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Formal Medical Studies by Researchers,
Universities and Hospitals concerning Magnesium from Around the World
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The Benefits of sufficient
Magnesium, curative effects of Magnesium supplementing, and dangers of Magnesium
deficiency has been established by formal medical studies across the globe.
Studies and results listed below include from the
USA, France, German, Japan, Great
Britain, South Africa, Netherlands, Denmark, Hungary and Switzerland.(Start by scrolling
down the page to spot topics of interest to you...)
Magnesium and carbohydrate
metabolism
<THERAPIE (France), 1994, 49/1 (1-7)
<>The
interrelationships between magnesium and carbohydrate metabolism have
regained considerable interest over the last few years. Insulin secretion
requires magnesium: magnesium deficiency results in impaired insulin
secretion while magnesium replacement restores insulin secretion. Furthermore, experimental
magnesium deficiency reduces the tissues sensitivity to insulin. Sub
clinical magnesium deficiency is common in diabetes. It results from both
insufficient magnesium intakes and increase magnesium losses, particularly
in the urine. In type 2, or non-insulin-dependent, diabetes mellitus, magnesium
deficiency seems to be associated with insulin resistance. Furthermore, it
may participate in the pathogenesis of diabetes complications and may contribute
to the increased risk of sudden death associated with diabetes. Some studies suggest
that magnesium deficiency may play a role in spontaneous abortion of diabetic
women, in fetal malformations and in the pathogenesis of neonatal hypocalcemia
of the infants of diabetic mothers. Administration of
magnesium salts to patients with type 2 diabetes tend to reduce insulin resistance.
Long-term studies are needed before recommending systematic magnesium supplementation
to type 2 diabetic patients with subclinical magnesium deficiency.
Disorders of magnesium metabolism
Endocrinology and Metabolism Clinics of North America (USA), 1995, 24/3
<>Magnesium depletion is more common than previously thought. It seems
to be especially prevalent in patients with diabetes mellitus. It is usually
caused by losses from the kidney or gastrointestinal tract. A patient with magnesium
depletion may present with neuromuscular symptoms, hypokalemia, hypocalcemia,
or cardiovascular complication. Physicians should maintain a high index of
suspicion for magnesium depletion in patients at high risk and should implement
therapy early.
Magnesium deficiency produces insulin
resistance and increased thromboxane synthesis
HYPERTENSION (USA), 1993, 21/6 II (1024-1029)
<>Evidence
suggests that magnesium deficiency may play an important role in cardiovascular
disease. In this study, we evaluated the effects of a magnesium infusion
and dietary-induced isolated magnesium deficiency on the production of thromboxane
and on angiotensin II-mediated aldosterone synthesis in normal human subjects.
Because insulin resistance may be associated with altered blood pressure,
we also measured insulin sensitivity using an intravenous glucose tolerance
test with minimal model analysis in six subjects. The magnesium infusion
reduced urinary thromboxane concentration and angiotensin II-induced plasma
aldosterone levels. The low magnesium diet reduced both serum magnesium and
intracellular free magnesium in red blood cells as determined by nuclear
magnetic resonance (186plus or minus10 (SEM) to 127plus or minus9 mM, p<0.01).
Urinary thromboxane concentration measured by radioimmunoassay increased
after magnesium deficiency. Similarly, angiotensin II-induced plasma aldosterone
concentration increased after magnesium deficiency. Analysis showed that
all subjects studied had a decrease in insulin sensitivity after magnesium
deficiency (3.69plus or minus0.6 to 2.75plus or minus0.5 min- 1 per microunit
per milliliterx10-4, p<0.03). We conclude that dietary- induced magnesium
deficiency 1) increases thromboxane urinary concentration and 2) enhances
angiotensin-induced aldosterone synthesis. These effects are associated with
a decrease in insulin action, suggesting that magnesium deficiency may be
a common factor associated with insulin resistance and vascular disease.
Magnesium and glucose homeostasis
DIABETOLOGIA (Germany, Federal Republic of), 1990, 33/9 (511-514)
<>Magnesium
is an important ion in all living cells being a cofactor of many enzymes,
especially those utilising high energy phosphate bounds. The relationship
between insulin and magnesium has been recently studied. In particular it
has been shown that magnesium plays the role of a second messenger for insulin
action; on the other hand, insulin itself has been demonstrated to be an
important regulatory factor of intracellular magnesium accumulation. Conditions
associated with insulin resistance, such as hypertension or aging, are also
associated with low intracellular magnesium contents. In diabetes mellitus,
it is suggested that low intracellular magnesium levels result from both increased
urinary losses and insulin resistance. The extent to which such a low intracellular
magnesium content contributes to the development of macro- and microangiopathy
remains to be established. A reduced intracellular magnesium content migth
contribute to the impaired insulin response and action which occurs in Type
2 (non-insulin-dependent) diabetes mellitus. Chronic magnesium supplementation
can contribute to an improvement in both islet Beta-cell response and insulin
action in non-insulin-dependent diabetes subjects.
