Magnesium Supplementation Dosing

by Herbert C. Mansmann, Jr. M.D.


1. The Recommended Daily Allowance (RDA) for Mg is between 350 and 450 milligrams (mg) – (6mg per kg per day). One pound of spinach and its cooking water a day will meet this requirement for a normal adult. Green vegetables with their chlorophyll, which contains Mg are good choices, as are nuts, legumes, unpolished rice, and whole grains. But the American diet contains too many refined ingredients. If you are pregnant or ill 600 mg of Mg/day – (10 mg/kg/day), is usually required.

2. The diet of high-income American women contains 120 mg of Mg per 1,000 calories. (Am Col Nutr 1993;12:444). Who today eats 3,000 to 4,500 calories per day in America? If you diet how much Mg do you get per day?

3. Chronic diarrhea is a common cause of Mg deficiency (MgD) and constipation is a common symptom of MgD.

4. Studies have shown that only 25% of Americans receive the RDA of Mg in their diet and 39% get less than 70% of the RDA.

5. Therefore, most healthy Americans need at least 350 mg or as much as 600 mg per day of supplemental elemental Mg, just to remain in positive Mg balance (PMgB). Which means, one takes in and absorbs more Mg than one loses in the urine. Unfortunately, many have other causes of negative Mg balance (NMgB), which commonly results in MgD.

6. If one tolerates 1,000 or more mg of Mg per day and has a normal serum Mg (sMg) level, that person must have at least the mildest form of MgD, an intracellular MgD. This is referred to as normomagnesemia MgD, a very frequent event, the part below the tip of an iceberg. Only 10-20% of those with MgD have a low sMg level, the only test of MgD, many doctors recognize and/or ever test. The other 80-90% with normal sMg, need tests for intracellular Mg content, or for Mg wasting.

COMMON CAUSES OF MgD is very complicated situation, for example: the drug Neurontin binds Mg in the GI tract and results in a malabsorption of both oral Mg and Neurontin (PDR says 24%). While the Company claims to have no information on Neurontin binding of Mg in the blood, clinical experience has shown that sMg levels must be lowered causing symptoms of MgD. While maybe not causing low sMg levels, per se, this drug does cause hypertension due to catecholamine (adrenalin type hormones for example, from stress) release (a known cause of redistribution of Mg) and hyperglycemia (an increase in blood sugar/glucose) both of which result in sMg loss by redistribution of Mg (into tissue) and by an increased urinary Mg wasting (uMg). Thus, this very important medication can cause MgD through three of the four mechanisms listed below the illustration. The following illustration shows the relationships of this complicated situation, in that an excess (a surge) of alcohol, catecholamine or glucose. *Note extra alcohol and extra glucose both result in an increase in catecholamine which ultimately leads indirectly to additional increase in urinary magnesium wasting.

1. Oral intake problems such as dieting, starvation, intravenous (worse when saline, NaCl, is used), tube feeding, eating the Mg poor American foods, vomiting, etc.

2. Malabsorption for example chronic diarrhea, and many other intestinal problems. Two cans of soda per day, (all of which contain phosphates), bind and prevent absorption of Mg ions from the GI tract. This is worse if one takes an Aspartame containing diet sodas, because in the GI tract the Mg binds Aspartame, which it does in the test tube in our laboratory. (If any Aspartame is also absorbed, say, after a large oral dose, it then would bind more ionized blood Mg, which is excreted in the urine). (Migraine is frequently caused by Aspartame in sensitive persons, a disease frequently helped by oral Mg supplementations and/or intravenous Mg sulfate {MgSO4}). Many drugs do the same thing.

3. Redistribution in the body of Mg follows 2 oz. of Alcohol, 2 cups of coffee/tea, or hot chocolate per day and the use of nicotine. Caffeinated diet soda is thus a triple problem. In diabetes, the intermittent high blood glucose seen in this disease enters many cells and displaces the Mg into the serum, which is then rapidly excreted in the urine. In stress catecholamines are released into the serum. Free fatty acids are then released that bind Mg, which is then stored in the tissues. Catecholamines also cause uMg wasting. The net effect is the loss of ionized Mg from the circulation. Ionized Mg is there to protect vital biochemical functions, and it is a co-factor in over 300 enzyme systems and their actions, including the CYP45O enzymes, which metabolize many toxins and drugs. Many drugs cause hyperglycemia, (the release of glucose into the serum), one new such drug is Zyprexa, and many others cause the release of catecholamines and as mentioned above some medications do both.

4. Increased urinary Mg wasting occurs in association with binding of many drugs. In drugs used for asthma, and epilepsy, and some antibiotics, steroids, etc. bind with Mg, and some cause the release of high levels of glucose (sugar), and catecholamines. Adrenaline is one type of catecholamine, which is released as a side effect of many drugs, including some pain medications, anti-cancer drugs and anti-convulsants, as well as during stress. Even an intravenous infusion of normal saline (salt solution) causes uMg wasting.

5. Other Causes; T3, triiodothyronine, and T4, thyroxin, increase uMg (Durlach p20) and an increase in T4 is protective against nephrocalcinosis by its increase in uMg, which dissolves the Ca in kidney tissue (Durlach p26), and a T4 increase uMg wasting supports the fact that hyperthyroidism is a cause of uMg wasting and therefore a cause MgD. Thus it is essential, when taking thyroid hormone; one must have a normal TSH level. I have seen the same said about hypothyroidism, maybe because that is stressful.

