Cardiovascular Risk Factors and Magnesium

[Guest guest]

Cardiovascular Risk Factors and Magnesium JoAnn Guest Jan 11, 2005 18:34 PST

Relationship to

Atherosclerosis, Ischemic Heart Disease and Hypertension

 

http://www.mgwater.com/alturacv.shtml

--

B.M. Altura, B.T. Altura

Department of Physiology, State University of New York Health Science

Center at Brooklyn, N.Y., USA

---

Key Words.- Atherogenesis - Coronary vasospasm Bioenergetics, cellular -

Dietary Mg intake - Lipid accumulation- Modulation of Ca metabolism in

cardiac and vascular muscle

 

Abstract.

Hypertension and atherosclerosis are well-known precursors of ischemic

heart disease, stroke and sudden cardiac death. Although there is

general agreement that the " atheroma " is the hallmark of atherosclerosis

and is found in coronary 'obstruction', there is no agreement as to its

etiology.

 

It is now becoming clear that a lower than normal dietary intake of

Magnesium can be a strong risk factor for hypertension, cardiac

arrhythmias, ischemic heart disease, atherogenesis and sudden cardiac

death.

 

Deficits in serum Magnesium appear often to be associated with

arrhythmias, coronary vasospasm and high blood pressure.

 

Experimental animal studies suggest interrelationships between

atherogenesis, hypertension (both systemic and pulmonary) and ischemic

heart disease.

 

Evidence is accumulating for a role of Mg2+ in the modulation of serum

lipids and lipid uptake in macrophages, smooth muscle cells and the

arterial wall.

 

Shortfalls in the dietary intake of Mg clearly exist in Western World

populations, and men over the age of 65 years, who are at greatest risk

for development and death from ischemic heart disease, have the greatest

shortfalls in dietary Mg.

 

It is becoming clear that Mg exerts multiple cellular and molecular

effects on cardiac and vascular smooth muscle cells which explain its

protective actions.

 

Introduction

 

Globally, among the leading causes of death, hypertension and

atherosclerosis rank at the top of the list. These cardiovascular

diseases, obviously, are the forerunners or precursors of ischemic heart

disease, stroke and sudden cardiac death.

 

Among mortality and morbidity indices for man, ischemic heart disease

ranks at the top of the list.

 

In the industrialized world ischemic heart disease is the leading

killer and accounts for approximately 35% of all deaths each year. The

incidence of this disorder rises to 80% in people over 70 years of age.

 

The most common cause of death results from " insufficient " coronary

blood flow.

 

Some deaths can occur rather suddenly, for example, sudden-death

ischemic heart disease. Possibly, as many as 40-60% of the latter may

occur in the complete absence of any prior atherosclerosis, " thrombus

formations " or " cardiac arrhythmias "

[for review, see 1].

 

These syndromes are often referred to as nonocclusive sudden-death

ischemic heart disease.

 

Other forms of ischemic heart disease can result in death as a

consequence of an " acute coronary occlusion " or " ventricular

fibrillation " ,

whereas others are still thought to come about from slow, progressive

occlusion of coronary vessels over a period of weeks to years.

 

Although there is general agreement that the " atheroma " is the hallmark

of atherosclerosis and is found in " coronary obstruction " , there is no

agreement at present as to either the characterization of the early

intimal changes or their etiology.

 

Hallmarks of Atherosclerosis

 

Irrespective of the etiology of atheromas, the " lesions " usually consist

of a " fibrous " cap containing smooth muscle cells, " macrophages " , " foam

cells " and " lymphocytes "

[for reviews, see 2, 31.

 

In addition, there appears formation of dangerous " necrotic centers "

consisting of " cholesterol crystals " , " cholesterol esters " , " calcium

ions " and dying foam cells.

 

What produces these characteristics is not completely known.

 

Although vascular smooth muscle cells in atheromas change from a

contractile to a noncontractile state and become responsive to

platelet-derived growth factor and elaborate connective tissue, no one

knows how these cells are transformed.

 

Finally, although " T lymphocytes " , " platelets " , " neutrophils " and

" macrophages " are found in developing 'atherosclerotic plaques', it is

not known what allows such cells to enter the vessel wall or be

attracted to the potential " plaque " site.

 

Theories on the Etiology of Hypertension

 

Although many theories have been suggested in the etiology of

hypertension, it is not known why peripheral blood vessels exhibit

increased responsiveness to pressor substances

[for review, see 4].

 

It is not known why peripheral blood vessels undergo " vasoconstriction "

either.

 

And, of course, it is not known why hypertension leads to a high

incidence of strokes and sudden cardiac death.

 

Is it possible that the atherosclerotic and hypertensive events are

related to the diet or the dietary intake of a particular food

substance, metabolite or element?

 

Are these vascular disease processes related to " mineral metabolism " ,

per se?

 

Why is the incidence of hypertension, atherosclerosis, sudden-death

ischemic heart disease and stroke low, in South African Bantu natives,

Bedouins in the Arabian desert, Aborigines in Australia and

Greenlanders?

 

And why, when these indigenous populations move to Western

civilizations, do the incidences of these cardiovascular diseases equal

those of Western civilized populations?

 

Relation of Soil Magnesium Content and Water Hardness to Incidence of

Cardiovascular Disease

 

If one divides the US into Eastern and Western halves, you begin to see

several interesting " phenomena " .