Magnesium content of erythrocytes
in patients with vasospastic angina
CARDIOVASC. DRUGS THER. (USA), 1991, 5/4 (677-680)
<>The
possibility that a magnesium deficiency might be the underlying cause of
vasospastic angina (VA) and the efficacy of Mg administration in its treatment
were studied. Subjects included 15 patients with VA and 18 healthy
subjects as the control group. The erythrocyte Mg content was measured by
atomic absorption, and serum Mg was measured by conventional chemical assay.
The efficacy of Mg administration was studied in seven patients with VA.
The results were as follows: (a) The mean erythrocyte Mg content was less
in the group with frequent episodes of angina (1.59 plus or minus 0.11 mg/dl)
than in the group without angina (2.11 plus or minus 0.38 mg/dl, p < 0.01)
and in the control group (2.22 plus or minus 0.29 mg/dl, p < 0.01). There
was no significant difference between the control group and patients of each
group with respect to serum Mg. (b) Coronary arterial spasm was induced by
ergonovine maleate in seven patients and was completely inhibited by the
administration of Mg sulfate (40-80 mEq, hourly) in six of these patients;
in the remaining patient neither obvious ST change nor chest pain occurred.
Thus, it was concluded that the measurement of erythrocyte Mg content is
useful to determine how easily vasospasm might occur in VA and that the administration
of Mg might be developed as a new therapy for spasm associated with a low
erythrocyte Mg content.
Variant angina due to deficiency
of intracellular magnesium
CLIN. CARDIOL. (USA), 1990, 13/9 (663-665)
<>A 51-year-old
man was diagnosed as having variant angina by documentation of typical ST
elevation during anginal attack and also by showing coronary arterial spasm
(#2 and #12) during hyperventilation on coronary arteriography. Large
quantities of calcium blocking agents and nitrates could not improve his
symptoms. Lack of intracellular magnesium was suspected from a daily excretion
of urine magnesium (5.3 mEq) and magnesium tolerance test (56.7%). After
hourly infusion of magnesium sulfate (80 mEq), coronary spasm could not be
induced by ergonovine.
Magnesium and sudden death
S. AFR. MED. J. (SOUTH AFRICA), 1983, 64/18 (697-698)
<>Magnesium deficiency may result from reduced dietary intake of the
ion increased losses in sweat, urine or faeces. Stress potentiates
magnesium deficiency, and an increased incidence of sudden death associated
with ischaemic heart disease is found in some areas in which soil and drinking
water lack magnesium. Furthermore, it has been demonstrated experimentally
that reduction of the plasma magnesium level is associated with arterial
spasm. Careful studies are required to assess the clinical importance
of magnesium and the benefits of magnesium supplementation in man.
Magnesium deficiency
produces spasms of coronary arteries: Relationship to etiology of
sudden death ischemic heart disease
SCIENCE (USA), 1980, 208/4440 (198-200)
<>Isolated coronary arteries from dogs were incubated in Krebs-Ringer
bicarbonate solution and exposed to normal, high, and low concentrations
of magnesium in the medium. Sudden withdrawal of magnesium from the medium
increased whereas high concentrations of magnesium decreased the basal tension
of the arteries. The absence of magnesium
in the medium significantly potentiated the contractile responses of both
small and large coronary arteries to norepinephrine, acetylcholine, serotonin,
angiotensin, and potassium. These data support the hypothesis that magnesium
deficiency, associated with sudden death ischemic heart disease, produces
coronary arterial spasm.
Magnesium and potassium in diabetes
and carbohydrate metabolism. Review of the present status and recent results.
Magnesium. 1984. 3(4-6). P 315-23
<>Diabetes
mellitus is the most common pathological state in which secondary magnesium
deficiency occurs. Magnesium metabolism abnormalities vary according
to the multiple clinical forms of diabetes: plasma magnesium is more often
decreased than red blood cell magnesium. Plasma Mg levels are correlated
mainly with the severity of the diabetic state, glucose disposal and endogenous
insulin secretion. Various mechanisms
are involved in the induction of Mg depletion in diabetes mellitus, i.e.
insulin and epinephrine secretion, modifications of the vitamin D metabolism,
decrease of blood P, vitamin B6 and taurine levels, increase of vitamin B5,
C and glutathione turnover, treatment with high levels of insulin and biguanides.
