THE ROLE OF MAGNESIUM

IN CLINICAL PRACTICE:
Benefits Supported By Research
Author: Petra Hunter, ND BHSc (Nat)
Editor: Michelle Batson, ND

Electronic
Configuration

Atomic
Numer

12

2
8
2

Name

Magnesium

Symbol

Mg
24.305
Atomic Mass

Advanced Clinical Insights

BioCeuticals Copyright 2005

INTRODUCTION
Magnesium is an essential mineral in human health where it is involved in a wide range of biological
functions, including energy production, nucleic acid and protein synthesis, electrolyte balance,
maintenance of cell membrane integrity, regulation of muscle contraction and relaxation, nerve
conduction and the regulation of vascular tone.
Total body stores of magnesium are estimated to be between 21-28 g in the average adult.1 The
mineral is distributed principally between bone (53%), muscle (27%) and other soft tissues (19%).2 Less
than 1% is found in serum and red blood cells.2
Magnesium deficiency has been implicated in numerous disease states, including cardiovascular
disease, diabetes, obstetric complications, osteoporosis, migraines, and neurological and muscular
problems.

Studies done on
young students and
older adults indicate
that a significant
number of
Australians fail
to meet the
recommended
daily intake of
magnesium.4,5

DEFICIENCY CAUSES AND

CLINICAL MANIFESTATIONS
FACTORS THAT MAY CAUSE MAGNESIUM DEFICIENCY 2
Reduced dietary intake
Poor gastrointestinal absorption or increased gastrointestinal losses (due to diarrhoea, vomiting, or laxative use)
Increased renal losses (including diabetes and alcoholism)
Drug induced (please see drugs & interactions section for more information)
Increased requirements (such as in pregnancy and growth)
Excessive sweating

CLINICAL MANIFESTATIONS
It has been
established that
magnesium intake
has declined by
more than half
during this century;
primarily due to
food processing.2

Magnesium deficiency, unless it is severe, is usually asymptomatic.1 However, it should be kept in

mind that the serum level of magnesium (the common way of testing for a magnesium deficiency)
is only low in a severe deficiency state, as the body preserves serum levels at the expense of
magnesium in cells and bone. For this reason, serum level may appear normal on testing, but a mild
to moderate deficiency state may be present. If a test is performed, the recommended screening
method is for red blood cell magnesium level.
Symptoms, when they do occur, include cardiovascular effects such as hypertension, arrhythmias,
ventricular tachycardia, and coronary and cerebral vasospasms; neurological effects including
dizziness, vertigo, seizures, tremors, ataxia, confusion, delirium, personality changes, depression and
coma; and systemic effects such as generalised muscle spasticity, muscular cramping, anorexia,
nausea, vomiting, hyperglycaemia, and hypercholesterolaemia.1,3

SOURCES OF MAGNESIUM
DIETARY
Common dietary sources of magnesium include cereals, legumes, nuts and green leafy vegetables.1,2
Food processing may lead to a severe depletion of the mineral, leaving only 3-28% of the original
content.2 It has been estimated that magnesium intake has declined by more than half during this
century.2 Meat, fish, dairy and fruits are quite low in magnesium.

SUPPLEMENTAL
Magnesium supplements are available in numerous salt forms as well as amino acid chelates; these
include magnesium carbonate, magnesium chloride, magnesium citrate, magnesium oxide, magnesium
phosphate, magnesium sulfate, and magnesium diglycinate. Magnesium hydroxide is used as an
ingredient in a number of antacids, including Mylanta.

The absorption rate and tolerability may vary greatly between the different supplemental
forms. 6,7

PHARMACOKINETICS
Absorption of magnesium occurs primarily from the ileum and colon.2 The efficiency of absorption of
a magnesium salt appears to largely depend on its solubility in intestinal fluids, as well as on the
amount ingested.3 Salts with a high solubility, such as magnesium citrate, appear to be better absorbed
than salts with poor solubility, such as magnesium oxide.3
Magnesium in its inorganic state (simple salt) is absorbed only to the extent of about 5-10%.6 Inorganic
minerals must be altered from their natural state before they can penetrate the intestinal barrier.
The most efficient way to achieve this goal is by coating them with amino acids.6 This process which
forms a complex composed of the mineral and the amino acid is called chelation. As the amino acid
surrounds the mineral, it neutralises its positive charge shielding it from the attraction of the intestinal
wall, which has a strong negative charge and would otherwise bind the mineral, denying it passage
into the blood stream.6
Moreover, the chelation of magnesium to an amino acid allows the mineral to be absorbed, at least in
part, like an amino acid, resulting in faster and more efficient absorption.
The diglycinate chelate (a covalently bonded dipeptide chelate) is a superior form of
magnesium chelate supplementation that has been designed for maximum absorption and
tolerance.
The results of in vitro and in situ studies show that magnesium diglycinate represents a highly
available form of magnesium that is absorbed in part as an intact dipeptide.7
Even in individuals with known malabsorption, magnesium diglycinate absorption has been
shown to be substantially greater than inorganic magnesium salts and is better tolerated.7
The exact mechanism of magnesium absorption (not absorbed as an amino acid) is not fully
understood. However, it is thought that the mineral is absorbed by an active transport mechanism as
well as by passive diffusion across the intestinal mucosa.8 It is possible that the active transport
system may account for greater magnesium absorption at a lower dietary intake, while absorption at
high dietary intakes may continue due to the passive absorption component.8 Excretion occurs via the
kidneys.2

MECHANISMS OF ACTION

Several types of
supplemental
magnesium are
poorly tolerated at
therapeutic doses
due to the minerals
cathartic effect.7
This problem can be
overcome by using
the diglycinate form.

Magnesium is involved in more than 300 enzyme systems and has a fundamental role to play in energy
metabolism and nucleic acid synthesis. It is also essential for the regulation of ion movements across
cell membranes, maintaining nerve and muscle electrical potentials and transmitting impulses across
neuromuscular junctions.

