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Associations of Serum Ca and Mg Levels with Mental Health in Adult
Women Without Psychiatric Disorders
Jung KI, et al.
Biol Trace Elem Res (2010)
133:153-161.
(AA)
Several lines of evidence from previous studies suggest that Calcium (Ca) and
Magnesium (Mg) may be involved in intracellular and interneuronal processes
associated with affective disorders. However, there have been inconsistent
results on the effect of Ca and Mg on depressive mood disorder. This
cross-sectional study was conducted to determine whether serum Ca and Mg
levels, as well as serum Ca/Mg ratio, are associated with mental health in
relatively healthy, adult women without psychiatric disorders. One hundred and
twelve adult women were recruited from the outpatient clinic in a university
hospital setting. Serum Ca and Mg levels were measured and indicators of mental
health such as depression, anxiety, and stress were evaluated using two
validated questionnaires; the Hospital Anxiety Depression Scale and the
Modified Brief Encounter Psychosocial Instrument Stress Scale. After
categorizing the serum Ca and Mg levels, and the Ca/Mg ratio into tertiles, the
mean scores on each mental health scale were compared using analysis of
covariance. The risk of depressive mood disorder according to the tertiles of
serum Mg level and serum Ca/Mg ratio was assessed using logistic regression
analysis. Women in the middle tertile of serum Ca/Mg ratio had significantly
lower scores on depression and stress scales (p = 0.004 and p = 0.007,
respectively) and a lower odds ratio (OR) for the risk of depressive mood
disorder (OR = 0.31, CI(95%) 0.10-0.93) than those in the highest tertile. The
OR for the risk of depressive mood disorder was higher in women in the lowest
tertile of serum Mg than in those in the highest tertile (OR = 3.92, CI(95%)
1.11-13.83). Serum Mg level and serum Ca/Mg ratio may be involved in the
mechanism for the progression of depressive mood or stress perception in
relatively healthy, adult women.
Short-term Oral Magnesium Supplementation Suppresses Bone Turnover in Postmenopausal Osteoporotic Women
Aydin H, et al.
Biol Trace Elem Res (2010) 133:136-143.
(AA)
Magnesium has been shown to increase bone mineral density when used in
the treatment of osteoporosis, yet its mechanism of action is obscure.
In this study, the effects of daily oral magnesium supplementation on
biochemical markers of bone turnover were investigated. Twenty
postmenopausal women have been divided into two groups. Ten patients
were given magnesium citrate (1,830 mg/day) orally for 30 days. Ten
postmenopausal women of matching age, menopause duration, and BMI were
recruited as the control group and followed without any medication.
Fasting blood and first-void urine samples were collected on days 0, 1,
5, 10, 20, and 30, respectively. Total magnesium, calcium, phosphorus,
iPTH and osteocalcin were determined in blood samples.
Deoxypyridinoline levels adjusted for creatinine were measured in urine
samples. Thirty consecutive days of oral magnesium supplementation
caused significantly decrease in serum iPTH levels in the
Mg-supplemented group (p < 0.05). Serum osteocalcin levels were significantly increased (p < 0.001) and urinary deoxypyridinoline levels were decreased (p <
0.001) in the Mg-supplemented group. This study has demonstrated that
oral magnesium supplementation in postmenopausal osteoporotic women
suppresses bone turnover.
Dietary Fiber, Magnesium, and Glycemic Load Alter Risk of Type 2 Diabetes in a Multiethnic Cohort in Hawaii
Hopping BN, et al.
J Nutr (2010) Jan;140(1):68-74.
(AA)
The influence of dietary fiber, magnesium (Mg), and glycemic load (GL)
on diabetes was examined in the Hawaii component of the Multiethnic
Cohort. The 75,512 Caucasian, Japanese American, and Native Hawaiian
participants aged 45-75 y at baseline completed a FFQ. After 14 y of
follow-up, 8587 incident diabetes cases were identified through
self-reports and health plans. We applied Cox regression stratified for
age at cohort entry and adjusted for ethnicity, BMI, physical activity,
education, and total energy with further stratifications by sex and
ethnicity. When comparing extreme quintiles, total fiber intake was
associated with reduced diabetes risk among all men [hazard ratio (HR):
0.75; 95% CI: 0.67, 0.84; P-trend <
0.001) and women (HR: 0.95; 95% CI: 0.85, 1.06; P-trend = 0.05). High
intake of grain fiber reduced diabetes risk significantly by 10% in men
and women. High vegetable fiber intake lowered risk by 22% in all men
but not women. Mg intake reduced risk (HR = 0.77 and 0.84 for men and
women, respectively) and, due to its strong correlation with fiber (r =
0.83; P < 0.001), may explain
the protective effect of fiber. The top GL quintile was associated with
a significantly elevated diabetes incidence in Caucasian men and in all
women except Japanese Americans. Overall, several associations were
more pronounced in Caucasians than in the other groups. These findings
suggest that protection against diabetes can be achieved through food
choices after taking into account body weight, but, due to differences
in commonly consumed foods, risk estimates may differ by ethnic group.
The Role of Zinc in Neurodegenerative Inflammatory Pathways in Depression
Szewczyk B, et al.
Prog Neuropsychopharmacol Biol Psychiatry (2010 Feb 13) [Epub ahead of print].
