peroxides measure oxidative stress, which is often elevated in active inflammatory bowel conditions.
- Antioxidant capacity:
- Why it matters: Oxidative stress accompanies and intensifies gut inflammation.
Urine Markers:
- Oxalates:
- Why it matters: Secondary for most, but sometimes monitored in gut inflammation due to absorption/processing changes.
Expert outreach
- [ ] Contact GI doctor for escalated meds? - [ ] James dillingham- uc health, POTS, ehlers? Person Meg met that had those. - [ ] Need to find better doctors - [ ] Integrative gastroenterologists - Wholistic approach doctor - [ ] Integrative Medicine Clinics and Functional Medicine Doctors - Reach out to a doctor about peptide BPC-157 - will they prescribe peptides?Things to eat?
- A study in mice showed that supplementing diets with tryptophan (found in turkey, nuts, and seeds) doubles anti-inflammatory T-regulatory cells in the colon, potentially easing colitis by guiding immune cells to inflamed areas.
Things to test
- [ ] Oral TUDCA induced microscopic remission in 45% of patients after 6 weeks. - [ ] “This makes me think that most cases of UC are down to bile acid deficiency’s. low bile → dysbiosis → barrier breakdown → immune activation → chronic ulcerative colitis” - [ ] Carrot salad from ray peat? - [ ] Ashwaganda (link)? - [ ] Oranges for Fatty Liver?Research
- [ ] BPC-157 with Tirzepatide? - [ ] See the chatgpt research here. - [ ] What the heck are peptides? Why is it a whole field? {color=“yellow_bg”} - [ ] Fecal Matter Transplant?Social dominance is gut mediated?
- Transplanting microbiota from dominant rats—particularly those rich in butyrate-producing bacteria like Clostridium butyricum—can restore dominance, highlighting a causal role. This effect is mediated by histone deacetylase 2 (HDAC2) in the medial prefrontal cortex (mPFC), which responds to microbial signals and modulates synaptic activity to influence competitive outcomes - Fecal microbiota transplantation (FMT) experiments provide strong evidence: germ-free mice receiving microbiota from submissive donors develop anti-social, depressive-like behaviors (e.g., reduced sociability in chamber tests and increased immobility in forced swim tests), mimicking submissiveness, while those receiving dominant microbiota do not. - Conversely, social dominance loss in mice perturbs the microbiota-gut-brain axis, altering gut composition (e.g., reduced Muribaculaceae and butanoate metabolism) and prefrontal cortex gene expression, particularly in interneurons involved in GABAergic transmission. - Depleting the microbiome with antibiotics mitigates these effects, increasing resistance to hierarchical demotion and reducing retreat behaviors, suggesting the microbiome amplifies stress responses to status loss. - Multi-omics analyses link these changes to disruptions in pathways like PI3K-Akt signaling and glutamatergic synapses, correlating with behaviors such as pushing or retreating. - The relationship is bidirectional: not only does the microbiome shape dominance, but social status and behaviors also influence microbiome composition. For instance, in zebrafish, dominant individuals show microbiome shifts favoring certain taxa, while chronic subordination or isolation leads to reduced diversity. - Gut microbiome diversity positively correlates with sociability (a composite of extraversion, social skills, and communication), with higher abundances of genera like Akkermansia, Lactococcus, and Oscillospira in more sociable individuals, and lower levels of Desulfovibrio and Sutterella. - Larger social networks are associated with greater microbiome diversity, while traits like anxiety and stress (linked to neuroticism) show negative correlations with diversity. - My levels: - % Butyrate: 19% (reference range 11 – 32) - Considered normal - Don’t know the other things.To follow up on
- [ ] My Iron absorption is pretty low. That can be associated with shortness of breath, also can be caused by IBD. - [ ] Find a dietitian with experience with IBD?For in person
- [ ] Microdosing, ketamine, neurofeedback, and EMDR? “I really want to know more about your perception of pain, how it plays into anxiety, and that condition he mentioned” - [ ] Should I buy a juicer? Recommend one? - [ ] Zinc Carnosine repairs the gut? - [ ] Why does cabbage juice work? - [ ] We ordered half a cow. Is that a no go? Studies seem to show carnivore is good? - [ ] Psychedelic Mushrooms Reduced Human Cellular Aging by 57%, Increased Lifespan in Mice 30% - Thoughts on psilocybin? - [ ] Family cholesterol numbers are high. - [ ] When I run, my lungs hurt, throat flares up, and I start getting phlegm or discharge. My voice cracks and I have a lazy cough for a day or two after - it feels like there’s something wrong with my throat/lungs. - [ ] What testing makes sense? E.g. food sensitivity? - [ ] What about all the people using carnivore to get better and saying plant based diets were worse? - [ ] Should I take Indigo Naturalis (Qing Dai)? - [ ] “For example, transplantation of colitic mouse microbiota to healthy mice led to transmission of disease markers and colitis.” - [ ] Should I still get scanned for PSC (more info, more info, more info)? {color=“green_bg”} Diagnosis relies on blood tests showing elevated liver enzymes (especially alkaline phosphatase), cholangiographic imaging (MRCP or ERCP), and sometimes liver biopsy. - [ ] Is there a test to tell me if I can’t break down some animal proteins such as milk and meat? - The point about protien powder causing problems is interesting. - A2 Milk? This helped Will with skin issues.Other
Is pomogranate juice worth doing? - [ ] Mold/environmental test (histimine triggers) - [ ] Citris vergomont for high cholesterol? - [ ] Beet root candy?! Beet roots? - [ ] Immune tea; phytrust.com. Phyto-teas. Guy had crohns 50 years ago. - [ ] DSMO worth considering? - [ ] He likes food sensitivtiy tests over stool. Skin prick tests for LEAP MRT. What happens to your white blood cells before and after coming into contact with an antigen in food. He likes this test a lot - there are false negatives and positives. - [ ] Best test; food diary.
Optional
- [ ] Can I get vitamin (intracellular vitamin level) testing done? - [ ] Check parathyroid hormone levels (PTH) as last test was in 2016 (perBacklog
- [ ] Get DNA tests done for the kids? - [ ] Medical Medium (the celery juice guy) says UC is caused by the shingles virus. - [ ] Should I try Methylene Blue since it helps with oxygen uptake and ROS? - [ ] Buy a human body replica I can disassemble? - [ ] Try out EFT - tapping on a place in the body and then thinking certain thoughts. Is this effective? Emotional Freedom Technique. - [ ] Could try the Fast Tract Diet, which is for LPR and Crohns. - [ ] Read this long thread - [ ] Send messages to my doctors asking if I might have Crohn’s disease. Why is my ALP elevated for so long? - [ ] Low Dose Naltrexone (LDN)? - [ ] SIBO test? Could contribute to LPR as well. - [ ] Buy hydrogen waterOutstanding Questions (for Swize)
- Genetically predicted UC was found to be causally associated with decreased levels of albumin (ALB) and decreased liver iron content. - Genetically predicted CD was found to be causally associated with increased levels of alkaline phosphatase (ALP). - Liver Disease Risk: - Both UC and CD were found to increase the risk of primary sclerosing cholangitis (PSC). - CD was also found to increase the risk of primary biliary cholangitis (PBC).Done
- [x] Wheat Zoomer (leaky gut) - [x] Talk to doctors about PEMT gene and PC deficiency..Should I be supplementing PC and Liposomal Glutathion? Eggs may not work. Take these. {color=“green_bg”} The PEMT Gene, Phosphatidylcholine, and Liposomal Glutathione: A Breakthrough Approach for Crohn’s Disease and Liver Health
Helios
- [x] Do GI Map test w/gluten peptide testing - [x] Stop Y-Formula, Artemisia, TMG, and probiotic 7-10 days prior {color=“orange_bg”} - [x] Test for H. Pylori happens in this test. Chronic H. pylori can mimic or worsen LPR, GERD, and dysbiosis symptoms by weakening stomach acid. - [x] What Zoomer test (showed high intestinal permeability) - [x] Upload Helios neurotransmitter questionnaireConsumables
- Nicotine helps a lot of people -FMT
Gut-directed hypnotherapy
Traditional Chinese Medicine (TCM) is more effective than prednisone (84%)
Hydrogen Peroxide can induce ulcerative colitis; some microbes produce h2o2
Low acid levels in the stomach are associated with IBD and worsened symptoms
Phosphatidylcholine levels in the gut mucus are 70% lower in people with ulcerative colitis even when not actively flaring
- Phosphatidylcholine in Intestinal Mucus Protects against Mucosal Invasion of Microbiota and Consequent Inflammation - Saturated phosphatidylcholine as dietary additive for colonic mucus: an open label prospective clinical observation trial - Delayed-Release Phosphatidylcholine Is Effective for Treatment of Ulcerative Colitis: A Meta-Analysis - Supplying PC to the colon is challenging; it’s absorbed in the SI. Need to use enteric-coated PC to have a chance.Active IBD is associated with mild to severe metabolic alkalosis. This means the body’s pH becomes too high (more alkaline).
Having no appendix reduces the odds of developing UC by 50-70%.
Removing the appendix early in life lowers the odds of developing ulcerative colitis because the appendix plays an immune-priming and microbiome-reservoir role that can help trigger UC in predisposed people. Studies show the appendix of UC patients produces high levels of: These cytokines are key drivers of UC. - IL-17 - IL-23 - TNF-α Appendix removal outcome varies by age: - Appendectomy before age 20 reduces the lifetime risk of ulcerative colitis by 50–70%. - Appendectomy after colitis develops does not help UC. - Appendectomy for causes other than appendicitis (like incidental removal) gives minor or no protection. - Appendectomy for actual appendicitis gives the strongest protective effect Note that the cecum is ALSO where the small intestine empties into the colon. So that could be another confounding thing.The microbiome exacerbates symptoms
Carnivore diet appears to help some, vegetarian for others, and for others - nothing helps.
