I am sure you have noticed that I write essays for my friends, and I have two friends with these problems. The standard medical practice is to treat them with toxic agents, and when this fails, operate on them, so a large number of the system’s victims end up with either a colostomy, a total colectomy, or both. However, this doesn’t have to happen, because both of these diseases are potentially curable.
Just imagine my experience. After a year of research, I cured my wife’s fatal AL amyloidosis by having her mouth abscesses removed. I refuse to believe that these two “idiopathic autoimmune” entities—or my Parkinson’s disease—are beyond our understanding or all hope.
Inflammatory bowel disease afflicts roughly 1.5 million Americans, most of them young, and the standard treatment ladder climbs from 5-aminosalicylates to corticosteroids to immunomodulators like azathioprine to mesalamine to biologics and finally to surgery. Many patients reach a workable remission on this ladder. The problem is that the rungs above mesalamine all involve trade-offs the patient is not always told about in plain terms, and the long-term natural history of the disease, even with treatment, is sobering. This review covers what the published evidence shows about alternatives and adjuncts, with an emphasis on interventions backed by randomized trials, formal case series, or strong mechanistic rationale.
The audience here is patients in remission on immunosuppression who are wondering what else might be possible, and their families. I’m not telling anyone to stop a working medication. The argument is narrower: when a young person is in remission on azathioprine, the pressing question is what other tools exist.
The numbers on long-term outcomes
A patient newly told she has ulcerative colitis often hears that the disease can be controlled with medication. That is largely true. What is rarely discussed in the same conversation is what control means at five, ten, and twenty-five years.
The best long-term data come from population-based cohorts. A systematic review of 17 such cohorts covering more than 15,000 UC patients found that 70 to 80 percent will relapse within ten years, about half will require hospitalization, and the cumulative risk of colectomy is roughly 10 to 15 percent at ten years in modern cohorts. Older Stockholm data showed colectomy rates of 20 percent at five years, 28 percent at ten years, and 45 percent at twenty-five years, though contemporary numbers are lower, partly because of earlier diagnosis and partly because of more aggressive medical therapy. Patients who stay on azathioprine successfully for more than five years have very low colectomy rates, roughly 1.4 percent in one large cohort, but only about a third of patients who start the drug are still on it at that point. Many discontinue for intolerance, infection, or loss of response.
For Crohn’s disease, the picture is rougher. Most patients require surgery within ten to twenty years of diagnosis, fistulization and stricturing complicate the late phase, and the recurrence rate after surgical resection is high.
These numbers are not a reason to panic and they are not a reason to dismiss conventional therapy. They are a reason to take seriously any intervention that might shift them, particularly interventions that could be added to existing treatment without obvious harm.
Azathioprine: what it does well, what it costs
Azathioprine (Imuran) is a purine analog that suppresses lymphocyte proliferation. It induces and maintains remission in UC and Crohn’s, allows steroid sparing, and, in patients who tolerate it long-term, reduces the need for biologics or surgery. None of that is in dispute.
The costs are also documented. A meta-analysis of population-based and referral-center studies found roughly a fourfold increased risk of lymphoma among IBD patients on thiopurines compared with the general population. The absolute risk is low in young patients and returns to baseline after the drug is stopped, but it is not zero. Men under 35 appear to be a higher-risk subgroup, partly because of the very rare hepatosplenic T-cell lymphoma that has been linked to combined thiopurine and anti-TNF therapy. Non-melanoma skin cancers are also increased. Pancreatitis affects 3 to 5 percent of patients, hepatotoxicity another 5 percent, and myelosuppression requires regular blood monitoring throughout treatment.
For pregnancy, the data are mixed and partly reassuring. Animal studies show clear teratogenicity at relevant doses, with cleft palate, skeletal anomalies, and urogenital defects reported, and the FDA category is D. In human IBD cohorts, however, the drug appears to cross the placenta without producing a consistent congenital anomaly signal, though it does correlate with increased rates of low birth weight, preterm birth, and small-for-gestational-age infants, particularly when combined with corticosteroids. Most current IBD guidelines now recommend continuing azathioprine through pregnancy if it has been controlling the disease, on the reasoning that an active flare during pregnancy poses worse risks to the fetus than the drug does. Breastfeeding is generally considered acceptable.
The rational position is that azathioprine is a real drug with real benefits and real costs, but that a patient who has reached remission on it is reasonable to ask whether the same outcome could be achieved with less.
