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MAGNESIUM THERAPY
©1993 Patricia Ann Braun, M.D.
Magnesium is indispensable for all life. It is integral to the function
of Adenosine-triphosphate (ATP). ATP is the energy molecule of life and is present in
everything that lives. In man, magnesium is responsible for over 300 critical metabolic
reactions, any of which, if deficient or faulty, can result in disease or even death. It
is highly concentrated in the myocardium, particularly the septum and is the relaxing
agent needed to relax the muscles after contraction. (spasm).
The question arises: How can a person be magnesium or mineral deficient
when their serum measurement is within the normal range? It is because serum represents
the medium through which homeostasis is maintained. Essentially all body tissues perform
functions that help to maintain these constant conditions. It is often done at the expense
of specific tissues due to the generalized needs of the body as a whole. An excellent
example of this is calcium mobilization from mother's tissues to her child in the womb
while her serum remains "normal" or homeostatic. Without sufficient dietary
intake, assuming adequate absorption, mother will suffer a calcium deficiency long before
the baby even though her serum remains "normal". Dietary intake of minerals and
nutrients, if absorbed, go directly into the serum, where it is processed by the liver and
other organs. It then becomes the responsibility of the tissues to assimilate or discard
these nutrients and minerals even when in excess in order to maintain body homeostasis as
measured in the serum. Magnesium may become deficient in several ways. The primary
deficiency is probably the lack of dietary intake. To understand dietary deficiency it is
helpful to understand the relationships between the individual minerals.
United States Government sources have shown that the average American
gets less than 40% of the RDA for magnesium. This deficiency of magnesium is somewhat
social in nature and is based in modern agriculture practices. Since it is a water soluble
element, freely bonding in ionic solutions, it is mobile in the soil and may be adversely
affected by other elements.
DEFICIENCY due to MINERAL COMPETITION
or IMBALANCE
It is commonly known, particularly in soil agronomy and generally in
medical science, that the ionic character of minerals create agonistic and antagonistic
effects on each other. It has been shown that calcium, phosphorus, iron, manganese and
potassium have an inverse relationship with magnesium. When the concentration of Ca+2,
P-3, Fe+, Mn+ or K+ increase a negative ionic
effect takes place resulting in a deficiency or relative deficiency of Mg+2.
The deficiency may result if just one antagonizing element is in excess! In short there
exists a balance which allows all the necessary minerals to be available to enzymes so
that the biologic work necessary to have a healthy organism can ensue. If not balanced a
deficiency results.
There are other notable inverse relationships that exist in tissue
minerals. Most notable are Ca/P, Ca/K, Ca/Na, Ca/Fe, Na/Mg, Na/K, Fe/Cu and Zn/Cu. It is
not the scope of this essay to discuss these relationships other than to mention that
there is a body of scientific knowledge available for study.
DEFICIENCY due to DIETARY AVAILABILITY
Modern agricultural practices are centered around Nitrogen, Phosphorus
and Potassium. Excess Potassium and Phosphorus on calciferous soils creates a relative
(bound or unavailable) magnesium deficiency while on loam or sandy soils which tend to be
acid, actual magnesium deficiency will exist. Acid rain also contributes to the leaching
of magnesium from the soil. Nitrogen, usually sprayed to excess in commercial farms,
causes increased metabolism of the plants, resulting in greater metabolic (enzymatic)
activity and increased need for magnesium. As soils have become depleted, science has
given man the ability to continue growing with "hybrid vigor" plants custom
tailored to grow on mineral deficient soils. If the soils are deficient in minerals, the
plants will be deficient in minerals. Whether we eat the plants directly or they are
processed through a cow or chicken, we fail to get the necessary minerals to maintain our
enzyme systems. When this happens, disease results.