Generally the science indicates that the introduction of red meat into diets might increase hydrogen sulfide. Preventing Ulcerative Colitis with Diet More meat = more sulfide.Inflammation appears in other places in the body for some with UC; bile ducts, lungs, skin, eyes, etc. We don’t know why.
A lot of people with UC don’t actually have autoimmune antibodies present. This seems to indicate an auto-immune like response that isn’t strictly autoimmune.
“There are some experts on IBD that question whether it even is autoimmune, but rather an autoimmune like response. They say most people with IBD don’t have autoimmune antibodies. It’s an interesting theory that makes a lot of sense when you look into it”Bifidobacteria breaks down sugar
Colonocytes (colon cells) run on 70% butyrate; not sugar. Butyrate is produced exclusively by bacteria. In UC, they have metabolic impairment that Ulcerative Colitis .
- Colonocytes preferentially oxidize butyrate, a short-chain fatty acid (SCFA) produced by bacterial fermentation of fermentable carbohydrates (especially fibers and resistant starch).
- They can get some energy from sugar, but not much and this is considered a dysfunction generally.
There is an interesting overlap between Pravda’s theory and the **Ulcerative Colitis . Roediger stipulates that hydrogen sulfide (H2S) and nitric oxide (from nitrogen) impairs energy metabolism which prevents them from adequately using butyrate for energy. Pivotal research round that CoA is “locked” by oxidation inside of the cell, impairing butyrate metabolism. **
- Roediger proved that the engine was stalled. Pravda (Radical Induction) proved that a stalled engine doesn’t just sit there—it “smokes” (H2O2), and that smoke is what calls the immune system to the scene
- If Roediger’s hypothesis is that the colon is “starving to death,” the Radical Induction Theory is that the colon is “poisoning itself” as a side effect of that starvation.
- A major validation of both theories came from the 2007 study Santhanam et al., which confirmed that the specific enzyme involved (thiolase) was inhibited by 80% in UC patients. This study specifically mentioned Roediger’s work and showed that the enzyme could be “restarted” using the exact type of reducing agents that the Radical Induction Theory advocates for.
**Faecalibacterium prausnitzii **appears to be the bacterium that downregulates the immune response; but, that’s low or gone in most people with colitis.
Reduced LXRβ signaling in the colon appears to accelerate immune aging and worsen ulcerative colitis, suggesting that impaired lipid and phospholipid regulation—rather than inflammation alone—may be a key driver of disease progression, particularly with aging.
Red and white meat are associated with 2x relapse risk rate. Oddly, no Ulcerative Colitis between objective flares and ultra-processed foods, dietary fibre, polyunsaturated fatty acids, or alcohol.
The PREdiCCt Study: Can we predict IBD flares?
Jobs that involve work in the open air and physical exercise appeared to offer protection against these diseases.
- Work outside where possible - Use a standing desk, incorporate “walking meetings”, get vigorous movement daily - Open windows to allow for natural ventilation and fresh air (this would reduce mold!)Children with newly diagnosed ulcerative colitis (UC) had higher serum levels of lipocalin‑2 (LCN-2), matrix metalloproteinase‑9 (MMP-9), and MMP‑9/LCN‑2 complex than their healthy peers, with LCN-2 showing the best diagnostic performance.
Some people appear to recover from UC after having their Mercury fillings removed.
Faecalibacterium prausnitzii is lacking in colitis patients; this seems like the cornerstone to re-populate.
That physicist also noted this in his research paper.| **Helps a lot** | **Helps a little** | **Hurts** | **Unknown** |
| Mesalamine enema | Deep stretch of pelvis | **Cow’s milk (dairy?)** | Cognitive Behavioral Therapy? |
| Walking/standing | Sitting on exercise ball | Wheat (Gliadin, or Fructans) | Rowing machine? |
| Mindfulness | Castor oil packs? | Lamb? | |
| Fasting! | **Alcohol** | ||
| Good sleep | NSAIDS | ||
| L-Glutamine powder | Antibiotics | ||
| Psyllium Husk powder | Running too hard (oxidative stress) | ||
| Fatty foods? Floating stools.. | |||
| Chicken thighs/legs! | |||
| Sitting / Flexing | |||
**Mouth taping** (at night)
- Improves sleep quality - 47% reduction in apnea symptoms - Oxygen saturation improves by \~30%**Sauna**
- Improved cardiovascular health - Detoxification through sweating - Reduced inflammation and muscle recovery - Stress reduction and mental clarity**Workout/movement**
- Combats stress - Decreases inflammation**Hydrate often** (coconut water, or electrolyte mix)
- Enhances short term memory - Reduces anxiety; increases stress tolerance by regulating cortisol - Improves emotional regulation - Essential for skin health**Sunlight exposure** (10-11am)
- Anti-inflammatory - Vitamin D - Metabolic improvements**Castor Oil Packs (at night)**
- Reduced inflammation - Improved digestion - Lymphatic circulation**Deep Breathing** (4-7-8 method)
- Reduces stress and anxiety (+vagal nerve stimulation) - Reduces blood pressure by 3-4mmHg!**Stelo Glucose Biosensor**
Tracks glucose levels[CAR-T cell therapy](https://www.ddw-online.com/first-use-of-car-t-therapy-to-treat-ulcerative-colitis-37427-202510/) (revolutionary if it works; reprograms the immune response)
Researchers reported the initial use of CAR-T cell therapy to target inflamed gut tissue in UC, showing potential to reset immune responses and promote mucosal healing in preclinical models. CAR-T could revolutionize UC treatment by offering a one-time intervention for refractory cases, though further human trials are needed**BOOM-IBD (or BOOM-IBD2) clinical trial** using a sacral nerve stimulation (SNS)
[A Game-Changing Wireless Implant for Personalized Chronic Pain Relief - USC Viterbi \| School of Engineering](https://viterbischool.usc.edu/news/2025/06/a-game-changing-wireless-implant-for-personalized-chronic-pain-relief/) [www.facebook.com](https://www.facebook.com/groups/UlcerativeColitisSupport/permalink/26199791642951001/#) MB310 Synthetic microbiome modulation: [Microbiotica Announces Impressive Results in its Phase 1b Trial of MB310 in Ulcerative Colitis](https://microbiotica.com/microbiotica-announces-impressive-results-in-its-phase-1b-trial-of-mb310-in-ulcerative-colitis/)
“Potential to become a new modality in the treatment of ulcerative colitis offering prolonged remission without immune suppression” - Clinical remission achieved in 63.2% (12/19) MB310 treated patients vs 30.0% (3/10) in placebo treated patients (ITT analysis) - All MB310 treated patients who entered follow-up (n=12) achieved sustained clinical remission and complete resolution of rectal bleeding - MB310 treatment improved objective histological measures of disease activity with striking improvements in microscopic markers of mucosal damage - MB310 treatment reduced the key bowel inflammation biomarker, faecal calprotectin - “If confirmed in larger studies, MB310 has the potential to transform the management of ulcerative colitis by restoring a healthy gut barrier thereby changing the natural history of the disease resulting in long-term clinical remission”[**MRM Health’s MH002 Microbiome Therapy**](https://www.biopharminternational.com/view/microbiome-based-therapy-gains-fda-fast-track-in-ulcerative-colitis)
[NIH Finds Cells Protecting Against Bowel Disease](https://www.miragenews.com/nih-finds-cells-protecting-against-bowel-disease-1688338/)
Scientists at the National Institutes of Health (NIH) have discovered a crucial regulatory pathway that protects the intestine from chronic inflammation. The study revealed that rare, harmful mutations in the **GPR15 gene** prevent protective regulatory T cells (called CD8+ TIGR cells) from migrating into the colon lining. When these cells are missing, inflammatory cells accumulate and drive severe, early-onset inflammatory bowel disease (IBD). This finding opens up new possibilities for targeted treatments that can restore this homing mechanism without the broad side effects of traditional immune-suppressing therapies.AI Prompts
1. Research the most effective lifestyle changes that can lead to remission or long-term control of ulcerative colitis, preferably without medication. Include both evidence-based (clinical studies, trials) and credible anecdotal or alternative medicine sources. No need to limit to specific categories—diet, stress, exercise, sleep, and microbiome therapies are all relevant. Focus on ulcerative colitis rather than proctitis unless there’s strong overlap. Prioritize what actually works best.[ChatGPT Project](https://chatgpt.com/g/g-p-683b8e23ca148191bd0110c04e3f4232-ulcerative-colitis/project)
- [ ] [ChatGPT - Eastern Medicine for UC](https://chatgpt.com/share/686af9ad-fdc0-8001-99df-9a5f6bc370db) - [ChatGPT - Lifestyle Changes for IBD](https://chatgpt.com/share/68649c6e-0e94-8001-af25-54d6ced0f566) {color="green_bg"} - [ChatGPT - Colonic hydrogen peroxide research](https://chatgpt.com/share/68f41a91-5528-8001-ba6c-c7ccd3d39516) {color="green_bg"} - [Perplexity summary of the theory - very good](https://www.perplexity.ai/search/please-research-colonic-epithe-T4aZCa_xSo6zXRpiTTw9yA#0) - [**ChatGPT**](https://chatgpt.com/share/686b3c70-ad68-8001-9bbc-866ad7e205ae)[: BPC-157 and Ulcerative Colitis](https://chatgpt.com/share/686b3c70-ad68-8001-9bbc-866ad7e205ae) - [**ChatGPT**](https://chatgpt.com/s/dr_688ed63674f48191b5483556264e5b5e)[:Preventing and Managing Proctitis through Microbiome Support](https://chatgpt.com/s/dr_688ed63674f48191b5483556264e5b5e) - [Please research the best non-pharmecutical cures for proctitis.](https://www.perplexity.ai/search/please-research-the-best-non-p-BrRyXFgmTmW.MCA.ykd0FQ)[HBOT](https://x.com/bryan_johnson/status/1902044120807567436) ([Sample at-home device](https://www.hpotech.com/hyperbaric-chambers/zeugma-monoplace-hyperbaric-chamber/))?
