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Viggo Holm, MD
Kronprinsensvej 4A DK-2000 Copenhagen, Denmark

Arch Neurol. 1978;35(7):478.

	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.—

would like to propose the hypothesis that an abnormally pronounced decomposition of inositol is important in the pathogenesis of multiple sclerosis (MS). The resulting intermittent deficiency of inositol compromises the synthesis of the phosphoinositides, the only myelinlipides with a fast turnover,^1.2 resulting in demyelinization.

It has been demonstrated³ that a reversible process, inositol glucose, exists in the organism. The question arises whether this equilibrium in cases of active MS is displaced abnormally far to the right, leading to an inositol deficiency.

The hypothesis is tested in a study by determination of the difference between the most negative redox potential (maximal metabolism) obtained in a blood sample without and with inositol added, respectively.

If the addition of inositol exclusively was able to abnormally increase the potential reduction, this would mean an abnormally pronounced metabolism of inositol, most likely via glucose.

Four parts of blood . . . [Full Text PDF of this Article]

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