The mesalamine baseline that gets skipped
Before discussing any of the alternative approaches, here is a brief note on conventional first-line therapy. 5-aminosalicylates (mesalamine, balsalazide, sulfasalazine) are the standard first-line medical therapy for mild-to-moderate UC for good reason. Up to 70 percent of patients reach symptom improvement on adequate doses within two months, the safety profile is excellent, and the drug is considered safe in pregnancy and lactation with the single caveat that Asacol HD contains dibutyl phthalate in its coating, which has shown teratogenicity in rabbits and should be switched to another formulation before conception.
Mesalamine alone is not enough for everyone, particularly those with extensive colitis or steroid-dependent disease, and it has a minimal role in Crohn’s of the small bowel. Some patients on azathioprine were originally placed on it when mesalamine alone could not maintain remission. Others were stepped up because of a single severe flare. The question of whether a stable patient might be maintained on mesalamine plus dietary and microbiome interventions, with azathioprine reserved for breakthrough disease, is one a thoughtful gastroenterologist will engage on the merits.
Diet: the strongest body of evidence outside the drug literature
The most consistent finding in the alternative IBD literature is that what people eat matters, often dramatically. Several distinct dietary approaches have shown formal benefit, and they share a common pattern: elimination of grains, refined sugars, processed foods, industrial seed oils, and most fermentable carbohydrates, with emphasis on animal protein, eggs, fats, and well-tolerated whole foods.
Carnivore and ketogenic diets
The most striking recent data come from a case series of ten IBD patients published in Frontiers in Nutrition in 2024 by Norwitz and Soto-Mota. All ten patients (six with UC, four with Crohn’s) had histologically confirmed disease and reached durable remission on a ketogenic, mostly carnivore diet, with several stopping all medication. Diets ran 67 to 82 percent fat with under 21 grams of carbohydrate daily. Quality-of-life scores on the Inflammatory Bowel Disease Questionnaire improved by 72 to 165 points. One Crohn’s patient remained 99 percent symptom-free for five years with no disease activity on follow-up colonoscopy. A UC patient with twenty-two years of disease activity reached remission and stayed there for over a year on a diet of roughly 90 percent red meat, eggs, and cheese with limited low-carb vegetables. The lead author notes that no patient who responded to the survey reported the diet making them worse.
A case series is not a randomized trial, and selection bias is real. People who join social media groups and report dramatic improvement on a diet are not a representative sample. But the size of the effect is hard to dismiss, the patients had biopsy-confirmed disease, and the durability (up to eleven years for one UC patient) is notable. The mechanism is plausible: removing fermentable substrates starves dysbiotic flora, ketones (particularly beta-hydroxybutyrate) reprogram macrophages toward an anti-inflammatory phenotype via STAT-6 signaling, and elimination of plant lectins, oxalates, and pesticide residues removes potential mucosal irritants.
A reasonable trial of carnivore or strict ketogenic eating runs four to eight weeks. Improvement, when it happens, is usually evident within the first two to four weeks. If symptoms worsen the diet should be stopped.
Specific carbohydrate diet
The Specific Carbohydrate Diet (SCD), developed by Sidney Haas in the 1920s and popularized by Elaine Gottschall’s Breaking the Vicious Cycle, eliminates all grains, sugars except honey, all dairy except aged hard cheese and 24-hour fermented yogurt, and most processed foods. The mechanism is the same as for the carnivore approach: starve the dysbiotic flora, particularly carbohydrate-fermenting bacteria.
The DINE-CD trial, a multicenter randomized comparison of SCD versus a Mediterranean diet in Crohn’s patients, found symptomatic remission rates of 46.5 percent on SCD and 43.5 percent on the Mediterranean diet at six weeks, statistically equivalent. A pediatric randomized trial of three SCD variants achieved clinical remission in all ten participants who completed twelve weeks, with C-reactive protein falling from 1.3 to 0.9 in the strict SCD group. A retrospective case report described an adult Crohn’s patient unresponsive to medical therapy who remained asymptomatic for 40 months on SCD monotherapy, with normal endoscopic and histologic findings at month 12, fecal calprotectin dropping from 493 to 70, and a 94 percent reduction in healthcare costs.
SCD is more sustainable for most people than strict carnivore because it allows fruit, vegetables, nuts, and legumes (after a starter phase). It requires home cooking and label reading. The learning curve is real but not prohibitive.