 

First, the soil Magnesium content in the Eastern USA is about one third

that of the Western USA

(table 1).

 

Second, the water hardness of the Eastern USA is one half that of the

Western USA

(table 1).

 

Third, although the death rate for cardiovascular diseases in the

Eastern USA is significantly higher than that of the Western USA,

noncardiovascular death rates are equivalent (table 1).

 

Similar phenomena have been observed in Canada, Finland and South

Africa [6-11]. In 1983, Leary and Reves [10] published findings from 12

magisterial districts in South Africa demonstrating that as the

concentration of Mg in the drinking water was found to be less and less,

in various geographical regions, the death rate from ischemic heart

disease was seen to rise more and more.

 

Studies such as these and others like them [6-9, 11] suggest that maybe

there is an important relationship between dietary Mg intake and the

incidence of heart disease.

 

 

Importance of Dietary Mg versus Ca Intake

 

Approximately, 12 years ago, Karppanen et al. [12] in Finland published

interesting findings in which it was suggested that the " ratio " of

'dietary' calcium to magnesium may be linked to ischemic heart disease.

 

According to the most recent USA dietary surveys, the Calcium:Magnesium

ratio in average American diets is rising.

 

Incidence of Hypomagnesemia in Hospitalized Patients:

Possible Relationship to Incidence of Cardiovascular Disease

 

During the past 10 years, a considerable number of studies have appeared

which indicate that hospitalized patients have incidences of

" hypomagnesemia " ranging from 7 to 60%, depending upon the type of

patient

[for reviews, see [1, 14].

 

What is particularly important to note here is that many of these

patients are in acute coronary care units and intensive care units.

 

Many of these patients present with numerous " cardiovascular

abnormalities " including " cardiac arrhythmias " , " atrial fibrillation " ,

" hypertension " , " strokes " and " myocardial infarctions " (heart attacks).

 

Deficit of Myocardial Magnesium Content and Ischemic Heart Disease

 

Ever since the early studies of Iseri et al. [15] in 1952, there has

been an increasing number of case reports and studies which indicate

that hearts of patients who die of sudden-death ischemic heart disease

exhibit " deficits " of Magnesium [for reviews, see 9, 11, 14].

 

On the average. there appears to be about a 20% deficit in cardiac

Magnesium content in these patients.

 

Magnesium is the only metal to be decreased to this extent consistently.

 

It is important to note that we and others have found that coronary

arteries of such victims often exhibit " deficits " of 30-40% in total

Magnesium content.

 

These deficits in Mg content do not appear to be a consequence of

cardiac necrosis for several reasons. First of all, nonnecrosed cardiac

tissue areas clearly exhibit approximately the same 20% reduction in

myocardial Mg, unlike the necrotic areas which can exhibit deficits of

almost 50% in Mg content of [9, 11, 16-181.

 

Anginal History and Myocardial Mg Content

 

It is rather interesting to note that patients with a history of angina

on autopsy exhibit severe " cardiac deficits " in Mg, whereas patients

without a history of angina appear to exhibit a near-normal myocardial

Mg content.

 

Is deficiency of myocardial Magnesium limited only to angina pectoris

and sudden-death ischemic heart disease, or is Mg deficiency also found

in other myocardial syndromes?

 

Loss of Myocardial Mg in Cardiac lschemic Syndromes

 

An examination of the literature reveals a growing body of evidence to

indicate that loss of myocardial Mg is seen in a host of " myocardial

lschemic " syndromes from " myocardial infarction " , " arrhythmias " ,

" torsades de pointes " to experimental and " iatrogenic ischemic " injuries

[for reviews, see 9, 11, 14].

 

Many of these are clearly associated with prior histories of

atherosclerosis and/or hypertension.

 

Hypertensive Vascular Disease and Mg Deficiency

 

Is hypertensive disease associated with Mg deficiency in blood and/or

tissues?

 

If so, hypertensive disease should be brought about in some cases solely

by Mg deficiency, and hypertension should be exacerbated by Mg

deficiency.

Finally, a variety of hypertensive syndromes should be amenable to

treatment with Mg (cell)salts.

 

At this point, we would like to take the opportunity to review some of

this evidence, including some of our own findings.

 

A number of studies in spontaneously hypertensive rats clearly

demonstrate (except for one study by Overlack et al.)

that the serum content of total Mg is " significantly reduced " in

'hypertensive' animals [for review, see 21].

 

An examination of most of the clinical studies on hypertensive patients,

so far studied, who received " diuretics " , where blood pressure often

continued to rise,

demonstrates that serum Mg is clearly, " reduced " by about 15-20% [for

review, see 21].

 

A few years ago, Resnick et al. [22] examined red blood cells from

hypertensive subjects and found that the ionized Mg2+ determined by 31P

nuclear magnetic resonance (NMR) spectroscopy was inversely related to

the diastolic blood pressure.

 

That is. the greater the " elevation " in diastolic blood pressure, the

" lower " the " ionized red blood cell Mg2+ content " [22].

 

Salt-Induced Hypertension and Mg

 

If all of this is so, then even " salt-induced " hypertension might be

expected to be associated with " Mg deficiency " and should be treatable

with 'Magnesium salts'.

 

We, therefore, utilized various groups of uninephrectomized male Wistar

rats given weekly implants of deoxycorticosterone acetate in order to

produce malignant salt-induced hypertension.

 

Some animals were allowed to drink Mg aspartate HCl freely, daily, for

periods up to 12 weeks.

