Could This Popular Pain-Killer Be Causing Celiac Disease?
http://www.greenmedinfo.com/blog/could-popular-pain-killer-be-causing-celiac-disease?page=2
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Saturday, June 28th 2014 at 5:45 pm
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A new study published in the American Journal of Physiology reveals that a popular NSAID drug known as indomethacin may be triggering celiac disease in those who eat gluten-containing foods such as wheat.
Titled, "Gliadin intake alters the small intestinal mucosa in indomethacin-treated HLA-DQ8 transgenic mice," the animal study concluded that the protein gliadin (one of several prolamine proteins in wheat together colloquially known as a 'gluten'), '...in combination with COX inhibition [produced through indomethacin treatment] caused a basal inflammatory status and an oxidative stress condition in the small intestine of DQ8 mice [a celiac disease susceptibility gene], thus triggering the mucosal lesion and, subsequently, an antigen-specific immunity."
Rats with the celiac disease susceptibility gene (DQ8), were treated with both gliadin (a gluten protein) and indomethacin, resulting 10 days later in celiac disease-associated intestinal changes, such as "a significant reduction of villus height, increased crypt depth, increased number of lamina propria activated macrophages and high basal interferon-γ." The pathological intestinal changes (enteropathy) were associated with "high levels of oxidative stress markers, similar to CD."
The researchers found that, "Notably, after a 30-day treatment enteropathic mice developed serum antibodies toward gliadin (IgA) and tTG (IgG). We concluded that gliadin intake in combination with COX inhibition caused a basal inflammatory status and an oxidative stress condition in the small intestine of DQ8 mice, thus triggering the mucosal lesion and, subsequently, an antigen-specific immunity."
The researchers stated their findings, "clearly indicated inhibition of COX-2 activity [with indomethacin] is required to generate the gliadin-driven mucosal lesion in DQ8 mice." In other words, the wheat protein gliadin alone was not capable of inducing celiac disease like lesions in the mice. Co-administration of the COX-2 inhibitor indomethacin was required to generate celiac disease like enteropathy:
"In the present study, we showed that intestinal adaptive immunity toward gliadin was not an essential prerequisite to trigger the mucosal damage in this model. In particular, we found that the simultaneous specific inhibition of COX-2 and gliadin intake were sufficient conditions to generate an even more marked lesion in the small intestine."
If this animal model reflects accurately human physiology, those who take the NSAID drug indomethacin -- and perhaps other pharmaceutical COX-2 inhibitors -- may be increasing their risk for developing intestinal lesions associated with celiac disease.
Discussion
We know that celiac disease prevalence is increasing worldwide at an alarming rate. According to the the Mayo Clinic, "celiac disease is four times more common now than 60 years ago, and affects about one in 100 people." Furthermore, non-celiac gluten sensitivity may afflict everyone, as demonstrated by our research project at Greenmedinfo.com that has identified over 200 health conditions validated in the biomedical literature to be linked to the consumption of wheat, in addition to research that shows that wheat harms the intestines of everyone, regardless of the presence of the classical DQ8/DQ2 celiac disease susceptibility genes.
Stefanie Seneff, MIT researcher, has made a convincing argument for the role of GMO foods contaminated with the herbicide glyphosate contributing to this modern day epidemic. Read her paper, "Glyphosate, pathways to modern diseases II: Celiac sprue and gluten intolerance," to get perspective on the topic. This author has also co-authored an article with Seneff, Jeffrey Smith, Dr. Tom O'Bryan, and Tom Malterre on Roundup herbicide contributing to the explosion of celiac disease epidemics, which can be viewed here.
Glyphosate toxicity likely figures as a primary driver of the increased rates of celiac disease observed over the past few decades, but it is also feasible that the popular use of NSAID drugs contributes to the accelerating epidemic as well, especially considering the manner in which they induce intestinal permeability – which is to say opening up the juncture between enterocytes (intestinal cells) resulting in the infiltration of luminal contents (bacteria and their immunotoxic components such as LPS) and undigested proteins from foods like wheat, which represent over 23,000 different proteins, each one of which is capable of inducing an adverse immune response.
Aspirin, for instance, has been found at low doses to cause small bowel injury consistent with increased intestinal permeability.[1] Ibuprofen has also been found to increase intestinal permeability,[2] while also being linked to cardiovascular disease, responsible for thousands of deaths each year.
Could widespread use of NSAID drugs be fomenting the increased prevalence of celiac disease?
Further research will be needed to know for certain whether or not NSAID drugs are contributing to the significant uptick in celiac disease incidence. For now, the best solution for those who would like to take back control of their health is to incorporate a gluten-free diet, alongside an approach that uses NSAID alternatives to reduce inflammation and pain.
With this in mind, you can deepen your understanding by reading any of the following articles:
For those already suffering from intestinal permeability, Greenmedinfo.com has a research page dedicated to identifying natural substances which heal up intestinal permeability: 50+ Potential Intestinal Permeability Aids.
REFERENCES
[1] Lynne M Howells, Barbara Gallacher-Horley, Catherine E Houghton, Margaret M Manson, E Ann Hudson. Evaluation of small bowel blood flow in healthy subjects receiving low-dose aspirin.World J Gastroenterol. 2011 Jan 14 ;17(2):226-30. PMID: 21245996
[2] T Khazaeinia, F Jamali. Evaluation of gastrointestinal toxicity of ibuprofen using surrogate markers in rats: effect of formulation and route of administration. Clin Exp Rheumatol. 2000 Mar-Apr;18(2):187-92. PMID: 10812490