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Magnesium for the Next Millennium

Magnesium is a trace mineral in several hundred chemical reactions in the body

Magnesium for the Next Millennium

Randall Swain, MD, Barbara Kaplan-Machlis, PharmD, New Millennium Wellness and Sports Medicine, and the Departments of Family Medicine and Clinical Pharmacy, West Virginia University, Charleston.

[South Med J South Med J 92(11), 1999. © 1999 Southern Medical Association]

 

Abstract

Background. Magnesium is a trace mineral in several hundred chemical reactions in the body. It has therapeutic potential in many medical conditions. In this review, we attempted to clarify the current information on the role of magnesium as a therapeutic agent.
Methods. A MEDLINE search from 1966 through March 1999 was conducted, using PubMed and "Magnesium" and "Therapeutic Usage" as the two initial key headings. Important articles were also identified from the bibliographies of the initial articles.
Results. A total of 51 articles were included in this review. Articles were excluded if they were based on animal study or were in a language other than English.
Conclusion. Magnesium has long been used as an ingredient in laxatives and antacids. It seems clear that intravenous magnesium also is effective for the suppression of ventricular ectopy in the hospital setting and is a first-line agent for torsades de pointes. It is less clear whether it is useful in patients with congestive heart failure or acute myocardial infarction (MI). Although effective for treatment of preeclampsia/eclampsia, its use in the termination of preterm labor has recently been questioned. In asthma and chronic lung disease, intravenous magnesium may be useful when conventional treatment has failed. Finally, magnesium may have a role in the prevention and treatment of vascular headaches.

 

Introduction

Magnesium is a trace mineral involved in more than 300 chemical reactions in the body. Similar to potassium, magnesium is predominantly an intracellular ion. More than two thirds of the total amount of magnesium is stored in bone, and about 25% is present in muscle. About one third of the total amount ingested in the gut can be absorbed, and the remaining two thirds is excreted in the feces. Magnesium absorption is proportional to the total magnesium status, ie, the higher the body stores, the lower the amount absorbed. Magnesium is similar to calcium in that it is dependent on vitamin D for absorption in the small intestine. Magnesium also acts competitively for calcium channels; therefore, it simulates a calcium channel blocker's mechanism of action. Magnesium is required for proper functioning of the Na+-K+ ATPase pump; thus, when potassium levels do not increase with supplementation, magnesium deficiency should be suspected.

 

Magnesium Deficiency

Magnesium is predominantly an intracellular and skeletal ion; less than 1% is located in the extracellular compartment. Therefore, serum magnesium levels correlate poorly with total body stores.[1] Magnesium is bound to plasma proteins, complexed to anions, and found as the ionized, physiologically active form. Additionally, serum levels do not equilibrate with tissue magnesium. Current assay methods of serum magnesium and 24-hour urine magnesium excretion do not provide information about intracellular magnesium. Because assay results appear to reflect relatively acute changes in magnesium status, evaluation of renal function, diuretic usage, and dietary intake of magnesium is necessary to determine the risk of chronic deficiency.[2,3]

Symptoms of magnesium deficiency generally fall within four categories: neuromuscular hypertonicity, psychiatric disturbances, potassium or calcium problems, or cardiac effects.[4] Before administration of supplemental magnesium, some experts have recommended a parenteral loading test to determine a deficiency state.[5] This is done by infusing 60 mEq or 3.6 g (1 mEq = 60 mg) of intravenous magnesium sulfate (MgSO4) over 12 hours in conjunction with a 24-hour urine collection for magnesium. Retention of more than 50% of the magnesium is considered evidence of deficiency, whereas less than 20% retention is unlikely to be deficiency. However, the test's complexity obviously makes it impractical. Alternative methods of magnesium determination include erythrocyte, mononuclear, and ionized magnesium. A method of measuring ionized magnesium levels, though not yet available, may eventually replace serum magnesium determinations as a more accurate assessment of true magnesium status.

