THE ROLE OF MAGNESIUM IN THE PREVENTION OF CORONARY DISEASE
AND OTHER DISORDERS
By Tom Miller
(909) 594-1862, tmiller@tstonramp.com (5/24/97)
Introduction
In the United States, heart disease kills more people each
year than any other disease. Many of us have good reason to
better understand its causes and how to prevent it. This document
is the result of hundreds of hours research on the subject. There
is something you should know. Magnesium deficiency is
very common in this country and may be the single most
correctable factor to prevent heart and other
diseases.
Although my father suffers from congestive heart failure, this
work really started when Howard Cassidy, my uncle, had a serious
heart attack and nearly died. He is fine now but his father, my
maternal grandfather, died from heart disease at age 66. As my
uncle described his own condition, it encouraged me to begin
reading. With the advent of the Internet medical research is now
readily available, literally at our fingertips.
Please accept this in the spirit with which it is offered. The
bad news is, you are probably magnesium deficient. The good news
is, it’s cheap and easy to fix. Unless you have kidney
disease, there is sufficient legitimate medical evidence for you
to begin taking a daily magnesium supplement.
Our diets and lifestyles are much different from our
ancestors. Living in a modern industrialized country the food is
processed (depletes mineral content by 80%); drinking water is
softened (bottled water is usually very mineral deficient);
beverages are made from de-ionized water (often phosphated); and
the soils our fruits and vegetables come from are lower in
magnesium than 75 years ago. We also get less physical exercise
and deal with more day to day stress than our long departed
relatives. For these reasons, chances are very high, (over 95%),
that you do not get enough magnesium from your diet.
As a result, nearly everyone in the U.S. is magnesium
deficient to an alarmingly high degree. It won’t kill you
immediately, but over the years even a relatively small shortfall
in magnesium will gradually contribute to serious health
problems. If you are male, it will most likely be your heart. If
you are female, hormones often protect your heart until
menopause. However, since pre-menopausal women are subject to
many other maladies related to magnesium deficiency, females also
benefit from magnesium supplementation.
Chances are very high that heart disease will touch your life
in some way. Unfortunately preventing heart disease is not as
simple as taking a daily dietary magnesium supplement. There are
other factors that can cause a heart attack in spite of optimal
magnesium levels. Magnesium is not a cure all. However, the
probabilities are very high that magnesium supplementation will
prevent, or substantially delay the onset of heart and other
diseases.
Background
If you do not suffer from kidney disease, consider taking an
oral daily dietary magnesium supplement. There is a vast and
undiscovered body of well-documented research that clearly
establishes a causal link between magnesium deficiency and heart
disease. After a few weeks of daily magnesium supplementation,
even if you are used to a well-balanced diet, your body will
begin to correct metabolic deficiencies that routinely occur in
the absence of magnesium. These changes are subtle, but they will
quietly help you live longer and your quality of life will be
higher than it would have been otherwise.
Although medical research continues to define exactly how
magnesium is used by our bodies, magnesium supplementation is
among the most important things we, the general public, can do to
prevent the onset of heart and other diseases. For generally
healthy people the only known side effect from taking too much
magnesium is diarrhea. Your body continuously discards excess
magnesium through urine and feces.
If you would like to learn more I encourage you to visit the
following web site:
http://www.mgwater.com
This site offers many complete papers by the world’s
leading magnesium experts. Medical doctors have conducted a wide
array of research on magnesium deficiency beginning in the
1950’s. Dr. Mildred Seelig, a respected medical doctor and
nutritionist, has studied the subject for over 40 years. Her
book, Magnesium Deficiency In The Pathogenesis Of
Disease, Plenum, NY, 1980, is among the best works on this
subject.
Dr. Jean Durlach has performed many experiments and written
papers and books on magnesium deficit and magnesium deficiency.
Dr. Burton Altura is also a very well respected expert on this
subject with many years of experience. These doctors have worked
with credible universities and medical research facilities around
the world.
An impressive number of their research papers together with a
host of others haves been compiled and made available to the
public, at no charge, by Paul Mason, sponsor of this very
important web site.
The U.S. recommended daily allowance (RDA) for magnesium (Mg)
is 350 mg (milligrams) per day for men and 280 mg/day for women.
Most researchers studying hypomagnesemia (not enough Mg) are now
convinced the RDA is insufficient to maintain an adequate amount
of biologically available Mg for all body functions. Magnesium is
necessary for normal functioning of over 300 enzymes that are
present in your body. (Enzymes are chemical substances necessary
for normal metabolism).
Without sufficient magnesium the body loses its capacity to
move potassium into the cells where it plays very important roles
in the maintenance of good health. Magnesium is also needed to
shift calcium into and out of cells. Cells require a small amount
of calcium, however too much calcium is a problem. Magnesium
serves to regulate these essential cellular minerals.
