jimmylegs wrote:re documentation - there's actually a 'journals' section of this site, but i don't know how well-used it is or even if it is working properly :S
Zinc profiles were examined in 68 patients with multiple sclerosis, 62 normal volunteers, and 13 patients with other neurological diseases. Plasma zinc levels were slightly increased in patients with multiple sclerosis and significantly increased in those with other neurological impairments (p <0.01), compared with control subjects. Albumin-bound as well as protein-bound zinc levels were normal in all groups tested. The α2 macroglobulin-bound zinc level was significantly lower (p < 0.01) in patients with multiple sclerosis than in control subjects. Erythrocyte-bound zinc levels were significantly increased (p < 0.05) in patients with multiple sclerosis when compared with control subjects. Erythrocyte-bound zinc was normal in patients with other neurological impairments. Because erythrocyte-bound zinc levels are relatively independent of daily fluctuations in dietary zinc intake, an increase in these values may suggest alterations in the control mechanisms governing zinc compartmentalization in patients with multiple sclerosis.
Previous studies have shown that zinc levels in erythrocytes are significantly elevated in patients with multiple sclerosis (MS). To examine the correlation between erythrocyte Zn levels and disease activity, we measured erythrocyte Zn levels longitudinally. Levels were dramatically decreased during a clinically documented exacerbation of MS. To determine the localization of increased Zn levels in MS erythrocytes, we employed standard techniques for the isolation of nonhemoglobin erythrocyte membrane ghosts. Patients with MS had three times more Zn in ghost material than did controls. Chloroform–methanol extraction in erythrocyte ghosts followed by determination of Zn levels indicated that most of the membrane-bound Zn was associated with the lipid-soluble fraction. Non-lipid-associated Zn and total membrane protein concentration were similar in MS and control samples. Results suggest that mechanisms which govern cellular availability, compartmentalization of Zn, or the binding of Zn to cell surface membranes may be altered in patients with MS, and that these mechanisms vary with disease activity.
The proposed aetiologies of multiple sclerosis (MS) have included immunological mechanisms, genetic factors, virus infection and direct or indirect action of minerals and/or metals. The processes of these aetiologies have implicated magnesium. Magnesium and zinc have been shown to be decreased in central nervous system (CNS) tissues of MS patients, especially tissues such as white matter where pathological changes have been observed. The calcium content of white matter has also been found to be decreased in MS patients. The interactions of minerals and/or metals such as calcium, magnesium, aluminium and zinc have also been evaluated in CNS tissues of experimental animal models. These data suggest that these elements are regulated by pooling of minerals and/or metals in bones. Biological actions of magnesium may affect the maintenance and function of nerve cells as well as the proliferation and synthesis of lymphocytes. A magnesium deficit may induce dysfunction of nerve cells or lymphocytes directly and/or indirectly, and thus magnesium depletion may be implicated in the aetiology of MS. The action of zinc helps to prevent virus infection, and zinc deficiency in CNS tissues of MS patients may also be relevant to its aetiology. Magnesium interacts with other minerals and/or metals such as calcium, zinc and aluminium in biological systems, affecting the immune system and influencing the content of these elements in CNS tissues. Because of these interactions, a magnesium deficit could also be a risk factor in the aetiology of MS.
Dysregulation of the HPA axis activity has been found in psychiatric diseases, with hyperactivity leading to hypercortisolism being found in melancholic depression (Ehlert, Gaab, Heinrichs 2001) and anorexia nervosa (Young & Korszun 2002) and reduced activity of the HPA axis being associated with post traumatic stress disorder (Ehlert, Gaab, Heinrichs 2001). Stress also activates the sympathetic-adrenal medullary (SAM) system which causes an increase in blood pressure, heart rate, constriction of peripheral blood vessels (Cohen & Rodriquez 1995) and higher levels of circulating epinephrine and norepinephrine (Tsigos & Chrousos 2002). The compensation stage is sustained activation of the sympathetic nervous system known as adrenal hyperfunction and the final stage occurs when the body’s ability to synthesize cortisol is diminished resulting in adrenal hypofunction (Meletis & Centrone 2002).
Users browsing this forum: No registered users