Others were allowed to drink the Mg salt 4 weeks after salt hypertension

for an additional 12 weeks.

 

Table 2 summarizes some of our data. By 3 weeks, mean arterial blood

pressure was elevated in all deoxycorticosterone acetate + salt groups.

 

However, by 9 weeks, the groups which received " Mg supplements "

exhibited significant " lowering " of blood pressure.

 

Many of the untreated animals with malignant hypertension died at 4-7

weeks of blood pressure levels in excess of 245 mm Hg.

 

Figure 1 clearly shows that there is a deficit in serum Mg in

uninephrectomized rats with salt-induced hypertension and that serum Mg

levels are restored to normal in rats allowed to drink Magnesium.

 

Interestingly, serum phosphate levels are also reduced in animals with

malignant hypertension, whereas rats given Mg exhibit a restoration of

phosphate to normal levels.

 

Hypophosphatemia itself is known to produce high blood pressure.

Whether or not this contributes to salt-induced hypertension in these

animals is under investigation.

-

 

In view of these experiments, we wondered whether pulmonary hypertension

is amenable to Mg therapy and whether the vascular remodeling that

normally takes place in the pulmonary circulation in this syndrome can

be " ameliorated " or " prevented " by Mg.

 

Rats were administered 40 mg/kg of monocrotaline. This plant extract is

known to produce specific pulmonary hypertension in all mammals so far

investigated, and a pulmonary, vascular remodelling takes place within

14-21 days. We examined all animals 21 days after monocrotaline [23].

 

Animals which received monocrotaline exhibited significant elevation in

pulmonary blood pressure [23]. Controls and control animals which

received oral " Mg aspartate HCl " exhibited no alteration in pulmonary

pressure. However, monocrotaline-treated animals which received Mg

aspartate HCl for 21 days exhibited a significant amelioration of

pulmonary hypertension.

 

If true pulmonary hypertension is observed in human subjects or animals,

the right ventricular to left ventricular ratio should be elevated. Our

monocrotaline- treated animals clearly manifested a right ventricular to

left ventricular ratio that was increased as expected .

 

The monocrotaline-treated animals, however, which received Mg therapy,

clearly exhibited reduction in the elevated right ventricular to left

ventricular ratio suggesting a " reversal " of the pulmonary hypertension

[23, 24].

 

If the latter is true, then we would expect to see attenuation of the

pulmonary hyperplasia of the arterial wall normally seen in pulmonary

hypertension.

 

Arteriolar and arterial walls clearly underwent significant hyperplasia,

after monocrotaline, with encroachment of the lumens [23-25].

 

Mg therapy, reversed the monocrotaline-induced hyperplasia. Obviously,

elevated levels of Mg must exert significant attenuating effects on

collagen and elastin synthesis and smooth muscle cell hyperplasia

[23-25].

 

These actions might therefore be of value in the treatment of

atherosclerosis.

 

Genetic Predisposition to Hypertension and Tissue Magnesium Levels

 

Is there any evidence to indicate that teenagers, that is children below

the age of 20 years, may exhibit Mg deficits which could be a risk

factor for the development of hypertensive vascular disease?

 

In the past 2 years, a group in Japan (headed by Shibutani in Hyogo

Medical College) has begun to publish a number of reports which suggest

that male children of parents with a genetic history of familial

hypertension exhibit significant deficits in red blood cell Mg content .

 

 

This may be the first study to clearly suggest that a predilection for

high blood pressure could develop in young males if, genetically, they

exhibit " deficits " in tissue Magnesium.

 

Dietary Mg Intake and Atherogenesis

 

If atherosclerosis is a strong risk factor for hypertension, ischemic

heart disease and stroke, and these are truly interrelated, then Mg

should exert strong effects on atherogenesis.

 

We, therefore, decided to examine rabbits given 1 or 2% cholesterol with

varying Mg intake [27]. The Mg intake was varied from 40% of normal to

normal or 2.5 times the normal intake.

 

The animals were followed serially for up to 10 weeks. Aortas were

excised and stained with Sudan 4 and examined histologically for

lesions.

 

No lesions could be found from rabbits ingesting normal chow with normal

lipid and Magnesium intake or normal synthetic chow .

 

High cholesterol intake in the presence of normal dietary Mg resulted in

significant atherosclerotic lesions.

 

The animals receiving low dietary Mg and 2% cholesterol exhibited

lesions far in excess of those observed with normal Mg intake.

 

However, if the intake of Mg was raised to 2.5 times normal, despite the

high cholesterol intake, the " atheromas " were greatly 'attenuated',

suggesting that Mg intake can " modulate " atherogenesis.

 

Overall, the data clearly indicate that the greater the lipid intake,

the greater the number of atherosclerotic lesions .

 

In addition, these data indicate that the lower the dietary intake of

Mg, the greater the risk for developing atheromas.

 

 

Stating this another way, it is also clear that the higher the intake of

Magnesium, the less chance for developing atheromas despite high lipid

intake.

 

Our data would seem to suggest that Mg must exert significant effects on

smooth muscle, macrophage and monocyte " accumulation " of " lipids " and

might affect chemotaxis and the activity of growth factors 'implicated'

in atherogenesis.

 

If this is all true, then dietary intake of Mg would be an important and

maybe critical factor in the prevention of atherosclerosis,

hypertension, cardiac disease, stroke and sudden cardiac death.