Autoimmune Protocol diet
The Autoimmune Protocol (AIP) is an extension of the paleolithic approach that eliminates grains, legumes, nightshades, dairy, eggs, coffee, alcohol, nuts, seeds, refined sugars, industrial oils, NSAIDs, and food additives during a six-week elimination phase, with controlled reintroduction afterward.
A Scripps Clinic uncontrolled trial of fifteen IBD patients under Konijeti showed mean partial Mayo scores improving from 5.8 to 1.0 in UC patients and Harvey-Bradshaw index from 7 to 3.4 in Crohn’s patients over eleven weeks. Mean fecal calprotectin dropped from 471 to 112. Among seven patients with follow-up endoscopy, six showed mucosal healing improvements. Four participants discontinued some or all medications during the study. A follow-up RNA expression study showed normalization of inflammatory pathway gene expression on biopsy specimens. The diet was associated with significant quality-of-life improvements by week three.
AIP is more restrictive than SCD during the elimination phase. Many patients use it as a diagnostic tool to identify their own trigger foods rather than as a permanent diet.
Exclusive enteral nutrition for Crohn’s
For pediatric Crohn’s disease, exclusive enteral nutrition (EEN) using a polymeric formula as the sole calorie source for six to eight weeks induces remission rates equivalent to corticosteroids, with mucosal healing that steroids do not achieve. EEN is established standard of care in European pediatric guidelines and a regrettably underused option in adults. The Crohn’s Disease Exclusion Diet (CDED), which combines partial enteral nutrition with a structured whole-food regimen excluding suspected pro-inflammatory foods, has produced similar results with better tolerability.
What the diet evidence collectively shows
Different elimination diets produce similar improvement, suggesting that the active mechanism is the removal of something rather than the addition of any specific food. Candidate culprits include processed seed oils, emulsifiers like polysorbate-80 and carboxymethylcellulose (which degrade the mucus layer in animal models), refined sugars, gluten in susceptible patients, and fermentable fibers in patients with severe dysbiosis. The improvement is often substantial, the side effect profile is favorable, and the cost is grocery money rather than a $40,000-a-year biologic.
Any of these dietary approaches can be combined with current medication. None requires stopping anything. The question for a patient in remission on azathioprine is whether a sustained dietary remission could eventually allow medication tapering with the agreement of her gastroenterologist. That is a reasonable question to ask.
Microbiome restoration
If diet works partly by reshaping gut flora, the next logical question is whether direct microbial interventions add value.
Fecal microbiota transplantation
My post about that is here. I went to a conference sponsored by Sabine Hazan, possibly the most prominent authority on stool transplant in the United States.
FMT is an established standard of care for recurrent Clostridioides difficile infection. Its role in UC has been studied in multiple randomized trials. A 2024 meta-analysis of fourteen studies and 600 UC patients found odds ratios of 2.25 for combined clinical and endoscopic remission and 2.02 for clinical remission, with no increase in adverse events compared to controls. Earlier meta-analyses showed similar magnitudes. Pooled-donor preparations (mixing stool from multiple healthy donors) outperformed single-donor FMT, and oral capsule delivery was superior to enema or colonoscopic delivery in head-to-head comparisons. The effect is more consistent in UC than in Crohn’s.
FMT is not yet FDA-approved for IBD outside of clinical trials. Patients pursuing it generally do so through participation in research protocols, through clinics in countries with more permissive regulation, or by working with a sympathetic gastroenterologist willing to use it off-label. Stool screening of the donor for pathogens is essential, as adverse events from inadequately screened donors have included transmission of multidrug-resistant E. coli and SARS-CoV-2.
For someone with severe established dysbiosis, FMT can produce a dramatic improvement that diet alone cannot match. Some patients have used a healthy family member (such as a sibling or parent) as the donor, with informal home preparation. The risk profile of this approach depends entirely on donor screening.
Probiotics
The probiotic data in IBD are uneven. Most consumer probiotics fail rigorous trials. Two preparations have produced consistent positive results.
VSL#3 (now sold as Visbiome in the United States) is a high-potency mixture of eight bacterial strains, including four lactobacilli, three bifidobacteria, and Streptococcus thermophilus. The Tursi 2010 randomized trial of 144 mild-to-moderate UC patients on stable 5-ASA or immunosuppression showed UCDAI improvement of greater than 50 percent in 63 percent of VSL#3 patients versus 41 percent of placebo, at 8 weeks on 3.6 trillion CFU per day. A separate Sood 2009 trial showed similar induction effects. VSL#3 also reduces the risk of pouchitis after colectomy with ileal pouch-anal anastomosis, with a randomized trial showing acute pouchitis rates of 10 percent versus 40 percent on placebo over the first year.
