Significant Magnesium Deficiency in Depression

Significant Magnesium Deficiency in Depression...

Significant Magnesium Deficiency in Depression

By Richard H. Cox, Ph.D.,C. Norman Shealy, M.D., Ph.D. Roger K. Cady, M.D., Diane Veehoff, R.N., M.S.W., Ph.D., Mariann Burnetti Awell, Psy.D., Rita Houston, L.P.N.

Abstract. Magnesium levels were tested in a total of 457 patients suffering either chronic primary depression or chronic pain with depression. The magnesium load or tolerance test is considerably more reliable than serum, red blood cell, whole blood, or white blood cell magnesium levels. Virtually all significantly depressed patients are deficient in magnesium. Clinicians should consider the potential of therapeutic benefit from magnesium replacement therapy in chronic depression. Although magnesium deficiency has been reported in depression, this association is not widely recognized (Ref. 1). Over the past 7 years we have investigated magnesium levels extensively in patients with primary depression and chronic pain with depression. The current report summarizes the frequency of magnesium deficiency in depressed patients as well as the greater

accuracy of the magnesium load test over various blood levels for measuring metabolic competency of this critical mineral.


Patients and Methods Testing Procedure

All depressed patients were diagnosed by a positive Zung Test for Depression (Ref.2) as well as the MMPI and clinical evaluations. The chronic pain patients labeled depressed were those who showed depression on the Zung test.

In 475 patients seen for either chronic depression or chronic pain with depression, magnesium levels were assessed. Three hundred fifty women and 107 men had blood drawn and sent by overnight mail to Meridian Valley Chemical Lab in Kent, Washington for cell magnesium levels. They ranged from 22 to 78 years of age. Twenty-six patients had whole blood magnesium levels done at another reference lab and 26 patients had red blood cell magnesium levels done at a third reference lab.

One hundred of the depressed patients who had standard cell magnesium tests (Ref. 3) also underwent magnesium load testing to allow comparison of the cell magnesium test with the somewhat more commonly recommended magnesium load test (Ref. 4).

Results

All 100 of these patients retained well over 50% of the magnesium load; indeed they commonly retained 85% to 100%.

An additional 46 chronic pain patients with depression also underwent magnesium load testing. Thirty-one of these were deficient; 15 were not.

White Blood Cell Magnesium

Magnesium Load
Normal levels 0.098-2less than 50% retention
RBC range (4.2-6.8 meq/L)Whole blood range (1.6-2.5 meq/L)
Patients Test Normal Low LowNormalHigh
Red Blood Cell10691
Whole Blood115100
White Blood Cell
(General Clinic Patients)
99185201
Magnesium Load
(Significantly Depressed Patients)
0100
Magnesium Load
(Chronic Pain Patients)
1531

Discussion

The magnesium load or tolerance test (Ref. 3) is apparently much more likely to detect deficiency of magnesium than any blood test. Although the white blood cell magnesium test is much simpler to perform, it picks up deficiency on only 60% of those who are demonstrated to be deficient by magnesium load testing.

The red blood cell magnesium test and the whole blood magnesium test may pick up only about 50% of those who are deficient. Others have reported the extreme lack of usefulness of serum magnesium levels which reflect only the most serious magnesium deficiencies (Ref. 5). Over the past 2 years we have used the buccal intracellular test for magnesium by Intracellular Diagnostics, Inc. and find it as reliable as the load test.

 NormalLow
WBC (in the depressed 100 who
had magnesium load
4060

The most striking finding is that all 100 of those patients with significant primary depression were deficient in magnesium by magnesium loading testing, although the white blood cell magnesium picked this up only 60% of the time. Interestingly, in 47 chronic pain patients who were depressed, only 31 patients (67%) were deficient by magnesium load testing. Obviously, there will be some depressed patients who are not deficient in magnesium, as seen in 15 chronic pain patients who were depressed but had normal magnesium load tests. Nevertheless, in those who suffer from significant depression, magnesium deficiency

appears to be virtually universal. Even if the 46 chronic pain patients with depression are included, of 146 depressed patients who underwent magnesium load testing, 131 or over 89.7% were magnesium deficient.

The finding of significant magnesium deficiency in depressed patients is of considerable interest, both scientifically and clinically. Magnesium is the natural calcium channel blocker. Clinically, magnesium deficiency has been associated with cardiac arrthymia, hypertension, myocardial infarction, strokes, anxiety, migraine, panic attacks, epilepsy, osteoporosis, immune dysfunction, as well as chronic fatigue, acute musculoskeletal pain and reflex sympathetic dystrophy; all illness with high incidence of concomitant depression. (Refs. 6-14).

Magnesium is significantly affected by blood levels of lithium, calcium, phosphorus, potassium and sodium. Intestinal absorption of magnesium is inhibited by high levels of intestinal calcium, fat, protein pr phosphorus. Urinary excretion of magnesium is increased by most diuretics as well as by stress, epinephrine, nonepinephrine and caffeine. All lead to urinary magnesium loss (Refs. 15-18).

