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An excerpt from:

Cereal Grains: Humanity's Double Edged Sword
Loren Cordain; World Review of Nutrition & Dietetics, 1999;84:19-73


There is increasing recognition that molecular mimicry is a highly likely mechanism underlying the development of multiple sclerosis (305,306). A number of viral and bacterial proteins have been shown to cross react with myelin basic protein (MBP) (305), one of the suspected target antigens in multiple sclerosis (MS). Because the blood brain barrier limits access to the CNS to activated T cells, invasion of the CNS requires auto-reactive T cells to be stimulated in the peripheral immune system. Therefore, it is possible that dietary antigens causing persistent T cell stimulation, and bearing similar amino acid homologies to the various myelin and non-myelin target antigens, could cause polyclonal expansion of autoreactive T cells in the peripheracy, in a manner similar to that observed for bacterial and viral antigens. Although no homologous amino acid sequences have yet been identified between dietary antigens and suspected autoantigens in MS patients, there are epidemiological reports which link both wheat (307) and milk (308) consumption to the incidence of multiple sclerosis, consistent with the observations that MS is positively correlated to latitude (309). There are a number of case reports showing remission of MS on gluten free diets (310,311,312). Further some MS patients have altered intestinal mucosa (313,314), suggestive of increased intestinal permeability to dietary antigens. However, MS patients generally do not show increased antibodies to gliadin (315), and a number of case studies have not shown beneficial effects of gluten free diets (316,317). If dietary antigens containing amino acid sequences similar to putative self antigens, indeed, do stimulate peripheral T cells, then interventions evaluating the influence of diet upon MS would need to consider the potential confounding influence of multiple dietary antigens (dairy products, grains, legumes, and yeast) capable of either molecular mimicry and/or T cell stimulation.

Psychological and Neurological Illnesses Associated with Cereal Grain Consumption Neurological complications have long been recognized in celiac patients and can include epilepsy, cerebellar ataxias, dementia, degenerative central nervous system disease, peripheral neuropathies (of axonal or demyelinating type), and myopathies (318). A recent study showed that 57% of patients with neuropathies of unknown cause (25 ataxia, 20 peripheral neuropathy, 5 mononeuritis multiplex, 4 myopathy, 3 motor myopathy, 2 myelopathy) demonstrated positive titres for antigliadin antibodies, and 16% (40 times higher than the general population) of this group also had celiac disease (315). The cause of neurological dysfunction associated with celiac disease and antigliadin antibodies is unknown, however it has been suspected that an immunological mechanism may be involved (315,318). Although no clinical trials have yet been conducted of strict adherence to a gluten free diet, it has been suggested that such a diet may result in stabilization or even improvement of neurological dysfunction (315).


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