Gerhard N. Schrauzer, PhD (Professor of Chemistry, University of California, La Jolla), an authority on selenium, has credited Revici with "having discovered pharmacologically active selenium compounds of very low toxicity," appraising him as "an innovative medical genius, outstanding chemist, and a highly creative thinker" (personal communication to the Board of Regents of the University of the State of N.Y., 2/14/86, in an administrative proceeding that is a matter of public record).
Dr. Revici was the first physician to develop selenium compounds, Lipid Bound Selenium, low enough in toxicity to give cancer patients doses far in excess of safety limits for ordinary forms of selenium. He was among the first research clinicians to treat cancer with naturally derived Omega 3 fatty acids.
He also appears to have been a pioneer in utilizing lipids to transport cytotoxic agents, Lipid Bound Selenium, through the bloodstream to sites of abnormal tissue.
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The formulation of lipid-based nanomedicines against cancer has been hypothesized to improve drug localization into the tumor tissue and to increase the anticancer efficacy of concentional drugs, while minimizing their systemic adverse effects
Se - Selenium is found in igneous rocks at 0.05 ppm; shale at 0.6 ppm; sandstone at 0.05 ppm; limestone at 0.08 ppm; fresh water at 0.02 ppm; sea water at 0.00009 ppm; soils at 0.2 ppm (not universally distributed, vast areas of Earth are deficient or even totally devoid of Se; Se is found in the humus of alkaline soils when present); marine plants at 0.8 ppm; land plants at 0.2 ppm; land animals at 1.7 ppm (highest concentrations found in liver, kidney, heart, and skeletal muscle).
Selenium is the most efficient antioxidant (anti-peroxidant) and is found at the subcellular level in the glutathione peroxidase enzyme system and metallo amino acids (selenomethionine, etc.). Selenium prevents cellular and subcellular lipids and fats from being peroxidized which literally means it prevents body fats from going rancid (seen externally as "age spots" or "liver spots" - this brown gold peroxidized lipid is known as ceroid lipofucsin).
Selenium also functions to protect cellular and organelle bi-lipid layer membranes from oxidative damage - the cover illustration is an electron photomicrograph of a selenium deficient rhesus monkey liver mitochondria magnified 126,000 times. The inner membrane of the mitochondria (made up of enzymes and RNA) has precipitated out of the normal structure to become a nonfunctioning organic crystalloid. This type of damage seen through the standard light microscope is called "age pigment". High intakes of vegetable oils including salad dressing, margarine and cooking oils concurrent with a selenium deficiency is the quickest route to a heart attack and cancer. The polyunsaturated configuration of the oils when heated or treated with hydrogen ("trans fatty acids") literally causes the rancidity free radical damage) of cellular fat.
Selenium Deficiency Diseases
- HIV (AIDS)
- Anemia (RBC fragility)
- Age Spots" & Liver
- Fatigue
- Muscular weakness
- Myalgia (muscle pain and soreness)
- Scoliosis
- Muscular Dystrophy (MD, White Muscle Disease, Stiff Lamb Disease)
- Cystic Fibrosis (congenital)
- Cardiomyopathy (Keshan Disease, Mulberry head" Disease)
- Multiple Sclerosis (MS) - associated with Hg poisoning
- Heart palpitations
- Irregular heart beat
- Liver cirrhosis
- Pancreatitis
- Pancreatic atrophy
- Lou Gehrig's Disease (ALS) - associated with Hg poisoning
- Parkinson's Disease - associated with Hg poisoning
- Alzheimer's Disease – associated with high vegetable oil consumption
- Adrenoleucodystrophy (ALD -Lorenzo's Oil" Syndrome)
- Infertility
- Low birth weight
- High infant modality
- Sudden Infant Death Syndrome (SIDS)
- Cancer - associated with carcinogen contact as well as high vegetable oil intake
- Clinical AIDS (HIV infection)
- Sickle cell anemia
The clinical diseases associated with selenium deficiency are diverse and to the uninformed (allopathic physicians) shrouded in mystery. Selenium deficiency is one of the more costly mineral deficiency complexes affecting embryos, the newborn, toddlers, teens and adults alike.
Selenium deficiency can result in infertility in both men and women. Congenital selenium deficiency during pregnancy can result in a wide variety of problems ranging from miscarriage, low birth weight, high infant mortality, cystic fibrosis muscular dystrophy and liver cirrhosis.
