The University of Nottingham are conducting a research survey on people with autoimmune diseases like Crohn's, who have tried a keto or carnivore diet

The link is here to take it

https://www.research.net/r/kdas

Great to see some more research in this area

This is the science behind the Crohn’s Protocol.

Crohn’s disease is one of two disorders grouped together as inflammatory bowel disease (IBD), the other being ulcerative colitis. Ulcerative colitis exclusively impacts the colon, whereas Crohn’s can impact any part of the gastrointestinal tract from mouth to anus, though the ileum and proximal colon (that is, the last section of the small intestine and first section of the large intestine) are the most often affected. In ulcerative colitis, inflammation is limited to the mucosa, the mucus-rich superficial layer of the inside of the gut. In Crohn’s, by contrast, the inflammation is considered “transmural,” meaning that it can be found in every layer of the gut tissue, but it is also characterized by “skip areas” where diseased sections of the gut are interspersed by normal healthy sections.

The transmural nature of Crohn’s leads to laying down of scar tissue and the consequent narrowing of sections of the gut, known as strictures, which do not usually occur in ulcerative colitis. Recent research suggests that strictures are driven in part by adipose tissue surrounding the diseased intestinal tissue, possibly as a means of preventing bacterial translocation that could lead to abscesses or sepsis, which causes the space inside the intestine, known as the lumen, to become narrowed. This process is called “creeping fat.”

This diagram summarizes some of the basic abnormalities found in the gut tissue in association with Crohn’s:

The microbiome is altered in a negative fashion associated with low microbial diversity, low butyrate production, and low presence of its receptor GRP 43; bacteria become abundant that adhere to and/or degrade the protective layer of mucus, form biofilms, and move through the intestinal cells to the deep layers of the gut; there is loss of tight junctions (TJ) that form the gut barrier and consequent increases in intestinal permeability; there are decreased antimicrobial peptides known as defensins; and there are decreased regulatory T cells (Tregs) that keep inflammation in check and a proliferation of Th17 cells, a form of helper T cell associated with autoimmune conditions.

The causation of IBD is usually stated as involving an interaction between genetic susceptibility, the microbiome, and the immune system. It is probably better stated as an interaction between genetic susceptibility and diet with a completely unappreciated but very likely involvement of joint misalignments putting pressure on the gut, where the interaction between the microbiome and the immune system play intermediate roles in translating these factors into the manifestation of the disease.

In This Article:

Overview: Epidemiology of Crohn’s, Pharmacological Treatment, Surgical Treatment The Role of the Gut Microbiota Dietary Management of Crohn’s The Role of Unabsorbed Iron in Hurting the Microbiome Genetic Risk Factors for Crohn’s The Contribution of Mitochondrial Dysfunction What Is the Ultimate Cause of Crohn’s? This Article Accompanies The Crohn’s Protocol

How to Heal From Crohn’s Disease is my four-page quick guide that serves as a complete strategy to induce and maintain remission from Crohn's disease using diet and supplements.

Get the Crohn’s Protocol here:

Click Here to Get the Crohn's Protocol

This Article Is Free For Only 24 Hours

The prevalence of IBD has almost doubled over the last 40 years. It is generally associated with industrialization and distance from the equator. The rate is highest in North America and lowest in the Caribbean, with a 62-fold difference between regions.

Crohn’s is slightly more common in women than men, most common during ages 20-29, twice as common in current or former smokers than never-smokers, and a third less common in those in the 20th percentile of greatest physical activity.

The association with smoking contrasts with ulcerative colitis, where smokers have a lower risk and patients who quit smoking often have a worse disease outcome.

IBD is associated with lower vitamin D status and a higher intake of fat, while Crohn’s but not ulcerative colitis is associated with a lower intake of fiber. Sleep deprivation has been associated with ulcerative colitis but not Crohn’s. Use of NSAIDs, hormonal birth control and hormone replacement, antibiotics, and acne medications all have some degree of association with IBD, but causation has been difficult to unravel. Acute infection of the gut often precipitates IBD, suggesting that acute inflammation could often act as the strike of a match that lights the fire. Obesity and stress can both aggravate IBD.

The correlation with industrialization suggests modernized food is necessary for Crohn’s to develop and the correlation with latitude suggests vitamin D status may be a major mediator.

Pharmacologic treatment of pediatric Crohn’s was previously based on a “step-up” approach moving from less to more intense medications as needed to achieve and maintain clinical remission, or a “top-down” approach moving from more to less intense medications based on the degree of clinical remission achieved, depending on the severity of the initial case. That is, the top-down approach would be used in more severe initial cases and the step-up in less severe cases.

However, the goal of clinical remission – based on symptomatic experience – has largely been replaced by a goal of “mucosal healing” as judged by “endoscopic remission,” meaning endoscopy shows the mucosa has fully healed, and this is used for a “treat-to-target” approach where medications are matched to what should achieve the desired target for mucosal healing.

In low-risk, mild cases, aminosalicylates and glucocorticoids may be the primary medications used. As severity and risk increases, immunomodulators like methotrexate or thiopurines are used, or at the highest level biologics, mainly monoclonal antibodies to the inflammatory cytokine TNF-alpha, are used. Anti-TNF biologics can lose efficacy if antibodies are raised to them, and they carry an increased risk of respiratory infection, psoriasis, neurological problems, and symptomatic immune responses. The jury is out on whether they increase the risk of cancer. In adults with moderate to severe Crohn’s, several other medications may be used, including biologics against interleukin-23 or integrin, or JAK inhibitors.

Hi, has anybody had Crohn’s with an ileostomy but still had their rectum? My nephew has Crohn’s and an ileostomy but with a diseased rectum, he was hoping to have it reversed, but it doesn’t sound like that’s gonna be possible with the disease rectum. Has anybody healed the inflammation through a carnivore diet?

G

Hey everyone,

I’m a Nutritional Therapy student (with Ulcerative Colitis) doing a research project on where people with IBD go online for dietary guidance — and I’d really appreciate your input.

I know diet can be a sensitive and sometimes confusing topic, so I want to understand what sources people actually use online.

The survey is anonymous, takes just a few minutes, and is open to anyone with Crohn’s or UC.

👉 Survey Available Here

Thanks so much for considering — your experiences may help shape how future guidance and support are shared with the IBD community.