Magnesium is a pivotal mineral nutrient that facilitates
the actions of over 300 enzymes, and the number increases with new
discoveries in molecular biology.(1) As an electrolyte, magnesium is the
most abundant divalent mineral caution in cells and is second only in
electrolyte quantity to monovalent potassium.(1) Uncorrected magnesium
depletion can lead to serious metabolic biochemical inefficiencies
adversely affecting cellular performance, and thereby health.
Canadian dietary intake of magnesium has been compared to the US
intake.(6) In the US, it is estimated that the daily intake is below the
newer 1997 Food and Nutrition Board Dietary Reference Intakes of 320
mg/day for women and 420 mg/day for men.
The analyzed mean daily
intakes in the Total Diet Study for females ages 14 to 16, 25 to 30 and 60
to 65 years old were respectively, 194 mg, 189 mg, and 187 mg. For males
in the same age groups, the intakes were respectively 297 mg, 294 mg, and
250 mg.(1) It is estimated that at the turn of the twentieth century
Americans (and probably Canadians) were consuming approximately 1200 mg
per day due to the high percent of plant food in their diet.(7) Today
plant food comprises less of the typical North American diet and a
significant amount of food processing reduces the pristine nutritional
value of plant foods, including magnesium content. It is also hypothesized
that fertilizers can precipitate soil magnesium preventing its absorption
by food plants.
Clinical hypomagnesemia is rare except in those
individuals who have medical conditions that lead to renal magnesium
wasting, including the hypercalcemia of hyperparathyroidism and
malignancy, genetic disease, alcoholism, and diabetes mellitus.(1)
However, wide spread relative tissue depletion is hypothesized by most
natural medicine leaders because the average daily intake is below the
recommended levels and because practitioner interventional magnesium
supplementation ameliorates a wide spectrum of health problems.
Low levels of magnesium are common in the elderly, but go unnoticed
because most physicians rely on serum magnesium levels to indicate
magnesium status.(11) However, most of the body's magnesium concentration
is intracellular and its status cannot be reliably indicated by blood
testing since blood levels remain somewhat constant. Low blood levels
represent end-stage deficiency, in which even the intracellular
concentration can no longer keep the blood level at the normal range. A
more sensitive test for magnesium status is the level of magnesium in red
blood cells which is readily available and is intracellular.(11)
Magnesium homeostasis is based on dietary intake, fractional intestinal
absorption, and renal regulation. Fractional absorption has been shown to
be curvilinear reflecting a saturation process and passive diffusion, with
an approximate 65 to 70% absorption with intakes of 7 to 36 mg, and an
approximate absorption of 11 to 14% with intakes of 960 to 1000 mg.(1)
Renal excretion is modulated to maintain homeostasis and decreased
magnesium intake in experimental animals and in humans rapidly decreases
magnesium excretion, even before blood levels fall below the normal
range.(1)
Before fractional absorption can occur, magnesium must be in an ionized
state. The absorbability of magnesium salts in humans varies based on how
soluble they are in the first place in the normal gastric pH, but also on
the gastric acid status of the individual. Two extremes are represented in
magnesium citrate and magnesium oxide. Magnesium citrate has high
solubility even in water (pH of 7), but the most common commercial
magnesium salt is magnesium oxide, which is poorly soluble, even in acid
solution.(1) An age-related hypochlorhydria coupled with alkaline
magnesium oxide is particularly troubling when improved magnesium
nutriment is imperative for general metabolic benefits, and for
ameliorating osteomalacia and osteoporosis, and glycemic control in
diabetics. Chronic use of H2 blockers or proton-pump inhibitors could
theoretically frustrate the goals of magnesium supplementation if alkaline
magnesium oxide is being used. Magnesium citrate is more expensive
relative to magnesium oxide, but it is expected to be significantly more
absorbed irrespective of gastric pH, which is a bonus in 40 percent of
postmenopausal women. Because magnesium citrate is soluble in water
irrespective of the pH, it is more reliable in the goal of realizing
optimal magnesium homeostasis in special needs cases.