Selenium deficiency in growing children can result in crib death or SIDS (Sudden Infant Death Syndrome) slow growth, small size (failure to reach genetic potential for size and mass), muscular dystrophy, scoliosis cardiomyopathy (muscular dystrophy of the heart muscle or Keshan Disease), anemia, liver cirrhosis muscular weakness, lowered immune capacity and neuromuscular diseases such as ALD (Adrenoleucodystrophy or "Lorenzo's Oil type syndromes).
In young adults, selenium deficiency appears as anemia, chronic fatigue, muscular weakness, myalgia, muscle tenderness, pancreatitis, infertility, muscular dystrophy scoliosis, cardiomyopathy (this is especially common in young athletes such as basketball players and football players at the high school, college, university and professional levels), part of the anorexia nervosa complex, multiple sclerosis (adequate Se protects against Hg poisoning), Lou Gehrig's Disease (ALS) and liver cirrhosis.
Selenium deficiency in adults appears as reduced immune capacity, anemia, infertility, "age spots" or "liver spots)," myalgia, muscle weakness multiple sclerosis, ALS, Parkinson's Disease, Alzheimer's Disease, palpitations or irregular heart beat, cardiomyopathy, hypertrophy or thickening of the cardiac muscle, liver cirrhosis, cataracts and cancer.
In a review of the anti-cancer effects of selenium Dr. Gerhard N. Schrauzer, head of the Department of Chemistry, UCSD states:
Selenium is increasingly recognized as a versatile anticarcinogenic agent. Its protective functions cannot be solely attributed to the action of glutathione peroxidase. Instead, selenium appears to operate by several mechanisms, depending on dosage and chemical form of selenium and the nature of the carcinogenic stress. In a major protective function, selenium is proposed to prevent the malignant transformation of cells by acting as a "redox switch" in the activation- inactivation of cellular growth factors and other functional proteins through the catalysis of oxidation-reduction reactions of critical ~SH groups or -S-S- bonds. The growth -modulatory effects of selenium are dependent on the levels of intracellular glutathione peroxidase and the oxygen supply. In general, growth inhibition is achieved by the Se-mediated stimulation of cellular respiration (more oxygen less cancer). Selenium appears to inhibit the replication of tumor viruses and the activation of oncogenes by similar mechanisms. However, it may also alter carcinogen metabolism and protect DNA against carcinogen-induced damage. In additional functions of relevance to its anticarcinogenic activity, selenium acts as an acceptor of biogenic methyl groups, and is involved in detoxification of metals and certain xenobiotics. Selenium also has immunopotentlating properties. It is required for optimal macrophage and natural killer cell functions.
The school of pharmacy from the University of Georgia released a report in August of 1994 that concludes a human selenium deficiency is related to the onset of full blown AIDS in chronically infected HIV patients. According to their report, HIV requires large amounts of selenium for replication, and in selenium deficient patients, the virus competes with the patient for limited amounts of the essential mineral. The HIV patient actually dies of selenium deficiency encephalopathy, liver cirrhosis or cardiomyopathy. Long term HIV patients (20 years or more) that never developed full-blown AIDS had supplemented with relatively large amounts of selenium.
Selenium is a trace mineral nutrient with anticancer and antiaging properties. Selenium helps protect cells against oxidative stress. As a part of the enzyme glutathione peroxidase, selenium serves as an antioxidant by destroying highly reactive chemicals that can form free radicals. Glutathione peroxidase destroys hydrogen peroxide, a naturally occurring chemical that is a powerful oxidizing agent. Hydrogen peroxide is produced for antimicrobial defense by macrophages, a type of white blood cell that engulfs foreign invaders, and it is a by-product of another antioxidant system (superoxide dismutase) that destroys a highly reactive form of oxygen called superoxide. Glutathione peroxidase neutralizes oxidative damage to lipids in cell membranes, thus limiting their damage due to free radical attack. Selenium may possess other antioxidant properties as well.
