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Chapter: Introduction to Human Nutrition: Minerals and Trace Elements

Magnesium: Absorption, transport, tissue distribution, Metabolic function, essentiality, Deficiency symptoms

Like calcium, magnesium is an alkaline earth metal. Magnesium is the eighth most abundant element in the Earth’s crust.


Like calcium, magnesium is an alkaline earth metal. Magnesium is the eighth most abundant element in the Earth’s crust. It does not occur uncombined, but is found in large deposits in the form of magnesite, dolomite, and other minerals. The metal is used in flashlight photography, flares, and pyrotechnics. It is one-third lighter than aluminum, and in alloys is essential for airplane and missile construction. Magnesium is used in producing nodular graphite in cast iron and as an additive to conventional propel-lants. The hydroxide (milk of magnesia), chloride, sulfate (Epsom salts), and citrate are used in medicine.


Magnesium was first shown to be an essential dietary component for rats in 1932 and later for humans. This essentiality is a reflection of the role that magnesium plays in the stabilization of ATP and other molecules. Since then, nutritionists have come to realize that frank magnesium deficiency is rare and that it only occurs in clinical settings as a secondary consequence of another disease. More recently, mod-erate or marginal deficiency has been proposed as a risk factor for chronic diseases such as osteoporosis, cardiovascular disease, and diabetes. These associa-tions are controversial.

Absorption, transport and tissue distribution

Magnesium is the second most common cation found in the body (about 25 g). It is evenly distributed between the skeleton (50–60% of total) and the soft tissues (40–50% of total). In the skeleton, about one-third of the magnesium is on the surface of bone. This magnesium pool is thought to be exchangeable and thus may serve to maintain serum or soft-tissue magnesium concentrations in times of need. Body magnesium is most closely associated with cells; only 1% of total body magnesium is extracellular. Within the cell, magnesium is found in all of the compartments.


Magnesium homeostasis is maintained by control-ling the efficiency of intestinal absorption and mag-nesium losses through the urine. The latter process is a stronger regulatory control mechanism for magne-sium. Magnesium absorption is presumed to occur throughout the small intestine of humans. In normal, healthy individuals, magnesium absorption is between 20% and 70% of magnesium in a meal. Magnesium crosses the intestinal epithelium by three different mechanisms: passive diffusion, solvent drag (i.e., fol-lowing water movement) and active transport. Regu-lation of intestinal nutrient absorption is generally thought to occur only for the active component of absorption. The mechanisms controlling intestinal magnesium absorption are unclear at this time. Because of the chemical similarity of magnesium to calcium, scientists have examined whether vitamin D status regulates magnesium absorption. It appears that only large changes in vitamin D status lead to alterations in magnesium absorption. Only limited information is available on the influence of dietary components on magnesium in humans. Phosphate may be an inhibitor of magnesium absorption. Free phosphate may form insoluble salt complexes with magnesium; phosphate groups in phytate may also inhibit magnesium absorption. Fiber-rich foods have been shown to lower magnesium bioavailability. However, it is not clear whether this was an indepen-dent effect of fiber or a reflection of the phytate content of these foods. Protein and fructose may enhance magnesium absorption.

As mentioned above, the kidney is the principal organ involved in magnesium homeostasis. The renal handling of magnesium in humans is a filtration– reabsorption process. Approximately 70% of serum magnesium is ultrafiltrable, and the normal healthy kidney reabsorbs about 95% of filtered magnesium. When an individual is fed a low-magnesium diet, renal output of magnesium is reduced. Excessive magnesium loss via urine is a clinical condition con-tributing to magnesium depletion in patients with renal dysfunction.

Metabolic function and essentiality

Magnesium is essential for a wide range of funda-mental cellular reactions, and is involved in at least 300 enzymic steps in intermediary metabolism, for example in the glycolytic cycle converting glucose to pyruvate, in β-oxidation of fatty acids, and in protein synthesis. Magnesium plays an important role in the development and maintenance of bone; about 60% of total body magnesium is present in bone. Magnesium has also been demonstrated to enhance the condensation of chromatin, and given the role of chromosomal condensation in the regulation of gene activity, magnesium depletion could indirectly affect gene transcription.

Deficiency symptoms

Magnesium homeostasis can be maintained over a wide range of intakes in normal, healthy individuals. Thus, magnesium deficiency does not appear to be a problem in healthy people. Frank magnesium defi-ciency is only seen in humans under two conditions: as a secondary complication of a primary disease state (diseases of cardiovascular and neuromuscular func-tion, endocrine disorders, malabsorption syndromes, muscle wasting) and resulting from rare genetic abnormalities of magnesium homeostasis. Symptoms of frank magnesium deficiency include:


      progressive reduction in plasma magnesium (10– 30% below controls) and red blood cell magnesium (slower and less extreme than the fall in plasma magnesium)


      hypocalcemia and hypocalciuria


      hypokalemia resulting from excess potassium excre-tion and leading to negative potassium balance

      abnormal neuromuscular function.

All of these symptoms are reversible with dietary mag-nesium repletion. Disrupted calcium metabolism is also evident from the effect of magnesium depletion on serum PTH and 1,25(OH)2D3 concentrations.

 Scientists have attempted to demonstrate that suboptimal intake of magnesium [e.g., below the rec-ommended dietary allowance (RDA) but not frank deficiency] is a contributor to the development of chronic maladies such as cardiovascular disease, diabetes mellitus, hypertension, eclampsia and pre-eclampsia, and osteoporosis. However, the results of studies in this area are ambiguous. The lack of positive findings may reflect the lack of sensitive and reliable tools for assessing magnesium status, the failure to account for magnesium intake from water (in dietary studies), or the difficulty in attributing causality to a single nutrient owing to the apparent heterogeneity of causes arising from epidemiological data relating to most chronic diseases. The fact that in 1997 the US RDA for magnesium was raised for most groups is a reflection that nutrition scientists believe that there is a negative consequence to sub-optimal magnesium intake. Additional research is needed to justify this concern.

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