In addition, certain genetic kidney tubular diseases with limited reabsorption ability, such as Bartter’s and Gitelman’s syndrome and Distal Renal Tubular Acidosis, among others, result in uMg wasting. The rest of the kidney functions well, but the reabsorption defects involving Mg, calcium, potassium, and zinc vary in degrees and consequences. A 24 hr urine Mg content is an important diagnostic test.

Any human can develop MgD, if two or more of the above causes are present frequently enough. Each day’s loss of Mg needs to be made up eventually by oral Mg intake, to remain healthy in PMgB. The bones, which contain 50% of the total body Mg, can keep our sMg levels normal for a long time. But this is just like money in the bank and continued uMg loss will ultimately break the bank, ending in osteoporosis, while the sMg falls. Thus, a low sMg, called hypomagnesemia, means one has a serious MgD. A low red blood cell Mg (rbcMg), is often found with a normal sMg. In addition, a low rbcMg is most likely seen when there is also a low sMg. Yet, a low rbcMg alone, is abnormal and an obvious excellent test showing intracellular MgD, although it is a less severe stage of MgD than a low sMg. However it is important to remember that total body MgD may be present when both the sMg and the RBCMg are normal, yet can be proven by doing a Mg Load Test.


1. Because of the tendency to diet, the occurrence of pregnant and lactation (nature gives the mother’s Mg, preferentially to infants), and the slow recovery of the Mg storage sites in the bones, women frequently develop MgD.

2. The following, sequential conditions in a female’s life are associated with MgD: amenorrhea (absence of menses), oligomenorrhea (markedly diminished frequency of menses) which is often seen in athletes, premenstrual syndrome (PMS), menstruation, pelvic floor dysfunction (painful muscle spasms called vulvodynia),premature labor, preeclampsia, eclampsia, lactation, and postmenopausal osteoporosis, (shown to be associated with a past history of PMS-see Lee. Bone & Mineral, 1994:24(2); 127-34).

Women who had irregular menstrual bleeding duration had a 40% increased risk of hip fracture and women with both irregular menstrual cycles and irregular menstrual bleeding had an 82% increased risk of hip fracture compared with women who reported neither irregularity (Folsom, AR. Am J Epidemiol 2001;153:251-255).

3. Some of the following are possible consequences of maternal MgD; miscarriage, pre-term labor, premature babies have many MgD related problems and this probably includes apnea, the onset of cerebral palsy, stillbirth, sudden infant death in utero, and sudden infant death.

4. The following conditions, which are associated with MgD, occur statistically and significantly more frequently in females as compared to males; Alzheimer’s disease, Carpel Tunnel Syndrome, competitive swimmers symptoms of MgD, diabetes, heart disease (worse types), migraine, Mitral Valve Prolapse Syndrome, osteoporosis and Status Asthmaticus (life-threatening asthma).

5. These women, as well as everyone, must try to maintain orally NATURE’S BALANCE, which is calcium (Ca) to Mg intake ratio of 2 to 1. Even when one is taking medications for osteoporosis Mg is needed for the matrix of the bones and gives bones their tensile strength, while calcium gives bones it’s hardness. Those with MgD will often need a larger amount of Mg than Ca. See the Topic on Mg, Ca and Osteoporosis in the patient information page on our web site.


1. Constipation, having hard formed stools, may be as infrequent as every 3-4 days, and require a real conscious effort, sometimes even needing help, like glycerin suppositories or enemas.

2. Other major common symptoms are hair loss, high blood pressure, kidney stones, migraine and/or some types of heart disease, one or all may be symptoms of MgD

3. Neuromuscular symptoms of MgD are prominent. They may include nystagmus and thigh muscle and/or lower leg and toe muscle soreness, pain and cramps, as well as dysphasia (painful swallowing), fasciculations, (involuntary movements under the skin, inside of the muscles, which feels like something crawling under the skin), tremors and unsteadiness. There may also be numbness and/or tingling of the fingers and/or toes in some patients.

4. Nervous symptoms may be present in some patients and include anxiety, apathy, confusion, depression, difficulty concentrating and/or remembering, dizziness in elderly (Geriatrics 1999;54:67-8, 73) and fatigue. The neuropathic pain called burning feet, (erythromelalgia), is associated with MgD in 30-50% of cases.

5. Ca is deposited, in the absence of sufficient Mg, in the drainage tubes of the kidneys to cause kidney stones. Ca can also be deposited in the soft tissue of the kidney, resulting in nephrocalcinosis when there is MgD.

6. Many have several symptoms at the same time. Those on Mg show a sequence of symptoms from the time for the next dose: 1st hour, the feeling of wearing boots and/or gloves, due to histamine release. 2ndrd hour fasciculations and at the 4th hour, trouble swallowing. Migraine, PMS, and muscle cramps are often acute, while hair loss and other are slow to be manifested. One needs to observe oneself, to see when more Mg is needed to prevent symptoms due to MgD. hour, burning pain, in some with erythromelalgia due to Substance P release in MgD. and muscle cramps, spasms, or pain, at 3 diagnosis of magnesium deficiency.

Mostly, this is a clinical diagnosis base of the presence of one or more of the causes of MgD, plus the presence of one or more of the symptoms of MgD. It is natural for doctors to want to confirm the diagnosis, so we are providing an additional, but separate comprehensive document on the laboratory diagnosis of MgD for your physician. However everyone should understand its content. In addition your physician will want to know that what we say is legitimate. Therefore we have prepared a letter to your doctor and a list of our medical publications to help reassure medical professionals. All of these are posted on web pages.

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