“Success is often just an idea away.” Frank Tyger
Introduction
Amphetamine psychosis has intrigued investigators for years. It is thought to provide a clue to schizophrenia. The authors A. Randrup and I. Munkvad have observed this. They published a report in Journal of Orthomolecular Psychiatry in the first 1972 issue.
“The symptoms of the “amphetamine psychosis” differ among individuals but in many cases they are very similar to those seen in certain forms of schizophrenia, particularly the paranoid form. The similarity is such that misdiagnoses have frequently been made (Connell 1958; Hampton 1961; Breitner 1963; Mendels 1964; Rickman et al. 1961; Beamish and Kiloh 1960; Bell and Trethowan 1961; Ellinwood 1969; Welsh 1962).” A. Randrup and I. Munkvad, Sct. Hans Hospital, DK 4000 Roskilde, Denmark
Dopamine
Dopamine theories have dominated psychiatry for decades and for very good reasons. It seems that the chemical structure of amphetamine is very similar to that of dopamine. Methamphetamine is even more potent than amphetamine. Huntington’s chorea first presents with psychiatric symptoms. Then neurological symptoms develop. Pathology is seen in the basal ganglia, which are areas high in dopamine. Parkinson’s disease patients treated with L-DOPA have experienced psychiatric side effects. All of this information seems to support the “pink spot” theory of Friedhoff & van Winkle. According to this theory a toxic O-methylated derivative of dopamine called DMPEA causes schizophrenia.
The “Pink Spot”
“We have compared our methods with those used by other workers and have found that those who reported positive findings for normal urine were using procedures (Takesada et al.16) which separated more material isographic with DMPE on chromatograms than did our method. This material can be separated from pink spot and when this is done pink spot is only found to be present in schizophrenics. Our findings indicate that the material responsible for these reports of positives in urines from control subjects is of dietary origin.” A. Pauline Ridges, Ph.D., M.Sc, A.R.I.C. (1972)
Ridges and her group were from Liverpool. Her article was entitled “Biochemical Research into Schizophrenia in Relation to Pink Spot Excretion”. It was published in the Journal of Orthomolecular Psychiatry.
A Unifying Hypothesis
This author has attempted a unifying hypothesis to explain the various data from different investigators. Dohan had found that an excess of one amino acid can wreak havoc in the brain in celiac disease. This disease is treated by a diet which excludes wheat gluten.
But what would happen if a toxin caused many amino acids to flood the brain cells? The results could be disastrous. Amino acids are found in the diet. For example, tryptophan is found in the following foods: Bananas, beans, brewer’s yeast, brown rice bran, caseinate, cottage cheese, dairy products, dates, eggs, fish, lactalbumin, legumes, meat, milk, nuts, peanuts, protein (hydrolysis), seafood, seeds, soy, turkey, whey, whole grains.
If there were an excess of tryptophan in the brain, these foods should be avoided. There is a pattern. Most of the foods high in tryptophan are animal foods. However some plant foods are also a problem. Dates and bananas are the only foods considered fruits on the list. No berries are on the list. Therefore berries and fruits might be the foods best to eat. Some vegetables have tryptophan and some are low in tryptophan.
Conclusions
The orthomolecular view is that drug abuse should be avoided. A toxic metabolite of dopamine causes schizophrenia. This toxin, DMPEA, causes amino acids to flood the brain cells. This unifying theory makes much of the data fall into place. It seems that all it takes is an excess of one amino acid to foul up the brain. This is seen in PKU, celiac disease, porphyria (where tryptophan floods the brain), hyperagininemia, etc. What if a number of amino acids were flooding the brain?
This theory explains the Detroit data. Detroit workers found a slowing of glucose metabolism in schizophrenia. The excess amino acids can cause this. More information is given in the references.
References
1. ANGRIST, B. and GERSHON, S.: A pilot study of pathogenic mechanisms in amphetamine psychosis utilizing differential effects of D and L amphetamine. Pharmakopsychiatrie. Neuro-Psychopharmakologie 4,63-75, 1971.
