The Science Behind the Crohn's Protocol

Anyone who has Crohn's or has a first-degree relative with Crohn's needs to understand the science of Crohn's and the extraordinary power of nutrition.

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.

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