Selenium is generally recognized as an anticancer agent. In selenium-deficient experimental animals, liver cells become defective and more prone to become cancerous when activated. Studies show that populations with a low selenium intake are more prone to gastrointestinal, breast and rectal cancers. Deficiency of selenium leads to lowered glutathione peroxidase activity. Furthermore, extensive Chinese studies have suggested that selenium supplementation provides protection against hepatitis B and liver cancer. Selenium may inhibit the development of cancer by blocking the activation of certain cancer-promoting genes, by inhibiting viruses linked to cancer or by supporting healthy cell division and protecting cells against oxidative damage that could damage their DNA.
Selenium supports a healthy immune system, where it stimulates antibody production and defensive cells (lymphocytes, macrophages and natural killer cells). Some AIDS patients may be selenium deficient. Selenium can block mercury, arsenic and cadmium poisoning. Damaged heart muscle (cardiomyopathy) has occurred in patients fed intravenously mixtures that lacked selenium, and populations in areas of China characterized by regional selenium deficiency are more disease prone. Osteoarthritis in Chinese children has also been linked to selenium deficiency.
Recommended Dietary Allowances (RDA) published in 1989 proposed a selenium RDA for the first time as 70 mcg/day for men and 55 mcg for non-pregnant, non-lactating women. Obtaining adequate selenium is a growing problem in the United States. Regions like the Pacific Northwest, the Great Lakes region and some southern states (Georgia and the Carolinas) possess low soil concentrations of selenium, and vegetables and grains growing in depleted soils contain only low levels of selenium. Possibly acid rain prevents plants from taking up this mineral from soil. For insurance, some may wish to supplement with no more than 200 mcg of organic selenium per day. This doubles the average U.S. intake of about 100 mg/day.
Chemically combined selenium represents the most prevalent form of the selenium in the typical diet. Selenium can replace sulfur in the amino acids cysteine and methionine to form the analogs, selenocysteine and selenomethionine. Selenocysteine occurs in a variety of proteins including glutathione peroxidase and is found in meat. Selenomethionine cannot be synthesized by the body and is supplied in the diet by a variety of foods. It can substitute for methionine in a variety of the body's proteins. The breakdown of methionine and selenomethionine releases cysteine and selenocysteine, respectively.
Biochemical function
Until recently, the only known metabolic role for selenium in mammals was as a component of the enzyme glutathione peroxidase which, together with vitamin E, catalase and superoxide dismutase, is a component of one of the antioxidant defense systems of the body. Recently, Burk and his colleagues have made great strides in the purification and characterization of their "selenoprotein-P", but so far they have been unable to clarify its function in people or in animals. Several different selenium-containing enzymes have been described in microorganisms, and it is likely that selenoproteins other than glutathione peroxidase remain to be discovered in higher animals. There is, for example, growing evidence that an additional selenoenzyme protein is involved in the synthesis of the hormone triiodothyronine from thyroxine.
The Use and Importance of Selenium
By Herb Boynton
Early in December, 1988, a report in the Sacramento Bee warned that millions of Americans might be at risk of being poisoned by foods containing high levels of selenium. This story raised fears concerning the safety of the foods we eat, suggested that our regulatory agencies are lax and grossly exaggerated the toxicity of selenium.
Selenium is a rare element which has many properties resembling those of sulfur. It is widely but unevenly distributed on the earth's crust. Because it is taken up by plants, it has always been in our food chain. Organisms not only adapted to its presence, but also through evolution they even learned how to put it to good use.
Without selenium, mammalian cells cannot grow, and life as we know it could not exist. Farmers in many parts of the United States learned this the hard way: For many years they had to face huge annual losses of livestock due to selenium deficiency diseases. These persisted until the Food and Drug Administration permitted the addition of selenium to feed.
In humans, selenium deficiency causes degenerative changes of the heart and a fatal cardiomyopathy. In China, thousands of children and young women died each year until large-scale selenium supplementation programs were instituted. Other studies have linked a lack of selenium with a diminished resistance to cancer. Several supplementation trials are underway to establish the value of selenium in cancer prevention.
The Sacramento Bee claimed, on the basis of the data it collected, that some common foods consumed by Americans are contaminated by potentially toxic levels of selenium. The FDA, which has been monitoring the selenium levels in U.S. foods on a regular basis since 1974, disagrees. It appears that some of the newspaper's high estimates arose because of errors in the conversion of selenium levels expressed on a dry-weight basis to fresh-weight food portions.