These effects, and many more, impact a wide array of body
functions. Potassium and magnesium are the primary cations
(positively charged elements) inside cells, whereas calcium is
the major mineral in bone.
Thousands of years ago our ancestors ate foods high in
magnesium and low in calcium. Because calcium supplies were
scarce and the need for this vital mineral was great, it was
effectively stored by the body. Magnesium, on the other hand, was
abundant and readily available, in the form of nuts, seeds,
grains, and vegetables, and did not need to be stored internally.
If you do not have enough available magnesium (magnesium
deficiency), it slowly degrades your general health in a variety
of ways. Magnesium deficiency is directly linked to heart
disease. Moreover, because of the many ways your body employs
magnesium, it plays a role in diabetes, cancer, stroke,
osteoporosis, arthritis, asthma, kidney stones, migraine, leg and
menstrual cramps, eclampsia, PMS, chronic fatigue syndrome,
tetany, and a host of other problems. How magnesium deficiency
manifests itself in your body depends upon hereditary,
susceptibilities and combinations of other conditions.
Dietary Magnesium Supplementation (Dosages)
To stop or dramatically slow the onset of disease, begin
taking a daily magnesium supplement today. The rule of thumb for
men is 3.0 to 4.5 mg/pound of body weight per day as
Mg2+. That is, total dietary magnesium (Mg2+) of
600 to 900 mg per day for a 200 pound man. This includes all the
magnesium you get from food, water, vitamins and supplements.
Normal diets provide about 300 mg of magnesium per day, so the
200 pound man example would require 300 to 600 additional
milligrams (mg) per day.
Magnesium supplements (as Mg) are commonly available in 100 to
250 mg magnesium oxide (MgO) tablets or capsules. It’s
available without prescription at drug and health food stores
everywhere. For men over 150 pounds, try starting with 250 mg per
day. Take the supplement with your largest meal.
After 2 weeks increase your daily dose by a convenient
increment, say, 100 or 125 mg. (Tablets are easily snapped in
half)..) If frequent bowel movements or gas become a problem,
reduce the amount and gradually increase again by spreading the
dose over three meals.
Pre-menopausal women do not require as much Mg as men.
2.3 to 3.0 mg per pound of body weight per day is
usually sufficient to maintain adequate magnesium in
women. However, after menopause, women should
increase the dose to the same level as men.
Notes About Supplements
The symbol for magnesium is Mg. It is often also written as
Mg2+ or Mg++. The superscripts indicate its valence or electrical
charge. The doses given are for elemental Mg but we do not take
magnesium as a metal. Oral supplements are usually, but not
always in the form of MgO (Magnesium Oxide). Most supplements
will be corrected for the weight of oxygen but you should read
the label. Elemental Mg weighs 24.3 and oxygen (O) weighs 16. MgO
therefore has a total weight of 24.3 + 16 = 40.3. So it follows
that one unit of MgO contains 24.3/40.3 percent Mg. This is
roughly 60% as Mg. When examining the package, it’s good to
fully understand what you are taking. Don’t be overly
concerned about this; it’s not that big of a deal but could
cause you to be taking less Mg than you thought. 250 milligrams
as Mg requires an MgO dose of 250/0.6 = 417 mg. 100 milligrams as
magnesium requires 167 mg of MgO. Most, but not all, of the
supplement manufacturers take this into account already.
I do not want to complicate the issue but I’m obligated
to explain one other item about the bioavailability of MgO
supplements. The availability of Mg through the intestinal wall
is influenced by several factors. One of the external factors is
the reactivity of the MgO itself. That is, not all MgO’s
are the same. MgO can have varying reactivity depending on how it
was produced. High surface area MgO (low density) is more
reactive than low surface area (high density) MgO. One is not
necessarily better than the other and mineral supplement
manufacturers rarely put reactivity on the label. In fact, one
supplier that I spoke with wasn’t aware that MgO could vary
in reactivity. Their product is a "heavy" MgO, meaning that it is
more hard burned (higher density) and less reactive (easier on
the stomach). For this reason Mg availability can vary from
manufacturer to manufacturer and even from batch to batch.
Although MgO activity will vary, don’t be too concerned
about it either. Just recognize that there are some differences
and one brand may work differently for you than another. The best
way you can tell is with your bowel movements. If you are doing
too much bathroom reading, back your dosage down. If you observe
no apparent effect you may be able to take more. You have to find
your own comfort level. Your body will get rid of the excess, but
in any case I wouldn’t suggest more than 800 mg per day as
MgO. This should be plenty to get the job done.
If you are interested, there is a way to determine if you are
getting enough magnesium. I would not recommend going to the
trouble unless you suspect an electrolyte balance problem but
here’s the information.
