Written by Ananda S. Prasad, MD
A Modern Detective Story
As presented at Wise Traditions Conference 2012
We know of eight trace elements that are essential to human health.
Iodine, as we all well know, is essential for thyroid function; iron is
essential for hemoglobin synthesis; and copper is essential for collagen
synthesis. Chromium is involved in glucose metabolism, although it is
not very well established how important it is for management of
diabetes. Selenium is very important because it is a part of glutathione
peroxidase, which works as an antioxidant. Fluoride is not essential
for life but considered important for dental health. Manganese is also
considered to be essential as it is involved in cartilage synthesis;
however, it’s deficiency has not been observed.
As
for zinc, its recognition as an essential mineral came only recently.
The story of how zinc achieved acceptance is a very interesting one. Not
long ago scientists derided the premise that zinc played a role in
human health. Today we know that zinc plays many important roles. For
example, zinc is a part of the super oxide dismutase enzyme, so it also
has a role as an antioxidant. In addition, zinc takes part in
neurotransmitters, and plays a key role in immune function, sound growth
and development. In fact, zinc is really a miracle element in many
ways.
EARLY ZINC RESEARCH
The first hint that zinc played an important role in life processes
came in 1869, when the mineral was found to be essential for the growth
of a fungus,
Aspergillus niger. It was a chemist from the
University of Lyon, France, Professor Jules Raulin, who reported in 1869
that zinc was needed for the growth of this organism. Prior to that
zinc was not considered to be important for biology.
In 1926 scientists found zinc to be essential for the growth of
higher plant life, and in 1934 Wilbert Todd, Conrad Elvehjem and Edwin
Hart from Wisconsin reported that zinc was also important for growth in
rats. In 1955, a disease called parakeratosis in swine was reported by
Tucker and Salmon, who showed that zinc could cure skin lesions. And
then O’Dell and Savage showed that zinc was needed for the growth of
poultry in 1958.
HOW I CAME TO STUDY ZINC
I was born in India, and some years later I came to the University of
Minnesota (USA) for my medical training. In 1958, I finished my
training, received my PhD and became a hematologist. At that time, I was
contacted by Professor Hobart Reimann, Chief of Medicine at Jefferson
at that time and formerly Chief of Medicine at Minnesota. He was invited
by the Shah of Iran, who was a personal friend, to set up a medical
curriculum for a university in Shiraz, Iran. And he was looking for some
young person who could go and help him set up the curriculum.
Cecil Watson, who was my boss, said that perhaps I might be
interested in doing this job. Hobart contacted me, but I was reluctant
because my research was going very well at the University of Minnesota, I
was happy, I did not speak the Iranian language, and I had no interest
in going to Iran. So I said to Hobart, “Hobart, why do you want to
disrupt my career for two years for something that would be a waste of
my time?”
But he was a very convincing person. He told me, “You’re a young man,
you should go for two years. You never know what you will see in terms
of diseases, and you’re a clinical investigator. You might enjoy seeing
something new. If nothing else happens, you will at least see a
different country.”
I finally accepted his challenge, went there and within two weeks of
my arrival, an Iranian physician presented a patient to me in a medical
center grand rounds. He was twenty-one years of age but looked like an
eight- or ten-year-old boy. He had extremely retarded growth, he had
hypogonadism, that is, no secondary sexual characteristics (his
genitalia were infantile) and the skin on his face appeared rough.
Superficially, it looked as if he might have suffered from vitamin A
deficiency, but we ruled this out later. He also had anemia; his
hemoglobin was 5 gram percent. As a hematologist, my first job was to
look at the red blood cells to see what was causing the anemia. I
determined very quickly that the anemia was due to iron deficiency.
But there were two problems: by reading the
Textbook of Medicine and Hematology
I learned that adult males don’t become anemic to this extent unless
there is a blood loss. And this patient had absolutely no evidence of
blood loss, so my first question was; how did he become iron deficient?
And the second major problem was that I could not explain this
extreme degree of growth retardation and hypogonadism based upon iron
deficiency. If you take rats, pigs or even elephants and make them iron
deficient, nothing happens to their growth or gonads. So those were the
two puzzles that I could not easily resolve.
