Magnesium RDA and Its Impact on Aging
Magnesium RDA How Much is Enough?
The National Research Council recommended minimum daily consumption for Magnesium RDA is 150 – 250 mg for children under 10 years of age, and 300 – 400 mg for adults. Current statistics show that only 25% of surveyed populations meet or exceed the Magnesium RDA. Almost 40% consume less than 70% of the RDA. It is fair to say that the majority of the North American population has a sub-optimal intake of magnesium.
Magnesium RDA is about 2 mg per pound body weight. The American diet typically provides 1.2 – 1.5 mg per pound of body weight. Many magnesium experts believe that an intake range of 2.7 – 4.5 mg per pound (about 400 – 700 mg a day) is optimal. Some on the forefront of Magnesium RDA research are recommending up to 1000 mg per day for healthy people, using the clinical symptom of diarrhea as a target marker. Once the marker is achieved, magnesium intake can be reduced. Asians, for example, are already taking 3 – 4.5 mg of magnesium per pound of body weight
- Musculo-Skeletal Symptoms: osteoporosis, chronic fatigue and weakness, muscle spasms, tics, tremors, and restlessness.
- Cardiovascular Symptoms: atherosclerosis, cardiac arrhythmias, sudden death, and vasospasms.
- Female Issues: PMS (Premenstrual Syndrome) and eclampsia.
- Psychiatric Symptoms: irritability, depression, and bipolar disorders.
- Neurological Symptoms: migraine headaches, excessive noise and pain sensitivity.
- Endocrine Symptoms: insulin resistance.
Clinical Uses of Magnesium
A. Prevention and Management of Primary Postmenopausal Osteoporosis (PPMO)
The use of calcium supplementation for the management of Primary Postmenopausal Osteoporosis (PPMO) has increased significantly since 1987, the year when the National Institute of Health increased their recommended daily intake of calcium to 1,500 mg for prevention of PPMO. This recommendation was made in spite of the different conclusions made by some clinical studies presented in the same proceedings. Results of some of these controlled studies presented showed no significant effect of calcium intake on mineral density on trabecular bone and only a slight effect on cortical bone. Since PPMO is predominately due to demineralization of trabecular bone, there is no justification for calcium mega-dosing in post-menopausal women. In fact, soft tissue calcification can be a serious risk factor during calcium mega-dosing under certain conditions. Certain investigators, notably Dr. Guy Abraham, postulated that a total dietary program emphasizing magnesium instead of calcium for the management of PPMO would be more effective for preventing bone loss. His concerns about low magnesium for osteoporosis are similar to his concerns for women with premenstrual tension syndrome.
To test Dr. Abraham’s hypothesis, 19 postmenopausal women on hormonal replacement were given a supplement consisting of 500 mg calcium (50% of RDA) and 600 mg of magnesium (200% of RDA). Serial bone density studies were conducted every 3 months. Subjects receiving the treatment showed an 11% increase in mean bone density versus 0.7% in the untreated group. Results also showed that in postmenopausal women on hormonal replacement therapy, the magnesium emphasized program resulted in a calcaneous bone density 16 times greater than that of dietary advice alone. At the start of the study, 15 subjects were below the fracture threshold. After a year of treatment with magnesium supplementation, only 7 of them were below the fracture threshold.
Researchers such as Dr. Abraham further postulate that PPMO is predominately a skeletal manifestation of chronic magnesium deficiency, facilitated by estrogen withdrawal during the postmenopausal period. He suggested raising magnesium RDA to 1000 mg/day and lowering the RDA for calcium to 500 mg/day. His proposed daily intake for calcium would be more in line with the World health Organization’s “practical allowance” of 400 – 500 mg daily for adults. Such a reversal of the magnesium/calcium ratio would most probably lower the incidence and prevalence of many other degenerative diseases as well.