Blood and urine levels of minerals and ions do not necessarily
reflect what is happening in the working cellular tissues. One
test, a buccal cell smear has high correlation between altered
mineral levels and pathophysiological conditions. (If
what’s going on in your body is good or bad.)
A sublingual smear is obtained by the health professional, by
briskly scraping the mucous membranes on the floor of the mouth
close to the frenulum. (The connecting fold or membrane under
your tongue.) Buccal cells have a high cytoplasm to nucleus
structure facilitating mineral analysis. They offer a rapid
renewing homogenous cell population which reflects current total
body intracellular mineral status. Analysis is performed using
scanning electron microscopy (SEM) and elemental X-ray analysis.
(EXA).
Diseases and Issues Associated With Magnesium Deficiency
Heart Disease
Magnesium deficiency plays several critical roles in the
maintenance of a healthy heart. Heart muscle cells require
magnesium as do smooth muscle cells and elastica in coronary
arteries. I’ve included a separate section on how magnesium
deficiency causes atherosclerosis and arteriosclerosis (hardening
of the arteries; athero is caused by fats, and arterio is caused
by mineral deposits).
Although most doctors are unaware, magnesium chloride is the
single best treatment following myocardial infarction (heart
attack) prior to reperfusion (getting blood back to the affected
area). The protocol for a major clinical study by the National
Institute of Health (NIH) has been written, accepted and recently
funded. The study will be known as the MAGIC study (MAGnesium In
Coronaries) and will include 10,500 MI (Myocardial Infarction)
patients across the country.
Mitral Valve Prolapse
The mitral valve or bicuspid valve is a heart valve that
consists of two triangular flaps between the left auricle and
ventricle. Magnesium deficiency has been linked to a condition
where the mitral valve malfunctions due to slippage from its
normal position. Mitral valve prolapse causes the heart to become
less effective in pumping blood and some researchers believe
magnesium helps to prevent and even correct this condition.
Cancer
There is evidence that magnesium deficiency plays a role in
oncogenesis in certain types of cancers. Changes in cell
chemistry have a direct impact on RNA and DNA. Magnesium plays a
role in polypeptide chains and is suspected of performing a role
as an oxygen free radical scavenger.
Diabetes
The role of magnesium in diabetes has been scientifically well
established for over 35 year. Magnesium influences insulin
production and function. I have spoken with Dr. Jerry Nadler of
the City of Hope here in Los Angeles. Although research into this
area is not well accepted, it is not new. Magnesium has been
effectively used to treat brittle diabetics. (Diabetics who
frequently oscillate between high and low blood sugar.)
In Europe, magnesium has long been used to treat insulin
resistant diabetes and decompensated diabetics developing
acidosis and ketosis. (Acidosis is low blood and body tissue pH.
Ketosis is an abnormal increase in ketone bodies).
Asthma and Allergies
The role of magnesium in lung function is currently being
investigated by a number of researchers. Low magnesium intake is
strongly correlated with the etiology (causes) of asthma and
chronic obstructive airway diseases. Patients treated with simple
dietary magnesium supplementation have reported marked
improvement. Inhalation of soluble magnesium compounds has also
been reported to provide relief.
Magnesium is also reported to suppress histamine production.
Some allergy sufferers have reported relief through dietary
magnesium supplements.
Arthritis
Because magnesium suppresses PTH (a mineral transport hormone)
and stimulates calcitonin (a polypeptide of 32 amino acid
residues), it helps remove calcium from soft tissues eliminating
some forms of arthritis. Copper is a metal ion long suspected as
playing a role in preventing arthritis. Copper is complementary
to magnesium uptake and may therefore reduce calcitic arthritis
by providing more magnesium absorption.
Osteoporosis
Research has clearly established a link between osteoporosis
and magnesium deficiency. Although most women have heard of the
need for calcium supplementation following menopause, few are
aware that magnesium is equally important. In fact, increasing
calcium without increasing magnesium can actually cause more harm
than good. According to Seelig and other researchers, calcium to
magnesium ratios in excess of 2:1 should be avoided.
Dr. Guy Abraham, M.D. has found strong evidence to suggest
that women with osteoporosis have a deficiency of a chemical that
is made when they take twice as much magnesium as calcium. In
fact, he found that when calcium intake is decreased, it is
utilized better than when it is present in high levels. Dr.
Abraham advocates taking more magnesium to correct calcium
deficiency related diseases.
Kidney Stones
Seelig and Bunce have clinically proven the relationship
between kidney stones and magnesium deficiency. The most common
form of kidney stones is calcium oxalate. As early as 1964 Moore
and Bunce reported the benefits of administering 420 mg of MgO
per day to patients with long histories of frequent stone
formation.