 

In addition, such a hypothesis would suggest that a suboptimal dietary

intake of Mg should put human subjects at risk for development of

cardiovascular disease.

 

Progressive Decline in Dietary Intake of Mg over the Past 90 Years

 

It is rather interesting that if one examines the intake of Mg over the

past 90 years, we note that there is a progressive and alarming decline

in Mg intake at the present time (table 3).

 

An examination of a recent US Department of Agriculture HANES dietary

survey reported in 1985 indicates clear and significant shortfalls in

dietary Mg, assuming an intake of 350 mg/day is needed for normal Mg

balance.

 

It is also clear from this survey that men over the age of 65 years,

who are known to present the greatest risk for death from ischemic heart

disease (vide supra), exhibit the greatest shortfalls for dietary Mg of

all male age groups.

 

This may be more than coincidental.

 

Protective Mechanisms of Mg Action against Death from Ischemic Heart

Disease

 

If Mg can ameliorate atherosclerosis and hypertension, and promote

coronary vasodilation and unloading of the heart, are these the primary

mechanisms of the protective actions of magnesium ions against death

from ischemic heart disease, or does Mg exert direct actions on

" myocardial bioenergetics " as well?

 

We will therefore present and discuss some of our recent experiments on

intact perfused hearts which may have direct bearing on this question.

 

31P NMR Spectroscopy, Myocardial Bioenergetics, [Mg2+]i and [pH]i

 

In order to get an assessment of cellular bioenergetics, we have

employed 31P NMR spectroscopy and near-infrared spectroscopy [28, 29].

 

When the perfusate magnesium ion concentration is " elevated " to

hypermagnesemic levels (2.4-4.8 mM), " coronary flow " , stroke volume,

" cardiac output " and aortic pressure are seen to

" rise " rather significantly, suggesting that Mg ions can exhibit

inotropic-like effects.

 

At the same time, the heart rate and rate-pressure product are

decreased, suggesting that Magnesium unloads the heart and " increases

its efficiency " .

 

The 31P NMR spectra for elevated magnesium indicated that elevated

[Mg2+]o results in elevated phosphocreatine levels (by 22-40%). Second,

inorganic phosphate levels were decreased, and there were chemical

shifts in the 31P NMR spectra produced by elevated Mg [28, 29].

 

Clearly, elevated Mg resulted in spectral shifts, which suggest that

alterations in myocardial intracellular, free Mg ions and intracellular

pH must have occurred.

 

Elevation in [Mg2+]o (i.e. 2.4-4.8 mM) clearly resulted in elevation of

intracellular, free Mg ions and alkalinization of the cytosol. Elevation

of the intracellular pH in the presence of elevation of intracellular,

free Mg ions would increase the creatine kinase reaction, resulting in

more phosphocreatine, contractile force and stroke volume, exactly as we

have observed.

 

It was clear from our data that elevation in extracellular Mg ions to

4.8 mM resulted in a 40% rise in phosphocreatine.

 

 

Influence of [Mg2+]o on Mitochondrial Levels of Cytochrome Oxidase and

Oxymyoglobin

 

Using a noninvasive near-infrared spectroscopic technique, we have

clearly found that the mitochondrial levels of oxidized cytochrome aa3

and oxymyoglobin are increased by elevation in extracellular Mg ions 31P

NMR [28]. These data coupled with the data suggest that the efficiency

of the myocardium is enhanced by Mg ions.

 

Reduction in [Mg2+]o Results in Myocardial Cellular Reduction in

[Mg2+]i, [pH]i, Oxymyoglobin and Oxidized Cytochrome aa3

 

If, however, the extracellular Mg ions are reduced below normal, the

cytosol becomes acidic and the intracellular free Mg ion level is

significantly altered [30].

 

Preliminary experiments indicate that reduction in extracellular Mg ions

or hypomagnesemia leads to rapid falls in oxymyoglobin levels.

 

Finally, our recent near-infrared experiments indicate that subjection

of intact rat hearts to hypomagnesemia clearly, results in increased

mitochondrial levels of reduced cytochrome oxidase aa3.

 

Conclusions

 

It is becoming clear that a large body of epidemiologic data supports

the idea that lower than normal dietary intake of Mg can be a strong

" risk factor " for hypertension, cardiac arrhythmias, ischemic heart

disease and sudden cardiac death.

 

Lower than normal myocardial and coronary vascular Mg content seems to

pose " serious risks " for angina, coronary vasospasm, ischemic heart

disease and sudden cardiac death.

 

" Deficits " in serum Mg appear often to be associated with arrhythmias,

coronary vasospasm and high blood pressure.

 

Experimental animal studies seem to suggest interrelationships between

atherogenesis, hypertension and ischemic heart disease.

 

Evidence is clearly accumulating to implicate a role for Mg in the

modulation of serum lipids, lipid uptake in macrophages, smooth muscle

cells and the arterial wall.

 

There clearly appear to be considerable shortfalls in dietary intake of

Mg in Western world populations, and that men over the age of 65 years,

who are at greatest risk for death from ischemic heart disease, have the

greatest " shortfalls " in dietary Mg.

 

Although Mg clearly influences calcium uptake and distribution in

vascular smooth muscle cells which can modulate vasomotor tone, it is

now becoming clear that Mg ions can directly " alter " myocardial cellular

bioenergetics and influence (possibly dictate)

efficiency of the myocardium.