Escherichia coli Nissle 1917 (Mutaflor) has been shown in randomized trials to be equivalent to mesalamine in maintaining UC remission. It is widely available in Europe and harder to obtain in the United States.
The dose matters. Most pharmacy-shelf probiotics deliver 1 to 10 billion CFU per dose. The trials that show benefit use 100 to 3,600 billion CFU. A patient who takes a generic probiotic and concludes that probiotics do not work has not properly tested the intervention.
Helminth therapy
This is a visible parasitic worm (such as a tapeworm, roundworm, or fluke) that infects humans and animals.
The hygiene hypothesis predicts that the rise in IBD in industrialized countries is partly driven by the disappearance of intestinal worms, which historically modulated host immunity toward a tolerant phenotype. This led to a series of trials using Trichuris suis ova (TSO), the porcine whipworm, which colonizes humans transiently without causing disease. The Summers 2005 randomized trial in 54 patients with active UC showed a 43 percent improvement with TSO versus 17 percent with placebo over 12 weeks, with no adverse events. An open-label Crohn’s disease trial showed 79% remission after six months of TSO. Industrial development of TSO as a regulated drug subsequently stalled when larger Phase III Crohn’s disease trials by Coronado Biosciences failed to meet endpoints, partly due to changes in the dosing protocol. The biology is intriguing, and a small underground community of patients self-treats with ova obtained from European sources.
Comment: I think this is crazy, and anyone considering it should research carefully before swallowing any damn worms.
Counterpoint: Like most of the Indian subcontinent, my dog, my wife, and I deworm every few months with a few days of fenbendazole at 225 mg a day. Fortunately, none of the three of us has inflammatory bowel disease. Getting rid of your worms is probably the better bet to treat that, and a course of fenbendazole, which may last three to four weeks, is harmless and at least decreases their numbers.
If you think that the worm thing is improbable, have a look at this video. Note that Dr. Ardis, the expert commentator, says that 70% of us have them living inside us. He sells proprietary herbal supplements. I believe that conventional drugs such as fenbendazole are more effective and equally safe, and you don’t have to take herbals like this three times a day for a month. To learn more about that sort of thing, see my interview with the Worm Queen. She developed a multi-million dollar business selling herbal worm treatments.
I concluded after interviewing her that her vulnerability to worms and her nearly fatal experience with them had more to do with her 7 root canals damaging her immunity than worms.
You can purchase fenbendazole over the counter at fenbenLab.com. It isn’t approved for human use, but mebendazole, a drug with a single-molecule difference, is approved in the United States.
Anti-inflammatory adjuncts with study data
Several botanicals and small molecules have randomized-trial evidence for adjunctive use in IBD.
Curcumin
Curcumin is the principal active compound in turmeric. Its bioavailability is poor, which has led to formulations using piperine, liposomes, or phospholipid complexes (Meriva, Theracurmin) to improve absorption.
The Hanai 2006 Japanese randomized maintenance trial gave 89 quiescent UC patients curcumin 2 g per day or placebo on top of sulfasalazine or mesalamine for six months. Relapse rates were 4.65 percent on curcumin versus 20.5 percent on placebo, a clinically and statistically significant difference. The Lang 2015 induction trial added curcumin 3 g per day or placebo to mesalamine in fifty mild-to-moderate active UC patients who had failed maximal-dose mesalamine alone. Clinical remission at four weeks was 53.8 percent on curcumin versus zero percent on placebo. A meta-analysis of randomized trials found pooled odds ratios of 2.9 for clinical remission and 2.3 for endoscopic response with curcumin added to mesalamine, with minimal side effects.
Curcumin at gram-level doses appears to work both for induction and for maintenance of UC remission. The dose is higher than that delivered by standard turmeric capsules, and the formulation matters. A reasonable trial uses 2 to 3 g per day of a high-bioavailability preparation for at least eight weeks.
