Gluten sensitivity, like most conditions, (including MS), can be mild (slight bloating) to severe, (Coeliac disease).
In my case, it causes terrible fatigue and makes my nerve pain go nuclear.
I’ve been gluten-free (I do cheat at times) since 2006, after a challenge here by the lovely Lollipop, to try diet for a while.
I was at rock-bottom after a 9 month relapse and went a bit far, actually eating a raw food diet for 6 months, but it really did help. I got very tired of this difficult diet in the end and now, I’m gluten-free. (I have to eat low-carb as well, but that’s another story).
Not everyone responds to cutting gluten from their diet.
Some do well on Swank, or Professor Jelink’s diet, some on Best Bet Diet and there are other diets, all of which will work for someone, somewhere.
It’s worth a try, but only if you feel you really want to, or else you’ll hate your new diet and cheat wherever possible.
The way that MS manifests itself is so different from person to person, makes it very frustrating to deal with. Very.
The Lancet Neurology, Volume 9, Issue 7, Pages 653 - 654, July 2010
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doi:10.1016/S1474-4422(10)70149-6Cite or Link Using DOI
Gluten sensitivity and the CNS: diagnosis and treatment
In their Personal View, Hadjivassiliou and colleagues1 indicate that some cases of gluten sensitivity are associated with white matter lesions in the brain and the spinal cord, and that these lesions are indistinguishable from those seen in patients with multiple sclerosis.
We would like to speculate whether, in a patient with multiple sclerosis and coeliac disease, treatment of one condition could lead to an improvement in the other disorder.
We have described a case report2 of a 29-year-old woman with relapsing-remitting multiple sclerosis. After treatment with interferon beta for 1 year, she had another relapse that was, for the first time, associated with gastrointestinal symptoms (diarrhoea and abdominal pain) and weight loss. The patient was diagnosed with coeliac disease (as proven by duodenal biopsy samples). Interferon beta was stopped and a gluten-free diet was started as a single treatment. She has followed this diet for the past 7 years and has been in good health during that time without any further relapses. Since the first year of being on a gluten-free diet, concentrations of anti-transglutaminase IgA antibodies have returned to normal. In 2004, after 2 years of being on this diet, gastrointestinal endoscopy showed normal duodenal mucosa. In 2009, a clear decrease in spinal and brain lesions was confirmed by use of MRI. The patient is now fully asymptomatic and results from neurological assessments are normal.
Although the favourable response of the neurological and gastrointestinal symptoms to the gluten-free diet of this case strongly indicates coeliac disease as the primary cause of the CNS effects, we believe that this patient presented both diseases. Coeliac disease appeared as an associated condition rather than as the main cause of the neurological disorder. Moreover, coeliac disease is often associated with other autoimmune diseases and its association with optical neuromyelitis or multiple sclerosis has been described.3
The complex causes of autoimmune diseases not only present a challenge to the development and testing of new therapies but also offer the potential to identify subgroups of patients who might benefit from particular approaches. Consuming gliadin for several years, starting in infancy, might not only be the cause of activation of coeliac disease but, in some patients, could also be an additional factor to trigger the beginning of other autoimmune diseases. Continued studies of such diseases are needed to help identify the most appropriate strategies for each disorder.4
We have no conflicts of interest.