ENERGY PRODUCTION
Magnesium serves as a cofactor for many intracellular enzymes that are part of mitochondrial energy
production. The mineral is heavily involved in the synthesis and function of the universal energycarrying molecule adenosine triphosphate (ATP), and plays a critical role in the control of glycolysis
and the Krebs cycle.2, 9 *Please see diagram on page 4
In addition, magnesium plays an important role in the integrity of the mitochondrial membrane.
A deficiency state is associated with swelling and disruption of mitochondrial cristae and a reduced
number of mitochondria per cell.9 A magnesium deficiency is also associated with increased
permeability and decreased selectivity of mitochondrial inner membrane and uncoupling of oxidative
phosphorylation.9
In addition to magnesium, nutrients such as malic acid and several of the B vitamins are also
essential in the respiratory chain involved in ATP synthesis.9

SYNTHESIS OF ESSENTIAL MOLECULES

The presence of magnesium is important to maintain an adequate supply of nucleotides
required for the increased DNA and RNA synthesis that occurs during cell proliferation.10
Replicating cells must be able to synthesise new protein and this process is highly sensitive to
magnesium depletion.10

 Many hormones and neurotransmitters exert their effects on cellular activity via the adenylate
cyclase (also known as cyclic AMP synthetase) system.10 The presence of magnesium is
required to activate this enzyme.10
Magnesium also facilitates the endogenous synthesis of glutathione.11,12 Magnesium deficiency
may rapidly reduce cellular glutathione levels.12

GLYCOLYSIS
Glycogen
Glucose 1-phoshate

Glucose

Mg

Mg

Glucose 6-phosohate
Mg

Fructose 6-phosphate
Mg

Fructose 1,6-bisphosphate
Dihydroxyacetone phosphate

Glyceraldehyde 3-phosphate

1,3-Bisphosphoglycerate
Mg

Clinical observations
support the view
that uncorrected
magnesium
deficiency impairs
repletion of cellular
potassium.13,14
For this reason,
patients with
refractory
hypokalaemia may
not respond to
potassium
supplementation
until magnesium
deficiency is
corrected.
Magnesium deficiency
should be considered
whenever severe
potassium deficiency
is encountered.13

3-Phosphoglycerate
Mg

2-Phosphoglycerate
Mg

Phosphoenolpyruvate
Mg

Pyruvate

Lactate

Mg

Acetyl-CoA
Oxaloacetale

Citrate

Malate

Isocitrate

Fumarate

2-Oxoglutarate

Mg
Mg

Succinate

Succinyl-CoA
Mg

KREBS (CITRIC ACID) CYCLE

Figure adapted from Abraham, 1992 (Reference 9)

ION TRANSPORT ACROSS CELL MEMBRANES

The co-existence of secondary electrolyte abnormalities plays a key role in the clinical manifestations
of magnesium deficiency. Magnesium appears to influence the properties of various cell membranes;
a process that is thought to occur by means of calcium channels and ion transport mechanisms.1
Through its role in ion transport systems, magnesium affects the conduction of nerve impulses,
muscle contraction, and the normal rhythm of the heart.11

Calcium and magnesium connection

Magnesium has been referred to as natures physiological calcium channel blocker. During
magnesium depletion, intracellular calcium levels raise.10 Calcium plays an important role in skeletal
and smooth muscle contraction; hence a state of magnesium depletion may result in muscle cramps,
hypertension, and coronary and cerebral vasospasms.10

Sodium, potassium and magnesium connection

Magnesium is also responsible for the maintenance of transmembrane gradients of sodium and
potassium by regulating sodium/potassium-ATPase activity. The arrhythmogenic effect of magnesium
deficiency may be related to magnesiums role in maintaining intracellular potassium.10 Higher
intracellular sodium levels may be the cause of hypertension.1

STRUCTURAL ROLES
4

Magnesium plays a structural role in bone, cell membranes, and chromosomes.11

EFFECTS OF MAGNESIUM:
BENEFITS SUPPORTED BY RESEARCH
Supplemental magnesium has been reported to be beneficial in a wide range of medical conditions, including:
Asthma, COPD
Cardiovascular Disease
- Angina/ Coronary Artery Disease
- Arrhythmias
- Congestive Heart Failure
- Hypertension
- Myocardial Infarction & Ischaemic Heart Disease
- Stroke/ TIA
Behavioural Problems
Chronic Fatigue Syndrome & Fibromyalgia
Dysglycaemia
- Magnesium & Metabolic Syndrome
- Magnesium Deficiency & Insulin Resistance in Obese Children
- Synergistic Effects of Chromium
Glaucoma
Hearing Loss
Migraine
Muscular Complaints
- Cramps
- Restless Leg Syndrome
- Intermittent Claudication
- Physical Endurance
Osteoporosis
Pain
Pregnancy Complications & Infant Health
- Pre-eclampsia (toxaemia)/ eclampsia
- SIDS
Premenstrual Syndrome (PMS)
Stress

CLINICAL APPLICATIONS

Oral magnesium
supplementation may
significantly lower
the need for
bronchodilator use
in those with mild to
moderate asthma.20

ASTHMA
Asthma is a chronic inflammatory disorder of the airways leading to airflow limitation. A decrease in
blood and tissue magnesium levels is frequently reported in asthma sufferers.15 Several different forms
of magnesium administration have been shown to be beneficial in the management of the asthmatic patient:
A review of randomised controlled clinical trials shows that the use of nebulised magnesium sulfate,
particularly if used in addition to a beta(2)-antagonist in the treatment of an acute asthma
exacerbation, may improve pulmonary function and reduce the number of hospital admissions.16
Intravenous (IV) magnesium sulfate, which relaxes smooth muscle resulting in bronchodilation,
is considered adjunctive therapy for severe asthma in patients with poor response to beta(2)antagonists.17 Global Initiative for Asthma (GINA) guidelines confirms the use of IV magnesium
sulfate for hospital management of severe episodes of asthma exacerbation.17
Magnesium is thought to inhibit airway smooth muscle contraction by inhibiting calcium influx
via the voltage-dependent calcium channels.18
A multicentre (emergency departments of eight hospitals) randomised controlled trial showed
that the administration of IV magnesium sulfate improves pulmonary function when used as an
adjunct to standard therapy in patients with very severe acute asthma.19
Oral magnesium supplementation is beneficial in mild to moderate asthma and is recommended
as a concomitant treatment in patients with a stable condition.20
A randomised, double-blind, placebo-controlled prospective study of 89 children with
mild or moderate persistent bronchial asthma, showed that oral magnesium
supplementation (200- 290mg magnesium citrate daily for 12 weeks) may significantly
lower the need for bronchodilator use compared to placebo.20

It has been well documented that experimental hypomagnesaemia in animals evokes, as an early
consequence, an inflammatory response.21 This also leads to an increased production of reactive
oxygen species resulting in oxidative damage of tissues.21 Several studies have shown that lungs might
be a specific target of magnesium deficiency.
Researchers speculate that this may have implications for at least several different lung pathologies,
including allergies, asthma, SIDS (Sudden Infant Death Syndrome) or facilitate formation of lung
metastases.21