I also wondered how often these cases came to the attention of
physicians. I was told by the Iranian physician who brought me the
patient that such cases were very frequent in the villages around
Shiraz; he said that if I wanted any number of cases like this they
could bring them to my service.
I was located in Nemaze Hospital, a very modern hospital in Shiraz,
Iran; it was actually a show piece for the Shah of Iran. I controlled
twelve beds under my care, so I told them to bring me twelve patients.
And sure enough, within two weeks, I had twelve such patients. I
studied them in great detail. One very interesting thing was their
nutritional history. It turned out that they were eating only bread,
made of unleavened flour. There was no animal protein intake; they had
some vegetables but very little dairy products or animal protein.
And most interestingly, they were also eating a pound of clay every
day. Shiraz is surrounded by hills and they would go there and get the
clay and eat it. I’d never seen a clay-eater in all my life, not in
Minnesota or anywhere else, and I did not quite understand why they were
eating clay, but that was the story.
PUBLISHED PAPER
I studied these twelve patients in great detail. I did not have very
good laboratory facilities in Iran but I did a very good clinical study.
I put all the clinical findings in a paper entitled, “Syndrome of Iron
Deficiency, Anemia, Hepatosplenomegaly, Hypogonadism, Dwarfism, and
Geophagia.” I submitted this paper to Professor Gutman, the editor of
the
American Journal of Medicine, and it was published in Volume 31, 1961.
In that paper, I speculated that perhaps because of the high
phosphate content in the clay and cereal protein, iron was being
chelated. I also went to the periodic table, looked at the transitional
elements and speculated that perhaps if iron is being chelated, other
trace minerals may be be affected similarly. I suggested that zinc may
be another mineral that is similarly chelated and thus unavailable for
absorption.
Zinc was very attractive to me because of earlier studies showing
that it was a growth factor for microorganisms, for plants and for
animals. So I thought that if there were a zinc deficiency in humans, I
was looking at it right there in Iran.
I included this speculation in the
American Journal of Medicine
article, and I also told the editor that if he thought that I was
speculating too far or too much and he did not like it, I’d revise my
article. Still, I urged him to publish the description of the syndrome
because this syndrome did not exist in any textbook of medicine.
Well, Dr. Gutman was a very brave editor. He reviewed the paper
himself. He wrote to me that the part he liked the most was the
speculation about zinc and he did not want to remove anything I had
written. The whole article was published completely unaltered. It’s a
sixteenpage article with great detail and information, and includes my
speculation about zinc. In 1983, this article was cited as a nutrition
classic and republished in Nutritional Review. By then, zinc deficiency
was an accepted phenomenon.
DWARFISM IN EGYPT
My paper attracted the attention of a lot of physicians,
nutritionists and biochemists in the United States. One of them was
Professor William Jefferson Darby, Chief of Biochemistry at Vanderbilt
University. He liked my idea that zinc deficiency might be contributing
to the symptoms and invited me to meet with him in Cairo, Egypt.
In Cairo, there is an institution called the United States Naval
Medical Research Unit, which was established by Franklin D. Roosevelt
for studying infectious diseases. Just before I arrived there, a
Rockefeller group had worked on typhus fever. The American army used to
be stationed in Egypt, and many soldiers died because of infections.
At that time, the Rockefeller group had left so the institute was
available to study zinc. I went there and talked to Bill Darby, but my
main concern was whether I would find these dwarfs in Egypt? I saw them
in Iran but maybe this happens only in Iran and not in Egypt or any
other country.
So I went with Bill Darby on a tour of several villages. I did not
speak the language, but I had a translator with me. To my great
surprise, I found that after visiting five villages that day, I saw
three or four patients in every village who looked like eight- or
ten-year-olds, but their chronological age was eighteen to twenty. It
shocked Bill Darby completely. He asked me, “Why do you ask the ages?”
But that was how I made my discovery.
