Monthly Archives: November 2010 - Page 5

More on Fecal Transplants

Posted by on November 3, 2010 43 comments

We’ve had ongoing interest in the topic of fecal transplants from readers of our bowel disease series, and we’ve recently had comments from two biomedical professionals reminding us that it is desirable to have fecal transplants performed by doctors after screening of the stool for pathogens.

Coincidentally, The Scientist ran a nice story today on fecal transplants. [1]

Fecal transplants are effective against C. difficile, ulcerative colitis, and probably other inflammatory bowel disorders:

By producing sturdy spores that can linger in the intestinal tract even after repeated antibiotic treatment, C. difficile can continually give rise to new toxin-producing colonies that wreak havoc on the colon. But these colonies prove no match for fecal transplants, which boast a cure rate of up to 95 percent….

Borody did his first fecal transplant back in the mid 1980s, when he was confronted with one of the most difficult cases he had seen at the time: a woman who had vacationed at Fiji and had developed an incurable colitis through an unknown pathogen.

While searching the literature for alternative treatments, he stumbled upon a paper published in 1958 in the journal Surgery that described four cases in which a similar condition was cured by infusing the inflamed guts of the patients with fecal samples from healthy donors. “So I looked at the method and I kind of made up the rest of it,” Borody said.…

The stool, now turned into slush, was administered to the patient — who had her gastrointestinal tract previously flushed — via two enemas over the course of two days.

The results were nothing short of surprising, Borody said. Within days her colitis was gone, never to return.

It’s a well-proven procedure in animals. Veterinarians don’t bother to screen rumen fluid for pathogens, and yet the procedure is almost always healthful for the recipient:

The procedure, which has deep roots in veterinary science, has been tried and tested in animals for centuries. Farmers handling livestock have long realized, for example, that indigestion following a change in diet in grazing animals, such as cows, can be treated by feeding the sick cow rumen fluid that has been sucked out of a healthy cow’s stomach.

Yet it’s hard to find doctors who will perform the procedure for any ailment except C. difficile infections:

Currently, while most fecal transplants in the U.S. are performed exclusively to treat C. difficile, a growing list of doctors, such as Lawrence Brandt, chief of Gastroenterology at Montefiore Medical Center in New York, are beginning to expand to other gut disorders such as inflammatory bowel diseases….

“It is currently considered a last resort,” he said. But he hopes that will soon change. “It’s relatively simple, relatively inexpensive, and it’s very rapid in its actions.”

Conclusion

In chronic infections of the colon, fecal transplants should be among the first treatments resorted to, not the last resort.

This is one treatment where experience with animals and human patients, demonstrating that fecal transplants are fairly safe and often highly effective in colonic disorders, should trump the normal regulatory barriers to new procedures.

However, given the cautious nature of regulators and most doctors, it seems unlikely that the therapy will be widely available any time soon.

It’s good to hear that there is a “growing list” of doctors who will perform a fecal transplant. Anyone with a seemingly incurable colonic disease should seek one of them out.

References

[1] Cristina Luiggi, “Same Poop, Different Gut,” The Scientist, Nov 3, 2010, http://www.the-scientist.com/news/display/57795/.

Thinking With Your Gut Bacteria

Posted by on November 2, 2010 18 comments

Is your personality really yours – or is it your bacteria’s?

What prompts this thought is a new paper that studied mate preference in fruit flies. It turns out that the gut bacteria in fruit flies influence their mate preference. [1]

Image source: Wikimedia commons.

It’s been known for 20 years that fruit flies raised on one type of food prefer to mate with fruit flies raised on that same food. Now, researchers have proven that the preference is dictated by gut bacteria. When fruit flies are given antibiotics, they forget their mate preference and will mate with fruit flies that eat different diets. [2]

Mating preference seems to be dominated by a single species:  Lactobacillus plantarum. This species is common in probiotic supplements and in fermented vegetables. So if you find yourself developing an attraction to starch-fed fruit flies, your probiotic could be to blame.

Personality-Altering Pathogens

Personality-altering pathogens may not be that rare. In the book we mention that Toxoplasma gondii, a protozoal parasite, infects 20% to 60% of the population in most countries, forms cysts throughout the body including the brain, and makes its victims behave recklessly:

  • Rats infected with T. gondii lose their fear of cats. [3]
  • Humans infected with T. gondii are 6 times more likely to get in traffic accidents. [4]

Conclusion

If people seem to be behaving increasingly oddly lately, perhaps it’s not your misanthropism. It might be a bug going around.

References

[1] “Gut Bugs Affect Mating,” The Scientist, Nov 2, 2010, http://www.the-scientist.com/news/display/57793/.