CARDIOVASCULAR DISEASE
The term cardiovascular disease (CVD) refers to all heart disease, cerebrovascular disease, and diseases
of the arteries, arterioles and capillaries. According to the Australian Institute of Health and Welfare,
heart, stroke and vascular diseases kill more Australians than any other disease group. In 2002, these
conditions accounted for 37.6% of all deaths (a total of more than 50,000 deaths).22
As mentioned under the mechanisms of action section, magnesium exerts numerous effects on the
cardiovascular system through its role in the ion transport systems, including regulation of normal
heart rhythm and blood pressure. By regulating intracellular calcium levels, magnesium also plays an
important role in smooth muscle contraction and hence coronary and cerebral vasospasms.
Actions noted by magnesium supplementation supportive to cardiovascular health include improved
myocardial metabolism, inhibition of calcium accumulation and myocardial cell death; improvement
of vascular tone, peripheral vascular resistance, afterload and cardiac output; reduced cardiac
arrhythmias; and improvement of lipid metabolism.23 Magnesium also reduces vulnerability to oxygenderived free radicals, improves endothelial function and inhibits platelet aggregation and adhesion.23

It has been shown

that the degree
of magnesium
deficiency is closely
related to the
frequency of chest
pain in patients
with variant angina.32

Epidemiologic studies have shown an inverse relationship between magnesium levels in

drinking water and the frequency of cardiac events and cardiovascular mortality.24,25 One
study of more than 15,000 individuals indicates that low serum and dietary magnesium may
be related to the aetiologies of several cardiovascular disorders, including hypertension and
atherosclerosis.26

ANGINA/ CORONARY ARTERY DISEASE

Angina (angina pectoris) is a type of transient chest pain/pressure/or discomfort that occurs when the
heart is not getting enough oxygen-rich blood supply. The most common underlying cause of angina
is coronary artery disease (CAD). CAD is a chronic condition in which there is a build up of plaque
on the coronary arteries, causing a gradual hardening and narrowing (atherosclerosis) of these blood
vessels.
Magnesium deficiency has been shown to trigger vasoconstriction and enhance vascular
endothelial injury, thus promoting the development and progression of atherosclerosis.27
Additionally, an experimentally induced low plasma level of magnesium has been noted to
accelerate atherogenesis by increasing LDL concentrations and their oxidative modifications,
and by promoting inflammation.28
A 10-year study of 400 high-risk subjects predisposed to CAD found that magnesium may be
important in the pathogenesis of coronary heart disease and sudden death.29
Oral magnesium therapy has been shown to improve endothelial function in patients CAD.28,30
Angina may also be caused by spasm of a coronary artery; a condition known as variant angina. This
type of angina usually responds well to magnesium supplementation; some reports even suggest that
magnesium is the treatment of choice for this condition.31
Japanese researchers have demonstrated that the degree of intracellular magnesium deficiency
in female patients with variant angina is closely related to the frequency of chest pain.32
An earlier study also found the magnesium status of patients with variant angina to be closely
related to disease activity.33

ARRHYTHMIAS
Arrhythmia is a condition of abnormal heartbeat. There are two major types of arrhythmias; tachycardia
(the heart beats too fast) and bradycardia (the heart beats too slow). Arrhythmias can be life-threatening
if they cause a severe decrease in the pumping function of the heart.

Arrhythmias are generally classified by the location in the heart that they occur (atria or ventricles).
Arrhythmias that start in the atria are referred to as atrial or supraventricular (above the ventricles)
arrhythmias. Ventricular arrhythmias begin in the ventricles.

Numerous clinical studies show that magnesium may be of benefit in several types of
arrhythmias. It is considered a first-line agent for torsades de pointes (a type of ventricular
tachycardia).34
Atrial fibrillation (AF) is one of the most common complications after coronary artery bypass
surgery.35 A recent meta-analysis of eight randomised controlled trials showed that magnesium
is associated with a significant reduction in the incidence of AF in these patients.35
Another meta-analysis of 17 randomised controlled trials noted that prophylactically
administered magnesium reduced the risk of supraventricular arrhythmias after
cardiac surgery by 23% (AF by 29%) and of ventricular arrhythmias by 48%.36
In experimental models, magnesium deficiency results in a number of electrocardiographic alterations,
as well as changes in automaticity and conduction.1 Among the electrocardiographic changes
are prolonged PR interval and QT interval, premature atrial complexes, atrial tachycardia, and
fibrillation.1
A probable mechanism by which magnesium acts is by slowing inward calcium current block, thus
decreasing sinus node rate, prolonging AV conduction time and increasing AV node refractoriness
without major changes in ventricular physiology.2 Magnesium depletion within the heart muscle also
leads to potassium depletion,31 which in its own right may lead to cardiac arrhythmias.
Potassium and magnesium deficiencies have been linked in clinical studies to an increased
frequency in serious arrhythmias and mortality in acute myocardial infarction.37 Magnesium
repletion has been shown to increase both magnesium and potassium levels and to decrease
the frequency of ventricular ectopic beats.37

CONGESTIVE HEART FAILURE

Congestive heart failure (CHF) is the inability of the heart to pump a sufficient amount of blood
throughout the body. Signs and symptoms of heart failure may include pulmonary and peripheral
oedema, shortness of breath, exertion, and fatigue.
Magnesium deficiency and other electrolyte abnormalities are common in patients with CHF.38 Low
serum magnesium concentrations are associated with frequent arrhythmias and high mortality in these
individuals.39 Since magnesium depletion is prevalent in CHF and magnesium has anti-arrhythmic and
beneficial cardiovascular effects, magnesium supplementation should be considered in the patients
suspected to be deficient.38
In addition, common conventional therapies for heart failure (such as digoxin, diuretics, and vasodilators)
are influenced by, or associated with, significant alteration in magnesium balance.40 In patients with
CHF, the presence of an adequate magnesium store serve as an important prognostic indicator, not
only because of an amelioration of arrhythmias, but also due to digitalis toxicity (see under drug/
nutrient interactions) and haemodynamic abnormalities.40

HYPERTENSION
Numerous studies indicate that magnesium may help lower elevated blood pressure and possibly even
have a preventative effect.42 The mechanisms involved include its regulatory effects on the cellular
placement of cations important to blood pressure (sodium, potassium and calcium) and its relaxant
effect on vascular smooth muscle.43

Magnesium
deficiency is one
of the most frequent
serum electrolyte
abnormalities seen
in clinical practice.41
Failure to respond
to conventional
treatment of recurrent
ventricular
tachycardia or
fibrillation in patients
with CHF or acute
myocardial infarction
should alert the
clinician to consider
administering
magnesium.41

