Coronary Disease, Cancer, Diabetes... and Niacin

[Guest guest]

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

 

Coronary Disease, Cancer, Diabetes... and Niacin

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.

 

 

 

 

AN IMPORTANT NOTE: This page is not in any way offered as prescription,

diagnosis nor treatment for any disease, illness, infirmity or physical

condition. Any form of self-treatment or alternative health program necessarily

must involve an individual's acceptance of some risk, and no one should assume

otherwise. Persons needing medical care should obtain it from a physician.

Consult your doctor before making any health decision.

Neither the author nor the webmaster has authorized the use of their names or

the use of any material contained within in connection with the sale, promotion

or advertising of any product or apparatus. Single-copy reproduction for

individual, non-commercial use is permitted providing no alterations of content

are made, and credit is given.

 

 

 

 

 

 

 

Hotjobs: Enter the " Signing Bonus " Sweepstakes