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--an
American, 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. |