Still following MAP...

Just ran across this. Hope it hasn't already been posted.

http://www.ncbi.nlm.nih.gov/pubmed/18789596?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum

"The plausibility of a causal role of Mycobacterium avium subspecies paratuberculosis (MAP) in Crohn's disease has gone from controversial to compelling."

The full article is published, but you would have to pay for a subscription to look at it. There is an interesting linked abstract on the right side of the page titled "Molecular evidence for Mycobacterium avium subspecies paratuberculosis (MAP) in Crohn's disease correlates with enhanced TNF-alpha secretion." In that article, the author reports that TNF levels for Crohn's patients that were MAP positive were higher than in ulcerative colitis patients that were also MAP positve. The implication is that in Crohn's there is an abnormal macrophage response to MAP. I would expect that there are several bacteria capable of causing this abnormal reaction - based on the number of different candidates in the literature.

Rider Fan,

do you know what kind of treatment and how long the treatment lasted? I heard from an Australian doctors report that MAP reproduces very very slowly (something like that) and it takes 2-3 years of antiobiotic treatment to effectively kill it.

This aussie doctor treats pple with severe CD with powerful antiobiotics and probiotics resulting in high remission rates (and based on MAP theory).

http://www.crohns.org/treatment/borody.htm

these studies looked at different depths of the intestinal wall. they should show different numbers based on how deep each study went.

The studies that show a poor or zero correlation with MAP may be flawed in that mycobacteria have traditionally been a very difficult bacterial genus with which to work. Koch's postulates have never been fulfilled with leprosy, for example, which is a mycobacterium. They are slow to grow, slow to die, and very tricky to culture; it seems likely that even sensitive PCR tests may not be effective in finding their DNA in many cases; cattle shed much larger quantities of MAP than do humans, and the veterinary tests are substantially more effective than similar tests on human biopsy and fecal samples.

If the correlation between MAP colonization and Crohn's were so poor, then we would not have startling results like those of Warwick Selby, whose anti-mycobacterial protocol put some 95% of patients in remission. Moreover, it would explain why so few of them (perhaps 15%) remained disease-free months or years after the antibiotics were stopped: either they were re-infected with MAP, or the organism was never really gone. Mycobacteria are very slow to grow, and very hard to kill without harming the host. If the gastric environment is not changed (which presumably entails a change in diet to prevent the entire gastric flora from simply combing back, giving an ideal environment for MAP to grow), the disease reoccurs.

Another way of looking at it: take a look at the symptoms of a cow with Johne's disease, which is known to be caused by MAP. Then look at human Crohn's and the symptoms of the disease in us. For those that wish to believe it's a coincidence- more power to you. That's fine by me. But when I lost weight, it was as muscle mass. It wasn't for a couple of years that I finally became overtly sick, and after reading about MAP infection I realized it was more than just similar to the protein-losing enteropathy (PLE) of cattle with Johne's.

Rider Fan> I agree with you that it is unlikely that MAP is the sole contributor to this disease, which is why it can be modulated- at least in the short run- with antibiotic treatments. However, I would contend that the findings by Selby- that such a large proportion of the Crohn's patients treated in this manner go into remission- who used a regimen that is highly specific to mycobacteria indicate that he's on to something.

Moreover, that the disease returns in a high proportion of the patients- but not all- is also highly interesting in that I doubt any of the patients were coached to change their eating habits. The one person who I know firsthand who has been in remission (cured?) some 4-5 years after ending the antibiotic therapy informs me their diet is very low in carbohydrates. There are several studies that advance that theory, and at least one gastroenterologist has published on the subject that he has an 85-90% "cure" rate (his word, not mine) by using carbohydrate restriction. The literature is virtually unanimous on the subject of carbohydrate restriction and Crohn's, even while other studies involving diet and the disease are all over the place, and contradict each other.

Unfortunately, there are no recent studies on the subject, and none done in large populations. I've been trying to convince gastroenterologists that this needs to be studied, but they simply comment that it's interesting and wander off.

Ah, well. Perhaps I'm just a lunatic. :)