2. BABREAU, A.: Dopamine and disease. C.M.A.J. 103, 824-832, 1970.
3. BEAMISH, P. and KILOH, L. G.: Psychoses due to amphetamine consumption. J. Ment. Sci. 106, 337-343, 1960.
4. BEJEROT, N.: Discussion p. 140 in Abuse of Central Stimulants by F. Sjoqvist and M. Tottie. Almqvist & Wiksell, Stockholm 1969.
5. BELL, D. S. and TRETHOWAN, W. H.: Amphetamine addiction. J. Nerv. Ment. Dis. 133, 489-496, 1961.
6. BREITNER, C: Appetite suppressing drugs as an etiologic factor in mental illness. Psychoso-matics 4, 327-333, 1963.
7. GRIFFITH, J. D., CAVANAUGH, H. H., HELD, J. and OATES, J. A.: Experimental psychosis induced by the administration of d-amphetamine. Symposium on Amphetamines and Related Compounds, pp. 897-904 edited by E. Costa and S. Garattini. Raven Press, New York, 1970.
8. HAMPTON, W. H.: Observed psychiatric reactions following use of amphetamine-like substances. Bull. NY Acad. Med. 37, 167-175, 1961.
9. www.associatedcontent.com/article/1340193/advances_in_affective_disorder_research.html
10. http://www.associatedcontent.com/article/381054/using_nutrition_to_fight_against_disease.html
11. JENKINS, R. B. and GROH, R. H.: Mental symptoms in Parkinsonian patients treated with 1-dopa. Lancet, II, 177, 1970.
12. JONAS, W. and SCHEEL-KRUCER, J.: Amphetamine induced stereotyped behaviour correlated with the accumulation of O-methylated dopamine. Arch. Int. Pharmacodyn. 177, 379-389, 1969.
13. UTENA, H.: Behavioural aberrations in methamphetamine intoxicated animals and chemical corelates in the brain. In: Correlative Neuro-sciences, vol. 21B, pp. 191-207 edited by T. Tokizane and J. P. Schade. Elsevier, Amsterdam, 1966.
14. WELSH, A. L.: Side effects of anti-obesity drugs. Charles C. Thomas, Springfield, Ill., U.S.A. 1961.
15. BERGEN, J. R.: Possible relationship of a plasma factor to schizophrenia. Trans. N.Y. Acad. Sci. 28:40, 1965.
16. DOHAN, F. C: Cereals and schizophrenia, data and hypothesis. Acta Psychiat. Scand. 42:125, 1966.
17. DOHAN, F. C: Coeliac disease and schizophrenia. Lancet 1:897, 1970.
18. DOHAN, F. C: Wartime changes in hospital admissions for schizophrenia. Acta Psychiat. Scand. 42:1, 1966.
19. DOHAN, F. C, GRASBERGER, J. C, LOWELL, F. M.,JOHNSTON, H. T. and ARBEGAST, A. W.: Relapsed schizophrenics: More rapid improvement on a milk and cereal-free diet. Brit. J. Psvchiat. 115:595, 1969.
20. BUSCAINO, V. M.: Biologia E terapia della schizophrenia. Acta. Neurol. 25:1, 1970.
21. FROHMAN, C. E., HARMISON, C. R., ARTHUR, R. E. and GOTTLIEB, J. S.: Conformation of a unique plasma protein in schizophrenia. Biological Psychiatry 3:113, 1971.
22. Cooperative Study: Plasma factors in schizophrenia. Arch. Gen. Psychiat. 18:471, 1968.
23. GREINER, A. C: Schizophrenia, melanosis iatrogenic-congenital defect? Dis. Nerv. Svst. 29:14, 1968.
24. GREINER, A. C. and NICHOLSON, G. A.: Schizophrenia-melanosis, cause or side effects? Lancet 2:1165, 1965.
