Multiple Sclerosis and Dietary Intervention

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Below is what I've collected on diet and MS. The real focus should be on getting the gluten and casein out of the diet.


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From the Celiac Perspective

Cook, Gupta, Pertschuk, Nidzgorski "Multiple Sclerosis and Malabsorption" Lancet; June 24, 1978, p. 1366

Fantelli, Mitsumoto & Sebek "Multiple Sclerosis and Malabsorption" Lancet May 13, 1978 p. 1039-1040

Davison, Humphrey, Livesedge et al. "Multiple Sclerosis Research" Elsevier Scientific Publishing New York, 1975

It is curious that the connection between malabsorption and MS stopped at about the same time that prednisone and other such steroids became the treatment of choice for MS. As is known, prednisone incites the re-growth of the villi despite the ingestion of gluten, in the celiac gut. Investigators who did endoscopies on MS patients admit that they have not asked about the patients' use of such drugs.

Drs. Cooke & Holmes in Coeliac Disease 1984; Churchill Livingstone, NY say that 10% of celiacs have neuropathic symptoms. Many appear to be associated with demyelination. Fineli et. al. echo that figure in "Adult celiac disease presenting as cerebellar syndrome" Neurology 1980; 30: 245-249.

Cooke & Holmes come right out and express some of their frustration with neurologists for ignoring the potiential for neuropathic celiac.

In this article:

Beversdorf D, Moses P, Reeves A, Dunn J "A man with weight loss, ataxia, and confusion for 3 months" Lancet 1996 Feb 17;347(8999):446

They discuss the neurological manifestations of adult celiac disease which include cerebellar ataxia, sensory neuropathy, myopathy, hyporeflexis, and seizures. These symptoms resemble those of Vitamin E deficiency. Patients with abetalipoproteinaenemia, who lack the lipoproteins necessary to carry fat-soluble vitamins, have similar symptoms. These patients respond to water-miscible Vitamin E supplementation.

In this article:

Cooke WT, Neurologic manifestations of malabsorption. In Handbook of clinical neurology, volume 28 (metabolic deficiency diseases of the nervous system, part II), Amsterdam; North Holland Publishing Company, 1976; 225-41.

They discuss the many neurological manifestations that are associated with coeliac disease, including ataxia, peripheral neuropathy, myelopathy, myopathy, and dementia.

A new school has emerged, on the heels of the following report:

Hadjivassiliou, et. al. "Does cryptic gluten sensitivity play a part in neurological illness?" Lancet 1996; 347: 369-371

They found that 57 percent of those with neurological problems of unknown cause also had antibodies to gliadin, which is a component of gluten. Sixteen percent of them had coeliac disease, a much higher level than normally found. Most of the patients with the anti-gliadin antibodies did not have other symptoms of coeliac disease such as poor absorption of vitamins.

Hadjivassilou et. al. "Clinical, radiological, neurophysiological, and neuropathological characteristics of gluten ataxia" The Lancet 1998; 352: 1582-1585.

The abstract summary reads, "Gluten sensitivity is an important cause of apparently idiopathic ataxia and may be progressive. The ataxia is a result of immunological damage to the cerebellum, to the posterior columns of the spinal cord, and to peripheral nerves. We (the authors) propose the term gluten ataxia to describe this disorder."

Patients with ataxia (a neuromuscular disorder) who attended a neurology clinic were screened for celiac disease (biopsy and HLA). The authors identified 28 patients with gluten sensitivity and ataxia with no other predisposing cause. The neurological symptoms preceded the diagnosis of celiac disease.

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