K depletion in diabetes mellitus is well known. Some of its mechanisms are
concomitant to those of Mg depletion. But their hierarchic importance is
not the same: i.e., insulin hyposecretion is more important versus K+ than
versus Mg2+. Insulin increases the cellular inflow of K+ more than that of
Mg2+ because there is more free K+ (87%) than Mg2+ (30%) in the cell. The
consequences of the double Mg-K depletion are either antagonistic: i.e. versus
insulin secretion (increased by K+, decreased by Mg2+) or agonistic i.e.
on the membrane: (i.e. Na+K+ATPase), tolerance of glucose oral load, renal
disturbances. The real importance of these disorders in the diabetic condition
is still poorly understood. Retinopathy and microangiopathy are correlated
with the drop of plasma and red blood cell Mg. K deficiency increases the
noxious cardiorenal effects of Mg deficiency. The treatment should primarily
insure diabetic control.
Hypocalcemia associated with estrogen
therapy for metastatic adenocarcinoma of the prostate
J. UROL. (USA), 1988, 140/5 PART I (1025-1027)
<>We report 2 cases of true hypocalcemia (not caused by decreased binding
protein) associated with metastatic prostate cancer and review previously
reported cases. Hypocalcemia is a common but frequently unrecognized complication
of prostatic cancer. Estrogen therapy often is associated with the hypocalcemia,
which may be asymptomatic. The hypocalcemia is always associated with osteoblastic
metastases and usually it is associated with increased serum alkaline phosphatase
activity, acid phosphatase activity and serum parathyroid hormone concentration.
Serum concentrations of magnesium, phosphorus and vitamin D frequently
are decreased. Patients are in a positive calcium balance. The osteoblastic
metastases seem to act as a calcium sink, creating a 'hungry tumor phenomenon'.
The role of estrogens may be to stop the resorption of normal bone resulting
in lower serum calcium concentrations.
[Overview--suppression effect of
essential trace elements on arteriosclerotic development and it's mechanism]
Saito N
Nippon Rinsho (JAPAN) Jan 1996, 54 (1) p59-66
<>It is known that the peroxidation of LDL is a trigger for developing
arteriosclerosis. The oxidized LDL is produced by either oxidative stress
or a few oxidant. Selenium decreased in serum and some organs of stroke-prone
spontaneously hypertensive rats (SHRSP), which is a cofactor of glutamine
peroxidase. Serum
magnesium decreased in patients with diabetes mellitus, with ischemic heart
disease, with essential hypertension and with cerebral vascular lesions.
Calcium to magnesium ratio was higher in some organs of SHRSP as compared
to Wistar Kyoto rats (WKY). These changes accelerated vascular lesions in
SHRSP. (21 Refs.)
Magnesium hormonal regulation and
metabolic interrelations
PRESSE MED. (France), 1988, 17/12 (584-587)
<>Magnesium ion is of great importance in physiology
by its intervention in 300 enzymatic systems, its role in membrane structure and its function in neuromuscular
excitability. The skeleton is the first pool of magnesium in the body.
Intestinal absorption, renal metabolism, bone accretion and resorption of
magnesium are very similar to those of calcium. Magnesium metabolism
is accurately controlled, in particular by parathyroid hormone, 25 - dihydroxy
vitamin D3, calcitonin, catecholamine and estrogens. The main regulation
mechanisms of magnesium metabolism are located in the kidney which is the
principal excretory organ.
Magnesium deficiency: Possible
role in osteoporosis associated with gluten-sensitive enteropathy
Osteoporosis International (United Kingdom), 1996, 6/6 (453-461)
<>Osteoporosis
and magnesium (Mg) deficiency often occur in malabsorption syndromes such
as gluten-sensitive enteropathy (GSE). Mg deficiency is known to impair parathyroid
hormone (PTH) secretion and action in humans and will result in osteopenia
and increased skeletal fragility in animal models. We hypothesize that Mg
depletion may contribute to the osteoporosis associated with malabsorption.