- Wound healing - Severe autism - Lyme disease - Systemic inflammation?[BPC-157’s benefits for proctitis](https://notebooklm.google.com/notebook/e6fbb0d8-a0c5-439b-ace0-5e37b649b769)
[Rectal Ozone Therapy is promising](https://www.417integrativemedicine.com/articles/what-is-rectal-ozone)
[The IBD Therapeutic Pipeline Is Primed to Produce - Practical Gastro](https://practicalgastro.com/2019/04/10/the-ibd-therapeutic-pipeline-is-primed-to-produce/)
\[Physicist\] [(PDF) Understanding the Pathogenesis of Inflammatory Bowel Diseases, and moving towards a "Functional Cure"](https://www.researchgate.net/publication/370419818_Understanding_the_Pathogenesis_of_Inflammatory_Bowel_Diseases_and_moving_towards_a_Functional_Cure)
**Roediger Hypothesis (“Starved Gut” theory)**
[Revisiting the “starved gut” hypothesis in inflammatory bowel disease](https://pmc.ncbi.nlm.nih.gov/articles/PMC9831042/) This alternative theory suggests that UC might be caused by an **intracellular deficiency of coenzyme A** in colonic cells, potentially due to toxins like hydrogen sulfide and nitric oxide. Based on the Roediger hypothesis, diets high in **sulfur** (meat, eggs, cheese) and **nitrogen** (certain vegetables) may contribute to the condition. - The **Roediger Hypothesis** proposes that **ulcerative colitis is fundamentally a disease of impaired energy metabolism in colonocytes**, specifically due to **defective utilization of short-chain fatty acids (SCFAs), especially butyrate**. > **In ulcerative colitis, colon epithelial cells are unable to adequately use butyrate as an energy source, leading to epithelial dysfunction and inflammation.** - The hypothesis helps explain several UC features: - Why UC is limited to the colon - Why **smoking** (which increases butyrate oxidation) is protective - Why **diversion colitis** occurs when fecal SCFAs are absent - Why **topical therapies** (e.g., rectal meds) are effective - Why early disease is mucosal rather than transmural - The Roediger Hypothesis remains **highly relevant**, particularly for: - Distal disease (proctitis) - Early UC - Diet- and microbiome-focused adjunct therapies - From Roediger’s own framework, remission requires: 1. **Adequate butyrate** 2. **Ability to oxidize it** 3. **Low sulfide burden** 4. **Reduced epithelial stress** 5. **Time for mucosal repair** - From a Roediger-aligned lens, your disease is driven by: 1. **High epithelial energy demand** 2. **Impaired butyrate oxidation** 3. **Localized metabolic stress points** (rectum + cecum) 4. **Secondary immune activation** - He says to**Dr. Jay Pravda’s “hydrogen peroxide theory of UC”**
RECOMMENDED TREATMENT PROTOCOL:
- **Topical Multicomponent Enema:** Administered once daily (usually at bedtime) for two weeks, then once every other day for two weeks. - **Formulation:** Add the following to a standard 60-milliliter enema bottle containing **4 g of mesalamine (5-ASA)** (after removing 20 mL of solution): - **15 mL of 1 molar sodium butyrate** (1.7 g) - **5 mL of sodium cromolyn** (total 100 mg) - **1 mL of budesonide** (5 mg/mL) - **Rationale:** Each component targets H₂O₂ and inflammation: - **Mesalamine (5-ASA):** Neutralizes extracellular H₂O₂ - **Sodium Butyrate:** Increases colonocyte glutathione (GSH), enhancing intracellular H₂O₂ neutralization - **Sodium Cromolyn:** Stabilizes mast cells, preventing histamine release and conversion to H₂O₂ - **Budesonide:** Inhibits neutrophil infiltration and decreases neutrophil H₂O₂ production - **Systemic Oral Reducing Agent:** - **Medication:** R-dihydrolipoic acid (RDLA) 300 mg twice daily (total 600 mg daily). *Note: Use the reduced form (RDLA), not the oxidized form (alpha-lipoic acid)* - **Duration:** Start with enema therapy and continue for 4–6 months. For long-term remission maintenance, continue RDLA indefinitely - **Rationale:** RDLA is an amphipathic antioxidant that directly reduces H₂O₂ and recycles other antioxidants like GSH, restoring cellular redox homeostasis and preventing relapse - **For Severe UC:** Consider intravenous **Sodium Thiosulfate (STS)** to rapidly reduce systemic and colonic H₂O₂ and restore redox homeostasisHis youtube comment: Where is the H2O2 coming from in UC Patients?
Where is the H2O2 coming from in UC patients?I explain this in detail in an upcoming publication, which is currently winding its way through the review process. In brief, all cells in the body produce H2O2. The intracellular site of excess H2O2 production depends upon the nature of oxidative stress the patient is exposed to. For instance, stress is a common oxidative stressor involved in relapse. Stress causes colonic hypercontractility, which releases large amounts of serotonin from enterochromaffin cells in the colonic epithelium. Serotonin is internalized by colonocytes and metabolized to H2O2 via monoamine oxidase. Acute or chronic stress can increase intracellular H2O2 and overwhelm cellular reductive capacity causing extracellular diffusion of H2O2 and subsequent UC. Dietary fat is metabolized by peroxisomal beta-oxidation, which generates large amounts of H2O2; thus high fat diets are oxidative stressors that increase the risk of UC. Smoking cessation removes the electron transport chain (ETC) inhibition caused by chemicals in tobacco. ETC hyperactivity increases electron leakage leading to increased H2O2 production etc.
And, why is it higher (or, is it higher in UC patients vs the healthy cohort)?
Yes, H2O2 production is higher in UC patients. Check out this study.
Impairment of mitochondrial acetoacetyl CoA thiolase activity in the colonic mucosa of patients with ulcerative colitis. GUT 2007;56:1543-1549. [https://pubmed.ncbi.nlm.nih.gov/17483192/](https://www.youtube.com/redirect?event=comments&redir_token=QUFFLUhqbEtSMUUxYk5NX0FnSFZWNjBqekZJMTRBQ3Bud3xBQ3Jtc0tsS19mQWJyQUNmSXFVeWJZNzRxZElJdVFqTEdBQ1NvUDdwc1FQUE4zbll0SUZQYVBLTHVmQkZ6cUVNX0VTazFHdjIzOERuMG1JNXY3QmFfVDRVblVXZ2xfa2x4cW5DSnZmelNadjZBVjZtVkFIVjRvUQ&q=https%3A%2F%2Fpubmed.ncbi.nlm.nih.gov%2F17483192%2F) H2O2 production is higher in UC patients because the initial rise in colonocyte H2O2 subsequent to oxidative stress exposure leads to mitochondrial oxidative damage resulting in mutations of the mitochondrial genome (mitochondrial heteroplasmy). This increases electron transport chain leakage, which generates additional H2O2 that causes addition mitochondrial genetic damage and mutations. The end result is a vicious cycle of ever increasing colonocyte H2O2 and more frequent (and severe) bouts of relapse. Here's a general review:
Can Ulcerative Colitis Be Cured? Discovery Medicine. 2019;27;197-200. [http://www.discoverymedicine.com/Jay-Pravda/2019/05/can-ulcerative-colitis-be-cured/](https://www.youtube.com/redirect?event=comments&redir_token=QUFFLUhqbVhpcnVNMVdjak5SUHRFUURuNmluaGlUTVhQd3xBQ3Jtc0ttZnBvVnNrMm14dl9mY0NTT1dHdUVlSVFRSVV2cGkxOHRXeHAtLXhPQ08zcFpyeVRRTXpyMkppRXNRZk1aNFZsaUhZWWQ5dnlJWGRrT1pYUFZMNm9VeTdMYnBSejZOaWZhSFVTemh4dG5GeXB3M1g2aw&q=http%3A%2F%2Fwww.discoverymedicine.com%2FJay-Pravda%2F2019%2F05%2Fcan-ulcerative-colitis-be-cured%2F) It is a dysbiotic bacteria causing a rise in H2O2? Or, another pathogen? Or, is it an environmental trigger, i.e., mold or heavy metal build-up affecting the cells negatively causing them to release H2O2?
It can be any of the above. Any environmental factor that increases H2O2 production in or in contact with the colonic epithelium can lead to UC. For example, bacterial infectious colitis attracts neutrophils into the colonic epithelium. The neutrophilic generated H2O2 can diffuse into colonocytes leading to mitochondrial damage with a subsequent rise in colonocyte H2O2 that can manifest as UC after the infection is resolved.
Another example is mercury that irreversibly binds and inactivates thiols such as glutathione, which is needed to neutralize cellular H2O2. The result is increased cellular H2O2 and UC when the H2O2 leaks out of the colonocyte. Here’s the reference:
Ulcerative colitis reactivation after mercury vapor inhalation. Am J Ind Med. 2006;49:499-502. [https://pubmed.ncbi.nlm.nih.gov/16691608/](https://www.youtube.com/redirect?event=comments&redir_token=QUFFLUhqbnMtWHlHXzJhMnNmRTdtVFRxM21TcXZCX0VtZ3xBQ3Jtc0tsSUYwS0JuUGx0aGNNTklkeGQ3cVljTWRucEhNcndYV2s1R1FBRG5WWHdhczZmT3YtbkRuTi1HMl96WTl6WUEtVjhJMWw2MHVXTXp6TUl2STRZVUNjNFJ0ejF5STFRelNDeHljdXBEQ1pKb21fMWN2QQ&q=https%3A%2F%2Fpubmed.ncbi.nlm.nih.gov%2F16691608%2F) What neutralizes the H2O2 in a UC patient's colon? The ALA and butyrate???
I explain this in detail in my upcoming publication. i have ran out of space.
Youtube comment: Do antibiotics cause oxidative stress?
