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COMMENTARY
Magnesium Research

(1995) 8, 4, 403-405


Commentary on recent clinical advances:
Magnesium depletion, magnesium deficiency and asthma


Key words: Asthma, magnesium, deficiency and depletion

The basic differences between the two types of magnesium deficit, magnesium deficiency and magnesium depletion, have been highlighted for several years (see reviews1,2. In the case of magnesium deficiency, the disorder results from an insufficient magnesium intake and merely requires oral physiological magnesium supplementation. In the case of magnesium depletion, the disorder which induces magnesium deficit is related to a dysregulation of the control mechanisms of magnesium metabolism: either a failure of the mechanisms which ensure magnesium homeostasis, or intervention of endogenous or iatrogenic factors that disturb magnesium status. Magnesium depletion requires a more or less specific correction of its causal dysregulation.

The differential diagnosis between these two types of magnesium deficit is of major importance. Distinguishing between magnesium deficit, deficiency and depletion is closer to a heuristic concept than a semantic specification2. Recent clinical data on disturbances of magnesium items in asthma testify to this.

A study by Fantidis et al.3 aims to determine whether asthma per se may affect magnesium status. Their exclusion criteria include any subjects with pathological or iatrogenic causes for potential secondary magnesium deficit (that is, pregnancy, breast-feeding, gastrointestinal, cardiovascular or metabolic diseases, recent convalescence; treatment with contraceptives, calcium antagonists, diuretics, digoxin, laxatives, vitamin D, and so on), or with signs suggestive of potential primary magnesium deficit (that is, frequent cramps, palpitations or spasms, tumour, asthenia, anorexia, anxiety, etc). All the subjects of the control group (n = 21) were healthy and had neither allergic disturbances nor asthma. The study group (n = 50) included asthmatic patients who may be divided either into three subgroups according to the severity of the disease (mild, moderate, and severe asthma), or into two sub-groups differentiating intrinsic (n = 33) and extrinsic (n = 17) asthma. In all study subjects serum, plasma, erythrocyte and polymorphonuclear magnesium concentrations were measured by atomic absorption spectrophotometry, and serum sodium, potassium and calcium concentrations and erythrocyte potassium concentrations were also measured. Polymorphonuclear cell magnesium content (pn Mg) was expressed as mg Mg/ng DNA. In patients with asthma the dosages were carried out in the interval between attacks.

While the magnesium concentrations and those of the other ions were normal in serum and erythrocytes, the (pn Mg) was lower (0.88 mg Mg/ng DNA ± 0.61; m with a line over it 1 s ± 1 SD) than in the control group (1.84 ± 0.9). There was no correlation between the different types of asthma or the degree of asthmatic severity and low pn Mg. This intracellular magnesium investigation enables the patients with asthma to be divided into two subgroups: one with a normal pn Mg (around one third of the cases; pn Mg = 1.88 ± 0.9), and another (around two thirds of the cases) with a highly significant decrease in pn Mg (pn Mg = 0.38 ± 0.28; P < 0.001). Stepwise discriminant analysis showed that pn Mg content discriminated between the control group and either the whole group of asthmatics or the low pn Mg subgroup of asthmatics.

Unaware of the basic difference between magnesium depletion and magnesium deficiency, the authors stress that "in view of the fact that serum and erythrocyte magnesium were normal and that the levels of other ions in erythrocyte were also normal, the reason of the low pn Mg content of (asthmatic) patients is unclear. One explanation may be that the regulation of magnesium flux differs from one cell type to another". We entirely agree with this remark: an isolated decrease in cellular magnesium should originate from a dysregulation of magnesium status, which exactly defines magnesium depletion. This magnesium depletion, present in two thirds of the cases of asthma and absent in one third of the cases must be either a marker of polynuclear disturbances in asthmatic individuals or a pathophysiological mechanism which contributes to the pathogenesis of some symptoms in two thirds of asthma cases. Further research will be necessary to elucidate the reason for and possibly cure the dysregulation of pn Mg in two thirds of asthma cases. It seems premature to write: "in asmathics with low pn Mg content magnesium may improve the condition by normalizing intracellular magnesium content'. Appropriate intervention trials may yield valuable information on this". It should be remembered that simple and non-toxic oral physiological magnesium supplementation never controls magnesium depletion. Pharmacological magnesium interventions may induce toxicity. Beneficial effects of intravenous magnesium therapy have only been observed in the treatment of acute asthma and not in bronchial asthma between attacks4.

In addition, it is well established that basophils are target cells for IgE molecules in asthma. Basophils only constitute a small proportion of the polymorphonuclear cells and it is hazardous to infer from a decreased total in pn Mg content that the basophil pn Mg content is consequently reduced.

These interesting data only allow us to conclude that between attacks and in two thirds of asthma cases a dramatic magnesium depletion is observed in the bulk of pn Mg, the origin and significance of which are so far unknown.

