Gluten and wheat sensitivity have become much more prevalent in the general population.

There is no definitive lab test for food sensitivities, as they differ from true allergies. True food allergies are an immediate response mediated by the immunoglobulin, IgE; whereas, food sensitivities are delayed reactions that occur as a result of a different set of immunoglobulins, IgG, IgM, and IgA. In my clinic, I recommend a celiac profile for every patient, as even slightly elevated serum levels can provide clues for a sensitivity reaction and provide a baseline measure.

According to the Annals of Allergy and Immunology:

Antigliadin and antiendomysial (transglutaminase) anti-bodies have been studied extensively in gluten-sensitiveenteropathy. The presence of antigliadin antibodies strongly suggests that gluten-sensitive enteropathy is due, in part, to a dietary element. Both serum and secretory levels of IgA are increased, whereas IgG levels are only minimally elevated and the IgM level is often decreased.

Sayer Ji’s article, “Opening Pandora’s Box: The Clinical Role of Wheat in Human Disease,” is a wonderful read that links the concept of food leptins (made popular by the Blood Type Diet) with nutriogenomics (food as information to your body which modifies gene expression). Due to wheat’s protective outer coating, it is very hard to digest in the body. The lectin in wheat (WGA) can cause damage to various tissues in the body, initiating inflammation and leading to diseases that extend outside the gastrointestinal tract.

the time has come to draw attention to the powerful little chemical in wheat known as ‘wheat germ agglutinin’ (WGA) which is largely responsible for many of wheat’s pervasive, and difficult to diagnose, ill effects. Not only does WGA throw a monkey wrench into our assumptions about the primary causes of wheat intolerance, but due to the fact that WGA is found in highest concentrations in “whole wheat,” including its supposedly superior sprouted form, it also pulls the rug out from under one of the health food industry’s favorite poster children.

What is unique about the WGA glycoprotein is that it can do direct damage to the majority of tissues in the human body without requiring a specific set of genetic susceptibilities and/or immune-mediated articulations. This may explain why chronic inflammatory and degenerative conditions are endemic to wheat-consuming populations even when overt allergies or intolerances to wheat gluten appear exceedingly rare. The future fate of wheat consumption, and by implication our health, may depend largely on whether or not the toxic qualities of WGA come to light in the general population.

Furthermore, WGA has opioid like properties which make it not only non-nutritive (for most of us who are sensitive), but also addictive.

These pharmacologically active, opiate-like proteins in gluten are known as gluten exorphins (A5, B4, B5, C) and gliadorphins. They may effectively anesthetize us, in the short term, to the long term, adverse effects of WGA. Gluten also contains exceptionally high levels of the excitotoxic l-aspartic and l-glutamic amino acids, which can also be highly addictive, not unlike their synthetic shadow molecules aspartame and monosodium glutamate.

This effect on your brain chemistry explains why I have actually had clients yell at me for suggesting a gluten free diet. For most, it’s simply an initial hesitancy and a look of panic in their eyes.  As explained, this is because gluten and wheat not only affect your brain, but also the brain-gut connection.

As you’ll recall in past articles,  your gastrointestinal tract has its own nervous system, called the enteric nervous system.  This gut nervous system holds up to 70% of your serotonin and contains more neurotransmitters than the brain!  Therefore,  withdrawal from food sensitivities can not only be a hard habit to break, but painful for a lot of people. Furthermore, it’s true that what you are craving is usually most intense for what you are sensitive to.

In this way, food sensitivities cause intense cravings as our bodies run the roller coaster ride of hypo and hyperglycemia, associated with insulin resistance, increased inflammation, and the malabsorption of intestinal permeability. This is similar to an addict who continually medicates him or herself to reach an artificial high point after they have experienced a low.

