Bipolar disorder and orthomolecular treatment.
Article Type: Clinical report
Subject: Bipolar disorder (Research)
Bipolar disorder (Care and treatment)
Bipolar disorder (Diagnosis)
Orthomolecular therapy (Health aspects)
Author: Hoffer, A.
Pub Date: 12/01/2009
Publication: Name: Townsend Letter Publisher: The Townsend Letter Group Audience: General; Professional Format: Magazine/Journal Subject: Health Copyright: COPYRIGHT 2009 The Townsend Letter Group ISSN: 1940-5464
Issue: Date: Dec, 2009 Source Issue: 317
Topic: Event Code: 310 Science & research
Geographic: Geographic Scope: Canada; United States Geographic Code: 1CANA Canada; 1USA United States
Accession Number: 213722863
Full Text: Introduction

Many people have asked me whether I have ever written about bipolar psychosis and orthomolecular treatment. I have not, mainly because I have focused on schizophrenia (Hoffer, Osmond, Callbeck, and Kahan 1957). We started our research program in Saskatchewan in 1952 and discovered that the results of any treatment program for patients were much better if one included the optimum doses of vitamin B3. We did not explore the use of this vitamin for manic-depressives, as they were then called, because it was a different category of illness.

Over the years, the distinction between manic-depressive and schizophrenic disease has gradually vanished, and I now am convinced they are both forms of the pellagra. Pellagra is caused by a deficiency of vitamin B3 in the diet of people who have normal needs for this vitamin, whereas these major psychotic diseases are deficiencies of the same vitamin due to internal factors that generate an increased need for it. When the deficiency is primarily in the diet, it is called a deficiency; when the need is a result of a biochemical problem in the body, it is called a dependency. The psychoses in both conditions are identical (Hoffer 1967, 2006). Logically, these psychoses should be called pellagra, schizophrenic type; pellagra, schizoaffective type; or pellagra, bipolar type.

In this article, I will propose that there is a continuum between manic-depression (hereafter called bipolar) and schizophrenia, with an in-between syndrome called schizoaffective psychosis. I suggest that a bipolar patient who never has perceptual changes even in the manic phase differs from a schizophrenic in the oxidation of adrenalin to adrenochrome. If there is excess adrenalin, this may be a causal factor for the manic state if the adrenalin is not converted into adrenochrome. If the manic state is characterized by perceptual changes (sensory illusions and hallucinations) and thought disorder, more of the adrenalin has been oxidized into adrenochrome. There are several oxidized derivatives of the catecholamines such as dopachrome from dopamine, nor-adrenochrome from noradrenalin. When I use the term adrenochrome, I refer to any or all of these oxidized derivatives. There is a continuum from no conversion or very little conversion of adrenalin into adrenochrome in the bipolar patients, to more conversion in the schizoaffective state, to a lot more in the schizophrenic state.

The Continuum: Bipolar to Schizoaffective to Schizophrenia

Clinical research in a non-research oriented psychiatric ward is never easy. For our double-blind controlled therapeutic trials, we tested the activity of the two vitamin B3 forms, niacin and niacinamide, against placebo. This study was on schizophrenic patients only. As director of psychiatric research, I did not make the first diagnosis; that was made by the treating psychiatrist, but I would not accept patients into the study unless I agreed that they were schizophrenic. That meant that at least three doctors were involved in the diagnosis, the treating psychiatrist, his superior, and me. From counting the proportion of patients admitted to this ward, I expected that it would not take very long to have enough subjects. However, to my surprise, once the study got under way, the number of patients diagnosed with schizophrenia suddenly decreased. It was obvious that the treating doctors did not want their patients placed in this treatment trial.

I became interested in the long-term stability of diagnosis, Did a manic-depressive remain manic-depressive on subsequent admissions, or did a schizophrenic remain so after many years? As director of psychiatric research, I had free access to all the patients files. I started to keep track of patients to study this effect. I found that manic-depression was not a stable diagnosis, meaning that with subsequent admissions (and often there were many), there was a gradual shift from manic-depressive to schizoaffective to schizophrenia. But the reverse was not true. Once a patient was diagnosed schizophrenic, he remained so on subsequent diagnosis, except he would eventually be called chronic. The diagnosis of schizophrenia was stable, but that of manic-depression was not. The meaningless term borderline personality disorder, given to schizophrenic patients who are disliked or who do not respond to treatment, had not yet been invented.