 

Noninvasive techniques such as 31P NMR spectroscopy, near-infrared

spectroscopy and image analysis should aid in the clarification of the

role of Mg as an important risk factor in cardiovascular disease.

 

Acknowledgement

 

The original work received herein was supported in part by NIAAA

research grant AA-08674.

 

References

 

1 Altura BM: Ischemic heart disease and magnesium. Magnesium

1988;7:57-67.

 

2 Ross R: The pathogenesis of atherosclerosis. N Engl J Med

1986;314:488-500.

 

3 Lee KT, Onodera K. Tanaka K (eds): Atherosclerosis II. Recent Progress

in Atherosclerosis Research. Ann NY Acad Sci 1990;598:1-589.

 

4 Laragh J, Brenner BM: Hypertension: Pathophysiology, Diagnosis and

Management. New York, Raven Press, 1990, vol 1 and 11.

 

5 Masironi R: Geochemistry and cardiovascular diseases. Philos Trans R

Soc Lond 1979;288:193-203.

 

6 Marier J, Neri LC, Anderson TW: Water hardness, human health and

importance of magnesium, rep No 17581. Ottawa, Natl Res Council

Canada,1979.

 

7 Marier J, Neri LC: Quantifying the role of magnesium in the

interrelationship between human mortality/morbidity and water hardness.

Magnesium 1985;4:53-59.

 

8 Altura BM: Magnesium and regulation of contractility: in Altura BM

(ed): Advances in Microcirculation: Regulation of the Microcirculation.

Basel, Karger. 1982, pp 77-113.

 

9 Altura BM, Altura BT: Magnesium-calcium interaction and contraction of

arterial smooth muscle in ischemic heart diseases, hypertension and

vasospastic disorders. in Wester P (ed): Electrolytes and the Heart. New

York, Transmedica, 1983, pp 41-56.

 

10 Leary, WP, Reyes AJ: Magnesium and sudden death. S Afr Med J

1983;64:697-698.

 

11 Altura BM, Altura BT: New perspectives on the role of magnesium in

the pathophysiology of the cardiovascular system. I. Clinical aspects.

Magnesium 1985;4:226-244.

 

12 Karppanen HR. Pennanen R. Passinen L: Minerals, coronary heart

disease and sudden coronary death. Adv Cardiol 1978;25:9-24.

 

13 Morgan KJ, Stampley GE, Zabik ME, Fischer DR: Magnesium and calcium

intakes in the US population. J Am Coll Nutr 1985;4:195-206.

 

14 Altura BM, Altura BT: Magnesium and the cardiovascular system:

Experimental and clinical aspects updated: in Sigel H, Sigel A (eds):

Metal Ions in Biological Systems. New York, Dekker, 1990, vol 26:

Compendium on Magnesium: Its Physiology, Biochemistry, and Nutrition. pp

359-416.

 

15 lseri LC, Alexander EC, MacCaughey RS, Boyle AJ, Meyers G: Water and

electrolyte content of cardiac and skeletal muscle in heart failure and

myocardial infarction. Am Heart J 1952;43:215-227.

 

16 Heggtveit MA, Tanser P, Hunt B: Magnesium content of normal and

ischemic hearts. Proc 7th Int Congr Clin Pathol, Montreal, 1969, p 53.

 

17 Speich M, Bousquet B, Nicholas G, Delajartre AY: Incidences de

l'infarctus du myocarde sur les teneurs en magnesium plasmatique

erythrocytaire et cardiaque. Rev Fr Endocrinol Clin 1979;20:159-163.

 

18 Speich M, Bousquet B, Nicholas G: Concentrations of magnesium,

calcium, potassium and sodium in human heart muscle after acute

myocardial infarction. Clin Chem 1980;26:1662-1665.

 

19 Johnson CJ, Peterson DR, Smith EK: Myocardial tissue concentration of

magnesium and potassium in men dying suddenly from ischemic heart

diease. Am J Clin Nutr 1979;32:967-970.

 

20 Overlack A, Zenzen JG, Ressel C, Muller HM, Stumpe KO: Influence of

magnesium on blood pressure and the effect of nifedipine in rats.

Hypertension 1987;9:139-143.

 

21 Altura BM, Altura BT: Role of magnesium in pathogenesis of

hypertension. Relationship to its actions on cardiac and vascular smooth

muscle: in Laragh JH, Brenner BM (eds): Hypertension: Pathophysiology.

Diagnosis and Management. New York, Raven Press, vol 1, 1990, pp

1003-1025.

 

22 Resnick LM, Gupta RK, Laragh JH: lntracellular magnesium in

erythrocytes of essential hypertension relation to blood pressure and

serum divalent cations. Proc Natl Acad Sci USA 1984;81:6511-6515.

 

23 Mathew R, Gloster ES, Altura BT, Altura BM: Magnesium aspartate

hydrochloride attenuates monocrotaline pulmonary artery hypertension in

rats. Clin Sci 1988;75:661-667.

 

24 Mathew R, Altura BM: Magnesium and the lungs. Magnesium

1988:7:173-187.

 

25 Mathew R, Altura BT, Altura BM: Strain differences in pulmonary

hypertensive response to monocrotaline alkaloid and the beneficial

effect of oral magnesium treatment. Magnesium 1989;8:110-116.

 

26 Shibutani Y, Sakamoto MK, Katsuno S, Yoshimoto S, Matsura T: Serum

and erythrocyte magnesium levels in junior high school students:

Relation to blood pressure and a family history of hypertension.