A meta-analysis of 20 randomised trials detected a dose-dependent reduction of blood pressure

from magnesium supplementation.44
A Japanese study of 17 patients with untreated, uncomplicated mild-moderate hypertension
showed that oral magnesium supplementation (600mg elemental magnesium; taken for
a period of two weeks) can be a useful approach to treat patients with uncomplicated
essential hypertension.45
A four week study of 21 patients receiving oral magnesium supplementation (same dose
as above) also supports the findings that oral magnesium intake may be effective in the
management of essential hypertension.46 The researchers of this trial also noted that magnesium
may reduce serum lipid concentration.
In a double-blind controlled trial, 91 middle-aged and elderly women with mild-moderate
hypertension who were not on antihypertensive medication were randomly assigned to
treatment with magnesium aspartate-HCl (20 mmol Mg/d) or placebo for 6 months. The results
of the study suggest that oral supplementation with magnesium may lower blood pressure in
subjects with mild to moderate hypertension.47

 15 patients with uncomplicated mild-moderate primary hypertension were submitted to

a double-blind randomised crossover study, receiving either 600mg elemental magnesium per
day (in three divided doses) or placebo for a period of 6 weeks. Even though the results were
not homogenous, those who benefited from the treatment noted significantly reduced systolic,
diastolic, and mean blood pressures.48 40% of subjects had their blood pressure effectively
controlled (10 mmHg reduction in mean blood pressure).
60 patients with office blood pressure >140/90 mm Hg were assigned to an 8-week
magnesium supplementation period or an 8-week control period in a randomised crossover
trial.49 The subjects were given 20mmol/d magnesium in the form of magnesium oxide
during the intervention period. Results were measured for office, home and ambulatory
blood pressures. All of these parameters were significantly lower in the supplementation
period than in the control period. The results also indicated that the blood pressure
lowering effects of magnesium supplementation is greater in subjects with higher blood
pressure.
Unfortunately, the results of clinical studies are inconsistent.1 Some of the negative clinical trials for
magnesium replacement did have patients on low salt diets.1 The hypotensive effect of a rigorously
followed low-salt diet decreases the need for magnesium supplementation to improve blood
pressure- even in the face of magnesium deficiency.

MYOCARDIAL INFARCTION AND ISCHAEMIC HEART DISEASE

The success of
magnesium
supplementation in
an acute myocardial
infarction is
dependent on the
correct timing of
administration.50
Magnesium has been
demonstrated to
be protective only if
present before or
at the time of
reperfusion.53

Myocardial infarction, also commonly referred to as a heart attack, is an event in which one of the
coronary arteries becomes blocked, usually by a blood clot, resulting in damage to the heart muscle
(myocardium). The outcome of this event depends on the extent of the tissue damage and on the
treatment that is given within a short time of the attack.
Evidence suggests that acute myocardial infarction (AMI) is associated with low magnesium levels.50
Because trials have reported varying results, analysis of the literature suggests that successful
supplementation in patients with AMI is dependent on correct timing of administration.50
Two large randomised and controlled trials led to different conclusions about whether magnesium
therapy is beneficial in AMI:
The LIMIT-2 study of 1992 found a 24% reduction in 28-day mortality and a 25% reduction in
heart failure during the first month after an AMI in the magnesium treated group.50,51 These
results led to the conclusion that the efficacy of IV magnesium administration is comparable to
that of thrombolytic or antiplatelet therapy in reducing early mortality of AMI.
However, the ISIS-4 study found no differences in the mortality rate in any subgroups of the
patients (the elderly, those at risk for magnesium depletion, and those receiving thrombolytic
or antiplatelet drugs).50,52
The chief difference in the methodology between the two trials was that magnesium was started
concurrently with reperfusion therapy in LIMIT-2, but after reperfusion therapy in ISIS-4. Animal
studies have shown that magnesium is protective only if present before or at the time of
reperfusion.53
Eight early randomised trials, involving nearly 1000 patients, suggested that
magnesium supplementation reduced mortality by as much as 50%.50
A study of 7172 men examined the relationship between magnesium intake and future risk
of coronary heart disease (CHD). The investigators found that within 15 years after dietary
assessment higher intakes of dietary magnesium is associated with less risk of CHD.54
The age-adjusted incidence decreased significantly from 7.3 to 4.0 per 1,000 person-years
in the lowest (50.3-186 mg/day) versus highest (340-1183 mg/day) quintiles of magnesium
intake.

STROKE/ TRANSIENT ISCHAEMIC ATTACK

A stroke, also known as a cerebrovascular accident, is a life-threatening event in which part of the
brain is deprived of adequate oxygen. There are two main types of stroke; ischaemic and haemorrhagic.
Ischaemic stroke occurs when the blood supply to the brain is interrupted, commonly by a blood clot.
Haemorrhagic stroke occurs when there is bleeding into or around the brain.

A transient ischaemic attack (TIA) is the result of a temporary interruption of blood flow to the brain;
the condition is sometimes also called mini-stroke.

Magnesium is involved in multiple physiological processes that may be relevant to cerebral ischaemia.
It may act as a neuroprotective agent through its vascular effects (increasing blood flow to ischaemic
tissue, anticonstrictor effects against vascular mediators, vasodilatation of the cerebral circulation) or
exert neuronal effects. Neuronal effects include block of the NMDA receptor ion channel, calcium
antagonism at voltage-gated channels, and enhanced regeneration of adenosine triphosphate.55
Significant neuroprotection with magnesium has been observed in different models of focal
cerebral ischaemia, with infarct volume reductions between 25-61%.56
One study on the prognostic impact of magnesium serum levels with respect to the occurrence
of neurological events in patients with advanced atherosclerosis showed that individuals in
the lowest tertile of magnesium serum levels exhibited a 3.29-fold increased adjusted risk for
neurological events compared to those in the highest tertile.57
Intravenous magnesium sulfate has been shown to have a significant positive effect on the
outcome in patients with acute stroke.58
Elevated homocysteine levels are considered a risk factor for cardiovascular disease. It has been
suggested that an increased serum homocysteine concentration causes abnormal metabolism of
magnesium in cerebral vascular smooth muscle cells, thus priming these cells for
homocysteine-induced atherogenesis, cerebral vasospasm and stroke.59 Research indicates that vitamins
B6, B12 and folic acid may act in synergy with magnesium in occlusive cerebral vascular diseases
induced by elevated homocysteine levels.59 Homocysteine has been noted to cause a dose-dependent
loss of magnesium in cultured cerebral vascular smooth muscle cells.59

SYNERGISTIC EFFECTS OF TAURINE IN CARDIOVASCULAR HEALTH

Several studies indicate that taurine is an effective therapeutic tool in the management of various
types of CVD:60
Taurine assists in the regulation of intracellular calcium levels, thereby protecting the
heart from intracellular calcium imbalances, which can lead to cell death and subsequent
myocardial damage;

Clinical studies show

that oral magnesium
supplementation may
be of great benefit in
children with
ADHD.62,63,64,64

Taurine may also prevent cardiac arrhythmias by regulating potassium flux in and out of
cardiac muscle cells;
Due to its positive inotropic effects, taurine is also capable of lowering blood pressure;
Taurine may improve the clinical manifestations of CHF, including the severity of dyspnoea,
palpitations, and oedema, as well as increase exercise capacity in these patients.

