LE Magazine January 2003

Vitamins and Minerals Help Fight Off Diseases of The Mind and The Body
Interview with Abram Hoffer, M.D., Ph.D.

Abram Hoffer, M.D., Ph.D., is an internationally recognized physician, author, medical researcher and pioneer in the use of vitamins and nutrients to treat disease. His research focusing on the use of vitamin megadoses as a schizophrenia treatment in the 1950's led to some startling observations.

Patients suffering from schizophrenic-related psychosis were able to lead normal lives after high-dose vitamin therapy. These schizophrenic patients had failed all conventional treatments, but most of them completely recovered after several months on Dr. Hoffer's therapy.

Dr. Hoffer has spent the past five decades conducting research related to the practice of orthomolecular medicine, which emphasizes the use of nutrients in optimum doses for the treatment of a wide range of diseases. His medical discoveries have been the topic of more than a dozen books and literally hundreds of research papers. Today, in his mid eighties, Dr. Hoffer continues to practice medicine, prescribing orthomolecular regimens to patients in Victoria, British Columbia, Canada. He is also the Editor-in-Chief of the Journal of Orthomolecular Medicine.

Life Extension contacted Dr. Hoffer to ask him about his 50 years of research, and how the medical profession is slowly beginning to accept his once-ignored theories of disease. In the following pages, we see why scores of patients have consulted Dr. Hoffer, and why he advocates this unique vitamin regimen to not only fight off disease, but to keep the toxins in our everyday surroundings at bay.

Life Extension Foundation: How did you get started with your research into orthomolecular medicine?

Dr. Abram Hoffer: In 1950, I had just finished my general hospital internship, and I was interested in doing some research in psychiatry. I became excited about psychosomatic medicine, which was then very popular. I approached the government of Saskatchewan, and asked them if they had a job for me. After a few months, they said yes. I didn't have any psychiatric training, but the condition was that I would take the training while on the job. My mission was to start a research program in psychiatry.

At that time, we were desperately short of psychiatrists, so the government of Saskatchewan hired a number of psychiatrists to join us. One of these was Humphrey Osmond. He brought with him a student who was a young colleague: Dr. John Smythies. These doctors had been studying mescaline, an akaloid drug that induces the [hallucinogenic] experiences in normal volunteers, which is present in peyote. They had concluded that the experience was similar to that induced by schizophrenia on normal people. Schizophrenic patients have many of the symptoms that are present in normal people when they take mescaline, or even LSD.

Drs. Osmond and Smythies had also observed that mescaline has a [biochemical] structure similar to adrenaline. They had developed the hypothesis that perhaps in the body of the schizophrenic, there might be a compound somehow related to adrenaline, which had the properties of mescaline. This was a very exciting hypothesis.

In 1950, there was no treatment for schizophrenia. Insulin coma [therapy] was disappearing; electric shock treatment was being used, but even when the results were good, they were always temporary, and you'd have to repeat it. Eventually it wouldn't work anymore. We were hopeless. Half our patients in the mental hospital were chronic schizophrenics, and we had no treatment, no drugs, nothing.

So, we decided to look at this hypothesis very carefully. I began to study all the known hallucinogens of that day. There weren't that many. One day, when I was jotting down the formula of these compounds, it suddenly struck me. They were all indoles. An indole is a chemical with a double ring. This made it much easier. If I tell the best biochemist in the world to search the schizophrenic body for a compound that causes schizophrenia, he'll think you're nuts. Of the 50,000 compounds or more, how many psychiatrists are willing to spend their whole lifetime chasing one, when they haven't got a lead? But when you're talking about indoles, you bring it down to about five or six [compounds], which makes it a lot easier.

Also, Dr. Osmond had observed oxidized adrenaline [in his research]. When some of their asthmatic patients took this discolored adrenaline, they also had some [of the same] reactions that they would get from mescaline.

LEF: That's adrenochrome, right?

Hoffer: That's right, but we didn't know it then. It turned out that, on our team, was a professor who had done his Ph.D. on adrenochrome. As we were talking about this [oxidized] compound, he told us what it was. We jotted down the structure of adrenochrome, and sure enough, it's an indole. So we said, "Now we have the right hypothesis. Let's search the human body for a compound which is an indole, which is derived from adrenaline, and which has the properties of mescaline." That was called the "adrenochrome hypothesis." That's what really started our research off.

We couldn't leave it at that, because we weren't interested in the hypothesis.

We wanted a treatment. And I knew at that time that the odds against us being correct were maybe a thousand to one. But we said we had to do something. So, we whittled down three characteristics. We said, first of all, it would have to be present in the body. Secondly, we said it must be a hallucinogen. And, thirdly, we said if we can somehow prevent the body from making it, maybe we would have a therapy.