Reliable estimates indicate that the selenium intakes of the great majority of Americans lie between 50 and 200 micrograms per day, an amount declared to be "adequate and safe" by the Food and Nutrition Board of the National Academy of Sciences. Other scientists believe that the optimal selenium intake level lies somewhere between 300 and 500 micrograms per day or at roughly twice the average U.S. intake. Selenium intakes of this magnitude are typical for adults in Japan.
In regions with locally excessive levels of selenium, toxic intake levels are occasionally reached. Symptoms of selenium poisoning appeared among the inhabitants of Enshi, a town in central China, after they had unknowingly ingested 5,000 micrograms of selenium per day for several months. This poisoning episode occurred when, as an emergency measure, seleniferous corn had to be consumed due to the failure of a rice crop.
Even at these high selenium intakes, the toxic symptoms were mild and reversible, and they disappeared after the normal diet was resumed.
The Enshi incident, which occurred about 10 years ago, shows that the threshold level of chronic selenium toxicity is about 10 to 20 times higher than the nutritional intake. The margin of safety for selenium thus is actually remarkably wide. Toxic levels are hardly ever reached since, even in the high-selenium regions of South Dakota, only a few people obtain more than 600 micrograms of selenium per day.
Author: Gerhard N. Schrauzer, Ph.D., is a professor of chemistry at the University of California, San Diego, and is one of the world's leading authorities on selenium.
Selenium Deficiency and Increased Risk of Lung Cancer
Serum samples were taken from 21,172 Finnish men between 1968-1972. Within 11 years, lung cancer was diagnosed in 143 of these people. These cancer victims were matched by age and region with 264 control subjects. The stored serum samples of these people were then analyzed for selenium content. The subjects who eventually developed lung cancer showed lower serum selenium than did the controls.
When the group as a whole was analyzed, subjects with selenium in the lowest 20% had 3.3 times the subsequent risk of lung cancer seen in those subjects with selenium in the highest 20%.
These results are in accord with other studies strongly suggesting that poor selenium nutrition may possibly be a significant risk factor for lung cancer.
Authors: Paul Knekt, Georg Alfthan, Arop Aromaa, Matti Hakama, Timo Hakuhnen, Jouni Maatela, Richard Peto, Erkki Saxen, Lyly Teppo.
Social Insurance Institution, National Public Health Institution, Finnish Cancer Registry, Department of Public Health, University of Tampere, Tampere, Finland.
Selenium, Aflatoxin and Cancer
(Experimental Study on Selenium Blockade of Primary Hepatocarcinoma Induced by Aflatoxin in Rats)
Aflatoxin is an extremely potent carcinogen produced by molds that contaminate peanuts and other foods. It is considered to be a major cause of liver cancer in the Third World.
This study demonstrated that supplementary selenium protects rats from aflatoxin-induced liver cancer; cancer incidence was 65% in rats receiving the control diet, but only 26% in those fed extra selenium.
In addition, the onset of liver cancer was delayed in the selenium-fed group. Improved selenium nutrition may offer a practical approach to prevention of liver cancer in Third World countries and perhaps, to some extent, in developed countries as well.
Author: Li Wenguang, Shou Longqi, Qidong LiverCancer Institute, Jiangsu, China.
Selenium and Heart Function (Effect of Selenium on the Function of Cultured Rat Heart Cell)
When rat heart cells are grown in 1 culture, the addition of selenium to the medium increases the frequency and amplitude (strength) of contractions, while promoting the synthesis of nucleic acids (RNA) and enhancing membrane stability. These effects are especially marked when the cells are deprived of oxygen and glucose for 60 minutes.
Good selenium nutrition may thus help to preserve the structural and functional integrity of heart tissue subjected to a temporary loss of blood flow, as in the case of heart attack or occlusion of one or more coronary arteries.
Author: Guangyuan Li, Yingyun Ren, Wei Cheng, Institute of Integrated Traditional and Western Medicine, I Man Medical University, Xian, China.
Selenium Supplementation, Heart Attack and Stroke (Effects of Selenium Supplementa- tion on Platelet Function as As- sessed by Platelet Aggregation and Glutathione Peroxidase Activity)
Platelets are the blood cells that aggregate, or clump, to trigger blood clots. Several previous studies have suggested that good selenium nutrition helps to control platelet aggregation. In this study, young men were supplemented for four weeks with 200 mcg selenium daily as high selenium yeast. An increase in platelet glutathione peroxidase activity was observed during supplementation.
