Laboratory Diagnosis of Magnesium Deficiency

BY Herbert C. Mansmann, Jr., MD

Everyone needs magnesium. Well persons also, yet the American diet of middle class women provides much less than the 360 mg per day, the old RDA, and our American diet gives us only 120 mg per 1,000 calories per day. Now will all of you that eat 3,000 cal a day please rise!! Therefore all Americans need Mg.

Many diseases and medications cause urinary Mg wasting, so these patients need more. Now you can say, I am lucky I have no symptoms of Mg deficiency so what should I do? Take it any way, it cannot hurt you and every day you take more than you need, called positive Mg balance (PMgB) which nature intended, your bones gain additional tensile strength. All the calcium in the world will not prevent osteoporosis, because Ca without Mg makes the bones hard, but brittle. Osteoporosis is a disease characterized by low bone mass and microarchitectural deterioration of bone tissue, leading to enhanced bone fragility and an increase in fracture risk. (Kanis, J Bone Miner Res. 1994;9:112). Mg helps bones stand impact. The Ca to Mg ratio through out-life should be at least 2 parts of Ca to 1 part of Mg. The only exception is never to take more than 2,500 mg of Ca/day, in spite of the need for higher doses of Mg. Those younger than 45 with two or more fractures in a year, are likely candidates for osteoporosis, or osteopenia (decreased mineralization of bones).

Taking Ca and Mg together

Ca and Mg are found together in nature, which occurs in food, in a 3 or 2 to 1 ratio. That means that if the RDA for Mg is 350 mg per day then Ca must be at least 700 or up to 1050 mg per day. For normals over 50, and if one is ill and under 50, most suggest 1,200 mg of Ca per day. This is to be taken in two divided doses with Vit D 400 IU with each Ca dose, this helps absorption of both Ca nd Mg. Do not take more than 2,500 mg of Ca per day, even if one thinks one needs much more, because of the nature-induced ratio. The Mg amount would be 1/2 the 1,200, the amount of Ca, or only 600 mg of Mg per day. Using the above nature’s ratio anyone taking 1,500 mg of Mg would need to take 3,000 mg of Ca, which is a mistake

Type Calcium Salt

Citracal has a very good record and is my choice, but it only contains 200 mg of Ca per pill, so one needs 7 a day. Yes it is true Ca citrate might give more Ca than the same amount of Ca carbonate. Ca in food has a protective effect for humans for million of years and food does not matter, it is Natures way. See below about Mg and Ca at the some time, this does not apply when using Ca citrate in Citracal, because citrate slows the absorption of Mg. This is prevented by separating the Mg and the Citracal by a 1-2 hours since the citrate in the Citracal binds Mg, thus decreasing the amount of Mg absorbed.

Magnesium and osteoporosis abstracts

The following several references supporting the theory that magnesium is pivotal in the development, prevention and treatment of osteoporosis are below, mostly for doctors, but as everyone should knows I believe all patients need to be one’s own advocate. Check this out.

I did a MEDLINE (a medical literature) search back to 1995, to up grade my Mg and Osteo Pro-Cite Database. There were 270 matches from 2001 back to 1966 and this list is updated as necessary. ________________________________________________________________________

#1, Authors, Johnson S.

Title, The multifaceted and widespread pathology of magnesium deficiency.

Source, Medical Hypotheses. 56(2):163-70, 2001 Feb.


Even though Mg is by far the least abundant serum electrolyte, it is extremely important for the metabolism of Ca, K, P, Zn, Cu, Fe, Na, Pb, Cd, HCl, acetylcholine, and nitric oxide (NO), for many enzymes, for the intracellular homeostasis and for activation of thiamine and therefore, for a very wide gamut of crucial body functions. Unfortunately, Mg absorption and elimination depend on a very large number of variables, at least one of which often goes awry, leading to a Mg deficiency that can present with many signs and symptoms. Mg absorption requires plenty of Mg in the diet, Se, parathyroid hormone (PTH) and vitamins B6 and D. Furthermore, it is hindered by excess fat. On the other hand, Mg levels are decreased by excess ethanol, salt, phosphoric acid (sodas) and coffee intake, by profuse sweating, by intense, prolonged stress, by excessive menstruation and vaginal flux, by diuretics and other drugs and by certain parasites (pinworms). The very small probability that all the variables affecting Mg levels will behave favorably, results in a high probability of a gradually intensifying Mg deficiency. It is highly regrettable that the deficiency of such an inexpensive, low-toxicity nutrient result in diseases that cause incalculable suffering and expense throughout the world. The range of pathologies associated with Mg deficiency is staggering: hypertension (cardiovascular disease, kidney and liver damage, etc.), peroxynitrite damage (migraine, multiple sclerosis, glaucoma, Alzheimer’s disease, etc.), recurrent bacterial infection due to low levels of nitric oxide in the cavities (sinuses, vagina, middle ear, lungs, throat, etc.), fungal infections due to a depressed immune system, thiamine deactivation (low gastric acid, behavioral disorders, etc.), premenstrual syndrome, Ca deficiency (osteoporosis, hypertension, mood swings, etc.), tooth cavities, hearing loss, diabetes type II, cramps, muscle weakness, impotence (lack of NO), aggression (lack of NO), fibromas, K deficiency (arrhythmia, hypertension, some forms of cancer), Fe accumulation, etc. Finally, because there are so many variables involved in the Mg metabolism, evaluating the effect of Mg in many diseases has frustrated many researchers who have simply tried supplementation with Mg, without undertaking the task of ensuring its absorption and preventing excessive elimination, rendering the study of Mg deficiency much more difficult than for most other nutrients.