Most hybrid corn will not bind the trace mineral cobalt. This cobalt
deficient corn is fed to feedlot cows resulting in reduced cobalamine in its tissues. Man
becomes deficient in B12 (cyanocobalamine) because his primary source for the
vitamin (red meat) is also deficient. Since commercial farmers have had to rely more and
more on plants that will grow under less-than-ideal conditions man's health has suffered.
DEFICIENCY due to LOSS
Secondary to dietary insufficiency, magnesium may be lost through
sweating, eating white refined sugar, excessive cooking, fluoridated water, high doses of
vitamin C, mitral valve prolapse, aging, increased intake of dietary fats, increased
dietary phosphates, medications, malabsorption, hypochlorhydria, renal insufficiency or
defect and food allergy.
TREATING SPASM with MAGNESIUM
Calcium is required for muscular contraction and it is now known to have
an important triggering role in initiating contraction. A "relaxing factor"
isolated from muscle homogenates has been shown by electron microscopy to consist of
membrane bounded vesicles derived by fragmentation of the sarcoplasmic reticulum. In
vitro, these vesicles, in the presence of ATP, rapidly and reversibly bind calcium. It is
now speculated that, in the resting state, most of the calcium in muscle is concentrated
within the sarcoplasmic reticulum. Excitation of the sarcolemma is conducted inward by the
membranes of the T system, somehow causing the sarcoplasmic reticulum to release calcium
ions to the myofibrils, triggering their contraction. When contraction is completed,
calcium ions are recaptured by the sarcoplasmic reticulum and relaxation ensues. Enzymes
splitting ATP and ADP have been demonstrated by histochemical methods at the electron
microscope level to be responsible for this recapture. The mechanism is still not fully
known, but it is apparent that ATP (and hence Mg++) is required for relaxation.
The neuromuscular irritability of muscle may be expressed in terms of
the following ratio:
Irritability is proportional to Na+ + K+
/ Ca++ + Mg++ + H+
A deficiency in calcium or magnesium as given above will result in
increased tendency towards spasm. It has been shown that calcium can displace magnesium
from cell surfaces at a critical concentration ratio of 1:20. For years calcium has been
given for low calcium tetanal cramps. For those patients that are not calcium deficient
magnesium is indicated. Magnesium is more effective in these cases because it serves
several functions.
1. Magnesium drives the irritability equation towards more stability.
2. Magnesium is required for the production of ATP which is required for
RELAXATION of muscles.
3. Magnesium acts as a calcium channel blocker ionically inhibiting the
release of calcium from the sarcolemma.
4. Magnesium inhibits ATP-ase in the myosin (contractile area where
calcium activates ATP-ase) yet stimulates ATP-ase in the sarcoplasma (re-capture area
where calcium inhibits ATP-ase.
In summary those patients who present with spasm due to trauma (skeletal
muscle spasm), asthma (bronchial spasm), migraine (cerebral-arteriol spasm), bowel/uterine
cramps (smooth muscle spasm), hot flashes (vascular instability with associated spasm),
coronary artery spasm (arteriole spasm), hypertension and some arrhythmia's, magnesium is
indicated and the treatment of choice. It is safe, extremely effective and inexpensive.
Often after a short IM or IV course of therapy to replenish lost magnesium, and allow the
muscles to relax and heal, only a maintenance dose of oral magnesium is necessary until
complete remission is achieved.
REFERENCES: MAGNESIUM DEFICIENCY
MAGNESIUM ABSORPTION DEFECTS
Arnold JD, Oldfield RK, Pollard AC, Silink M. Primary hypomagnesemia:
case report Aust Paediatr J 1983;19:45.
Teebi AS. Primary hypomagnesemia, an X-borne allele? Lancet 1983;1:701.
Hennekam RCM, Donckerwolcke RA. Primary hypomagnesemia, an autosomal
recessive inherited disease? Lancet 1983;1:927.
Seelig, MS. The Requirements of Magnesium by the Normal Adult. Am. J.
Clin Nutr. 1964;14:342-390.
Seelig, MS. The Requirements of Magnesium; Factors that Increase Needs.
lnternational Symposium on Magnesium 1971.
