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Magnesium and the inflammatory
response: Potential physiopathological implications.
Mazur A, et al.
Arch Biochem Biophys. 2006 Apr 19.
The purpose of this review is to summarize experimental
findings showing that magnesium modulates cellular events
involved in inflammation. Experimental magnesium deficiency
in the rat induces a clinical inflammatory syndrome
characterized by leukocyte and macrophage activation,
release of inflammatory cytokines and acute phase proteins,
excessive production of free radicals. Increase in
extracellular magnesium concentration, decreases
inflammatory response, while reduction in the extracellular
magnesium results in cell activation. Because magnesium acts
as a natural calcium antagonist, the molecular basis for
inflammatory response is probably the result of modulation
of intracellular calcium concentration. Magnesium deficiency
induces a systemic stress response by activation of neutron
endocrinological pathways. As nervous and immune systems
interact directionally, the roles of neuromediators have
also been considered. Magnesium deficiency contributes to an
exaggerated response to immune stress and oxidative stress
as the consequence of the inflammatory response.
Inflammation contributes to the proatherogenic changes in
lipoprotein metabolism, endothelial dysfunction, thrombosis,
hypertension, and explains the aggravating effect of
magnesium deficiency on the development of metabolic
syndrome. Further studies are still needed to assess more
accurately the role of magnesium in immune response in
humans, but these experimental findings in animal models
suggest that inflammation is the missing link to explain the
role of magnesium in many pathological conditions.

Oral magnesium administration prevents
thermal hyperalgesia induced by diabetes in
rats.
Hasanein P, et al.
Diabetes Res Clin Pract. 2006 Jul;73(1):17-22.
Peripheral
neuropathy is a common complication of diabetes mellitus. It
has been shown that hyperglycemia may contribute to its
development but the exact pathophysiology underlying this
complication is not fully understood. Since oral magnesium
supplementation can normalize hyperglycemia induced by
diabetes in rats, this study was designed to examine the
effect of oral magnesium administration on thermal
hyperalgesia (pain hypersensitivity) in streptozocin-induced
diabetic rats. Twenty-four male adult wistar rats were
divided equally into control, magnesium-treated control,
diabetic and magnesium-treated diabetic groups. In
magnesium-treated diabetic rats, magnesium sulfate was added
into the drinking water once diabetes was established and
continued for 8 weeks. Magnesium-treated control animals
received magnesium sulfate in the same dose and over the
same time period. The other two groups; control and diabetic
animals, only received tap water. At the end of the 8 weeks,
thermal pain threshold was assessed by tail flick test and
magnesium and glucose plasma levels were measured in all
groups. A significant decrease in thermal pain threshold and
plasma magnesium levels and an increase in plasma glucose
levels were seen in diabetic rats 8 weeks after diabetes
induction. After 8 weeks of oral magnesium, thermal
hyperalgesia was normalized and plasma magnesium and glucose
levels were restored towards normal. It is concluded that
oral magnesium administration given at the time of diabetes
induction may be able to restore thermal hyperalgesia,
magnesium deficiency and hyperglycemia and in diabetic rats.

Bioavailability of zinc glycinate in
comparison with zinc sulphate in the presence of
dietary phytate in an animal model with Zinc labeled rats.
Schlegel P, and Windisch W.
J Anim Physiol Anim Nutr (Berl). 2006 Jun;90(5-6):216-22.
The objective of this study
was to quantify the bioavailability of zinc (Zn) from
sulphate and glycinate as representatives of inorganic
and organic zinc sources. The semi-synthetic basal diet
contained 2 mug/g of native Zn and was fortified with
pure sodium-phytate (8g/kg) in order to simulate
conditions of common cereal-based meals. The basal diet
was supplemented with either 53 mug/g of Zn from
sulphate (control) or 10 mug/g of Zn from either
sulphate (ZnSulphate) or glycinate (ZnGly). Twenty-four
(65) Zn-labelled, growing rats weighing 133 g were
allotted to the three diets (eight animals pretreatment)
and were kept pair-fed to ZnSulphate for 15 days. Zn
contents in blood plasma, femur and whole body, as well
as, plasma alkaline phosphatase activites were reduced
compared with control indicating zinc deficiency in
ZnSulphate and ZnGly treatment. This allowed their
differentiation in zinc bioavailability. True absorption
of dietary Zn was significantly higher in ZnGly than in
ZnSulphate (51% vs. 44%) while losses of endogenous
faecal Zn and urinary Zn were not affected to a
quantitatively relevant extent. This resulted in a +30%
significantly improved Zn retention for ZnGly (33% vs.
25%) and a lower severity on Zn deficiency symptoms
compared with ZnSulphate. Metabolic utilization
accounted for 95% of absorbed dietary Zn for both Zn
sources. Overall, the bioavailability of zinc glycinate
was significantly superior by 16% to zinc sulphate (49%
vs. 42%), mainly because of a higher absorptive
potential at presence of a strong antinutritive
component (phytate) in the diet.

