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<td><b><font face="Arial,Helvetica"><font size=+1>Coronary Disease, Cancer,
Diabetes... and Niacin</font></font></b></td>
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<td VALIGN=TOP WIDTH="132"><font color="#FF0000">Bypass a Coronary</font>
<br><a href="index.html">Home</a></td>
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<td VALIGN=TOP><b><font face="Arial,Helvetica">Niacin, Coronary Disease
and Longevity</font></b>
<br><b><font face="Arial,Helvetica">by Abram Hoffer, M.D., Ph.D.</font></b>
<p><b><i><font face="Arial,Helvetica">Background</font></i></b>
<br><font face="Arial,Helvetica">In 1954, it was impossible to predict
or even to think that my bleeding gums would one day, 31 years later, lead
to additional useful life to people with coronary disease related to cholesterol
and lipid metabolism. That year, malocclusion of my teeth had broken down
the ability of my gum tissue to repair itself quickly enough. Because my
bite was not correct there was too much wear and tear on tooth sockets
and my gums began to bleed. No amount of vitamin C and no amount of dental
repair helped. Eventually I reconciled myself to the idea I would soon
have all my teeth extracted.</font>
<p><font face="Arial,Helvetica">But at this time I had been treating schizophrenics
and seniles and a few other diseases with niacin, and I began also to take
this vitamin, 1 gram after each meal, i.e. three grams per day. I did so
because I wanted to experience the flush which comes when one first takes
niacin and its gradual waning with continuing use so I could discuss this
reaction more knowledgeably with my patients. There was also a legal issue
- most doctors' defence against malpractice suits is that they were doing
what any other similar physician would do it like circumstances. If I were
sued (I have never been sued) because of unusual discomfort or because
of adverse effects from niacin, I would not be able to use that defence
since only a handful of physicians had ever used these large quantities
of niacin. I had concluded that if the unlikely did occur and I was charged
with malpractice, one of my defences would be that I had tried it myself
for at least three months without suffering any serious consequences. I
must admit I had not discussed this with any litigation lawyer. My reasons
were therefore both practical and paranoid. I had no intention of treating
myself or my bleeding gums.</font>
<p><font face="Arial,Helvetica">Two weeks after I had started taking niacin
my gums were normal. I was brushing my teeth one morning and suddenly awakened
in surprise there was no bleeding whatever! A few days later my dentist
confirmed my gums were no longer swollen, and I still have most of my teeth.
Eventually I reasoned that the niacin had restored the ability of my gum
tissue to repair itself faster than I could damage it by chewing with my
crooked teeth.</font>
<p><font face="Arial,Helvetica">A few months later I was approached by
Prof. Rudl Altschul, Chairman, Department of Anatomy, College of Medicine,
University of Saskatchewan. He had taught neurohistology and I had been
one of his students. Prof. Altschul had discovered how to produce arteriosclerosis
in rabbits. He fed them a cake baked by his wife, Anna, which was rich
in egg yolks. Rabbits fed cooked egg yolk promptly developed hypercholesterolemia
and later arteriosclerotic lesions on their coronary vessels (Altschul
and Herman, 1954). Altschul had also discovered that irradiating these
hypercholesterolemic rabbits with ultraviolet light decreased their cholesterol
levels. He wanted to extend this research by irradiating human subjects,
but not one internist in Saskatoon would allow him access to their patients.
People who bake in the southern sunshine may wonder why this "dangerous"
treatment received such a negative response. Prof. Altschul thus approached
me, as Director of Psychiatric Research, Department of Health, Saskatchewan,
I had access to several thousand patients in our two mental hospitals.
I agreed to this provided that Dr. Humphry Osmond, Superintendent of the
Saskatchewan Hospital at Weyburn also agreed. This treatment was innocuous,
would not cost us anything and would help us create more of an investigative
attitude among our clinical staff. But before we started I requested
that Prof. Altschul meet with our clinical staff and present his ideas
to them.</font>
<p><font face="Arial,Helvetica">A few weeks later he came to Regina by
train and I drove him to Weyburn in my car to meet Dr. Osmond and his staff.