I did not do a formal study; but this was unnecessary, as one was done by Prof. Nolan D. C. Lewis, chairman of the Department of Psychiatry at Columbia University, and his research psychologist Dr. Piotrowski (1954) who followed 70 patients. Lewis was one of North America's most distinguished psychiatrists. His interests were eclectic and ranged from psychoanalysis to pathology. He was even interested in the effect of mescaline (peyote), which he had taken. He was chair of the Dementia Praecox Committee of the Scottish Rites Masons. Osmond and I were invited to one of their meetings in 1952 held in the Canada Room (I thought that was very kind) of the Waldorf Astoria Hotel, where we for the first time reported our new hypothesis about adrenochrome and schizophrenia. Lewis had supported the slender efforts being made by American psychiatrists to prevent being swamped by psychoanalysis, which was galloping into North America. We became good friends, and later he wrote the foreword to our first American edition of How to Live with Schizophrenia. Our first application for a grant from Ottawa to test our hypothesis was turned down by the three Canadian professors of psychiatry on the committee then vetting federal grants, but we were given a small grant after Lewis reviewed it and recommended that we should get 20 years of support and not just 2 (Hoffer 2005).

All the patients studied by Lewis and Piotrowski had been diagnosed manic-depressive on their first admission, but on following them up several years, the two researchers found that half of them eventually were rediagnosed schizophrenic. This raised the question, had the condition really changed its nature, or had the diagnosis been missed in the first admission? Lewis and Piotrowski found that, had the original diagnosticians taken seriously the presence of hallucinations, they would have been able to predict accurately those patients who eventually were clearly schizophrenic. The difficulty with this diagnosis was that these patients usually showed schizophrenic features when they were in a manic phase, and seldom when they were depressed or more or less normal. They analyzed the symptoms present in the first admission history and found ten factors that, if they had been taken into account, would have accurately predicted the manic-depressives who eventually became schizophrenic. Half of the factors were perceptual. This chapter by Lewis and Piotrowski should be required reading for every psychiatrist, but most of them are not even aware it has been published. Here are some of their conclusions:

a. The essential psychological trait of schizophrenia is a defect in one's criterion of reality. If this is present, the patient does not have bipolar psychosis. Conolly defined insanity as: "a disease of perception combined with an inability to judge that these changes are real or not." (1830)

b. The diagnosis of manic-depressive psychosis (bipolar) can be made only by eliminating schizophrenia.

c. The practice appears to be to diagnose schizophrenia only when the schizophrenic features are predominant and to ignore the diagnosis when the schizophrenic features are not prominent, as in spurious manic-depressives.

d. Even a trace of schizophrenia is schizophrenia. Many patients with few and mild schizophrenic signs and with a strong affective element fail to improve and spend years in institutions. (Written in 1954)

In about 1952, the great psychoanalyst Dr. Karl Menninger (Menninger Clinic) gave us a series of seminars in Saskatchewan. He had with him a little manual he had written describing in a logical and systematic way how to do the mental-state examination. During those two weeks, he, his wife, my wife, Rose, and I played a lot of bridge. When he left, he gave me this manual, which I cherished. (Unfortunately, I lent it to someone, and, as is too often the case, it never found its way back to me.)

Menninger listed four areas of mental activity that need to be examined: perception, thinking, mood, and behavior. Perception covers the senses by which we are aware of the world and of our own bodies, including vision, hearing, taste, touch, and smell. Examples of visual changes are hallucinations; examples of auditory changes are voices; but there are many more. Thinking may be disordered: the process of thinking may be compromised, as well as the content, delusions being an example. Mood may high or low or inappropriate, and the same applies to behavior, which may be overly active, too passive, or inappropriate. (These are all described in detail in our book How to Live with Schizophrenia.) This is a remarkable scheme for examining the mental state and one that I have used ever since I read his book. Unfortunately, it now appears to me that very few psychiatrists are aware of this work. Menninger's ideas of the value of perceptual changes in diagnosis are given short shrift, and too much weight is given to mood. This is a pity, as it has been known for several hundred years that perceptual changes are the key to many patients' bizarre changes in behavior (Conolly 1830).

Smith (2007) found that a substantial proportion of normal people hear voices and do not believe that they are sick and need treatment, and many are correct. Had Smith been aware of Conolly's definition of insanity, he would have been less puzzled, since hearing voices (perceptual changes) is only half of the correct definition. The person hearing voices must also believe that they are real, and may or may not act upon them resulting in psychotic behavior. Hearing voices that the person recognizes are not real does not indicate that the person is schizophrenic.