At that point I decided to join Vanderbilt University to do the
research on zinc in Egypt. I was helped by the National Institutes of
Health, which gave me very good support, and also Admiral Galloway of
the U.S. Navy was able to provide support for my research. In addition, I
had help from the Egyptian Ministry of Public Health. With all that
help I was able to set up a good laboratory where I could measure zinc.
I did not see females when I was in Iran and Egypt; the reason was
that females would not come to me to be examined. They refused to come
to my ward but later on I had an Iranian physician working with me who
was able to examine these female dwarfs. He kept them in his own house
and found that indeed they had ovarian hypo-function and were growth
retarded. These results were reported in 1974 in the
American Journal of Clinical Nutrition.
Zinc deficiency not only affects males but also females. Other
symptoms include rough skin, poor appetite, mental lethargy, and
frequent infections. Now, this last symptom is very important: I never
saw a dwarf beyond the age of twenty-five in the Middle East, either in
Iran or Egypt. I went to the villages, asked the physicians what
happened to them, and was told that they died of infections: pneumonia,
meningitis, viral, parasitic, all kinds of infections. That convinced me
that zinc probably has a very important effect on immune cells.
TREATING ZINC DEFICIENCY
Back in those days, in 1961-1962, the measurement of zinc was very
difficult. We did not have the atomic absorption spectrometer, so you
had to do the dithizone technique. That meant shaking the tubes all day
for eight hours and at the end of eight hours, you’d get two results,
two patients. It was very arduous and difficult, and the contamination
problem was very difficult to deal with, but in spite of these problems
we were able to study forty dwarfs in great detail. Not only did we
measure zinc in the plasma, we also looked at zinc levels in the red
cells, hair and urine. By use of Zn-65, we also measured the zinc
turnover rate and exchangeable pool.
We put all these things together and showed for the first time that
indeed zinc deficiency occurs in humans. Prior to this, all the
textbooks said that zinc deficiency was never seen in human subjects.
We wanted to see whether by giving zinc we could make these dwarfs
grow, although I had never seen any such example in the textbooks of
medicine, any instance of someone aged eighteen or twenty years who
would grow just because you are giving a simple inorganic element like
zinc. I did not believe it was possible; nonetheless what we gave them
15 mg of zinc a day. We studied about forty dwarfs in Egypt.
At that time zinc capsules were not available in the market. I had to
take zinc sulfate and put it into a capsule. I also needed special
permission from the U.S. Navy and the Egyptian government to give the
dwarfs zinc. I had to argue with them that the amount of zinc I was
giving was not toxic.
To my great surprise I found that within three weeks they were
developing secondary sexual characteristics, they started growing
hair―mustache, beard and axillary hair―and within six months the
genitalia became completely normal. Even more surprising, within one
year the gain in height was five to six inches.
When I saw those results, I was truly thrilled. I knew that this was
something very important for medicine. We published several papers from
Egypt. One thing we were able to do was to discriminate between the
effect of iron and the effect of zinc. When we gave them iron, just iron
sulfate, we corrected the anemia, the hemoglobin became normal, iron
became normal, iron binding capacity returned to normal, but nothing
happened to their growth or gonads. But when we gave them zinc they
remained anemic, hemoglobin did not change, but they grew in height and
developed normal adult genitalia within six months.
CONTROVERSY AND ACCEPTANCE
Those were the basic reports that we published from Egypt. Some of my
colleagues praised the observation; they thought that it was a great
discovery. But there were several scientists who thought that it could
not happen, that zinc had no effect, and the topic became very
controversial. I had to live with controversy for almost ten years. I
constantly had to defend the thesis: why did I think it was zinc? As a
matter of fact, some of my colleagues told me that I had become a
lunatic to think that zinc was needed by humans.
In 1973, I got a call from National Academy of Sciences to appear
before the National Research Council to talk about zinc. I told the
chairman, “You read English, I have written everything in English, you
can decide on your own whether my evidence is good enough or not.”
“We have done that,” he said, “and we all in the committee agree that
zinc is important and is essential for humans, and we are planning to
submit this to the U.S. Congress to declare zinc as an essential
element. We need to establish the recommended dietary allowance (RDA)
and we want you to tell us what the recommendation should be.” And that
was a great relief for me, the controversy was ended and I had a
peaceful life after that. Based on our input the RDA was set at 15 mg
per day for adult males.