In terms of risk reduction for, or the amelioration of, osteomalacia and
osteoporosis, the role of magnesium is multifactorial and complicated
without adequate understanding. In experimental animal models, magnesium
deficiency has been associated with depressed bone growth, abnormal bone
formation, and osteopenia.(1) More specifically, magnesium deficiency
blunts the action of 1,25-dihydroxy-vitamin D3, even when it is present in
high doses.(1) This form of vitamin D3 is produced in the proximal tubules
of the kidney and probably accounts for essentially all of the biological
activity of the vitamin D3 group. It is approximately 1000 times more
active than its liver produced precursor, 25-hydroxy-vitamin D3.(8) It is
instrumental in the absorption of calcium from the gut, and to a lesser
extent from the glomerular filtrate.(8) Beyond blunted action, magnesium
deficiency appears to partially impair the stimulatory effect of
parathyroid hormone (PTH) on the kidney hydroxylation of
25-hydroxy-vitamin D3 to 1,25-dihydroxy-vitamin D3, reducing its
formation.(1)
Adequacy of 1,25-dihydroxy-vitamin D3 formation and
action is crucial to maintaining the concentration of ionized calcium in
the blood. To the degree that calcium is not adequately absorbed from the
gut or reabsorbed form the filtrate, to that extent the bones must give up
calcium to maintain blood calcium homeostasis. Chronic degrees of
magnesium depletion is an important contributing factor in the confluence
of age-related factors that bring about and promote compromised bone
tissue.(9,10)
Adequate magnesium status appears to be important in the formation of
optimally strong bone calcification, from a crystal structural point of
view not just from a mineral density point of view.9 Researchers
investigated 19 osteoporotic women by first giving them a magnesium
intravenous load test with a standard amount of magnesium, monitoring the
amount of magnesium homeostatically thrown-off in the urine.
Sixteen of the women retained 90 percent of the administered magnesium,
demonstrating significant magnesium depletion. Every one of these 16
magnesium depleted women also demonstrated abnormally large and abnormally
shaped bone calcium crystals, presenting structurally altered
calcification that was viewed as compromising to bone strength. The three
women who demonstrated adequate magnesium status also demonstrated normal
calcification crystals. While this study is small and should be repeated,
it does suggest two important ideas. Firstly, the incident and extent of
magnesium depletion is probably significant in a large percent of the
osteoporotic population. This at least impacts on the adequacy of
1,25-dihydroxy-vitamin D3 formation and action. Sparing the bones from
inordinate sacrificial calcium donation to maintain extra cellular calcium
homeostasis because of poor gut and filtrate calcium absorption is at the
heart of risk reduction and disease avoidance.
Secondly and less often broached, concerns over risk reduction by
elevating bone mineral density does not address risk associated with the
nature of the crystal design itself. Greater density but at compromised
load bearing capacity may not be adequate risk reduction at
all.
Many other health problems can often be ameliorated by overt
magnesium supplementation, and more salient examples are given here:(11)
angina, arrhythmias, cardiomyopathy, congestive heart failure, some cases
of high blood pressure, intermittent claudication, low HDL cholesterol,
mitral valve prolapse, prevention of transient ischemic attacks (TIA's),
poor glycemic control, inappropriate chronic fatigue, firomyalgia,
glaucoma, some cases of hearing loss, kidney stones, migraine and tension
headaches, and PMS.
People with kidney disease
should not take magnesium supplements without physician approval to avoid
the risk of developing hypermagnesemia. Heart patients with
atrioventricular block should not self-select magnesium supplements
without physician approval to avoid the risk of exacerbating SA and AV
block secondary to unrecognized impaired kidney excretion of
magnesium.(5)
Contraindications
Supplementation of magnesium is contraindicated in those with impaired
renal magnesium excretion.
Ordinary daily supplementation of magnesium citrate is
not associated with adverse effects when the intake falls in the commonly
recognized supplementation range of 300 to 400 mgs of elemental
magnesium.