Magnesium 1988;7:188-194.

 

27 Altura BT, Brost M, Bloom S, Barbour RL, Stempak JK, Altura BM:

Magnesium dietary intake modulates blood lipid levels. Proc Natl Acad

Set USA 1990;87:1840-1844.

 

28 Altura BM, Barbour RL, Reiner SD, Zhang A, Cheng TP, Down JL, Gupta

RK, Wu F, Altura BT: Influence of Mg2+ on distribution of ionized Ca2+

in vascular smooth muscle and on cellular bioenergetics and

intracellular free Mg2+ and pH in perfused hearts probed by digital

imaging microscopy, 31P NMR and reflectance spectroscopy: in Zhakari S,

Witt E (eds): Imaging Techniques in Alcohol Research. Monograph 21,

Washington, NIAAA, pp 235-272.

 

29 Barbour RL, Altura BM, Reiner SD, Dowd TL, Gupta RK, Wu F, Altura BT:

Influence of Mg2+ on cardiac performance, intracellular free Mg2+ and pH

in perfused hearts as assessed with 31P-NMR spectroscopy. Magnes Trace

Elem 1992;10:99-116.

 

30 Barbour RL, Gupta RK, Dowd TL, Reiner SD, Wu F, Altura BT, Altura BM:

Response of cardiac energetics to elevated and low magnesium in perfused

rat hearts. J Magn Reson Imaging, in press.

 

31 Altura BM, Altura BT: Magnesium and vascular tone and reactivity.

Blood Vessels 1978;15:5-16.

 

32 Altura BM, Altura BT: Magnesium, electrolyte transport and coronary

vascular tone. Drugs 1984; 28(suppl 1): 120-142.

 

33 Altura BM, Altura BT, Carella A, Turlapaty PDMV: Ca2+ coupling in

vascular smooth muscle: Mg2+ and buffer effects on contractility and

membrane Ca2+ movements. Can J Physiol Pharmacol 1982;60:459-482.

 

Prof. Dr. B.M. Altura

Box 31

SUNY Health Science Center 450 Clarkson Avenue

Brooklyn, NY 11203 (USA)

 

--

 

THE MAGNESIUM WEB SITE

=====================================================================

 

From the 1996 FDA Science Forum. Abstract.

---

http://www.mgwater.com/mgrda.shtml

 

Is the RDA for Magnesium Too Low?

N.A. Littlefield and B.S. Hass, NCTR, FDA, Jefferson AR 72079

 

Since magnesium (Mg), an essential nutrient, is abundant in the

environment and food supply, it is generally assumed that Mg deficiency

is not a problem.

 

However, the literature indicates that deficiencies may exist in both

third world and industrialized nations and may influence cardiac and

vascular diseases, diabetes, bone deterioration, renal failure,

hypothyroidism, and stress.

 

Because Mg in certain forms is not easily absorbed and no classical

symptoms exist, the problem of Mg deficiency is readily masked,

especially in high risk groups such as diabetics, alcoholics, those

taking hypertension medication, and some athletes.

 

The current Recommended Daily Allowance (RDA) for the US is 6 mg/Kg/day,

which translates to 420 mg for a 70 Kg man. The estimated intake in the

US is 300 mg/day.

 

Studies show that as much as 3 times this amount may be needed by the

general population and especially by those predisposed to cardiac

disease states. This report summarizes recent research on Mg in human

diets and the results of Mg deficiencies.

====================================================================

What Really Causes Heart Attacks?

--

 

What Really Causes Heart Attacks?

http://coldcure.com/html/dep.html#reactive

 

Everyone knows that high cholesterol and high blood pressure cause heart

attacks. We have been taught that we must use diet and expensive statin

drugs to lower our bad cholesterol if we don't want a heart attack.

 

We have been taught that we must get our blood pressure down by diet

(reduce our salt and fat intake and exercise) and take a variety of

expensive drugs including diuretics (lowers blood volume), beta-blockers

(inhibits adrenaline), alpha-blockers (makes heart beat with less force

and relaxes blood vessels), ACE - angiotensin-converting enzymes (spares

magnesium and potassium, but looses sodium, and relaxes arteries),

vasodilators (relaxes arteries), central adrenergic inhibitors (blocks

certain signals from brain), calcium-channel-blockers (relaxes

arteries).

 

However, magnesium deficiency is the real disease, and heart problems

are the symptoms of magnesium deficiency.

 

This seems wrong, but it is a fact well hidden by the pharmaceutical

drug pushers.

 

It is vital to your heart health that you verify this claim by reading

The Magnesium Factor .

 

Briefly stated, all of the above medicines are poor substitutes for

magnesium, because magnesium naturally does each of these " drug "

functions far better than the drugs themselves.

 

These drugs are poor in performance compared with magnesium, and make us

poor in terms of both our recovery and our pocket books.

 

The only reason to use drugs instead of magnesium is to make the

pharmaceutical drug-pushers rich.

 

How much magnesium? That is the catch.

 

We must take enough magnesium each and every day to combat the effects

of stress in its action in depleting magnesium, and this amount is

higher than has been historically true.

 

Our " modern " way of life is very stressful, and we all leak magnesium

becasue of stress, some more than others. I can't personally see how we

can get our blood pressure down to 100/60 (like it was when we were

teenagers) with less than about 500 mg of supplemental magnesium per

day.