Answer: I have seen this before. Antibiotics are meant to eradicate pathogenic (disease causing) bacteria but they can also damage mitochondrial in our cells because mitochondria are descended from bacteria. When mitochondria in the cells lining the inner surface of the large intestine (called colonocytes) get damaged they produce excess hydrogen peroxide. Antibiotics can also reduce the “good” bacteria in our large intestine, which are collectively called the microbiome. This can also cause the colonocytes to produce excess hydrogen peroxide. I developed a therapy whose known mechanism of action is to neutralize hydrogen peroxide. I will soon be submitting a paper for publication that explains this in detail.His opinion on Crohn’s disease
Crohn’s disease is very different from ulcerative colitis. The evidence indicates that UC is caused by too much hydrogen peroxide in the cells that line the inner surface of the large intestine. On the other hand, the evidence points to an antigenic overload of the inner layer of the intestinal lining called the lamina propria as the cause of Crohn’s disease. I added a link (below) to my paper explaining this. I initially focused on developing a treatment for UC because all the components to treat and induce long-term remission were available “off the shelf”. Crohn’s disease can also be effectively treated to induce long term remission but development of this type of new treatment would take specialized resources, which I do not have.In any case, It’s very difficult to develop cures for any disease because not everyone likes cures. JP [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3070014/](https://www.youtube.com/redirect?event=comments&redir_token=QUFFLUhqbWgyUzh1cE1MTUs2SXFTendyREQ0cGJjS01vQXxBQ3Jtc0trM3dWSTYySVpyVGg5cHI0NVFqVzlBbFowLVJrTElEbUVOVUZRM2tzS1FQcHp3ajQ4S2NtTUR0M0NMR1lKdjZ1ZDRSNDVPc2MtRHNZWk4yWHdxelRBZ1lBRzRjcEhXcDZMUks0N0ZuaEREb0FFT3o4RQ&q=https%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC3070014%2F)
**Phosphatidylcholine deficiency**
Dysbiosis
This [Crohn’s Disease test](https://otakaropathways.co.nz/order-tests/) looks for a specific bacteria that they believe to be causing Crohn’s in some people.
[Antibiotic Use](https://x.com/RiverRising1/status/1991174000567894113?referrer=grok-com)
[EBV Virus mimics colitis](https://www.reddit.com/r/UlcerativeColitisRDLA/comments/1ecttch/viral_colitis_or_ulcerative_colitis/)
[These are the things](https://www.reddit.com/r/UlcerativeColitisRDLA/comments/1ecttch/comment/lfn0g74/?utm_source=share&utm_medium=web3x&utm_name=web3xcss&utm_term=1&utm_content=share_button) one person was taking for EBV.[Aerolysin bacteria causes some cases of it?](https://www.newscientist.com/article/2505175-common-type-of-inflammatory-bowel-disease-linked-to-toxic-bacteria/?utm_term=Autofeed&utm_campaign=echobox&utm_medium=social&utm_source=Twitter#Echobox=1763772691)
[Toxic Bacteria Spur Colon Inflammation in Ulcerative Colitis](https://www.medscape.com/viewarticle/toxic-bacteria-spur-colon-inflammation-ulcerative-colitis-2025a1000wgk) “Finally, the researchers looked for *Aeromonas *bacteria in stool samples. They found them in 72 per cent of 79 people with ulcerative colitis, but only 12 per cent of 480 people without the condition. This test couldn’t reveal whether these bacteria were MTB and therefore if they produced aerolysin.”[Aeromonas Bacteria (macrophage-toxic bacteria) were present in many UC patients](https://pubmed.ncbi.nlm.nih.gov/41264716/) (not me, though)
**MAP Virus**: [UC & Crohn's disease: is ](https://pmc.ncbi.nlm.nih.gov/articles/PMC3031217/#B60)[*Mycobacterium avium *](https://pmc.ncbi.nlm.nih.gov/articles/PMC3031217/#B60)[subspecies ](https://pmc.ncbi.nlm.nih.gov/articles/PMC3031217/#B60)[*paratuberculosis *](https://pmc.ncbi.nlm.nih.gov/articles/PMC3031217/#B60)[the common villain?](https://pmc.ncbi.nlm.nih.gov/articles/PMC3031217/#B60)
The article "[Ulcerative colitis and Crohn's disease: is Mycobacterium avium subspecies paratuberculosis the common villain?](https://doi.org/10.1186/1757-4749-2-21)" proposes a unified hypothesis that **Mycobacterium avium subspecies paratuberculosis (MAP)** is the single infectious agent responsible for both Crohn’s disease (CD) and ulcerative colitis (UC). The key findings and arguments presented in the paper include: - **MAP as the Etiologic Agent:** MAP, which causes Johne’s disease in animals, has been consistently identified in humans with both CD and UC. The author argues that the two conditions are different clinical expressions of the same infection rather than separate "idiopathic" diseases. - **Evidence from Disease Clusters:** Studies of both related families and unrelated individuals (such as school classmates) show that CD and UC often appear in the same clusters. This suggests an environmental, infectious transmission—likely through contaminated water or milk. - **Factors Influencing Disease Phenotype:** The author identifies five main factors that determine whether a MAP infection manifests as UC or CD: - **Bacterial Dose:** Small doses of MAP typically result in UC, while larger doses lead to CD. - **Age at Infection:** Adults tend to develop UC shortly after infection, whereas children often develop CD after a long latency period. - **Smoking:** While smoking is often thought to "protect" against UC, the author suggests it actually switches the disease phenotype from UC to CD. - **Genetics and Sex:** Specific genes and gender-based immune responses also influence which disease type an individual develops. - **A New Path for Treatment:** The paper concludes that if MAP is accepted as the cause, public health priorities should shift toward the [prevention](https://pmc.ncbi.nlm.nih.gov/articles/PMC3031217/#abstract1) of infection (such as through vaccination and water treatment) and the development of effective antibiotic treatments to cure already infected individuals.An infection of the [lining with a bacteria](https://centrefordigestivediseases.com/ulcerative-colitis/#:~:text=The%20postulated%20causal%20agent%20is%20said%20to%20be%20an%20infection%20of%20the%20lining%20with%20a%20bacteria%2C%20Fusobacterium%20varium%20identified%20by%20researchers%20from%20Japan), Fusobacterium varium (identified by researchers from Japan)
Researchers observed that: - **Fusobacterium varium**, an anaerobic, gram-negative bacterium normally found in the gut and oral cavity, was: - Found in **higher abundance** in colonic mucosa of some UC patients - Able to **adhere to and invade epithelial cells** - Capable of producing **butyrate-related toxins** (notably high levels of butyric acid in the wrong context), which can damage epithelial cells In animal models: - Instillation of *F. varium* or its metabolites caused **colitis-like inflammation** - In small human trials, **antibiotic regimens** targeting anaerobes (e.g., amoxicillin + tetracycline + metronidazole) led to **temporary symptom improvement** in some UC patients This led to the **postulation** (not proof) that *F. varium* might act as: - A **trigger** in susceptible hosts - Or an **amplifier** of inflammation once disease is established **What this hypothesis does NOT establish** Crucially, the evidence **does not meet criteria for causality**: - *F. varium* is also found in **healthy individuals** - Its presence does **not precede disease onset** in longitudinal studies - Eradication does **not result in durable remission** - Relapse occurs without re-infection - No Koch’s postulates (modern or molecular) are satisfied As a result, the consensus interpretation is: > Fusobacterium varium is more likely an opportunistic or secondary organism that thrives in the inflamed UC environment, rather than the primary causeRed meat → hydrogen sulfide theory
This theory states that red meat consumption increases hydrogen sulfide content in the gut, which is toxic.PSC potentially
Autoimmune theory
Antibodies associated with Crohn’s and Colitis
Genes associated with Crohn’s and Colitis
Schistosoma Ulcerative colitis (parasites)
C Difficil infection
[The Microbiome and Clostridium Difficile - Practical Gastro](https://practicalgastro.com/2017/12/02/the-microbiome-and-clostridium-difficile/) Josh Dech ([Gut Solution](https://gutsolution.ca/))
[Steven Root](https://stevenroot.co/) (has IBD, reflux himself)
Crohn’s Colitis Lifestyle
[**Dr. Chanu Dasari, MD**](https://www.youtube.com/@MindGutImmunity)**; phytonutrient diet**
Dr. Snow ([The Natural Gastro Solution](https://www.thenaturalgastrosolutions.com/))
He’s very cheap, only 400\$. Sells supplements from **Moss Nutrition** - [InflammaSelect 120 VC](https://www.mossnutrition.com/product/inflammaselect-120-vc-m017/) Thinks that: - All IBD/IBS is the same, varying forms of the same thing - Caused by antibiotics - Need to eat the same things that make up the gut lining in order to repair - Some people on FB say he helped them - Has a free ebook, does not tell you what to take though[Jacob Coulson](https://www.facebook.com/jacocowellness)
Seems to have some sort of mix that he sells that improves colitis or cures it.[Dr. Jackie McEwen-Powel](https://www.facebook.com/profile.php?id=61563906296060) (wrote [Well Now](https://www.wellnow.co.za/))
[Dr. Mark Davis ND](https://www.markdavisnd.net/) - [**Book Here**](https://www.foundational-medicine.com/ourapproach) (Naturopath, IBD/FMT)
[High Carb Health](https://www.highcarbhealth.com/)
[Healthy With Nicole](https://www.youtube.com/watch?v=mAOivA266Wg)
Wrote “How I healed my ulcerative colitis” which advocated a carnivore diet initially, but she’s since been influenced by Peat’s work and healthy ingestion of sugar and carbs.Traditional Chinese Medicine (LOOK AT THIS)