Boswellia serrata
Indian frankincense resin contains boswellic acids that inhibit 5-lipoxygenase, the enzyme that produces leukotriene B4, a key inflammatory mediator in UC. The Gupta 1997 trial compared Boswellia serrata gum resin 350 mg three times daily for six weeks against sulfasalazine in active UC. Remission rates were 82 percent on Boswellia and 75 percent on sulfasalazine. A subsequent Gupta trial in 30 chronic colitis patients showed remission in 14 of 20 on Boswellia 900 mg per day versus 4 of 10 on sulfasalazine. A German maintenance trial in Crohn’s found Boswellia non-inferior to mesalamine but did not meet superiority criteria. Tolerability is excellent.
Standardized extracts (such as 5-Loxin or AprèsFlex) provide more consistent dosing than crude resin. The mechanism is complementary to mesalamine (which acts on cyclooxygenase pathways) rather than redundant with it.
Vitamin D
Vitamin D deficiency is endemic among IBD patients, and the relationship is bidirectional: malabsorption from inflamed gut lowers levels, and low levels drive immune dysregulation that worsens inflammation. A meta-analysis of supplementation trials found vitamin D reduced clinical relapse risk with a relative risk of 0.64, an effect strongest in Crohn’s patients in remission (RR 0.47). The target serum 25-hydroxyvitamin D level in IBD appears to be in the 50 to 80 ng/mL range, higher than the 30 ng/mL conventionally considered “sufficient.” Most patients require 5,000 to 10,000 IU daily of cholecalciferol to reach this range, with periodic testing to verify levels.
Comment: This is the usual blather you get from medical journals. I believe that vitamin D levels well above 100 ng/mL are better for patients with inflammatory bowel disease and for anyone else with chronic disease. I keep mine at 130. See this reference. It requires 50,000 IU capsules, and taking them at least several times a week. You need to check your vitamin D levels to ensure your dosing is appropriate. This may be the most important tip in this article.
Low-dose naltrexone
Naltrexone at 4.5 mg per day (one-tenth the addiction-medicine dose) acts as a transient opioid antagonist that triggers a rebound increase in endogenous opioid signaling, with downstream anti-inflammatory effects on toll-like receptor 4 and microglia. The 2007 randomized trial by Smith in 34 adult Crohn’s patients showed clinical response rates of 83 percent on LDN versus 38 percent on placebo at 12 weeks. A pediatric crossover trial showed similar benefit. A Cochrane reviewnoted that the trials are small and that further randomized evidence is needed, but the safety profile is excellent, and the drug is cheap when obtained from a compounding pharmacy. Side effects are mostly limited to vivid dreams in the first few weeks.
LDN requires a prescription. Compounding pharmacies in most states fill it for $30 to $50 per month. Patients on chronic opioids cannot use it.
Wormwood
A German double-blind trial of Artemisia absinthium (wormwood) 500 mg three times daily added to standard therapy in active Crohn’s disease produced near-complete remission in 13 of 20 patients on wormwood versus zero of 20 on placebo at eight weeks, with documented steroid sparing. The mechanism is uncertain but may involve direct anti-inflammatory effects and modulation of gut flora. The dose is high enough that quality control of the preparation matters.
BPC-157 is a peptide that potentially improves inflammatory gut conditions
These include pancreatitis and Crohn’s disease.
It is a synthetic 15-amino-acid peptide derived from human gastric juice, widely studied in animal models for its potential to promote tissue healing and reduce inflammation, particularly in the gastrointestinal tract, including conditions such as IBD. It is believed to work by enhancing angiogenesis and fibroblast activity and by protecting the gut lining, though rigorous human clinical trials are currently lacking and it is not FDA-approved.
Key Aspects of BPC-157 for Gut Health:
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Mechanism: It acts as a “Body Protective Compound,” supporting gastric mucosa integrity, increasing blood flow to damaged areas, and enhancing collagen synthesis.
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Gut Applications: Research suggests it may help treat inflammatory bowel disease (IBD), leaky gut, fistulas, and NSAID-induced ulcers.
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Administration: It is often administered via subcutaneous injection for systemic effects or orally to target gut-related issues.
It is over-the-counter and in the gray market and is unlikely ever to reach a pharmacy, for a cured patient is a lost customer.
Chlorine dioxide is the elephant in the room.
Chlorine dioxide (ClO2), produced by activating sodium chlorite (NaClO2) with citric or hydrochloric acid, has been used in alternative medicine for several decades for a variety of infections and chronic illnesses. Jim Humble’s MMS protocols introduced it to a wide audience, and protocols have been adapted for IBD by clinicians and patients on the basis that dysbiotic flora and intracellular pathogens may contribute to disease.
