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Hi! Jim, Since we are on the topic of IRON, lets take a look at what can happen when the liver has been damaged. It may seem like it has nothing to do with Parkinson's, but bear with me and look for my comments below. My comments begin with *** J Gastroenterol Hepatol 1997 Oct;12(9-10):S272-S282 Pathogenesis of alcoholic liver disease with particular emphasis on oxidative stress. Ishii H, Kurose I, Kato S 1)Oxidative stress is well recognized to be a key step in the pathogenesis of ethanol-associated liver injury. ***Oxidative stress was noted by Floor E,Wetzel MG J Neurochem 1998 Jan;70(1):268-275Increased protein oxidation in human substantia nigra pars compacta in comparison with basal ganglia and prefrontal cortex measured with an improved dinitrophenylhydrazine assay. ***where he says... 2)These degenerative processes are hypothesized to involve oxidative stress. *** One would already begin to expect that the liver is fundamental in ***the development of Parkinson's. Since this oxidative stress is ***found both in ethanol associated liver injury and Parkinson's ***disease. ***But lets go on.... there is more to come. <smile> Ethanol administration induces an increase in lipid peroxidation either by enhancing the production of oxygen reactive species and/or by decreasing the level of endogenous antioxidants. ***Sound a little familiar? However, there could also be many reasons ***for this,aging alone probably has some influence. But aging alone ***does not produce Parkinson's disease. This might be why we see ***improvements with antioxidant therapy, et. liver damage. ***Please proceed...<smile> Numerous experimental studies have emphasized the role of the ethanol-inducible cytochrome P450 in the microsomes and the molybdo-flavoenzyme xanthine oxidase in the cytosol. This review shows the putative role of ethanol-induced disturbances in iron metabolism in relation to iron as a pro-oxidant factor. Ethanol administration also affects the mitochondrial free radical generation. ***Again, when the liver is not functioning in a normal manner, et. ***ethanol-induced changes, there is a change in iron metabolism. ***continue...<smile> Neurology 1997 Sep;49(3):714-717 Altered systemic iron metabolism in Parkinson's disease.Logroscino G, Marder K, Graziano J, Freyer G, Slavkovich V, LoIacono N, Cote L, Mayeux R *** Dietary intake did not seem to make a difference ***in the amount of iron that was deposited in the substantia nigra. ***But now we know that iron metabolism can be disturbed by liver ***functioning,and the liver is a site where apoptosis normally occurs. *** ***It could be that subtle changes in the liver could cause a change ***in iron metabolism, or it could be due to some uninvited guests. ***Whatever the reason there are many conditions in which this can ***occur. The purpose of this, was to show that the liver can effect ***iron metabolism. So it may not be all in your head.<smile> *** Best Wishes, Linda Forrest's Mom Many previous studies suggest a role for active oxygens in ethanol-induced mitochondrial dysfunction in hepatocytes. Recent studies in our laboratory in the Department of Internal Medicine, Keio University, using a confocal laser scanning microscopic system strongly suggest that active oxidants generated during ethanol metabolism produce mitochondrial membrane permeability transition in isolated and cultured hepatocytes. In addition,acetaldehyde, ethanol consumption-associated endotoxaemia and subsequent release of inflammatory mediators may cause hepatocyte injury via both oxyradical-dependent and -independent mechanisms. These cytotoxic processes may lead to lethal hepatocyte injury. Investigations further implicate the endogenous glutathione-glutathione peroxidase system and catalase as important antioxidants and cytoprotective machinery in the hepatocytes exposed to ethanol. ***Here it is suggested that the antioxidants are protective, ***protecting what...the liver. Yes. PMID: 9407347, UI: 98071238 Jim Slattery wrote: > > Hi Linda, > > >Envir.M.D.but I can assure you that it was natural > medicine. We were > >instructed that this would in no way be comprised by the > use of > >antioxidants, mineral or amino acids, etc. (not into > herbs<smile>) > > That raises another point. Analysis of post-mortem PD > brains shows an excess of non-absorbable iron, and a > depletion of the substance that cconverts this iron to a > form usable by the body, in comparison to non-PD controls. > I don't know which is cause or effect, nor how this is > related > to PD, but it may be wise to watch the iron intake, also the > types chellating agents in vitamin/mineral supplements. > > > I believe that their are many causes to Parkinson's > disease > > That appears to be the case; many causes with one effect, to > knock out the dopamine-producing cells. > > > We directed most of his treatments towards > detoxification, however, > >since we know that any illness can cause stress on the > host, not > > There is a very strong link between stress-produced > brain-affecting chemicals and both "freezing" (akinesia) and > spasmodic movement (dyskinesia). > > > I believe that what many patients fail to realize is a > doctor is > >not always going to suggest that tests be run. But that is > no reason > >why the patient cannot request these tests. > > Many older patients are still living with the impression, > created in their younger years, that "doctor knows best", > and that it is somehow impudent to suggest otherwise. I am > grateful for what my present doctors do to keep me alive and > functioning (and believe you me, if I wasn't taking my PD > meds, I would have been dead years ago - so much for "PD is > not life-threatening). But there are so many > disorders,medications, side-effects, etc., that a doctor > would have to have an Einstein-sized brain just to keep up. > However, I would much prefer a doctor who said "I don't know > the answer, let's see if we can find out", than one who > claimed to know everything. > > >even cold medicines. However, most drug stores give you a > list > >of known adverse reactions, but if I was to begin to worry > about > > As far as they are aware of them. I have seen labels on > Sinemet saying to take them with meals, and I even saw an > advisory note to GPs recommending the same thing. But, as > Kathryn(sp?) Holden and others have pointed out, taking > Sinemet with animal protein can lead to a lessened intake of > l-dopa, or even an absence. > > We all, sufferers, primary carers, health professionals, and > members of the general public, need to be better educated > about health disorders, their effects, and treatments, not > only with PD, but with other chronic illnesses. Perhaps > then we might be healthier, wealthier, and more tolerant. > <silent prayer> > > Jim 59/13 > [log in to unmask]