BEHAVIOUR PROBLEMS

Supplementation
with magnesium and
vitamin B6 has also
led to remarkable
improvements in
autistic patients.66

Magnesium deficiency occurs more frequently in children with attention deficit hyperactivity disorder
(ADHD) than in healthy controls.
Researchers studied 116 children aged 9-12 years with recognised ADHD for blood serum, red
blood cell, and hair levels of magnesium. A deficiency was found in 95% of the subjects.61
In a recent trial, a combination of magnesium and vitamin B6 was shown to reduce the
symptoms of hyperexcitability (including physical aggressiveness, instability, and scholar
attention) in all study participants (52 children) after 1-6 months of treatment.62
50 children (7-12 years) with diagnosed ADHD who had low magnesium (determined by
serum, red blood cell, and hair levels) were given standard treatment together with 200mg of
magnesium per day for six months. A further 25 magnesium deficient children with ADHD,
receiving standard therapy without magnesium, served as a control. Compared to their clinical
state before supplementation and the control group, the children in the magnesium
supplemented group showed a significant decrease in hyperactivity. At the same time,
among the children given standard treatment alone, hyperactivity was intensified.63,64
It has also been suggested that magnesium deficiency may play a central role in Tourettes syndrome
and comorbid conditions.65
Magnesium, together with vitamin B6, may also be beneficial for autistic patients. While no
cure for autism is known, magnesium and B6 supplementation has led to remarkable
improvement in many cases.66

CHRONIC FATIGUE SYNDROME & FIBROMYALGIA

Despite considerable efforts by scientists worldwide, no single aetiology has been identified to explain
the occurrence of chronic fatigue syndrome (CFS). However, a review of literature suggests that
a number of marginal nutritional deficiencies may have aetiological relevance.67 These include
deficiencies of various B vitamins, vitamin C, magnesium, sodium, zinc, coenzyme Q10, essential fatty
acids, and amino acids such as L-carnitine and L-tryptophan.67
Although findings have been mixed, several studies have found lower erythrocyte magnesium levels
in CFS patients than in controls.67,68
32 patients with CFS were randomly allocated to receive either intramuscular magnesium
sulfate (n=15) or placebo (n=17) for a period of six weeks.68 At the end of the study, 12 of the
15 patients treated with magnesium reported to have improved energy levels,
better emotional state and less pain. In contrast, only three of the 17 placebo patients said
they felt better and only one reported improved energy levels.

Observations by
clinicians find that
patients with fatigue
may take a couple
of weeks to respond
to treatment, while
patients with
fibromyalgia may
respond in only
a couple of days.67

This study confirms results obtained in clinical trials already during the 1960s.31 These studies
used oral magnesium and potassium (1 g of each) rather than the injectable form. Out of
almost 3,000 patients studied, 75-91% experienced relief during treatment, in contrast
to only 9-26% of those taking placebo.
When fibromyalgia is a substantial component of the clinical picture, magnesium
supplementation may be combined with malic acid. Malate also plays an important role in
energy metabolism; specifically the generation of mitochondrial ATP, which may be reduced in these
patients.9,67
In an open-label trial, patients with primary fibromyalgia were treated orally for an average
of eight weeks with 200-600 mg magnesium and 1200-2400mg malate daily.67,69 The subjects
exhibited a significant decrease in mean tender point index from 19.6 to 6.5. However, only
two days after six of the 15 patients were switched to placebo, they reported a worsening in
muscle pain. After two weeks, their mean tender point index had risen to 21.5.

DYSGLYCAEMIA
Research indicates
that magnesium
supplementation
or increased intake
of magnesium-rich
foods may be an
important clinical
tool in the prevention
of type 2 diabetes
in obese children.75

Magnesium is known to play a major role in the secretion and effect of insulin. Supplementation with
magnesium has been noted to improve insulin response and action, as well as glucose tolerance.
Several studies in patients with blood sugar problems have shown this mineral to be of significant
clinical value.

MAGNESIUM & THE METABOLIC SYNDROME

A strong relationship between decreased serum magnesium and the metabolic syndrome has been
established.70 Key features of the metabolic syndrome include abdominal obesity, raised triglycerides,
reduced HDL cholesterol, raised blood pressure, and raised fasting plasma glucose level. It was
recently estimated that 20-25% of Australian adults have the syndrome.71
A growing number of studies suggest that intracellular magnesium plays a key role in modulating
insulin action and insulin-mediated glucose uptake.72
A randomised, double-blind, placebo-controlled trial of 63 subjects with type 2 diabetes found
oral magnesium supplementation to improve insulin sensitivity and metabolic control.73
In a recently published article, Japanese researchers observed that not only does a deficiency
of magnesium decrease insulin sensitivity and secretion, but also contributes to the pathogenesis
and development of lifestyle related diseases, including hypertension and hyperlipidaemia.74

MAGNESIUM DEFICIENCY & INSULIN RESISTANCE IN OBESE

CHILDREN
Magnesium deficiency has been associated with insulin resistance and increased risk for type 2
diabetes in adults.75 The problem has now also been found to extend to obese children.

10

In a study designed to determine whether obese children exhibit serum magnesium deficiency
and its potential association with insulin resistance, researchers found that the connection
between magnesium deficiency and the risk for type 2 diabetes may begin already in
childhood.75

The researchers observed 24 obese non-diabetic children and 24 sex- and puberty-matched
lean control subjects. Serum magnesium was found to be significantly lower in the obese
children compared with lean controls and the serum magnesium level was inversely correlated
with fasting insulin and positively correlated with quantitative insulin sensitivity check index.
It was concluded that magnesium supplementation or increased intake of magnesiumrich foods may be an important tool in the prevention of type 2 diabetes in obese children.