On the way down and back we discussed our work. He gave me an interesting
review of how he saw the problem of arteriosclerosis, which he considered
to be a disease of the intima, the inner lining of the blood vessels. He
hypothesized that the intima had lost its ability to repair itself quickly
enough. As soon as I heard this I thought of my bleeding gums and of my
own repair hypothesis. I then told him of my recent experience. I asked
him if he would be willing to test niacin which if it had the same effect
on the intima as it had had on my bleeding gums might have antiarteriosclerotic
power. Prof. Altschul was intrigued and agreed to look at the idea if he
could get some niacin. I promptly sent him one pound of pure, crystalline
niacin from a supply I had received earlier, courtesy of Merck and Company,
now Merck, Sharp and Dohme.</font>
<p><font face="Arial,Helvetica">One evening about three months later I
received a call from Prof. Altschul who began to shout, "It works! It works!"
Then he told me he had given niacin to his hyperlipidemic rabbits and within
a few days their cholesterol levels were back to normal. He had discovered
the first hypocholesterolemic substance. Drug companies were spending millions
to find such a compound.</font>
<p><font face="Arial,Helvetica">But did it also work in humans? The next
day I approached Dr. J. Stephen, Pathologist, General Hospital, Regina.
I was a biochemical consultant to him. I outlined what had been done and
wanted his help in some human experiments. I assured him niacin was safe
and we would only need to give a few grams to patients. He promptly agreed.
He said he would order his technicians to draw blood for cholesterol assay
from a large variety of patients, would then given them niacin and would
follow this with another cholesterol assay. I suggested we discuss this
with the patients' physicians but Dr. Stephen laughed and said they did
not know what went on in hospital and that to contact each one would probably
make the study impossible. A few weeks later the data poured in: niacin
also lowered cholesterol levels in people. The greater the initial or baseline
level, the greater the decrease.</font>
<p><font face="Arial,Helvetica">We published our results (Altschul, Hoffer
and Stephen, 1955). This report initiated the studies which eventually
proved niacin increases longevity. Because of its importance, this paper
is reproduced here. Note, it was not double blind. However, patients did
not know what they were getting or why they were getting it. This type
of impromptu research is forever impossible with ethics committees, informed
consent and so on. Thirty years ago only the integrity of physicians protected
patients against experimental harm.</font>
<p><font face="Arial,Helvetica">At the same time we were examining the
effect of niacin on cholesterol levels, Russian scientists were also measuring
the effect of vitamins on blood lipids but they used very little niacin
and found no significant decreases, Simonson and Keyes (1961).</font>
<p><font face="Arial,Helvetica">The finding that niacin lowered cholesterol
was soon confirmed by Parsons, Achor, Berge, McKenzie and Barker (1956)
and Parsons (1961, 1961a, 1962) at the Mayo Clinic which launched niacin
on its way as a hypocholesterolemic substance. Since then it has been found
to be a normalizing agent, i.e. it elevates high density lipoprotein cholesterol,
decreases low density and very low density lipoprotein cholesterol and
lowers triglycerides. Grundy, Mok, Zechs and Berman (1981) found it lowered
cholesterol by 22 percent and triglycerides by 52 percent and wrote, "To
our knowledge, no other single agent has such potential for lowering both
cholesterol and triglycerides."</font>
<p><b><i><font face="Arial,Helvetica">The Coronary Study</font></i></b>
<br><font face="Arial,Helvetica">The only reason for being concerned about
elevated cholesterol levels is that this is associated with increased risk
of developing coronary disease. The association between cholesterol levels
in the diet and coronary disease is not nearly as high even though the
total diet is a main factor. The kind of diet generally recommended by
orthomolecular physicians will tend to keep cholesterol levels down in
most people. This diet can be described as a high fiber, sugar-free diet
which is rich in complex polysaccharides such as vegetables and whole grains.</font>
<p><font face="Arial,Helvetica">Once it became possible to lower cholesterol
levels even with no alteration in diet, it became possible to test the
hypothesis that lowering cholesterol levels would decrease the risk of
developing coronary disease. Dr. E. Boyle, then working with the National
Institute of Health, Washington, D.C., quickly became interested in niacin.
He began to follow a series of patients using 3 grams (3,000 milligrams)
of niacin per day. He reported his conclusions in a document prepared for
physicians in Alcoholics Anonymous by Bill W (1968). In this report Boyle
reported that he had kept 160 coronary patients on niacin for ten years.