Osmond and Smythies (1952) originated the hypothesis that the experience induced in normal volunteer subjects by mescaline, the active ingredient in peyote, was in many ways a model of what happened in schizophrenic patients, and that there is a relationship between adrenalin, a catecholamine, and mescaline in chemical structure. In other words, this suggested that in the bodies of these patients, toxic substances were found that had the hallucinogenic properties of mescaline (or LSD and similar substances) and might be related to or derived from adrenalin. We did not know enough about transmethylation of noradrena-lin and its derivatives to pursue this any further. It was generally assumed that transmethylation could not occur in the body. But the basic idea was extraordinarily sound and productive, leading to our adrenochrome hypothesis (Hoffer, Osmond, and Smythies 1954)

The hallucinogenic experience, whether it was psychotomimetic or psychedelic, almost always impressed the volunteers by the striking changes in perception. This immediately drew attention to the perceptual symptoms in this psychosis. Osmond and I read many books written by patients who had recovered from the illness, and hundreds of charts about patients who were ill. The more we studied this phenomenon, the more convinced were we that perceptual changes were extremely important if we were to understand what it was like to be schizophrenic. This led to the development of the Hoffer Osmond Diagnostic (HOD) test, which we standardized on thousands of patients at four different hospitals in Saskatchewan. These results were announced in the Journal of Neuropsychiatry: editor in chief Dr. L. J. Meduna gave us the entire August 1961 vol. 2 issue.

The HOD test is a simple card-sort test with 145 cards, each one containing a statement or question. Sixty-two cards test the subjects' experiential world with perceptual changes, 38 deal with thinking and its disorders, and 44 with mood changes. It is really an examination of the way subjects experience their sensory world. Schizophrenic patients and subjects under the influence of the hallucinogens score very high. There is a very close correlation between the diagnosis of schizophrenia and the scores. But it was not a diagnostic test for schizophrenia. High scores suggest that schizophrenia should be considered seriously, but they can also be high in other conditions. We found that most schizophrenic patients scored high when sick, and as they recovered the scores decreased. During a relapse, the scores go up again. But we also found that up to one-third of other psychiatric groups also scored high. This is not surprising, considering the difficulty making clinical diagnosis. The manic-depressive patients of Lewis and Piotrowski would have also scored high. It is a simple test, easy to give, does not tire the patients, and may be used as often as one wishes. It is an excellent way to measure relapse before the patients may become aware of it. It is also cross-cultural; for example, it is being used successfully in Japan. Prof. Masaki Kakitani described its value in diagnosis and in following treatment below:

The test results also correlate very significantly with the presence of the "mauve factor" in patients' urine. With Osmond, I described a syndrome we called malvaria, as the mauve factor had not yet been identified (Hoffer and Osmond 1963). These are patients who score high on the HOD test; that is, have a lot of perceptual changes, have the mauve factor in their urine, and when treated with vitamins respond as if they were schizophrenic, no matter what their clinical diagnosis.

Carl Pfeiffer (1975) showed that the mauve factor combined with pyridoxine and zinc to produce a deficiency of both nutrients, which were thus needed in the treatment program. Before this discovery, patients with this factor were treated in Saskatchewan for schizophrenia, mainly with vitamin B3. But the addition of these two nutrients greatly improved the treatment results and decreased the need for as much vitamin B3. Pfeiffer described the syndrome under the term pyrroleuria. The dose of pyridoxine is less than 1 gram each day. It is also useful for some patients with severe premenstrual tension. Pfeiffer found that patients with this condition had clear signs such as white areas in their fingernails, stria, pain in their knees, changes in their skin, and PMS. Very few laboratories are doing this test. If patients improved, the amount of kryptopyrrole went down to normal, very low levels. A relapse was usually preceded by a recurrence of the urinary factor.

There will never be any test that will correlate perfectly with the clinical diagnosis schizophrenia, as the diagnosis is too vague, uncertain, and transient. If one day by consent physicians agree to diagnose depending upon the results of a laboratory test, then the correlation will be high. This happened with syphilis, which became a simple diagnosis after the serological blood test was developed and used as the diagnostic test. I look upon these malvarians as having a form of pellagra. I have found that mentally ill patients who score high on the HOD test, or who have above normal levels of mauve factor in their urine, or both, respond best to a program that includes vitamin B3.

