Abstract
A highly significant decrease in ability to metabolize an oral load of tyramine to its sulphate conjugate compared with controls is characteristic of patients with endogenous unipolar depressive illness. Neurotic depressives do not differ from controls. The biochemical deficit persists after clinical recovery from depression and is also present in about half the first-degree relatives of endogenously depressed probands. Thus, it is likely to be a trait marker for the disease and a predictor of vulnerability to it.
About half of a small group of acute schizophrenics without overt depression also manifested with a tyramine conjugation deficit. A number of methodological questions related to precision of diagnosis, drug status and completeness of urine collection need to be answered before these findings can form the basis of a unitarian hypothesis of functional mental illness.
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© 1985 The Human Press Inc
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Sandler, M., Hale, A.S., Walker, P.L., Bridges, P.K. (1985). Tyramine-Conjugation Deficit as a Trait-Marker in Endogenous Depressive Illness. In: Boulton, A.A., Maitre, L., Bieck, P.R., Riederer, P. (eds) Neuropsychopharmacology of the Trace Amines. Humana Press. https://doi.org/10.1007/978-1-4612-5010-4_43
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DOI: https://doi.org/10.1007/978-1-4612-5010-4_43
Publisher Name: Humana Press
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