ABNORMAL RENAL EXCRETION
Booth BE, Johanson A. Hypomagnesemia due to renal tubular defect in
reabsorption of magnesium. J Pediatr 1974;85:350.
Gastrointestinal Disorders
Galland L. Magnesium and inflammatory bowel disease. Magnesium
1988;7:78-83.
Review: Magnesium (Mg) deficiency may occur in inflammatory bowel
disease as a result of 1) decreased oral intake due to pain or anorexia, 2) restrictive
diets (low-residue diets are low in Mg), 3) decreased absorption due to disease or
surgery,4) steatorrhea with the formation of Mg soaps, 5) Mg losses in diarrheal fluid, 6)
magnesuria induced by corticosteroids or surgery, and 7) increased requirements for
healing and for rapid cell turnover. Mg concentration in diarrheal fluid averages 5.8
mEq/1, about 3 times that of serum. Complications of Mg deficiency include muscle cramps,
bone pain, delirium, acute tetany, fatigue, depression, cardiac abnormalities,
urolithiasis, impaired healing, and colonic motility disorders. Hirsch found Mg deficiency
in 7 of 11 patients with chronic intestinal pseudoobstruction. Parenteral Mg markedly
improved or relieved this condition in all patients who were Mg-deficient. Parenteral and
oral Mg requirements in patients with IBD may be as high as 120 and 700 mg/day,
respectively, depending on fecal losses and on the severity of malabsorption.
MAGNESIUM AS A TREATMENT FOR CERTAIN DISORDERS
Magnesium Deficiency Can Cause Sudden Unexplainable Death
Magnesium is one mineral that is in just about every single phase of the
detox pathway. In fact, magnesium is in over 300 enzymes and metabolic pathways. It is the
most under- recognized electrolyte disorder in the U.S. One magnesium authority suspects
80% of the population is deficient (Science News, vol. 133, June 1988). It is
responsible for the resistance of many therapies, like hypokalemia, (uncorrectable low
potassium, as from using diuretics, "fluid pills", heart and blood pressure
pills), uncorrectable vitamin D3 deficiencies (as with osteoporosis and osteomalacia), or
resistant iron deficiencies. I suspect it accounts for much of the sudden death in
athletes. Several joggers and other athletes who were very healthy and had no coronary
arteriosclerosis, suddenly dropped dead. When one sweats, much magnesium is lost. But if
the cardiologist or family doctor doesn't check it and replace it (protocol for physicians
in Appendix), a mystifying death results from cardiac arrhythmia (irregular heart beat
that becomes so chaotic that it becomes fatal as insufficient blood is pumped to the rest
of the body).
The average American consumes less only 40% of the RDA
(recommended daily allowance) of magnesium, a recent United States government survey has
shown (Science News, volume 133, June 4, 1988). This causes no overt
symptoms, but can not be considered benign when over 300 enzymes depend on it. In
laboratory animals, for example, rarely supplementing magnesium has cleared - salt induced
hypertension, chemically induced pulmonary hypertension, and high cholesterol induced
hyperlipidemia. Dr. Mildred Seelig, one of the country's leading authorities on magnesium
(along with Dr. William J. Rea), suggests that 80%-90% of the population is notably
magnesium deficient. This is truly an epidemic in disguise in its own right, since this
deficiency can cause nearly any symptom one can think of (see Chapter 7).
Jogging is one way to commit the perfect crime if you don't know your
magnesium status. For sweating causes excessive loss of magnesium and sets the runner up
for developing a fatal cardiac arrhythmia. Please do the magnesium loading test, for your
sake.