Only six died against a statistical expectation that 62 would have died
with conventional care. He stated, "From the strictly medical viewpoint
I believe all patients taking niacin would survive longer and enjoy life
much more."</font>
<p><font face="Arial,Helvetica">His prediction came true when the National
Coronary Drug Study was evaluated by Canner recently. But E. Boyle's data
spoke for itself. Continuous use of niacin will decrease mortality and
prolong life. Perhaps Boyle's study was one of the reasons the Coronary
Drug Project was started in 1966. Dr. Boyle was an advisor to this study
which was designed to assess the long term efficacy and safety of five
compounds in 8341 men, ages 30 to 64, who had suffered a myocardial infarction
(heart attack) at least three months before entering the study.</font>
<p><font face="Arial,Helvetica">The National Heart and Lung Institute supported
this study. It was conducted at fifty-three clinical centres in twenty-six
American states and was designed to measure the efficacy of several lipid
lowering drugs and to determine whether lowering cholesterol levels in
patients with previous mycardial infarcts would be beneficial. Niacin,
two dosage strengths of estrogens, Clofibrate, dextrothyroxine and placebo
were tested.</font>
<p><font face="Arial,Helvetica">Eighteen months after the study began,
the higher dose estrogen group in the study was discontinued because of
an excess of new non-fatal myocardial infarctions compared to placebo.
The thyroxine group was stopped for the same reason for patients with frequent
ectopic ventricular beats. After thirty-six months dextrothyroxin was discontinued
for the rest of this group, again because myocardial infarcts were increased.
After fifty-six months the low dose estrogen group study was stopped. There
had been no significant benefit to compensate for the increased incidence
of pulmonary embolism and thrombophlebitis and increased mortality from
cancer. Eventually only niacin, Clofibrate and placebo groups were continued
until the study was completed.</font>
<p><b><i><font face="Arial,Helvetica">Canner's Study (1985)</font></i></b>
<br><font face="Arial,Helvetica">Dr. Paul L. Canner, Chief Statistician,
Maryland Medical Research Institute, Baltimore, examined the data for the
Coronary Drug Project Research Group. About 8000 men were still alive at
the end of the treatment trial in 1975. This new study was begun in 1981
to determine if the two estrogen regimens and the dextrothyroxine regimen
had caused any long term effects. High dose estrogen had been discontinued
because it increased non-fatal myocardial infarctions, low dose estrogen
increased cancer deaths and dextrothyroxine increased total mortality,
i.e. compared to placebo, Clofibrate and niacin. None of the subjects continued
to take the drugs after 1975.</font>
<p><font face="Arial,Helvetica">The 1985 follow-up study showed no significant
differences in mortality between those treatment groups which had been
discontinued and placebo or Clofibrate. However, to the investigator's
surprise, the niacin group fared much better. The cumulative percentage
of deaths for all causes was 58.4%, 56.8%, 55.9%, 56.9% and 50.6% for low
dose estrogens, high dose estrogens, Clofibrate, dextrothyroxine, placebo
and niacin, respectively. </font>
<p><font face="Arial,Helvetica">The mortality in the niacin group was 11
percent lower than in the placebo group (P = 0.002). The mortality benefit
from niacin was present in each major category or cause of death: coronary,
other cardiovascular, cancer and others. Analysis of life table curves
comparing niacin against placebo showed the niacin patients lived two years
longer. With an average followup of fourteen years, there were 70 fewer
deaths in the niacin group than would have been expected from the mortality
in the placebo group. Patients with cholesterol levels higher than 240
mg per 100 mL benefited more than those with lower levels.</font>
<p><font face="Arial,Helvetica">What is surprising is that the niacin benefit
carried on for such a long period even after no more was being taken. In
fact the benefit increased with the number of years followed up. It is
highly probable the results would have been much better if patients had
not stopped taking niacin in 1975. Thus, E. Boyle's patients who remained
on niacin for ten years and received individual attention had a<b><i> 90
percent decrease in mortality.</i></b> With the huge coronary study this
type of individual attention for the majority of patients was not possible.