Even when used in higher amounts up to 600 mg per day,
it is observed to be well tolerated.(3) It is estimated that at the turn
of the twentieth century Americans (and probably Canadians) were consuming
approximately 1200 mg per day due to the high percent of plant food in
their diet.(7) As much as 1000 mg of elemental magnesium per day as
magnesium oxide has been used to enhance glycemic control in Type 2
diabetics without adverse effect.(4) However, diabetics have a recognized
propensity towards magnesium depletion,(1) and 1000 mg/day of magnesium
oxide for a diabetic may be necessary. Magnesium oxide is not absorbed as
well as magnesium citrate, thus lower amounts of the citrate form are
predicted to accomplish the same enhancement of glycemic control, but this
would have to be established empirically.
Magnesium supplementation
(or the use of magnesium containing antacids or magnesium containing
cathartics) when there is an impaired renal function may predispose one to
magnesium toxicity. One of the earliest signs of toxic magnesium blood
levels is a fall in blood pressure, progressing with increased
hypermagnesemia, with later effects including nausea, lethargy, confusion,
deterioration of renal function, ECG changes with either tachycardia or
bradycardia, muscle weakness, hypocalcemia, hypokalemia, heart block and
cardiac arrest.(1)
Use 1 to 2 capsules per day, or as indicated by a health
care professional.
The newer 1997 Food and Nutrition Board Dietary Reference Intakes for
magnesium is 320 mg/day for women and 420 mg/day for men. The mean daily
analyzed intakes in the Total Diet Study for females ages 14 to 16, 25 to
30 and 60 to 65 years old were respectively, 194 mg, 189 mg, and 187 mg.
For males in the same age groups, the intakes were 297 mg, 294 mg, and 250
mg.(1) These intake figures are lower than would be predicted from only
food content estimates and disappearance data.(1) Thus the need to
practice
daily supplementation may be appropriate for a wide section of
adults.
1. Shils, Maurice E., Magnesium, in Modern Nutrition in
Health and Disease, ed, Maurice E. Shils, James A. Olson, Moshe Shike, A
Catharine Ross, ninth edition, Lippincott Williams & Wilkins, New York,
1999 2. Graedon, Joe and Tersa Graedon, Deadly Drug Interactions, St
Martin's Griffin, New York, 1995 3. Jellin, J.M., et al, Pharmacist's
Letter/Prescriber's Letter Natural Medicines Comprehensive Database, 3rd
edition, Stocton, CA, Therapeutic Research Faculty, 2000 4. Lima, M de
L, et al, The effect of magnesium supplementation in increasing doses on
the control of type 2 diabetes, Diabetes Care, 21(5):682-
686,1998 5. Rardon, David P., Charles Fisch, Electrolytes and the
Heart, in Hurst's The Heart Companion Handbook, eighth edition, Editors,
Robert C. Schlant and R. Wayne Alexander, McGraw-Hill, New York,
1995 6. Report of the Scientific Review Committee, Nutrition
Recommendations, Canadian Government Publishing Centre, 1990, p 136 7.
Firshein, Richard, The Nutraceutical Revolution, Riverhead Books, New
York, 1998 8. Goodman, H. Maurice, Hormonal Regulation of Calcium
Metabolism , in Essential Medical Physiology, ed. Leonard R. Johnson,
Lippincott-Raven Publishers, New York, 1998, pp 597-615 9. Cohen, L.
and R. Kitzes, Infrared spectroscopy and magnesium content of bone minerzl
in osteoporotic women, Israeli Journal of Medical Science,17:1123-1125,
1981 10. Rude, R.K., et al, Low serum concentration of
1,25-dihydroxyvitamin D in human magnesium deficiency, Journal of Clinical
Endocrinology and Metabolism, 61:933-940, 1985 11. Murray, Michael T.,
Encyclopedia of Nutritional Supplements, Prima Printing, Rocklin, CA, 1996
WN Products Magnesium Citrate
These statements have not been evaluated by the Food and Drug Administration (FDA). Products are intended to support general well being and are not intended to treat, diagnose, mitigate, prevent, or cure any condition or disease. If conditions persist, please seek advice from your medical doctor.
