January 22, 2013
Dr. William Davis, author of the NY Times bestseller, Wheat Belly, recently attended a conference in which Dr. Alessio Fasano spoke. Dr. Fasano is a noted celiac disease investigator who has dissected out the details of bowel “leakiness” characteristic of the disease.
Among the issues he highlighted was the fact that Homo sapiens have a gene that no other species possesses, a gene for a modified form of the protein haptoglobin. Ordinarily, haptoglobin is responsible for “cleaning up” free hemoglobin in the bloodstream. Hemoglobin is contained within red blood cells but, when damaged, free hemoglobin is released which is toxic; haptoglobin then “cleans” up the hemoglobin for disposal.
Humans are the only species with a modified form of haptoglobin, programmed by a gene acquired after human predecessors, Australopithecus, diverged from “Pan” apes, chimpanzees and bonobos, and transitioned towards ancestral Homo species. This protein is haptoglobin 2. The functions of this protein are distinct from haptoglobin’s role of hemoglobin scavenging.
Haptoglobin-2 has another name: zonulin. Zonulin proteins are found within intestinal cells, or enterocytes, with production/release triggered by various foreign bacteria, such as strains of E. coli and Salmonella Once triggered by bacteria, zonulin is responsible for creating bowel “leakiness,” allowing water to leak into the bowel: diarrhea, an adaptive response that develops in response to foreign invaders to flush them out. (Cholera toxin is the penultimate example of this effect, resulting in gallons of watery diarrhea.)
By a quirk of nature, the wheat protein, gliadin, mimics the effects of foreign bacteria and it, too, triggers zonulin. But this function is flawed in that it generates a two-way response: Not only can water exit, but intestinal contents are able to gain entry in the opposite direction: into the bloodstream.
Among the most fascinating findings of Dr. Fasano’s work: The gliadin-zonulin leak effect occurs not just in people with celiac disease or gluten-sensitivity; it occurs in everybody. The effect is longer and more pronounced (5-fold greater) in the enterocytes of people with celiac disease, but the effect of increased two-way leakiness spares nobody.
Only humans have the gene for haptoglobin-2 or zonulin. Chimpanzees and other primates do not have this gene. Interestingly, humans experience 75 different forms of autoimmune disease, while chimps experience none. Dr. Fasano presented compelling evidence, including increased zonulin blood levels, that this mechanism of intestinal leakiness underlies multiple inflammatory and autoimmune conditions, such as rheumatoid arthritis, autoimmune hemolytic anemia, Crohn’s disease, celiac disease, and type 1 diabetes.
Dr. Fasano was reluctant to declare that, based on his findings, bowel leakiness induced by wheat gliadin was sufficient reason to banish all wheat from the human diet, as he is a very careful scientist who feels he has to further explore this avenue and chart out all the details before making such a bold pronouncement. But I have no such qualms. And, besides, the potential for bowel leakiness is only one among many reasons to lose the wheat.
Lose the wheat, lose the zonulin-triggered bowel leakiness that can lead to the myriad forms of autoimmune and inflammatory diseases.
Learn more at http://www.wheatbellyblog.com/