Gut bacteria theory for adult onset celiac disease

[Zizzle]

Wall Street Journal Article quoting Dr. Alessio Fasano:

http://blogs.wsj.com/health/2010/09/27/ ... -bacteria/

Probably explains MC too.

[tex]

Zizzle,

They sort of proved that the diagnostic markers of celiac disease can present at virtually any age, (which I thought we already knew ), but IMO they did not prove that the prevalence of celiac disease is increasing, (though the incidence of official diagnoses may indeed be increasing). Increased prevalence of a disease in a fixed cohort of subjects can simply be due to a time-dependent disease, (IOW, low-sensitivity diagnostic tests are not capable of early detection of the disease).

Please don't misunderstand me, I do believe that celiac disease is probably on the increase. I'm just saying that IMO, this research project did not prove that claim, due to a critical invalid assumption in their methods.

Here's why I disagree with their conclusion. Looking at what they did, they studied the same cohort of subjects, at two different times in their lives, and concluded that since more of them presented with the classic diagnostic markers of celiac disease at advanced age, that means that the prevalence of celiac disease is increasing. That is simply an incorrect conclusion, because it assumes that their diagnostic process is 100% accurate, and the truth is, it is far short of that. Their theory may be correct, but some of their methods were not scientifically sound. While it is true that they demonstrated that their ability to medically diagnose celiac disease is a time-dependent process, (IOW, they can't diagnose celiac disease, until the disease is mature), that does not prove that those individuals who were diagnosed later in life, did not have the disease earlier - it simply proves that their diagnostic procedures were inadequate to diagnose the disease earlier. I'm kind of surprised that Dr. Fasano would make such an elementary mistake. He, of all researchers, should know better.

There is good evidence that they are correct that a change in gut bacteria population demographics may indeed be the reason why celiacs become symptomatic, but the shortcomings of the classic tests that they use to diagnose celiac disease, preempt their ability to claim that this research project actually proves that celiac disease presents later in life for many people. The disease is there, but they simply can't detect it earlier, because the "official" diagnostic criteria require certain outdated procedures, which result in doctors looking for antibodies in the wrong place, (in the blood). By the time antibodies become numerous enough in the blood, to show a positive test result, the disease has been developing for years, (probably decades, in some cases).

This helps to elucidate the problem with mainstream medicine's methods regarding celiac disease/gluten-sensitivity:

We tested 227 normal volunteers with blood tests for celiac disease. Twenty-five of these people (11%) had either antigliadin IgG or IgA in their blood versus only one (0.4%) that had antiendomysial, antitissue transglutaminase, and antigliadin IgA in the blood. So for every one person in a population that has the antibodies that have 100% specificity for celiac disease of the intestine (antiendomysial and antitissue transglutaminase), there are 24 that have antibodies to gliadin that may not have celiac disease. So what is going on with the 11% with antigliadin antibodies in blood? Are these false positives (rhetorically)? You�re telling me that there is a disease called celiac disease and it is associated with antibodies to gliadin in the blood and sometimes it damages the intestine? But people with antigliadin antibody in their blood but no other antibodies do not have a clinically significant immunologic reaction to gluten? Do you see the problem? How can 11% be false positives? What about the 89% with none of these antibodies? You cannot equate having no antibodies at all (a negative test) with having antigliadin antibodies alone. If you have antibodies to gliadin, something is going on here. Where there�s smoke there�s fire. The purpose of this study was to test this hypothesis: that an antigliadin antibody alone does indicate the presence of an immune reaction to gluten that may be clinically important. Using tests for intestinal malabsorption and abnormal permeability (i.e., tests of small bowel function, unlike a biopsy which says nothing about function), we found that 45% of people with only an antigliadin IgG or IgA antibody in blood (without either antiendomysial or antitissue transglutaminase antibody) already had measurable intestinal dysfunction, compared to only 5% of people with no antibodies to gliadin in their blood. When we did biopsies of these people�s intestines, none had villous atrophy with only a few showing some early inflammation. Thus, having an antigliadin antibody in your blood does mean something: that there is nearly a 1 in 2 chance that functional intestinal damage is already present even though it may not be visible structurally at the resolution attained by a light microscope assessment of a biopsy.

