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Remained very tense and uncomfortable all the time. This group did not profit from their experience. In a few patients an injection of adrenochrome after two hours would, within a few minutes, bring on the typical LSD reaction. We concluded that LSD did not act as an hallucinogen per se but that it induced an increase in the production of adrenochrome which was the hallucinogen. An individual who could not make enough adrenochrome would not be able to have the typical LSD reaction. This conclusion was supported by our earlier finding that vitamin B3 markedly reduced the intensity of LSD reactions whether given before or during the LSD reaction. By blocking the adrenochrome effect it would also block the effect of LSD. It would also explain why Brom LSD, a very potent antiserotonin, would not be an hallucinogen. Brom LSD probably has no effect on adrenalin oxidation and would not increase the formation of adrenochrome. These are interesting speculations. Perhaps now with increasing interest in free radical hypotheses and in oxidized derivatives of the catecholamines, scientists will direct their interest back into these areas. Will Blocking the Production of Aminochromes be Therapeutic for Schizophrenia? Our two basic equations immediately directed our attention in 1952 to the need for compounds which would decrease the formation of adrenochrome. We needed compounds that were safe, could be taken over a lifetime and which had no side effects. We realized that any treatment for schizophrenia must be life long. It is impossible to give ECT or insulin for life, which explains why these treatments were successful for short periods. We wanted to decrease the formation of adrenalin, not stop it, by pulling methyl groups away from noradrenalin. We also knew that adrenochrome was a respiratory enzyme inhibitor and that the respiratory enzymes were made in the body from thiamin, riboflavin 53.
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Application of self-regulation. The potentially harmful effects of inappropriate promotion of pharmaceutical products are so great that there is no room in the DTCA regimen for `testing the boundaries', or fringe advertising, which has occurred already in DTCA, and is known to occur in advertising of other products.' 53 Consequently the NZMA supports the outcome of the review.54 General practitioners have adopted a similar position. The Royal New Zealand College of General Practitioners RNZCGP ; welcomed the review, saying that while DTCA can be positive and empower patients with information, `problems arise when the advertising encourages patients to seek medicines which they do not need or which are unsuitable for their particular situation'.55 It stopped short of arguing that GPs are pressurised into prescribing inappropriately because of DTCA, but highlighted damage to the doctor-patient relationship and detracting from the care a GP is able to give. In its submission to the review the RNZCGP said it: `applauds any measure that assists consumers to better understand the choices available to them provided that such information is presented in a balanced manner.' 56 However, it said the arguments for DTCA of prescription medicines weren't persuasive, arguing that the quality of information provided through advertising is inadequate and lacks balance. It believes existing legislation is inadequate and that conventional television advertising is not the proper medium to present complete prescribing information. As a result the RNZCGP preferred retaining DTCA, but under more stringent rules and regulations, with continued self-regulation the route favoured by the Ministry of Health.
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The Johns Hopkins tests prompted a researcher at the University of Leeds to comment that: "This compound is very actively metabolised in man but inefficiently so in the rat and squirrel monkey, which leads to much higher brain concentra tions in these animals than would be found in man. For these reasons, the changes seen in the squirrel monkey are unlikely to be of any greater relevance for man than were the earlier spec ulations from rat data"17. He continued: "Allegations arising from inappropriate high-dose studies in rats fenflu ramine ; and squirrel monkeys dexfenfluramine ; are not backed up by any serotonergi cally mediated central nervous system pathology in man, yet dexfenfluramine has been used by more than 5 million patients for 6 years, and the parent compound by more than 20 million patients for 26 years"17. In 1991 researchers at the pharmaceutical company Wyeth, studied fenfluramine in mice and rats; they added rats to their research because they had already studied fenfluramine in mice and had "noted deviations from the expected results" in that species. They wrote: "Fenfluramine, which is considered to act via serotonergic mechanisms is a potent anorectic at doses which do not affect behaviour in the rat, while in the mouse there is no separation between anorectic and sedative doses. These data illustrate further and propecia.
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