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
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.
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
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
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
By 1960, a large
number of American psychiatrists had joined
us, and by 1970, I think we had a collective
experience of over 100,000 schizophrenic
patients treated. The results were really
good. They weren't perfect-we've never
claimed that-but they were certainly an
awfully lot better than what you get today
by simply taking drugs.
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
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
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
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
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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