Platelet aggregation in response to the triggering agent (collagen) was decreased, as was production of the clot-promoting compound thromboxane. By helping to stabilize platelets, good selenium nutrition may promote cardiovascular health and may reduce the risk of both heart attack and stroke.
This effect is somewhat similar to that of aspirin. However, aspirin is a drug that produces a pharmacological effect, whereas selenium is a nutrient which functions to normalize platelet activity.
Authors: H.W. van der Torre, J. Veenstra, H. van de Pol, H. van Steenbrugge, S. Pelupessy and G. Schaafsma, the Ockhuizen Department of Nutrition,
TNO-CIVO Toxicology and Nutrition Institute, P.O. Box 360, 3700 Aj Zeist, The Netherlands.
Selenium, Vitamin E and Conges- tive Heart Failure (Selenium and Vitamin E Defi- ciency in Mini Pigs as an Animal Model for Keshan Disease)
Antioxidant deficiency in mini pigs is being studied as a possible model for Keshan disease, a syndrome of heart failure triggered by selenium deficiency and common in selenium-depleted regions of China.
In mini pigs, combined deficiency of selenium and vitamin E leads to inefficient functioning of the left chamber of the heart (left ventricle), with a compensatory thickening of the heart wall. This poor heart function leads to blood pooling in the liver and lungs. Heart glutathione peroxidase activity was 30% of that seen in normally fed animals.
This animal model underlines the crucial importance of antioxidant nutrition (selenium and vitamin E) to efficient heart function.
Authors: K.H. Konz, M. Haap, Y. Xia, K.E. Mill, R.A. Walsh*, and R.F. Burk, Dept. of Medicine, Vanderbilt University, Nashville, TN 37232.
The following info on Selenium is from Julian Whitaker, MD's Health & Healing newsletter; Vol. 7, No.2, Feb 1997
The Selenium Saga Started With Skin Cancer
Selenium's role as an anti-cancer nutrient was first published by Dr. Raymond Shamberger in 1965. Knowing that skin cancer was caused by free radical damage, he used selenium, which is a potent antioxidant, on the skin of animals subjected to ultraviolet light and reported a marked reduction in cancer incidence. This started a flurry of animal studies with selenium, which clearly demonstrated that this unique mineral could prevent carcinogens from causing cancer, and also stop the process once cancer had been introduced.
Selenium Protects You Against Cancer on Three Levels
Selenium seems to have several mechanisms of anti-cancer activity.
1. First are the antioxidant properties of selenium. It is essential for your body's generation of glutathione, an important antioxidant that mops up hydrogen peroxide, a potent free radical produced in your body by normal metabolic processes.
2. Selenium's ability to protect you against cancer goes beyond this. At somewhat higher levels, selenium facilitates the quick repair of free radical damage to the DNA molecule. Our current understanding of cancer is that a damaged DNA molecule replicates, carrying with it this "spark" that ignites the growth of a tumor. If adequate selenium is present, however, the DNA molecule is repaired-and normal cellular function ensues.
3. Perhaps the most dramatic property is that selenium initiates apoptosis, or cell death, in cancerous and precancerous cells. Cancer cells generally divide rapidly and die early. Selenium appears to cause cancer cells to die before they replicate, thereby short-circuiting again the generation of malignancy, tumor growth and cancer spread.
Research on Selenium and Cancer in Humans Started with Soil Analysis
Even though the research on animals was convincing and consistent, Dr. Shamberger looked for a connection between selenium with human cancers. In the early 1970s, noting that selenium's presence in American soil varied from region to region, Dr. Shamberger demonstrated that cancer rates were significantly higher in areas of the country where soil selenium levels were lower.
This finding had been convincingly confirmed by studies in China. China is unique in that there are areas of the country in which the soil selenium levels are so high they're almost toxic, and other areas where selenium 'is almost absent.
An Analysis in China Showed a Clear Correlation
Blood levels of selenium are an excellent means of gauging selenium intake. By examining selenium blood levels in samples from blood banks in 30 different regions of China, scientists were able to classify the soils in the various regions as either 1) low, 2) medium or 3) high selenium. They then looked at the total death rates from cancer in these three defined regions and found a ratio of 3:2:1!