B. Prevention of Cardiovascular Diseases (CVD)
Cardiovascular diseases have been often linked to magnesium depletion. One of the most alarming trends in the past half-century is the sharp increase in sudden deaths from ischemic heart diseases, particularly in middle-aged men who suddenly develop myocardial infarction, cardiac arrhythmia, or cardiac arrest. It has been postulated that magnesium deficiency may be a common etiologic factor.
Magnesium is found in high amounts in nuts like almonds and peanuts. Research has found than nut lovers (those who eat nuts 5 times a week) have half the chance of developing a heart attack compared to those who eat nuts only once a week.
Epidemiological studies provide compelling evidence. The lower death rates from coronary heart diseases (CHD) in Japan, China, India, and Italy versus those in Europe and America point to differences in cholesterol and saturated fat consumption as being the primary causative factor.
Not to be forgotten, and perhaps even more critical, is the role of dietary salt in contributing to these differences in death rate. In countries with lower CHD death rates, most of the magnesium comes from table salt that is derived from seawater through an evaporative process. This type of table salt contains calcium, potassium, and large amounts of magnesium, in addition to the sodium. Table salt used by North Americans comes primarily from salt mines. As a result of being washed with hydrochloric acid and recrystallization, this purified salt contains almost pure sodium chloride. The Japanese consume 10 grams of ocean salt a day. This provides approximately 1500 mg of magnesium. This is almost four times the magnesium recommended in the RDA and five times more than the average American gets. People from the countries using sea salt suffer a higher incidence of hypertension and stroke (probably due to the higher sodium intake) but lower rate of CHD (probably due to their higher magnesium intake). With increasing use of pure sodium chloride in these countries over the past 20 years, it is interesting to note that the incidence of CHD has increased accordingly.
A variety of cardiac arrhythmias have been associated with magnesium dis-equilibrium, including ventricular tachycardias, fibrillations, and ectopic beats. Coronary spasm is also a major pathogenic feature of hypo-magnesemia. For patients with variant angina, 24-hour magnesium retention after intravenous magnesium loading was 60%, while it was only 36% in control subjects. Substantial evidence has associated magnesium deficiency with sudden cardiac death, a condition that claims 300,000 lives every year.
Deficiency in magnesium, aside from having a negative impact on the energy production pathway required by mitochondria to generate ATP, also reduces the threshold antioxidant capacity of the cardiovascular system and its resistance to free-radical damage. Vitamin E has been found to have strong protective properties against magnesium deficiency-induced myocardial lesions and cardiomyopathy. Magnesium acts as an antioxidant against free radical damage of the mitochondria. It has been called nature’s “calcium channel blocker” because of its ability to prevent coronary artery spasm, arrhythmias, and to reduce blood pressure.
C. Pre-menstrual Syndrome, Diabetes, Depression, and Chronic Fatigue
Women affected by premenstrual syndrome have been found to have reduced magnesium levels. Since magnesium is a cofactor in hundreds of enzymatic reactions, many of which govern cell membrane function, it is easy to see how magnesium can play a fundamental role in multiple organ systems, although there is no conclusive proof that links low magnesium levels directly to PMS.
Magnesium plays the role of a second messenger for insulin action.Insulin itself has been shown to be an important regulatory factor for intracellular magnesium accumulation. Dietary magnesium supplements have been shown to improve both insulin response and insulin action in non-insulin dependent diabetics.
Getting the Magnesium RDA also helps regulate nerve cell function. Its presence in adequate amounts in the synaptic gap between nerve cells controls the rate of neuron firing. Nerves fire easily when magnesium levels are too low. The effect of this rapid firing is increased sensitivity to stimulation of all kinds. Noise will sound excessively loud, emotional reactions will be exaggerated, and the brain may be too stimulated to sleep. Magnesium deficiency may cause excessive muscle tension (such as spasms, tics, and restlessness) because magnesium is needed at the neuro-muscular junction to allow muscles to relax. Chronic fatigue is another common clinical entity associated with deficiency of magnesium.