In high-risk patients with suspected deficiency, supplementation of magnesium is given empirically regardless of the measured serum level, unless it is elevated. Specifically, empiric magnesium replacement may be considered in patients taking diuretics (especially loop), patients who are malnourished or alcoholic, patients with low potassium levels, or those who are diabetic. Supplementation is best accomplished in a hospital setting by the parenteral route. Supplementation with 1 to 4 g of MgSO4 over 1 to 4 hours is usually adequate, depending on the extent of deficiency; the administration rate should be slower for infusing increasing amounts in nonemergency situations to avoid hypotension. Outpatient supplementation is generally accomplished with oral magnesium oxide, beginning with 400 to 800 mg per day. Dosing may be limited by diarrhea.

 

Magnesium Excess

Magnesium excess is rare but has been reported subsequent to use of over-the-counter laxatives and antacids.[6] Patients often have concomitant renal insufficiency. Clinical presentation includes pseudocoma, hyporeflexia, muscle weakness, ataxia, confusion, nausea and vomiting, flushing, bradycardia, hypotension, widened QRS, AV block, and respiratory arrest. Magnesium is associated with central nervous system toxicity at serum concentrations more than 6 mEq/L; it is manifested as lethargy and sedation, nausea and vomiting, depressed deep tendon reflexes, followed by muscle paralysis, respiratory depression, coma, and death. Cardiotoxicity (hypotension, bradyarrythmia, first-degree heart block, complete heart block, or asystole) occurs with severe hypermagnesemia (10 to 15 mEq/L). Unfortunately, since symptoms of magnesium toxicity are often nonspecific, they may be mistaken for other, more common clinical causes of decreased mental status (ie, substance abuse, extreme illness, or trauma). Treatment consists of removal of magnesium supplementation and if necessary, calcium infusion, which may block some of magnesium's effects.

 

Laxatives/Antacids

Antacids containing magnesium may be formulated as hydroxide, oxide, carbonate, phosphate, trisilicate, or citrate salts. The salt used influences the antacid onset and duration of action. Magnesium ions react with gastric acid to produce magnesium chloride. Magnesium hydroxide (milk of magnesia) readily reacts with gastric acid, producing a potent, short-acting neutralizing effect. Magnesium carbonate's crystal structure is responsible for its slower onset of action. Magnesium trisilicate is a relatively weak antacid that is poorly soluble and produces the slowest onset of action and longest duration of action of all the magnesium preparations. Only about 5% to 10% of the total amount of ingested magnesium is absorbed from the small intestine, and it is renally excreted.[7]

Magnesium compounds alter gastrointestinal motility and secretion and can result in a dose-limiting diarrhea. Alkalization of gastric contents stimulates gastrin to increase gastric motility. Osmotic diarrhea results from poorly absorbed, unreacted magnesium salts in the small intestine.[8] In contrast, aluminum relaxes gastric smooth muscle, delays gastric emptying, and has a constipating effect. Therefore, magnesium salts are often combined with aluminum salts in antacids to balance their effects.[7,8] Aluminum reacts relatively slowly in the stomach, so combination aluminum/magnesium antacids provide a rapid, sustained acid neutralizing capacity. Although overall bowel function is not significantly changed, the laxative effect of aluminum/magnesium combinations most often predominates.

Magnesium laxatives are indicated for acute bowel evacuation before diagnostic evaluation, for treatment of severe constipation from chronic opioid or laxative abuse, or for occasional use in healthy adults. Onset of laxative effect is observed within 30 minutes to 3 hours. Magnesium's mechanism of action is as an oral saline laxative and cathartic primarily by its osmotic effect in the colon. Magnesium increases gastric motility by stimulation of cholecystikinin, thus increasing fluid and electrolyte retention in the intestinal lumen. Magnesium salts are formulated as the sulfate salt (Epsom salt), hydroxide salt (milk of magnesia), and citrate salt (Bicitra). Sulfate salts are the most potent. Usual doses of Epsom salt for laxative use range from 5 to l5 g (at least 40 mEq) of magnesium dissolved in a solution of at least 8 oz of liquid. Fruit juice or a carbonated drink can be mixed with it to hide the bitter taste. Milk of magnesia is available as a chewable tablet or aqueous suspension taken at a dose of 15 to 40 mL (40 to 110 mEq) followed by at least 240 mL of water. Bicitra is available as an oral solution. A 240-mL dose is equivalent to 4 g of magnesium hydroxide. With any of the laxative formulations, a large volume of water may be lost with passing the stool, so drinking a full glass of water after each dose is recommended. Magnesium salts are effective laxatives for acute bowel evacuation resulting in a dose-dependent increase in bowel movements and stool water.[9,10]

