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Magnesium supplementation and the
potential association with mortality rates among
critically ill non-cardiac patients
Dabbagh OC , et al.
Saudi Med J. 2006; 27(6):821-5
Recent literature showed that development of hypomagnesemia
is associated with higher mortality. The objective of this
study is to evaluate the impact of magnesium supplementation
on mortality rates of critically ill patients. All patients
admitted to the Intensive Care Unit (ICU) of King Abdul-Aziz
Medical City, Riyadh, Saudi Arabia since September 2003 were
included. We recorded the demographics data, APACHE score,
daily magnesium levels and magnesium supplementation. We
collected the data for 30 days or until discharge from ICU.
Statistical analysis was performed using the student t-test
for continuous data and the Fischers exact test for
categorical data. Nothing was carried out to influence the
behavior of intensivists in replacing magnesium. During the
study period, 71 patients (45 males and 26 females) were
admitted to the ICU, the mean age was 54 +/- 18 years for
males and 56 +/- 19.2 years for females. The mean magnesium
level on admission was 0.78 +/- 0.2 mmol/L and the majority
of the patients were medical admissions. Approximately 39.4%
had hypomagnesemia on admission and the overall mortality
rate was 31%. In able to standardize the supplementation of
magnesium among groups, the daily magnesium supplementation
index (DMSI = total magnesium supplement in grams/length of
stay in days) was calculated. The mortality rates for DMSI
with <1 grm/day (low groups) was statistically significant
higher than that of DMSI with >1 grm/day (high group) (43.5%
versus 17%). There were no statistically significant
differences between magnesium levels of both groups of DMSI
except at admission where DMSI group had higher magnesium
levels <1 grm/day). Daily magnesium supplementation
index higher than 1 grm/day is associated with lower
mortality rates for critically ill patients. This effect was
not found to be independent and may be related to severity
of illness. Given that magnesium levels were similar between
the 2 groups of DMSI at almost all points of the study,
magnesium supplementation per se may be beneficial in
lowering mortality rates. The exact cause of this effect is
unknown. An aggressive magnesium supplementation protocol
may be warranted. A larger scale randomized study is
necessary to evaluate this effect.
Iron and exercise induced alterations
in antioxidant status. Protection by dietary milk
proteins
Zunquin G, et al.
Free Radic Res. 2006; 40(6):535-42.
Lipid peroxidation stress induced by iron
supplementation can contribute to the induction of gut
lesions. Intensive sports lead to ischemia reperfusion,
which increases free radical production. Athletes frequently
use heavy iron supplementation, whose effects are unknown.
On the other hand, milk proteins have in vitro antioxidant
properties, which could counteract these potential side
effects. The main aims of the study were: (1) to demonstrate
the effects of combined exercise training (ET) and iron
overload on antioxidant status; (2) to assess the protective
properties of casein in vivo; (3) to study the mechanisms
involved in an in vitro model. Antioxidant status was
assessed by measuring the activity of antioxidant enzymes
(superoxide dismutase (SOD); glutathione peroxidase (GSH-P~)),
and on the onset of aberrant crypts (AC) in colon, which can
be induced by lipid peroxidation. At day 3D, all ET animals
showed an increase in the activity of antioxidant enzymes,
in iron concentration in colon mucosa and liver and in the
number of AC compared to untrained rats. It was found that
Casein's milk protein supplementation significantly reduced
these parameters. Additional information on protective
effect of casein was provided by measuring the extent of
TBARS formation during iron/ascorbate-induced oxidation of
liposomes. Free casein and casein bound to iron were found
to significantly reduce iron-induced lipid peroxidation. The
results of the overall study suggest that iron
supplementation during intensive sport training would
decrease anti-oxidant status. Dietary milk protein
supplementation could at least partly prevent occurrence of
deleterious effects to tissue induced by iron overload.
Calcium intake and 10-year weight
change in middle-aged adults.
Gonzalez AJ, et al.
J Am Diet Assoc, 2006; 106(7):1066-73.
The goal of this study was
to examine the purported effects of calcium on
modulating body weight. Retrospective data was used to
assess the relationship between calcium intake and
weight change over an 8- to 12-year period among
middle-aged adults. Participants were 10,591 men and
women aged 53 to 57 years recruited during 2000-2002.