How We Became Deficient In Magnesium
There are many factors that contribute to the lowering of magnesium and
other minerals in the diet:
1. Poor soils, which become depleted as we feed much of the world. You know that
a tomato from your garden doesn't taste the same as one fran the grocery store because
they don't have the same minerals in them. Commercial growers fertilize with the minerals
that make the tomato look plump and red, but not necessarily the minerals for good taste
or good nutrition. Studies now demonstrate what we know through taste: Commercially grown
produce often has less than 75% of the nutrients that organically grown produce has. With
organic produce, man-made chemical formulations are not relied upon to restore what was
taken from the soil. Instead mother nature makes the formula, since real manures and
compost materials are used. There are many trace minerals, some of whose roles in plant
physiology are not yet understood. Mother nature always has the wisdom to include them,
but man hasn't yet reached her level of biochemical sophistication.2. Acid rain will leach
out minerals from the soil just as water softeners remove them from our drinking water.3.
Cooking, destroys some vitamins and removes minerals that are lost to the water.4. High
fat diets.5. Aging depletes nutrients.6. Chronic exposure to chemicals (which we are all
getting more of).7. Chronic diseases deplete nutrients.8. High phosphates in soda or soft
drinks; as well as in other processed foods, compete for absorption of minerals.9.
Medications (diuretics, digitalis, etc.) use up or deplete nutrients.10. Competitive
inhibition from many other minerals by not balancing them. For example, you way read about
zinc and decide to take some, but in an unbalanced form, you will eventually create an
iron or molybdenum or copper deficiency. Too high a dose of vitamin C will inhibit the
uptake of many minerals, and high levels of calcium (commonly prescribed in an unbalanced
form by gynecologists and family doctors) can actually cause a magnesium deficiency. Every
time you have a food that has low nutrient density (very low vitamin/mineral to caloric
ratio), you fall further behind in nutrient debt.
How To Diagnose magnesium Deficiency
So how do you diagnose magnesium deficiency? It is difficult. Blood
tests like the rbc or red blood cell magnesium and the plasma magnesium are practically
useless because if they are positive that is wonderful; but they miss about 80% of the
people who are magnesium deficient. Dr. Jon Pangborn, Ph.D. suggests that if specific
amino acids are low in a 24 hour urine amino acid analysis, that you can be pretty sure
that you have a magnesium deficiency. This is probably a better criteria, but the best one
is published in volume IV, issue 4 of Clinical Ecology, 1986 (Rea, W.J., Magnesium
Deficiency and Chemical Sensitivity). Dr. Rea presented cases that had symptoms suggestive
of magnesium deficiency, but whose rbc (red blood cell) magnesiums were normal. He then
gave them an intravenous (injected into the blood stream) challenge of magnesium and their
symptoms clear. This showed that they were indeed magnesium deficient, and that the blood
test was useless. Before and after urine tests for magnesium also further proved that they
were deficient.
One of the most common symptoms of magnesium deficient patients are back
and neck pain. In fact, at one time I had chronic back pain with insufferable spasm for
months. foolishly blamed it on old horseback and lifting injuries of 20 years earlier
because I had x-ray evidence of a destroyed disc, collapsed vertebral bodies (back bones)
and arthritic spurs. But when Dr. Rea suggested I give myself an I.V. trial of magnesium,
the constant pain of months miraculously melted away. Once more this shows us that
regardless of what blood tests and x-rays demonstrate, there is usually a correctable
abnormality in the here and now. We just need to be smart enough to find it.
The other common symptoms, besides chronic pain, relieved by the
magnesium challenge test in this study were fine tremors, muscle spasm, anxiety, panic
disorder, and nervousness, Raynaud's spastic vessels (cold white fingers), arrhythmia
(irregular heart beat), and of course, you guessed it: fatigue.
Many people with years of-chronic back pain are delighted to find they
get marked improvement when they correct an unsuspected magnesium deficiency. After all,
many people have damaged their backs. But to keep muscle spasm going, there has to be
something else wrong. Magnesium deficiency is one of the causes of protracted muscle
spasms.