 

Magnesium and Chronic Respiratory Diseases

The initial modern, controlled study using MgSO4 for asthma was published in 1987 by Okayama et al.[11] The investigators studied 10 patients with mild asthma and gave 0.5 mmol/min MgSO4 IV over 20 minutes, or a total of 1.2 g. Treatment resulted in improvements in FEV1 and FVC. Subsequently, a double-blind crossover study by Rolla et al[12] examined the effects of 2 g of IV MgSO4, administered over 20 minutes, in 10 asthmatic patients. Only a mild bronchodilating effect, much smaller than that obtained with a beta agonist inhalation, was observed. McNamara et al[13] reported the case of a 72-year-old man who received a magnesium infusion in the emergency room (ER) during a severe asthma attack after not responding to standard treatment. The authors concluded that impending intubation of the patient was avoided due to the efficacy of the magnesium. They subsequently conducted a study of acute asthma in 38 ER patients who were randomized to receive either placebo saline infusion or 1.2 g of intravenous MgSO4. Magnesium therapy resulted in an increased peak flow from 225 to 297 L/min and a significantly better discharge rate.[14] All patients entered into the study were unresponsive to conventional treatment with aerosolized beta agonists, methylprednisolone sodium succinate (Solu-Medrol), and aminophylline infusions. In a European trial, Tiffany et al[15] studied 48 asthmatic patients who did not respond to two albuterol nebulizer treatments. No positive effects of magnesium were observed, but all of the severe asthmatics were excluded. In another ER study, 135 patients were entered and distributed randomly to placebo and magnesium treatment groups.[16] The study group received 2 g of IV MgSO4 in addition to standard therapy with beta agonists, and intravenous steroids. Although not statistically significant, hospital admission rates were slightly lower for the treatment versus the placebo groups, 25% vs 35%, respectively (P = .21). When results were stratified by severity, the severe asthmatics (FEV1 <25% of baseline) receiving magnesium showed statistically significant improvement. Hospitalization rate was 78.6% for the placebo group and 33% in the treatment group (P = .009). The FEV1 was also increased more in magnesium-treated patients versus the placebo group both at 2 hours (P = .014) and 4 hours (P = .026) after magnesium infusion. Noppen et al[17] also studied 6 patients admitted to the hospital with severe asthma. MgSO4 at 0.615 mmol/min IV over 20 minutes or 1.5 total grams was added to conventional treatments, and a significant improvement in FEV1 from 0.94 ± 0.39 L to 1.3 ± 0.44 L (P = .05) was observed. Clinical symptoms also improved in all patients; however, greater improvements were noted with nebulized beta agonists. A larger trial on 120 patients seen in the ER showed no significant differences between treatment (2 g of IV MgSO4) and control (standard therapy).[18] None of the asthmatics entered into the trial had complete improvement with only one nebulized beta agonist treatment.

Another European trial, using magnesium for the treatment of asthma, studied[17] adult asthmatics who were instructed to consume a low magnesium diet for 3 weeks.[19] Subsequently, patients received either placebo or an oral dose of 400 mg per day of magnesium oxide, and FEV1 was measured. Asthma symptom scores were lower in the treatment group, but no other significant changes occurred in FEV1, peak flow, or use of rescue inhalers. However, the low magnesium diet used in the study may have been a confounding variable, since it may have produced a temporary deficiency state.