ZINC IN PARENTERAL SOLUTIONS
After my stay in Egypt, I came to the U.S. and started doing my work
on zinc in the laboratory. At that time, there was a lot of research
going on in developing parenteral solutions to give to patients who
could not eat or who had malabsorption and could not sustain life. At
that time, the rehydration solution and the parenteral nutrition
solution (TPN) were almost as perfect as you could get for all the animo
acids, vitamins, and so on. But if patients received this TPN for three
months, they would die of infection.
I was shown one patient at Harper Hospital whose hemoglobin had
dropped from twelve to nine. When I saw this patient, she was psychotic;
she had a lot of parakeratotic lesions around her eyes, mouth and
orifices, the same lesions as you see in severe zinc deficiency, in
patients with acrodermatitis enteropathica. I told the resident not to
worry about the hemoglobin but to worry about her life, and to give her
zinc. He said, “Dr. Prasad, where do I find zinc to give parenterally?”
There was no solution available so I got on the phone, called the FDA
and asked their special permission to prepare parenteral zinc solution
to give to this lady or else she would be dead within three to four
days. They gave me permission to do that. My pharmacy helped me get the
solution and the patient recovered completely.
This kind of experience had been observed by many other scientists
throughout this country and also elsewhere. FDA, USDA, NIH and U.S.
Pharmacopeia, they all decided to have a very urgent meeting in 1977 in
Chicago, and at that time it was made mandatory for the physicians to
include zinc in their parenteral solution, and this has continued to the
present time. The addition of zinc has made TPN completely successful.
Now you see patients who have been on TPN for five to ten years and are
doing very well. This is a very important story in terms of the impact
of zinc on health.
PREVALENCE OF DEFICIENCY
When I came back to the U.S., all my colleagues told me that I had
described a very important disease, made some very interesting
observations, but predicted I would never see zinc deficiency in the
United States. “What are you going to do here?” they asked.
As a matter of fact, Professor William Bean, Chief of Medicine at
Iowa University, wrote a book called Rare Diseases, and he included my
syndrome in that book. I saw him in one of the meetings and I told him I
liked his book very much but I thought he was wrong regarding zinc. I
told him I believed that zinc deficiency was not a rare syndrome and
that as time went on, we would find that zinc deficiency was more
prevalent than we realized. In developing countries, zinc deficiency may
affect as many as 50-70 percent of the population. The WHO estimate is
that two billion people have zinc deficiency.
What about the United States? We have found that in the elderly
population, 30 percent have zinc deficiency. For this reason they have
immune dysfunction, they are oxidatively stressed, and they also
generate increased amounts of inflammatory cytokines.
What about women during pregnancy, and the need for zinc for fetal
growth? The requirement under those conditions, according to the RDA, is
something like 25 mg; however, if we just look at the diet and examine
how much zinc you get in a standard American diet, there’s no way that
you can get 25 mg of available zinc. So there is a lot of zinc
deficiency in that age group.
My colleague Harold Sandstead and I published a paper on the Mexican
population of Galveston, Texas. We found that zinc deficiency affected
Hispanic children and young women at rates of approximately 25-30
percent. And then Dr. Hambidge published a paper about a Hispanic group
in Denver, Colorado, also showing widespread zinc deficiency. And I have
seen a lot of Black Americans in Michigan, particularly the patients
with sickle cell disease and others, where zinc deficiency is fairly
common.
So to say that there is no zinc deficiency in the U.S. is wrong.
There is plenty, but in most cases it is not recognized; you would have
to be very alert to find it.
As Chief of Hematology making rounds in five different hospitals, I
found that zinc deficiency was common in many other diseases. For
instance, we found that patients with liver disease have hyperzincuria;
alcoholics excrete a lot of zinc in their urine so they become zinc
deficient; patients with malabsorption syndrome become zinc deficient
very rapidly; patients with chronic renal disease also have
hyperzincuria; and we find zinc deficiency in patients with nephrotic
syndrome, glomerulonephritis and so on, even in several patients with
malignancies.
