In my last post, I explained there is too much of a compound called TNF (tumor necrosis factor-alpha) in the guts of Crohn’s sufferers and this compound prevents or delays the inflammation and ulcers from healing.

Here’s another study I didn’t mention in my last post, that, again, emphasizes too much TNF is linked to chronic wounds (non healing or slow healing) and inflammatory diseases such as Crohn’s.

Tumor necrosis factor-alpha (TNF-(alpha)) is an important mediator during the inflammatory phase of wound healing. Excessive amounts of pro-inflammatory cytokines such as TNF-(alpha) are associated with inflammatory diseases including chronic wounds.
Read more: http://www.ncbi.nlm.nih.gov/pubmed/11112697

All Crohn’s drugs (steroids, immunosuppressants, biologics, etc), in one way or another, may help to reduce the TNF so the healing process can begin and inflammation/ulcers start to heal. For example:

• Corticosteroids can improve Crohn’s and corticosteroids inhibit TNF (study).
• Naltrexone can improve Crohn’s and Naltrexone inhibits TNF (study).
• Mesalamine can improve Crohn’s and Mesalamine inhibits TNF (study).
• Enbrel, Remicade and Humira can all improve Crohn’s and all are anti-TNF drugs.
• Ect.

But where does the high level of TNF in the gut come from? TNF is normally produced at low-levels when inflammation occurs, but high levels of TNF have been found in non-inflamed tissues as well as inflamed tissues.

“Our results highlight an important role of cytokines such as IL-12 and TNF-α in CD, as there was an increased expression of these cytokines in both inflamed CD and noninflamed CD tissues compared to non-CD samples. Upregulated cytokine expression in CD suggests that there are links between cytokine expression and disease severity. The highest level of expression of these cytokines was observed consistently with the fistulizing type of disease”.
Read more: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3165214/

What the above study found was startling. The more TNF Crohn’s sufferers have in their guts, the greater the severity of the disease! The simple diagram below sums it up.

So, if the level of TNF is so high, higher than what is normally expected of inflamed tissue, where is it all coming from?

Are you ready for this? If you’re not already aware of this, you’ll be SHOCKED! Are you sure you are ready for this? Before I explain any more, do you think Crohn’s could be caused by a stubborn gut infection where certain bacteria indirectly produce high amounts of TNF in the guts of Crohn’s sufferers?

Here we go. There are two types of bacteria linked to Crohn’s disease: MAP and AIEC.

Mycobacterium avium paratuberculosis (MAP) is also the cause of Johne’s disease, a gut inflammatory disease similar to Crohn’s. Adherent-invasive E. Coli (AIEC) has been found in Crohn’s sufferers for decades.

Here’s an interesting paper about Crohn’s and AIEC.

“The role of adherent-invasive E. coli (AIEC) in Crohn disease (CD) has been in debate for decades. AIEC bacteria are found in the small intestine of patients with chronic CD, but it has remained unclear whether this infection is causal or secondary to underlying immune deficiencies in CD patients. In this issue of the JCI, Chassaing and colleagues demonstrate that AIEC bacteria express an adherence factor called long polar fimbriae (LPF) that aids in the binding of these bacteria to M cells overlying Peyer’s patches and subsequent entry into lymphoid tissue.”
Read more here: http://www.jci.org/articles/view/46333

Here’s an interesting paper about Crohn’s and MAP

“Although Crohn’s disease is considered to be autoimmune in origin, there is increasing evidence that it may have an infectious cause. The most plausible candidate is Mycobacterium avium subspecies paratuberculosis (MAP). Intriguingly, Koch’s postulates may have been fulfilled for MAP and Crohn’s disease, even though they still have not been met for Mycobacterium leprae and leprosy. In animals MAP causes Johne’s disease, a chronic wasting intestinal diarrhoeal disease evocative of Crohn’s disease.”
Read more here: http://www.ncbi.nlm.nih.gov/pubmed/12901893

With Crohn’s, MAP and AIEC have a LOT in common! They both prefer the gut and they invade and replicate inside immune cells in the gut. But, here’s the most important thing that happens. The immune cells invaded with MAP or AIEC produce high levels of TNF. Let me say that again, the immune cells invaded with MAP or AIEC produce high levels of TNF!!

Before we go any further, how common is MAP and AIEC in Crohn’s sufferers?

This study found MAP in 92% of Crohn’s sufferers.

“Detection of M. avium subsp. paratuberculosis in mucosal biopsy specimens was also evaluated by using mycobacterial growth indicator tube (MGIT) cultures (Becton Dickinson). IS900[L/AV] PCR detected M. avium subsp. paratuberculosis in 34 of 37 (92%) patients with CD”.
Read more: http://www.ncbi.nlm.nih.gov/pubmed/12843021

This study found up to 36% of Crohn’s sufferers infected by AIEC.

“In neoterminal ileal specimens, AIEC strains were found in 36.4% of CD early lesions”.
Read more: http://www.ncbi.nlm.nih.gov/pubmed/15300573

These two studies prove that MAP/AIEC infected immune cells produce high levels of TNF.

“AIEC LF82-infected cells release high levels of TNF-alpha.”
Read more: http://www.ncbi.nlm.nih.gov/pubmed/11500426

“high production of TNF-α from macrophages infected with viable MAP might contribute to the pathogenesis of CD”.
Read more: http://onlinelibrary.wiley.com/doi/10.1002/ibd.21750/full

MAP has been found in water tanks, rivers feeding domestic water supply, milk and cheese. It’s very likely that AIEC is found in the food chain.

Do you think it’s fair to say that probably all Crohn’s sufferers are infected by either AIEC or MAP or both? I think that’s very probable. Here’s an updated diagram of what’s really happening in Crohn’s.

In this study, the author discusses CURING Crohn’s with antibiotics.

“If infectious in origin, Crohn’s disease should be curable with appropriate antibiotics… Rational studies to evaluate appropriate therapies to cure Crohn’s disease are proposed.”
Read more: http://www.ncbi.nlm.nih.gov/pubmed/12901893

A few years ago, a study put around 70% of Crohn’s sufferers in long-term remission or permanent remission with a specific antibiotic. If Crohn’s was really an incurable autoimmune disease (like everyone is told), why did about 70% of them in that study experience long-term remission or perhaps permanent remission without using drugs such ASAs, steroids, biologics, etc? Antibiotics only kill bacteria!

Is Crohn’s disease really just a very stubborn gut infection?

My ebook explains what antibiotic was used in the above study, how to get it from your doctor, how much to take and when to take it.