The pediatric asthmatic population has received less attention in the literature on magnesium. One small trial involved 22 asthmatic children and showed that nebulized MgSO4 was an ineffective bronchodilator.[20] One recent study on both adults and adolescents compared nebulized salbutamol and nebulized magnesium sulfate.[21] In this randomized double-blind controlled trial, 33 asthmatic patients ranging from 12 to 60 years were studied. All patients were given 100 mg of hydrocortisone IV. Patients were randomized to receive nebulizers of either 3 mL of a 3.2% solution or 95 mg of MgSO4 solution or 3 mL (2.5 mg) salbutamol solution. Both the magnesium sulfate and salbutamol groups had significant increases in peak flow rates (35% and 42%, respectively). No significant difference occurred in peak flow between groups. In India, Rama Devi et al[22] studied 47 asthmatic children who responded poorly to inhaled beta agonists. Treatment with 50% MgSO4 at a dose of 0.2 mmol/kg over 35 minutes produced significant early improvements in both asthma score and peak flow measurements as compared with placebo. A retrospective chart review reported the effects of 40 to 50 mg/kg of IV MgSO4, administered over 20 minutes, in 4 children who failed to respond to conventional therapy.[23] The subjects showed clinical improvements in asthma scores, respiratory rates, CO2 retention, and peak flow rates. Finally, Ciarallo et al[24] studied 31 patients from the ER who failed to have peak flow rates >60% of predicted values after three albuterol nebulizer treatments. Magnesium infusions were then given at a rate of 25 mg/kg over 20 minutes up to a 2-g maximum. Children receiving the magnesium bolus had significantly greater increases in peak flow (59% vs 20% at both 30 and 90 min, P = .05) as well as FEV1 (34% vs -1% at 30 min, P = .05; 75% vs 5% at 90 min, P = .01).

Another population that has been minimally studied is the intubated asthmatic. One case report has related magnesium's use in this situation. The patient failed standard therapy for asthma but showed clinical improvement and was weaned from the ventilator after intravenous magnesium administration.[25]

More recently, a population with chronic obstructive pulmonary disease (COPD) was studied to determine the usefulness of magnesium.[26] The trial involved 72 patients who received either standard therapy alone or standard therapy in addition to IV MgSO4 for COPD exacerbation. Patients in the study group were given 1.2 g of magnesium sulfate after receiving albuterol by nebulizer and had significantly greater improvements in peak flow than the control group (22% vs 6%, P = .01). The investigators also observed a trend toward decreased hospitalization in the treatment group versus the control group (28% vs 42%, respectively), though this difference was not statistically significant (P = .25).

The majority of data indicate that MgSO4 infusions of 1 to 2 g over 20 to 30 minutes are the most effective in moderate to severe asthmatics not responding to standard therapy. In addition, though there is a paucity of data, magnesium infusions may be effective for patients having COPD exacerbations. However, there is minimal data involving COPD patients. Intravenous MgSO4 has been useful in the pediatric population in small studies, but the exact dosing is uncertain. The efficacy of nebulized magnesium is uncertain at this point, since absorption may be a problem and studies have shown conflicting results. Therefore, this treatment should be considered experimental.

 

Magnesium and Cardiac Disease

Magnesium has become an important treatment option in the management of certain arrhythmias, but its use in ischemic heart disease has been limited in the United States. Several European trials have recommended the use of magnesium for patients with MI despite the lack of convincing data to show a statistically significant difference in outcomes. Even meta-analysis has failed to resolve the question. Therefore, a second Leicester Intravenous Magnesium Intervention Trial (LIMIT-2) was conducted to resolve this issue.[27] The LIMIT-2 recruited 2,316 patients with suspected MI and randomized them to receive either magnesium bolus and subsequent 24-hour infusion or saline placebo. Mortality at 28 days was 7.8% in the magnesium group and 10.3% in the placebo group (P = .04), a relative reduction of 24% in the magnesium group. The incidence of ventricular failure was also reduced by 25% (P = .009). Side effects were minimal, but these included flushing related to the speed of the infusion and an increased incidence of sinus bradycardia (P = .02). However, the overall difference, though statistically significant, appears small (7% to 10%). The mechanism of magnesium's effect on patients having MI is thought to be due to a cellular protective effect on the myocardium. Magnesium may help to reform ATP lost during ischemia, thereby helping the myocardium recover.[28] Magnesium has been used in cardioplegic solutions during bypass surgery for some time for the same purpose.[29]