Many dropped out because of the niacin flush, of these many could have
been persuaded to remain in the study if they had been given more individual
attention. This is very hard to do in a large scale clinical study of this
type. Dr. Boyle, in discussions with me, referred to this as one of the
defects in the Coronary Drug Study. I would conclude that the proper use
of niacin for similar patients should decrease mortality somewhere between
11 and 90 percent after a ten year follow-up, with the reduction in mortality
increasing as the safe natural substance which will decrease mortality
and increase longevity especially in patients with elevated cholesterol
levels.</font>
<p><font face="Arial,Helvetica">The National Institute of Health (1985)
released the conclusions reached by a consensus development conference
on lowering blood cholesterol to prevent heart disease held December 10
- 12, 1984. This was followed by an NIH conference statement, "Lowering
Blood Cholesterol to Prevent Heart Disease," Volume 5, No. 7. This statement
reports that heart disease kills 550,000 Americans each year and 5.4 million
are ill. Total costs of heart disease are $60 billion per year. Main risk
factors include cigarette smoking, high blood pressure and high blood cholesterol.
NIH recommends that the first step in treatment should be dietary and their
recommendations are met by the orthomolecular diet. But when diet alone
is not adequate, drugs should be used. Bile-acid sequestrants and niacin
are favoured while the main commercial drug, Clofibrate, is not recommended
"because it is not effective in most individuals with a high blood cholesterol
level but normal triglyceride level. Moreover, an excess of overall mortality
was reported in the World Health Organization trial of this drug." </font>
<p><font face="Arial,Helvetica">Since niacin is effective only in megavitamin
doses, 1 gram three times per day, NIH is at last promoting megavitamin
therapy. The National Institute of Health asked that their conference statement
be "posted, duplicated and distributed to interested staff ". Since every
doctor has patients with high blood cholesterol levels, they should all
be interested. In fact, if they are not, some of them will be facing litigation
from angry wives whose husbands have not been treated with niacin for their
elevated cholesterol levels.</font>
<p><b><i><font face="Arial,Helvetica">Niacin Combined With Other Drugs
Which Lower Cholesterol</font></i></b>
<br><font face="Arial,Helvetica">Familial hypercholesterolemia is an inherited
disease where plasma cholesterol levels are very high. Illingworth, Phillipson,
Rapp and Connor (1981) described a series of 13 patients treated with Colestipol
10 grams twice daily and later 15 grams twice daily. Their cholesterol
levels ranged from 345 to 524 and triglycerides from 70 to 232. When this
drug plus diet did not decease cholesterol levels below 270 mg/100 mL they
were given niacin, starting with 250 mg three times daily and increasing
it every two to four weeks until a final dose of 3 to 8 grams per day was
reached. To reduce the flush patients took aspirin (120 to 180 mg) with
each dose for four to six weeks. With this dose of niacin they found no
abnormal liver function test results. This combination of drugs normalized
blood cholesterol and lipid levels. They concluded, "In most patients with
heterozygous familial hypercholesterolemia, combined drug therapy with
a file acid sequestrant and nicotinic acid (niacin) results in a normal
or near normal lipid profile. Long term use of such a regimen affords the
potential for preventing, or even reversing, the premature development
of atherosclerosis that occurs so frequently in this group of patients."</font>
<p><font face="Arial,Helvetica">At about the same time Kane, Malloy, Tun,
Phillips, Freedmand, Williams, Rowe and Havel (1981) reported similar results
on a larger series of 50 patients. They also studied the combined effect
of Colestipol and Clofibrate. Abnormalities of liver function only occurred
when the dose of niacin increased rapidly. The first month they took 2.5
grams per day, the second month 5.0 grams per day and 7.5 grams per day
the third month and thereafter. In a few blood sugar went up a little (from
115 to 120 mg), and uric acid levels exceeded 8 mg percent in six. None
developed gout. All other tests were normal. They concluded, "The remarkable
ability of the combination of Colestipol and niacin to lower circulating
levels of LDL and to decrease the size of tendon xanthomas suggests that
this combination is the most likely available regimen to alter the course
of atherosclerosis." The combination of Colestipol and Clofibrate was not
as effective. For the first time it is possible to extend the life span
of patients with familial hypercholesterolemia.</font>
<p><font face="Arial,Helvetica">Fortunately, niacin does not decrease cholesterol
to dangerously low levels. Cheraskin and Ringsdorf (1982) reviewed some
of the evidence which links low cholesterol levels to an increased incidence
of cancer and greater mortality in general. Ueshima, Lida and Komachi (1979)
found a negative correlation between cholesterol levels between 150 and
200 and cerebral vascular disorders (r = .83). Mortality increased for
levels under 160 mg.</font>
<p><font face="Arial,Helvetica">Hoffer and Callbeck (1957) reported that
the hypocholesterolemic action of niacin was related to the activity of
the autonomic nervous system. We referred to a previous study by Altschul
and Hoffer where we found on normal volunteers (medical students) that
there was a linear relationship between the effect of niacin in lowering
cholesterol, the initial cholesterol levels and body weight. The regression
equation was Y = 0.95X - 0.39Z - 90 where Y is the decrease in cholesterol
level in milligrams, X is the initial cholesterol value and Z the body
weight in pounds. The multiple correlation coefficient is 0.83. When Y
= 0 niacin has no effect on cholesterol levels. When Y is negative it means
the cholesterol levels were elevated by niacin. This might then be a good
indication of the optimum cholesterol levels. For a 200 pound patient Y
= 0 when X is 176 mg, and for a 150 pound subject Y = 0 when X is 156 mg.