NOTE: The many symptoms and signs of MgD, as well as the link between MgD induced occurrence of CaD induced osteoporosis.


#2. The lead author Bob Rude is one of the very best and one of my personal MgD consultants.

Authors, Rude RK. Kirchen ME. Gruber HE. Meyer MH. Luck JS. Crawford DL.

Title, Magnesium deficiency-induced osteoporosis in the rat: uncoupling of bone formation and bone resorption.

Source, Magnesium Research. 12(4):257-67, 1999 Dec.


Magnesium (Mg) intake has been linked to bone mass and/or rate of bone loss in humans. Experimental Mg deficiency in animal models has resulted in impaired bone growth, osteopenia (decreased bone mass), and increased skeletal fragility. In order to assess changes in bone and mineral homeostasis that may be responsible, we induced dietary Mg deficiency in adult Simonsen albino rats for 16 weeks. Rats were fed either a low Mg diet (0.002 percent) or a normal control Mg diet (0.063 percent). Blood was obtained at baseline, 4 weeks, 8 weeks, 12 weeks and 16 weeks in both groups for serum Mg, calcium, PTH, and 1.25(OH)2-vitamin D determinations. Femurs were harvested at 4 weeks and 16 weeks for mineral analysis and histomorphometry. Serum Mg fell in the Mg depleted group to 0.6 mg/dl (mean) by 16 weeks (controls = 2.0 mg/dl). The serum calcium (Ca) concentration was higher in the Mg depleted animals at 16 weeks, 10.8 mg/dl (controls = 8.9 mg/dl). Serum PTH concentration fell progressively in the Mg deficient rats to 30 pg/ml by week 16 (control = 96 pg/ml). Serum concentration of 1.25(OH)2-vitamin D also fell progressively in the Mg deficient animals by 16 weeks to 14 pg/ml (control = 30 pg/ml). While the percent ash weights of Ca and phosphorus in the femur were not different at any time point, the percent ash weight of Mg progressively fell to 0.54 percent vs control (0.74 percent) by 16 weeks. The percent ash weight of potassium also fell progressively in the Mg deficient group to approximately 30 percent of control by 16 weeks. Histomorphometric analyses showed a significant drop in trabecular bone volume in Mg deficient animals by 16 weeks (percent BV/TV = 13.2 percent vs 17.3 percent in controls). Evaluation of the endosteal bone surface features showed significantly greater bone resorption in the Mg depleted group as reflected in increased number of tartrate-resistant positive osteoclasts/mm bone surface (7.8 vs 4.0 in controls) and an elevated percent of bone surface occupied by osteoclasts (percent OcS/BS = 12.2 percent vs 6.7 percent in controls. This increased resorption occurred in the presence of an inappropriate lowered bone forming surface relative to controls; a decreased number of osteoblasts per mm bone surface (0.23 vs 0.94 in control) and a decrease in percent trabecular surface lined by osteoid (percent OS/BS = 0.41 vs 2.27 percent in controls) were also noted. Our findings demonstrate a Mg-deficiency induced uncoupling of bone formation and bone resorption resulting in a loss of bone mass. While the fall in PTH and/or 1.25(OH)2-D may explain a decrease in osteoblast activity, the mechanism for increased osteoclast activity is unclear. These data suggest that Mg deficiency may be a risk factor for osteoporosis.

#3, Authors

Rude RK. Kirchen ME. Gruber HE. Stasky AA. Meyer MH.

Title, Magnesium deficiency induces bone loss in the rat.

Source, Mineral & Electrolyte Metabolism. 24(5):314-20, 1998.


Disorders in which magnesium (Mg) depletion is common have an associated high incidence of osteoporosis. Mg depletion in humans results in hypocalcemia, low serum parathyroid hormone (PTH) and 1, 25(OH)2-vitamin D levels, as well as PTH and

vitamin D resistance which may serve as mechanisms for the development of osteoporosis. In order to determine if isolated Mg depletion will result in bone loss, we have induced dietary Mg deficiency in the rat. Adult (290 g) female rats were given either a low-Mg diet (2 mg/100 g chow; n = 6) or a normal control Mg diet (63 mg/100 g chow; n = 6). Dietary calcium (Ca) was normal in both groups (592 mg/100 g chow). At 12 weeks, blood was obtained for serum Mg, Ca, PTH,1,25(OH)2-vitamin D, and