Any neurotic symptoms can result from a magnesium deficiency since not
only the synthesis but the breakdown of brain chemicals or hormones is critically
dependent upon it. The toxic brain syndrome symptoms (spacey, dizzy, dopey, confused,
depressed for no reason, can't think straight, irritable, depressed, abnormally
aggressive, and more) can be duplicated by a magnesium deficiency just as easily as by a
chemical exposure.
Top Drawer treatment of any cardiac arrhythmia or chronic muscle spasm
should include assessment of magnesium status. Since several scientific papers demonstrate
that blood tests are worthless in ruling out a deficiency, a magnesium loading test
followed by a therapeutic trial is recommended.
Magnesium deficiency also causes mast cells to release much more
histamine. This is the stuff responsible for much hayfever misery. So the more deficient
one is, the worse the allergies. Obviously correcting a solitary magnesium defect can
often greatly improve one's allergies.
So a trial of magnesium is indicated for any spastic condition.
Remember, in order for a muscle to contract, it needs calcium. In order to relax it
needs magnesium. Many people have spastic conditions which smack of magnesium deficiency,
like asthma, migraine, colitis, angina, chronic back pain, muscle spasm, arrhythnia,
vasculitis, hypertension, cystitis, eye twitches, tremors seizures, Raynaud's, infertility
and nystagmus. But vertigo, psychosis, confusion, depression, eclampsia, diabetes,
phlebitis, exhaustion, TIA's (small strokes), refractoriness to potassium therapy and
insulin can also be due to magnesium deficiency.
The bottom line on magnesium is, the physician should think about it in
everybody. Because chances are he is going to be right. Then an oral or injectable
magnesium loading test will provide the proof (see Appendix for magnesium loading test).
Studies now show that the blood tests are not sensitive enough to diagnose magnesium
deficiency with certainty. Only a therapeutic trial can do that. For if the blood test is
abnormal that's wonderful information. But if it's "normal", it does not mean
the other unmeasured storage sites of magnesium. are, for the magnesium in the blood serum
accounts for only 1% of the body total. We must remember the blood test is only
measuring one area where magnesium "hangs out" . And only before and after urine
tests (see Appendix) will show you when you have finally saturated all the pools or
storage sites.
But each nutrient has an optimal dose for each person and on either side
of this optimal dose is a dose that becomes progressively more harmful. Furthermore, each
nutrient must be in balance with all the others.
Sherry Rogers. M.D., Tired or Toxic, Prestige Publishing
1990:153-160
MAGNESIUM AND INFARCTION
Smith L, Heagerty A, Bing RF, Barnett DB. Magnesium sulfate infusion
after acute myocardial infarction: effects on arrhythmias and mortality. Clin Sci
1985;68(Suppl 11):56.
In this double blind study, patients with acute myocardial infarction
(MI) received intravenous infusions of either magnesium sulfate (2.7 mmol/hour) or saline
placebo during the first 24 hours following acute myocardial infarction (MI). Treatment
was begun within 1 hour of admission to the coronary care unit. Patients with renal
impairment complete heart block, or inability to give informed consent were excluded. All
patients also received standard therapy; hypokalemia was corrected by IV potassium
administration. Magnesium (Mg) infusions doubled serum Mg after 6 hours. In the first 24
hours. 2 deaths occurred in the Mg group (n = 92; 2.2% mortality rate) compared to 7 in
the placebo group (n = 93; 7.5% mortality rate). This 71% reduction in death rate was not
quite statistically significant (p < 0.1). Serious ventricular arrhythmias (ventricular
tachycardia or fibrillation) occurred in 5.4% and 9.7% of the Mg and placebo groups,
respectively (44% reduction in the Mg group; p < 0.1). Total cardiac events
(arrhythmias and death) were reduced by 56% in the Mg group (p < 0.02). No evidence of
Mg toxicity was seen. This study suggests that intravenous Mg administration is safe and
reduces the incidence of serious early squelae following acute MI.
MAGNESIUM AND VITAMIN B6 for CARPAL TUNNEL SYNDROME
Ellis JM, Presley J. Vitamin B6: the Doctor's Report. Harper and Row,
New York, 1973.