In other words, the cancer death rate in the high selenium regions was only one third of that in the low selenium regions. This finding, which was published in 1985, was criticized for technical reasons and, not surprisingly, received very little serious attention from scientists or the media. However, a reduction in cancer death rate of 66% is a finding that only an idiot would dismiss on technicalities.
Two Studies Provided Further Evidence...
In the 1980s, Dr. Shu-Yu Yu and colleagues at the Cancer Institute, Chinese Academy of Medical Sciences in Beijing, China set out to test these findings with more controlled research. With support from Nutrition 21, a small nutritional supplement company, they examined the effects of selenium in a double-blind, placebo-controlled trial of 226 people known to be at high risk for liver cancer because they carried the hepatitis B antigen in their blood. These patients were given either a placebo or 200 mcg of high selenium yeast (a food form of selenium) every day. At the end of four years there were five cases of liver cancer in the placebo group and none among those taking daily selenium.
Dr. Yu also recruited 2,474 family members of people who had developed liver cancer and so were judged to be at higher risk for the disease. Half received 200 mcg of high selenium yeast, and the other half received a placebo. During the two years of the study, 13 of the 1,030 controls developed liver cancer, compared to only 10 of the 1,444 on selenium. That's a 45% reduction in cancer incidence in the selenium group.
... But No One Was Interested in These Astonishing Results...
The results of both of these studies were statistically significant, yet they failed to generate interest in the United States. Our conventional mindset toward cancer is to simply ignore the significance of nutritional elements, and consequently, no money is allocated for studies of this nature.
Again, Nutrition 21 responded by giving a small grant to Dr. Clark, chief researcher of the most recent study, who was committed to discovering the truth about selenium. All of the evidence, both animal and human, pointed to an incredibly powerful anti-cancer effect, but the acid test for American physicians--anAmerican, double-blind, placebo-controlled trial--had not been done.
... So an American Double-Blind, Placebo-Controlled Study Was Done
Dr. Clark then recruited patients' in several dermatology clinics who had had either squamous cell or basal cell carcinomas removed. From 1983 through 1991, 1,312 patients were enrolled and given either a placebo or 200 mcg of high selenium yeast daily. Blood selenium levels initially averaged 114 ng/ml, and remained at this level, in the placebo group. Those taking selenium experienced a 67% increase in their blood selenium, to a level of 190, which remained more or less constant throughout the test. This blood level was in the range of those of people living in areas with selenium-rich soil, and was far below the 1,000 ng/ml level identified as possibly toxic by the Environmental Protection Agency.
The Results Were Rapid and Dramatic.
Most remarkable was the rapidity with which the investigators noted a reduction in serious cancers: In fact, selenium seems to offer cancer protection almost immediately, as the study showed. The overall cancer rate in the selenium group was 37% lower than in the placebo group, and the total cancer death rate was 50% lower in the selenium group, both astoundingly high differences.
The chances of this simply being a fluke were 3 in 10,000. Without question, selenium was the reason for this dramatic reduction in the incidence of, and death rate from, cancer.
Selenium's Protective Effects Were Clear for Certain Cancers
Selenium's effects on specific cancers were also identified. Interestingly, skin cancers, which the study was initially designed to evaluate, showed little response to selenium. However, the selenium group had a 63% reduction in the incidence of prostate cancer, a 58% reduction in colon or rectal cancer, and a 45% reduction in lung cancer.
The Study Was Terminated Early Because the Results We re So Clear
The results were so definitive that the study was ended early. The data were not supposed to be publicly viewed or published until 1998, but the study was stopped in 1996 because of the dramatic reduction in cancer incidence and death in the selenium group. The researchers felt it would be inappropriate to allow the placebo group to continue taking an agent which did nothing, while they could be taking a supplement that would reduce their risk of serious and deadly cancers.
I can't Emphasize Enough the Importance of These Results for You
It is difficult for me to articulate the magnitude of this study. Even if the results were only half as good as they were (25% vs. 50% reduction in death rate), you're still looking at saving close to 100,000 lives a year, just from taking an inexpensive, completely safe (at 200 mcg a day) nutritional supplement. This is one of nature's most powerful agents for protection against cancer.
