Magnesium Deficiency and CFS

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Magnesium Deficiency In Patients

With Chemical Sensitivity*

J. Rea, MD, FACS * *

Alfred R. , DO**

Ralph E. Smiley, MD**

Barbara Maynard, RD**

Ollie Dawkins-Brown, MEd, MS**

Abstract

Assessment of magnesium status in 51 consecutive chemically sensitive patients (12 males, 39 females, ages ranged from 13 to 67 years) in an environmentally controlled hospital unit was undertaken. The purpose of this study was to evaluate the magnesium status in chemically sensitive patients whose disorders were closely associated with the symptoms of magnesium deficiency. The symptoms included back and neck pain, fine tremors, muscle spasm, anxiety and nervousness, spastic vascular phenomena, ventricular arrhythmia, and fatigue. Results of laboratory tests and IV magnesium challenges showed that some patients with chemical sensitivities may have a disturbance of intracellular magnesium. RBC and plasma levels proved to be poor indicators of magnesium status: 2.8% (1/35 positive) and 15% (5/33 positive) respectively. Intravenous magnesium challenge appeared to be a more accurate assessment of total body magnesium status (76% positive 39/51). Overall clinical improvement with magnesium treatment appears to be somewhat low, (45% or 23 of 51) but it is worthy of consideration in those chemically sensitive patients who are magnesium deficient.

Keywords: Magnesium deficiency, chemical sensitivity, intravenous magnesium challenge.

Introduction

A group of chemically sensitive patients exists who exhibit many of the signs and symptoms similar to those seen in magnesium deficient patients. The following case illustrates this point.

Case Study

A 55-year-old female treated for chemical sensitivity for 8 years developed low back pain after a fall. Medication did not relieve her pain which had persisted for two years. Her orthopedist thought that she was not absorbing sufficient amounts of magnesium. Challenge with magnesium sulfate relieved her symptoms

Discussion

Magnesium deficiency is probably more wide spread in the general population than originally suspected. This appears to be primarily due to poor dietary intake.2, 4 Increased phosphate also contributes to magnesium deficiency states.5 Segments of the population are at risk due to the large consumption of high phosphate containing soft drinks. Others who have poor protein or high fat6 metabolism tend to be more likely afflicted with magnesium deficiency. Some disease states such as advancing age7 diabetes mellitus, 8, 9 alcoholism,10 heart failure, 11, 12 or use of diuretics,13,14 may cause magnesium depletion. Hypoxia and drugs such gentamycin, cylclosporin and angiotensin 15-17 can also deplete the body of magnesium. Excess vitamin C may effect a drop in magnesium levels.18, 19 Malabsorption of magnesium has been associated with gastrointestinal problems such as functional bowel disorder,20 ulcerative olitis,20 and Crohn’s disease.21,22 Acute magnesium deficiency can occur after epinephrine, cold stress, and stress of serious injury or extensive surgery.23 The average daily amount of magnesium intake is around 120 mg/100 calories in the adult U.S. population.24 The need may be increased with any of the aforementioned conditions.

Many patients with chemical sensitivity have poor dietary intake, poor protein metabolism, or fall within the aforementioned conditions. Recent research has suggested that certain chemicals tiny alter the body's magnesium or its catalyzed products. For example, ethanol and carbon tetrachloride24 have been shown to disturb liver collagen in rats. Exposures to some pesticides can disturb muscle and nerve physiology with muscular spasm and tetany occuring.26, 27 Most chlorinated hydrocarbons are also lipophilic. Exposures can lead to disturbances in membrane stability. Magnesium plays an integral role in membrane stability. It is also a co-factor in many metabolic reactions. 28, 29 Additionally, it has been shown to counteract the diuretic inducer of catecholamine.30 Consideration of the above facts suggests that some chemically sensitive patients may be magnesium deficient.

Some interesting facts came to the forefront as we further considered this group of patients. It appeared that serum and red blood cell measurements of magnesium may not reflect a true state of magnesium depletion unless it is extremely low. Further, if serum levels fell within the "normal' range, a depleted state may still be a possibility. This was in agreement with the World Conference on Magnesium (1985) consensus that the best way to define deficiency was by magnesium challenge.31

We found a great disparity between alleviation of signs and symptoms control (45%) and calculated magnesium deficiency (76%). There may be several reasons for this disparity: 1) The patient's symptoms may have been caused by other factors; 2) In some cases, the magnesium deficiency may not have been severe enough in light of biochemical individuality to produce symptoms originally; 3) The patient may not have been treated with sufficient amount of magnesium to relieve the symptoms; 4) Lower levels of magnesium retention may not reflect a true magnesium deficiency based on current thinking of what normal values of retention are; and 5) The lack of a precise calculated value for dietary intake may be a further complication although assessment of oral intake would have tended to bias the study toward higher levels of magnesium excretion.

The results of this study suggest that there possibly be some degree of magnesium deficiency in people who are chemically sensitive and that for enhancement of their treatment, attention should be paid to their magnesium intake.

References

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