This is remarkably close to the optimum values recommended by Cheraskin
and Ringsdorf and others, i.e, 180 to 200 milligrams.</font>
<p><font face="Arial,Helvetica">Hoffer and Callbeck found that niacin also
lowered cholesterol levels of schizophrenic patients, but the schizophrenic
response was represented by a different equation Y = 0.28X -0.43Z + 53.
This is shown in the following table where expected decreases in cholesterol
are calculated from two equations. (See Table 3 page 220.) i.e. at higher
levels niacin decreases cholesterol levels more in normal subjects while
at lower levels niacin did not increase the level of cholesterol. Again
niacin elevated levels in normal subjects from 150 to 176, decreased it
from 200 to 178 and from 250 to 181 mg.</font>
<p><b><i><font face="Arial,Helvetica">How Does Niacin Work?</font></i></b>
<br><font face="Arial,Helvetica">Niacin, but not niacinamide, lowers cholesterol
levels even though both forms of Vitamin B3 are anti pellagra and are almost
equally effective in treating schizophrenia and arthritis and a number
of other diseases. Niacin also differs from niacinamide because it causes
a flush to which people adapt readily while niacinamide has no vasodilation
activity in 99</font>
<br><font face="Arial,Helvetica">percent of people who take it. For reasons
unknown, about 1 in 100 persons who take niacinamide do flush. They must
be able to convert niacinamide to niacin in their bodies at a very rapid
pace. There must be a clue here somewhere. It is believed that niacin causes
a flush by a complicated mechanism which releases histamine, interferes
in prostaglandin metabolism, may be related to serotonin mechanism and
may involve the cholinergic system, Rohte, Thormahlen and Ochlich (1977). </font>
<p><font face="Arial,Helvetica">Histamine is clearly involved. The typical
niacin flush is identical with the flush produced by an injection of histamine.
It is dampened down if not prevented entirely by anti-histamines and by
tranquilizers. The adaptation to niacin is readily explained by the reduction
in histamine in the storage sites such as the mast cells. When these are
examined after a dose of histamine, these cells contain empty vesicles
which contained the histamine and also heparinoids. If the next dose is
spaced closely enough there will have been no time for the storage sites
to be refilled and therefore less histamine will be available to be released.
After there is complete adaptation to niacin a rest of several days will
start the flushing cycle again. This decrease in histamine has some advantage
in reducing the effects of rapidly released histamine. Dr. Ed Boyle found
that guinea pigs treated with niacin were not harmed by anaphylactic shock.
Because the flush is relatively transient it can not be involved in the
lowering of cholesterol which remains in effect as long as medication is
continued. Prostaglandins appear to be involved. Thus, aspirin, Kunin (1976),
and indomethacin, Kaijser, Eklund, Olsson and Carlson (1979) reduce the
intensity of the flush, Estep, Gray and Rappolt (1977).</font>
<p><font face="Arial,Helvetica">In 1983 I suggested that niacin lowered
cholesterol because it releases histamine and glycosaminoglycans. Niacinamide
does not do so (Hoffer, 1983). Mahadoo, Jaques and Wright (1981) had earlier
implicated a histamine-glycosaminoglycan histaminase system in lipid absorption
and redistribution. Boyle (1962) found that niacin increased basophil leukocyte
count. These cells store heparin as well as histamine. He suggested that
the improvement caused by niacin is much greater than can be explained
by its effect on cholesterol. "Possibly," he wrote, "it is due to release
of histamine and also to the eventual marked diminution in the intravascular
sludging of blood cells."</font>
<p><font face="Arial,Helvetica">It is possible the beneficial effect of
niacin is not due to the cholesterol effect but is due to a more basic
mechanism. Are elevated cholesterol levels and arteriosclerosis both the
end result of a more basic metabolic disturbance still not identified?