This book reports one of the authors' many years of successful clinical
use of pyridoxine for treatment of carpal tunnel syndrome, "rheumatic"
musculoskeletal complaints, problems related to the menstrual cycle and exogenous
estrogens, and (using magnesium along with pyridoxine) pre-eclampsia and eclampsia.
CHEMICAL SENSITIVITY
Rea WJ, Magnesium deficiency and chemical sensitivity. Clin Ecol
1986;IV,4
HYPOGLYCEMIA
Harris S. Gastrointestinal manifestations of hyperinsulinism. Am I Dig
Dis 1935-6; 2:557.
Veverbrants E, Otsen W, Arky A. Role of gastro-intestinal factors in
reactive hypoglycemia. Metabolism 1969;18:6.
Wilkerson CF. Recurrent migrainoid headaches associated with spontaneous
hypoglycemia. Am J Med Sci 43. 1949,218:209.
NUTRIENT TREATMENT OF HYPOGLYCEMIA
Stabbing IB, Turner MO, Franz KB. Reactive hypoglycemia and magnesiuim.
Magnesium Bulletin 1982;2:131.
The Influence of Venous Occlusion and Exercise on Serum Magnesium
Concentration. Clin. Res. 1964;12:203
FATIGUE: EFFECT OF VITAMINS
Annand JC. Pyridoxine and magnesium in the treatment of shock. Lancet
1957;2:340.
FATIGUE: EFFECT OF POTASSIUM MAGNESIUM ASPARTATE
Hicks JT. Treatment of fatigue in general practice: a double-blind
study. Clin Med 1964(Jan.):85.
Formica PE. The housewife syndrome: treatment with the potassium and
magnesium salts of aspartic acid. Curr Ther Res 1962;4:98.
Shaw DL, et al. Management of fatigue: a physiologic approach. Am J Med
Sci 1962;243:758.
Crescente FJ. Treatment of fatigue in a surgical practice. J Abdominal
Surg 1962;4:73.
Friedlander HS. Fatigue as a presenting symptom. Curr Ther Res
1962;4:441.
Kruse CA. Treatment of fatigue with aspartic acid salts. Northwest Med
1961(June):597.
Council on Drugs. New drugs and developments in therapeutics. JAMA
1963;183:362.
MINERAL LABORATORY ANALYSIS
TRACE MINERALS USING WHITE BLOOD CELL ANALYSIS
MAGNESIUM - Magnesium is an intracellular mineral. It can be considered
a macro-mineral as there are approximately 25 grams stored in the body. In the past few
years our appreciation for this extraordinary mineral has abundantly grown, as
deficiencies are becoming more recognized. Magnesium is a cofactor in nearly all enzyme
reactions requiring ATP in the body. It also serves the important functions of protein
formation, DNA production, nerve conduction and relaxation of heart and artery muscle
walls. Magnesium has been found to slow the release of both adrenaline and noradrenaline,
and to partially block adrenergic receptors. Mildred Seeling, M.D. documents several
hundred cases of infant ischemic heart disease related to magnesium deficiency. More
recently Dr. Sherman Bloom at the annual meeting of American College of Cardiology (1982)
stated that magnesium is "natures own calcium channel blocker." Magnesium by
injection can replace calcium channel blockers for angina and cardiac arrhythmias. Other
clinical uses responsive to magnesium include esophageal spasm, some cases of high blood
pressure, menstrual and leg cramps, seizure- disorders, and urinary stones.
Measurement of magnesium status, like other minerals has many problems.
One of the foremost experts on this mineral states that the magnesium retention test is
probably the most accurate method of assessment. An injection of two ml of 50% MgSO4
and a 24 hour pre and post urine magnesium and creatinine is collected. Retention of
greater than 25% indicates magnesium deficiency. However, this is a cumbersome procedure.