It was our objective to determine Mg status and bone mass in GSE patients
who were clinically asymptomatic and on a stable gluten-free diet, as well
as their response to Mg therapy. Twenty-three patients with biopsy-proven
GSE on a gluten-free diet were assessed for Mg deficiency by determination
of the serum Mg, red blood cell (RBC) and lymphocyte free Mg2+, and total
lymphocyte Mg. Fourteen subjects completed a 3-month treatment period in
which they were given 504-576 mg MgCl2 or Mg lactate daily. Serum PTH, 25-hydroxyvitamin
D, 1,25-dihydroxyvitamin D and osteocalcin were measured at baseline and
monthly thereafter. Eight patients who had documented Mg depletion (RBC Mg2+
< 150 microM) underwent bone density measurements of the lumbar spine
and proximal femur, and 5 of these patients were followed for 2 years on
Mg therapy. The mean serum Mg, calcium, phosphorus and alkaline phosphatase
concentrations were in the normal range. Most serum calcium values fell below
mean normal and the baseline serum PTH was high normal or slightly elevated
in 7 of the 14 subjects who completed the 3-month treatment period. No correlation
with the serum calcium was noted, however. Mean serum 25-hydroxyvitamin D,
1,25-dihydroxy vitamin D and osteocalcin concentrations were also normal.
Despite only 1 patient having hypomagnesemia, the RBC Mg2+ (153 + or - 6.2
microM; mean plus or minus SEM) and lymphocyte Mg2+ (182 plus or minus 5.5
microM) were significantly lower than normal (202 + or - 6.0 microM, P <
0.001, and 198 + or - 6.8 microM, p < 0.05, respectively). Bone densitometry
revealed that 4 of 8 patients had osteoporosis of the lumbar spine and 5
of 8 had osteoporosis of the proximal femur (T-scores less than or equal
to -2.5). Mg therapy resulted in a significant rise in the mean serum PTH
concentration from 44.6 + or - 3.6 pg/ml to 55.9 plus or minus 5.6 pg/ml
(p < 0.05). In the 5 patients given Mg supplements for 2 years, a significant
increased in bone mineral density was observed in the femoral neck and total
proximal femur. This increase in bone mineral density correlated positively
with a rise in RBC Mg2+. This study demonstrates that GSE patients have reduction
in intracellular free Mg2+, despite being clinically asymptomatic on a gluten-free
diet. Bone mass also appears to be reduced. Mg therapy resulted in a rise
in PTH, suggesting that the intracellular Mg deficit was impairing PTH secretion
in these patients. The increase in bone density in response to Mg therapy
suggests that Mg depletion may be one factor contributing to osteoporosis
in GSE.
Energy and nutrient intake in patients
with CF
Monatsschrift fur Kinderheilkunde (Germany), 1996, 144/4 (396-402)
<>Background: Nutritional assessment and management remain important
issues in the treatment of CF patients despite newer developments as lung
transplantation, inhalation with DNase and gene therapy. Methods: The nutritional
status of 26 patients (mean age 15,8 years; 16 male; 46% homozygous, 38%
heterozygous for DeltaF 508, remaining unknown; 3 pancreas sufficient, Shwachman
score intermediate to excellent) of our CF clinic was analyzed using a three
days protocol, the precise weighing method and comparison of data with the
official dietary recommendations. Results: The average energy intake was
below the 130% officially recommended and the fat intake was below the aimed
40% of total energy intake. The regression analysis revealed positive correlations
between energy intake and SDS(Height) and Shwachman score and SDS(Weight)
respectively. Food contained an insufficient amount of unsaturated fatty
acids. Water soluble vitamins were supplemented adequately besides folic
acid, but intake of fat soluble vitamins E and A often was insufficient despite
extra vitamin capsules. Every second patient did not take enough minerals
as calcium, magnesium or iron. Conclusions: This analysis underlines how
important the regular assessment of the nutritional status can be for the
individual nutritional management of CF patients even if clinical symptoms
of deficiencies could not be detected. An increase of fat intake as a main
source of energy, essential fatty acids and fat soluble vitamins has to be
encouraged as well as the increased use of milk and milk products for the
prevention of osteoporosis. Iron and folic acid are further critical nutrients.
Kidney stone clinic: Ten years
of experience
Nederlands Tijschrift voor de Klinische Chemie (Netherlands), 1996, 21/1
(8-10)
<>Experiences are described at a kidney stone clinic which was established
as part of the Department of Clinical Biochemistry ten years ago. During
this period, the investigational protocol has changed from an in-patient
to an out-patient scheme. The most important metabolic abnormalities among
calcium oxalate kidney stone formers were hypercalciuria, hypernatriuria,
hyperuricosuria, increased blood urate, decreased blood phosphate and hyperphosphaturia
with decreased renal phosphate threshold. These abnormalities were found
in the majority of patients. Oxalate output was, however, increased in less
than 50 percent of the patients. The effectivity of thiazides, allopurinol,
magnesium and phosphate supplementation was tested, and it was concluded
that (a) the effect of thiazides was significant, but calciuria normalized
only in a few cases, (b) the withdrawal of allopurinol led to a significant
increase of urate parameters only in patients without a low-purine diet,
(c) a sufficient dose of magnesium and phosphate is necessary to achieve
a therapeutie effect. Preliminary data indicate that some patients with hypercalciuria
and kidney stones are at risk of decreased bone mass, and the role of bone
markers monitoring is mentioned.