Zinc status in infantile wheezing.
Tahan F, and Karakukcu C..
Pediatr Pulmonol. 2006 Jul;41(7):630-4.
The increase in
prevalence of asthma is strongly dependent on environmental
factors, including diet. Significant decreases in the intake
of dietary zinc may be an important contributing factor to
the increasing incidence of wheezing and asthma, but there
have been no studies evaluating zinc levels in wheezy
infants. Our objective was to investigate the zinc status of
wheezy infants. Wheezy infants (n = 34) and healthy children
(n = 14) were included in the study. Total IgE and
eosinophil counts were obtained, and skin testing was done
with a battery of 25 antigens with appropriate positive and
negative controls. Levels of zinc were determined in hair.
No significant difference was observed in peripheral blood
eosinophil counts and total IgE levels among groups. Hair
zinc levels were significantly lower in wheezy infants (P <
0.001). In conclusion, hair zinc levels were lower in wheezy
infants than in healthy controls, suggesting that zinc
deficiency may influence the risk of wheezing in early
childhood.

Rapid
recovery from major depression using magnesium treatment.
Eby GA, Eby KL.
Med Hypotheses. 2006 Mar 14; [Epub ahead of print]
Major depression is a mood disorder characterized by a
sense of inadequacy, despondency, decreased activity,
pessimism, anhedonia and sadness where these symptoms
severely disrupt and adversely affect the person's life,
sometimes to such an extent that suicide is attempted or
results. Antidepressant drugs are not always effective and
some have been accused of causing an increased number of
suicides particularly in young people. Magnesium deficiency
is well known to produce neuropathologies. Only 16% of the
magnesium found in whole wheat remains in refined flour, and
magnesium has been removed from most drinking water
supplies, setting a stage for human magnesium deficiency.
Magnesium ions regulate calcium ion flow in neuronal calcium
channels, helping to regulate neuronal nitric oxide
production. In magnesium deficiency, neuronal requirements
for magnesium may not be met, causing neuronal damage which
could manifest as depression. Magnesium treatment is
hypothesized to be effective in treating major depression
resulting from intraneuronal magnesium deficits. These
magnesium ion neuronal deficits may be induced by stress
hormones, excessive dietary calcium as well as dietary
deficiencies of magnesium. Case histories are presented
showing rapid recovery (less than 7 days) from major
depression using 125-300mg of magnesium (as glycinate and
taurinate) with each meal and at bedtime. Magnesium was
found usually effective for treatment of depression in
general use. Related and accompanying mental illnesses in
these case histories including traumatic brain injury,
headache, suicidal ideation, anxiety, irritability,
insomnia, postpartum depression, cocaine, alcohol and
tobacco abuse, hypersensitivity to calcium, short-term
memory loss and IQ loss were also benefited.
Dietary deficiencies of magnesium, coupled with excess
calcium and stress may cause many cases of other related
symptoms including agitation, anxiety, irritability,
confusion, asthenia, sleeplessness, headache, delirium,
hallucinations and hyperexcitability, with each of these
having been previously documented. The possibility that
magnesium deficiency is the cause of most major depression
and related mental health problems including IQ loss and
addiction is enormously important to public health and is
recommended for immediate further study. Fortifying refined
grain and drinking water with biologically available
magnesium to pre-twentieth century levels is recommended.

Effects of
zinc supplementation on 1- to 5-year old children.
Zilva AP, Vitolo MR, Zara LF,
Castro CF.
Pediatr (Rio J), 2006 May 26;82(3).
To assess the
impact of zinc supplementation on nutritional and
biochemical parameters among children aged 12 to 59
months. A blinded randomized clinical trial was carried
out with 58 children aged 12 to 59 months included in
the National Child Nutritional Program, which provided
them with 2 kg of iron-fortified milk. The
supplementation group (n = 28) received 10 mg/day of
zinc sulfate for four months, and the control group (n =
30) received placebo. The following
parameters were used to assess the nutritional status:
weight-for-height and height-for-age expressed as z
scores, according to National Center for Health
Statistics standards, biochemical measurements of serum
iron and serum zinc, and hemoglobin and hematocrit
levels. Zinc supplementation did not have a remarkable
influence on anthropometric parameters. Baseline serum
zinc levels were low in both groups. After
supplementation, variations in mean hemoglobin,
hematocrit, serum zinc, and serum iron levels
significantly increased in the zinc supplementation
group. Zinc supplementation improved hemoglobin response
and normalized serum zinc concentration. The results
show the importance of establishing policies for
nutritional care that can tackle zinc deficiency as
well.

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