Coronary Disease, Cancer, Diabetes... and Niacin, Bypass a Coronary

[Guest guest]

http://www.doctoryourself.com/hoffer_cardio.html

 

Coronary Disease, Cancer, Diabetes... and Niacin

Bypass a Coronary

 

 

Niacin, Coronary Disease and Longevity

by Abram Hoffer, M.D., Ph.D.

 

Background

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.

 

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.

 

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.

 

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.

 

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.

 

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.

 

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.

 

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.

 

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).

 

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. "

 

The Coronary Study

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.

 

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. "

 

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.

 

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.

 

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.

 

Canner's Study (1985)

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.

 

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.

 

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.

 

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 90 percent

decrease in mortality. 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.

 

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. "

 

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.

 

Niacin Combined With Other Drugs Which Lower

Cholesterol

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. "

 

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.

 

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.

 

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.

 

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.

 

How Does Niacin Work?

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

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).

 

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).

 

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. "

 

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.

 

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.

 

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.

 

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.

 

Niacin as a Treatment for Acute Coronary Disease

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.

 

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.

 

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.

 

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. 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.

 

Conclusion

Niacin increases longevity and decreases mortality in

patients who have suffered one myocardial infarction.

The Medical Tribune, 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.

 

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.

 

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.

Inositol hexanicotinate is an ester of inositol and

niacin. In the body it is slowly hydrolyzed releasing

both of these important nutrients. The ester is more

effective than niacin in lowering cholesterol and

triglyceride levels, 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.

 

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.

 

One of the most exciting findings is that niacin will

protect against cancer. 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.

 

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.

 

Jacobson and Jacobson (Hostetler (1978) believe niacin

(more specifically, NAD) prevents processes which lead

to cancer. They found that 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. Cancer cells are

low in NAD.

 

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).

 

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 Type I

diabetes, 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

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

refused. She started on niacin 3 grams per day. She is

still well twenty-five years later.

 

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.

 

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

the body?

 

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.

 

Literature Cited

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.

 

Hoffer A: The psychophysiology of cancer. J. Asthma

Research, 8:61-76, 1970.

 

Hostetler, D: Jacobsons put broad strokes in the

niacin/cancer picture. The D.O., Vol. 28, August 1987,

pp. 103-104.

 

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.

 

Titus K: Scientists link niacin and cancer prevention.

The D.O., Vol. 28, August 1987, pp. 93-97.

 

Vague PH, Vialtettes B, Lassmanvague V and Vallo JJ:

Nicotinamide may extend remission phase in insulin

dependent diabetes. The Lancet, 1:619-620, 1987.

 

Wahlberg G, Carlson LA, Wasserman J and Ljungqvist A:

Protective effect of nicotinamide against nephropathy

in diabetic rats. Diabetes Research, 2:307-312, 1985.

 

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.