When it was identified in collaboration with Pfeiffer, the term for mauve factor was changed to kryptopyrrole. They are close but not identical. It is closer to OHHPL (hydroxyhemoppyrrolin-2-one). It is a member of the pyrrole family, and may be correctly referred to as urinary pyrrole. Today, many investigators are studying this compound. Dr. Woody McGinnis heads a large study group. It appears to be a measure of oxidative stress. There is no doubt that many patients who are mentally ill suffer from oxidative stress. These include schizophrenic patients, autistic children, and a substantial proportion of other diagnostic groups.

Conolly's description of insanity, as a disease of perception combined with an inability to judge whether these changes are real, is a remarkable working diagnosis that I have found most helpful. Not only is this definition so valuable, but it also helps one to understand why schizophrenic patients have delusional symptoms. For example, if an individual lost his sense of taste (zinc deficiency) and everything tasted flat or bitter, he might ascribe this to poison being put into his food. This was a very common delusion caused by a taste misperception. It is a pity that modern psychiatry has ignored Conolly's definition in favor of that of Eugen Bleuler, which downplayed perceptual changes and emphasized thought disorder. Ironically, most modern psychiatrists, while paying lip service to Bleuler, still depend upon gross auditory and visual hallucinations before they will diagnose schizophrenia. But the modern trend is to give ever more emphasis to mood, and whenever patients are depressed, they are immediately called bipolar, and the gross perceptual changes are missed or ignored. The history of schizophrenia over the past 150 years would have been very different, and in my opinion much more positive, if Conolly's diagnostic criteria had been accepted.

Schizophrenia is characterized by the combination of perceptual changes and thought disorder. The mood changes that are almost always present are due to the biochemical changes in the body and the psychological reaction to this very serious disease. The mood disorder must be secondary to the perceptual and thought disorder. Schizoaffective disorder is present when the perceptual and thought disorder changes are present but only during the manic phase. And finally, bipolar disorder is present when there are no perceptual changes or thought disorder. Using the HOD test and similar perceptual tests will alert the clinician to the presence of these perceptual changes.

The Three Main Psychotic Disorders

Bipolar disorder is characterized by a series of mood swings, which fluctuate from mania to depression and are normal in between. There are no perceptual symptoms and thought disorder. The cycle varies tremendously from once a month to once every few years. Modern drugs will distort the typical cycle and in many cases convert depression into mania. When normal or depressed, bipolar patients do not suffer the typical schizophrenic symptoms, but when they are manic may often hear voices and see visions, which clear as the mania clears. There are thus at least two types of bipolar patients: those who never have any schizophrenic symptoms and those who do when they are manic. What, then, are we to call them? Psychiatry got around this by giving them both diagnoses. They are called schizoaffective.

They also respond differently to orthomolecular therapy. The nonschizophrenic bipolars need mood-stabilizing treatment, while the schizoaffective patients need this plus treatment for the schizophrenic component of their disease. I find that schizoaffective patients are much easier to treat than are bipolar patients and schizophrenic patients, and their response is much better.

Diagnosis can be very difficult, and often this depends more on the orientation of the diagnostician than on the disease itself. The diagnosis "schizophrenia" is so dismal and carries such a poor prognosis that many physicians prefer not to even think about it; and if their patients have mood swings, minor or major, they will call them bipolar. A large proportion of the schizophrenic patients referred to me were originally called bipolar, and their perceptual changes had been either not elicited or were ignored. In a major recent study (Weiser et al. 2001), it was found that nearly 30% of a schizophrenic population had been diagnosed with affective disorder during adolescence compared with only 7% of the general population. This confirmed what I have observed for the past 50 years, having seen over 5000 schizophrenic patients.

The Adrenochrome Hypothesis

Are the three main types of psychotic patients--bipolars, schizoaffective, and schizophrenics--related?

The adrenochrome hypothesis provides an explanation. Hoffer, Osmond, and Smythies (1954) hypothesized that schizophrenia was caused by the formation of adrenochrome in the body. Adrenochrome is the oxidized derivative from adrenalin. The reaction is activated by oxygen, accelerated by oxidizing enzymes and by copper or iron. Our research division showed how to synthesize pure crystalline adrenochrome, which later was identified in blood and other tissue and can be measured, usually by its conversion to adrenolutin. We showed that it is a hallucinogen. We based our vitamin B3 trials on the hypothesis that anything that might inhibit the formation of adrenochrome from adrenalin would be therapeutic. But adrenochrome is only one member of a class of chrome indoles that is readily made from the catecholamines: dopachrome from dopamine, noradrenochrome from noradrenalin, and adrenochrome from adrenalin.