SYNERGISTIC EFFECTS OF CHROMIUM IN DYSGLYCAEMIA

Numerous studies demonstrate that supplemental chromium may have significantly beneficial
effects on blood glucose and lipid metabolism in patients with mild to severe glucose intolerance,
as encountered in metabolic syndrome and diabetes.76,77,78,79,80,81,82
Some of the proposed mechanisms include an increased insulin binding and subsequent uptake of
glucose into the cell, increased number of insulin receptors, and activation of insulin receptor kinase
leading to increased insulin sensitivity.83

GLAUCOMA
A subgroup of glaucoma patients in whom vasospasm leads to reduced blood supply to the optic
nerve may benefit from supplemental magnesium. These patients are often treated with calcium
channel blocker drugs.
Ten patients (six with open-angle glaucoma, four with normal-tension glaucoma) were
supplemented with magnesium, a natural calcium channel blocker.84 Magnesium (121.5 mg
twice daily) was administered for a month. After the treatment, the visual fields tended to
improve, leading the researchers to the conclusion that magnesium has a beneficial effect in
glaucoma patients with vasospasm.
Although these results are very promising, a larger trial is warranted to confirm these results.

HEARING LOSS
Noise-induced hearing loss appears to result from energy depletion in the hair cells of the ear.
The problem may be further enhanced by hypomagnesaemia induced vasoconstriction.85
Magnesium treatment has been repeatedly shown to reduce the incidence of both temporary
and permanent noise-induced hearing loss.86
Researchers studied 300 young, healthy, and normal-hearing military recruits who underwent
2 months of basic training, which includes repeated exposures to high levels of impulse noise
while using ear plugs. The recruits were assigned to receive either 167mg magnesium
aspartate daily or placebo. The study results demonstrated that the rate of noise induced
hearing loss was significantly more frequent and more severe in the placebo group.87

Oral magnesium
supplementation
significantly reduces
the attack frequency
of migraine
headaches as well
as drug
consumption for
symptomatic relief.90

Magnesium may also improve hearing in patients with acute-onset hearing loss.
In a prospective, randomised, double-blind, placebo-controlled trial, 28 patients with idiopathic
sudden sensorineural hearing loss were treated with either steroids and oral magnesium
(study group) or steroids and a placebo (control group).86 Compared to the control group,
the magnesium treated group had a significantly higher proportion of patients with improved
hearing. Further analysis of the data also suggested that the magnesium treated individuals
experienced hearing improvement at a larger magnitude than the control subjects.

MIGRAINE
Migraine-type headaches are common; Australia is home to 2 million sufferers.88
The activities of magnesium in the body include counteracting vasospasm, inhibiting platelet aggregation,
and stabilising cell membranes, all of which are involved in migraine pathogenesis.89 In addition,
magnesium concentration has an effect on serotonin receptors, nitric oxide synthesis and release,
inflammatory mediators, and a variety of other migraine related receptors and neurotransmitters.89
In order to evaluate the prophylactic effect of oral magnesium, 81 patients with migraine (mean
attack frequency 3.6 per month) were given oral magnesium (600mg daily) or placebo for 12
weeks. In weeks 9-12 the attack frequency was reduced by 41.6% in the magnesium group and
by 15.8% in the placebo group compared to baseline. The number of days with migraine and
the drug consumption for symptomatic treatment per patient also decreased significantly in the
magnesium group.90

11

 The intravenous (IV) use of magnesium to abort an acute attack has also been studied in a
randomised, single-blind, placebo-controlled trial including 30 patients.91 15 patients received
1g of IV magnesium sulfate given over 15 minutes; 15 patients served as controls. However,
those in the placebo group with persisting complaints of pain accompanying symptoms (such
as nausea and vomiting) after 30 minutes also received the same dose of magnesium as those
in the treatment group.
All patients in the treatment group responded to treatment with magnesium sulfate.
The pain disappeared in 13 patients (86.6%); it was diminished in 2 patients (13.4%);
and in all 15 patients (100%), accompanying symptoms disappeared.
In the placebo group, a decrease in pain, but persistent accompanying symptoms was noted
in 1 patient. Accompanying symptoms disappeared in 3 patents 30 minutes after placebo
administration.
All patients who initially received placebo were subsequently treated with magnesium.
All of these patients responded to treatment. In 14 patients (93.3%), the attack
ended; in 1 patient (6.6%), pain intensity decreased; and in all 15 patients (100%),
accompanying symptoms disappeared.

MUSCULAR
Adequate magnesium levels are required at neuromuscular junctions to permit muscles to relax.
Chronic magnesium deficiency increases the likelihood of excessive muscle tension, and may lead to
muscle spasms, tics, restlessness, and twitches.92

CRAMPS
Magnesium
deficiency should
always be included
in the differential
diagnosis of patients
who present with
persistent or severe
muscle pain.97

Muscle cramps are involuntary and often painful contractions of the muscles. During magnesium
depletion, intracellular calcium levels raise; calcium plays an important role in skeletal and smooth
muscle contraction, hence a state of magnesium depletion may result in muscular cramping.10
Muscle cramps, muscle strains (and damage), and headaches due to muscle tension are all
associated with a magnesium deficiency state.93
Bartl et al. demonstrated that nightly muscle cramps during pregnancy may be a sign of a latent
magnesium deficiency which can be influenced by oral magnesium supplementation.94
Swedish researchers have also found oral magnesium supplementation to be a valuable
therapeutic tool in the management of pregnancy-related leg cramps in magnesium deficient
patients.95
Magnesium supplementation may also be of benefit to non-pregnant individuals. Volunteers
suffering regular leg cramps were given magnesium citrate (equivalent to 300 mg magnesium)
or placebo for 6 weeks in a randomised, double-blind, cross-over placebo-controlled trial.
While no difference in cramp severity or duration was recorded between the groups, there was
a trend towards fewer cramps experienced by those taking magnesium. Significantly more
subjects thought that the treatment had helped after magnesium than after placebo (78% and
54% respectively).96

RESTLESS LEG SYNDROME

Restless leg syndrome (RLS) is a sleep disorder primarily characterised by leg discomfort during sleep,
which is only relieved by movement of the legs. RLS can result in decreased quality of sleep with
subsequent daytime sleepiness, anxiety, depression, and confusion or slowed thought processes from
lack of sleep.
Researchers have shown oral magnesium supplementation to be a useful therapy in patients
with mild to moderate RLS as well as periodic limb movement during sleep (PLMS) related
insomnia.98

INTERMITTENT CLAUDICATION

12

Intermittent claudication occurs when the leg muscles do not receive enough oxygen rich blood
during walking or exercise, causing painful cramping. The condition is caused by atherosclerosis and
therefore shares similar risk factors as for coronary artery disease and is characterised by magnesium
deficiency.31

