John P. Cleary, M.D.
For 99 percent of his existence man lived in stone-age cultures
eating mainly meat. About 10,000 years ago the diet began to vary,
Cultures like the Amerinds and Esquimox have only recently changed
their dietary habits. These population groups are subject to extremely
high alcohol addiction rates.
Niacin.
In a total meat diet there is as high as 250 mg of niacin per
day while the mixed or vegetarian diet is much lower. The present
recommended daily allowance for niacin is only 20 mg. A metabolic
system which has evolved predominantly on a mostly meat diet,
and which at present only receives 20 mg of niacin daily, could
be under duress.
In 1980 a patient being treated for hyperlipidemia with 500 mg
of nicotinic acid a day (250 mg time release capsules twice daily)
reported after 4 weeks of treatment that he had stopped drinking
alcohol! After trying the niacin on ten more patients with success,
the author searched biochemical publications to see if other researchers
had discovered a possible mechanism of action.
History of niacin use.
Late in the l930s nicotinic acid was used to treat the recognized
deficiency state called pellagra in doses of 500 mg daily. Cases
of pellagra were found in chronic alcoholics, but apparently the
disease has frequently gone undetected because the skin lesions
were absent or late in appearance.
Ishil and Nishihars' research.
Recent work discusses unsuspected and undiagnosed pellagra in
terminally ill alcoholics. In 1981. Ishii and Nishihara1 reported
twenty alcoholic patients with pellagra; the pellagra was discovered
only after autopsy. Autopsies revealed classical neuropathological
findings of pellagra in brain sections of these patients. Typically
these alcoholics would enter the hospital confused, disoriented
and agitated. Later diarrhea occurred which did not respond to
any treatment and the patient expired from bronchopneumonia. This
occurred despite treatment with antibiotics, vitamins B1, B6,
B12, and C and the use of antidiarrheal agents. After reviewing
these twenty patients, Ishii and Nishihara found four new patients
with pellagra who had identical symptoms as the first twenty.
These four people were treated with all of the previous medications,
but niacin was added. The four niacin-treated patients recovered.
Typical pellagrin skin lesions had not appeared at any time on
these last four patients, just as they had not appeared on the
twenty patients who died and were autopsied.
Smith's research.
Dr. Russell Smith carried on an early investigation of the niacin
treatment for alcoholism in the 1960s.2 Smith was inspired by
Hoffer and 0smond who treated patients with schizophrenia, and
alcoholics with schizophrenia, with very high doses of niacin
(3-20 grams a day). The latter alcoholic-schizophrenic group had
good success as a result of this niacin treatment. Smith reported
500 such patients treated over a five year period using three
or more grams of niacin daily. Smith had a 50-60% success rate.
Smith's work was apparently ignored, perhaps because he could
not offer a biochemical explanation for the mechanism of action,
The biochemistry of action of niacin in the treatment of alcohol
addiction.
Acetalaldhyde is the key to understanding the biochemistry of
alcohol addiction. Lindros in 1982 , 3 explained that acetaldehyde
is the first intermediate step in the pathway to the oxidation
of ethanol. Alcohol is metabolized in two stages: (1) by the enzymes,
alcohol dehydrogenase and aldehyde dehydrogenase. These enzymes
require NAD (nicotinamide adenine dinucleotide) as a coenzyme.
In alcoholics the first stage reaction is faster than in normal
or control subjects, (2) The second stage involves metabolism
of acetaldehyde to acetate. In alcoholics this reaction is decreased
compared to normal. The net result is the accumulation of acetaldehyde
and the elevation of acetaldehyde in the blood and (more importantly)
in the brain tissues. The reason for alcohol addiction in humans.
Davis in 1970,4 showed that acetaldehyde condenses with dopamine
in the brain to form morphine-like compounds. These substances
bind to opiate receptors. This is the cause for addiction to alcohol
in humans.
Unwin's contributions.7
In the course of investigating the effects of acetaldehyde and
alcohol on mice, Unwin, 1982, in England, noted that there was
no observable difference between giving a 4.5 grams per kilogram
dose of ethanol subcutaneously or a 0.3 ml of acetaldehyde per
kilogram, subcutaneously. Both caused sedation for two hours with
loss Of MUSCU14T co-ordination. Thus the active substance is the
acetaldehyde. Alcohol is just a means for generating acetaldehyde.
It is the acetaldehyde that then condenses with dopamine.
Eriksson's study.5
In 1974 C.J. Eriksson showed that Acetalaldhyde levels in rats
could be cut in half by using an increase of nicotinamide. The
probable mechanism of action for niacin treatment of alcohol addiction
in humans is that niacin also reduces acetaldehyde levels in the
brain. This interrupts acetaldehyde and dopamine condensations
to the morphine-like compounds, thus stopping the patient's addiction
to alcohol.
McElfresh and McDonald's experiments.6
The most recent work has been done by biochemical geneticists.
In 1983, McElfresh and McDonald showed that fruit flies exposed
to lO% alcohol in the air had reduced levels of nicotinamide adenine
dinucleotide (NAD). NAD is the alcohol-exposed fruit flies was
reduced to 20% compared with the controls. Both Eriksson's and
the McElfresh-McDonald studies suggest that giving excess NAD
in the form of niacin has an impact on lowering the acetaldehyde
levels in organisms exposed to recurrent alcohol use.
Conclusion.
It is concluded that at least 10% of the population suffers from
a niacin deficiency that manifests itself in the disease state
known as alcohol addiction. This group's minimum daily requirement
of niacin appears to be about 125 mg to 250 mg. Treatment of active
alcohol addiction requires about 500 mg of niacin per day,
References