Blaine Company has marketed an MgO tablet under the tradename
Uro-Mag for over 40 years. It is a well-established treatment for
kidney stones.
Migraine
Magnesium deficiency has been linked to the onset of migraine
headaches. Magnesium plays a role in vasodilation and is thought
to behave like a calcium channel blocker at the cellular level.
Calcium channel blockers are frequently prescribed to migraine
sufferers.
Eclampsia
Magnesium deficiency has been directly linked to eclampsia, a
condition which causes life threatening convulsions and severe
hypertension which may necessitate early termination of pregnancy
with low birth weight babies. Mg treatment is classic for control
of Eclampsia.
More recently magnesium has been shown to decrease the
likelihood of pre-term birth. It has been suggested that pregnant
mothers supplement their magnesium intake to meet the high
magnesium needs placed on them by the fetus. Clinical trials have
demonstrated that mothers supplementing with MgO have larger,
healthier babies.
In Germany there have been thousands of cases demonstrating
this effect. (Conradt, Staepling and Weideinger recommend oral Mg
supplements during pregnancy)
Menstrual Cramps and PMS
Increasing dietary magnesium often decreases menstrual
cramping as well as PMS. Calcium causes muscles to contract,
while magnesium helps them to relax. Dietary calcium gives
temporary relief of menstrual cramps. However, calcium also
depletes the body of magnesium and ensures cramping will occur in
the following month if magnesium is not replenished.
Athletic Stamina
Magnesium supplementation has been used to enhance the
performance of endurance athletes such as long distance
marathoners, swimmers, and cross country skiers. Magnesium shifts
the cellular energy production from anaerobic to aerobic. This is
a more efficient mode of energy production and greatly reduces
production of lactic acid.
Triglyceride and LDL/HDL Reduction
Dietary magnesium supplementation has been reported to reduce
triglyceride levels and reduce the ratio of LDL to HDL. These are
two critical factors closely related to heart disease.
Skin Tone
It has been reported that Mg supplementation may play a role
in maintenance of skin flexibility and tone. Connective tissue is
reportedly more flexible when magnesium levels are correct.
Bone Mass and Flexibility
Magnesium imparts flexibility to bone predominately because of
its role in the bone matrix. (The organic portion of the bone.)
Magnesium behaves like flexible glue in bones. Industrial cements
produced from magnesium rather than calcium are up to 6 times
stronger and more flexible than conventional calcium-based
Portland cement.
Tetany
Farmers currently supplement cattle feed with MgO to prevent
grass tetany, milk fever, or grass staggers. Loss of brain
magnesium induces cerebral dysfunction, convulsions and death in
beef and dairy cattle. Similar conditions are observed in
hypomagnesiemic human patients.
Cerebral Palsy
A very interesting and exciting new finding is that women with
other complications, that were treated with magnesium, had 1/7
the likelihood of their low birth weight babies developing
cerebral palsy.
Leg Cramps
Leg and muscle cramping can be caused by magnesium deficiency
through production of lactic acid or reduction of arterial blood
flow. Both can be improved and often eliminated through dietary
magnesium supplementation.
Stress
Magnesium is used by some doctors to treat mental stress. On
the periodic chart, magnesium appears near lithium. Lithium is
often used to treat stress and related disorders. Magnesium plays
a role in mediating calcium dependent synapse reactions relating
to neurotransmissions.
Delirium Tremors
Alcohol depletes magnesium and can cause magnesium deficiency.
This has been tied to hallucinations and convulsions recognized
as delirium tremors.
Alzheimer’s and dementia are also suspected to be linked
to magnesium deficiency.
Atherogenesis and Magnesium Deficiency (An Hypothesis)
Back to my uncle. In describing his condition he explained
that his blockage was small and located in one of his coronary
arteries. The coronary arteries are only about 3 millimeters in
diameter so it doesn’t take much to plug them up. They
bring blood from the aorta (a large manifold at the top of the
heart) to the heart muscle itself. These coronary arteries split
into two, then four, then eight and so forth as they descend
toward the bottom of the heart. Each of these splits, or forks in
the road if you will, are called bifurcations.
My uncle’s blockage was at a bifurcation in the left
anterior descending coronary artery near the top of his heart.
This stopped blood from getting to a large portion of his heart,
and really spoiled his afternoon. It is very interesting to note
that according to cardiologists who work on this every day, about
85% of the time sclerotic plaques (gunk) form near bifurcations
first.
This pattern of injury seems to suggest (at least to me) a
strong relationship to hemodynamics. (The hydrodynamics of blood
flow.)
The following includes more terms that may not be familiar to
you. I apologize in advance however, the field of medicine like
any profession has its own language to accurately convey
information in a concise form. I’ll try to explain each
term the first time it is used. It should also be mentioned that
although the relationships detailed here are accurate, I have
found no research tying this all together as I have done here.
