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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.

Tom Miller figure 1

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:

Other factors that may be protective include:

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:

Tom Miller table 1

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



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