RobinN
Super Mom
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The April 2007 issue of the American Journal of Clinical Nutrition published the finding of researchers at Harvard University that having a greater intake of magnesium is associated with lower levels of some markers of inflammation and endothelial dysfunction in healthy women. The two conditions often precede atherosclerosis and type 2 diabetes, and are involved in the metabolic syndrome. Magnesium intake has been associated by some studies with a decrease in metabolic syndrome features.
Y. Song of Harvard Medical School and colleagues included 657 participants in the Nurses' Health Study for the current investigation. Blood samples drawn between 1989 and 1990 were analyzed for inflammation markers C-reactive protein, interleukin 6, and soluble tumor necrosis factor alpha receptor 2, and endothelial biomarkers E-selectin, soluble intercellular adhesion molecule 1, and soluble vascular cell adhesion molecule 1. Dietary questionnaires completed by the subjects in 1986 and 1990 were averaged to provide the dietary intake of magnesium and other nutrients.
After adjusted analyses, higher intake levels of magnesium were associated with lower levels of C-reactive protein and E-selectin. The authors write that the direct effect of magnesium on glucose and insulin homeostasis may be responsible for the associations, however they suggest that, alternatively, magnesium may modulate systemic inflammation and endothelial function to influence insulin resistance, explaining that there is increasing evidence implicating the two conditions as its antecedents.
"These observed associations, albeit generally modest, may represent a pathophysiologic mechanism for the pleiotropic effects of magnesium intake on the features of the metabolic syndrome and its associated chronic diseases," the authors conclude.
—D Dye
http://www.lef.org/whatshot/2007_04.html
Endothelial dysfunction is a physiological dysfunction of normal biochemical processes carried out by the endothelium, the cells that line the inner surface of all blood vessels including arteries and veins (as well as the innermost lining of the heart and lymphatics.) Compromise of normal function of endothelial cells is characteristic of endothelial dysfunction. Normal functions of endothelial cells include mediation of coagulation, platelet adhesion, immune function, control of volume and electrolyte content of the intravascular and extravascular spaces. Endothelial dysfunction can result from disease processes, as occurs in septic shock, hypertension, hypercholesterolaemia, diabetes as well as from environmental factors, such as from smoking tobacco products.
Endothelial dysfunction is thought to be a key event in the development of atherosclerosis and predates clinically obvious vascular pathology by many years. Endothelial dysfunction has also been shown to be of prognostic significance in predicting vascular events including stroke and heart attacks.
A key feature of endothelial dysfunction is the inability of arteries and arterioles to dilate fully in response to an appropriate stimulis. This can be tested by a variety of methods including iontophoresis of acetylcholine, intra-arterial administration of various vasoactive agents, localised heating of the skin and temporary arterial occlusion by inflating a blood pressure cuff to high pressures. Testing can also take place in the coronary arteries themselves but this is invasive and not normally conducted unless there is a clinal reason for intracoronary catheterisation. These techniques are thought to stimulate the endothelium to release nitric oxide (NO) and possibly some other agents, which diffuse into the surrounding vascular smooth muscle causing vasodilation.
Dysfunctional endothelial cells are unable to produce NO to the same extent (or there is increased and rapid destruction of NO) as healthy endothelial cells and therefore vasodilatation is reduced. This creates a detectable difference in subjects with endothelial dysfunction verses a normal, healthy endothelium.
http://en.wikipedia.org/wiki/Endothelial_dysfunction
This mineral has eliminated 30 yrs of severe migraines for me. There is evidence in other research stating that we as a society are deficient. I have been giving Rebecca this in pill form, but I think I will go back to the Ionic since this is absorbed directly into the cells.
I see it being suggested as an alternative on many headache sites.
As I understand, it helps the blood vessels "control of volume and electrolyte content of the intravascular and extravascular spaces". We are speaking of electrolytes
in another thread, and I also was under the impression that it is the constriction and expansion of the vessels that put strain on the nerves during a headache.
I hope this is of interest to others. I thought I might start some discussion on this subject and how it might relate to seizures.