Many factors influence serum magnesium. The degree of binding,
complexing or chelating of magnesium and protein bound factions are subject to multiple
variables. Thus, serum magnesium is of no value. A value as low as 1.2 mEq/L. has been
shown without a depletion of total body magnesium.
It has also been shown that RBC magnesium may vary by a factor of five
depending on the age of the red blood cells, making this a very unreliable measurement.
Seeling and others have examined WBC magnesium. The evidence indicates this may be nearly
as accurate as the magnesium retention test.
Mildred S. Seeling. M.D., M.P.H., FACN, Magnesium Deficiency in the
Pathogenosis of disease. Plenum Medical Books, New York, 1980.
TRACE MINERALS USING HAIR ANALYSIS:
CALCIUM/MAGNESIUM
Calcium and Magnesium need to be discussed in the same paper since they
usually maintain in hair, an approximate ratio of 8:1 (Ca/Mg).
The physician using hair element analysis is Particularly concerned when
Calcium and Magnesium deviate from the mean by 2 standard deviations or more.
Unpublished data developed at Doctor's Data, Inc., in conjunction with
their physician-clients, indicates that a very low (-2 standard deviations) Calcium and
Magnesium is indicative of systemic deficiency. This is a good indicator of malabsorption
of elements when two or more additional divalent elements are also low. A very high (+2
standard deviations) Calcium and Magnesium is indicative of maldisposition of these
elements and has been associated with osteoporosis and periodontal disease.
Hair element analysis provides a simple, inexpensive, noninvasive test
for early detection of these problems. A study of 40 individuals, by Jeffrey Bland, Ph.D.
found elevated hair Calcium and Magnesium to be consistent with nutritionally induced
secondary (low Ca/high Phosphorus diet) hyperparathyroidism.
At the present time, hair Calcium and Magnesium levels provide valuable
information to the practicing physician knowledgeable in interpreting the results. As more
studies are completed, their value will increase.
The published reports presented here are merely to verify that studies
of hair Calcium and Magnesium levels are related to nutritional intake, specific disease
syndromes and other metabolic conditions.
An experienced clinician is necessary to properly relate the levels of
Calcium and Magnesium in the hair with the patient's other laboratory tests, history, diet
and symptoms. These two elements are reduced by approximately 15% in naturally gray hair.
SUMMARY OF THE LITERATURE:
HAIR CALCIUM/MAGNESIUM
Hair Calcium levels were significantly elevated in patients with chronic
renal failure whether nondialyzed, hemodialyzed, or hemofiltered. Secondary
hyperparathyroidism was suggested. Plasma Calcium levels were not significantly affected.1
Hair Calcium levels of patients with Psoriasis affecting the scalp were
depressed; those with Psoriasis not affecting the scalp had elevated hair Calcium levels.
The findings suggested that scalp hair as part of the integument may suffer from
Psoriasis. Moreover, the authors noted that the psoriatic process should not be considered
only as a cutaneous disorder affecting both skin and nails but as a cutaneo-ungulopilary
metabolic disease.2
Hair Calcium levels of midshipmen were higher than those in an Eskimo
population, possibly as a result of milk consumption. Variation of hair Calcium and other
elements in the midshipmen were significantly reduced after months of eating the same food
suggesting a relationship between hair levels and ingestion.3
Elevated hair Calcium and Magnesium were correlated with behavioral
problems in a review of 51 studies.4
In a comparison between Indian college students, Indian village young
men, and U.S. males- the villagers had increased levels of Calcium, the college students
had significantly lower Magnesium levels than the villagers, but much higher levels than
the U.S. males. The major difference was their diet.5
There was a negative correlation between Lead and Magnesium in the