I had taken my Ph.D. at the University of Minnesota in vitamins. And so, in 1950, I knew the vitamins as of that day. There was one vitamin, in particular, called B3 or niacin, which is a methyl acceptor; it picks up methyl groups. We felt that if we could prevent the body from making enough adrenaline by binding the methyl groups, we would prevent the methylation of noradrenaline to adrenaline, and therefore we could decrease the production of adrenochrome. We knew that niacin was very safe, so we decided to try niacin to see if it might help. We also knew that vitamin C tended to stabilize adrenalin. So, we felt if we also gave our patients vitamin C, we would cut down on the oxidation of adrenalin to adrenochrome.

Then, we got hold of some vitamins. I wrote to Merck & Company-they were the leaders in the field of vitamins at that time-and said, "This is what we're trying to do, and we're desperately poor, please, could you send us some of the vitamins?" And I listed the ones I wanted. To my amazement, two weeks later, I got a 50 pound drum of niacin, a 50 pound barrel of niacinamide and a 50 pound barrel of vitamin C.

So then, we had to make them up into 500-milligram tablets because we had concluded that the tablets then available on the market were no good. These commercial vitamins were only 100 mg in potency and they were so full of fillers that it would make people sick. Now, we had the idea let's try niacin. We also felt we'd have to give a lot because if it had been active in small quantities, someone else might have reported it [in another study].

I can recall the first patient who I treated. This was a young woman who was the head secretary of a major corporation in our city. She became psychotic, and was admitted to a hospital. She was given shock treatments; she appeared to recover, and went back to work. She had a recurrence the following Christmas, and had another one the third Christmas. By this time, I was at the hospital, and when she came in [the third] time, she was under my care. She said she had failed to respond to at least three series of ECT [electro shock therapy]. I decided she would be a good subject to test on niacin. So, I started her on niacin, 1 gram taken three times a day after meals, and also the same amount of vitamin C.

LEF: Did you titrate it up, or did you just start it three times a day?

Hoffer: I just did it [three times a day]. I kept her on it for a month, and I thought I began to see some improvement. She had been extremely paranoid and delusional. Gradually, the delusion began to disappear, and after two months, I discharged her from the hospital. I saw her again as an outpatient. She remained well, but about a year or two later, on her own, she stopped taking her vitamins. Her sister brought her in, and said, "My sister is sick again." So, I yelled at her, put her back on the same vitamins, and she made another recovery. She did this about three or four times. Finally, after she had been well for about five years, she came to me again, and said, "Dr. Hoffer, do you think I can now go off [the vitamins] without having to go back on?" I said, "Let's try." So, she went off the vitamins, and she stayed well thereafter. She went back to her job as the senior secretary at this large firm.

LEF: What took place that caused her to be able to go off of her vitamins?

Hoffer: I would say about 20% to 30% [of those who have] been well off can go off it. I don't understand it either. But that's an observation. Schizophrenia is a disease like diabetes where you have to take [the proper therapy] forever. It's not like an infection. If you have an infection, you take antibiotics for ten days, and it's gone.

So we then ran eight patients in an open pilot study, and all eight recovered. At that time, we were getting quite excited. So, then we ran the first double-blind, controlled experiments in the history of psychiatry.1 We divided 30 patients into three groups; niacin, placebo and niacinamide. Niacinamide is the other form of [vitamin] B3, but we put that in because it doesn't flush [episodic redness of the face and neck] the patients. [Otherwise], the nursing staff would assume that every patient who flushed was on niacin, and every patient who didn't flush was on placebo. It was what we called a "blind control."

Editor's Note: In studies, "control" groups include patients who are given non-therapeutic interventions to be compared with the product being tested. The "dummy" intervention is included as a control to ensure that the outcome was caused by the effect of the therapeutic intervention, and not by other means. For example, aspirin might be given to a group of patients with a headache, and an antacid is given to a "control" group of patients, who also have headaches. The likely outcome is that more patients in the "intervention" group (those who took the aspirin) will report relief than those in the "control" group. In that way, investigators can conclude that it was the aspirin that provided the effect, not the antacid.

In a "blinded" study, the patients, the investigators, or sometimes both (double-blind study) do not know whether a patient is receiving the therapy or the "dummy" intervention. In this way, scientists can ensure that the results of the study are not affected by the so-called "placebo effect." In some cases, a placebo, which has no pharmacological action but is used as a control in scientific research, can create therapeutic effects through the power of suggestion. For example, a patient might be given a sugar pill and told that it is a non-steroidal anti-inflammatory drug (NSAID) that will ease inflammatory pain. In some cases, the pain may actually subside because the patient believed the dummy pill was actually an NSAID.

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