zinc and magnesium are two of the essential nutrients known to be depleted in ms patients. medications can sometimes, by various mechanisms, exacerbate this problem. careful informed dietary change - and, if necessary, supplementation - has the potential to help
two related studies:
Release of glutamate and GABA in the hippocampus under zinc deficiency (2003)http://www.ncbi.nlm.nih.gov/pubmed/12704815
"Zinc homeostasis in the brain is affected by dietary zinc deficiency, and its alteration may cause brain dysfunctions. On the basis of the previous evidence that hippocampal zinc was responsive to 12-week zinc deprivation, responsiveness of hippocampal zinc to dietary zinc deficiency was examined in rats fed a zinc-deficient diet for 4 weeks. ... In the brain of the zinc-deficient rats, ... zinc concentration in the hippocampal extracellular fluid was approximately 30% of that of control rats. These results demonstrate that vesicular zinc is responsive to dietary zinc and may decrease easily under zinc deficiency. ... Gamma aminobutyric acid (GABA) concentration
in the hippocampal extracellular fluid during stimulation with high K+ was increased in the control rats, but not in the zinc-deficient rats
. The present study suggests that the excitability of hippocampal glutamatergic neurons is enhanced by dietary zinc deficiency"
Anxiety and stress among science students. Study of calcium and magnesium alterations (2006)http://www.jle.com/e-docs/00/04/1D/1B/article.phtml
"...The present results showed that the evaluated students did not experiment a stress increase during exams but suffered a significant anxiety increase. It is interesting to observe that the psychological findings agree with urinary biomarkers studied. It is known that anxiety is related to partial magnesium decrease associated with an increase in urinary magnesium excretion [12-17]. This might be partially attributed to the plasmatic glucose decrease caused by anxiety that leads to catecholamine secretion in order to restore glucose levels. These hormones are implicated in hypomagnesemia [9-11]. Also, an increase in aldosterone secretion might be able to explain the findings of this paper, as aldosterone leads to an increased renal excretion of magnesium [27-29]. The noticeable increase in muscular tension linked to anxiety consumes an important amount of energy that is partially due to the ATP-ADP transformation. A high increase in urinary phosphate excretion [30-32] also contributes to the magnesium reduction. Indeed, magnesium has been proposed for treatment in different anxiety disorders [33-38]. Stress correlates with a urinary calcium increase resulting from cortisol liberation [39, 40]. Cortisol blocks the calcium tubular reabsorption mediated by aldosterone, and as a consequence increases calcium urinary excretion [5-8]. Moreover, aldosterone causes an increase in renal magnesium excretion. In the present paper, we did not observe changes in stress and no correlatively significant increases were detected in urinary calcium concentration or excretion.
It must be pointed out that no differences were observed in urinary concentrations and excretion of magnesium and phosphate (phosphorus) when the first urine of the morning was studied (2h urine). This can be linked to the relaxation induced by sleep that must be accompanied by a decrease in anxiety.
The present results showed that the evaluated university science students did not experience stress increase as a consequence of exams but suffered a significant increase in anxiety.
This was associated to a urinary magnesium excretion increase responsible for partial magnesium depletion