Adrenochrome Hypothesis and Treatment of Schizophrenia
In 1951, there were only three acceptable treatments for schizophrenia: (1) psychotherapy based upon psychoanalysis, which did not work; (2) insulin coma, which was rapidly being displaced by electroconvulsive therapy; and (3) ECT, which aborted many acute psychotic reactions but in the long run did not change the course of the illness very much. There was nothing else on the horizon except a few workers who were investigating steroids, histamine, thyroid, and the newly discovered antihistamines. Pellagraologists had found that a few patients in southern mental hospitals recovered when given niacin, but they were promptly re-diagnosed pellagrins, thus retaining the sacred principle that only pellagrins responded to this vitamin, vitamin B-3. We confirmed that histamine treatment helped many acute patients, but it was no more practical to use it on a sustaining basis than it was to use insulin coma or ECT for chronic control of psychosis.
Humphry Osmond and I agreed we should base any new treatment on our adrenochrome hypothesis for two reasons. If such a treatment were successful it would bolster the hypothesis, but much more important, we would have a way of helping our patients. We decided to use compounds that were safe, available, could be taken easily, and would prevent or decrease the oxidation of adrenalin to adrenochrome. This was the first example of antioxidant therapy applied to medicine. We hoped that vitamin B-3 would decrease the production of adrenochrome or prevent its toxic effect on the respiratory enzymes. Adrenochrome was known to be a powerful inhibitor of these enzymes. We also hoped that ascorbic acid, as one of nature’s best water-soluble reducing substances, would act in a like manner.
Both vitamins were and are safe and fit our requirements for a treatment that could be taken for a lifetime if necessary. But in order to be effective we concluded we would have to use doses larger than those already reported, for if smaller doses had been effective this would have been reported. We decided to begin with 3 to 10 grams per day of each vitamin.
A few preliminary studies soon showed these doses were safe and acceptable to patients. Our first pilot study included eight severely ill acute cases, two under my care and six under Dr Osmond’s care at a mental hospital. All had not responded to previous treatment. All recovered on these vitamins. I am still surprised. Perhaps in 1952 schizophrenics were not as badly damaged by high-tech nutrition as they are today. Pritchard found no difference in outcome between patients treated before and after tranquilizers were introduced,66 but Bockoven and Solomon concluded schizophrenics treated between 1947 and 1952 had a better long-term outlook than patients treated with tranquilizers between 1967 and 1972.67 They concluded, “psychotropic drugs may not be indispensable to the success of community-based mental health services and that their extended use in aftercare may prolong the social dependency of many discharged patients.” They were, in fact, made as dependent then as they are now on tranquilizers alone. It is impossible to function normally in any activity requiring energy, initiative and concentration on tranquilizers alone. Would you allow a heavily tranquilized surgeon to operate on your heart? Two factors have made the outcome worse: (1) malnutrition and (2) tranquilizers alone.
We started a double dummy experiment to test our ideas. These experiments had been done in England but had not yet come across to North America. In fact, the first report in North America that tranquilizers were helpful in the treatment of manic states were open clinical experiments. According to modern clinical scientific dogma, these results should not have been published, should not have been read, and should not have been believed because they were anecdotal – that evil way of making observations. Yet H. Lehmann became the North American pioneer in introducing tranquilizers because of one anecdotal report. Thank God double-blind theorists did not exist then. By the time we finished our experiment, it had become “double blind,” overthrowing the British term “double dummy.”
In our experiment, the addition of 3 grams per day of either niacin or niacinamide to the treatment then available doubled the one-year cure rate of acute patients from the placebo rate of 35% to 70%. Three more double-blind controlled experiments gave us similar results. We also found and reported in 1955 that chronic patients did not respond to vitamin B-3, even in doses of 10 grams per day.17,68,69,70,71,23 Our method was described by Clancy, Hoffer, Lucy, Osmond, Smythies and Stefaniuk.72
Our main conclusions were:
1. That acute patients doubled their one-year recovery rate.
2. That chronic patients did not.
These findings have been confirmed by every study reported since then. Thus, the Montreal group using only chronic patients labeled newly admitted obtained mixed results. Generally, they did not respond, but they ignored evidence of improvement. The New Jersey studies were also mixed. The initial report on chronic patients was negative. However, Dr J. Wittenborn later reviewed his data, pulled out 24 patients who were chronic, less ill, and found that compared to placebo 70% had responded — i.e., double the placebo rate.73 Every psychiatrist since 1960 has been able to find similar responses, provided they took the pains to follow the basic treatment protocols. So far I have not known any psychiatrists who, having used the nutritional approach for at least one year, have given it up, in spite of massive harassment by local, state, and national psychiatric establishments. There is one exception – a northeastern psychiatrist gave up all use of vitamins after 6 months because, if he had not, he would have lost his hospital privileges and his practice. He, in the end, merely lost his self-respect, for in his sign-off letter to me he bemoaned the fact he was not permitted to treat his schizophrenic patients in the most efficacious way.
Vitamin therapy is advancing very quickly because it works, even when there are no drug companies to push it, and arrayed against it are all the establishment organizations, including nutritionists, psychiatrists, psychologists and social workers. Our main support has come from the thousands of families hit by schizophrenia who have compared results when their relatives were on tranquilizers only and then treated more effectively with orthomolecular therapy. Politics, not science, has inhibited the advance of orthomolecular therapy, and it is politics as practiced by our patients that will force you to eventually become orthomolecular psychiatrists. Until then, our poor schizophrenics will be treated in tranquilizer institutions or condemned to the streets, while the wealthy will be able to seek out orthomolecular hospitals and practitioners and be given their chance for recovery.
Treatment today is much more than vitamin B-3 and ascorbic acid, even though these two vitamins remain basic components. Treatment today is to our original treatment as a Japanese Cressida is to a Model T. Ford. This does not mean the Adrenochrome Hypothesis is proved, but it does provide further support; it is a viable theory and must continue to be examined.
Conclusion
The Adrenochrome Hypothesis has been tested experimentally by a large number of scientists since it was first reported in 1952 in New York before the Dementia Praecox committee of the Scottish Rites Masons. Three major sub-hypotheses have been confirmed; it is made in the body, it is an hallucinogen; and its antidotes are therapeutic for schizophrenia. What must still be done is to determine how schizophrenics and normals differ in the way they deal with the catecholamine/aminochrome pathways.
Schizophrenia is a syndrome.73,74,75 The Adrenochrome Hypothesis may account for the final clinical picture, but the abnormal changes are triggered by a number of factors, such as cerebral allergies, vitamin dependencies and deficiencies, and so on. The essential fatty acids76,77 and the prostaglandins78,79 are involved. One day all these factors will be examined and co-related so that we will have a clear picture of what happens when a person becomes schizophrenic.60.
All three known pathways by which the catecholamines are metabolized play a role in the body. What we must know is how they are related to each other and what factors direct these pathways.
