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DIETARY MAGNESIUM REDUCTION TO 25% OF
NUTRIENT REQUIREMENT DISRUPTS BONE AND
MINERAL METABOLISM IN THE RAT
Rude RK, et al.
Bone 2005 May 26; pS8756-3282
Low magnesium intake could be a risk factor in
osteoporosis. It has been reported that severe magnesium
deficiency
(0.04% Nutrient Requirement) and moderate magnesium
deficiency (10% of NR) result in bone loss. This study
examines the effect of a magnesium intake that is 25% of the
nutrient requirement on bone and mineral metabolism in
the rat. The following were monitored at 2, 4, and 6 months
in control and magnesium deficient animals: serum Mg,
Ca, PTH, 1,25(OH)(2)-vitamin D, alkaline phosphatase,
osteocalcin, and pyridinoline. Mineral content,
microcomputerized tomography, histomorphometry and
immunocytochemical localization were looked at for the
femurs andtibias of the animals. In the animals receiving
25% of the NR for magnesium, profound hypomagnesemia
developed, along with a 27% reduction in bone magnesium
content. The serum calcium levels were about the same for
both groups. Serum 1,25(OH)(2)-vitamin D and PTH were much
lower in the magnesium depleted group. The markers of bone
turnover were the same. Further testing showed a decrease in
bone volume and trabecular thickness in the magnesium
deficient. Osteoclasts and osteoblasts remained the same.
Immunocytochemical localization of TNFalpha in osteoclasts
increased 138-150%, which could result from the increase of
substance P that was elevated by 179-432%.
This all points to magnesium intake of 25% of NR causing
lower bone mass that could be related to increased release
of substance P and TNFalpha.
RELATIONSHIP BETWEEN MAGNESIUM LEVELS
IN DRINKING WATER AND SUDDEN INFANT DEATH
SYNDROME
Chiu HF; Chen CC; Tsai SS; Wu TN; Yang Cy.
Magnes Res 2005 Mar;18(1):12-8.
The possible association between
the risk of death from sudden infant death syndrome (SIDS)
and the levels of
magnesium in drinking water from municipal supplies was
investigated in a matched case-control study in Taiwan.
Characteristics for all SIDS deaths (501 cases) among Taiwan
residents from 1988 through 1997 were compared with
those of people who died from other causes (501 controls).
The levels of magnesium in the drinking water of these
residents were determined from data obtained from the Taiwan
Water Supply Corporation (TWSC). The controls were
pair-matched to the SIDS cases by sex, month and year of
birth. The results of our study show that there is a
significant trend towards a decreased risk of SIDS with
increasing magnesium levels in drinking water.
MAGNESIUM IN CONGESTIVE HEART FAILURE
Ohtsuka S; Yamaguchi I
Clin Calcium 2005 Feb;15(2):181-6
Magnesium deficit and other
electrolyte abnormalities is a frequent disorder in
patients with congestive heart failure.
Over stimulation of the rennin-angiotensin-aldosterone
system, long-term administration of diuretics, digoxin,
poor
oral intake and impaired absorption contribute to these
electrolytes abnormalities. Hypomagnesaemia and
depletion of
intracellular magnesium stores have been held
responsible for a variety of cardiovascular and other
functional
abnormalities, including various arrhythmias, impairment
of cardiac contractility, and vasoconstriction. Because
sudden death is prevalent in congestive heart failure, a
causal relationship between arrhythmias and magnesium
deficiency has been proposed. Reportedly, administration
of magnesium can suppress ventricular arrhythmias;
however, it remains to be elucidated whether
administration of magnesium prevents sudden death and
improves prognosis of the patients with congestive heart
failure. Nevertheless, since magnesium depletion may be
prevalent in congestive heart failure and magnesium has
anti-arrhythmic and beneficial cardiovascular effects,
magnesium should be supplemented to the patients
suspected to have its deficiency.
MAGNESIUM DEFICIENCY IS ASSOCIATED
WITH INSULIN RESISTANCE IN OBESE CHILDREN
Huerta Mg; et al.
Diabetes Care 2005 May;28(5):1175-81.
Magnesium deficiency has been
associated with insulin resistance (IR) and increased risk
for type 2 diabetes in adults.
This study was designed to determine whether obese children
exhibit serum or dietary magnesium deficiency and its
potential association with IR. In the study, 24 obese
non-diabetic children and 24 sex-and puberty-matched lean
control subjects were evaluated. Researchers measured serum
magnesium, indexes of insulin sensitivity, dietary magnesium
intake (using a food frequency questionnaire), and body
composition. Serum magnesium was significantly lower in
obese children (0.748 ± 0.015 mmol/l, means ± SE) compared
with lean children (0.80 ± 0.012 mmol/l). Serum magnesium
was inversely correlated with fasting insulin and positively
correlated with quantitative insulin sensitivity check index
(QuickI). Dietary magnesium intake was significantly lower
in obese children. Dietary magnesium intake was inversely
associated with fasting insulin and directly correlated with
QuickI. The association between magnesium deficiency and IR
is present during childhood. Serum magnesium deficiency in
obese children may be secondary to decreased dietary
magnesium intake. Magnesium supplementation or increased
intake of magnesium-rich foods may be an important tool in
the prevention of type 2 diabetes in obese children.
MANGANESE ACTS CENTRALLY TO STIMULATE
LUTEINIZING HORMONE SECRETION: A POTENTIAL
INFLUENCE ON FEMALE PUBERTAL DEVELOPMENT
Toxicol Sci 2005 Jun;85(2):880-5 (ISSN: 1096-6080)
Pine M; Lee B; Dearth R; Hiney JK; Dees WL
Manganese (Mn), an essential element considered
important for normal growth and reproduction, has been shown
in
adults to be detrimental to reproductive function when
elevated. Because Mn can cross the blood-brain barrier and
accumulate in the hypothalamus, and because it has been
suggested that infants and children are potentially more
sensitive to Mn than adults, the researchers wanted to
determine the effects of Mn exposure on puberty-related
hormones and the onset of female puberty. It was
demonstrated that MnCI(2) when administered acutely into the
third
ventricle of the brain acts dose-dependently to stimulate
luteinizing hormone (LH) release in prepubertal female rats.
Incubation of hypothalami in vitro showed that this effect
was due to a Mn-induced stimulation of luteinizing hormone
releasing hormone (LHRH). Further demonstration that this is
a hypothalamic site of action was shown by in vivo
blockade of LHRH receptors and lack of a direct pituitary
action of Mn to stimulate LH in vitro. To assess potential
short-term effects, animals were supplemented with MnCI(2)
(10 mg/kg) by gastric gavage from day 12 until day 29,
or, in other animals, until vaginal opening (VO). Mn caused
elevated serum levels of LH, follicle stimulating hormone,
and estradiol, and it initiated a moderate but significant
advancement in age at VO. Our results are the first to show
that Mn can stimulate specific puberty-related hormones and
suggest that it may facilitate the normal onset of puberty.
They also suggest that Mn may contribute to precocious
puberty if an individual is exposed to elevated levels of Mn
too early in development.
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