That’s why this part of the paper is titled an hypothesis.
It’s what I think might have happened to my uncle. Any
errors in this section are entirely mine, but it’s an
explanation that a few believe has at least some merit.
Step One
It is widely believed that atherosclerosis (hardening of the
arteries with fatty deposits) is an injury response. Meaning
something is actually damaging the arteries, rather than just
collecting stuff that is mechanically building up like silt in a
river.
Endothelial cells are a single layer of specialized cells that
form the inside of your arteries. The subendothelial layer is a
very thin connective tissue which contains elastin. As its name
implies, this is the layer responsible for providing much of the
elasticity in your arteries. It is a protein that is similar to
collagen (an insoluble fibrous protein that is the primary
component in connective tissue) and is a chief constituent in
elastic fibers. Your body requires magnesium to maintain
elastin.
Smooth muscle cells are the next layer. Smooth muscle cells
(SMC’s) provide integrity and control dilation of the
arterial cavity. Endothelial cells respond to pressure by
releasing agents that cause SMC’s to expand and contract.
This controls blood pressure and flow in the artery. One of the
earliest signs of magnesium deficiency is degeneration of the
subendothelium. Animals with low magnesium diets have been shown
to lose the elasticity of their arterial system. Coronary
arteries require more elasticity than other arteries because the
heart expands and contracts as it beats. Since these arteries are
on the heart muscle itself, they too must stretch and flex as the
heart beats. Continuing loss of elasticity results in
inflammation of the endothelial and subendothelial layers at
points that are most mechanically challenged by stretching.
Imagine a small rubber-band like tube shaped to form the letter
"Y". In your mind's eye grasp the two legs of the Y in one hand.
With your other hand, grip the single leg. Begin pulling them
apart just as though they were stretching on the surface of the
heart. Stretch it as far as you can. Where is the shape weakest?
If we left the rubber tube out in the sun for a week or so, what
would happen if you slowly stretched it again? Where might you
expect the first crack to appear? Maybe not always, but most of
the time I believe it would happen at or near where one tube
becomes two… at the bifurcation. If your artery loses
elasticity does it make sense that the problem might show up at
or near the bifurcation?
Step Two
Lipoproteins are fats that are combined with proteins
comprising cholesterol. Although not completely accurate, think
of lipoproteins as little sausages. They have a casing and inside
is the cholesterol. There are essentially two kinds of
lipoproteins (sausages); high density lipoprotein (HDL) and low
density lipoprotein (LDL). HDL is considered the good cholesterol
while LDL has been linked to heart disease. (VLDL is another
class of lipoprotein known as very low density lipoprotein.
It’s the really bad LDL.)
When inflamed, endothelium release cytokines (cellular
hormones) that can, like lipoproteins, have good or bad effects
on the artery. One type of cytokine constricts arteries and
increases coagulation; another dilates arteries and protects
against clumping of platelets on the endothelium. Cytokines
chemotactic (chemically activated) for monocytes (specialized
white blood cells), provide adhesion sites at the inflammation.
Monocytes burrow beneath the enodothelial monolayer, ingest
lipoproteins, and secrete agents to stop the inflammation.
It has been demonstrated that monocytes engorged with oxidized
low density lipoprotein (LDL) over-ingest. (They don’t know
when to stop eating the low density lipoprotein.) The term is
they are not "upward regulated", and therefore these cells burst
into foam cells. (They pig out on LDL sausages and rupture their
little membranes.) When this happens, they release free
cholesterol, cytokines, and procoagulants (thrombosis inducing
agents) into the surrounding area. This process forms plaque
which consists of a mass of lipid-engorged monocytes covered by a
fibrous cap. The whole ugly mess is pushed into the artery by the
smooth muscle cells. Injury to the endothelium is the first
pathogenic step, or genesis of atherosclerosis, therefore it is
called atherogenesis. (Literally "gruel origin"). This gruel is
usually referred to as arterial plaque. However, even before the
plaque begins, lesions are formed in the endothelium. The medical
world does not yet clearly understand what causes these lesions.
If they did, they might be able to prevent atherosclerosis and
maybe even arteriosclerosis. Since LDL ruptures monocytes when
they "eat" too much oxidized lipoprotein (LDL), lessening the
LDL/HDL ratio plays a role in lowering your risk of heart attack.
(A ratio higher than about 3.6 LDL/HDL is considered high). Some
believe that LDL/HDL ratio may be more important than your
cholesterol level. There are old people walking around today with
cholesterol levels in excess of 300 and they have no signs of
atherosclerosis. (Cholesterol levels above 240 are considered
dangerous).