Conversely, two other large trials provide some negative data regarding the use of magnesium in ischemic heart disease. The ISIS-4 trial reported the beneficial effects after 24 hours of intravenous magnesium administered to more than 2,000 patients with suspected acute myocardial infarction. Hypotension was a concerning side effect acutely. There was no favorable effect on mortality rates.[30] One trial using oral magnesium supplements (15 mmol of magnesium oxide per day or 375 mg) in 200 subjects surviving MI looked at major cardiac events over a 1-year period.[31] The authors found no decrease in cardiac events. Therefore, we cannot recommend routine use of either oral or intravenous magnesium for patients with MI.

Mortality rates among patients with congestive heart failure (CHF) and magnesium deficiency is a controversial issue. One study showed a decreased mortality among CHF patients with normal serum magnesium levels of the time of admission (71% survival rate) as compared with patients who had low magnesium levels (45% survival). However, patients with higher than normal serum magnesium levels had an even lower survival rate (37%) in this same study.[32] The PROMISE study was conducted in 1,088 patients with CHF and low serum magnesium levels; no increase in mortality was observed.[33] We do currently check and correct low magnesium levels in CHF patients, even though doing so may not decrease mortality rates. We believe the potential benefits far outweigh any risk of in-hospital infusions.

Magnesium infusion has many acute effects on the conduction system of the heart. A prolonged PR interval, increased sinoatrial node conduction time, or increased AV nodal refractory period could occur. No adverse effects on atrial or ventricular conduction have been observed.[34] Digitalis-associated arrhythmias respond well to magnesium infusion, even for patients with normal serum magnesium levels.[35] MgSO4 has also been shown to be effective for ventricular arrhythmias refractory to lidocaine in patients with normal serum magnesium levels.[36]

Along with potassium replacement, magnesium administration is often first-line therapy to treat ventricular ectopy, especially in patients taking loop diuretics. Magnesium is a second-line or third-line agent for ventricular arrhythmias and a first-line agent for torsades de pointes ventricular arrhythmias.[37] Magnesium's role in supraventricular and sustained ventricular arrhythmias is not well established but may be considered if standard therapies are ineffective. In summary, intravenous magnesium is a first-line agent in torsades and to extinguish ventricular ectopy when necessary. Its use in ischemic events and CHF is still under debate.

 

Preeclampsia/Tocolysis

Parenteral magnesium sulfate is administered in pregnancy for seizure prevention and control in severe preeclampsia/eclampsia and as a tocolytic for preterm labor. Magnesium's anticonvulsive effect may result from its depression of neuromuscular transmission, as a direct depressant effect on smooth muscle, or as a central nervous depressant.[38] The IV and IM routes are equally effective in achieving optimal serum concentrations for seizure prophylaxis, but IV infusion minimizes the pain associated with a large volume of solution and allows immediate discontinuance with signs of toxicity. Recommended dose for seizure prophylaxis is a loading dose of 4 to 6 g administered over 3 to 5 minutes, followed by an infusion of 1 to 3 g per hour to achieve a serum concentration of 4 to 7 mEq/mL.