Plasma copper, zinc and magnesium
levels in patients with premenstrual tension syndrome
ACTA OBSTET. GYNECOL. SCAND. (Denmark), 1994, 73/6 (452-455)
<>We measured plasma Cu, Zn and Mg levels in 40 women suffering from
premenstrual tension syndrome (PMTS) and in 20 control subjects by atomic
absorption spectrophotometer. Mean plasma Cu, Zn and Mg levels, the Zn/Cu
ratio were 80.2 plus or minus 6.00 microg/dl, 112.6 plus or minus 8.35 microg/dl,
0.70 plus or minus 0.18 mmol/l, and 1.40 plus or minus 0.10 in the PMTS group;
and 77.0 plus or minus 4.50 microg/dl, 117.4 plus or minus 9.50 microg/dl,
0.87 plus or minus 0.10 mmol/l, and 1.51 plus or minus 0.05 in the control
group respectively. The mean Mg level and the Zn/Cu ratio were significantly
lower in PMTS patients than in the control group. Plasma Mg and Zn levels
were diminished significantly during the luteal phase compared to the follicular
phase in PMTS group. Mg deficiency may
play a role in the etiology of PMTS.
Oral magnesium successfully relieves premenstrual mood changes
OBSTET. GYNECOL. (USA), 1991, 78/2 (177-181)
<>Reduced magnesium (Mg) levels have been reported in women affected
by premenstrual syndrome (PMS). To evaluate the effects of an oral Mg preparation
on premenstrual symptoms, we studied, by a double-blind, randomized design,
32 women (24-39 years old) with PMS confirmed by the Moos Menstrual Distress
Questionnaire. After 2 months of baseline recording, the subjects were randomly
assigned to placebo or Mg for two cycles. In the next two cycles, both groups
received Mg. Magnesium pyrrolidone carboxylic acid (360 mg Mg) or placebo
was administered three times a day, from the 15th day of the menstrual cycle
to the onset of menstrual flow. Blood samples for Mg measurement were drawn
premenstrually, during the baseline period, andin the second and fourth months
of treatment. The Menstrual Distress Questionnaire score of the cluster 'pain'
was significantly reduced during the second month in both groups, whereas
Mg treatment significantly affected both the total Menstrual Distress Questionnaire
score and the cluster 'negative affect'. In the second month, the women assigned
to treatment showed a significant increase in Mg in lymphocytes and polymorphonuclear
cells, whereas no changes were observed in plasma and erythrocytes. These
data indicate that Mg supplementation could represent an effective treatment
of premenstrual symptoms related to mood changes.
Magnesium and the premenstrual syndrome
ANN. CLIN. BIOCHEM. (UK), 1986, 23/6 (667-670)
<>Plasma and erythrocyte magnesium were measured in 105 patients with
premenstrual syndrome (PMS) using a simple atomic absorption spectroscopy
method. The erythrocyte magnesium concentration for the patients with PMS
was significantly lower than that of a normal population. The plasma magnesium
did not show this difference. The significant of this apparent cellular deficiency
of magnesium is discussed.
Magnesium concentration in brains from multiple sclerosis patients
ACTA NEUROL. SCAND. (Denmark), 1990, 81/3 (197-200)
<>Magnesium (Mg) concentrations were studied in the brains of 4 patients
with definite multiple sclerosis (MS) and 5 controls. The magnesium contents
were determined by inductively coupled plasma emission spectrometry in autopsy
samples taken from 26 sites of central nervous system tissues, and visceral
organs such as liver, spleen, kidney, heart and lung. The average Mg content
in the CNS tissues, as well as visceral organs except for spleen, of MS patients
showed a significantly lower value than that seen in control cases. The most
marked reduction of Mg content was observed in CNS white matter including
demyelinated plaques of MS samples. Whether or not these significantly lower
Mg contents found in CNS and visceral organs of MS patients may play an essential
role in the demyelinating process remain unclear, requiring further studies
on MS pathogenesis from the point of metal metabolism.