PHYSICAL ENDURANCE
Physical activity increases the bodys need for energy; magnesium plays many roles in energy metabolism.
Energy for muscle contraction is derived from the hydrolysis of ATP; the enzyme that drives the
hydrolysis of ATP, ATPase, requires magnesium. Thus adequate levels of magnesium are required for
skeletal muscle function.
187 patients with coronary artery disease were randomised to receive either 365mg
magnesium (as magnesium citrate; n=94) or placebo (n=93) for 6 months in a multicentre,
randomised, prospective, double-blind trial. Oral magnesium supplementation was
reported to significantly increase exercise duration time and lessened
exercise-induced chest pain in these patients.99
Serum and erythrocyte magnesium levels were determined in a group of 11 endurance athletes
before and after a 25 km running race and compared to 30 sedentary controls. The differences
encountered suggest that athletes suffer from a magnesium deficiency that is partially due to
physical exercise.100
A human study demonstrated that, when combined with strength training, supplemental
magnesium (8mg/kg body weight/day; including dietary intake) increases muscle strength to
a greater extent than strength training without supplementation.101
In addition to magnesium, nutrients such as malic acid (malate) and several of the B vitamins
are also essential in the respiratory chain involved in ATP synthesis.9
Malate plays an important role in generating mitochondrial ATP both under aerobic and hypoxic
conditions.9 It has been proposed that malate deficiency is a cause of physical exhaustion.9

THE SYNERGISTIC EFFECTS OF GLUTAMINE IN PHYSICAL ENDURANCE

The amino acid glutamine considered to have an anabolic effect on skeletal muscle, where it
stimulates the synthesis and inhibits the degradation of proteins.103
It has been noted that athletes suffering from overtraining syndrome appear to maintain low plasma
glutamine levels for months or years.104 Plasma glutamine responses to prolonged and high
intensity exercise are characterised by increased levels during exercise followed by significant
decreases during the post-exercise recovery period, with several hours of recovery required for
restoration of pre-exercise levels. If recovery between exercise bouts is inadequate, the acute effects
of exercise on plasma glutamine level may be cumulative. These observations have important
implications for organ functions in these athletes, particularly with regard to the gut and the cells
of the immune system, which may be adversely affected by glutamine deficiency.104

Magnesium
deprivation increases
oxygen requirements
to complete sub
maximal exercise
and reduces
endurance
performance.102

Researchers believe that reduced plasma concentrations of glutamine may be a good

indicator of severe exercise stress.104

OSTEOPOROSIS
Research indicates that magnesium may be just as important in the prevention and treatment of
osteoporosis as calcium.105,106,107 In addition, adequate serum magnesium levels are necessary for
proper calcium metabolism since a state of deficiency can result in hypocalcaemia. Magnesium affects
mineral metabolism in bone by a combination of effects on hormones and other factors that regulate
these processes. A deficiency of this mineral has an inhibitory effect on osteoblasts108 and may result
in increased osteoclast activity.109,110
The benefits of magnesium supplementation were investigated in postmenopausal women who
received two to six tablets daily of 125mg magnesium hydroxide for six months and then
two tablets for another 18 months in a 2 year, open, controlled trial. Twenty-three symptom-free
postmenopausal women who were found to have osteoporosis but refused treatment served as
controls. The mean bone density of all the treated women increased significantly, while
in the untreated controls, the mean bone density was significantly decreased.111
Magnesium deficiency occurs frequently in chronic alcoholism and may contribute to the increased
incidence of osteoporosis seen in this population.112 Additionally, magnesium deficiency may
contribute to osteoporosis associated with malabsorption.
In a study by Rude RK et al., where patients with a malabsorption syndrome were given
magnesium supplements for two years, a significant increase in bone mineral density was
observed.113 Furthermore, experimental magnesium deficiency in animal models has resulted in
impaired bone growth, osteopenia, and increased skeletal fragility.110

13

PAIN
Magnesium is known to block the N-methyl-D-aspartate (NMDA) receptors, which are involved in the
potentiation of pain. This effect is thought to contribute to magnesiums pain reliving action in
migraine headaches, postoperative pain, neuropathic pain, erythromelalgia, Raynauds phenomenon,
and possibly other vascular disorders and pain syndromes.
Neuropathic pain may respond poorly to morphine and is often difficult to relieve. Researchers
investigated the safety and efficacy of IV magnesium sulfate at two doses in 12 patients with
neuropathic pain.114
After receiving 500mg, three patients experienced complete pain relief and two experienced
partial pain relief for up to 4 hours duration; pain was unchanged in one patient. After
receiving 1g, one patient experienced complete relief and four experienced partial pain relief
of similar duration; pain was unchanged in one patient.
IV magnesium at these doses appeared to be safe and well tolerated.
In a randomised, double-blind study, 42 patients undergoing elective abdominal hysterectomy
with general anaesthesia received magnesium sulfate or placebo intravenously before and
20 hours following surgery. Compared to control subjects, magnesium-treated patients required
less morphine during the first 48 hours and experienced less discomfort during the first and
second postoperative days.115
In addition, while the control subjects experienced increased insomnia during the first and second
postoperative nights, the magnesium-treated patients showed no change in postoperative
sleeping patterns compared to preoperative patterns.
When a board member of the Erythromelalgia Association experienced complete remission of
his disabling erythromelalgia (EM) by taking oral magnesium sulfate (up to 1166 mg daily) after
only modest improvements on conventional medication, he encouraged other members to try
the same approach and report back to the association.116
Overall, 8 of 13 patients reported improvement (1 remission; 3 major improvements; 2 moderate
improvements; 2 mild improvements). Four patients (30.8%) reported no response to
magnesium therapy, and 1 patient's symptoms worsened. Two patients' magnesium dose was
limited because of diarrhoea. (However, this problem may be overcome by using a magnesium
diglycinate chelate; please refer to the pharmacokinetics section).
This informal survey demonstrates that the use of high dose oral magnesium supplementation
may produce good and sometimes dramatic results in patients unresponsive to many other
treatments. The author concluded that these results suggest a role for oral magnesium in the
treatment of EM and possibly other vascular disorders.