The amount of adrenochrome that can be formed must depend upon the amount of adrenalin that the body can make. That means that under stress, when adrenalin secretion is greatly enhanced, much more is available; and since adrenalin must be removed very quickly because of its dramatic effect on blood pressure, the body will convert as much as possible to substances that do not increase blood pressure. Adrenochrome is toxic to dividing cells, and probably is one of nature's methods for controlling excess growth, like cancer, and for destroying bacteria. It is toxic to heart muscle and to neurons, as are all hallucinogens. Schizophrenic patients are more prone to heart disease.

I suggest that bipolar patients excrete large amounts of the catecholamines but do not convert as much into adrenochrome. They will not suffer the usual changes induced by this hallucinogen. Schizoaffective patients produce too much catecholamine in the manic phase. They are under extreme stress, and that is why it is only in that phase that they will make enough adrenochrome to cause the schizophrenic symptoms. Patients with severe heart failure have increased amounts of adrenolutin in their blood. In blood, adrenochrome is converted into adrenolutin. Schizophrenic patients, on the other hand, make too much adrenochrome as long as they are sick, whether they are manic or depressed.

The main prodromal symptom of oncoming mania is lack of sleep. When the patient is getting only 4 hours of sleep or less, he is in grave danger of going manic. I advised my patients of this and discussed with them what they can do to prevent this from occurring. One of my patients under very good control went to Las Vegas. He got swept up in his gambling, did not go to bed (a very bad idea), and after 36 hours was wildly manic and had to be shipped back to Victoria, once more psychotic.

I think that one of the functions of the body during sleep is to destroy and remove the products of metabolism that are no longer needed or are harmful, and I think that removing these chrome indoles is one of the functions. Normally, if deprived of sleep long enough, people become psychotic with typical hallucinations. Sleep deprivation is well known as a harbinger of bad news. And is it not interesting that visual and auditory hallucinations during sleep are called dreams, and are considered to be perfectly normal? Menninger wrote that schizophrenia was like a dream from which one did not awaken. There is some relation between hallucinations and dreams. I have seen in many patients how hearing daytime voices becomes hearing thoughts, and after a while becomes hearing similar things in their sleep. By this time they are free of the auditory hallucinations. I suggest that it takes a minimum 5 hours' sleep out of 24 to be rid of excess adrenochrome and similar chrome indoles, and that it is wiser to be some distance from that minimum.

There are other oxidized derivatives of adrenalin and other catecholamines.

Adrenolutin is toxic, as is adrenochrome. But when adrenochrome is treated with ascorbic acid under certain conditions, some of it is converted into 5,6-dihydroxy-N-methyl-indole, which was called leukoadrenochrome. This substance has antitension or antianxiety properties.

For a more elaborate discussion of the relation between the catecholamines and mental disease, see Foster and Hoffer (2004a, 2004b), Smythies (1997, 1998, 2002), and Smythies and Galzigna (1998).

Orthomolecular Treatment

The orthomolecular component of treatment of schizophrenia is described in a International Schizophrenia Foundation treatment manual and in a book of case histories written by 18 patients (Hoffer 2007a, 2007b). This was the protocol developed on the basis of the adrenochrome hypothesis. Bipolar disorders wherein adrenochrome appears to play no role will need different treatment with much more emphasis on dealing with the excessive production of the catecholamines. Drugs are used to control mania and they are very helpful, especially lithium. They are xenobiotics and difficult for the body to deal with; they should be used with great care, in the lowest possible effective dose, and not forever.

Perhaps we should consider using much larger doses of niacin to control both, since it is one of the best antagonists to adrenalin. This idea occurred to me a few months ago. A middle-aged woman told me that during the previous two years she had been forced to have hospital treatment twice because of her manic behavior. During each admission she was treated with the usual medication, but after discharge she refused to continue with the drugs. After her second admission, six months before I saw her, she again stopped all drugs and instead took niacin--30 grams twice daily. This is an enormous dose and not one that I recommend, because high doses can cause nausea and vomiting. But she had no side effects. She was mentally normal. When I asked her why she was taking so much, she replied that she felt so good that she would sooner swallow 120 niacin pills (500 mg) each day than any of the drugs she had been forced to take. Other patients have taken as much niacin, but this is very rare. I recommended to her referring physician that she should decrease the amount very slowly, consistent with her present state of good mental health. This should be investigated. Bipolar and schizoaffective patients might respond well to high doses of niacin. The dose should be increased at the first indication that they are moving into a hypomanic and later manic phase.