From here:

http://www.finerhealth.com/Essay/

Otherwise, that's a good article. Thanks for the link, (which contains a link to the original article).

Tex

P. S. Joe posted about this same research project in the News Releases of Interest forum, but in that article, the writer took a somewhat different approach.

[Polly]

Hi Z!

I am 100% convinced that antibiotics (doxycycline over several weeks) brought on my MC, likely by permanently altering my gut bacteria. Of course, I'm sure I was genetically suspectible to gluten intolerance, but prior to those antibiotics, I went my whole life eating everything and anything. And I never had any of the significant GI problems (reflux, bloating, gallbladder disease, etc.) during my life that so many MCers experience prior to getting the disease. Sigh.
Medical research is really beginning to put lots of significance on the body's bacterial colonization, so hopefully we will benefit from new discoveries. I would like to learn more about the fecal transplants that some researchers are trying. Has anyone heard anything new about this? Thanks for sharing.

Love,

Polly

[mbeezie]

I haven't heard anything new but I agree with everyone's points. Now what would have been interesting it to see what Enterolab scores were in 1974 and 1989. I shudder to think of all the children, my son included, that are (or were) on antibiotic after antibiotic at such a young age and what it has done to their gut flora. The cocktail of genes, stress and dybiosis is a surefire way to get sick.

Mary Beth

[CAMary]

I'm in agreement with Polly - since my onset was right on the heels of a c-diff infection triggered by three courses of abx to treat a stubborn sinus infection....Yes I have the right genes for gluten sensitivity - but part of me also wonders if I'd used the neti pot at my first symptom of sinus trouble (like I do now!) if I'd never have developed this beast....

But then again, I'd never have met any of you all...gotta look for the silver lining!

Mary

[Gloria]

I trace my problems to being prescribed two concurrent antibiotics for diverticulitis.

Gloria

[wonderwoman]

I quit smoking almost three years ago. It was shortly after quitting that I began having loose stools. I have learned here there is a connection with quitting smoking and MC diagnosis.

Then about two years after quiting my D became so bad while taking Penicillin for a tooth abscess that I saw a gastroenterologist. A sigmoidoscopy was done immediately and three weeks later a colonoscopy at which time I was diagnosed with CC. Two weeks later I was pretty much GF, DF, & SF. By one month 100% free. 7 1/2 months later doing great on 1 Entocort a day and the GF, SF diet.

[Zizzle]

I totally agree with the antibiotic/gut flora connection. I don't know whether my MC was due to traveler's diarrhea or antibiotics taken. I do know that both of my autoimmune flares occured shortly after having children. The first was a itchy rash (possibly DH) that started 3 months after my son was born and lasted 9 months. My MC was diagnosed when my daughter was 2 yrs old. Has anyone on this board reported symptoms starting after childbirth?

Of course I took lots of antibiotics after my son was born for 3 rounds of mastitis. After my daughter, I had more antibiotics for a presumed bladder infection or mastitis early on. I was also prone to UTIs and took Macrobid (Nitrofurantoin) a couple of times a year. I suppose I should suspect the antibiotics more than the pregnancies...

[tex]

Zizzle,

Hormones have a huge influence on MC "activity", and, as we all know, antibiotics can trigger reactions as well. Together, the effects are bound to be even more potent.

Here is a prior discussion about the effects of hormones, (during pregnancy and postpartum), on MC symptoms:

http://www.perskyfarms.com/phpBB2/viewt ... +pregnancy

Here is a discussion on BC pills and MC:

http://www.perskyfarms.com/phpBB2/viewt ... +pregnancy

As you can see, during pregnancy, some MCers go into remission, while for others, their symptoms become worse. No one knows why.

Incidentally, even HRT patches can cause an MC reaction.

Tex