osteocalcin determinations. The rats were then euthanized and the femurs obtained for mineral analysis and histomorphometry. Serum Mg in the low-Mg group was less than control (0.4 +/- 0.2 vs. 1.9 +/- 0.2 mg/dl, p < 0.001; mean +/- SD) while serum Ca

was higher (11. 7 +/- 0.5 vs. 9.3 +/- 0.4 mg/dl, p < 0.001). PTH was suppressed in the Mg-deficient group (36 +/- 16 vs. 109 +/- 30 pg/ml in controls, p < 0.002). Serum 1,25(OH)2-vitamin D was also suppressed in the Mg-deficient animals (7.1 +/- 4.8 vs. 28.5 +/- 8.2 pg/ml in controls, p < 0.002). Serum osteocalcin levels were not different (19.8 +/- 2.5 ng/ml in Mg-deficient rats vs. 15.3 +/- 3.4 ng/ml in controls). While the ash weight of Ca and phosphorus in the femur did not change, the ash weight of Mg fell (low-Mg group 0.55 +/- 0.01%, controls 0.65 +/- 0.02%, p < 0.001). Histomorphometry

demonstrated reduction in bone mass; the trabecular bone volume in the femur of the low-Mg group was reduced from control (7.7 +/- 0.2 vs. 13.7 +/- 1.9%, p < 0.002). A surprising new observation was an increase in osteoclast (OC) bone resorption with Mg depletion. The number of OC per millimeter bone surface was 16.9 +/- 1.3 in the low-Mg group versus 7.8 +/- 1.5 in controls (p < 0.001). The percentage of bone surface occupied by OC was 38.3 +/- 3.7 in the low-Mg group versus 17.7 +/- 2.4 in controls (p < 0.001). This increased resorption occurred with an inappropriate non-altered bone-forming surface relative to control (% osteoid surface: low-Mg group 2.4 +/- 0.7 vs. controls 2.6 +/- 0.4; % osteoid volume: low-Mg group 0.25 +/- 0.09 vs. controls 0.38 +/- 0.06; number of osteoblasts per millimeter bone surface: low-Mg group 0.9 +/- 0.3 vs controls 1.3 +/- 0.3). No increase in bone-forming surface or osteoblast number despite an increase in OC resorbing surface and OC number strongly suggests impaired activation of osteoblasts and an uncoupling of bone formation and bone resorption. Our data demonstrate that Mg depletion in the rat alters bone and mineral metabolism which results in bone loss.




Sojka JE. Weaver CM.


Magnesium supplementation and osteoporosis.


Nutrition Reviews. 53(3):71-4, 1995 Mar.


Among other things, magnesium regulates active calcium transport. As a result, there has been a growing interest in the role of magnesium (Mg) in bone metabolism. A group of menopausal women were given magnesium hydroxide to assess the effects of magnesium on bone density. At the end of the 2-year study, magnesium therapy appears to have prevented fractures and resulted in a significant increase in bone density. [References: 32]


#5. This is the best clinical study by an excellent investigator.


Stendig-Lindberg G. Tepper R. Leichter I.


Trabecular bone density in a two year controlled trial of peroral magnesium in osteoporosis.


Magnesium Research. 6(2):155-63, 1993 Jun.


Since magnesium regulates calcium transport, and magnesium replacement in

magnesium-deficient postmenopausal patients resulted in unexpected improvement in documented osteoporosis, we investigated the effect of magnesium treatment on trabecular bone density in postmenopausal osteoporosis. Thirty-one postmenopausal patients (mean age +/- SD = 57.6 +/- 10.6 years), consecutively admitted to the Back Rehabilitation Unit with musculoskeletal pain of non-malignant origin and bone

density values of < or = 1.19 g/cm3 (measured by Compton Bone Densitometer), received two to six tablets daily of 125 mg each of magnesium hydroxide (Magnesium Magma USP/; ‘Mazor’, Israel) for 6 months and two tablets for another 18 months in a 2

year, open, controlled therapeutic trial. Twenty-three symptom-free postmenopausal women (mean +/- SD = 61.2 +/- 6.2 years) whose bone density was concurrently assessed at the same laboratory and who were found to have osteoporosis but refused treatment, served as controls. No new fractures occurred. Twenty-two patients (71 per cent)

responded by a 1-8 per cent rise of bone density. The mean bone density of all treated patients increased significantly after 1 year (P < 0.02) and remained unchanged after 2 years (P > 0.05). The mean bone density of the responders increased significantly both after one year (P < 0.001) and after 2 years (P < 0.02), while in untreated controls, the mean bone density decreased significantly (P < 0.001). The disparity between the initial mean bone density and bone density after one year in all osteoporotic patients and in

the responders differed significantly from that of the controls (both P < 0.001).





Makgoba MW. Datta HK.

The critical role of magnesium ions in osteoclast-matrix interaction: implications for divalent cations in the study of osteoclastic adhesion molecules and bone resorption.

European Journal of Clinical Investigation. 22(10):692-6, 1992

UI: 93093039

NOTE: No abstract available on line.

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