An important question to ask is why the elderly become zinc
deficient. When we started taking their history, it turns out that they
rarely eat three meals a day. They have a quick breakfast, maybe a
doughnut and coffee, no lunch and then they will have a meal they don’t
cook themselves, often eat at a restaurant. And the intake as we
calculated, in Michigan, would be around 8-10 mg of zinc per day.
Now this is not only my experience in Michigan but the same thing has
been reported in the elderly from Australia, Europe and many other
countries. The ainc intake is not optimal among the elderly subjects,
that’s the major problem. Also it turns out that the absorption of zinc
is also not optimal in this age group.
MORE RESEARCH
My next project was to set up a human experimental model of mild zinc
deficiency where there was nothing abnormal except zinc intake. I
succeeded in producing that model in Michigan, and we studied that model
for many years, publishing many significant papers on the functions of
zinc in humans.
What I did was to restrict zinc in the daily diet to around 3-5 mg.
If you consider the elderly eating some 8-10 mg, it was a marginal
deficiency that we were after, and that’s what we developed in the
volunteers. But in spite of the fact that the deficiency was very
marginal, they had a lot of evidences related to zinc defciency. For
instance, neurosensory changes: they had abnormal taste, called
dysgeusia. They could not taste sugar, salt and bitter properly. They
had problem with dark adaptation; they had decreased serum testosterone;
they developed low sperm count; and most interestingly we found that
the ammonia levels went down.
It turns out that zinc is involved and zinc-dependent enzymes are
required to utilize ammonia. We later proved this in our animal studies.
The subjects in our experiments had a lot of immunological changes.
We found that they had decreased production of interleukin-2, a very
important cytokine generated by T- helper cells. T-helper cells are a
type of white blood cell that play an important role in the immune
system.
The patients had decreased thymulin activity. Thymulin is a hormone
produced by the thymus gland that is very important for the
proliferation, development and differentiation of T-helper cells.
The thymulin story is very interesting. This hormone was isolated and
found to be a nano peptide that is zinc dependent. This work was done
by Jean-Francois Bach and Mireille Dardenne in France, and I went to
visit them. The discovery was reported, and I wanted to see whether or
not it is true in the deficiency model that I had set up.
In collaboration with Bach and Dardenne, we did a study on thymulin
in our patients here. It turns out that thymulin activity is highly
sensitive to zinc restriction. When we restricted zinc, within eight to
ten weeks, thymulin activity declined, even though there was no change
in plasma zinc. Blood levels of zinc stayed normal for twenty-four weeks
because we were restricting zinc slightly, but thymulin activity was
affected; interleukin-2 was affected as well.
These findings indicate that the immunological functions are far more
sensitive to zinc than anything that you can measure in the laboratory.
Regarding cognitive deficiencies, my colleague Professor Harold
Sandstead did some work on Chinese dwarfs, and he found that they had
impaired cognitive functions which were improved by zinc
supplementation.
ZINC THERAPY FOR ACUTE DIARRHEA
We went through the first stage where we thought that zinc was not
important for humans, then the second phase where we thought that
deficiency was very rare. Now we know that zinc deficiency is common.
And now we have learned that there are some very important therapeutic
effects of zinc in certain conditions.
The first one has to do with infants and children in developing
countries, where they frequently suffer from acute diarrhea and
respiratory tract infections. I was invited to Bangladesh about twelve
years ago, and I was shown a ward of one thousand babies with acute
diarrhea. The physicians told me that ninety percent would die within
three weeks. They were being given oral rehydration solution, which was
developed almost thirty years ago for treatment of diarrhea, but this
oral rehydration solution did not save their lives.
Professor Bob Black from Johns Hopkins University, became very
interested in zinc; he said since zinc is essential perhaps we should
add some zinc to the solution. He had his colleague Ken Brown and others
set up a program in India, Bangladesh and Pakistan. Indeed, they found
that once they added zinc to the oral rehydration solution, the children
lived, and the mortality went down very dramatically. They published
this important observation in several papers.