Certainly, niacin is much safer than lithium or any of the other such drugs currently in use. It is impossible to poison oneself with niacin as, if the dose is too high, the nausea and vomiting will soon persuade anyone to cut the dose down. Saul (2007) reported: "Over a twenty-three year period, vitamins have been connected with the deaths of a total of ten people in the United States. Poison control statistics confirm that more Americans die each year from eating soap than from taking vitamins." About half the population takes vitamins. If you are still concerned about the danger of taking niacin, read Hoffer and Foster (2007), and remember that I have been taking it since 1955, at least 3 grams daily.

References

Conolly J. An Inquiry Concerning the Indications of Insanity (1830). London: Dawsons of Pall Mall; 1964.

Foster HD, Hoffer A. Schizophrenia and cancer; the adrenochrome balanced morphism. Med Hypotheses. 2004[a];62:415-419.

--. The two faces of L-Dopa: benefits and adverse side effects in the treatment of encephalitis lethargica, Parkinson's' disease, multiple sclerosis and amyotrophic lateral sclerosis. Med Hypotheses. 2004[b];62:177-181.

Hoffer A, Osmond H. The Hallucinogens. New York: Academic Press; 1967.

Hoffer A. Adventures in Psychiatry. Toronto: Kos Press; 2005.

--. Schizophrenia Delenda Est. J Orthomol Med. 2006;21:123-139.

--. Treatment Manual. Toronto: International Schizophrenia Foundation; 2007a.

--. Mental Health Regained. Toronto: International Schizophrenia Foundation; 2007b.

Hoffer A, Foster HD. Feel Better, Live Longer With Vitamin B-3. Toronto: CCNM Press; 2007.

Hoffer A, Osmond H. Malvaria: a new psychiatric disease. Acta Psychiat Scand. 1963;39:335-366.

Hoffer A, Osmond H, Callbeck MJ, Kahan I. Treatment of schizophrenia with nicotinic acid and nicotinamide. J Clin Exper Psychopathol. 1957;18:131-158.

Hoffer A, Osmond H, Smythies J. Schizophrenia: a new approach. II. Results of a year's research. J Ment Science. 1954;100:29-45.

Kakitani M. My experience with HOD test. Personal communication. 2007.

Lewis NDC, Piotrowski ZA. Clinical diagnosis of manic-depressive psychosis. In: Hoch PH, Zubin, J, eds. Depression. New York: Grune & Stratton; 1954:25-38.

McGinnis WR. Urinary pyrrole (Mauve Factor): metric for oxidative stress in behavioral disorders. Poster presentation at: Diet and Optimal Health Conference; Linus Pauling Institute, Portland, OR; May 21, 2003.

Osmond H, Smythies J. Schizophrenia: a new approach. J Ment Sci. 1952; 98:309-315.

Pfeiffer CC. Mental and Elemental Nutrients. New Canaan, CT: Keats Publishing; 1975.

Saul A. Orthomolecular Medicine News Service. February 27, 2007. Available at: www.orthomolecular.org.

Smith DB. Muses, Madmen and Prophets. Penguin Press; 2007.

Smythies JR. Oxidative reactions and schizophrenia: a review-discussion. Schizophr Res. 1997;24:357-364.

Smythies J. Recent advances in the neurobiology of schizophrenia. Ger J Psychiatry. 1998;1;24-40.

--. The adrenochrome hypothesis of schizophrenia revisited. Neurotox Res. 2002;4:147-150.

Smythies J, Galzigna L. The oxidative metabolism of catecholamines in the brain: a review Biochim Biophys Acta. 1998;1380:159-162.

Weiser M, Reichenberg A, Rabinowitz J, et al. Association between nonpsychotic psychiatric diagnoses in adolescent males and subsequent onset of schizophrenia. Arch Gen Psychiatry. 2001;58:959-964.