Currently, TCM is widely used in the treatment of UC in Eastern Asian countries. Langmead *et al* has reported that herbal remedies for the treatment of IBD include ***slippery elm, fenugreek, devil's claw, Mexican yam, tormentil*, and *Wei tong ning* (a TCM)**.\[[16](https://www.google.com/url?sa=E&q=https%3A%2F%2Fpmc.ncbi.nlm.nih.gov%23ref16),[17](https://www.google.com/url?sa=E&q=https%3A%2F%2Fpmc.ncbi.nlm.nih.gov%23ref17)\] *Slippery elm, fenugreek, devil's claw, tormentil*, and *Wei tong ning* are novel drugs in the management of IBD. Chen et al reported that 118 cases of UC patients were treated with integration of TCM and that 86 cases of UC were treated with prednisone as controls.\[[18](https://www.google.com/url?sa=E&q=https%3A%2F%2Fpmc.ncbi.nlm.nih.gov%23ref18)\] The therapeutic effects were observed and compared after two therapeutic courses of 40 consecutive days. **As a result, there were 39 cases cured, 60 cases improved and 19 cases failed, with a total effective rate of 84% in TCM-treated group**. In contrast, there were 15 cases cured, 37 cases improved and 34 cases failed, with a total effective rate of 60.5% in prednisone-treated group (*P* \< 0.01). These data indicate that treatment of UC by the integrated TCM method is superior to that by simple Western drugs, such as prednisone and that it is also safe and effective in maintaining remission of UC.\[[16](https://www.google.com/url?sa=E&q=https%3A%2F%2Fpmc.ncbi.nlm.nih.gov%23ref16),[18](https://www.google.com/url?sa=E&q=https%3A%2F%2Fpmc.ncbi.nlm.nih.gov%23ref18)\][Dan Purser, MD](https://share.google/Xy73dELl0EZLyt8FW) (PEMT gene and PC as a cure for UC)
Recommends Liposomal Glutathione and Phosphatidylcholine, says it addresses PEMT/MTHFR issues in his colitis patients and functionally cures them.[Naturally Treating Ulcerative Colitis and Crohn's](https://www.youtube.com/watch?v=XL2NpGa_IDY)
Dr. Dan Purser discusses natural approaches to treating Ulcerative Colitis and Crohn's disease. He emphasizes that while he cannot cure these conditions, his methods have shown significant improvement in symptoms. Here are the key points of his approach: - **Genetic Testing (MTHFR and Glutathione Errors):** Dr. Purser highlights the importance of checking for genetic errors, particularly MTHFR and glutathione errors, which he has observed in almost all his Crohn's and ulcerative colitis patients (3:56). He suggests using the Foundation Methylation Wellness test or 23andMe's health and ancestry link (with privacy precautions) and then utilizing a platform like NutraHacker to interpret the raw data (5:50). - **Glutathione Supplementation:** He strongly recommends a patented glutathione supplement, which he claims is a "game changer" for his patients (7:11, 18:38). This supplement also helps heal rectal/anal fissures associated with Crohn's when applied topically (12:31). - **MTHFR Support (B Vitamins):** To address MTHFR errors and related B vitamin absorption issues, he suggests MTHFR Renew or Endure, or for sensitive individuals, "Pyramid Pure Melt" chewables (7:39, 9:08). - **Probiotics:** Dr. Purser stresses the crucial role of high-quality probiotics. He recommends Nature's Way Healthy Trinity (10:44) and Garden of Life Raw Probiotics Ultimate Care (17:12), suggesting taking them with yogurt. - **Micronutrient Testing:** He advocates for comprehensive intracellular micronutrient testing, like the CMA Micronutrient test by Cell Science, to identify specific vitamin deficiencies (14:57, 25:41). He notes that addressing these deficiencies is vital for healing (19:47). - **Diet:** While acknowledging that many patients are emaciated and struggle with absorption, he broadly suggests a paleo-like diet, but emphasizes that the primary focus should be on nutrient absorption (21:14). - **Addressing Anemia:** He explains that anemia in these patients often stems from bleeding in the colon and vitamin deficiencies, both of which need to be addressed (22:05). - **Toxic Element Testing:** Dr. Purser mentions toxic element testing, such as the Jupiter Nova test, to check for heavy metals like mercury, which some patients have linked to gut issues (25:08). - **Individualized Approach:** He reiterates that while these are general recommendations, severe cases might require a more in-depth, personalized approach, potentially including injectable B12 or IV nutrient therapy (23:00, 26:57).[PC can save your gut??](https://www.youtube.com/watch?v=ClF0WsDt45M)
[What can you do for your gut? Don’t suffer all your life](https://www.youtube.com/shorts/kxUT931PxOc)
[Natural Treatment for Crohn’s?](https://www.youtube.com/shorts/eDsBZLmwK-s)
[Heal the Gut by Addressing One Genetic Error?](https://www.youtube.com/watch?v=9zEB1m2p-Dw)
[Possible Cause of Crohn's Disease?](https://www.youtube.com/watch?v=I_jxDWgax6A)
[10K views · 92 reactions \| 🧬 Dealing with Crohn’s or ulcerative...](https://www.facebook.com/watch/?v=784980643882777)
[The Microbiome Expert](https://themicrobiomeexpert.com/)
Seen people on FB speaking highly of him.The Walter Clinic (now retired, dammit!)
[Walter Clinic \| Moose Jaw SK](http://facebook.com/WalterClinic) This guy seemed like the real deal. Was getting patients into remission, saying he was healing their immune systems. His old domain, **goodlifeagain.com**, is available to purchase. {color="green_bg"}[Nick Norwitz](https://x.com/nicknorwitz) healed his UC with Keto
Vegetable Police (funny guy)
- [How I Healed Myself From Ulcerative Colitis: A Step By Step Guide That Always Works!](https://www.youtube.com/watch?v=XcnRmt6hxyc) - **Diet Change Was Crucial:** The speaker claims to have put ulcerative colitis into remission through natural methods, primarily by changing his diet. He emphasizes that contrary to what some doctors say, diet plays a huge role in both triggering and healing this disease. He initially adopted a fruit-based raw vegan diet inspired by David Klein’s work, focusing on peeled fruits like papayas, mangoes, bananas, apples, and grapes as the most soothing and healing foods for the colon. - **Eliminating Dairy and Toxic Foods:** He found that dairy was a major trigger for his flare-ups. Removing all dairy from his diet led to sustained remission. Processed foods, fast food, and other toxins also contributed to his symptoms and required elimination. - **Celery Juice and Cabbage Juice:** Drinking plain celery juice every morning (about two cups, made from one whole head of celery) significantly improved his digestion over several months by rebuilding stomach acid and thus improving nutrient absorption. He also recommends cabbage juice for its purported ulcer-healing effects, though he admits it's unpleasant to drink. - **Water Fasting (Supervised):** He suggests that a supervised water fast is the fastest way to heal the colon, but recognizes this isn't practical for most people. For real-world healing, he recommends sticking to fruit, avoiding raw vegetables, nuts, seeds, beans, meat, eggs, and dairy during recovery. - **Discipline and Consistency:** Healing requires strict discipline and consistency, often for months at a time. He cautions against returning to trigger foods too soon, as this led to repeated setbacks in his own journey. He advocates for staying on healing foods well past the point of feeling better to truly complete the healing process. - If you need a **step-by-step protocol**, here’s his simplified version: - Wake up and drink water until hydrated - Drink 2 cups of plain celery juice every morning (no additives) - Optionally add cabbage juice (and consider cabbage juice enemas) - Drink soothing herbal teas (slippery elm, marshmallow root, licorice) - Eat only peeled, high-water fruits for an extended period, avoiding all harsh, scratchy, or high-protein foods (including beans, nuts, meat, dairy, eggs) - Persist with the diet for months, especially beyond when symptoms resolve, to ensure complete healing[Mark Hyman](https://drhyman.com/pages/function-health) (Functional Med, General)
C C on youtube (Matt recommended) talks SIBO
[Crohn’s Naturally](https://www.crohnsnaturally.com/)
[Dr. Sarah Myhill](https://www.youtube.com/watch?v=XpJkA-3XZlY&t=1218s)
Ray Peat &
Someone on [Reddit tried Ray Peat’s method](https://www.reddit.com/r/UlcerativeColitis/comments/1lmr136/peaty_approach_to_uc/) and reported improvements.
[Shawn Baker MD](https://www.youtube.com/watch?v=USJRSiJL9iA)
[Gut Optimized](https://x.com/GutOptimized)
[**This doctor**](https://ndnr.com/gastrointestinal/therapeutic-retention-enemas-an-underutilized-modality-for-uc/) has impressive knowledge of enema use
[IcyFrog on reddit had luck with FMT and fasting](https://www.reddit.com/r/UlcerativeColitis/comments/1iiu8o2/comment/mbdxy1l/?context=3) (and [eats raw fruits/veggies](https://www.reddit.com/r/UlcerativeColitis/comments/1iiu8o2/comment/mb8wb5d/?context=3))
Another user said “[Fasting, bone broth, high dose vitamin b, c, d zinc and organic Whole Foods](https://www.reddit.com/r/UlcerativeColitis/comments/1m8zxs7/comment/n56jpty/?utm_source=share&utm_medium=web3x&utm_name=web3xcss&utm_term=1&utm_content=share_button).”
Honnas ([**Biome Optima Course**](https://biome-optima.thinkific.com/courses/take/biome-optima/texts/19749883-the-importance-of-mental-toughness-resilience-envisioning-success)**, **offers [coaching](https://www.teamhonnas.com/resources/nutrition-coaching))
Medical Medium
[Crohn's, Colitis, & IBS - Radio Show Archive by Medical Medium](https://soundcloud.com/medicalmedium/crohns-colitis-ibs?in=eve-falco/sets/me)Jim Humble with MMS Theory & Chlorine Dioxide???
