Minerals and Trace Elements 195magnesium 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 effi ciency 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 infl uence 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 fi ber or a refl ection 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 fi ltration–
reabsorption process. Approximately 70% of serum
magnesium is ultrafi ltrable, and the normal healthy
kidney reabsorbs about 95% of fi ltered 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.Defi ciency symptoms
Magnesium homeostasis can be maintained over a
wide range of intakes in normal, healthy individuals.
Thus, magnesium defi ciency 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 defi ciency 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) 2 D 3 concentrations.
Scientists have attempted to demonstrate that
suboptimal intake of magnesium [e.g., below the rec-
ommended dietary allowance (RDA) but not frank
defi ciency] 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