WHEAT--- The myth that you need to have ‘bad genes’ to experience intestinal damage from consuming wheat was disproved years ago. It is a common myth that wheat only causes immune-mediated intestinal damage within those with a rare genetically based aberration called celiac disease. Still relatively unknown research from 2007 clearly demonstrated that everyone’s body likely experiences adverse intestinal effects from gluten (gliadin) exposure. As far as celiac disease, the specific mechanisms by which wheat causes damage are well-known, and they go like this… In celiac disease, an alcohol-soluble wheat storage protein known as gliadin is partially degraded (i.e. deamidated) by the enzyme tissue transglutaminase, the effect of which is to activate susceptible host T-cells to mistakenly identify and attack intestinal villi as if they were ‘foreign’ invaders. This highly destructive autoimmune process can be verified through blood tests, or through the so-called “gold standard” of an intestinal biopsy that clearly reveals destroyed villi and/or flattened intestinal surfaces, the hallmark pathology of celiac disease. The reality, however, is that one does not need to be celiac, or have a particular genetic mutation, in order to experience damage associated with exposure to wheat gliadin. In a study published in the journal GUT in 2007, a group of researchers asked the question: “Is gliadin really safe for non-celiac individuals?“ In order to test their hypothesis that an innate immune response to gliadin is common in both patients with celiac disease and without celiac disease, intestinal biopsy cultures were taken from both groups and challenged with crude gliadin, the gliadin synthetic 19-mer (19 amino acid long gliadin peptide) and 33-mer deamidated peptides. Results showed that all patients with or without celiac disease, when challenged with the various forms of gliadin, produced an interleukin-15-mediated response. The researchers concluded: “The data obtained in this pilot study supports the hypothesis that gluten elicits its harmful effect, throughout an IL15 innate immune response, on all individuals [my italics].” The primary difference between the two groups is that the celiac disease patients experienced both an innate and an adaptive immune response to the gliadin, whereas the non-celiacs experienced only the innate response. The researchers hypothesized that the difference between the two groups may be attributable to greater genetic susceptibility at the HLA-DQ gene locus (on chromosome 6) for triggering an adaptive immune response, higher levels of immune mediators or receptors, or perhaps greater permeability in the celiac intestine. It is also possible that over and above the possibility of greater genetic susceptibility, most of the differences are from epigenetic factors that are influenced by the presence or absence of certain nutrients in the diet, bacterial strains within the gut flora, and environmental exposures, which include NSAID drugs like naproxen or aspirin which can profoundly increase intestinal permeability in the non-celiac, rendering them susceptible to gliadin’s potential for activating secondary adaptive immune responses. This may explain why, in up to 5% of all cases of classically defined celiac disease, the typical HLA-DQ haplotypes are not found. However, determining the factors associated with greater or lesser degrees of susceptibility to gliadin’s intrinsically toxic effect should be secondary to the fact that it has been demonstrated to be toxic to both non-celiacs and celiacs.1 In other words, rather than look up the adverse gut responses associated with wheat, and particularly, wheat gliadin, as being a rare genetically-based aberration, we may want to reconsider the common, culturally reinforced view that wheat is an intrinsically healthy food that only an ‘abnormal’ subset of the human population has an ‘unhealthy’ response to. To the contrary, perhaps the immunoreactive effects that wheat gliadin induces indicates that we have a human species-specific intolerance to this ‘food,’ and that rather than look at these adverse effects as being ‘unhealthy reactions to a healthy food,’ perhaps we should look at them as ‘healthy reactions to an intrinsically unhealthy (or metabolically incompatible) food.’ Ultimately, intestinal damage is only the tip of the so-called “celiac” or “non-celiac gluten sensitivity” icebergs. GreenMedInfo.com has indexed research from the National Library of Medicine on over 300 adverse health effects associated with wheat and/or wheat components. You can view the first-hand research here: http://www.greenmedinfo.com/toxic-ingredient/wheat Also, learn more about wheat’s adverse effects to gastrointestinal health by reading our recent article:Wheat As A Common Cause of Dyspepsia and IBS, and a broader perspective on the dangers of wheat in our essay ‘The Dark Side of Wheat.’

