Role of Magnesium in Hypertension
Bruno Sontia, Rhian M. Touyz.
Arch Biochem and Biophy, 458 (2007) 33-39.
Magnesium affects blood pressure by modulating vascular tone
and reactivity. It acts as a calcium channel
antagonist, it stimulates production of vasodilator
prostacyclins and nitric oxide and it alters vascular
responses to vasoactive agonists. Magnesium deficiency has
been implicated in the pathogenesis of
hypertension with epidemiological and experimental studies
demonstrating an inverse correlation between
blood pressure and serum magnesium levels. Magnesium also
influences glucose and insulin homeostasis,
and hypomagnesemia is associated with metabolic syndrome.
Although most epidemiological and
experimental studies support a role for low magnesium in the
pathophysiology of hypertension, data from
clinical studies have been less convincing. Furthermore, the
therapeutic value of magnesium in the
management of hypertension is unclear. The present review
addresses the role of magnesium in the
regulation of vascular function and blood pressure and
discusses the implications of magnesium deficiency in
experimental and clinical hypertension, in metabolic
syndrome and in pre-eclampsia.
Racial Differences in Skeletal Calcium
Retention in Adolescent Girls with Varied Controlled Calcium
Intakes
Michelle Braun, et al.
Am J Clin Nutr 2007;85:1657-63.
Higher bone mass in blacks than in whites has been related
to greater calcium utilization efficiency. Dietary
calcium requirements for maximal skeletal calcium accretion
during puberty may differ between the races.
This study compared the relation between calcium intake and
calcium retention in black and white
adolescent girls. A range of controlled calcium intakes
(760-1981 mg Ca/d) were used in 3-week
controlled balance studies. Some subjects were studied more
than once; a total of 182 observations from 55
black girls and 66 white girls were analyzed. Blacks had 185
± 32 mg/d greater mean skeletal calcium
retention than did white (P<0.0001) at all calcium intakes
as a result of significantly greater net calcium
absorption (P<0.0001) and lower calcium excretion
(P<0.0001). Dietary calcium requirements did not
differ with race. Higher calcium retention at all calcium
intakes during adolescence may underlie the higher
bone mineral content of adult blacks than of adult whites.
MAGNESIUM METABOLISM IN TYPE 2 DIABETES MELLITUS, METABOLIC SYNDROME, AND INSULIN RESISTANCE
Barbagallo M, Dominguez LJ
Arch Biochem Biophys. 2007 Peb 1 ;458(1):40-7
Cellular and extracellular magnesium depletion is a characteristic of Type 2 diabetes. Epidemiologic research has
indicated a high prevalence of hypomagnesemia and lower intracellular magnesium levels in diabetics. Insulin and
glucose are involved in the regulation of magnesium metabolism. Intracellular magnesium is a key regulator of insulin
action, insulin-mediated glucose uptake, and vascular tone. Lower intracellular magnesium levels lead to a defective
tyrosine-kinase activity, post-receptorial impairment in insulin action, and an increased insulin resistance in diabetics.
Insulin resistance of certain metabolic syndromes has been proposed to be the result of magnesium deficit, and low
dietary magnesium is related to the development of Type 2 diabetes. A number of studies have shown that magnesium
supplementation has a positive impact on the metabolic profile of diabetics, but more, larger prospective studies are still
needed to support the use of magnesium supplementation as a public health strategy against the risk of diabetes.
Selenium Glycinate Supplementation
Effects on Gutathione Peroxidase and PSA in Healthy Middle
Aged Men
Robert A. DiSilvestro, et al.
The FASEB Journal 21, No 5, April 2007;227.2.
