Mg levels found to be greatly reduced in Calcified Mitral Valves

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Mg levels found to be greatly reduced in Calcified Mitral Valves

http://www.ctds.info/5_13_magnesium.html#calcification

 

Magnesium is a known treatment for a variety of types of calcification of soft

tissues.

 

Mg levels have been found to be greatly reduced in calcified mitral valves.

 

In a study of rats, Mg deficiency has been shown to cause aortic calcification.

Vitamin K deficiency has also been linked to calcification of soft tissues.

 

Also see my section on Calcium Deposits.

 

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Arterial calcification: a review of mechanisms, animal model

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Med Res Rev. 2001 Jul;21(4):274-301. Related Articles, Links

 

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_uids=1\

1410932 & dopt=Abstract

 

Arterial calcification: a review of mechanisms, animal models, and the prospects

for therapy.

 

Wallin R, Wajih N, Greenwood GT, Sane DC.

 

Section of Rheumatology, Department of Internal Medicine, Wake Forest University

School of Medicine, Winston-Salem, North Carolina, USA.

 

The causes of arterial calcification are beginning to be elucidated.

Macrophages, mast cells, and smooth muscle cells are the primary cells

implicated in this process. The roles of a variety of bone-related proteins

including bone morphogenetic protein-2 (BMP-2), matrix Gla protein (MGP),

osteoprotegerin (OPG), osteopontin, and osteonectin in regulating arterial

calcification are reviewed. Animals lacking MGP, OPG, smad6, carbonic anhydrase

isoenzyme II, fibrillin-1, and klotho gene product develop varying extents of

arterial calcification.

 

Hyperlipidemia, vitamin D, nicotine, and warfarin, alone or in various

combinations, produce arterial calcification in animal models.

 

MGP has recently been discovered to be an inhibitor of bone morphogenetic

protein-2, the principal osteogenic growth factor.

 

Many of the forces that induce arterial calcification may act by disrupting the

essential post-translational modification of MGP, allowing BMP-2 to induce

" mineralization " .

MGP requires gamma-carboxylation before it is functional, and this process uses

vitamin K as an essential cofactor.

 

Vitamin K deficiency, drugs that act as vitamin K antagonists, and oxidant

stress are forces that could prevent the formation of GLA residues on MGP.

 

The potential role of arterial apoptosis in calcification is discussed.

Potential therapeutic options to limit the rate of arterial calcification are

summarized. Copyright 2001 John Wiley & Sons, Inc.

 

Publication Types:

Review

 

PMID: 11410932 [PubMed - indexed for MEDLINE]

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Focus on Magnesium

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Introduction

 

Magnesium is second only to potassium in terms of concentration within

the individual cells of the body. The functions of magnesium primarily

revolve around its ability to activate many enzymes.

 

Magnesium deficiency is extremely common in Americans, particularly in

the geriatric population and in women during the premenstrual period.

Deficiency is often secondary to factors that reduce absorption or

increase secretion of magnesium such as: high calcium intake, alcohol,

surgery, diuretics, liver disease, kidney disease, and oral

contraceptive use.

 

Signs and symptoms of magnesium deficiency can include fatigue,

irritability, weakness, heart disturbances, mental confusion, muscle

cramps, loss of appetite, insomnia, and a predisposition to stress.

 

Magnesium Supplementation in Cardiovascular Disease

 

Magnesium supplementation has been shown to be an extremely effective

therapy or adjunctive measure in many common conditions especially

cardiovascular disease. Magnesium is absolutely essential in the proper

functioning of the heart. Magnesium's role in preventing heart disease

and strokes is generally well-accepted. In addition, there is a

substantial body of knowledge demonstrating that magnesium

supplementation is effective in treating a wide range of cardiovascular

diseases.

 

For example, magnesium was first shown to be of value in the treatment

of cardiac arrhythmias in 1935. More than seventy years later, there are

now numerous double-blind studies showing magnesium to be of benefit for

many types of arrhythmias including atrial fibrillation, ventricular

premature contractions, ventricular tachycardia, and severe ventricular

arrhythmias.

 

Magnesium supplementation has also been shown to be helpful in angina

due to either a spasm of the coronary artery or atherosclerosis. The

beneficial effects of magnesium in angina relate to its ability improve

energy production within the heart; dilate the coronary arteries

resulting in improved delivery of oxygen to the heart; reduce peripheral

vascular resistance resulting in reduced demand on the heart; inhibit

platelets from aggregating and forming blood clots; and improve heart

rate.

 

Magnesium supplementation is also critical in congestive heart failure

(CHF). Studies have shown that CHF patients with normal levels of

magnesium significantly live longer than those with lower magnesium

levels.

Many of the conventional drugs for CHF and high blood pressure

(diuretics, beta-blockers, calcium channel-blockers, etc.) deplete body

magnesium stores.

Magnesium supplementation generally produces a modest

impact in lowering high blood pressure (i.e., less than 10 mm Hg for

both the systolic and diastolic).

 

Other Conditions Benefited by Magnesium Supplementation

 

Because of magnesium’s critical role in many body processes, it is not

surprising that research has demonstrated magnesium supplementation to

benefit many other conditions. For example, since magnesium promotes

relaxation of the bronchial smooth muscles, magnesium supplementation is

a well-proven and clinically accepted measure to halt an acute asthma

attack (via intravenous administration) as well as acute flare-ups of

COPD.

 

Magnesium is known to play a central role in the secretion and action of

insulin. Several studies in patients with diabetes or impaired glucose

tolerance have shown magnesium to be of significant value. Magnesium

supplementation (usually 400 to 500 mg per day) improves insulin

response and action, glucose tolerance, and the fluidity of the red

blood cell membrane. In addition, magnesium levels are usually low in

diabetics and lowest in those with severe retinopathy. Diabetics appear

to have higher magnesium requirements.

