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Colitis and Crohn's is likely a reaction to fungus

Recent studies in both humans and mice suggest the immune system’s inflammatory response to fungus causes Crohn’s and colitis.

The major breakthrough came when researchers employed a different means of finding fungus in the intestinal tissue. Previously, doctors usually just looked at tissue cultures. Unfortunately, it is difficult to tease fungus out of tissue and get a culture of it. The lack of data lead mainstream doctors to believe that fungus / yeast had nothing to do with intestinal disease. Now with DNA testing, researchers have found fungus in the intestinal tissue of people with Crohn’s and Colitis.

Here is a German paper, from 2008, that says there is an increased fungal load in people with Crohn’s and Colitis.


Here is a 2012 paper by Iliyan Iliev, et al, from Cedars Sinai.


These researchers showed the severity of colitis in mice depends on the way the immune system responds to fungus. Genetics that cripple the immune system’s effectiveness against fungus can cause an increased inflammatory response. They also showed that a similar gentic weakness appears to cause the same problem in humans. When they gave the mice anti-fungals, this decreased the severity of the induced colitis.

Here is a few details of the study. Colitis was induced in wild mice and in Dectin-1 deficient mice. The mice that were deficient in Dectin-1 had a more severe form of colitis. This difference in colitis severity was not due to the different bacteria present in the Dectin-1 deficient mice. The researchers implanted bacteria from the Dectin-1 mice into the wild mice and this did not change the results.

Then why would the Dectin-1 deficient mice get a more severe form of colitis? It has to do with their immune response to fungus. Without Dectin-1, the immune system has a difficult time marking the fungus for destruction. This causes the immune system to increase the inflammation. When the researchers gave the Dectin-1 deficient mice some antifungals, this reduced the severity of the colitis.

The researchers then looked at the Dectin-1 gene variations in humans. They found a halotype associated with increased severity of colitis. Humans with this halotype of the Dectin-1 gene had a much more severe form of colitis that was very difficult to treat. Hence human genetics play a big part in the severity of colitis, and this has to do with the immune system’s inability to effectively control fungus without creating a lot of inflammation.

I think this is a huge discovery. Kudos to our researchers! :thumleft:
I placed the above in your multimedia section. Thank you for telling me about that section.

I found something else that is highly relevant to fungus and Crohn's. Crohn's is also associated with a bacteria called Mycobacterium avium paratuberculosis (MAP). The MAP bacteria interferes with macrophages getting rid of the Candida / yeast. I find it quite interesting that the lack of Dectin-1 also interferes with the macrophages getting rid of the Candida / yeast. In both situations, the immune system is being interfered with at the same point.

The fact that Rifaximin antibiotic seems to help with Crohn's may be due to this antibiotic's ability to get rid of the MAP bacteria. However, there is another way to help get rid of MAP. The lauric acid in coconut oil will help kill both the MAP and Candida. However, you have to get the coconut oil distributed throughout the intestine. You need some roughage with it. For a long time, Ray Peat, Ph.D. has suggested the use of a salad of gated carrots, warmed coconut oil, and vinegar. This would allow some of the coconut oil to travel the entire length of the intestines. Another idea is to use grated coconut to make macaroon cookies. People with Crohn's and colitis have already discovered that the macaroon cookies help. Here is a rating of the effectiveness of the cookies:


Here is the reference that says the MAP bacteria interfere with the macrophages getting rid of Candida.

"Glycolipid fractions from Mycobacterium avium serovar 2 (Mycobacterium
paratuberculosis 18) inhibited the killing of Candida albicans by activated
bovine peripheral-blood-derived macrophages."


Isolation and partial characterization of glycolipid fractions from Mycobacterium avium serovar 2 (Mycobacterium paratuberculosis 18) that inhibit activated macrophages.
Hines ME 2nd,