If it were entirely an effect arising from lowered cholesterol levels,
why did Clofibrate not have the same beneficial effect? An enumeration
of some other properties of niacin may one day lead to this basic metabolic
fault. Niacin has a rapid anti sludging effect. Sludged blood is present
when the red blood cells clump together. They are not able to traverse
the capillaries as well, as they must pass through in single file. This
means that tissues will not receive their quota of red blood cells and
will suffer anoxemia. Niacin changes the properties of the red cell surface
membrane so that they do not stick to each other. Tissues are then able
to get the blood they need. Niacin acts very quickly. Niacin increases
healing, as it did with my gums. Perhaps it has a similar effect on the
damaged intima of blood vessels.</font>
<p><font face="Arial,Helvetica">Within the past few years adrenalin via
its aminochrome derivatives has been implicated in coronary disease. If
this becomes well established it provides another explanation for niacin's
beneficial effect on heart disease. Beamish and his coworkers (1981, 1981a,
1981b) in a series of reports showed that myocardial tissue takes up adrenalin
which is converted into adrenochrome, that it is the adrenochrome which
causes fibrillation and heart muscle damage. They further found that Anturan
protects against fibrillation induced by adrenochrome and suggest this
is supported by the clinical findings that Anturan decreases mortality
from heart disease.</font>
<p><font face="Arial,Helvetica">Under severe stress as in shock or after
injection of adrenalin, a large amount of adrenalin is found in the blood
and absorbed by heart tissue. Severe stress is thus a factor whether or
not arteriosclerosis is present, but it is likely an arteriosclerotic heart
can not cope with stress as well. Fibrillation would increase demand for
oxygen which could not be met by a heart whose coronary vessels are compromised.</font>
<p><font face="Arial,Helvetica">Niacin protects tissues against the toxic
effect of adrenochrome, in vivo. It reverses the EEG changes induced by
intravenous adrenochrome given to epileptics, Szatmari, Hoffer and Schneider
(1955), and also reverse the psychological changes, Hoffer and Osmond (1967).
In synapses NAD is essential for maintaining noradrenalin and adrenalin
in a reduced state. These catecholamines lose one electron to form oxidized
amine. In the presence of NAD this compound is reduced back to its original
catecholamine. If there is a deficiency of NAD the oxidized adrenalin (or
noradrenalin) loses another electron to form adrenochrome (or noradrenochrome).
This change is irreversible. The adrenochrome is a synaptic blocking agent
as is LSD. Thus niacin which maintains NAD levels decreases the formation
of adrenochrome. It is likely this also takes place in the heart and if
it does it would protect heart muscles from the toxic effect of adrenochrome
and from fibrillation and tissue necrosis. None of the other substances
known to lower cholesterol levels are known to have this protective effect.
Niacin thus has an advantage: (1) in lowering cholesterol and, (2) in decreasing
frequency of fibrillation and tissue damage.</font>
<p><b><i><font face="Arial,Helvetica">Niacin as a Treatment for Acute Coronary
Disease</font></i></b>
<br><font face="Arial,Helvetica">Altschul (1964) reviewed the uses of niacin
clinically where it is used as soon as possible after an acute event. Goldsborough
(1960) used both niacin and niacinamide in this way. Patients with a coronary
thrombosis were given niacin 50 mg by injection subcutaneously and 100
mg sublingually. As the flush developed the pain and shock subsided. If
pain recurred when the flush faded another injection was given, but if
pain was not severe another oral dose was used. Then he used 100 mg three
times daily. If the flush was excessive he used niacinamide.</font>
<p><font face="Arial,Helvetica">Between 1946 and 1960 he treated 60 patients,
24 with acute infarction and the rest with angina. From the 24 patients,
six died. Four of the angina patients also had intermittent claudication
which was relieved. Two had pulmonary embolism and also responded.</font>
<p><font face="Arial,Helvetica">Niacin should be used before and after
every coronary bypass surgery. Inkeless and Eisenberg (1981) reviewed the