Major potential dietary sources of magnesium are hard water; dark green, leafy vegetables; carrots; beets; sesame seeds and legumes. Magnesium deficiency may result in inadequate intake of magnesium; high calcium intake; high intakes of sodium, protein, fat, potassium, wheat, alcohol, sugar, or caffeine; diarrhea; diuretics; laxative abuse; severe stress (Ref. 11,8). Interestingly, it has been demonstrated that 70% of men and 80% of women do not take in even the daily recommended allowance of magnesium (Ref. 11). And, as would be expected, the nutrition of depressed patients is usually very inadequate.

The neurological and metabolic consequences of magnesium deficiency are widespread. Magnesium is a major regulator of all membrane potentials, as well as neuronal and muscular tone. Thus, magnesium deficiency prevents normal nerve cell stability.

Magnesium also plays a synergistic role with taurine, both of them assisting in stabilization of cellular membrane potential as well as being natural calcium channel blockers (Ref. 19). The clinical use of calcium channel blockers in neurological disorders such as migraine may be obviated with far less “side effects” by administration of magnesium taurate.

Our personal clinical studies have indicated that at least 78% of chronically depressed patients are deficient in taurine (Ref.20). With an even higher incidence of magnesium deficiency, it is easy to understand some of the many symptoms accompanying depression.

Although intravenous magnesium, 2 grams per day for 5 days in 2 weeks, appears in our experience to assist significantly in the relief of depression, additional studies are needed in which depressed patients are treated only with magnesium taurate orally. It may well be that magnesium taurate alone will be as effective as the average antidepressant which helps no more than 50% of depressed patients (Ref. 21). Magnesium taurate is less expensive and has virtually no risk, as long as renal function is normal.

References

1. Seeling MS: Magnesium Deficiency in the Pathogenesis of Disease, New York, Plenum Publishing Corporation, 1980.

2. Zung, W.K.K. A self-rating depression scale. Arch. Gen. Psychiat. 12:63-70, 1965.

3. Ryzen E, Elbaum N, Singer FR, et al: Parenteral Magnesium Tolerance Testing in the Evaluation of Magnesium Deficiency. Magnesium 4:137-147, 1985.

4. Seeling, MS: Magnesium Deficiency in Two Hypertensive Patient Groups. Southern Medical Journal 83:739-42, 1990.

5. Reinhart RA: Magnesium Metabolism. Arch Intern Med 148:2415-2420, 1988.

6. Seeling CB: Magnesium Deficiency in Two hypertensive Patient groups. Southern Medical Journal 83:739-742, 1990.

7. Schoenen J, et al: Blood magnesium levels in migraine. Cephalalgia 11:97-9, 1991.

8. Seeling MS, Berger AR, Spielholz N: Latent Tetany and Anxiety, Marginal Magnesium Deficit, And Normocalcemia. Disease of the Nervous System 36:461-465, 1975.

9. Seeling MS: Increased need for magnesium with the use of combined oestrogen and calcium for osteoporosis treatment. Magnesium Research 3:197-215, 1990.

10. Seeling MS: Magnesium Deficiency in the Pathogenesis of Disease. New York, Plenum Publishing Corporation, 1980.

11. Morgan KJ, et al: Magnesium and Calcium Dietary Intakes of the U.S. Population. Journal of the American College of Nutrition 4:195-206, 1985.

12. Altura Bt, Altura BM: The Role of Magnesium in Etiology of Strokes and Cerebrovasospasm. Magnesium 1:277-291, 1982.

13. Cox IM, Campbell MJ, Dowson D: Red blood cell magnesium and chronic fatigue syndrome. The Lancet337:757-760, 1991.

14. Turlapaty PDMV, Altura BM: Magnesium Deficiency Produces Spasms of Coronary Arteries: Relationship to Etiology of Sudden Death Ischemic Heart disease. Science 208:198-200, 1980.

15. Flatman PW: Magnesium Transport across Cell Membranes. J. Membrane Biol., 80:1-14, 1984.

16. Spencer H, Osis D: Studies of Magnesium Metabolism in Man: Original Data and a Review. Magnesium 7:271-280, 1988.

17. Rude RK: Physiology of Magnesium Metabolism and the Important Role of magnesium in Potassium Deficiency. The American Journal of Cardiology 63:31G-34G, 1989.

18. Levine BS, Coburn JW: Magnesium, the Mimic/Antagonist of Calcium. The New England Journal of Medicine 310:1255, 1984.

19. Durlach J et al., Taurine and magnesium homeostasis: New data and recent advances. In Durlach A, Seeling MS (eds.) Magnesium and cellular process and medicine. Karger Basel, 1987.

20. Shealy, C. Norman, Cady, Roger K., Veehoff, Diane, Houston, Rita, Burnetti, Mariann, Cox, Richard and Clossen, William. The Neurochemistry of Depression. American Journal of Pain Management. Vol. 2, No. 1, pp. 13-16.

21. Weissman MM, Lieb J, Pursoff B, Bothwell S. A Double-Blind Trial of Maprotiline (Ludiomil®) and Amitriptyline in depressed Outpatients. Acta Psychiat Scand 52:225-236, 1975.

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