Because of organized medicine’s suppression, there are no published randomized controlled trials, but the evidence is so substantial that such trials would be unethical because of the placebo control group’s potential for harm. There is a mammoth body of patient case reports, including long-term remissions for UC and Crohn’s disease, attributed to MMS protocols. These patients often combined this treatment with dietary changes and other interventions.
Chlorine dioxide is a potent oxidative antimicrobial that kills bacteria, viruses, and fungi at concentrations that do not damage human tissue when used at the dilutions called for in standard protocols. Whether the profound benefits reported by users reflect a microbicidal effect, secondary effects on biofilm or hydrogen sulfide production, or non-specific mechanisms is unclear. We do know that the stool flora in inflammatory bowel disease is abnormal and that many inflammatory species are present.
Fifteen million people across the world use chlorine dioxide, and its documented cures include many disease entities, including even disseminated pancreatic cancer, which does not respond to anything else. Among the treatments in this article, it has the best chance of achieving a complete cure for inflammatory bowel disease.
Because chlorine dioxide threatens most treatments in standard medical practice, the captured mainstream literature and search results pretend it is poisonous, claiming that taking it is similar to drinking bleach.
Being sure about chlorine dioxide requires a learning curve. I started with theuniversalantidote.com, which I suggest for anyone seriously interested in this subject. I have written 21 posts on chlorine dioxide and have been building my knowledge base for over 1,000 hours.
A reference list is at the end of this article, and there are about a hundred thousand people in two Telegram groups for you to learn from and communicate with. Getting mentorship from people in those communities is a must. Dr. Pierre Kory, a mainstream author, has written a book about chlorine dioxide. HERE is a link to my book summary that I published on Substack.
Things that probably don’t help and may hurt
Several commonly-recommended interventions have either no evidence or active harm signals in IBD.
Aloe vera juice has limited evidence for mild UC induction, but it is a known cathartic and can worsen diarrhea. Kombucha and most fermented foods can flare disease in patients with severe dysbiosis. Fish oil at 3 to 4 grams of EPA plus DHA has marginal trial evidence in Crohn’s disease, with most studies failing to maintain remission, though general anti-inflammatory effects argue for moderate intake. Glutamine supplementation has not shown consistent benefit. Slippery elm and marshmallow root have anecdotal but no formal data. CBD has shown modest symptomatic improvement without affecting inflammation.
NSAIDs (ibuprofen, naproxen, aspirin in anti-inflammatory doses) can trigger and worsen IBD flares and should be avoided. Acetaminophen is commonly recommended by gastroenterologists, but it is an unacceptable human drug because of its toxicity. Antibiotics for unrelated infections can disrupt the microbiome and provoke flares; when needed, the narrowest-spectrum agent for the shortest duration is preferable.
Smoking has a paradoxical relationship with the two diseases. Active smoking supposedly protects against UC and worsens Crohn’s. Transdermal nicotine patches at 15 to 25 mg have shown modest induction benefit in active UC in randomized trials, but no maintenance benefit, and the side-effect profile (skin irritation, sleep disruption) is real. This is a curiosity worth knowing about rather than a treatment recommendation. The Crohn’s patient who smokes should stop. The UC patient should not start. If you believe smoking is good for anything, you also believe in the Easter Bunny.
A composite approach for someone already in remission
For a patient currently doing well on azathioprine, interested in pregnancy and seeking what else is available, a reasonable framework is as follows. None of this requires stopping anything immediately.
First, fix the diet. A four-to-eight-week trial of strict elimination, whether carnivore-keto, SCD, or AIP, will reveal whether food sensitivity is a major driver of their inflammation. Improvement in fecal calprotectin and CRP, measured before and after the trial, is the objective endpoint. If symptoms and biomarkers improve, the dietary pattern can be sustained long-term by gradually reintroducing well-tolerated foods to identify each person’s specific triggers.
Second, repair the microbiome. Visbiome at therapeutic doses for at least three months. Vitamin D titrated to over 100 ng/mL on serum testing. (See this vitamin D post.) Consideration of FMT through a research protocol or through a willing gastroenterologist if dysbiosis is severe and the dietary response is incomplete.
