THOMAS A. BAN
Books Authored/Coauthored
1. Thomas A. Ban: Conditioning and Psychiatry. Aldine, Chicago 1964; Unwin, London 1966; Conditioning Behavior and Psychiatry London/New York: Aldine; 2008
2. Thomas A. Ban: Psychopharmacology. Williams and Wilkins: Baltimore; 1969
3. Heinz E. Lehmann and Thomas A. Ban: Pharmacotherapy of Tension and Anxiety. Springfield: Charles C. Thomas; 1970
4. Thomas A. Ban: Nicotinic Acid in the Treatment of Schizophrenias: Introduction. Toronto: Canadian Mental Health Association; 1970
5. Thomas A. Ban and Heinz E. Lehmann: Nicotinic Acid in the Treatment of Schizophrenias: Progress Report No. I. Toronto: Canadian Mental Health Association; 1971
6. Thomas A. Ban: Nicotinic Acid in the Treatment of Schizophrenias: Complementary Report A. Toronto: Canadian Mental Health Association; 1971
7. Thomas A. Ban and Heinz E. Lehmann: Experimental Approaches to Psychiatric Diagnoses. Springfield: Charles C. Thomas; 1971
8. Thomas A. Ban: Schizophrenia: A Psychopharmacological Approach. Springfield: Charles C. Thomas; 1972 (English original and Japanese translation)
9. Thomas A. Ban: Recent Advances in the Biology of Schizophrenia. Springfield: Charles C. Thomas; 1973 (English original and Japanese translation)
10. Morris Lipton, Thomas Ban, John Kane, Jerome Levine and Richard Wittenborn: Megavitamins and Orthomolecular Therapy in Psychiatry. Task Force Report No. 7. Washington: American Psychiatric Association; 1973
11. Thomas A. Ban: Depression and the Tricyclic Antidepressants. Montreal: Ronalds Federated; 1974
12. Thomas A. Ban: Introduction to the Psychopharmacology of Doxepin. Montreal: Pfizer; 1977
13. Thomas A. Ban: Psychopharmacology of Thiothixene. New York: Raven Press; 1978
14. Thomas A. Ban: Psychopharmacology for the Aged. New York: Karger; 1980 (English original and Japanese translation)
15. Thomas A. Ban: Psychopharmacology of Depression. New York: Karger; 1981 (English original and Italian translation)
16. Thomas A. Ban and Mark H. Hollender: Psychopharmacology for Everyday Practice. Basel: Karger; 1981 (English original and Dutch and Japanese translations)
17. Thomas A. Ban: Prolegomenon to the Clinical Prerequisite. Psychopharmacology and the Classification of Mental Disorders. Oxford: Pergamon Press; 1987 (Progress in Neuro-Psychopharmacology and Biological Psychiatry 1987; 11: 527-80)
18. Bertalan Petho and Thomas A. Ban in collaboration with A. Kelemen, G. Ungvari, I. Karczag, I. Bitter, J. Tolna, M. Jarema, F. Ferrero, E. Aguglia, G.L. Zurria, O.K. Fjetland: DCR Budapest-Nashville in the Diagnosis and Classification of Functional Psychoses. Basel: Kargr; 1988. (Psychopathology1988; 21: 153-239)
19. Thomas A. Ban: CODE-DD. Composite Diagnostic Evaluation of Depressive Disorders. Nashville: JM Productions; 1989. (English original and Estonian, French, Italian and Polish translations)
20. Thomas A. Ban: Declino Cognitivo Nell'Anziano Demenza e Sindromi Demenziali Epidemiologia, Diagnosi e Terapia. Milan: UTET;
21. Thomas A. Ban:Sostiutuire il Neurolettico. Rome: Il Pensiore. Scientifico Editore; 1992
22. Thomas A. Ban and Ronaldo Ucha Udabe: Clasificacion de las Psicosis. Buenos Aires: Editorial Salerno; 1995. (Spanish; English original Classification of Psychosis. INHN E-Books November 6, 2014)
23. Thomas A. Ban: Neuropsychopharmacology and the Forgotten Language of Psychiatry. Madness: From Psychiatry Neuronology. INHN E-Books Nov. 14, 2013
24. Thomas A. Ban: From Melancholia to Depression. A History of Diagnosis and Treatment. INHN E-Books March 6, 2014
25. Thomas A. Ban: CODE-SD Composite Diagnostic Evaluation of Schizophrenic Disorders. INHN E-Books April 17, 2014
26. Thomas A. Ban: History of Psychiatry INHN E-Books May 1, 2014
27. Thomas A. Ban: General Psychopathology. INHN E-Books May 8, 2014
28. Thomas A. Ban: Dementia: Differential Diagnosis. INHN E-Books May 15, 2014
29. Thomas A. Ban: DAS Diagnostic Assessment Scales for Diagnostic Criteria for Research. INHN E-Books August 21, 2014
30. Thomas A. Ban: Psychopharmacology of Anxiety Disorders CODE-AD. INHNE-Books October 16, 2014
31. Psychopharmacology and The Classification of Functional . INHN E-Books November 27, 2014
Thomas A. Ban
June 2, 2016
Gin S. Malhi: A critical analysis of concepts in psychiatry.