[2] Sharon G et al. Commensal bacteria play a role in mating preference of Drosophila melanogaster. PNAS, www.pnas.org/cgi/doi/10.1073/pnas.1009906107, 2010. http://pmid.us/21041648.

[3] Webster JP et al. Parasites as causative agents of human affective disorders? The impact of anti-psychotic, mood-stabilizer and anti-parasite medication on Toxoplasma gondii’s ability to alter host behaviour. Proc Biol Sci. 2006 Apr 22;273(1589):1023-30. http://pmid.us/16627289.

[4] Flegr J et al. Increased incidence of traffic accidents in Toxoplasma-infected military drivers and protective effect RhD molecule revealed by a large-scale prospective cohort study. BMC Infect Dis. 2009 May 26;9:72. http://pmid.us/19470165.

Why Wheat Is A Concealed Cause of Many Diseases, III: Adjuvant Activity

Posted by on November 1, 2010 34 comments

We’ve been looking into how wheat can cause autoimmune diseases other than the “classic” wheat-associated diseases, celiac disease and Hashimoto’s thyroiditis.

The first post in the series discussed how wheat can cause a leaky, permeable gut that lets toxins and bacteria into the body. The second post discussed how wheat can itself generate a variety of auto-antibodies that attack nerves, brain, connective tissue and joints.

Now, we want to look at how wheat can create diseases by binding to other molecules and causing the body to form antibodies to them. Wheat can thereby cause allergies against foods as well as autoimmune attacks on self molecules.

Adjuvant Activity of Wheat Germ Agglutinin

Immunologically speaking, an “adjuvant” is a molecule that when bound to another molecule makes it much more immunogenic. Adjuvants such as aluminum salts are used in vaccines to make the immune system produce antibodies more readily against the target protein. This lowers the vaccine dose needed for immunity.

Wheat germ agglutinin (WGA) is a wheat lectin. (It is not part of gluten.) WGA can act as an adjuvant, causing the body to generate antibodies against proteins that, in isolation, the body would not form antibodies against. 

For instance, antibodies against the egg protein ovalbumin are not generated if it enters the body alone, but are generated if it is accompanied by WGA. [1]

So don’t eat toast with your eggs! If you have a leaky gut, the wheat might give you an egg allergy.

Haptenization Activity of Wheat Gliadin

A similar process that helps create auto-antibodies is “haptenization.” The immune system forms antibodies more readily against large molecules than small ones. (This helps avoid autoimmunity, since small molecules are more likely to have similar human peers.)

When two small molecules bind together, so they look like one big one, the immune system is more likely to form antibodies against the large complex. These antibodies may then react against one of the molecules individually, even if it is not paired up. If the targeted molecule is human, then the antibody is an auto-antibody.

One reason wheat gliadin is so disruptive to the body is that it binds strongly to sugars. The average molecule of wheat gliadin is bound to 1 to 2 molecules of glucose and 2 molecules of sialic acid, another sugar. [2] Since a lot of human molecules have sialic acid residues, gliadin can bind to them.

One of the sialic acid-containing molecules gliadin binds to is called GM1 ganglioside. This molecule is found on the intestinal brush border, but it is also found in nerves. When wheat binds to GM1 ganglioside on the intestinal surface, it induces the formation of auto-antibodies that attack the ganglioside in nerves. In 65% of patients with gluten sensitivity and peripheral nerve damage, anti-ganglioside antibodies are found. [2]

Conclusion

Wheat could be a concealed cause of many food allergies, through WGA’s adjuvant activity. If so, then many food allergies may gradually disappear after wheat is given up.

Wheat proteins can also bind to an extraordinarily large number of human proteins, in part by binding to sialic acid or other carbohydrate residues of glycoproteins or glycolipids, and has a chance to induce antibody formation against many of those proteins.

The bewildering array of ways in which wheat can trigger attacks on human tissue makes it impossible to identify all the wheat-caused diseases.  The only thing we can say for sure is that if you have a disease, it’s a good idea to give up wheat. You may give up your illness at the same time.

Related Posts

Other posts in this series:

  1. Wheat Is A Cause of Many Diseases, I: Leaky Gut Oct 26, 2010.
  2. Why Wheat Is A Concealed Cause of Many Diseases, II: Auto-Antibody Generation Oct 28, 2010.

References

[1] Lavelle EC et al. The identification of plant lectins with mucosal adjuvant activity. Immunology. 2001 Jan;102(1):77-86. http://pmid.us/11168640

[2] Alaedini A, Latov N. Transglutaminase-independent binding of gliadin to intestinal brush border membrane and GM1 ganglioside. J Neuroimmunol. 2006 Aug;177(1-2):167-72.  http://pmid.us/16766047.