Aronson, H., Silverstein, A. B., & Klee, G. D. (1959). Influence of lysergic acid diethylamide (LSD-25) on subjective time. AMA archives of general psychiatry, 1(5), 469-472., 10.1001/archpsyc.1959.03590050037003
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The authors discuss the last five years work of the Saskatchewan group and develop their hypothesis relating adrenaline metabolites to schizophrenia. They also discuss work done in other centres. They indicate some of the difficulties encountered not only in synthesizing adrenochrome and adrenolutin but also in working experimentally with them in human subjects. The successful synthesis of pure stable adrenochrome and adrenolutin has made chemical assay possible. Using their adrenochrome assay, they have found differences between adrenochrome metabolism in normals and schizophrenics. While these require exploration the authors believe that their hypothesis is strong enough to warrant attention or to see whether others can confirm their findings. While adrenochrome and adrenolutin are at present the only metabolites of adrenaline which can be obtained as pure stable compounds and have psychotomimetic properties, there is suggestive evidence that others will be found.
Osmond, H., & Hoffer, A. (1959). Schizophrenia: A new approach (continued). The British Journal of Psychiatry, 105(440), 653-673. https://dx.doi.org/10.1192/bjp.105.440.653
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Despite 14 years of investigation, as intensive as accorded any biologically active chemical, a gap remains in the systematic description of human response to lysergic acid diethylamide (LSD-25). The dramatic schizophrenic-like symptoms after doses of 40μg to 100μg have drawn the main interest. The threshold for activity is placed at 20μg by general consensus, while perfunctory administration of smaller doses has left their effect uncertain. Accompanying those pharmacologic demonstrations has been the controversy whether LSD symptoms simulate the psychopathology of schizophrenia1 or can be better explained as a toxic organic psychosis.2 One of these alternatives might be favored by its resemblance to the complete dosage-response relationship of LSD. It is unfortunate for analogical comparison that early stages of toxic psychosis have rarely been described in a psychopathological framework3; on the other hand, there is a firm basis for comparison with various schizophrenic processes. This preliminary note reports
Greiner, T., Burch, N. R., & Edelberg, R. (1958). Psychopathology and psychophysiology of minimal LSD-25 dosage: A preliminary dosage-response spectrum. AMA Archives of Neurology & Psychiatry, 79(2), 208-210., 10.1001/archneurpsyc.1958.02340020088016
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Horita, A., & Dille, J. M. (1954). Pyretogenic effect of lysergic acid diethylamide. Science, 120(3131), 1100-1101., 10.1126/science.120.3131.1100
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Anderson, E. W., & Rawnsley, K. (1954). Clinical studies of lysergic acid diethylamide. European Neurology, 128(1-2), 38-55.
Deshon, H. J., Rinkel, M., & Solomon, H. C. (1952). Mental changes experimentally produced by LSD (d-lysergic acid diethylamide tartrate). Psychiatric Quarterly, 26(1), 33-53., 10.1007/BF01568448
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Guttmann, E. R. I. C. H., & Maclay, W. S. (1936). Mescalin and depersonalization: Therapeutic experiments. Journal of Neurology and Psychopathology, 16(63), 193.
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Mitchell, S. W. (1896). Remarks on the effects of Anhelonium lewinii (the mescal button). British Medical Journal, 2(1875), 1625.
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