college youth but not observed in the village youth. The college youth had significantly
higher levels of Lead. In the limited age group (16-25), there was no variation in
reference range.5
Females have significantly higher hair Calcium levels than males. After
the age of 10, the level is quite stable with a slight decrease with age. Abnormally high
hair Calcium correlates with clinically diagnosed hypoglycemia.6
Clinically diagnosed hypoglycemia patients had elevated Mg. Females had
higher Mg levels than males and levels were reasonably constant through life. The
conclusion is that "hair, with proper treatment and analysis, may be a good tissue
for probing trace element exposure, abnormal nutritional intake or the development of a
trace element responsive metabolic disorder.6
Elevated hair Calcium and Magnesium was correlated to depressed systolic
and diastolic blood pressure. Hair elements have been associated with some disease states
such as depressed Magnesium and diabetes. Some elements may have an effect on a small
percent of population while others may need to interact with other elements to have a
clinical effect. Hyperlipidemia patients had depressed hair Calcium levels. Anthropometric
factors had more effect on blood pressure than elements.7
Hair Calcium levels were lower in an area surrounding a refinery. 8
Autistic children had significantly lower hair Calcium and Magnesium
levels.9
The hair of new borns with Cystic Fibrosis had significantly lower
Calcium and Magnesium although the amniotic fluid levels of the mothers delivering the
Cystic Fibrosis children was similar to that of mothers of normal children. It was also
noted that virtually all Calcium and 80% of the Magnesium found in the hair of CF children
was water-soluble whereas only a small fraction is water-soluble in healthy infants.10
PKU children had significantly lower Calcium and Magnesium hair levels.11
Dyslexic children have elevated hair Magnesium and hair Calcium levels
at 60% of controls. Other elements were also significantly varied.12
The authors note that early hair analysis was criticized due to
interlaboratory variations of results, but many of these factors have been recognized and
may be technically eliminated by proper sampling and analysis. The deviation of Mg could
have been from elevated toxics. 13
REFERENCES:
CALCIUM/MAGNESIUM
(1) Marumo, F.; Tsukamoto, Y.; Iwanami, S.; Kishimoto, T.;
Yamagami, S. 1984. Trace element concentrations in hair, fingernails and plasma of
patients with chronic renal failure on hemodialysis and hemofiltration. NEPHRON 38:267-272
(2) Abdel-Aal, H.; Soliman, A.; El Mahdy, H. and El Saiee, L.
1976. Study of some minerals in scalp hair and blood sera of psoriatics. ACTA DERMATOVENER
(Stockholm) 56:265-267.
(3) Gordus, A. 1973. Factors affecting the trace-metal
content of human hair. JOURNAL OF RADIOANALYTICAL CHEMISTRY, 15:229-243.
(4) Rimland, Bernard, Ph.D. and Larson, Gerald E., M.A. 1983.
Hair mineral analysis and behavior: An analysis of 51 studies. JOURNAL OF LEARNING
DISABILITIES. 16:279-285.
(5) Barker, Dee H.; Rancher, Alvin C.; Mittal, B.M.;
Shanbhag, S.V.; Sharma, V.N. and Sharma, L.S. Metal concentrations in human hair from
India (Pilani, Rajasthan). Study supported by a grant from the Research Division of the
Brigham Young University and by a research grant from the Birla Institute of Technology
and Science, Pilani, Rajasthan, India.
(6) Eatough, Delbert J.; Christensen, James J.; Izatt, Reed
M. and Hartley, Charles. Level of selected trace elements in human hair. FIRST HUMAN HAIR
SYMPOSIUM. Algie C. Brown, ed. Medcom Press.
(7) Chattopadhyay, A. and Jervis, R. 1974. Hair as an
indicator of multielement exposure of population groups. TRACE SUBSTANCES IN ENVIRONMENTAL
HEALTH - VIII, Columbia: Univ. Missouri, pp. 31-38.
(8) Medeiros, D., Ph.D. and Bergman, R., DVM. 1982. Blood
pressure in young adults as associated with dietary habits, body conformation, and hair
element concentrations. NUTRITION RESEARCH. 2:455-465.
(9) Marlowe, M., Ph.D. et al. Decreased magnesium in the hair
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