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SEYMOUR REICHLIN, M.D., Ph.D.,

AMA Arch Gen Psychiatry 1959;1(4):434-440.

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

In the search for metabolic causes or manifestations of schizophrenia, much attention has been paid to the abnormally low oxygen consumption rate which is found in the majority of schizophrenic patients.^1-7 This disturbance is not caused by thyroidgland hypofunction, as is shown by normal thyroid radioiodine uptake or plasma protein-bound iodine in most schizophrenics.^7-17 Evidence that the thyroid gland is not necessarily responsible for hypometabolism in schizophrenics comes also from the observation that a few patients appear able to tolerate enormously large doses of thyroxine or thyroid extracts without manifesting thyrotoxicosis.^5,18,19 These findings, if they are generally applicable, indicate, among other possibilities, that in schizophrenia there is a depression of tissue responsiveness to thyroxine effects, as suggested by Hoskins,^5,6 or that there is an abnormality of thyroxine metabolism in these patients.

The hypothesis that there is an abnormality of thyroxine . . . [Full Text PDF of this Article]

Author Affiliations
St. Louis With the Technical Assistance of Mtanios G. Koussa, A.B.

Departments of Medicine and of Psychiatry, Washington University School of Medicine.

Abbott Laboratories, Oak Ridge, Tenn.

Footnotes
Submitted for publication Jan. 9, 1959.

This work was supported in part by U. S. Public Health Service Grant B834, and by a grant from the Commonwealth Fund.

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