Zinc, copper and magnesium concentration
in serum and CSF of patients with neurological disorders
ACTA NEUROL. SCAND. (Denmark), 1989, 79/5 (373-378)
<>Zinc (Zn), copper (Cu) and magnesium (Mg) concentrations in cerebrospinal
fluid (CSF) and serum were determined with atomic absorption spectrophotometry
in 74 patients suffering from various neurological diseases, and in 28 healthy
controls. Increased CSF zinc levels were found in the group of peripheral
nervous system diseases (P < 0.01) and in the cases of different neurological
syndromes with increased CSF protein concentration (P < 0.001). Increased
CSF and serum copper levels were found in the cases with increased CSF protein
levels (P < 0.05). It is probable that damaged blood-brain-barrier (BBB)
permits the passage of the trace elements Zn, Cu and of Mg into the subarachnoid
space. Decreased serum Cu levels (P < 0.01) were found in the group of
multiple sclerosis (MS). The findings are correlated to those of previous
communications.
The susceptibility of the centrocecal
scotoma to electrolytes, especially in multiple sclerosis
IDEGGYOG.SZLE (HUNGARY), 1973, 26/7 (307-312)
<>A study of the action of magnesium on the centrocecal scotoma in
multiple sclerosis revealed that the scotomas were transiently reduced by
magnesium infusions or that calcium ionization was modified by alkalinization
or Na EDTA.
Experimental and clinical studies
on dysregulation of magnesium metabolism and the aetiopathogenesis of multiple
sclerosis.
Magnes Res (ENGLAND) Dec 1992, 5 (4) p295-302
<>The proposed aetiologies of multiple sclerosis (MS) have included
immunological mechanisms, genetic factors, virus infection and direct or
indirect action of minerals and/or metals. The processes of these aetiologies
have implicated magnesium. Magnesium and zinc have been shown to be decreased
in central nervous system (CNS) tissues of MS patients, especially tissues
such as white matter where pathological changes have been observed. The calcium
content of white matter has also been found to be decreased in MS patients. The interactions
of minerals and/or metals such as calcium, magnesium, aluminium and zinc
have also been evaluated in CNS tissues of experimental animal models. These
data suggest that these elements are regulated by pooling of minerals and/or
metals in bones. Biological actions of magnesium may affect the maintenance
and function of nerve cells as well as the proliferation and synthesis of
lymphocytes. A magnesium deficit may induce dysfunction of nerve cells or
lymphocytes directly and/or indirectly, and thus magnesium depletion may
be implicated in the aetiology of MS. The action of zinc helps to prevent
virus infection, and zinc deficiency in CNS tissues of MS patients may also
be relevant to its aetiology. Magnesium interacts with other minerals and/or
metals such as calcium, zinc and aluminium in biological systems, affecting
the immune system and influencing the content of these elements in CNS tissues.
Because of these interactions, a magnesium deficit could also be a risk factor
in the aetiology of MS. (51 Refs.)
Magnesium concentration in plasma
and erythrocytes in MS
Acta Neurologica Scandinavica (Denmark), 1995, 92/1 (109-111)
<>There are few reports of Mg in MS and none dealing with Mg content
in erythrocytes. Mg concentration was determined in serum and in erythrocytes
with the help of a BIOTROL Magnesium Calmagite colorimetric method (average
sensitivity: 0.194 A per mmol/I) and a Hitachi autoanalyzer in 24 MS patients
(7 men and 17 women, age 29-60; 37 years on average with the duration of
the disease: 3-19; 11 years on average, at clinical disability stages according
to the Kurtzke scale: 1-7; 3.2 on average, in remission stage. A statistically
significant decrease (p < 0.001) of Mg concentration in erythrocytes and
no changes in plasma of MS patients were found. The results obtained suggest
the presence of changes in membrane of erythrocytes which could be connected
with their shorter life and with affection of their function.
Comparative findings on serum IMg2+
of normal and diseased human subjects with the NOVA and KONE ISE's for Mg2+
SCAND. J. CLIN. LAB. INVEST. SUPPL. (United Kingdom), 1994, 54/217
<>It is clear now that although different ionophores for ionized Mg
(Img2+) have been designed by several groups, each of these has a distinctly
different K(MgCa). In view of this, it is important to determine whether
each of these ion selective electrodes (ISE's) yield identical results for
IMg2+ in sera from healthy and diseased humans. Using such an approach, we
determined, in a blinded-and random manner, IMg2+ with both the NOVA and
KONE ISE's for IMg2+ in two independent laboratories. No significant differences
were found either for sera from healthy human volunteers or diseased patients.
We did, however, note several interesting findings: 1. randomly, selected
hospitalized patients exhibit a much higher incidence of abnormalities for
IMg2+ (57-71%) than that noted previously for total Mg (TMg) measurements;
and 2. coronary heart disease, rectal cancer and multiple sclerosis patients
exhibit extracellular deficits in ionized free Mg.