[KliniPharm Facebook group](https://www.facebook.com/KliniPharmShop/)
- Creates enteric-coated Phosphatidylcholine - See their “SpongiCol” line of products[Carnivore & Keto Diet](https://pmc.ncbi.nlm.nih.gov/articles/PMC11409203/)
**Clinical improvement was universal:** All 10 patients with inflammatory bowel disease (IBD), including both ulcerative colitis and Crohn's disease, who adopted a ketogenic or carnivore diet experienced significant clinical improvement. **Dietary composition:** The diets of the patients primarily consisted of meat, eggs, and animal fats. The study highlights that the elimination of plant matter and processed foods may be a key factor in symptom relief.**Autoimmune Protocol (AIP) Diet (73% remissions in study)**
An elimination diet derived from paleo principles, AIP removes grains, dairy, legumes, nightshades, and processed foods, focusing on meats, vegetables, and healing broths. **Notably, a 2017 pilot trial **(open-label) tested the AIP diet in 15 adults with active IBD (5 UC, 10 Crohn’s). The results were remarkable: *73% (11/15) achieved clinical remission by week 6*, and all remained in remission through the 5-week maintenance phase. This rapid improvement rivaled typical drug response rates, despite patients having long-standing disease (mean 19-year duration). Some participants even discontinued steroids or biologics during the diet and still improved. These findings, while from a small uncontrolled study, suggest that AIP (coupled with lifestyle guidance on sleep/stress) can induce remission in a subset of UC patients. **Evidence level***: *Moderate (one small but positive trial and many anecdotal successes). The AIP diet’s effectiveness warrants further research, but it underscores the potential of comprehensive dietary elimination in IBD.**Ulcerative Colitis Exclusion Diet (UCED)**
This is a newer diet that shows promise, but requires more research. A pilot study on pediatric patients with mild to moderate UC found that UCED helped induce clinical remission in some cases, especially when combined with antibiotics.**Biome Optima Diet (Honnas Health) (**[**coaching**](https://www.teamhonnas.com/resources/nutrition-coaching)**)**
**Biome Optima Notes**
**Related**: [Granola Chat Version!](https://notes.granola.ai/d/37ab6310-ecca-4dec-ae46-b693490e4518) This presentation outlines a theoretical approach to treating Inflammatory Bowel Disease (IBD) by optimizing the gut microbiome. The speaker presents a comprehensive explanation of how gut dysbiosis contributes to IBD and offers seven specific strategies to restore gut health. ### Understanding the IBD-Microbiome Connection The central theory proposes that IBD is caused by gut microbiome dysbiosis (imbalance), which leads to intestinal hyperpermeability ("leaky gut"). When the gut barrier becomes compromised, pathogenic entities cross into systemic circulation, triggering an immune response and chronic inflammation. Healthy intestinal epithelial cells are connected by tight junctions that are regulated by microorganisms in the gut. When the microbiome is balanced (eubiosis), these tight junctions function properly; when imbalanced (dysbiosis), inflammation occurs. ### The Mental Approach to Healing Resilience and positive thinking are emphasized as crucial components of recovery. Visualizing a healthier future self and setting health goals provides motivation during difficult periods. Continuous effort toward improvement is presented as superior to surrendering to the disease. ### Recommended Strategies for Gut Microbiome Optimization ### Drink Clean Water Chlorinated tap water may damage the gut microbiome. Recommended alternatives include: - Spring or mineral water (preferably in glass bottles) - Reverse osmosis water (with added minerals) - Distilled water (with added minerals) ### Consume Prebiotic Fiber Prebiotics promote beneficial microorganisms in the gut. The speaker distinguishes between: - Soluble fiber: dissolves in water, fermented by gut bacteria to produce inflammation-reducing short-chain fatty acids - Insoluble fiber: doesn't dissolve, can irritate inflamed intestines - Roughage: mostly insoluble fiber, may aggravate intestinal wounds A phased approach is recommended, starting with soft, soluble fiber foods and gradually expanding based on tolerance. ### Consume Probiotics Probiotic foods directly improve gut microbiome composition by introducing beneficial microorganisms that regulate intestinal permeability. Research shows probiotics can improve IBD remission rates. Sources include: - Milk kefir - Lacto-fermented vegetables - Coconut milk kefir and yogurt - Probiotic supplements The speaker notes that introducing probiotics may cause a Herxheimer reaction (temporary symptom worsening) as pathogenic organisms die off. ### Supplement with Psyllium Husk Psyllium husk forms a gelatinous substance that: - Acts as a prebiotic when combined with probiotics - Creates a soothing "salve" for irritated intestinal tissue - Helps form well-structured stools - Improves both constipation and diarrhea Important precautions: - Don't take with medications (may affect absorption) - Mix with adequate water (25ml per gram) - Begin with small amounts (½ tablespoon) and gradually increase - Maximum recommended dose is 30g daily (about 2 tablespoons) - Consult a doctor before use if you have GI obstructions or strictures ### Practice Intermittent Fasting Benefits include: - Modulating the gut microbiome toward eubiosis - Increasing beneficial bacteria and short-chain fatty acid production - Reducing daily bowel movements by triggering the gastrocolic reflex less frequently A 16:8 fasting schedule (16 hours fasting, 8-hour eating window) is recommended. ### Exercise Consistently Moderate exercise: - Promotes gut microbiome diversity - Increases short-chain fatty acid production - Improves lymphatic system function (reducing trapped inflammation) - Enhances immune system function Recommendations include exercising 3-4 times weekly with 24 hours between sessions, avoiding excessive endurance training. ### Action Items - [ ] Replace tap water with clean water alternatives - [ ] Begin incorporating tolerable prebiotic foods according to the phased approach - [ ] Add probiotic foods gradually to avoid severe Herxheimer reactions - [ ] Discuss psyllium husk supplementation with doctor, particularly regarding medication interactions - [ ] Implement a 16:8 intermittent fasting schedule if approved by doctor - [ ] Establish a moderate exercise routine 3-4 times weekly
**Plant-Based Diets (High-Fiber/Vegetarian/Vegan)**
Diets rich in whole plant foods (fruits, vegetables, whole grains) are associated with reduced inflammation. In a prospective study, patients who adopted a plant-based diet (PBD) had significantly lower relapse rates than those on a regular diet. For example, one trial reported only 27% five-year relapse rate in UC patients maintaining a PBD, versus 53% among those on a conventional diet. Anecdotally, a 2024 case series documented three UC patients who achieved remission on a whole-food plant-based diet – two stopped all medications and remained symptom-free. Notably, symptoms returned when one patient reverted to a meat-based diet. A whole food, plant-based approach (emphasizing fruits, vegetables, legumes, and whole grains while minimizing animal products) has demonstrated up to 98% effectiveness in maintaining remission in some observational data. A case series of three UC patients achieved full remission within months on this diet, with symptoms recurring upon reintroducing meat. Another trial found a semi-vegetarian diet (mostly plant-based with limited animal protein) effective in both active and quiescent UC stages, preventing relapse in over 90% of participants over two years. **Evidence level:** Moderate (one controlled study with long-term follow-up, plus case series and mechanistic support). Plant-based diets appear beneficial for many, but larger trials are needed.**Specific Carbohydrate Diet (SCD)**
The SCD is a strict grain-free, sugar-free diet aiming to alter gut flora. It has garnered extensive anecdotal support from patient communities and some clinical observation. In a small pediatric study, 8 of 12 children with IBD (including UC) achieved remission within 12 weeks on SCD. A survey-based case series of 50 adults reported that 44% were able to discontinue medications on SCD and maintain remission, with an average 95% dietary adherence. One notable case report described a 73-year-old UC patient who, after 3 months on SCD, saw symptom resolution and had a completely normal colonoscopy at 2 years, confirming deep remission. However, not everyone improves on SCD – a randomized trial in children found mixed results (some improved fecal inflammation, others did not). **Evidence level**: Low to moderate (multiple case reports/series and small uncontrolled studies, but lack of large RCTs). SCD can induce remission in some individuals, though its strictness limits compliance**Mediterranean Diet**
A Mediterranean-style diet (high in vegetables, fruits, whole grains, olive oil, and fish) is widely viewed as anti-inflammatory. Observational research suggests it may promote milder disease activity in IBD. In a 2025 cohort of \~700 IBD patients in remission, those with *good Mediterranean diet adherence *(along with exercise) had a \~75% lower risk of moderate/severe relapse over 2 years. Other studies note improved liver fat, body weight, and quality of life in UC patients following a Mediterranean diet. While direct trials in active UC are limited, experts consider this diet beneficial for overall health and possibly disease control. **Evidence level***: *Moderate (epidemiological and cohort data; no dedicated RCT in UC flares yet). Given its general health benefits and some positive signals, a Mediterranean diet is often recommended as part of a “healthy lifestyle” for UC.**Low FODMAP Diet**
