Whenever we put up information on
alternative treatments that have not been properly/Scientifically
tested, we receive a few angry emails.
There have been 7 international conferences on the theme niacin and cancer. This vitamin is an essential component of the enzyme systems that repair broken DNA molecules. The dose ranges from 100 milligrams three times daily to 1000 milligrams three times daily. Several studies in Detroit have found that the response rate of cancer around the head and neck was 10% on radiation alone but increased to 80% when patients were given large doses of niacinamide. Very rarely niacin will cause obstructive jaundice which clears when the niacin is stopped. For details see my book Orthomolecular Medicine for Physicians.
A.Hoffer PhD MD FRCP(C)
One vitamin Gerson liked was niacin. It "helps to bring back sufficient glycogen into the liver cells," (page 209) open[s] the small arteries and capillaries;" (page 209) and "raises the electrical potentials in the cells." (page 209) He also recommended discontinuing taking niacin in cases of bleeding. (page 209)
Q Is there any danger in taking niacin?
A Dr. Gerson felt strongly about the use
of increased amounts of Niacin (Vitamin B3) in cancer patients
from the beginning of treatment and without too much interruption.
However after using 50mg six times a day for four to six months,
it should not be diminished too fast as well. Niacin helps to
bring back sufficient glycogen into the liver cells. It also
helps in protein metabolism, acts to open small arteries and
capillaries (of course it would be discontinued with any bleeding
problems.) It raises electrical potential in cells. In addition,
this information can be found on page 209 of "A Cancer Therapy:
Results of Fifty Cases" (Dr. Max Gerson, Gerson Institute,
ISBN 0-9611526-2-1) The best to you and your healthy children.
Studies of cultured cells in vitro provide evidence that NAD content influences the cellular response to DNA damage, an important risk factor for cancer. Cellular NAD is consumed in the synthesis of ADP-ribose polymers, which play a role in DNA repair, and cyclic ADP-ribose may mediate cell-signaling pathways important in the prevention of cancer (10). Additionally, cellular NAD content has been found to influence levels of the tumor suppressor protein, p53, in human breast, skin, and lung cells (11). Neither the cellular NAD content nor the dietary intake of NAD precursors (niacin and tryptophan) necessary for optimizing protective responses following DNA damage has been determined, but they are likely to be higher than required for the prevention of pellagra. Niacin deficiency was found to decrease bone marrow NAD and poly-ADP-ribose levels and increase the risk of chemically induced leukemia (12), and niacin supplementation decreased the risk of ultraviolet light-induced skin cancers in mice (13). However, little is known regarding cellular NAD levels and the prevention of DNA damage or cancer in humans. Elevation of NAD levels in blood lymphocytes after supplementation of two healthy individuals with 100 mg/day of nicotinic acid for eight weeks reduced DNA strand breaks in lymphocytes exposed to free radicals in a test tube assay compared to those of non-supplemented individuals (14). More recently, nicotinic acid supplementation of up to 100 mg/day in 21 healthy smokers failed to provide any evidence of a decrease in cigarette smoke-induced genetic damage in blood lymphocytes compared to placebo (15).
Generally, relationships between dietary
factors and cancer are established first in epidemiologic studies
and followed up by basic cancer research on the cellular level.
In the case of niacin, research on biochemical and cellular aspects
of DNA repair have stimulated an interest in the relationship
between niacin intake and cancer risk in human populations (16).
Recently, a large case-control study found increased consumption
of niacin, along with antioxidant nutrients, to be associated
with decreased incidence of oral (mouth), pharyngeal (throat),
and esophageal cancers in northern Italy and Switzerland (17,
18). An increase in niacin intake of 6.2 mg was associated with
about a 40% decrease in cases of cancers of the mouth and throat,
while a 5.2 mg increase in niacin intake was associated with
a similar decrease in cases of cancer of the esophagus.
Niacin, Coronary Disease
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
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)
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
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?
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
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.
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
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
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.
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,
A recent study also found that the combination of niacin and a cholesterol-lowering drug called simvastatin (which belongs to a class known as HmG CoA reductase inhibitors or statins) may dramatically slow the progression of heart disease, reducing risk of heart attack, and even death.
Daily recommendations for niacin from the diet for healthy individuals are listed below.
It is important to note, however, that only extremely high doses of niacin (in the range of 1,500 to 3,000 mg per day in divided doses) are helpful for most medical conditions. Such high doses are considered "pharmacologic" and must be prescribed by a qualified healthcare practitioner. The practitioner will instruct you on increasing the amount of niacin slowly, over the course of 4 to 6 weeks, and to take the medicine with meals to avoid stomach irritation.
Infants birth to 6 months: 2 mg (adequate intake)
Males 19 years and older: 16 mg (RDA)
High doses (75 mg or more) of niacin can cause side effects. The most common side effect is called "niacin flush," which is a burning, tingling sensation in the face and chest, and red or "flushed" skin. Taking an aspirin 30 minutes prior to the niacin may help reduce this symptom.