Aristo Vojdani, Ph.D., M.Sc., M.T, famous immunology researcher describes how permeability, or “leaky gut” plays a big role in  systemic and chronic diseases through the following pathway:

Mucosal immune abnormalities–>
Imbalanced gut flora (big players in your immune system) –>
Induction of intestinal barrier dysfunction–>
Release of inflammatory mediators into circulation –>
Enhanced systemic inflammation and damage to tissues –>
Open Blood Brain Barrier resulting in neuroinflammation–>
Causing neuro invasion & neurodegeneration
This is not just a theory, according to the Academy of Science, wheat enteropathy can be linked to chronic disease, specifically multiple sclerosis.
We determined the level of serum immunoglobulin A and immunoglobulin G antigliadin and antitissue transglutaminase antibodies in 98 patients with multiple sclerosis. We found a highly significant increase in titers of immunoglobulin G antibodies against gliadin and tissue transglutaminase in the multiple sclerosis patients. Seven patients had a positive IgG AGA, whereas only 2 controls presented positive titers (P = 0.03). Four patients had positive IgG anti-tTG while all the controls tested negative (P = 0.02).

Therefore, wheat sensitivity can effect you beyond your gastrointestinal tract. Most of my clients get confused and believe that because they don’t have digestive symptoms, wheat is not an issue. However, the systemic effect of chronic inflammation and irritation of eating a food that overloads your immune system on a consistent basis can cause a variety of symptoms that aren’t just digestive related. Many studies are now indicating that rheumatid arthritis and other autoimmune disorders can be linked to leaky gut and chronic irritation to the muscosa.

Does this mean that most are doomed to never eating out again and enjoying their mom’s homemade wheat pasta? I feel that if the body is healthy, moderation is the key. In providing a tailored and individualized nutritional support protocol for each patient, I feel that catching a gltuen sensitivity early can prevent future damage and even celiac disease down the road. I also have a little nutritional trip and digestive support aid up my sleeve for those times when the birthday cake is too inviting and deprivation effects kick in.

Still, I have found that most people tend to stay gluten free, because they “just feel better and have more energy.” Some even report, “I don’t like the taste anymore and what it does to my body.” What a gift! To get back in tune with the body and follow how you feel. Healing and getting to the root of the issue vs. fixing and curing- a Naturopathic dream patient!

FYI- What’s the Difference between celiac disease manifestations and gluten sensitivity? How much immune response is initiated by the host:

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 locus for triggering an adaptive immune response, higher levels of immune mediators or receptors, or perhaps greater permeability in the celiac intestine. It is 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. Other factors such as exposure to NSAIDs like naproxen or aspirin 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 greater or lesser degrees of susceptibility to gliadin’s intrinsically toxic effect should be a secondary to the fact that it is has been demonstrated to be toxic to both non-celiacs and celiacs.

References:

Decreased levels of heat shock proteins in gut epithelial cells after exposure to plant lectins.Gut. 2000 May;46(5):679-87.PMID: 10764712

Syer Ji. Opening Pandora’s BreadBox. GreenMedInfo.com

NEJM. Celiac Disease: The Villian Unmasked? 348:2573, June 19, 2003 Clinical Implications of Basic Research

Gut-Brain Connection:
Ducrotte’,P. [Irritable bowel syndrome: from the gut to the brain-gut] Gastroenterol Clin Biol. 2009 Aug-Sep;33(8-9):703-12. PMID: 19682813
Iwan M. et al. Transport of micro-opioid receptor agonists and antagonist peptides across Caco-2 monolayer. Peptides. 2008 Jun;29(6):1042-7. Epub 2008 Feb 6. PMID: 18355944
Maes M, Kubera M, Leunis JC. The gut-brain barrier in major depression: intestinal mucosal dysfunction with an increased translocation of LPS from gram negative enterobacteria (leaky gut) plays a role in the inflammatory pathophysiology of depression. Neuro Endocrinol Lett. 2008 Feb;29(1):117-24. PMID: 18283240
Inflammation & Mood Disorders: Aristo Vojdani, Ph.D., M.Sc., M.T. The Mucosal Barrier Function Test. Functional Medicine teleseminar experts 2009 (Sept) Sponsor: BioHealth Diagnostic.
Gareau MG, Silva MA, Perdue MH. Pathophysiological mechanisms of stress-induced intestinal damage. Curr Mol Med. 2008 Jun;8(4):274-81. PMID: 18537635
AAAAI. Food Allergies. Practice Parameters. Accessed January 2010.

Gluten Sensitivity in MS: experimental myth or clinical truth? Ann N Y Acad Sci. 2009 Sep;1173:343-9.