Gin S. Malhi, Erica Bell and Richard J. Porter: Serial quelling the typical use of atypical antipsychotic drugs
Ken Gillman’s comment on Aitor Castillo’s comment
Aitor Castillo’s response to Gin Malhi starts by stating, “In this very polemic paper, the central question is: ‘how can one agent treat so many different psychiatric disorders? The authors try to debate this issue choosing quetiapine as a scapegoat. I wonder why they did this, because the same thing could be applied to olanzapine or many other psychiatric drugs.’”
I have several major problems with Castillo’s response which over-extrapolates from sparse and poor data to make assertions that are little more than speculations which require more substantive scientific evidence to be taken seriously.
The characterisation of Malhi’s writing as a “polemic” is inappropriate, both because it is a loaded use of the word polemic and because it suggests the writer has an emotional reaction to what is being written, which further hints at bias and non-scientific thinking.
The word polemic originates from an argument against established religious doctrine. Doctrine is belief, not evidence. A fundamental building block of science is arguing against “established” views — that is an essential and important part of scientific discourse — especially since most ideas put forward in psychiatry are in dire need of rebuttal, through polemical writing if necessary. The modern use of the word polemic disparagingly distorts it, giving it a subtext insinuation of substandard dialectical quality. Indeed, use of the word “polemic” has parallels with use of the term “sic” for which I criticised Charles Beasley in my previous response to another comment — such usage often says as much about the writer as it does about the discussion. Castillo then follows up with the word “scapegoat” which is equally biased, emotive and unjustified. They are using it as an egregious exemplar — which indeed it is.
Next comes an obvious “straw man” argument, that the same thing can be applied to lots of other drugs. No, it cannot, they are all different pharmacologically and any logical view about their supposed effects must follow on from their basic pharmacology — the basic pharmacology of quetiapine is that it is a specific H1 antagonist — the best data we have indicates that property is 20 times greater than any other property it possesses. It is around 100 times greater than its potency as a dopamine receptor antagonist. Any rational view of its pharmacology must, prima facie, assume that it works solely as an antihistamine, at least if given in any sensible, non-injurious, clinical dosage. A reminder: its neuropharmacological profile is almost identical to that of promethazine — talk about returning to the past!
The speculation that it is an AD because the metabolite is “a potent NRI” is just that, pure speculation, not established scientific fact (Jensen, Rodriguiz, Caron et al. 2008). Its affinity for the NET, which is not unequivocally established by independent replicated work, is not established in therapeutic use in humans and it has not been shown to attenuate the tyramine pressor response.
The most astonishing fact about the literature on this drug is that not a single paper about it mentions the fact that it is an H1 antagonist at all, and that property is hugely more potent than any other property it possesses — that clearly indicates that everybody writing about it is doing it in a totally one-eyed fashion which completely goes against what Castillo himself mentions (Zohar, Stahl, Moller et al. 2015), which is the laudable recent proposition that all these drugs should be categorised strictly by their neuropharmacological properties, thus classifying it as a highly selective centrally acting H1 antagonist!
It is the first drug in the modern era to be prescribed widely for sleep, anxiety, depression, mania, dementia and schizophrenia: it is either a miracle, or the most stupendous con-job ever perpetrated on patients and the eternally gullible psychiatric fraternity. Unless you believe in miracles. And in the mercury-in-a-sieve miracle of “atypicality” you must also believe, because good scientific evidence simply does not exist, except in the minds of people who work all day with rats (and the marketing department).
If the company believed that the metabolite was an anti-depressant, they could have re-marketed it and enabled a new patent — they have not. That is despite the fact with that they have gotten tens of billions of dollars from this drug, so they are flush with funds to do some extra work! It reminds me of the little-known story about bupropion and its metabolite hydroxybupropion, which was named Radafaxine and tested, failed and was never marketed. All subsequent papers by the drug company studiously failed to note those results. They were glossed over, perhaps because they would suggest that bupropion did not work either, since it is less potent than the metabolite. Indeed, bupropion is best regarded as a pro-drug.
Psychiatrists have had the pharmacological wool pulled over their eyes so many times now they could stuff a mattress with the waste.
One cannot leave this subject without noting that designating this drug as an atypical antipsychotic is to venture deep into the realm of Humpty Dumpty language — as he said in Alice Through the Looking Glass, “'When I use a word, it means just what I choose it to mean — neither more nor less..” I make other points related to this in a longer discussion of this drug elsewhere (Gillman 2021).
There are various other counterarguments to the contents of Castillo’s response which one could make, but I have said enough.
References:
Gillman PK. Quetiapine: The miracle of Seroquel, 2017 psychotropical.com/quetiapine-the-miracle-of-seroquel.
Jensen NH, Rodriguiz RM, Caron MG, Wetsel WC, Rothman RB, Roth BL. N-desalkylquetiapine, a potent norepinephrine reuptake inhibitor and partial 5-HT1A agonist, as a putative mediator of quetiapine's antidepressant activity. Neuropsychopharmacology 2008;33(10):2303-12.
Zohar J, Stahl S, Moller H-J, Blier P, Kupfer D, Yamawaki S, Uchida H, Spedding M, Goodwin GM, Nutt D. A review of the current nomenclature for psychotropic agents and an introduction to the Neuroscience-based Nomenclature. Eur Neuropsychopharmacol 2015;25(12):2318-25.
November 18, 2021