One interesting side story is that when Bill Gates was visiting
Bangladesh, he was told the story that these children with the diarrhea
would have died, but we are giving them zinc and with zinc they would
live. He went to India and he heard the same story; he went to Pakistan
and heard the same story; so he went back to Seattle and asked his
foundation to contact a zinc expert.
I got a call from his foundation to advise him about zinc. I went to
the foundation, and they were asking all kinds of questions as to why
they should invest money in treatment of diarrhea with Bill Gates
Foundation funds.
I told them that if you give twenty million dollars and go to twenty
countries, you would save millions of kids, you would see the result
very quickly. They bought the idea and they gave twenty million dollars,
and studies were done in twenty different countries.
A reporter for Time magazine was visiting Africa, going from one
village to another talking to families. The families would tell them
that they lost four children but the fifth one was living because they
received a small tablet of zinc. She published her article on zinc in
Time magazine. Now WHO has a program in seventy countries where zinc is
mandatory for treatment of acute diarrhea. Truly, zinc is a life-saving
element.
WILSON’S DISEASE
Wilson’s disease is a fatal genetic disorder. Normally the disease
expresses itself by the time you reach twenty, thirty or forty years,
and copper accumulates in the liver, brain and the kidneys. The patients
die by the time they reach forty or fifty years old. But we discovered
that if you give them zinc, you can decrease the copper burden.
This was an accidental discovery. In sickle cell anemia you find zinc
deficiency, and I was interested in giving zinc to decrease the
sickling of the red cells because when the red cells sickle, they
produce pain all over the body. They clog up the blood vessels and
there’s a pain crisis. In order to reduce the copper burden, however, I
had to give them 150 mg of zinc a day. At that level, we found that the
copper went down. Only then do you see low serum copper, low
ceruloplasmin and microcytosis (small red blood cells).
We published these finding in
The Journal of the American Medical Association
in 1978 or so, and this gave us the idea that perhaps in Wilson’s
disease and similar genetic disorders, we could use zinc to decrease the
copper burden.
Dr. Brewer, my colleague, has been working with this premise for
twenty years; he’s following about three hundred patients all over the
country. What he’s found is that zinc is a very effective mode of
therapy for Wilson’s disease.
The FDA has approved zinc as a therapy for Wilson’s disease, which used to be fatal but now can be managed very well.
ZINC AND THE COMMON COLD
Now a bit about zinc and the common cold. In 1984, George Eby from
Texas reported for the first time that if you take zinc acetate or zinc
gluconate lozenges, you can decrease the severity and duration of the
common cold. But between 1984 and 2000 many studies were carried out,
and the subject remained controversial. Half the reports said it works,
the other half said it doesn’t work.
I came into the picture in the year 2000, when I did two studies, one published in the
Annals of Internal Medicine and the other in
The Journal of Infectious Diseases.
There were a lot of problems with the previous studies. In the first
place was that the salts they were using for zinc lozenges were not
appropriate. You must have something where zinc is released properly in
the mouth when you take it as a lozenge. We found that gluconate or
acetate was the proper salt to use.
The second thing we found was that if you start within twenty-four
hours of the onset of a cold―there are eight to ten symptoms, and if you
have two symptoms you start immediately―the lozenges are effective, but
if you wait three or four days after the cold starts, then zinc is no
longer an effective mode of therapy, and the cold will last eight days.
The final thing that we found was that in the chemical formulation, a
lot of lozenges on the market have citric acid and many other binders;
all these binders prevent zinc from ionization and therefore render it
unavailable for action.
If all these three factors are taken care of we found that zinc is
very effective; it will reduce the duration of a cold by 50 percent and
severity by 50 percent. Recently, a big Cochrane review on zinc for the
common cold was published, and it was picked up by
The New York Times and the
Los Angeles Times among many others. The review confirmed our results that indeed zinc will be effective if all these precautions are taken.
Zinc works by decreasing the adhesion molecules where viruses attach.
So it makes sense that zinc works in the early stages of a cold, but
not later after the viruses have attached to adhesion molecules.
