'Aortic calcification' Magnesium Deficiency?

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'Aortic calcification' - Magnesium Deficiency?

JoAnn Guest

Mar 29, 2006 17:14 PST

 

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

 

Magnesium is a known treatment for calcification.

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.

---

Arterial calcification: a review of mechanisms, animal model

--

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=11410932 & 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.

 

Publication Types: Review

PMID: 11410932 [PubMed - indexed for MEDLINE]

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

Focus on Magnesium

 

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

diarrheaat 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

420mg, 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.

 

Possible Side Effects:

 

In general, magnesium is very well tolerated. Magnesium

supplementationcan sometimes cause a loose 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 " absorption of magnesium.

 

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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JoAnn Guest

mrsjo-

www.geocities.com/mrsjoguest/Diets

[Guest guest]

www.calcify.com

 

 

 

-

" JoAnn Guest " <angelprincessjo

 

Friday, April 14, 2006 5:29 PM

'Aortic calcification' Magnesium

Deficiency?

 

 

'Aortic calcification' - Magnesium Deficiency?

JoAnn Guest

Mar 29, 2006 17:14 PST

 

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

 

Magnesium is a known treatment for calcification.

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.

---

Arterial calcification: a review of mechanisms, animal model

--

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=11410932 & 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.

 

Publication Types: Review

PMID: 11410932 [PubMed - indexed for MEDLINE]

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

Focus on Magnesium

 

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.

 

D