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Robert F. Kushner, MD
Department of Medicine

Stephen A. Berman, MD, PhD
Department of Neurology University of Chicago School of Medicine 5841 S Maryland Ave Chicago, IL 60637

Arch Neurol. 1990;47(4):383-384.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.

—Recent articles have held forth hope that certain metabolic myopathies might undergo improvement with proper dietary therapy.^1-3 In particular, the simple expedient of a high protein diet has appeared to be remarkably effective in the disparate disorders of McArdle's disease,¹ debrancher deficiency,₂ and acid maltase deficiency.³ With respect to McArdle's disease, a single patient, described by Slonim and Goans, demonstrated marked improvement after consuming a high protein diet.¹ Indeed, 45 minutes after a high protein (25% to 35%) meal, his exercise tolerance improved 400%. Over a 3-year period, the patient also experienced a decrease in muscular atrophy and an increase in exercise tolerance. The investigators discussed the possibility that increased availability of branched-chain amino acids (BCAAs) contributed to the improvement by serving as an alternative energy source for exercising muscle. To focus on this possibility, we studied the functional and metabolic muscle . . . [Full Text PDF of this Article]

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