Third, layer in adjunctive anti-inflammatories with trial evidence. Curcumin 2 to 3 g per day in a high-bioavailability formulation. Boswellia 600 to 1,200 mg per day of a standardized extract. These can be added without changing the medication regimen.
Fourth, when stable on this combined approach for six to twelve months, with documented mucosal healing on endoscopy and normal inflammatory biomarkers, the question of medication taper becomes legitimate. A patient might step down from azathioprine to mesalamine alone, or to mesalamine plus low-dose naltrexone, with close monitoring. Some patients reach drug-free remission. Others find they need maintenance therapy, but at a lower toxicity tier than they started on.
For the specific case of a young woman planning a pregnancy, the discussion is sharper. The conventional approach is to stay on azathioprine through pregnancy. The alternative is to attempt a pre-pregnancy transition to mesalamine (safest of all IBD drugs in pregnancy) plus dietary control and adjunctive interventions, with the expectation that any flare during pregnancy can be addressed with mesalamine, oral steroids if needed, or restoration of azathioprine. Either path can be defended. Each woman has to make her own decision with her gastroenterologist.
Reasonable expectations
Patients sometimes hear about a dramatic remission story and conclude that the same outcome is available to them if they only try hard enough. Sometimes that is true. Often it is not. IBD is heterogeneous. Some patients have strong dietary triggers and respond to elimination almost completely.
The problem is that the typical course is decades of escalating immunosuppression with rising toxicity and a colectomy rate that approaches 20 to 30 percent over the course of a lifetime of UC. A patient who uses diet, microbiome work, and rational adjuncts in addition to conventional therapy is hedging in both directions. If the conventional therapy continues to work, the additions improve the quality of life and may allow tapering. If conventional therapy fails, the patient already has the framework in place to try harder on the lifestyle side.
The cost of trying these approaches is small. The upside is substantial.
Comment: I wish I could tell you that my friends carefully read this loving essay that I spent so many hours writing. I wish I could report that they were considering alternative therapies and studying chlorine dioxide. Unfortunately, they are still entirely hypnotized by their “physicians” and the depraved siren songs of conventional medicine.
When they received the draft of this work and my carefully edited cover letter, they DFR and DFL (didn’t f—-ing read or listen), and sent me an abusive text. I knew this was a likely outcome, but I made the effort on the off chance it might help them. Judy told me I was an idiot for trying. No man is a hero to his wife.
Chlorine Dioxide References
· HERE is the Rumble video link for my Dave Oates chlorine dioxide episode.
· HERE is Dave’s Telegram channel. THIS link features his interview with Mark Grenon, and THIS is the Rumble link.
Dave adds:
· Here are links for my platform, Chlorine Dioxide Testimonies:
· https://t.me/ChlorineDioxideTestimonies
· https://t.me/ChlorineDioxideTestimonies/1/501881
· Chlorine Dioxide Testimonies (CDT) on the Telegram Main Platform:
· Click HERE to join Chlorine Dioxide Testimonies (CDT) on the Skool Main Platform.
· Get Started Right with Chlorine Dioxide (CD) HERE.
· Chlorine Dioxide Testimonies (CDT) on Telegram
· Togoda.com is my new search engine for Chlorine Dioxide Testimonies on Telegram. For example, a Togoda.comkeyword search for “Chlorine Dioxide Testimonies on Telegram” brings up:
Chlorine Dioxide documentaries links:
· “The Universal Antidote” was made in 2020. (NASA used this name first.)
Stay connected and informed about CD & other simple solutions at home:
Appendix: The Robert Yoho Substack articles on chlorine dioxide
I have been writing about chlorine dioxide on my Substack, Surviving Healthcare, since late 2023. These posts go deep into many of the people, debates, and protocols summarized here. The interviews with Kerri Rivera, Mark Grenon, Dave Oates, Tanya Carmona Daniels, and the Curious Outlier are primary sources. The posts on my own protocols, the MMS1 versus CDS debate, and the clinical testimonials give texture and personal experience that no book summary can replace. If Kory’s book interests you, these articles are the logical next stop.
The posts below are listed in the order I wrote them.
1. KEY POST: “Chlorine Dioxide (CD) Is a Universal Antidote” — NASA (November 2023). The introductory post that started my series. Covers the compound’s history, mechanisms, suppression, and how to make it.
2. Kerri Rivera, the Mama Bear Who Started a Movement (December 2023). Rivera discovered chlorine dioxide to save her autistic son before Humble or Kalcker reached wider audiences. She has since helped over 100,000 children. Interview and background.