The Two Step Heart Attack
Step one is the loss of arterial elasticity. Step two is the
inflammation response. These steps occur slowly over time and are
not confined to the primary coronary arteries. Smaller arteries
can suffer the same fate and slowly kill off portions of the
heart muscle or tissue at the circulatory extremities. This is a
common problem in diabetics and explains why they must pay
careful attention to foot circulation for example.
In the case of arteriosclerosis (calcified blockages)
magnesium deficiency causes the deposition of calcium in the soft
tissue response to injurey. That’s why the blockage becomes
calcified. Atherosclerosis (fat blockages) are more influenced by
the LDL/HDL ratio. In both blockages the root cause is suspected
to be directly related to magnesium deficiency.
Dietary magnesium supplementation will not reduce cholesterol.
It will however, help maintain the elasticity of your arteries
and has been reported to raise the amount of HDL. This in turn
reduces your LDL/HDL ratio and reduces the risk of heart attack.
In addition, magnesium prevents the deposition of calcium along
the arterial wall at points of micro-injury. Thus magnesium may
play a crucial role in the prevention of both atherosclerosis and
arteriosclerosis.
Finally, magnesium is important in the maintenance of healthy
muscles. The heart muscle itself benefits from an adequate supply
of available magnesium. For these reasons, magnesium is critical
to the maintenance of a healthy heart.
Traditional Risk Factors
Although the progression of atherosclerosis is well
researched, the initiating event(s) responsible for lesion
formation are still a matter of speculation. Factors strongly
correlating with increasing risk of cardiovascular disease (CVD)
include:
- Male Sex
- Aging
- Family history
- High Saturated Fat Diet
- High Sodium Diet
- Smoking
- Obesity
- Stress
- Hypertension
- Diabetes
Other factors that may be protective include:
- Exercise
- Low fat and salt
- Diets high in fruits, vegetables, whole grains and
fish
- Aspirin
- Anti-oxidants
Among the leading factors currently under investigation areis
the role of oxidative stress (free radicals), viral or bacterial
infection, vasodilation dysfunction (relating to nitric oxide
synthase), and hypertension (high blood pressure).
Why magnesium deficiency, which has been studied for more than
50 years with literally thousands of written papers, has not been
taken seriously is still a mystery. Research and advertising goes
where the money is and historically that’s been fat,
calcium and sodium, not magnesium. Free radicals are believed to
induce injury through reactive oxygen species such as superoxide
radical anion, peroxyl radicals, hydrogen peroxide, lipid
hydroperoxides, hydroxyl radical, alkoxyl radicals, ozone,
singlet oxygen, and the nitrogen free radicals, i.e., nitric
oxide and nitrogen dioxide. Hydroxyl radical is extremely
reactive with a wide range of compounds. Second order reaction
rates are commonly on the order of 2.6 x 10 to the eleventh
M/sec. OH radical is a good candidate for consideration because
it is capable of causing extensive and indiscriminate biological
damage. The Haber-Weiss reaction when catalyzed by iron can
account for the production of OH through reaction of O2- and
H2O2. (These free radicals are all oxidizers. They’re not
always bad to have around and in some cases actually help the
immune system fight off foreign microbes.)
Recent research at Harvard suggests viral or bacterial
infection may play a role in atherogenesis. Analysis of plaque
formations reveals the presence of various microorganisms in 30%
of the cases examined. (I believe this is likely opportunistic
rather than causal.)
Dr. John Cooke of Stanford University School of Medicine
believes increased levels of nitric oxide (NO) in the bloodstream
via amino acid arginine (how endothelium produces NO) decrease
the incidence of CVD (cardiovascular disease). Research has
clearly demonstrated the role of NO is vasodilation (relaxation
or increased diameter of the artery). It is speculated that
endothelial NOS (nitric oxide syntase) dysfunction may be
responsible for atherosclerosis.
High blood pressure has long been suspected as a factor in
atherosclerosis. Fifty million Americans have systolic blood
pressure averaging greater that 140 mm Hg and/or diastolic
pressure of 90 mm Hg or greater. While epidemiologic
investigations fail to establish a causal link, most researchers
agree that hypertension plays a role in atherogenesis.
Considerable research has been performed attempting to link
oxidative stress, NO inhibition, or hypertension with
atherogenesis.
They may all be correct. That is, each plays a symptomatic
role. However, magnesium is the one common thread that links them
together. Magnesium has been proven to reduce oxidative stress
and therefore plays an anti-oxidant role in regulation of free
radicals. Vasodilation is controlled by nitric oxide, but it is
implemented by magnesium in the muscles. Bacteria and viruses in
the atheroma are there because these organisms attempted to
exploit the inflammation, and then got caught up in the
body’s immune/infection response.
This may be a bit oversimplified but it makes sense to me, and
to a lot of well-qualified doctors I have suggested the idea
to.
How is Magnesium Different from other Cations?