Linear regression was used to model associations of
10-year weight change and calcium intake, adjusted for
weight at age 45 years, energy intake, physical
activity, and other factors. Calcium intake was
associated with 10-year weight change only in women.
Women with current calcium supplement dose of >500
mg/day had a 10-year weight gain of 5.1 kg (95%
confidence interval 4.7 to 5.5) compared to 6.9 kg (95%
confidence interval 6.5 to 7.4) among nonusers (P for
trend=0.001). Trends were similar for total calcium
intake from diet plus supplements (P for trend=0.001).
Dietary calcium alone had no significant effect on 10-
year weight change. Increasing total calcium intake, in
the form of calcium supplementation, may be beneficial
to weight maintenance, especially in women during
midlife.
Cardiac fibrogenesis in magnesium
deficiency: a role for circulating angiotensin II and
aldosterone
Sapna S, et al.
Am J Physiol Heart Circ Physiol, 2006; 291(1):H436-40.
Mechanisms/underlying cardiac fibrogenesis in magnesium
deficiency are unclear. It was reported earlier from this
laboratory that serum from magnesium-deficient rats has a
more pronounced stimulatory effect on cell proliferation,
net collagen production, and superoxide generation in adult
rat cardiac fibroblasts than serum from rats on the control
diet. The profibrotic serum factors were, however, not
identified. This study tested the hypothesis that
circulating angiotensin II may modulate cardiac fibroblast
activity in hypomagnesemic rats. Male Sprague-Dawley rats
were pair-fed a magnesium-deficient or -sufficient diet for
6 days, and the effects of serum from these rats on
[3H]thymidine and [3H]proline incorporation into cardiac
fibroblasts from young adult rats were evaluated in the
presence of losartan, an angiotensin II type 1 (AT1)
receptor antagonist, and spironolactone, an aldosterone
antagonist. Losartan and spironolactone markedly attenuated
the stimulatory effects in vitro of serum from the
magnesium-deficient and control groups, but the inhibitory
effects were considerably higher in cells exposed to serum
from magnesium-deficient animals. Circulating and cardiac
tissue levels of angiotensin II were significantly elevated
in magnesium-deficient animals (67.6% and 93.1%,
respectively, vs. control). Plasma renin activity was 61.9%
higher in magnesium-deficient rats, but serum angiotensin-converting
enzyme activity was comparable in the two groups.
Furthermore, preliminary experiments in vivo using enalapril
supported a role for angiotensin II in magnesium deficiency.
There was no significant difference between the groups in
serum aldosterone levels. The findings suggest that
circulating angiotensin II and aldosterone may stimulate
fibroblast activity and contribute to a fibrogenic response
in the heart in magnesium deficiency.
Moderate iron deficiency in infancy:
biology and behavior in young rats
Beard Jl, et al.
Behav Brain Res, 2006 ; 170(2) :224-32.
Iron deficiency anemia in early childhood is associated with
developmental delays and perhaps, irreversible alterations
in neurological functioning. The goals were to determine if
dietary induced gestational and lactational iron deficiency
alters brain monoamine metabolism and behaviors dependent on
that neurotransmitter system. Young pregnant rats were
provided iron deficient or control diets from early in
gestation through to weaning of pups and brain iron
concentration, regional monoamine variables and achievement
of specific developmental milestones were determined
throughout lactation.
Despite anemia during lactation, most brain iron
concentrations did not fall significantly until P25, and
well after significant changes in monoamine levels,
transporter levels, and D2R density changed in terminal
fields. The changes in D2R density were far smaller than
previously observed models that utilized severe dietary
restriction during lactation or after weaning. Iron
deficient pups had normal birth weight, but were delayed in
the attainment of a number of milestones (bar holding,
vibrissae-evoked forelimb placing). This approach of iron
deficiency in utero and during lactation sufficient to cause
moderate anemia but not stunt growth demonstrates that
monaminergic metabolism changes occur prior to profound
declines in brain iron concentration and is associated with
developmental delays. Similar developmental delays in iron
deficient human infants suggest to us that alterations in
iron status during this developmental period likely affects
developing brain monaminergic systems in these infants
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