The myth that you need to have ‘bad genes’ to experience intestinal damage from consuming wheat was disproved years ago.

It is a common myth that wheat only causes immune-mediated intestinal damage within those with a rare genetically based aberration called celiac disease. Still relatively unknown research from 2007 clearly demonstrated that everyone’s body likely experiences adverse intestinal effects from gluten (gliadin) exposure.

As far as celiac disease, the specific mechanisms by which wheat causes damage are well-known, and they go like this…

In celiac disease, an alcohol-soluble wheat storage protein known as gliadin is partially degraded (i.e. deamidated) by the enzyme tissue transglutaminase, the effect of which is to activate susceptible host T-cells to mistakenly identify and attack intestinal villi as if they were ‘foreign’ invaders.  This highly destructive autoimmune process can be verified through blood tests, or through the so-called “gold standard” of an intestinal biopsy that clearly reveals destroyed villi and/or flattened intestinal surfaces, the hallmark pathology of celiac disease.

The reality, however, is that one does not need to be celiac, or have a particular genetic mutation, in order to experience damage associated with exposure to wheat gliadin.

In a study published in the journal GUT in 2007, a group of researchers asked the question: “Is gliadin really safe for non-celiac individuals?“  In order to test their hypothesis that an innate immune response to gliadin is common in both patients with celiac disease and without celiac disease, intestinal biopsy cultures were taken from both groups and challenged with crude gliadin, the gliadin synthetic 19-mer (19 amino acid long gliadin peptide) and 33-mer deamidated peptides.

Results showed that all patients with or without celiac disease, when challenged with the various forms of gliadin, produced an interleukin-15-mediated response. The researchers concluded:

“The data obtained in this pilot study supports the hypothesis that gluten elicits its harmful effect, throughout an IL15 innate immune response, on all individuals [my italics].”

The primary difference between the two groups is that the celiac disease patients experienced both an innate and an adaptive immune response to the gliadin, whereas the non-celiacs experienced only the innate response.

The researchers hypothesized that the difference between the two groups may be attributable to greater genetic susceptibility at the HLA-DQ gene locus (on chromosome 6) for triggering an adaptive immune response, higher levels of immune mediators or receptors, or perhaps greater permeability in the celiac intestine.

It is also possible that over and above the possibility of greater genetic susceptibility, most of the differences are from epigenetic factors that are influenced by the presence or absence of certain nutrients in the diet, bacterial strains within the gut flora, and environmental exposures, which include NSAID drugs like naproxen or aspirin which can profoundly increase intestinal permeability in the non-celiac, rendering them susceptible to gliadin’s potential for activating secondary adaptive immune responses.

This may explain why, in up to 5% of all cases of classically defined celiac disease, the typical HLA-DQ haplotypes are not found. However, determining the factors associated with greater or lesser degrees of susceptibility to gliadin’s intrinsically toxic effect should be secondary to the fact that it has been demonstrated to be toxic to both non-celiacs and celiacs.¹

In other words, rather than look up the adverse gut responses associated with wheat, and particularly, wheat gliadin, as being a rare genetically-based aberration, we may want to reconsider the common, culturally reinforced view that wheat is an intrinsically healthy food that only an ‘abnormal’ subset of the human population has an ‘unhealthy’ response to. To the contrary, perhaps the immunoreactive effects that wheat gliadin induces indicates that we have a human species-specific intolerance to this ‘food,’ and that rather than look at these adverse effects as being ‘unhealthy reactions to a healthy food,’ perhaps we should look at them as ‘healthy reactions to an intrinsically unhealthy (or metabolically incompatible) food.’

Ultimately, intestinal damage is only the tip of the so-called “celiac” or “non-celiac gluten sensitivity” icebergs. GreenMedInfo.com has indexed research from the National Library of Medicine on over 300 adverse health effects associated with wheat and/or wheat components. You can view the first-hand research here: http://www.greenmedinfo.com/toxic-ingredient/wheat

Also, learn more about wheat’s adverse effects to gastrointestinal health by reading our recent article:Wheat As A Common Cause of Dyspepsia and IBS, and a broader perspective on the dangers of wheat in our essay ‘The Dark Side of Wheat.’