 

An underlying magnesium deficiency can result in chronic fatigue and

symptoms similar to the chronic fatigue syndrome (CFS). Low red blood

cell magnesium levels, a more accurate measure of magnesium status than

routine blood analysis, have been found in many patients with chronic

fatigue and CFS. Double-blind studies in people with CFS have shown

magnesium supplementation significantly improved energy levels, better

emotional state, and less pain. Magnesium supplementation has also been

shown to produce tremendous improvements in the number and severity of

tender points in patients with fibromyalgia.

 

Magnesium increases the solubility of calcium in the urine.

Supplementing magnesium to the diet has demonstrated significant effect

in preventing recurrences of kidney stones. However, when used in

conjunction with vitamin B6 (pyridoxine) an even greater effect is

noted.

 

Magnesium supplementation is very important in preventing headaches.

There is now considerable evidence that low magnesium levels trigger

both migraine and tension headaches. In individuals with chronic

headaches that have low magnesium levels, magnesium supplementation has

been shown to produce excellent results in double-blind studies.

 

Magnesium needs increase during pregnancy. Magnesium deficiency during

pregnancy has been linked to preeclampsia (a serious condition of

pregnancy associated with elevations in blood pressure, fluid retention,

and loss of protein in the urine), preterm delivery, and fetal growth

retardation. In contrast, supplementing the diet of pregnant women with

additional oral magnesium has been shown to significantly decrease the

incidence of these complications.

 

Magnesium deficiency has also been suggested as a causative factor in

premenstrual syndrome. While magnesium has been shown to be effective on

its own, even better results may be achieved by combining it with

vitamin B6.

 

Available Forms:

 

Magnesium is available in several different forms. Absorption studies

indicate that magnesium is easily absorbed orally, especially when it is

bound to amino acids, aspartate, citrate, or malate. Inorganic forms of

magnesium such as magnesium chloride, oxide, or carbonate are less well

absorbed and are more likely to cause diarrhea at higher dosages.

 

Usual Dosage:

 

Many nutritional experts feel the ideal intake for magnesium should be

based on body weight (6 mg/2.2 pounds body weight). For a 110-pound

person the recommendation would be 300 mg, for a 154-pound person 420

mg, and for a 200-pound person 540 mg.

 

Cautions and Warnings:

 

If you suffer from a serious kidney disorder or are on hemodialysis, do

not take magnesium supplements unless directed to do so by a physician.

People with severe heart disease (such as high-grade atrio-ventricular

block) should not take magnesium (or potassium) unless under the direct

advice of a physician.

 

Possible Side Effects:

 

In general, magnesium is very well tolerated. Magnesium supplementation

can sometimes cause a looser stool, particularly magnesium sulfate

(Epsom salts), hyroxide, or chloride.

 

Drug Interactions:

 

There are many drugs that appear to adversely effect magnesium status.

Most notable are many diuretics, insulin, and digitalis.

 

Nutrient Interactions:

 

There is extensive interaction between magnesium and calcium, potassium,

and other minerals.

 

High dosages of other minerals will reduce the intake of magnesium and

vice versa.

 

A high calcium intake and a high intake of dairy foods fortified with

vitamin D results in decreased magnesium absorption. Vitamin B6 works

together with magnesium in many enzyme systems.

 

Key References:

 

Gums JG. Magnesium in cardiovascular and other disorders. Am J Health

Syst Pharm. 2004;61:1569-76.

Touyz RM. Magnesium in clinical medicine. Front Biosci. 2004;9:1278-93.

Fox C, Ramsoomair D, Carter C. Magnesium: its proven and potential

clinical significance. South Med J. 2001;94(12):1195-201.

Saris NE, Mervaala E, Karppanen H, Khawaja JA, Lewenstam A. Magnesium.

An update on physiological, clinical and analytical aspects. Clin Chim

Acta. 2000;294(1-2):1-26.

Jee SH, Miller ER 3rd, Guallar E, et al. The effect of magnesium

supplementation on blood pressure: a meta-analysis of randomized

clinical trials. Am J Hypertens. 2002;15:691-6.

Alter HJ, Koepsell TD, Hilty WM. Intravenous magnesium as an adjuvant in

acute bronchospasm: a meta-analysis. Ann Emerg Med. 2000;36(3):191-7.

Barbagallo M, Dominguez LJ, Galioto A, et al. Role of magnesium in

insulin action, diabetes and cardio-metabolic syndrome X. Mol Aspects

Med. 2003;24(1-3):39-52.

Manuel y Keenoy B, Moorkens G, Vertommen J, et al. Magnesium status and

parameters of the oxidant-antioxidant balance in patients with chronic

fatigue: effects of supplementation with magnesium. J Am Coll Nutr.

2000;19(3):374-82.

Howard JM, Davies S, Hunnisett A. Magnesium and chronic fatigue

syndrome. Lancet 1992;340:426.

Cox IM, Campbell MJ, Dowson D. Red blood cell magnesium and chronic

fatigue syndrome. Lancet 1991;337:757–60.

Russell IJ, Michalek JE, Flechas JD, Abraham GE. Treatment of

fibromyalgia syndrome with Super Malic: a randomized, double blind,

placebo controlled, crossover pilot study. J Rheumatol.

1995;22(5):953-8.

Schwille PO, Schmiedl A, Herrmann U, et al. Magnesium, citrate,

magnesium citrate and magnesium-alkali citrate as modulators of calcium

oxalate crystallization in urine: observations in patients with

recurrent idiopathic calcium urolithiasis. Urol Res. 1999;27(2):117-26.

 

 

 

 

 

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