Physiologically important cations (elements important to
electrolyte balance, pH and formation of enzymes) include sodium
(Na), calcium (Ca), magnesium (Mg), and potassium (K). The ionic
radii, and oxidation potentials are:
At the cellular level magnesium is important because of its
charge density (charge to size ratio). This may also account for
flexibility and elasticity imparted by magnesium in bone and
muscle.
Intracellular pH is maintained by ion transfer through the
cell membrane and magnesium has been identified to influence the
transport across each of the other cation pathways. (That’s
why magnesium and calcium, for example, can be antagonistic to
one another.) In cells, ion channels play a role in maintenance
of the optimum physiological Cation-Anion balance. This has to do
with pH control both inside (intracellular) and outside
(extracellular) the cell. Magnesium and calcium are both divalent
cations. (That means they have an atomic charge of plus two.)
Sodium and potassium are monovalent cations. (They have a charge
of plus one.) Electrolyte chemistry is very complex and requires
a careful balance of protons and electrons. Magnesium plays a
critical role because, on a mass basis, it is associated with
more anions than the other cations.
Magnesium and Energy Production
Muscle fibers take up glucose (sugars) and either use it
immediately, or store it in the form of glycogen. During
exercise, glycogen is broken down to glucose which then goes
through a sequence of enzymatic reactions that either require
oxygen for aerobic metabolism, or with sub-optimal oxygen, shifts
to anaerobic (in the absence of oxygen). With the presence of
magnesium, glucose is metabolized through the aerobic cycle
rather than the less efficient anaerobic cycle. These reactions
occur in the cytosol. (This is the fluid portion of the cytoplasm
inside cells.) In the absence of magnesium this pathway is the
anaerobic (no oxygen) glycolysis (glucose breakdown) pathway.
Glucose molecules that go through this sequence of reactions
generate lactic acid. Lactic acid is well recognized as being
responsible for sore muscles and cramping. Magnesium helps the
cells to maintain aerobic metabolism, even with heavy exercise,
which results in a decrease in lactic acid and a decrease in
muscle cramping. If you want a good example of this phenomenon
you need only perform an infrequent physical chore (like clipping
the hedges, throwing a baseball, lifting, etc.) with and without
a magnesium supplement. If the difference does not impress you,
you’ll be the first.
Summary
Magnesium deficiency is suspected to contribute to
atherogenesis by reduction of arterial elasticity. Medical
research has produced thousands of articles relating magnesium
with a wide array of problems including heart disease, cancer,
atherogenesis, diabetes, asthma, migraine, osteoporosis,
arthritis, chronic fatigue syndrome, kidney stones, leg cramps
and a host of other problems too numerous to mention.
J. K. Aikawa, a well-respected medical researcher, observed
the relationships between magnesium deficiency and disease in
humans and animals. Magnesium’s role in life has been
described as "biological glue". Photosynthesis and many important
biologic functions are impossible without Mg. It is essential for
plant and animal life. According to epidemiological research in
the United States and elsewhere, unless you currently take a
daily magnesium supplement, or drink magnesium-rich hard water,
there is a very high probability that you are magnesium
deficient. For this reason, daily oral supplementation with MgO
will delay the onset of a wide range of diseases. (If you have
kidney disease, consult your doctor first.)
Total daily dietary magnesium for men should be in the range
of 3.0 to 4.5 mg per pound of body weight per day. Pre-menopausal
women require less Mg than men. 2.3 to 3.0 mg per pound of body
weight per day is usually sufficient. Increased bowel movement
frequency will help you to determine your optimum dose. Spread
your supplements over all three meals if necessary.
Although unpopular, it is worth mentioning that reduction or
elimination of large amounts of phosphated beverages such as
Pepsi, Coke, and other carbonated phosphates will reduce
physiologic loss of essential minerals. Switching to beverages
such as citrus drinks, non phosphated sodas, cranberry and grape
juice will decrease this source of demineralization. Phosphate
tightly binds Mg and is an Mg waster that contributes to
magnesium deficiency. Most juices (except apple) are rich in
magnesium.
The medical community is slowly becoming aware of the benefits
explained herein. If you have any concerns, please consult your
family doctor. Feel free to give him/her a copy of this letter.
If they’ve not heard of the benefits of magnesium, I would
be happy to refer them to many excellent medical papers and
expert medical doctors familiar with the subject.
Acknowledgments
Thanks to Dr. Alan Heldman, Johns Hopkins Bayview Medical
Center for his friendship and continuing support. I also want to
thank Dr. Mildred Seelig for her extensive work on this subject
and the many hours she has willingly spent discussing the subject
with me. I especially want to thank Paul Mason for his work on
the web site. Few moments in life are as exciting as when I first
found their site on the Internet.