PREGNANCY COMPLCIATIONS AND INFANT HEALTH

Magnesium deficiency during pregnancy can induce maternal, foetal, and paediatric consequences that
may last throughout life.117
Animal studies of gestational magnesium deficiency show that it may have a marked effect on
parturition and post uterine involution. A deficiency state may also interfere with foetal growth and
development, and has been linked to an increased incidence of Sudden Infant Death Syndrome (SIDS).117
Furthermore, oral magnesium supplementation during pregnancy has been associated with significantly
fewer maternal hospitalisations, a reduction in preterm delivery, and less frequent referral of the
newborn to the neonatal intensive care unit.118

PRE-ECLAMPSIA (TOXAEMIA)/ ECLAMPSIA

Pre-eclampsia, or toxaemia, is a complication of pregnancy characterised by elevated blood pressure,
albuminuria and/or oedema that may develop between the 20th week of gestation and the end of the
first week postpartum. If the condition progresses to seizures or coma, it becomes known as eclampsia.
The aetiology for pre-eclampsia and eclampsia is unknown.
Magnesium sulfate is the agent of choice for reducing the rate of eclampsia and to prevent recurrent
convulsions.119,120,121

14

A literature search from 1966 to 2003 shows that magnesium sulfate has long been used in the
prophylaxis of eclampsia. Numerous randomised controlled trials and systemic reviews have
demonstrated its efficacy.122 Most studies to date have relied on intravenous administration.

 Oral supplementation of magnesium has been shown to prevent pregnancy induced

hypertension (PIH).123
A prospective randomised double-blind study was carried out in 102 pregnant women;
51 receiving 3g of magnesium gluconate daily from the 28th week of gestation to delivery, and
51 served as controls. Four per cent of the pregnant women developed PIH after magnesium
gluconate treatment, which was substantially lower than the 16 per cent in the control group.

SUDDEN INFANT DEATH SYNDROME (SIDS)

It has been suggested that SIDS might be due to the foetal consequences of a maternal magnesium
deficiency, which may be prevented by increased magnesium intake by the mother.124
A recently published study shows that there is a significant trend towards reduced risk of SIDS
with increasing levels of magnesium in drinking water.125
Different mechanisms for SIDS have been proposed:
It is thought that SIDS may be a foetal consequence of maternal magnesium deficiency through
impaired control of brown adipose tissue thermoregulation mechanisms leading to a modified
temperature set point. SIDS can result from dysthermia, both hypo- or hyperthermic types.117
Infants sleeping on their stomach (prone position) can be jeopardised if they lack the muscle
strength to shift their position or turn their heads to rescue themselves from potential suffocation.
Two major studies from the 1970s showed muscle weakness in the upper half of the body in
infants who died of SIDS and shoulder hypotonia in near-miss for SIDS infants.126
Muscle strength is seriously impaired in the young magnesium deficient subject, while
magnesium rapidly reverses muscle weakness.126
A review, published in 1991, of 19 retrospective case-control studies that investigated the relationship
between prone sleeping position and SIDS led to a change of recommended sleeping position for
infants away from the prone position. However, despite a decreased incidence of SIDS, it still remains
the leading cause of death in infants aged 1 month to 1 year of age in industrialised countries.126

Studies indicate
that gestational
magnesium
deficiency results
in suboptimal foetal
growth and
development and
may be linked to an
increased incidence
of SIDS.127

PREMENSTRUAL SYNDROME (PMS)

Several studies point to the effectiveness of oral magnesium supplementation in the clinical
management of PMS.
38 women with PMS symptoms were given 200 mg magnesium daily or placebo for two
menstrual cycles. While no effect was noted in the first month of treatment, in the second
month there was a greater reduction in the symptoms of PMS-H (weight gain, swelling of
the extremities, breast tenderness, and abdominal bloating) with magnesium
supplementation compared to placebo.128

Chronic stress leads

to a tissue depletion
of magnesium,
consequently
increasing the bodys
need for the mineral.

In a randomised double-blind trial, 32 women were supplemented with 360 mg magnesium

three times daily (during the second half of the menstrual cycle) or placebo for two cycles. In
the next two cycles both groups received magnesium.129
The results of this study indicate that magnesium supplementation could represent an
effective treatment for PMS-related mood changes.
In 20 patients with premenstrual migraine, supplementation with magnesium (360 mg/day) or
placebo during the second half of the menstrual cycle reduced the number of days with
headache.130

STRESS
Stress hormones, including both catecholamines (adrenalin and noradrenalin) and corticosteroids (e.g.
cortisol), can promote a reduction in tissue magnesium levels.67 Stress induces a shift of magnesium
from the intracellular to the extracellular space, increasing urinary excretion and eventually depleting
body stores.131 Consequently stress increases the bodys need for magnesium.
When magnesium deficiency exists, chronic stress can promote a further decline in health. Based on
human and animal research, it has been shown that a variety of nutrients in addition to
magnesium, such as vitamin C, a number of B vitamins, and tyrosine, may allow individuals
to minimise the systemic effects of stress.132

15

CONTRAINDICATIONS, PRECAUTIONS
AND ADVERSE REACTIONS
Magnesium is contraindicated in patients with renal failure.3 It is also contraindicated in those with
high-grade atrioventricular (AV) block.3
Individuals with myasthenia gravis should also avoid the use of magnesium supplements.133,134
The most common adverse reactions from high-dose supplemental magnesium is diarrhoea;3 this problem
can be overcome by taking a magnesium diglycinate chelate (please see pharmacokinetics section).

DRUG INTERACTIONS
Magnesium may decrease the absorption of the following drugs; take at least two hours apart:3,135

Bisphonates
Quinolone antibiotics
Tetracycline antibiotics
Warfarin

Magnesium may also interfere with the efficacy of the following:11,135

Chlorpromazine
Digoxin*
Nitrofurantoin
Penicillinamide
Oral anticoagulants

*However, magnesium has also been noted to reduce cardiac arrhythmias due to digoxin poisoning as
well as significantly decrease the frequency and complexity of ventricular arrhythmias in digoxin-treated
patients with congestive heart failure without digoxin toxicity.136
Caution may also be prudent in patients taking calcium channel blockers (potentiation of effect),
potassium-sparing diuretics (may also have magnesium-sparing effects), and skeletal muscle relaxants
(potentiating effect).
A large number of medications may lead to magnesium depletion, including cisplatin,
corticosteroids, digoxin, erythromycin, gentamycin, loop diuretics, neomycin, oral
contraceptives, theophylline, thiazide diuretics.135

SUMMARY
Magnesium plays a role in more than 300 enzyme systems and is critically involved in energy
production, synthesis of essential molecules, and regulation of ion transport across cell membranes.
Mild to moderate deficiency states are becoming more common due to modern food processing and
consequently a reduced dietary intake.
Conditions that may be associated with magnesium deficiency include cardiovascular disease, behavioural problems, fatigue, fibromyalgia, migraine headaches, muscular complaints, osteoporosis, pregnancy complications, premenstrual syndrome, and reduced tolerance to stress.
Clinicians should consider using magnesium supplementation to prevent deficiency in patients at risk
and to treat deficiency when it occurs.

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