evidence related to coronary artery bypass surgery and lipid levels. There
is still no consensus that this surgery increases survival. In most cases
the quality of life is enhanced and 75 percent get partial or complete
relief of angina. I believe a major problem not resolved by cardiovascular
surgery is how to halt the arteriosclerotic process. Inkeles and Eisenberg
report that autogenous vein grafts implanted in the arterial circuit are
more susceptible than arteries to arteriosclerosis. In an anatomic study
of 99 saphenous vein grafts from 55 patients who survived 13 to 26 months,
arteriosclerosis was found in 78 percent of hyperlipidernic patients. Aortic
coronary bypass grafting accelerates the occlusive process in native vessels.</font>
<p><b><i><font face="Arial,Helvetica">If patients were routinely placed
on the proper diet and if necessary niacin long before they developed any
coronary problems, most if not all the coronary bypass operations could
be avoided. If every patient requiring this operation were placed upon
the diet and niacin following surgery, the progress of arteriosclerosis
would be markedly decreased. </font></i></b><font face="Arial,Helvetica">Then
surgeons would be able to show a marked increase in useful longevity. One
would hope to have the combined skills of a top cardiac surgeon and a top
internist using diet and hypocholesterolemic compounds.</font>
<p><b><i><font face="Arial,Helvetica">Conclusion</font></i></b>
<br><font face="Arial,Helvetica">Niacin increases longevity and decreases
mortality in patients who have suffered one myocardial infarction. <i>The
Medical Tribune</i>, April 24,2985, properly expressed the reaction of
the investigators by heading their report, "A Surprise Link to Longevity:
It's Nicotinic Acid." Had they taken Ed Boyle's finding seriously they
would not have been surprised and would have gotten even better results.</font>
<p><font face="Arial,Helvetica">Note: In 1982 Keats published my review
of Vitamin B3 (Niacin). This present review concentrates in greater detail
on only one aspect of niacin's many beneficial properties. The two should
be read together as they are companion reports.</font>
<p><font face="Arial,Helvetica">Derivatives of niacin have been examined
for their ability to alter lipid levels as well as niacin. It would be
advantageous if the niacin vasodilation (flush) were eliminated or removed.
The main disadvantage of the niacin derivatives will be cost. <b><i>Inositol
hexanicotinate</i></b> is an ester of inositol and niacin. In the body
it is slowly hydrolyzed releasing both of these important nutrients. The
ester<b><i> is more effective than niacin in lowering cholesterol and triglyceride
levels</i></b>, Abou El-Enein, Hafez, Salem and Abdel (1983). I have used
this compound, Linodil, available in Canada but not the U.S.A. (at the
time this paper was written) for thirty years for patients who can not
or will not tolerate the flush. It is very gentle, effective, and can be
tolerated by almost every person who uses it.</font>
<p><font face="Arial,Helvetica">Niacin is effective in decreasing the death
rate and in expanding longevity for other conditions, not only cardiovascular
diseases. It acts by protecting cells and tissues from damage by toxic
molecules or free radicals.</font>
<p><font face="Arial,Helvetica">One of the most exciting findings is that
<b><i>niacin
will protect against cancer. </i></b>A conference at Texas College of Osteopathic
Medicine at Fort Worth early this year, was the eighth conference to discuss
niacin and cancer. (Titus,1987). The first was held in Switzerland in 1984.</font>
<p><font face="Arial,Helvetica">In the body niacin is converted to nicotinamide
adenine dinucleotide (NAD). NAD is a coenzyme to many reactions. Another
enzyme, poly (Adenosine adenine phosphate ribose) polymerase, uses NAD
to catalyze the formation of ADP-ribose. The poly (ADP-ribose) polymerase
is activated by strands of DNA broken by smoke, herbicides, etc. When the
long chains of DNA are damaged, poly (ADP-ribose) helps repair it by unwinding
the damaged protein. Poly (ADP-ribose) also increases the activity of DNA
ligase. This enzyme cuts off the damaged strands of DNA and increases the
ability of the cell to repair itself after exposure to carcinogens.</font>
<p><font face="Arial,Helvetica">Jacobson and Jacobson (Hostetler (1978)
believe niacin (more specifically, NAD) prevents processes which lead to