[ILLUSTRATION OMITTED]

by A. Hoffer, PhD, MD, FRCP (c), RNCP (1917-2009)

Abram Hoffer was born in 1917 on a farm in Saskatchewan, Canada. He earned his MD from University of Toronto and a PhD in agricultural biochemistry from the University of Minnesota. He was director of psychiatric research from 1950 to 1967 for the Department of Public Health, Saskatchewan, and associate professor, psychiatry (research), from 1955 to 1967. Then he was in private practice from 1967 to 1976 in Saskatoon, and in Victoria, BC, until 2005. From 2006 he was a consultant in nutrition and the proper use of vitamins. With H. Osmond, he developed the first comprehensive hypothesis of schizophrenia with their adrenochrome hypothesis; this led to megavitamin treatment and later to orthomolecular treatment in association with Linus Pauling. Sometimes criticized from afar for his controversial views, he was beloved by his many patients and close colleagues. He devoted his life to the goal of curing schizophrenia, and practiced until his death in May 2009.
My experience with HOD test
  by Prof. Masaki Kakitani
  School of Psychology,
  Rissho University

  I came to know somehow the work of Dr. Hoffer when I was a graduate
  student in the United States. I stayed in the States from 1968
  through 1978. The McGovern Report came to my notice in 1978. Through
  this report I became interested in problems caused by hypoglycaemia.
  Then I encountered with KYB (Know Your Body) Club and met Dr. Kaneko.
  I joined a tour sponsored by KYB Club and I met Dr. Hoffer in New
  York City. Since I had known the existence of HOD test, I approached
  Dr. Hoffer and got his permission to translate it into Japanese. I am
  a clinical psychologist teaching Choice Theory, Reality Therapy,
  Quality School, and Lead Management. I train graduate students to
  become clinical psychologists. I would like to share some of my
  experiences in which I used HOD test.

  Case 1: Thirty five years old man. Single. Under medications. The
  client had been diagnosed as schizophrenia two years before he came
  to me for counseling. He was under medications. He was given
  risperdal (risperidone), artane, miradol, lupox, and lexotan. I asked
  him to take HOD test and he agreed. He took it three times altogether
  at different occasions. The results are shown at table 1.

  In April he began to take 3 grams of Niacin and 3 grams of Vitamin C
  per day while maintaining medications. In May Vitamin B complex (B1
  level 150mg/day) was added. In June Vitamin B6 (250mg) was added. The
  sign of improvement was shown at the table 1. He described his
  conditions saying he used to function 30% level but now 60-70% level.
  He was able to ask his doctor to reduce medications. Medications were
  changed to three from five kinds and doses were also reduced. The
  final medicine was risperidone which was most difficult to secede
  from.

  Case 2: A female college student. 20 years old. Single. She came to a
  school counselor before summer vacation. After checking the HOD test
  results the school counselor asked her when she felt this way first
  time. She said that she felt like this since her grade school. The
  school counselor talked to her parents and got their informed
  consent. She started taking Vitamin C and Niacin 3 grams each per
  day, and some Zinc. She came back to school after summer vacation and
  took HOD test again. She was found to be in a normal state. The
  results are shown at table 2.

  It was fortunate that she had not received any medications. She was
  free from some possible complications from medications.

  Case 3: A man of 36 years old. Single. Under medications. He was
  referred to me by a counselor. He was under medications. He took HOD
  test. I asked him to take the test indicating his current conditions
  and recall the worst time, which was two years before, and answer his
  worst conditions. The results are shown at table 3.

  In case three I am rather confident through HOD test results that he
  should ask his psychiatrist to reduce his medications. He would be
  fine if he could maintain his conditions without brain drugs. He
  would be starting his supplement and reducing his medications.

  These three cases show that HOD test is a useful tool for monitoring
  the progress as well as diagnosing schizophrenia in Japanese culture.
  The HOD test has not been standardized in Japan yet. We have no
  intention to do so now since the most of the questions on the test
  seem to appeal similarly to people with different cultures. The
  counselor is able to determine the level of confusions the client is
  having by looking at the HOD test results. I can say that it is a
  very useful psychological test.

Table 1

      April 7, xxxx  June 22, xxxx  July 30

TS          69            35          13
PerS        13             5           1
PS           5             1           1
DS           8             6           0
RS          8.6           5.8         2.6
SF           7             3           1

Table 2
      June 10  September 22

TS       79         14
PerS     19          3
PS        3          0
DS       13          5
RS       5.8        2.8
SF        6          2

Table 2

      His guess at worst time  March 7

S               47               10
PerS             3                0
PS              11                0
DS               7                3
RS              6.7              3.3
SF               5                0
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