Re: Statins-Niacin

November 8, 2006

,

This is from doctoryourself.com, Dr. Saul's website, info on

niacin and cholesterol.

Coronary Disease, Cancer, Diabetes... and Niacin

Bypass a Coronary

Home 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,

, 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.

, 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. 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 , 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. L. Canner, Chief Statistician, land 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, on, 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, , Freedmand,

, 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 (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.

son and son (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, , 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: sons put broad strokes in the niacin/cancer

picture. The D.O., Vol. 28, August 1987, pp. 103-104.

Rabbani GH, 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.

Saul, PhD

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November 8, 2006

I have a comment on this below, quoted from this

article:

<< " 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,

, 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. " >>

------------------

I just finished two months straight of taking the

following dosages of Niacin and Niaciminide:

Niaminicide in a capsule containing:

400 mg. of Niacinimide

200 mg. GABA

1200 mg. of Inositol.

(Taken 3x a day)

20 mg. Niacin in a sublingual B Complex formula

15 mg. Niacin in a Women's Multivitamin, also taken

once daily.

So, altogether this would total, per day for the

Niacin and Niacinimide:

Niaminicide: 1200 mg.

Niacin: 35 mg.

I've had several interesting things happen from thi

that I'd like to report.

First, after two months of taking these amounts of

Niacin and Niaminicide, I developed severely painful

liver inflammation. It stopped when I stopped taking

the Niaminicide. I still get a bit of it when I take

the Women's Daily Vitamin and the Sublingual B Complex

containing Niacin, but not too bad. A few sharp pains

momentarily.

So I'd say to watch liver function when taking large

amounts of Niaciminide and Niacin, especially since I

wasn't even taking half of the 3000 mg. per day that

the doctor in this article says is safe.

The second thing that happened was that my Hashimoto's

antibodies completely disappeared. I assume this has

something to do with the methyl malfunction thing

which the B Vitamins and in particular either Niacin

or Niacinimide and Inositol (which is KIND of a B

Vitamin but kind of not) are supposed to have

something to do with fixing.

I'd had some fairly raised Hashi's antibodies, 179 out

of a range of 0-150 on the test taken in August. Now I

don't have any at all that could even be discerned as

of the latest test taken on October 31st.

Also, on my test results for Cholesterol levels from

this past Tuesday, after taking the Niacinimide and

Niacin for two months:

My " good " cholesterol was too low.

My " bad " cholesterols were high. Not HUGELY high, but

high by about 10-15 points over the top end of the

range.

HOWEVER, this was the very first test I've ever done

for my cholesterols, and it was done at the END of

taking the Niacin and Niaminicide for two months.

This means that the levels of bad cholesterol might

have been even higher than they are now, before

starting the N and N, and have actually been lowered

during these past two months of taking it.

Anyway, that's my own personal experience after taking

that amount of Niacin and Niaminicide for two months.

--- Linn wrote:

> ,

>

> This is from doctoryourself.com, Dr. Saul's

> website, info on

> niacin and cholesterol.

>

> Coronary Disease, Cancer, Diabetes... and Niacin

> Bypass a Coronary

> Home Niacin, Coronary Disease and Longevity

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

________________________________________________________________________________\

____

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November 8, 2006

Niacin has also been proven to keep Type 1 diabetes antibodies from

developing.

Linn

> I have a comment on this below, quoted from this

> article:

>

> << " 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,

> , 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. " >>

>

> .

>

November 8, 2006

From my research on niacin & treating cholesterol, it's my

understanding that one should not use the niaciminide form. It's not

effective, and as you saw, has regular side effects.

Regular niacin is ok. Don't get the non-flushing. The flushing form

is more effective. Flushing can be worked around by increasing

slowly (I think one of my prior links had a schedule) over the

course of about a month, give the body time to adjust. Or just start

right in with the 3g/day. The body adjusts after a week if you can

put up with the flushing short-term.

> I just finished two months straight of taking the

> following dosages of Niacin and Niaciminide:

>

> Niaminicide in a capsule containing:

>

> 400 mg. of Niacinimide

> 200 mg. GABA

> 1200 mg. of Inositol.

> (Taken 3x a day)

>

> 20 mg. Niacin in a sublingual B Complex formula

>

> 15 mg. Niacin in a Women's Multivitamin, also taken

> once daily.

>

> So, altogether this would total, per day for the

> Niacin and Niacinimide:

>

> Niaminicide: 1200 mg.

> Niacin: 35 mg.

>

> I've had several interesting things happen from thi

> that I'd like to report.

>

> First, after two months of taking these amounts of

> Niacin and Niaminicide, I developed severely painful

> liver inflammation. It stopped when I stopped taking

> the Niaminicide. I still get a bit of it when I take

> the Women's Daily Vitamin and the Sublingual B Complex

> containing Niacin, but not too bad. A few sharp pains

> momentarily.

>

> So I'd say to watch liver function when taking large

> amounts of Niaciminide and Niacin, especially since I

> wasn't even taking half of the 3000 mg. per day that

> the doctor in this article says is safe.

>

November 8, 2006

This is one of the most thorough pieces I've read about niacin! Even tells how

to dose it.

Thank you Linn!

Linn wrote: ,