Someone, Dr.Elena Verdu wondered if gluten might contribute to IBS and she did a study. She's discovering what others have discovered, that there is an entity, "non-celiac gluten sensitivity" where people who don't fit the diagnosis of celiac, get better on a gluten-free diet. I know it's real. It has a higher rate of morbidity and mortality, compared to the general population, according to Ludvigsson. He says:"Patients with mild inflammation and gluten sensitivity have a higher risk of death, even if their symptoms are not severe enough to warrant a diagnosis of full-blown celiac disease."
As for the notion that non-celiac gluten sensitivity is milder than celiac disease, Anderson et al, in their study titled “Malignancy and mortality in a population-based cohort of patients with coeliac disease or ‘gluten sensitivity’ World J Gastroenterol 2007 January 7; 13(1): 146-151, report a higher rate of malignancy and early mortality among those with non-celiac gluten sensitivity than among those with celiac disease. This finding may be the result of the common recommendation that patients ignore test results that show non-celiac gluten sensitivity, as many physicians believe that such results are “non-specific” and do not warrant a gluten free diet
Let's hope there are more studies to help us sort things out. This study is reported by Diana Gitig PhD at Celiac.com 05/18/2011
“Irritable bowel Syndrome (IBS) is based on a clinical description only; there are no pathophysiological pathways definitively associated with it. It is characterized as gastrointestinal symptoms with no discernable cause. A diagnosis of IBS depends on recurrent abdominal pain or discomfort for at least three days per month in the last three months, with the onset of the discomfort either associated with a change in frequency or appearance of stool or alleviated by defecation. A number of different mechanisms have been suggested as potential causes of IBS. These range from psychological origins, to increased visceral hyperalgesia (sensitivity to pain), to the low grade gut inflammation and altered gastrointestinal permeability and motility observed in IBS patients. Complicating matters is that most patients exhibit only a subset of symptoms. Since gluten has been demonstrated to negatively affect even people without celiac disease by an unknown mechanism (see Study Shows Gluten Intolerance Without Celiac Disease), and the underlying causes of IBS remain unclear, Dr. Elena Verdu wondered if gluten might contribute to IBS.
Like those with IBS, patients with gluten sensitivity lack the antibodies against tissue transglutaminase that are the hallmark of celiac disease but nonetheless suffer immune mediated inflammation in their gut. Interestingly, when IBS patients without celiac eliminated gluten from their diet, 68% of them reported more severe pain, bloating, and tiredness upon gluten rechallenge. But how? By what mechanism? No changes were detected in intestinal permeability or fecal lactoferrin, a marker of intestinal inflammation. However, it is possible that these phenomena persisted, just at below the level of detection.
Based on these data, and other evidence that is rapidly accruing suggesting that gluten can negatively affect those without celiac disease, Dr. Verdu suggests that IBS patients might be screened for anti-gliadin antibodies even if they lack antibodies against tissue transglutaminase. These nonspecific antibodies can indicate an immunological response to gluten, and thus their presence could used to determine if their symptoms might be alleviated by adherence to a gluten free diet. She makes sure to point out, though, that this is probably not the case for all IBS patients.
Read the abstract here Am J Gastroenterol 2011; 106:516–518
Intestinal Permeability
The trigger for so many diseases caused by gluten sensitivity appear to come from "intestinal permeability" which is found at the microscopic level. With or without villous damage. Here is a schematic representation of "intestinal permeability" and look at the bottom and see the influence on the immune system especially Th2CD4 and it's effects on Mast cells and ultimately the brain.