Magnesium's tocolytic effect is attributed to antagonism of calcium-mediated myometrial contractions. Tocolytic therapy can be initiated with a 4 g IV bolus administered over 20 to 30 minutes, followed by an infusion of 2 to 4 g per hour until contractions cease. Intravenous infusion of magnesium is then continued for 12 hours after the last contraction. The goal serum magnesium level is 5 to 8 mg/L. Reflexes and serial magnesium levels should be monitored, since decreased or absent reflexes may signal impending respiratory failure. In general, severe toxicity does not appear until levels are over 8 mg/mL. Although IV magnesium can be followed by oral administration as an oral oxide or gluconate salt, clinical limitations include erratic absorption and diarrhea. Magnesium toxicity is dose dependent. Urine output of at least 100 mL in 4 hours, indicating sufficient renal function, is necessary to avoid toxicity. Toxicity is readily monitored by assessing deep tendon reflexes, blood pressure, respirations, serum magnesium concentrations, and electrocardiograms.

Magnesium sulfate is also used to terminate preterm labor, but recent studies bring its effectiveness into question. This initially was reported in 1984 when a randomized study showed no differences between placebo, magnesium, and terbutaline in arresting preterm labor between 26 and 34 weeks' gestation.[39] This has also been supported by trials in which magnesium sulfate given for preeclampsia or eclampsia in patients near term had no significant impact on labor progress.[40] Higby et al,[41] after reviewing the literature available, recommended abandoning magnesium as a tocolytic. However, it still remains in widespread use. Complications are rare but can include hypocalcemia, hypothermia, hypotension, somnolence, and though rare, pulmonary edema. Tachyphylaxis, or the decreased effect of medication with continued use, is a problem with use of beta2 agonists for this condition, but tachyphylaxis does not occur with magnesium. Prolonged use is therefore possible. Short-term fetal effects can include decreased fetal tone and movement. Prolonged infusions (>1 week) have an association with some fetal skeletal changes.[42]

Some recent epidemiologic data indicate that magnesium infusions may benefit newborns weighing less than 4,500 g, since they had less incidence of cerebral palsy than non-exposed infants of low birth weight.[43] However, this initial hypothesis was proved inaccurate when a randomized, controlled, double-blind trial was discontinued because of increased neonatal mortality in the magnesium group.[44]

In summary, magnesium appears to be an effective treatment in preeclampsia and eclampsia but does not appear to be useful in tocolysis. Its use may need to be tempered in the future because of its possible negative effect on neonates.

 

Headaches

Magnesium is also gaining some attention for the treatment of vascular headaches. Changes in the ionized magnesium blood levels and an increase in the ionized calcium to ionized magnesium ratio have been postulated to be markers for certain patients with vascular headache.[45] Forty-two percent of migraine sufferers had low serum ionized magnesium and high ionized calcium to ionized magnesium ratios, whereas only 23% of patients with continuous daily headache had these findings. This observation was also confirmed by Mauskop et al,[46] who divided patients who had chronic daily headache into those with daily migraine headaches (DMH) and those with daily tension headaches (DTH) and found that 31% of DMH patients had low serum ionized magnesium levels and 62% had higher ionized calcium to ionized magnesium ratios. In the DTH group, only 4% had low serum ionized magnesium levels, and 37% had high ionized calcium to magnesium ratios. Abnormal visual evoked potentials, thought to be a marker for vascular headaches, have become normalized after oral magnesium supplementation.[47]

Oral magnesium has been used in two small trials for migraine prophylaxis. Both trials had small sample sizes and resulted in different conclusions. In the first trial, 135 patients received a small dose of 10 mmol of magnesium per day or 250 mg, resulting in no beneficial effects.[48] In the second trial, 43 patients received 600 mg/day, resulting in a 41.6% reduction in frequency (15.8% placebo response), and significant reductions in days with headache and less medicine use.[49] There was a nonsignificant trend in severity reduction. Both of these trials used smaller magnesium doses; routine supplementation or deficiencies often involve at least 800 mg per day (400 mg of magnesium oxide orally twice daily). Two trials have investigated acute use of 1 g of IV magnesium sulfate in the ER and have found benefits in small numbers of patients with vascular headaches or cluster headaches. Patients with low serum ionized magnesium levels responded best.[50,51]

The study of magnesium therapy for migraine is in the early stages, and we do not yet know whether it works and when to use it. Therefore, its use in this condition should probably be considered experimental for now since other, more specific effective agents are available. However, it is safe and without significant side effects and may be tried for prophylaxis if desired. The oral dosage would be 400 mg of magnesium oxide twice daily. The most common side effect is loose stool.