 

Wouldn't that be expensive? NO!

 

Certainly not compared to the cost of these drugs, and certainly not

when compared to the life-extending properties of magnesium compared

with these drugs. Expensive to Social Security? Maybe, because you will

live 30 to 40 years longer. Expensive to Medicare? NO. Your health care

expenses will plumet downward, and you may forget the name of your

doctor!

 

 

HEART BECOMES " IRRITABLE " WHEN DEPRIVED OF MAGNESIUM

*************************************************************

The Human Nutrition Research Center in Grand Forks, North Dakota has

released an alarming report that reveals when humans are deprived of

magnesium they may begin to experience abnormal heart beats.

[American Journal Clinical Nutrition 75: 550-54, March 2002]

 

The heart muscle of people who experience sudden-death heart attack

has been found to be low in magnesium. Areas of the world where

drinking water is low in magnesium (soft water areas) have higher

rates of heart attacks.

 

Magnesium is a muscle relaxant, while calcium is a muscle

constrictor.

 

Low magnesium intake is associated with muscle spasm, tremors and

convulsions.

 

Most Americans, particularly women, have been advised to consume

1200-1500 milligrams of calcium daily.

 

Virtually none of these women have been told that calcium in single

doses that exceed 500 milligrams are *not absorbed*

and that they only need an additional

200 milligramof supplemental calcium

since their " diet " already provides about 800 milligrams of this

mineral.

 

Since 99 percent of magnesium resides inside living cells, blood

serum levels are not a good indicator of magnesium deficiency.

 

In other words, your doctor can't easily tell you by a blood test if

your magnesium levels are low.

 

Most Americans, 8 in 10, do not consume enough magnesium.

 

The countries that have the highest mortality rates in the world are

the Scandinavian countries and New Zealand where more calcium is

consumed from dairy products, while for comparison the lowest mortality

rates in the world are in

Portugal and Japan

where calcium-rich dairy products are NOT consumed regularly.

 

Americans consume about 800 milligrams of calcium daily (milk

drinkers may get 1200-1500 mgs from their diet alone),

but only consume about 275 milligrams of magnesium.

 

Thus the dominance of calcium over magnesium produces symptoms of

" muscle spasm " .

 

Migraines, eyelid twitch, heart flutters, back aches, premenstrual

tension, leg cramps and constipation are all

 

linked to calcium *overload*.

 

 

A significant percentage of American adults consume more than 2000

milligrams of daily calcium, the point where side effects of

overdosage begin to be reported.

 

More than 300,000 sudden-death heart attacks are reported annually in

the US (more than 80 per day)

which are believed to be related to " excessive " calcium and a

" hortage " of magnesium.

 

Modern medicine's answer to the problem is to prescribe billions of

dollars of 'calciumblocker'drugs.

 

Magnesium is a " natural " calcium blocker,

 

but this goes unrecognized by most physicians

 

Researchers warn that adults who consume excessive amounts of

caffeine or alcohol, or who take water pills (diuretics), are prone

to experience irregular heart beats and should consume more

magnesium.

 

The same is true for diabetics and people with low thyroid.

 

Most Americans consume tap water that has been softened

(sodium added) which worsens the problem.

 

Sodium 'depletes' magnesium levels.

 

American adults need to supplement their diet with 200-400

milligrams of magnesium.

 

The only side effect of too much magnesium

is loose stool.

Reducing dosage resolves this problem.

 

Copyright Knowledge of Health, Inc., 2002

Written By: Bill Sardi

 

www.alternative-medicine-message-boards.info

Posted by Chrisgaren

" Magnesium Deficiency and Sudden Death "

-

Reprinted from:

http://www.drgrisanti.com/magnesium.htm

---

The Grisanti Report

A Reliable Source for Alternative Medical Advice

Report #1260

-

MAGNESIUM DEFICIENCY & SUDDEN DEATH

Written and Researched by Ronald J. Grisanti D.C., D.A.B.C.O.

 

An athletic 20 year man is playing basketball and suddenly collapses

on the court and dies.

 

On a hot July day, a young and vibrant college football player

suddenly makes a great tackle and never gets up.. only to be

pronounced dead 5 minutes later.

High School track runner dies after finishing second in a race.

 

The sad truth is 1 out of 50,000 young adults will fall victim to

Sudden Death.

 

Most sudden deaths have been linked to a thickened, enlarged heart

called hypertrophic cardiomyopathy (HCM), or by a condition that

disturbs the rhythm of the heart called an arrhythmia.

 

When one sweats, a significant amount of magnesium is lost.

Magnesium is

the most under-recognized electrolyte disorder in the U.S. Dr.

Mildred Seelig, one of the country's leading authorities on

magnesium suggests that 80%-90% of the population is deficient is

magnesium

 

It is beyond the extent of this article why the public is being

denied the truth of the seriousness of magnesium deficiency and

sudden death. The amount of medical research could fill a book, but

it is unfortunately being ignored.

 

According to Micheal A. Brodsky M.D., associate professor of

medicine at the University of Medicine and the director of the

Cardiac Arrhythmia Service at the University of California..

 

mineral imbalances interfere

with the heart's normal nerve function.

 

While most athletes have been conditioned to drink a potassium rich

drink after sweating.. very few have been educated on the dangers of

a magnesium deficiency.

 

Dr. Brodsky states that arrhythmia therapy should

focus on replenishing two key minerals: potassium and magnesium.

