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Arthritis – Rheumatoid

Rheumatoid Arthritis and the Gut: An Inflammatory Connection

Rheumatoid Arthritis patients display a greater propensity for food allergies and sensitivities, a link that evidence indicates may be more than coincidental (Hvatum 2006). In fact, studies suggest that reactions originating in the gut may fuel systemic inflammatory fires, thereby exacerbating RA symptoms. Support for this theory appeared in the peer-reviewed literature as early as the late 1940's (Zeller 1949).

Immunologic reactions to components of certain foods in many ways resemble the self-reactivity seen in RA and other autoimmune diseases; that is, the immune system mistakenly attacks non-pathogenic molecules. Therefore, it may be possible to calm the immune system by eliminating unnecessary molecular triggers found in certain foods. Studies have shown that RA patients produce significantly more intestinal antibodies against various foods than healthy controls (Hvatum 2006). In a 12-week clinical trial, adherence to an allergen-restricted or allergen-free diet corresponded with symptomatic improvement for a small number of subjects (van de Laar 1992). When allergens were reintroduced into their diets, symptoms reemerged. Vegetarian, vegan, and gluten-free diets have been linked to symptomatic relief in RA patients (Muller 2001; Hafstrom 2001). Interestingly, a recent review of genome-wide association studies revealed that people with celiac disease (characterized by gluten sensitivity) and those with RA shared genetic similarities (Zhernakova 2011).

Based on the connection between food and rheumatism, avoiding foods that result in elevated IgG antibodies in the blood may be an underappreciated method of relieving RA symptoms. Low-cost IgG blood testing allows RA patients to pinpoint potentially problematic foods and begin eating a diet that best suits their immunological profile.

Oral Tolerance and Undenatured Type-II Collagen

Immune system T-cells are tasked with recognizing and distinguishing between "self" and "foreign" molecules. They do this by responding to very specific molecular shapes and 3-dimensional structures (Bagchi 2002). If T-cells in the blood are simply exposed without any "training" to a previously unrecognized protein structure (such as those found in joint collagen), they react violently and trigger a massive inflammatory response to destroy the protein (Cremer 1998).

When scientists want to create an animal model of arthritis they inject collagen into their subjects, thereby sensitizing the T-cells in their blood to the collagen protein (Corthay 1998). Those circulating T-cells initiate inflammation in the animal's joints, which are rich in collagen.

With adequate preparation, T-cells can be "trained" to differentiate between friend and foe. One place this training happens is in the intestinal tract; specifically, the lower end of the small intestine, which is rich in collections of immune tissue called Peyer's patches. Peyer's patches contain T-cells, which become exposed to all sorts of molecular shapes that are natural components of the food we eat (Meyer 2000). In that fashion, we desensitize our immune systems and develop a natural tolerance to new foods without having constant allergic or inflammatory reactions.

By providing the correct 3-dimensional collagen to the digestive tract, we can "educate" our T-cells to ignore collagen when they encounter it in joints (Park 2009; Bagchi 2002). This phenomenon is dubbed oral tolerance to collagen.

Upon induction, oral tolerance to collagen suppresses joint inflammation, as has been demonstrated in numerous laboratory studies (Park 2009; Zhu 2007; Nagler-Anderson 1986). Oral administration of soluble type II collagen has even prevented experimentally induced arthritis by way of collagen injections (Min 2006; Nagler-Anderson 1986).

But not just any collagen will do. Typical commercial processing causes collagen to become denatured, uncoiling from its normal helical shape and losing its functional 3-dimensional structure. Denatured collagen has no beneficial effects on joint inflammation (Nagler-Anderson 1986).

A more natural form of collagen called undenatured type II collagen (UC-II®) has recently been developed (Zhao 2011). UC-II® retains its original 3-dimensional molecular structure, keeping it recognizable by T-cells in Peyer's patches. UC-II® is robust enough to survive the harsh conditions in the stomach and small intestine, arriving at Peyer's patches with its molecular structure intact (Bagchi 2002).

As mentioned previously, collagen exposure subsequent to joint deterioration is a key mechanism by which the immune system is driven to destroy joint tissue in arthritis. Therefore, retraining the immune system through induction of oral tolerance may be an effective means of easing the inflammatory rheumatic process.