I apologize for the length of this, but it is just bits and bytes after all. I compiled all this a year ago as a follow-up to the work Ron Hutton and I had done on the role of H. pylori bacteria in PD. I was about to post it when the infamous BT collapse occurred and that venue where it might mean anything to someone disappeared. I thought this info had been lost until a couple of hours ago, when I found it hiding in an obscure neighborhood on my hard disk. Rather than let it go to waste I will post it here for any who are interested.

The gist of it is that there is a strong case to be made for inflammation induced by common bacteria as one of the primary causes and aggravating factors for PD. This isn't just academic interest because, if so, then it becomes very important to think about anti-inflammatory therapies both to prevent further damage and, most exciting of all, to lessen symptoms. After all, those diseases that cause inflammation of the brain such as encephalitis have symptoms from that swelling. Why would PD be any different. So, without further ado, I present the "Ben Hur" of reports:


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.