Migraine--diagnosis,
differential diagnosis and therapy]
Ther Umsch (SWITZERLAND) Feb 1997, 54 (2) p64-70
<>Migraine is caused by intermittent brain dysfunction. Attacks result
in severe unilateral headache with nausea, vomiting, photophobia, phonophobia
and general weakness. The prevalence of migraine is 12 to 20% in women and
8 to 12% in man. Treatment of an acute attack is done by antiemetics in combination
with analgesics. Severe migraine attacks are treated with ergotamine or sumatriptan.
Parenteral treatment is performed most efficiently and safely with i.v. ASA.
Frequent and severe attacks require prophylaxis. Drugs of first choice are
metoprolol, propranolol, flunarizine and cyclandelate. Substances of second
choice are valproic acid, DHE, pizotifen, methysergide and magnesium. Homeopathic
remedies are not superior to placebo. Nonpharmacological treatment consists
of sport therapy and muscle relaxation techniques.
Prophylaxis of migraine with oral magnesium:
results from a prospective, multi-center, placebo-controlled and double-blind randomized study.
Cephalalgia (NORWAY) Jun 1996, 16 (4) p257-63
<>In order to evaluate the prophylactic effect of oral magnesium, 81
patients aged 18-65 years with migraine according to the International Headache
Society (IHS) criteria (mean attack frequency 3.6 per month) were examined.
After a prospective baseline period of 4 weeks they received oral 600 mg
(24 mmol) magnesium (trimagnesium dicitrate) daily for 12 weeks or placebo.
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 the baseline (p <
0.05). The number of days with migraine and the drug consumption for symptomatic
treatment per patient also decreased significantly in the magnesium group.
Duration and intensity of the attacks and the drug consumption per attack
also tended to decrease compared to placebo but failed to be significant.
Adverse events were diarrhea (18.6%) and gastric irritation (4.7%). High-dose
oral magnesium appears to be effective in migraine prophylaxis.
Electromyographical ischemic test and
intracellular and extracellular magnesium concentration in migraine and tension-type
headache patients.
Headache (UNITED STATES) Jun 1996, 36 (6) p357-61
<>Headache has often been described in the hyperexcitability syndrome
which recognizes an alteration of calcium and magnesium status in its etiopathogenesis.
Moreover,
in migraine patients magnesium has been shown to play an important role as
a regulator of neuronal excitability and, therefore hypothetically, of headache.
The present research involves a neurophysiological evaluation and magnesium
status assessment of a group of headache patients. Nineteen patients (15
women and 4 men) with episodic tension-type headache and 30 patients (27
women and 3 men) with migraine without aura were examined. An ischemic test
was carried out on the right arm with electromyographic (EMG) recording of
motor unit potential activity during the interictal period. The determination
of extracellular (serum and saliva) and intracellular (red and mononuclear
blood cells) magnesium was also performed. The EMG test was positive in 25
of 30 migraine patients and in 2 of 19 tension-type headache patients. Between
the two patient groups, there were no significant variations in the concentration
of extracellular and white blood cell magnesium, while the red blood cell
concentration of this mineral in the group of migraineurs was significantly
reduced with respect to that in the group of tension-type headache patients
(P < 0.05). The positive EMG test was significantly associated with a
low concentration of red blood cell magnesium (P < 0.0001). These results
confirm previous findings by demonstrating different etiopathogenic mechanisms
as the basis of migraine and tension-type headache. Migraine seems to be
related to an altered magnesium status, which manifests itself by a neuromuscular
hyperexcitability and a reduced concentration in red blood cells.
Magnesium supplementation and osteoporosis
Nutrition Reviews (USA), 1995, 53/3 (71-74)
<>Among other
things, magnesium regulates active calcium transport. As a result, there
has been a growing interest in the role of magnesium (Mg) in bone metabolism.
A group of menopausal women were given magnesium hydroxide to assess the
effects of magnesium on bone density. At the end of the 2-year study, magnesium
therapy appears to have prevented fractures and resulted in a significant
increase in bone density.
Calcium, phosphorus and magnesium
intakes correlate with bone mineral content in postmenopausal women
GYNECOL. ENDOCRINOL. (United Kingdom), 1994, 8/1 (55-58)
<>Qualitative and quantitative differences in the dietary habits of
postmenopausal women were studied to assess their influence on bone health
and osteoporosis. A total of 194 postmenopausal women were studied with forearm
DEXA densitometry. 70 were osteoporotic and 124 served as controls. Women
had been menopausal for 5-7 years and had never been treated with hormone
replacement or drug therapy. A 3-day dietary recall was completed on Sunday,
Monday and Tuesday after the examination: the results were processed by computer
and daily calcium, phosphorus and magnesium intakes were related to bone
mineral content (BMC). Data were compared with Student's t-test and significance
was assessed at p < 0.05. Regression analysis was performed to correlate
BMC and intake levels. The dietary intake of calcium phosphorus and magnesium
was significantly reduced in osteoporotic women and correlated with BMC.