3. Snoot Spray is Nose Magic (December 2023). Michelle Herman’s and Val Alliger’s companies produce commercial chlorine dioxide products that have systemic effects.
4. I am getting rich from Frontier Pharm and Snoot! multilevel marketing (MLM)(Jan, 2024). I wish, ha. I did clear $1800 in the first few weeks but give all profits to charities promoting chlorine dioxide (CD). If you get involved, you can keep whatever you make.
5. Kerri Rivera Returns to Reveal More Secrets of Natural Medicine (March 2024). Second interview. Covers Parkinson’s protocols, the MMS1 vs CDS debate, methylene blue, my own treatment regimen, and leaky gut.
6. Tanya Carmona Daniels Updates Us About Chlorine Dioxide (CD) (May 2024). Carmona Daniels is a top insider with COMUSAV Mundial and the Kalcker Institute. Interview covers the global movement, the MMS1/CDS distinction, and affiliate resources.
7. A Top Chlorine Dioxide (CD) Expert Says We Must All Take It If We Want to Live(June 2024). My anonymous source Steve, with decades of CD experience, shares his knowledge on mechanisms, cancer, dosing, and why MMS1 outperforms CDS.
8. Errors and Omissions in My Most Recent Chlorine Dioxide Post (July 2024). Corrections and clarifications on the MMS1 vs CDS debate, Herxheimer reactions, the role of hydrochloric acid as the preferred activator, and how to stop a reaction with orange juice.
9. As a Patient, I Am a Total Pain in the A** (August 2024). A patient case: a woman’s unstable insulin-dependent diabetes disappeared after one week of MMS1 protocol. Includes my personal regimen and a case series of CD against metastatic cancer.
10. Mark Grenon Is the Most Experienced Living Chlorine Dioxide (CD) Clinician (September 2024). Grenon’s history with Jim Humble, the Genesis II Church, the two documentaries, and his imprisonment. How MMS was discovered and why MMS1 is preferred over CDS.
11. Further Clinical Trials of Chlorine Dioxide Are Unethical Because “A Thousand Anecdotes Become Data” — Pierre Kory (December 2024). Case testimonials across many diseases. Kerri Rivera’s 15-year autism record. An argument for why the anecdotal dismissal is itself a methodological error.
12. Curious Outlier Repost: How to Use Chlorine Dioxide, Part 1 (December 2024). The fast-track series from the author of The Universal Antidote documentary. Starting procedure, suppliers, and the three golden rules.
13. Bonus post about a hero: Susan Raj promoted chlorine dioxide by herself alone in Indi for years. (January 2025)
14. Part 2 of Curious Outlier’s How to Use Chlorine Dioxide Series (January 2025). Protocol 1000 in detail. How to make CD from raw materials at home using muriatic acid and sodium chlorite.
15. A Curious Outlier Repost: Chlorine Dioxide for Skin Diseases and Skin Conditions (January 2025). Before-and-after testimonials for psoriasis, eczema, wounds, infections, and more. Topical protocols for superficial and deep skin conditions.
16. A Rare Interview with the Elusive Mark Grenon, One of Chlorine Dioxide’s Masterminds (February 2025). Extended interview with Grenon himself. His near-fatal poisoning and recovery using CD, his imprisonment, and his ongoing advocacy.
17. Dr. Andreas Ludwig Kalcker, one of the masterminds of chlorine dioxide. (early 2025) The proponent of chlorine dioxide solution (CDS).
18. Dave Oates — By Day, a Jet Mechanic, and by Night, a Caped Crusader for Chlorine Dioxide (CD) (May 2025). Oates saved his mother’s life with CDS when she was near death from Covid. He runs the largest CD testimonials channel on Telegram. His self-experimentation and personal protocols.
19. Midweek Repost: Live Blood Analysis Proves Chlorine Dioxide Works (November 2025). Curious Outlier documents real-time microscopic changes in blood cells before and after CD administration. Red cell morphology, rouleaux formations, and vaccine injury context.
20. Midweek Bonus: My Friend Kerri Rivera Is Being Shadow-Banned, and I Am Asking for Assistance (December 2025). Rivera is one of the three original pioneers of the CD movement alongside Grenon and Humble. This post documents the ongoing suppression of her autism work and calls for support.
21. Chlorine Dioxide for Lyme and Beyond: A Conversation with Mark Grenon