cancer. They found that <i>one group of human cells given enough niacin
and then exposed to carcinogens developed cancer at a rate only one-tenth
of the rate in the same cells not given niacin.<b> </b></i>Cancer cells
are low in NAD.</font>
<p><font face="Arial,Helvetica">It is not surprising that niacin also decreased
the death rate from cancer in the National Coronary Drug Study. The first
cancer case I treated was given niacin 3 grams per day and ascorbic acid
3 grams per day, Hoffer (1970).</font>
<p><font face="Arial,Helvetica">Niacinamide also increases the production
of NAD. Three grams per day given to juvenile diabetics produced remissions
in a large proportion of these young patients, Vague, Vialettes, Lassman-Vague,
and Vallo (1987). They concluded, "Our results and those from animal experiments
indicate that, in <b><i>Type I diabetes</i></b>, nicotinamide slows down
the destruction of B cells and enhances their regeneration, thus extending
remission time." See also Yamada, Nonaka, Hanafusa, Miyazaki, Toyoshima
and Tarui (1982). Kidney</font>
<br><font face="Arial,Helvetica">tissue is protected by niacinamide, Wahlberg,
Carlson, Wasserman and Ljungqvist (1985). It protected rats against the
diabetogenic effect of Streptozotocin. Clinically niacin has been used
to successfully treat patients with severe gIomerulonephritis. One of my
patients was being readied for dialysis. Her nephrologist had advised her
she would die if she</font>
<br><font face="Arial,Helvetica">refused. She started on niacin 3 grams
per day. She is still well twenty-five years later.</font>
<p><font face="Arial,Helvetica">Niacin and niacinamide are protective in
a large number of diseases. I will refer to one or more its ability to
reduce fluid loss in cholera, Rabbani, Butler, Bardhan and Islam (1983).
It inhibits and reverses intestinal secretion caused by cholera toxin and
E. coli enterotoxin. It reduces diarrhea associated with pancreatic tumors
in man.</font>
<p><font face="Arial,Helvetica">It is clear Vitamin B3 is a very powerful,
benign substance which is involved in numerous reactions in the body, and
which in larger doses is therapeutic and preventative for a large number
of apparently unrelated diseases. Are all these conditions really expressions
of minor and major Vitamin B3 deficiency states due to diet, or to accumulation
of toxins in</font>
<br><font face="Arial,Helvetica">the body?</font>
<p><font face="Arial,Helvetica">It is highly likely that any human population
which increased the intake of Vitamin B3 in everyone, by even 100 mg per
day and to much higher levels in people already suffering from a number
of pathological conditions, will find a substantial decrease in mortality
and an increase in longevity.</font>
<p><b><i><font face="Arial,Helvetica">Literature Cited</font></i></b>
<br><font face="Arial,Helvetica">Abou EI-Enein AM, Hafez YS, Salem H and
Abdel, M: The role of nicotinic acid and inositol hexanicotinate as anticholesterolemic
and antilipemic agents. Nutrition Reports International, 281:899-911, 1983.</font>
<p><font face="Arial,Helvetica">Hoffer A: The psychophysiology of cancer.
J. Asthma Research, 8:61-76, 1970.</font>
<p><font face="Arial,Helvetica">Hostetler, D: Jacobsons put broad strokes
in the niacin/cancer picture. The D.O., Vol. 28, August 1987, pp. 103-104.</font>
<p><font face="Arial,Helvetica">Rabbani GH, Butler T, Bardhan PK and Islam
A: Reduction of fluid-loss in cholera by nicotinic acid. The Lancet, December
24CE31, 1983, pp. 1439-1441.</font>
<p><font face="Arial,Helvetica">Titus K: Scientists link niacin and cancer
prevention. The D.O., Vol. 28, August 1987, pp. 93-97.</font>
<p><font face="Arial,Helvetica">Vague PH, Vialtettes B, Lassmanvague V
and Vallo JJ: Nicotinamide may extend remission phase in insulin dependent
diabetes. The Lancet, 1:619-620, 1987.</font>
<p><font face="Arial,Helvetica">Wahlberg G, Carlson LA, Wasserman J and
Ljungqvist A: Protective effect of nicotinamide against nephropathy in
diabetic rats. Diabetes Research, 2:307-312, 1985.</font>
<p><font face="Arial,Helvetica">Yamada K, Nonaka K, Hanafusa T, Miyazaki
A, Toyoshima H and Tarui S: Preventive and therapeutic effects of large-dose
nicotinamide injections on diabetes associated with insulitis. Diabetes,
31: 749753, 1982.</font>
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