(AA)
According to new hypothesis, depression is characterized by decreased
neurogenesis and enhanced neurodegeneration which, in part, may be
caused by inflammatory processes. There is much evidence indicating
that depression, age-related changes often associated with impaired
brain function and cognitive performances or neurodegenerative
processes could be related to dysfunctions affecting the zinc ion
availability. Clinical studies revealed that depression is accompanied
by serum hypozincemia, which can be normalized by successful
antidepressant treatment. In patients with major depression, a low zinc
serum level was correlated with an increase in the activation of
markers of the immune system, suggesting that this effect may result in
part from a depression-related alteration in the immune-inflammatory
system. Moreover, a preliminary clinical study demonstrated the benefit
of zinc supplementation in antidepressant therapy in both treatment
non-resistant and resistant patients. In the preclinical study, the
antidepressant activity of zinc was observed in the majority of rodent
tests and models of depression and revealed a causative role for zinc
deficiency in the induction of depressive-like symptoms, the reduction
of neurogenesis and neuronal survival or impaired learning and memory
ability. This paper provides an overview of the clinical and
experimental evidence that implicates the role of zinc in the
pathophysiology and therapy of depression within the context of the
inflammatory and neurodegenerative hypothesis of this disease.
Features of Central Neurotransmission in Animals in Conditions of Dietary Magnesium Deficiency and After Its Correction
Spasov AA, et al.
Neurosci Behav Physiol (2009); 39(7):645-53.
(AA)
Magnesium is important in the regulation of neurotransmitter metabolism
and the modulation of receptor function in the CNS, including
neurotransmitters and receptors involved in the pathogenesis of many
mental disorders. The aim of the present work was to perform a
pharmacological evaluation of the central mechanisms of action of
magnesium salts in the clofelin, phenamine, arecoline, nicotine,
apomorphine, and 5-hydroxytryptophan tests in conditions of dietary
magnesium deficiency. After reaching the magnesium deficiency state,
animals were given oral (via tube) magnesium L-asparaginate and
magnesium chloride lone and in combination with vitamin B(6), as well
as the reference agent Magne B6. Our assessments of phenamine
stereotypy in magnesium-deficient animals showed reductions in the
latent period by an average of 14.89% and a significant increase in the
duration of phenamine stereotypy by an average of 19.44% (from 268.23
+/- 8.17 to 320.36 +/- 19.90 min) as compared with intact rats. Studies
of hyperkinesia induced by 5-hydroxytryptophan showed a two-fold
reduction in its extent in the magnesium-deficient group (p <=
0.05). Administration of arecoline to magnesium-deficient animals
resulted in a statistically significant increase in the latent period
from a mean of 92.75 +/- 19.35 to 245.17 +/- 121.86 sec, with a
reduction in the duration of tremor from an average of 1175.58 +/-
127.87 to 703.83 +/- 89.33 sec (p < = 0.05) as compared with intact
rats. In terms of its influence on the hypothermic effects of clofelin
and apomorphine and the convulsive effect of nicotine, there were no
significant differences between the intact group and the
magnesium-deficiency animals. Administration of magnesium salts
compensated for the magnesium deficiency in plasma and erythrocytes,
which was accompanied by recovery of measures in the phenamine,
arecoline, and 5-HT tests to levels typical of intact controls. There
was a tendency for magnesium L-asparaginate and magnesium chloride
combined with pyridoxine to have greater activity, and the efficacies
of these treatments was no less than that of reference agent Magne B6.
Thus, dietary magnesium deficiency led to impairment of
neurotransmission in central serotoninergic, M-cholinergic, and
noradrenergic structures and administration of magnesium salts reversed
these changes.
The Role of Zinc Deficiency in Alcohol-induced Intestinal Barrier Dysfunction
Zhong W, et al.
Am J Physiol Gastrointest Liver Physiol (2010 Feb 18) [Epub ahead of print].
(AA) Disruption of the intestinal barrier is a causal factor in the
development of alcoholic endotoxemia and hepatitis. This study was
undertaken to determine if zinc deficiency is related to the
deleterious effects of alcohol on the intestinal barrier. Mice were
pair-fed an alcohol or isocaloric liquid diet for 4 weeks, and
hepatitis was detected in association with elevated blood endotoxin
level. Alcohol exposure significantly increased the permeability of the
ileum, but did not affect the barrier function of the duodenum or
jejunum. Reduction of tight junction proteins at the ileal epithelium
was detected in alcohol-fed mice, although alcohol exposure did not
cause apparent histopathological changes. Alcohol exposure
significantly reduced the ileal zinc concentration in association with
accumulation of reactive oxygen species. Caco-2 cell culture
demonstrated that alcohol exposure increases the intracellular free
zinc due to oxidative stress. Zinc deprivation caused epithelial
barrier disruption in association with disassembling of tight junction
proteins in the Caco-2 monolayer cells. Furthermore, minor zinc
deprivation exaggerated the deleterious effect of alcohol on the
epithelial barrier. In conclusion, epithelial barrier dysfunction in
the distal small intestine plays an important role in alcohol-induced
gut leakiness, and zinc deficiency due to oxidative stress may
interfere with the intestinal barrier function by a direct action on
tight junction proteins or by sensitizing to the effects of alcohol.
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