 

Summary

Magnesium is an interesting trace mineral that appears to be useful as a therapeutic agent in a number of conditions. We do not believe there is enough evidence to recommend it in the routine care of cardiac patients with acute MI or CHF. Its mainstream indications have included suppression of ventricular ectopy in a hospital setting, treatment of torsades de pointes, prevention of eclampsia, and arrest of premature labor, as well as its use as a laxative and antacid. The use of MgSO4 infusions in the hospital for treatment of asthma and COPD refractory to standard treatment is promising. The use of oral and intravenous magnesium in treating vascular headaches is experimental, but it may be tried in refractory cases since relatively few side effects appear to occur.

Reprint requests to Randall Swain, MD, Healthscope, 500 Donnally St, Suite 203, Charleston, WV 25301.

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  46. Mauskop A, Altura BT, Cracco RQ, et al: Chronic daily headache. one disease or two? diagnostic role of serum ion-ized magnesium. Cephalalgia 1994; 14:24-28
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  48. Pfaffenrath V, Wessly P, Meyer C, et al: Magnesium in the pro-phylaxis of migraine. a double-blind, placebo-controlled study. Cephalalgia 1996; 16:436-440
  49. Peikert A, Wilimzig C, Kohne-Volland R: Prophylaxis of migraine with oral magnesium: results from a prospective, multi-center, placebo-controlled and double-blind random-ized study. Cephalalgia 1996; 16:257-263
  50. Mauskop A, Altura BT, Cracco RQ, et al: Intravenous magne-sium sulfate relieves headaches in patients with low serum ionized magnesium levels. Headache 1995; 35:597-600
  51. Mauskop A, Altura BT, Cracco RQ, et al: Intravenous magne-sium sulfate alleviates headaches of various types. Headache 1996; 36:154-160

 

 

If you missed it, you can go to either a SHORT explanation of the whole story, or a detailed explanation on ONE PAGE.  On this page you are getting more detail on one part of the story, but on either of those pages you can get the broad picture.  Don't miss reading one of them.  You can actually spend many hours on this web site, depending on the depth of research and reading you want to do.  There are an amazing 4,000 pages here -- more information on these general subjects than almost all other web sites combined!  At some point along the way you will probably say, "Karl's crazy," and leave never to return to this site, or you will say "I want to try some of that oral chelation formula he writes about!"

 

Special Pages On The Various of 12 Web Sites Authored by Karl Loren
OC History Oral Chelation Testimonials
Family Of Three Oral Chelation Formulas Life Glow Basic Life Glow Basic Ingredient List
Life Glow Plus Life Glow Plus
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Super Life Glow Super Life Glow
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Karl Loren's Diet Guarantee Navigation Help Page
The Links Below Jump To Pages On Whatever Web You Are In
Table Of Contents Search This Web Navigation Help Page
Write To Karl Loren -- He Pledges To Answer EVERY Personal Message, Personally.  Click here or on his name in the box below.
The Links Below Are To Various Web Sites Published By Karl Loren
Karl Loren Web Vibrant Life Web Karl Loren's Book
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Emmessar Happiness Arthritis
Instead Of Chelation Therapy Super Colostrum (2)
Karl Loren's Catalog Store Central Page For All 12 Webs!
 

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Copyright © May 20, 2008 6:25 AM by Karl Loren on behalf of Vibrant Life, ALL RIGHTS RESERVED.  Permission is granted for non-commercial downloading, copying, distribution or redistribution on two conditions:  One, that some form of copyright notice is included in every copy distributed or copied, showing the copyright belonging to Vibrant Life, Burbank, CA, at www.oralchelation.com . The second condition is that the material is not to be used for any purpose contrary to the purposes and objectives of this site.  This permission does not extend to materials on this site which are copyrighted by others.