 

Almost all physicians have known for some time just how vital

potassium is for normal heartbeat.

 

Magnesium is an entirely different story, however. According to

Carla Sueta M.D., Ph.D., assistant professor of

medicine and cardiology at the University of North Carolina at

Chapel Hill School of Medicine " apparently,

many doctors still don't realize how important a role this mineral

can play in some heart patients.

 

In fact, most never check the magnesium level. She has shown through

her research that magnesium reduced the incidence of several types

of ventricular arrhythmia by 53 to 76 percent.

 

Magnesium deficiency can be induced by the very drugs meant to help

heart problems. Some types of diuretics (water pills) cause the body

to

excrete both magnesium and potassium, as does digitalis.

 

And magnesium deficiency is often at the bottom of what's called

refractory potassium deficiency.

 

The amount of magnesium in the body determines the amount of

a particular enzyme that determines the amount of potassium in the

body, " he explains.

 

So if you are magnesium-deficient, you may in turn be potassium-

deficient, and no amount of potassium is going to correct this

unless you are also getting enough magnesium.

 

The Best Test To Determine Your Level of Magnesium

 

Although most physicians rarely check this important mineral, the

few that do usually rely on test called Serum Magnesium.

 

Unfortunately, this

test only measures approximately 1% of the magnesium in your body..

a poor test at best. The " Gold Standard " and the most accurate test

is the RBC Minerals or more commonly called Elemental Analysis in

Packed

Erythrocytes. This test examines the levels of eight minerals and

seven toxic heavy metals.

 

The erythrocyte is the red blood cell that floats in our serum to

carry oxygen to our cells.

 

The minerals this test analyzes from inside the red blood cell

includes magnesium, manganese,

molybdenum, potassium, selenium, vanadium and zinc. Another test

which has proven to be extremely valuable in detecting magnesium

deficiencies is called the Urine Magnesium Loading Test.

 

In this test, the patient collects a 24-hour urine sample and the

total magnesium is measured. The patient is then given a dose

Magnesium Chloride 18% and another 24-hour urine specimen is

collected.

 

The magnesium is again measured. If the

body retains more than a certain amount of magnesium, then it is

concluded that the body is magnesium deficient.

 

Common Symptoms of Magnesium Deficiency

 

The most common symptoms include back and neck pain, muscle spasms,

anxiety, panic disorders, Raynaud's spastic vessels, arrhythmia,

fatigue, eye twitches, vertigo, migraines.

 

Best Sources of Magnesium

 

The best way of insuring enough magnesium is to eat a variety of

whole foods, including organic whole grains, nuts, seeds and

vegetables, preferably food grown on naturally composted soil. The

green color of green vegetables is due to chlorophyll, which is a

molecule that contains magnesium. Avoid refined processed foods,

especially white sugar and

white flour products, as most magnesium is removed from them.

 

Dr. Grisanti's Comments:

 

If you are suffering with a heart problem and have not had your

magnesium checked, then I want to urge you to have your physician

order the two tests listed above. Unless you have proof that your

magnesium is within normal levels, I want you to realize that you

are playing with your health!

 

 

 

References

 

1:Eisenberg MJ, Magnesium deficiency and sudden death (editorial),

AM Heart J 1992 Aug; 124(2):544-9

2:Magnes Res 1994 Jun;7(2):145-53

3:Tzivoni, Dan, M.D. and Keren, Andre, M.D., " Suppression of

Ventricular Arrhythmias by Magnesium " , The American Journal of

Cardiology, June 1, 1990;65:1397-1399.

4:Miner Electrolyte Metab 1993;19(4-5):323-36

5:Keller, Peter K. and Aronson, Ronald S., " The Role of Magnesium in

Cardiac Arrhythmias " , Progress in Cardiovascular Diseases, May/June

1990;32(6):433-448.

6:Biochim Biophys Acta 1993 Oct 20;1182(3):329-32

7:Biochim Biophys Acta 1994 Jan 11;1225(2):158-64

8: " Practical Briefings: Clinical News You Can Put Into Your Practice

Now. Ventricular Arrhythmias and Magnesium " , Patient Care, October

15, 1990;16-20

9:Magnes Res 1993 Jun;6(2):191-2

10:Hennekens (1987) Epidemiology Medicine, p.54-98

11:Schriftenr Ver Wasser Boden Lufthyg 1993;88:474-90

12:Am J Cardiol 1992 Oct 8;70(10):44C-49C

13:Fiziol Zh SSSR Im I M Sechenova 1992 Jul;78(7):71-7

 

 

 

© 2001 Ronald J. Grisanti D.C., D.A.B.C.O

 

NOTICE: This information is provided for educational purposes. Any

medical procedures, dietary changes, or nutritional supplements

discussed herein should only be undertaken on the advice of a

qualified

physician.

 

Ronald J. Grisanti, D.C., D.A.B.C.O

The Grisanti Center of Integrative Medicine

4200 East North Street, Suite 14 • Greenville, SC 29615

(864) 292-0226 • FAX: (864) 268-7022

 

 

Reprinted from:

http://www.drgrisanti.com/magnesium.htm

 

JoAnn Guest

mrsjo-

DietaryTi-

 

 

 

 

 

AIM Barleygreen

" Wisdom of the Past, Food of the Future "

 

http://www.geocities.com/mrsjoguest/Diets.html

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Meet the all-new My – Try it today!