George Jelinek gives a good insight in this coeliac discussion:
Quote:
There is a number of researchers who contend that, in an evolutionary sense, legumes, and gluten in cereals, are relatively recent additions to the human diet. These protein-rich foods may be implicated in a host of auto-immune diseases including MS. The most severe form of gluten intolerance is coeliac disease. Here, people develop serious digestive system disorders due to an immune response to the gluten in wheat. One might expect, if gluten was a key ingredient in the diet to avoid in MS that people with MS might have a higher than usual incidence of coeliac disease, or vice versa, that people with coeliac disease might have a higher than expected incidence of MS. A major population study published in mid-2007 examined 14 000 people in Sweden with coeliac disease and compared them with 70 000 other people without the disease acting as controls.1 One would have expected a higher rate of MS (or other CNS degenerative disease) in those people with coeliac disease than controls if gluten was involved in causing these diseases. In fact the researchers found no statistically significant association between coeliac disease and subsequent multiple sclerosis, Parkinson's disease, Alzheimer's disease, hereditary ataxia, the symptom ataxia, Huntington's disease, myasthenia gravis or spinal muscular atrophy. This is very strong evidence that there is no link with gluten.
If there was indeed a link, one should at least expect to find in people with MS antibodies to gluten which indicate intolerance. In fact, Italian researchers looking at 95 patients with MS found not a single patient with elevated antibody levels.2 UK researchers tested 49 patients with MS for their antibody levels and found 12% had raised levels; however this compared with 13% of unselected blood donors, so it was unlikely that people with MS had any special sensitivity to gluten.3 Iranian researchers tested 166 people with MS for antibodies and compared them to people without MS.4 They found no difference in antibody levels.
Italian researchers used an alternative approach to investigate this problem. They fed a gluten-free diet to animals with the experimental form of MS, EAE. The animals on the gluten-free diet initially had a more severe disease course.5 Later, they seemed to be doing better than those animals eating gluten. The study in my view provided an indeterminate result.
The molecular mimickry theory of MS causation is perfectly valid, and probably explains why cow's milk protein for example sets off the chain of events leading to myelin attack by the immune system. We now have good evidence from the laboratory that a segment of cow's milk protein is identical to a segment of myelin oligodendrocyte glycoprotein. The immune system, in setting up defence against this foreign protein, is 'tricked' into also attacking this part of myelin. Whenever something like this is proposed as an explanation for the immune attack on myelin, it is important to validate it against what we actually see in human populations.
For cow's milk, this is easy. The world map of MS distribution is almost exactly the same as the world map of cow's milk consumption. That is, there is almost a direct correlation epidemiologically between cow's milk consumption and MS incidence. This is a kind of 'cross check' if you like, that the theory is correct. As a result, I strongly advise people to avoid cow's milk.
For gluten for example (or tomato for that matter), there are several major problems with the theory. Firstly, there is no clear biochemical similarity between part of the gluten compound and myelin as far as I am aware. Secondly, when we run the epidemiological cross-check, populations that consume wheat do not appear to have a higher incidence than other populations. A further cross-check is to see whether people who do develop auto-immunity to wheat (those with coeliac disease) also get auto-immunity to myelin; the data show that there is not a higher incidence of coeliac disease in those with MS or vice versa. And finally, the animal data don't support a link either.
So I advise people that gluten should be relatively safe. It is important to try to base these recommendations on evidence, not just theory, and I feel comfortable that the evidence does not support a link with gluten sufficiently to make a recommendation to avoid it. Overall, the evidence of any effect of gluten in MS is not convincing enough to warrant changing my own diet to exclude wheat products.
References
1. Ludvigsson JF, Olsson T, Ekbom A, et al. A population-based study of coeliac disease, neurodegenerative and neuroinflammatory diseases. Aliment Pharmacol Ther 2007; 25:1317-1327
2. Salvatore S, Finazzi S, Ghezzi A, et al. Multiple sclerosis and celiac disease: is there an increased risk? Mult Scler 2004; 10:711-712
3. Pengiran Tengah CD, Lock RJ, Unsworth DJ, et al. Multiple sclerosis and occult gluten sensitivity. Neurology 2004; 62:2326-2327
4. Borhani Haghighi A, Ansari N, Mokhtari M, et al. Multiple sclerosis and gluten sensitivity. Clin Neurol Neurosurg 2007
5. Di Marco R, Mangano K, Quattrocchi C, et al. Exacerbation of protracted-relapsing experimental allergic encephalomyelitis in DA rats by gluten- free diet. Apmis 2004; 112:651-655