The importance of magnesium deficiency in the physiopathology of asthma has been recently claimed after a large epidemiological study conducted in 2,633 adults5. Britton showed that high dietary magnesium intake is associated with better lung function and a reduced risk of airway hyperreactivity and wheezing. It might be therefore inferred that a low magnesium intake, that is, magnesium deficiency, could be involved in the aetiology of asthma and chronic obstructive airways disease5. But this remains to be proven. Coexistence does not, mean causality. Only the specific reversibility of the symptoms through the control of the magnesium deficiency will really demonstrate the existence of an aetiopathogenic link. A study showing that plasma, erythrocyte and mononuclear leucocyte concentrations of magnesium do not differ significantly from those of healthy controls is at variance with the hypothesis of the existence of magnesium deficiency in asthmatic patients3,6. Nonetheless, though magnesium deficiency does not seem to be a cause for asthma per se, primary magnesium deficiency may coexist with asthma and constitute a 'decompensatory' factor for asthma through both nervous hyperexcitability and various disturbances of immunity, the biochemical bases of which may combine decreased nucleotidic ratio (AMPc/GMPc), increased intracellular Ca2+, degranulation of basophils, enhanced production of IgE, an inflammatory state which may depend on cytokines, neuropeptides, prostaglandin D2 and leukotdenes3,7-10. Over a half of the patients with reaginic allergy, which may induce asthma, present with chronic primary magnesium deficiency, most often associated with symptoms of tetany (Chvostek sign and repetitive EMG tracings). Conversely the frequency of allergic antecedents is high in cases of latent tetany due to primary magnesium deficit8. Oral physiological magnesium therapy may then enhance the effect of specialized treatment.

It is only when primary magnesium deficiency decompensates asthma that oral physiological magnesium supplementation becomes beneficial as an adjuvant treatment of asthma8.

To sum up, the dramatic decrease in pn Mg observed in two thirds of the cases of an asthmatic group constitutes a marker or a pathophysiological factor in these particular cases. The mechanism of this magnesium depletion being unknown, it does not involve any therapeutic consequences for the time being. Conversely, when chronic primary magnesium deficiency coexists with asthma it constitutes a decompensatory factor whose control with simple oral physiological magnesium supplementation must help in asthma therapy.

References

1. Halpern, M.J. (1985): Magnesium physiopathology II. Magnesium deficiency and depletion. In: Proceedings of 1st European Congress on Magnesium, eds. M.J. Halpern & J. Durlach, pp. 9-23. Basel: Karger.

2. Durlach, J. (1995): Editorial policy of Magnesium Research: General consideration the quality criteria for biomedical papers and some complementary guidelines for the contributors of Mag. Res. 8, 191-206.

3. Fantidis, P., Cacho, J.R., Marin, M., Jarabo, R.M., Solera, J. & Herrero, E. (1995): Intracellular (polymorphonuclear) magnesium content in patients with bronchial asthma between attacks. J. R. Soc. Med. 88, 441-445.

4. Durlach, J., Durlach, V., Bac, P., Bara, M. & Guiet-Bara, A. (1994): Magnesium and therapeutics. Magnes. Res. 34, 313-328.

5. Britton, J. (1994): Dietary magnesium, lung function, wheezing and airway hyperreactivity in a random population sample. Lancet 344, 357-362.

6. de Walk, H.W., Kok, P.T.M., Struyvenberg, A., Van Rijn, H.J.M., Halboom, J.R.E., Kreukniet, J. & Lammers, J.W.J. (1993): Extracellular and intracellular magnesium concentrations in asthmatic patients. Eur. Respir. J. 6, 1122-1125.

7. Durlach, J., Poenaru, S., Rouhani, S., Bara, M. & Guiet-Bara, A. (1987): The control of central neural hyperexcitability in magnesium deficiency. In: Nutrients and brain function. ed. W.B. Essman, pp. 48-71. Basel: Karger.

8. Durlach, J. (1988): Allergic forms of primary magnesium deficit. In: Magnesium in clinical practice, ed. J. Durlach, pp. 101-102; p. 245. London, Paris: John Libbey.

9. Hunziker, N. (1990): Magnesium and its role in allergy. In: Metal ions in biological systems, Vol. 26. Compendium on magnesium, eds. H. Sigel & A. Sigel, pp. 531-547. New-York: M. Dekker.

10. McCoy, H. & Kenney, M.A. (1992): Magnesium and immune function: recent findings. Magnes. Res. 5, 281-293.

Jean Durlach
President, SDRM
Editor-in-Chief Magnesium Research


All articles by Dr. Durlach are copyrighted, and permission is granted to Web users only to make single hard copies for personal use. Additional reprints should be obtained from the originating journals. Excerpts may be used by the media with attribution to Dr. Durlach.


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