Thanks to my family, and special thanks to doctors Mark Shand
and Ron Wardle. Finally, thanks to my uncle, Howard Cassidy. His
pain has benefited those of us who may now avoid the horror of a
heart attack.
References
(This is actually only a small fraction of the works reviewed.
If you would like more, give me a call.)
Heldman, A & Goldschmidt-Clermont, P. (1996): The
Molecular Biology of Coronary Disease, Bernard Laboratory for
Fundamental Research in Preventive Cardiology, Division of
Cardiology, Department of Medicine, Johns Hopkins University
School of Medicine.
Durlach J, Durlach V, Bac P, Bara M, Guiet-Bara. A Magnesium
and therapeutics. Magnes Res 1994 Dec; 7(3-4):313-28
Cardiovascular Consequences of Magnesium Deficiency and Loss:
Pathogenesis, prevalence and manifestations. Magnesium and
chloride loss in refractory potassium repletion, Mildred S.
Seelig, M.D., M.P.H. New York Medical College, Valhalla, and the
American College of Nutrition, Scarsdale, New York
Cooke, John P, MD, Ph.D. Anti-atherogenic effects of nitric
oxide: mechanisms of action. Stanford Univ Sch of Medicine,
Stanford, CA.
Reue, Karen L, Ph.D. Apolipoprotein A-IV expression and
function. West Los Angeles VA Med Center, Los Angeles, CA.
Sladek, Frances M, PhD. Transcription regulation
apolipoproteins by HNF- 4. Univ of California, Riverside,
Riverside, CA.
Smith, Jeffrey W, Ph.D. Structure-function relationships of
platelet and endothelial cell integrins. La Jolla Cancer Research
Fndn, La Jolla, CA.
Foy, Robyn A, Ph.D. Effect of pH on vascular-endothelial cell
interaction. University of Iowa, Iowa City, IA.
Moy, Alan, MD. The role of endothelial contraction and
adhesion in inflammatory edema. Univ of Iowa, Iowa City, IA.
Nelin, Leif D, MD. The role of endothelium in developmental
and pathologic changes in pulmonary hemodynamics. Medical College
of Wisconsin, Milwaukee, WI.
Moczydlowski, Edward G, Ph.D. Function and regulation of a
Ca2+-activated K+ channel in vascular smooth muscle. Yale
University, New Haven, CT.
Segal, Steven S, Ph.D. Microvascular hemodynamics: effects of
muscle mechanics. John B Pierce Laboratory Inc, New Haven,
CT.
Sinusas, Albert J, MD. Multimodality 3-dimensional assessment
of flow and functional reserve for determination of myocardial
viability. Yale University, New Haven, CT.
Welsh, Donald G, Ph.D. Effects of active and passive tension
on microvascular hemodynamics. Yale Univ School of Medicine, New
Haven, CT.
Adams, David J, Ph.D. Signal transduction and adhesion in
vascular endothelium. University of Miami, Miami, FL.
Harrison, Jeffrey K, Ph.D. Characterization of the ligand
binding site of the angiotensin (AT) receptor. Univ of Florida
Sch of Med, Gainesville, FL.
Haught, Walter H, MD. Common mechanisms of inhibition of
atherosclerosis by anti-oxidants, hypocholesterolemic agents, and
calcium blocker. Univ of Florida Sch of Med, Gainesville, FL.
Irby, Rosalyn B, BS. Differential expression of sterol carrier
proteins in diabetic hypercholesterolemia. Univ of S Florida Sch
of Med, Tampa, FL.
Visner, Gary A, DO. Endothelin-1 regulation in human pulmonary
endothelial cells. University of Florida, Gainesville, FL.
Kuppusamy, Periannan, Ph.D. Measurement of oxygen
concentration and distribution in the heart using electron
paramagnetic resonance spectroscopy. Johns Hopkins Medical
School, Baltimore, MD.
Gordon, David, MD. Vascular biology patterns of collagen gene
expression in human atherosclerosis. Univ of Michigan Med School,
Ann Arbor, MI.
Shayevitz, Jay R, MD. Endothelial oxidant injury and calcium
dysregulation: interactions with violatile anesthetics.
University of Michigan, Ann Arbor, MI.
Lerman, Amir, MD. Endothelin in coronary atherosclerosis in
humans. Mayo Clinic, Rochester, MN.
Daugherty, Alan, Ph.D. Myeloperoxidase: A putative mediator of
oxidative changes in atherogenesis. Washington University, St
Louis, MO.
Daugherty, Alan, Ph.D. Arterial lipoprotein receptor
modulation in atherogenesis. Washington University, St Louis,
MO.< /p>
This page was first uploaded to The Magnesium Web Site on May
24, 1997
http://www.mgwater.com/
Healthy Water
Association--USA