Originally developed for IBS, a low-FODMAP diet reduces fermentable carbs that can trigger gut symptoms. In UC, it does not cure inflammation but can alleviate bloating, gas, and diarrhea in those with IBS-like symptoms. A systematic review noted low-FODMAP diets improved overall GI symptoms and quality of life in IBD. This diet is considered adjunctive – helping symptom management – rather than a primary remission induction strategy. **Evidence level**: Low (no evidence for inflammation remission, but some benefit for symptom control). It may be useful for UC patients in remission who have persistent IBS-type symptoms.[Ayuverdic Medicine](https://gsconlinepress.com/journals/gscarr/sites/default/files/GSCARR-2023-0052.pdf) shows promise (see [case study](https://gsconlinepress.com/journals/gscarr/sites/default/files/GSCARR-2023-0052.pdf))
**Mindfulness-Based Stress Reduction (MBSR)**
This meditation and mindfulness training program has **strong evidence** in UC remission maintenance. In a randomized controlled trial (2022), 43 UC patients in remission were assigned to 8-week MBSR classes or an education control. **After one year**, none of the MBSR-trained patients experienced a disease flare, whereas 5 of 23 control patients had relapses. The MBSR group had significantly *fewer flare-ups* and reported lower perceived stress. Biological markers (fecal calprotectin, cortisol) also supported the link between stress and gut inflammation. *Evidence level:* Moderate to high (RCT showing reduced flare frequency). This suggests that mindfulness and meditation can prolong remission – likely by blunting stress-related inflammatory responses.**Relaxation Techniques (yoga, deep breathing)**
Practices such as yoga, deep-breathing exercises, tai chi, and gut-directed hypnotherapy are widely used by IBD patients to relieve stress. **Yoga**, for example, was tested in a German trial on UC patients in remission – it significantly improved patient-reported quality of life and energy levels compared to a control group, and trends toward reduced inflammation were observed. Hypnotherapy has shown promise in IBS and some IBD cases for reducing anxiety and possibly inflammation. *Evidence level:* Low (primarily anecdotal or small studies). Still, these mind–body techniques carry minimal risk and can be valuable complements to medical therapy, aiming to prevent the stress-related relapse cycle.**Psychotherapy and CBT**
Cognitive-behavioral therapy (CBT) and other talk therapies may help patients cope with UC and possibly impact disease activity. While results are mixed, some studies indicate psychotherapy can improve quality of life and perhaps lengthen remission. For instance, a small trial found **mindfulness-based cognitive therapy **reduced stress and improved mindfulness skills in inactive UC. Behavioral interventions overall have shown trends toward longer remission, though not all trials reach significance. *Evidence level: *Low to moderate (some supportive studies, but inconsistent). Nonetheless, many patients benefit from counseling to manage the emotional toll of UC, which indirectly can stabilize their condition.Within each phylum, organisms are sorted with overabundant species first, followed by normal, then low. --- - **Actinobacteria** Gram-positive bacteria that include beneficial Bifidobacterium, important for carbohydrate fermentation, vitamin production (B vitamins, K), and gut barrier integrity. Often reduced in ulcerative colitis and dysbiosis; supported by polyphenols (chocolate, tea, berries) and prebiotic fibers. - Actinobacteria: -1 (Low) - Actinomycetales: -1 (Low) - Bifidobacterium family: -1 (Low) - **Bacteroidetes** Gram-negative anaerobes specializing in breaking down complex plant fibers and polysaccharides; balance with Firmicutes is linked to body weight and metabolic health. Some species are protective against inflammation, while others may be associated with colon cancer risk. - Alistipes spp.: +2 (High) - Bacteroides stercoris: +2 (High) - Bacteroides fragilis: +1 (Slightly high) - Bacteroides spp.: +1 (Slightly high) - Parabacteroides johnsonii: +1 (Slightly high) - Parabacteroides spp.: +1 (Slightly high) - Alistipes onderdonkii: 0 (Normal) - Bacteroides spp. & Prevotella spp.: 0 (Normal) - Bacteroides pectinophilus: 0 (Normal) - Bacteroides zoogleoformans: 0 (Normal) - **Firmicutes** Largest gut phylum, including many butyrate producers (key for anti-inflammatory effects and gut barrier function) and lactic acid bacteria; often elevated in dysbiosis and altered in ulcerative colitis. Diets rich in resistant starch, whole grains, and diverse fibers support beneficial Firmicutes. - Dialister invisus & Megasphaera micronuciformis: +1 (Slightly high) - Mediterraneibacter gnavus: +1 (Slightly high) - Veillonella spp.: +1 (Slightly high) - Firmicutes: 0 (Normal) - Bacilli Class: 0 (Normal) - Catenibacterium mitsuokai: 0 (Normal) - Clostridia Class: 0 (Normal) - Clostridium methylpentosum: 0 (Normal) - Clostridium L2-50: 0 (Normal) - Coprobacillus cateniformis: 0 (Normal) - Dialister invisus: 0 (Normal) - Dorea spp.: 0 (Normal) - Holdemanella biformis: 0 (Normal) - Eubacterium siraeum: 0 (Normal) - Faecalibacterium prausnitzii: 0 (Normal) - Lachnospiraceae: 0 (Normal) - Ligilactobacillus ruminis & Pediococcus acidilactici: 0 (Normal) - Lactobacillus family: 0 (Normal) - Phascolarctobacterium spp.: 0 (Normal) - Ruminococcus albus & R. bromii: 0 (Normal) - Streptococcus agalactiae & Agathobacter rectalis: 0 (Normal) - Streptococcus salivarius ssp. thermophilus & S. sanguinis: 0 (Normal) - Streptococcus spp.: 0 (Normal) - Anaerobutyricum hallii: -2 (Very low) - Agathobacter rectalis: -1 (Low) - Streptococcus salivarius ssp. thermophilus: -1 (Low) - **Proteobacteria** Contains many opportunists and pathogens (e.g., E. coli, Salmonella); often elevated in inflammation, dysbiosis, and UC flares. Diets high in processed foods may increase Proteobacteria, while high-fiber, polyphenol-rich diets can reduce them. - Escherichia spp.: +1 (Slightly high) - Proteobacteria: 0 (Normal) - Enterobacteriaceae: 0 (Normal) - Acinetobacter junii: 0 (Normal) - **Mycoplasmatota** Cell-wall–less bacteria that can be commensal or pathogenic; less studied in gut health but sometimes linked to dysbiosis in chronic conditions. - Metamycoplasma hominis: 0 (Normal) - **Verrucomicrobiota** Includes Akkermansia muciniphila, a mucin-degrading bacterium linked to gut barrier health and reduced inflammation; often lower in ulcerative colitis. Supported by polyphenols, prebiotic fibers, and certain polyunsaturated fats. - Akkermansia muciniphila: -1 (Low) ### Culture Results – Sorted by Growth Level {toggle="true"} These results reflect viable organisms grown from stool cultures, categorized by pathogenic potential, balance, and yeast presence. Unlike PCR-based abundance, culture results highlight live bacteria and fungi, which may correlate more directly with current colonization and infection risk. --- - **Pathogenic Bacteria (Culture)** Known disease-causing organisms that should not be present in a healthy gut. Often linked to foodborne illness, gastroenteritis, and systemic infections. - (All tested species): NG (No Growth) - Aeromonas spp.: NG - Edwardsiella tarda: NG - Plesiomonas shigelloides: NG - Salmonella group: NG - Shigella group: NG - Vibrio cholerae: NG - Vibrio spp.: NG - Yersinia spp.: NG - **Imbalanced Bacteria (Culture)** Non-pathogenic bacteria present at elevated levels that may contribute to dysbiosis when beneficial species are lacking. Can be associated with mild inflammation or gut barrier disruption. - Streptococcus parasanguinis: 3+ (High) - Streptococcus salivarius: 3+ (High) - Klebsiella/Raoultella complex: 2+ (Slightly high) - Corynebacterium amycolatum: 2+ (Slightly high) - Corynebacterium aurimucosum: 2+ (Slightly high) - Streptococcus mitis/oralis group: 2+ (Slightly high) - **Dysbiotic Bacteria (Culture)** Opportunistic organisms considered harmful at elevated levels; may indicate disrupted microbiota or increased risk for inflammation. - Enterobacter cloacae complex: 3+ (High) - **Yeast (Culture)** Fungi that may overgrow in dysbiosis, especially with high sugar intake or after antibiotic use. - No yeast isolated: NG (Within reference: 0+ – 1+)
[Metagenomics - AI powered prediction of Inflammatory Bowel’s Disease and Probiotic Recommendation](https://www.medrxiv.org/content/10.64898/2026.02.12.26345333v1)
Probiotics (**important!!**)
Specific probiotic strains have demonstrated clinical efficacy in UC: - **E. coli Nissle 1917:** A landmark 12-month RCT with 327 UC patients showed this probiotic was ***equivalent to mesalamine*** for maintaining remission. Relapse rates after one year were similar (\~34-36%) in both groups, establishing Nissle 1917 as a legitimate maintenance therapy with Level 1 evidence. {color="green_bg"} - Genotoxin risk!! - [Biokult probiotics](https://x.com/DwightVoeks/status/1971334744437883277) cured this person’s Crohn’s in 4 days {color="green_bg"} - [**Multi-strain Probiotics (VSL#3)**](amazon.com/VSL-Probiotic-Management-Irritable-Refrigerated/dp/B07WX1LVHL/ref=cm_cr_arp_d_product_top?ie=UTF8)**:** This high-potency mixture of 8 bacterial strains has shown benefit in active UC. Multiple studies found high-dose VSL#3 induced remission in patients with mild-to-moderate UC, with one open-label trial reporting \~50% remission rates. Probiotics are also very effective in preventing pouchitis in post-surgery UC patients. *Evidence level:* High for maintenance, moderate for induction. {color="green_bg"} - [Florastor](https://www.amazon.com/Florastor-Daily-Probiotic-Supplement-Women/dp/B01NB0G1V8/ref=cm_cr_arp_d_product_top?ie=UTF8&th=1) has a number of amazon reviews citing improvement or remission of colitis - [Another one with great UC reviews, 10 strains](https://www.amazon.com/Probiotics-Formulated-Probiotic-Supplement-Acidophilus/dp/B079H53D2B/ref=cm_cr_arp_d_product_top?ie=UTF8&th=1) - Patients with proctitis have reported benefits from products like VSL#3 or homemade fermented foods (**yogurt, kefir, sauerkraut**) to complement their standard treatment. - Very highly rated! [Microbiome Plus Gastrointestinal Probiotics L Reuteri NCIMB 30242 GI Digestive Supplements Capsule, Allergy Safe & Gluten Free for Men and Women (1 Month Supply)](https://www.amazon.com/Microbiome-Plus-Gastrointestinal-Probiotics-Supplements/dp/B01MEG1Y9C/ref=cm_cr_arp_d_product_top?ie=UTF8)Prebiotics and Dietary Approaches
