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LOW-FAT DIET IN MULTIPLE SCLEROSIS

JAMA. 1961;177(10):702-703. doi:10.1001/jama.1961.03040360038008.
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Cruveilhier in 1835 described a pathological entity to which he referred as "sclérose en plaques," or multiple sclerosis. Important contributions to this entity were made by Carswell, Frerich, Rindfleisch, and Charcot. The characteristic pathological lesion of multiple sclerosis is demyelination of nervous elements of the brain and the spinal cord. The clinical symptoms correspond to the areas of demyelination. The cause of demyelination is not known and has given rise to many hypotheses.

Swank1 suggests that primary defect in multiple sclerosis is an erosion of the blood-brain barrier and that the defect in permeability of the barrier is produced by a disturbance in the suspension stability of the blood due to a high-fat intake. The early changes which precede demyelination are not known with any degree of precision. Putnam believed that the plaques were the result of occlusion of the central vein leading to the plaque and caused by thrombosis.

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