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This is a brief summary of an exciting new way of looking at PD that has been taking shape over the last five years and which holds promise of effective treatment via anti-inflammatory actions. I will be posting a large body of work exploring this over the next few days at – http://health.groups.yahoo.com/group/PDpower/ and welcome discussion. Part One: Summary I have been working on this for several months beginning with an interest in Helicobacter pylori. There is no original research on my part here other than the attempt to connect “the dots” generated by true researchers. There are gaps, particularly where it is necessary to make a leap from animal model or test tube to human. There are no doubt big flaws that I have overlooked. But this theory answers more questions about PD than I would ever have imagined. See if you agree. Evidence for and implications of endotoxin-induced inflammatory origins of Parkinson’s disease (PD): Hypothesis: Parkinson’s patients are part of a subset of the population who show a hypersensitivity to the endotoxin lipopolysaccharide (LPS) resulting from neonatal exposure and which results in a chronic inflammatory state in the brain. This inflammatory state results in both longterm damage to the substantia nigra (SN) and, perhaps more importantly, acute symptomology producing the typical Parkinson’s picture. In addition to providing a plausible framework for the causes and effect leading to PD, this hypothesis explains many seemingly unrelated facts about the condition. Among them are the observed gender difference in PD, the finding of iron in the SN, the geographical limitation of damaged neurons to the SN, the nature of manganese induced parkinsonism, the sleep disturbances common in PD, the amplification of symptoms by stress, the elevated levels of cortisol common in PD, the role of mercury, the problem of mitochondrial function, etc. In addition, numerous anecdotal reports by patients of temporary remission coinciding with use of drugs with known anti-inflammatory effects are explained by the hypothesis as are similar reports and epidemological data related to non-prescription medicines such as green tea, turmeric, alpha-lipoic-acid, etc. No other proposed hypothesis for the origins and course of Parkinson’s disease comes close to explaining all of the above. Nor does any offer the hope of such a quick test of the basic concept. Simply reproducing the anecdotal information referred to above would immediately verify the broader principle. Similarly, a move to clinical trials and even actual treatment by way of “off label” use of already approved drugs should allow speedy implementation. ---------------------------------------------------------------------- To sign-off Parkinsn send a message to: mailto:[log in to unmask] In the body of the message put: signoff parkinsn