A deficiency of magnesium can present common psychiatric symptoms including depression, anxiety, restlessness, and irritability. Depressed patients have been found to have lower levels of magnesium. Oral supplementation of magnesium has been tried as an adjunct treatment in psychiatric patients and been found to be successful in rapidly cycling bipolar affective-disorders.
Magnesium RDA Discussion
Magnesium is perhaps the most under-appreciated mineral in our lives. Over 75% of Americans are deficient, even by the low standards set by the RDA. Physicians and anti-aging researchers alike are now recognizing the growing clinical importance of magnesium.
Magnesium RDA supplementation is recommended for healthy patients as well as for those with osteoporosis, cardiovascular disease, depression, diabetes, chronic fatigue syndrome, premenstrual syndrome, and hypertension.
Magnesium deficiency, at the intra-cellular level, is difficult to measure. Blood tests using traditional laboratory methods do not give a good indication of magnesium level from an optimum health and disease prevention perspective. One’s blood test can be “normal” while the intracellular level is “deficient”.
The decision to give magnesium supplementation should therefore rely on evaluation on predisposing factors and symptoms. 100 – 200 mg supplemental magnesium with each meal (three times a day) seems a reasonable and safe recommendation for people with normal kidney function and for those not regularly taking magnesium containing laxatives or antacids. This level of supplementation, coupled with the average dietary magnesium intake, would bring the total daily consumption in line with the 400 – 700 mg a day advocated by many researchers and nutritionally oriented clinicians for optimum health.
Abraham GE, et al: A total dietary program emphasizing magnesium instead of calcium. J Reprod Med 35(5):503-7, 1990.
Abraham GE: The calcium controversy. J Appl Nutr 34:69-73, 1982.
Abraham GE: Nutritional factors in the etiology of the premenstrual tension syndromes. J Reprod Med 28:446-64, 1983.
Arsenian MA: Magnesium and cardiovascular disease. Progress in cardiovascular diseases 35(4):271-310, 1993.
Balch J, Balch P: Prescription for nutritional healing. Avery Publishing Group, New York, 1997.
Chesnut CH: Report from NIH Consensus Conference 1984, NIH/NOF Workshop, 1987. In Osteoporosis Update, 1987. Edited by Gernant HK: San Francisco Radiology Research and Education foundation, pp 3-6, 1987.
Dubey A, et al: Magnesium, myocardial infarctions and arrythmias: The role of magnesium in myocardial infarction. Drugs 37:1-7, 1989.
Ettinger B: Estrogen, progestogen, and calcium in treatment of postmenopausal women. Osteoporosis Update, 1987. Edited by Genant HK: San Francisco Radiology Research and Education Foundation, pp253-58.
Freedman AM, et al: Magnesium deficiency-induced cardiomyopathy: protection by vitamin E. Biochem Biophys Res Comm 170:1102-6, 1990.
Goto K, et al: Magnesium deficiency detected by intravenous loading test in variant angina pectoris. Am J Cardiol 65:709-12, 1990.
Jeppesen BB: Magnesium status in patients with acute myocardial infarction: a pilot study. Magnesium 5:95-100, 1986.
Kanis JA, et al: Calcium supplementation of the diet: I and II. Br Med J 298:137, 205, 1989.
Kummerow FA: Hypothesis: possible role of magnesium and calcium in the development of structure and function in the plasma membrane in mammalian cells and in human diseases. J Am Coll Nutr 11:410-25, 1992.
Saito K, et al: Effects of oral magnesium on blood pressure and red cell sodium transport in patients receiving long-term thiazide diuretics for hypertension. Am J Hypertens 1:715-45, 1988.
Seelig MS: Magnesium Deficiency in the Pathogenesis of Disease, New York.
Shilis ME: Magnesium in health and disease. Ann Rev of Nutr 8:429-60, 1988.
Wester P: Magnesium. Am J Clin Nutr 45:1305-10, 1987.
? Copyright 2015 Michael Lam, M.D. All Rights Reserved.
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