Prebiotics (fermentable fibers) nourish beneficial bacteria and increase short-chain fatty acids production: - A small study found combining **psyllium fiber with mesalamine** improved remission maintenance compared to mesalamine alone. {color="green_bg"} - The high-fiber "4-SURE" diet showed a 69% increase in butyrate output with clinical improvement in 46% of UC patients. *Evidence level:* Low to moderate. Some active UC patients may not tolerate high fiber until inflammation subsides.[Fecal Microbiota Transplantation](https://www.humanmicrobes.org/fecal-microbiota-transplant-fmt) (FMT)
Multiple randomized controlled trials support FMT efficacy in UC: - Moayyedi (2015): 24% remission with donor FMT vs. 5% with placebo at 7 weeks. - Paramsothy (2017): 27% remission with multi-donor FMT vs. 8% with placebo at 8 weeks. Using pooled donors increased microbial diversity. - Costello (2020): 32% remission with multi-donor FMT vs. 9% in controls at 8 weeks. - Combination therapy: One study combining FMT with an anti-inflammatory diet maintained deep remission for up to one year. *Evidence level:* High (multiple RCTs). FMT roughly doubles remission odds compared to placebo, though it remains experimental with logistical challenges (donor selection, safety screening, regulatory issues).Fermented Foods
Natural fermented foods (yogurt, kefir, kombucha, sauerkraut) may help maintain microbial diversity, though no UC-specific RCTs exist. These foods are generally recommended as part of an anti-inflammatory diet if tolerated.**Mirtazapine**
Mirtazapine is a prescription medication primarily used as an antidepressant that can also help with sleep issues. For UC patients, it may offer dual benefits: - Improves sleep quality through its sedating properties - May help reduce inflammation through its effects on certain neurotransmitters - Can stimulate appetite in patients who struggle with eating due to UC symptoms However, it should only be used under medical supervision and after discussing potential benefits and risks with your healthcare provider.**Sleep Hygiene Practices**
Several evidence-based practices can improve sleep quality for UC patients: - Maintain a consistent sleep schedule (go to bed and wake up at the same time) - Create a dark, cool, and quiet sleeping environment - Avoid blue light exposure from screens 1-2 hours before bedtime - Practice a relaxing bedtime routine (reading, gentle stretching, meditation) - Limit caffeine intake, especially in the afternoon and evening**Natural Sleep Aids**
Several natural supplements may help improve sleep quality: - Magnesium glycinate - helps relax muscles and calm the nervous system - Chamomile tea - known for its mild sedative effects - Melatonin - can help regulate sleep-wake cycles - L-theanine - promotes relaxation without drowsiness Always consult with your healthcare provider before starting any supplements, as they may interact with UC medications.**Environmental Modifications**
Creating an optimal sleep environment can significantly improve sleep quality: - Use blackout curtains or an eye mask to block light - Maintain room temperature between 60-67°F (15-19°C) - Consider using a white noise machine to mask disruptive sounds - Invest in a comfortable mattress and pillows that support good sleep posture[Wheat grass juice](https://x.com/i/grok/share/2gqsfZ8pfqtC0fbhELsx0QJYt)
A small randomized, double-blind, placebo-controlled trial involving 23 patients with active distal UC found that consuming 100 ml of wheatgrass juice daily for one month significantly reduced overall disease activity (measured by an index including rectal bleeding, bowel movements, sigmoidoscopic evaluation, and physician assessment) and the severity of rectal bleeding. In this study, 78% of participants showed clinical improvement compared to 30% in the placebo group. The juice was started at 20 ml per day and gradually increased to 100 ml.Tart cherry Juice 2x/day ([it can reduce inflammation by 40% in the gut!](https://www.perplexity.ai/search/why-is-tart-cherry-juice-thoug-FkeCieCiSZm2PI30KD457A))
Celery Juice
Cabbage Juice ([**super effective for flares**](https://www.youtube.com/watch?v=OztkuD09GGU))
Coconut water 1x/day ([reduces inflammation](https://www.perplexity.ai/search/why-is-it-thought-that-coconut-YOIpjFg1RW6yG9Nt7bzViw))
[Help for Crohn’s, Colitis, IBD And IBS](https://www.bhherbalsolutions.com/product/heal-ulcerative-colitis-naturally-heal-crohns-heal-ibd-heal-ibs/#reviews)
**Phosphatidylcholine **
I am extremely deficient in this according to my genetic test. Research shows that PC (correctly delivered) is a helpful adjunct for UC. - Tons of studies: [Experiences with (delayed release) phosphatidylcholine for treating Ulcerative Colitis?](https://www.reddit.com/r/UlcerativeColitis/comments/ubiu7i/experiences_with_delayed_release/) - [Saturated phosphatidylcholine as dietary additive for colonic mucus: an open label prospective clinical observation trial](https://amj.amegroups.org/article/view/6771/html) - Note that I should shoot for \~2G of PC/day. In between meals! Most PC is absorbed in the small intestine and doesn’t make it to the colon. Therefore it needs to be enteric coated or use another delayed release mechanism such as being hydrologized. **Where to buy** [KliniPharm](https://www.klinipharm.com/products/spongicol/) appears to have enteric coated PC. They’re a German company. They have a few versions: - [Traditional soy-lectin (30% PC)](https://klinipharmshop.com/produkt/spongicol-kollagen-lecithin-granulat-250g/). This was used in studies that showed efficacy. I think this is their oldest form. - [Capsule form](https://klinipharmshop.com/produkt/spongicol-kollagen-lecithin-kapseln-100-stk-2/) - [New egg-lectin version (80% PC) capsules](https://klinipharmshop.com/produkt/spongicol-kollagen-lecithin-kapseln-100-stk/). This is more concentrated, newer. - [SpongiCol version (90% PC) capsules. ](https://klinipharmshop.com/produkt/spongi-sunflower-100-st-2/) {color="yellow_bg"} - [x] I bought this version because of cost for results. - If this didn’t work, try the 30% version or look at the main [bowel health page again](https://klinipharmshop.com/produkt-kategorie/darmpflege/). Some evidence suggests the 30% version could be the most effective. {color="yellow_bg"} - • **LT-02:** A novel modified-release formulation, **LT-02**, which contained highly concentrated (\>94%) PC and a gastric acid-resistant coating (designed to release at pH 5.5 in the duodenum), was developed for larger trials - I also [bought this for systemic PC](https://bodybio.com/products/bodybio-pc-phosphatidylcholine). It should not double up with the other PC… {color="yellow_bg"} - Lastly, there is an interesting [enteric coated “PhosCholine” complex I might try at some point. Contains boswellia as well!](https://fullscript.com/catalog/products/phoscholine-complex-60t)RDLA
- Can get it from Digestive Warrior [R-Dihydrolipoic Acid (RDLA) by Redox BioScience](https://digestivewarrior.com/products/r-dihydrolipoic-acid-99-pure-by-redox-bioscience) - Or from Premier Lipoceutics [Back in Stock: R-DHLA --Super Antioxidant for Mitochondrial Health and Vitality!](https://premierlipoceutics.com/products/r-dhla-super-antioxidant-for-mitochondrial-health-and-vitality)**Curcumin / CureQD**
**Boswellia serrata**
- [Enteric version](https://klinipharmshop.com/en/produkt/boswellia-spongi/) An herbal resin with anti-inflammatory properties, boswellia has been compared to standard drugs in ulcerative colitis (UC). In one small trial,** 82% of UC patients on boswellia (350 mg thrice daily) achieved remission at 6 weeks, nearly equivalent to the 75% remission rate on sulfasalazine** (a standard UC 5-ASA drug). This suggests boswellia may induce remission similarly to 5-ASA medication for some patients. However, a separate placebo-controlled study in Crohn’s disease maintenance found boswellia no better than placebo, and overall research is limited. Another trial showed a boswellia formulation was **as effective as mesalamine in maintaining remission for chronic colitis.** **Evidence level:** Low (a few small trials with mixed results). Boswellia is intriguing as a therapy to reduce inflammation and has a long history in Ayurvedic medicine, but consistency of benefit is not yet confirmed.**Indigo naturalis (Qing Dai)**
[Quing Dai](https://academic.oup.com/ibdjournal/advance-article-abstract/doi/10.1093/ibd/izaf119/8161586?redirectedFrom=fulltext&login=false&utm_source=Klaviyo&utm_medium=email&utm_campaign=September%20%2725%20-%20Newsletter%201&utm_id=September%20%2725%20-%20Newsletter%201%20%2801K2Y8Z633T4EAGRTVYAEM8JXJ%29)[**Andrographolide**](https://pmc.ncbi.nlm.nih.gov/articles/PMC5835811/)
- Very bitter herb - [Presents therapeutic effect on ulcerative colitis through the inhibition of IL-23/IL-17 axis](https://pmc.ncbi.nlm.nih.gov/articles/PMC5835811/)[Tributyrin](https://pmc.ncbi.nlm.nih.gov/articles/PMC10389721/) seems superior to butyrate, it’s a precursor to it
[Tributyrin alleviates gut microbiota dysbiosis to repair intestinal damage in antibiotic-treated mice](https://pmc.ncbi.nlm.nih.gov/articles/PMC10389721/)[Zinc Carnosine](https://x.com/MCotterMD/status/1990585257788108885?s=20)
Keep hearing about this one. “The Mucosal Repair Agent”. - Accelerates epithelial repair (up to 3× faster in trials) - Protects against bile acid irritation - Increases mucin thickness and restores barrier integrity - Reduces micro-ulceration that leads to irregular stools[Zinc Carnosine](https://x.com/NickBardoukas/status/1956374100458238193)
[Analyze & Optimize on Twitter / X](https://x.com/Outdoctrination/status/1886067127586820548)[Taurine](https://x.com/MCotterMD/status/1990585257788108885?s=20) ([ONLY WITH PLANT DIET](https://www.youtube.com/watch?v=ihl1moq1l0M))
“The Hydration + Bile Modulation Specialist” 🔹 Stabilizes chloride channels → reduces secretory diarrhea🔹 Regulates bile acid conjugation → decreases urgent loose stools
🔹 Supports mitochondrial osmoregulation in colonocytes
🔹 Protects against oxidative damage that disrupts stool form