Hostname: page-component-78c5997874-fbnjt Total loading time: 0 Render date: 2024-11-14T22:37:05.680Z Has data issue: false hasContentIssue false

Adrenochrome As the Cause of Schizophrenia: Investigation of Some Deductions from this Hypothesis

Published online by Cambridge University Press:  08 February 2018

Extract

Osmond and Smythies (1952) have given reasons for reviving the view originally put forward by Bleuler (1950) that schizophrenia is essentially a disorder of metabolism, and have suggested that some substance chemically related to mescaline might be the causative agent. Hoffer, Osmond and Smythies (1954) have begun an investigation of this hypothesis and have found that adrenochrome, an oxidation product of adrenaline which is probably a normal intermediate metabolite, has active hallucinogenic properties. These authors do not regard adrenochrome as being unquestionably the toxic agent in schizophrenia, but suggest that it or some closely related substance, having the indole ring and derived from adrenaline, is involved. They also advance the opinion that the metabolic fault consists of an overproduction of adrenochrome or similar substances. Such a view necessarily implies either overproduction of adrenaline or a blocking of one or more of the paths of adrenaline detoxification in the body which do not lead through adrenochrome. As adrenaline is derived from tyrosine the hypothesis is essentially one of abnormal tyrosine metabolism. From this hypothesis certain deductions can be made.

Type
Original Articles
Copyright
Copyright © Royal College of Psychiatrists, 1955 

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Ackerman, L. V., and del Regato, J. A., Cancer, Diagnosis, Treatment and Prognosis, 1947. London.Google Scholar
Bacq, Z. M., Pharm. Rev., 1949, 1, 1.Google Scholar
Bellak, L., Dementia Praecox, 1947. New York.Google Scholar
Bickel, H., Gerrard, J., and Hickmans, E. M., Lancet, 1953, ii, 812.Google Scholar
Bleuler, E., Dementia Praecox, 1950. (Reprint). New York.Google Scholar
Churchman, R., Proc. Soc. Exp. Med. Biol., 1924, 22, 135.Google Scholar
Haden, R. L., and Orr, T. G., Johns Hop. Bull., 1924, 35, 58.Google Scholar
Heard, R. D. H., and Welch, A. D., Biochem. J., 1935, 24, 998.CrossRefGoogle Scholar
Himsworth, H. P., The Liver and its Diseases, 1947. Oxford.Google Scholar
Hoffer, A., Osmond, H., and Smythies, J., J. Ment. Sci., 1954, 100, 29.Google Scholar
Hoskins, R., Biology of Schizophrenia, 1946. New York.Google Scholar
Hutcheon, D. E., Personal communication from Dr. Hutcheon, 1955.Google Scholar
Lea, A. J., Nature, 1945, 155, 428.Google Scholar
Idem , Thorax, 1952, 7, 305.Google Scholar
Idem , Brit. J. Nutrii., 1953, 7, 224.Google Scholar
Idem , Science, 1955, 121, 608.Google Scholar
Loehner, C. A., Endocrinology, 1938, 23, 507.Google Scholar
Lucy, J. D., Arch. Neurol. and Psych., 1954, 71, 629.Google Scholar
MacConaill, M. A., Ann. Eugen., 1941–42, 11, 173.Google Scholar
Osmond, H., and Smythies, J., J. Ment. Sci., 1952, 98, 309.Google Scholar
Riddell, W. J. B., Ann. Eugen., 1942, 11, 245.Google Scholar
Steggerda, M., J. Heredity, 1941, 32, 402.CrossRefGoogle Scholar
Submit a response

eLetters

No eLetters have been published for this article.