At the very high doses used to lower cholesterol and the other conditions mentioned previously, liver damage and stomach ulcers can occur. When taking pharmacologic doses of niacin, your doctor or other healthcare practitioner will periodically check your liver function through a blood test. People with a history of liver disease or stomach ulcers should not take niacin supplements. Those with diabetes or gallbladder disease should do so only under the close supervision of a healthcare provider. Niacin should not be used if you have gout.
Taking any one of the B complex vitamins for a long period of time
can result in an imbalance of other important B vitamins. For this
reason, it is generally important to take a B complex vitamin with
any single B vitamin.
Blood Pressure Medications, Alpha-blockers
As described earlier, recent scientific evidence suggests that taking niacin with simvastatin (a drug that belongs to a class of cholesterol-lowering medications known as HMG-CoA reductase inhibitors or statins including atorvastatin and lovastatin as well), appears to slow down the progression of heart disease. However, the combination may also increases the likelihood for serious side effects, such as muscle inflammation or liver damage.
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Elam M, Hunninghake DB, Davis KB, et al. Effects of niacin on lipid and lipoprotein levels and glycemic control in patients with diabetes and peripheral arterial disease: the ADMIT study: a randomized trial. Arterial Disease Multiple Intervention Trial. JAMA. 2000;284:1263-1270.
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Gardner SF, Marx MA, White LM, et al. Combination of low-dose niacin and pravastatin improves the lipid profile in diabetic patients without compromising glycemic control. Ann Pharmacother. 1997;31(6):677-682.
Gardner SF, Schneider EF, Granberry MC, Carter IR. Combination therapy with low-dose lovastatin and niacin is as effective as higher-dose lovastatin. Pharmacother. 1996;16:419–423.
Garg A. Lipid-lowering therapy and macrovascular disease in diabetes mellitus. Diabetes. 1992;41(Suppl 2):111-115.
Goldberg A, Alagona P, Capuzzi DM, et al. Multiple-dose efficacy and safety of an extended-release form of niacin in management of hyperlipidemia. Am J Cardiol. 2000;85:1100-1105.
Guyton JR. Effect of niacin on atherosclerotic cardiovascular disease. Am J Cardiol. Dec 17, 1998;82:18U–23U.
Guyton JR, Capuzzi DM. Treatment of hyperlipidemia with combined niacin-statin regimens. Am J Cardiol. Dec 17, 1998;82:82U–84U.
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"Because vitamins in large doses may have drug like effects, they could compromise the effectiveness of standard medical treatment in the same way that taking two different drugs might." (McDonald)
"Pregnant women or those planning to become pregnant should not use megavitamin therapy. Congenital abnormalities and spontaneous abortions may occur." (Ontario) (Loescher)
"Megadose vitamin therapy may cause injury that is confused with disease symptom. High vitamin intake is more hazardous to peripheral organs than to the nervous system, because the central nervous system vitamin entry is restricted." (Snodgrass)
"Large doses of thiamine had been known for years to have neurological effects in animals." (Snodgrass)
Vitamin K: "Large amounts of vitamin K in pregnancy can cause jaundice in the newborn. Dietary supplements high in vitamin K can block the effects of oral anticoagulants." (Medical Letter)
Pyridoxine (Vitamin B6): Individuals taking several grams daily for prolonged periods developed severe peripheral neuropathies. Others developed ataxia (failure of muscular coordination), numbness around the mouth, and numbness and clumsiness of the hands and feet. Neurological examination showed profound loss of position and vibration sense in their distal limbs, with severe impairment of the senses of pain, temperature, pinprick, and touch, and loss of limb reflexes. (Medical Letter) (Berger) (Schaumburg)
Niacin (Nicotinic Acid): Niacin causes release of histamine, which in turn can cause severe flushing, itching, and gastrointestinal disturbances. In one trial, three grams of niacin daily increased serum uric acid (leading to gouty arthritis) and fasting blood glucose concentrations.
Large doses of niacin can cause liver toxicity; increased aminotransferase activity occurs frequently, and cholestatic jaundice that disappeared when the vitamin was discontinued has been reported with as little as 750 mg [milligrams] daily taken for less than three months. (Medical Letter)
Niacin 100mg 100T SN0501 $NZ10.70
Cancer cells hide after Chemotherapy
After the initial doses of radiation and/or chemotherapy, cancer cells start hiding.
" They develop a slime coating, and they become like Stealth bombers, and they can hide from future doses of radiation and chemotherapy. This is why repeated dose of radiation and chemotherapy become less effective".Dr. John Maras, Nu-Gen Educational Library.
" The way to get rid of this "slime coating" is to use large doses of plant and animal enzymes- especially bromelain and pancreatin. This allows an 'access point' for the immune system to attack the cancer cells".....Dr. John Maras, Nu-Gen Educational Library
What doctors say about Chemo Therapy ?
"The world is a dangerous place to live; not because of the people who are evil, but because of the people who don't do anything about it."
A Sad day for Alternative healing
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