SICKLE CELL DISEASE
Sickle cell disease is a genetic disorder. It turns out that these
patients hemolyze red cells at a higher-than-average rate. The
hemoglobin is very rich in zinc so they lose all the zinc in their
urine, and they becme very deficient. Zinc can be very helpful for the
the treatment of sickle cell patients.
MACULAR DEGENERATION
As we get older, at least 50 percent will develop macular
degeneration, and this causes blindness. The National Institutes of
Health has been conducting a study on eye diseases and zinc and other
antioxidants for the last ten years. It turns out zinc is very effective
in the prevention of blindness and the progression of macular
degeneration.
But most interestingly, they also observed that mortality was
decreased in those subjects who were receiving zinc alone versus those
who were receiving other vitamins and antioxidants.
CARBON MONOXIDE POISONING
In Russia, a zinc histidine compound called Acyizol is being used for
carbon monoxide poisoning very effectively. In mining and related
industries, people are already using zinc histidine for carbon monoxide
poisoning in Russia.
ZINC IN THE ELDERLY
The elderly are prone to pneumonia and upper respiratory tract
infection; the incidence is something like 5-6 per year. Our recent
study has shown that by supplementing them with zinc, you reduce the
incidence by 66 percent.
Zinc has three major effects on immunology. First, it affects
cell-mediated immunity; second, it is an antioxidant; and third it works
as an anti-inflammatory agent. Why are these observations so important?
Because if you look at the current concept of many chronic diseases
including atherosclerosis, cancer and some neuro- degenerative
disorders, it is oxidative stress and chronic inflammation that are
implicated in these conditions. I suspect that zinc may be very helpful
as a preventive agent for these diseases.
ZINC AND ENZYMES
When I started my research I knew of only three enzymes that required
zinc: carbonic anhydrase, carboxy peptidase and alcohol dehydrogenase.
Today, we know of over three hundred enzymes that require zinc, and we
know of two thousand zinc-dependent transcription factors that are
involved in cell biology.
One example of a zinc-dependent enzyme is super oxide dismutase,
which converts the super oxide into hydroxy ions. Zinc generates
metallothionein, and this protein detoxifies hydroxylione. Zinc is also
an inhibitor of NADPH oxidase, which is involved in generation of free
radicals.
In the past ten years we have learned that zinc works like a
molecular signal. Once zinc goes from outside to inside the cell, it
takes part in phosphorylation of many of components and participates in
very important roles in the cell biology.
THE ACCEPTANCE OF ZINC
From
an ignored mineral, zinc has now become so important in fifty years
that a new society of molecular zinc cell biology has been formed. It
has one hundred fifty members internationally. Our last meeting was in
Australia. More and more scientists are now interested in the study of
zinc, and there is considerable research on this subject. No doubt we
will be learning a lot more about zinc in the future.
(Source:
westonaprice.org)
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The omega-3 fats from fish and conjugated linoleic acid from dairy and meat are superior fat loss nutrients. They improve insulin sensitivity by building the outside layer of cells, which makes them more receptive to insulin. They decrease inflammation—CLA is a potent cancer fighting nutrient—and have a stress reducing effect, lowering cortisol.
If you're going to take one new habit from this list, let it be that you start getting some green tea in your diet. Green tea and yerba mate come from different plants, but they both contain extremely high levels of the catechin antioxidants that promote fat loss.
Seeds are jam packed with an array of nutrients that support leanness and energy, but the irresistible thing about seeds is how the improve hormone levels. Seeds tend to be high in zinc, boosting testosterone production. They also contain compounds that promote the elimination of estrogens from the body. Supplementation with flax seeds, for example, has even been shown to decrease belly fat gain on a high-fat, high fructose diet.
Fenugreek is a spice that deserves special attention because it is so effective at improving insulin health and energy use, while increasing free testosterone when combined with strength training. A study of young men showed that supplementing with 500 mg a day while training for 8 weeks led to significantly greater improvements in strength, fat loss, muscle gain, and free testosterone over a placebo group.
Garlic has been found to increase calorie use in the body by raising the ratio of brown fat to white fat (brown fat is considered good, white is very bad).