It is generally assumed that middle aged, healthy men in the
USA eat adequate amounts of selenium. In
contrast, 5 week supplementation with 200 ug selenium as
selenium glycinate (Albion Laboratories, Inc.)
increased plasma and erythrocyte glutathione peroxidase
activities (p<0.05 for plasma, p<0.01 for
erythrocytes). Although the increases were not big, small
increases in blood glutathione peroxidase
activities could be indicative of bigger increases in
prostate activities of this enzyme (contention based on a
rat study). Consistent with this concept, selenium glycinate
supplementation reduced plasma PSA values,
even though the supplementation period was not overly long
for a PSA study, and starting PSA values were
not abnormally high. An attempt was made to see if zinc
arginate supplementation could enhance the
selenium effects on glutathione peroxidase activities (zinc
status in rats can impact these activities). Zinc
supplementation produced a small increase in plasma
activities (p<0.05), as well as in markers of zinc
status, but the effects were not additive when zinc and
selenium supplementation were combined. In
conclusion, selenium intake may not be optimal in US middle
aged men, especially in regard to prostate
health; no evidence was found for improved zinc status
enhancing selenium function.
Zinc
Supplementation Decreases Incidence of Infections in the
Elderly: Effect of Zinc on Generation of Cytokines and
Oxidative Stress
Ananda S. Prasad, et al.
Am J Clin Nutr, 2007;85:837-44.
Zinc deficiency, cell-mediated immune dysfunction,
susceptibility to infections, and increased oxidative
stress have been observed in elderly subjects (ie, those
>55yo). Zinc is an effective anti-inflammatory and
antioxidant agent. The primary objective was to
determine the effect of zinc on the incidence of total
infections in healthy elderly subjects. The secondary
objective was to determine the effect of zinc on
cytokines and oxidative stress markers. A randomized,
double-blind, placebo-controlled trial of zinc
supplementation was conducted in elderly subjects. Fifty
healthy subjects of both sexes aged 57-88y and
inclusive of all ethnic groups were recruited for this
study from a senior center. The zinc-supplemented
group received zinc gluconate (45 mg elemental Zn/d)
orally for 12 months. Incidence of infections during
the supplementation period was documented. The
generation of inflammatory cytokines, T helper 1 and T
helper 2 cytokines, and oxidative stress markers and the
plasma concentrations of zinc were measured at
baseline and after supplementation. Compared with a
group of younger adults, at baseline the older
subjects had significantly lower plasma zinc, higher ex
vivo generation of inflammatory cytokines and
interleukin 10, and higher plasma oxidative stress
markers and endothelial cell adhesion molecules. The
incidence of infections and ex vivo generation of tumor
necrosis factor α and plasma oxidative stress
markers were significantly lower in the
zinc-supplemented than in the placebo group. After zinc
supplementation, the incidence of infections was
significantly lower, plasma zinc was significantly
higher,
and generation of tumor necrosis factor α and oxidative
stress markers was significantly lower in the
zincsupplemented
than in the placebo group.
Copper Supplementation Effects on
Erythrocyte Superoxide Dismutase
Activities in Middle Aged Men and Women
Robert A. DiSilvestro, et al.
The FASEB Journal 21, No 5, April 2007;698.8.
Based on the current RDAs for copper which fall below
older recommendations, fewer people show
inadequate copper intake than previously proposed.
However, 8-week copper supplementation (2 mg
copper as copper glycinate per day), in middle aged
adults (N-35), consistently raised values for
erythrocyte
activities of the copper enzyme superoxide dismutase.
Placebo had no effect. The copper supplementationinduced
changes in erythrocyte superoxide dismutase activities
correlated with changes in two plasma
copper enzyme activities, ceruloplasmin and diamine
oxidase. These results suggested that in this
population, copper intake was not typically high enough
to maximize copper enzyme activities. A number
of possible practical health consequences of this
behavior were investigated, but none of the measures
were
altered by copper supplementation. For example, copper
supplementation did not significantly alter plasma
cholesterol related parameters, though changes in HDL
cholesterol correlated with final superoxide
dismutase values in both the copper and placebo groups.
Copper supplementation did not alter C-reactive
protein, homocysteine, and LDL oxidation based on ELISA
analysis. LDL oxidation, when measured by lag
time ex vivo, had previously shown a relationship to
copper status. Values for the ELISA measure may be
slow to change since they were not affected by 8 weeks
of 400 IU/day of vitamin E supplementation
(plasma vitamin E did rise). A number of previous
studies had shown vitamin /E supplementation to affect
LDL oxidation lag time. In summary, copper
supplementation can readily raise copper enzyme activity
readings in middle aged adults, but the practical health
consequences remain unclear.
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