Celiac.com 03/09/2010 - Celiac disease is a vastly growing epidemic. Those suffering from celiac have varying levels of difficulty digesting wheat, rye and barley; as celiac primarily affects the small bowel and is considered to be an autoimmune intestinal disorder. However, compounding new evidence sited in the March 2010 edition of the The Lancet Neurology, suggests that celiac disease also affects the nervous system, indicating a wider systemic disorder than previously thought.
Thanks to modern science and years of testing, many neurological disorders are now being directly associated with gluten intolerance. The most common associations have been demonstrated to be, cerebellar ataxia and peripheral neuropathy. Although gluten has also been shown to impact drug resistant epilepsy, multiple sclerosis, dementia, and stiff-man syndrome among others. To accurately determine the effects gluten has on neurological health, testing by Hadjivassiliou and colleagues was done in three areas: serology, genetics, and clinical response to gluten withdrawal.
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As far as serological tests are concerned, IgG antibodies to gliadin (AGA) have long been considered the most accurate indicators of neurological gluten sensitivity. However, researchers are now finding that IgG AGA is no longer a relevant test for gluten sensitivity, and it is now being replaced with more dependable tests. In fact, researchers recently became aware of IgG DGP AGA as an nearly absolute marker for the connection between gluten sensitivity and celiac disease. Initial data also indicates that TG6 are markers for gluten sensitivity, while TG3 appears to be markers for dermatitis herpetiformis. Additionally, IgA antibodies to TG2, if they are detectable in the intestine, have also been shown to effectively connect neurological disease with gluten intolerance.
Genetics is another important correlation between gluten intolerance and neurological disorders. Clinically speaking, the recognition of HLA DQ2 combined with a positive serology, increases the probability that gluten plays a roll in the manifestation of neurological pathogenesis.
Evaluating gluten withdrawal is crucial when establishing the gluten/neurological abnormalities connection. The link has been clearly noted in patients newly diagnosed with cerebellar ataxia or peripheral neuropathy. After establishing a gluten-free diet, the patients showed considerable improvement of their neurological symptoms. However, patients that had neurological symptoms lasting longer than 12 months, did not typically show signs of neurological improvement once a gluten-free diet was initiated. The reason for this is thought to be a result of irreversible neural cell damage, such as a loss of Purkinje cells accompanied by prominent T-lymphocyte, as seen in patients with ataxia.
While the findings of these studies indicated that gluten is a major factor associated with neurological disorders, further studies are needed to show conclusive evidence of the direct correlation between the two. Such findings may provide the key to determining if autoimmunity is fundamental in evoking gluten-sensitive neurological impairment.
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