Calcium and magnesium intakes were lower than the recommended daily allowance
even in normal women. The results suggest that nutritional factors are relevant
to bone health in postmenopausal women, and dietary supplementation may be
indicated for the prophylaxis of osteoporosis. Adequate nutritional recommendations
and supplements should be given before the menopause, and dietary evaluation
should be mandatory in treating postmenopausal osteoporosis.
Magnesium in the physiopathology
and treatment of renal calcium stones
PRESSE MED. (FRANCE), 1987, 16/1 (25-27)
<>The
inhibitory effect of magnesium on the first stages of renal calcium stone
formation is modest in vitro and more pronounced in experimental in vivo
studies. Magnesium deficiency has not yet been convincingly demonstrated
in man. However, urinary magnesium concentrations are abnormally low
in relation to urinary calcium concentrations in more than 25% of patients
with kidney stones. A supplementary magnesium intake corrects this abnormality
and prevents the recurrence of stones. Magnesium seems
to be as effective against stone formation as diuretics. The modalities
of magnesium therapy still have to be determined and its results confirmed.
Magnesium, possibly added to drinking water, may well play a role in the
primary prevention of renal calcium stones.
Urinary factors of kidney stone
formation in patients with Crohn's disease
KLIN. WOCHENSCHR. (Germany, Federal Republic of), 1988, 66/3 (87-91)
An increased frequency of kidney stone formation is reported in patients
with imflammatory bowel disease. In order to investigate its pathogenesis,
the concentrations of factors known to enhance calcium oxalate stone formation
(oxalate, calcium, uric acid) as well as of inhibitory factors for nephrolithiasis
(magnesium, citrate) were determined in the urine of 86 patients with Crohn's
disease and compared with those of 53 metabolically healthy controls. Six
patients with Crohn's disease already had experienced calcium oxalate nephrolithiasis.
Patients with Crohn's disease had significantly higher urinary oxalate and
lower magnesium and citrate concentrations. Among all patients
magnesium and citrate were significantly lower in those with a positive history
of kidney stones. Our results demonstrate that the increased propensity
for renal stone formation in patients with Crohn's disease is a result not
only of increased urinary oxalate, but also of decreased urinary magnesium
and citrate concentrations.
Renal stone formation in patients
with inflammatory bowel disease
SCANNING MICROSC. (USA), 1993, 7/1 (371-380)
Kidney stones are more common in patients with inflammatory bowel disease
(IBD) than in the general population. The main lithogenetic risk factors
were evaluated in patients affected by Crohn's disease and ulcerative colitis.
Our results show the presence of several factors, besides hyperoxaluria,
in patients with IBD although their behaviour appears different in Crohn's
disease and ulcerative colitis at pre- and post-operative stages. Before
surgery in patients with Crohn's disease we found a decreased citrate (p
< 0.001) and magnesium (p < 0.005) excretion together with a low urinary
volume (p < 0.001) and pH (p < 0.005). After surgery patients with
Crohn's disease showed a further reduction of magnesium and citrate. Patients
with ulcerative colitis before surgery showed a reduced citrate excretion
(p < 0.05) and a more acidic pH (p < 0.05) than healthy subjects. Surgical
treatment of proctocolectomy with ileal pouch-anal anastomosis seems to increase
the risk of stone formation; in fact, after surgery we observed a relevant
decrease of urinary volume (p < 0.001), pH (p < 0.0001) and urinary
excretion of citrate (p < 0.0001) as well as magnesium (p < 0.005).
Patients with IBD seem to be at greater risk of stone formation than patients
with idiopathic calcium lithiasis; in fact, they show a lower excretion of
citrate (p < 0.001) and magnesium (p < 0.001) together with a low urinary
pH (p < 0.001) and volume (p < 0.001). Urinary volume reduction is probably
one of the major risk factors together with the decrease of small molecular
weight inhibitors that is a constant finding in all patients with IBD.
The studies above
collectively present the great importance in a person having a sufficient
Magnesium intake. Magnesium is a necessary mineral to process calcium, in
physical and mental process, in 300 enzymatic systems, in membrane structure
and in the neuromuscular system and in proper kidney functions. They clearly
establish that Magnesium is a cornerstone mineral in virually every human
body function.
Some of the studies additionally point to key minerals of magnesium, zinc,
potassium, calcium and the importance of trace minerals.
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