See
http://www.doglore.net/2009/02/15/th...accine-debate/
and scroll down past all the info on dogs, and read,

"Gary Smith explains what observant healthcare practitioners have been saying for a very long time, but perhaps didn’t understand why their observations led them to say it. His theory, incidentally, is causing a huge stir within the inner scientific sanctum. Some believe that his theory could help to cure diseases, including cancer. For me, it explains why the vaccine process is inherently questionable.

Gary was learning about inflammation as part of his studies when he struck upon a hypothesis so extraordinary that it could have implications for the treatment of almost every inflammatory disease – including Alzheimer’s, Parkinson’s, rheumatoid arthritis, and even HIV and Aids.

Gary’s theory questions the received wisdom that when a person gets ill, the inflammation that occurs around the infected area helps it to heal. He claims that, in reality, inflammation prevents the body recognising a foreign substance and therefore serves as a hiding place for invaders. The inflammation occurs when at-risk cells produce receptors called At1 (known as angiontensin II type I receptors). While At1 has a balancing receptor, At2, which is supposed to switch the inflammation off, he says that in most diseases this does not happen"

So inflammation could be totally different to the established theory. Now this is the innovative thinking that will find the cure
Ron

Interesting. I know that at one point my doctor ran a test on me for inflammation. I can't remember what in the world the name of the test was that he ran, but I do know that my results were elevated. He explained to me that it meant that I had inflammation inside of my body. I never heard any more about it.

There is a summary of 2 separate studies concerning immune cells
which has direct implication for the use of vaccines, and why they
may result in undesired/unanticipated effects. The summary appears in New Scientist magazine:
http://www.wemove.org/stayconnected/article.asp?ID=1161

Could vaccines result in immune responses in which
the correct immune cell Th1, morphs into the wrong cell, Th17,--causing
inflammation or autoimmunity when none was wanted?

The original J.Inflammation article is at

http://www.biomedcentral.com/content...6-9255-1-3.pdf

Ron

Hi all,
Inflammation is a topic that has been of my interest for a long time. It is a double edged sword sort of thing. It has to be the right amount, right combination of cytokines and at the right place for it to be useful.
Amazingly, most often human body manages to do that.

'Gary’s theory questions the received wisdom that when a person gets ill, the inflammation that occurs around the infected area helps it to heal. He claims that, in reality, inflammation prevents the body recognising a foreign substance and therefore serves as a hiding place for invaders. The inflammation occurs when at-risk cells produce receptors called At1 (known as angiontensin II type I receptors). While At1 has a balancing receptor, At2,'

I havent followed Gary's papers or work , but from what I read today, this theory doesnt seem right to me. Inflammation is a process that has several components, and proinflammatory cytokines are one part of it and they are the major players. These factors are made in response to infection (Pathogen recognizing receptors called TLR). this is sort of a alarm for the body to know that there are intruders and get ready to defend the body. Wihtout inflammation and subsequent activation of cells, pathogens will not be cleared, vaccines will not work. There is plenty of data supporting this. On the other hand, acute and high level of inflammation is a different story, can lead to even death (Toxic shock syndrome). I agree that chronic and elevated levels of cytokines and other factors do contribute to inflammation, might mislead the immune system and lead to autoimmune responses and other disorders too.

Thanks
Girija

[/I][/I]QUOTE=Ronhutton;466281]The original J.Inflammation article is at

http://www.biomedcentral.com/content...6-9255-1-3.pdf

Ron[/QUOTE]

I, too, have been more and more interested in inflammation's role in PD. I am convinced that the immune and endocrine systems are at the heart of the problem. A model with prenatal exposure to bacterial endotoxins results in a hypersensitivity to future exposures that triggers the innate defenders in the brain but leaves them with an impaired ability to shut down normally. The same fetus can be exposed to maternal stress hormones and be born with a poorly regulated endocrine system. The natural response to inflammation is for the endocrine system to pump out stress hormones which signals the immune system to cool it. But the altered immune system responds poorly if at all in the brain, so the hormones keep coming until they become a problem themselves. They are cut back but then the immune response flares up again and so a new round begins. This see-saw goes on and on alternately damaging the brain and exhausting the system via the stress response.

By the time we know something is wrong, the immune system has done enough damage to start our motor symptoms and the endocrine system, the most marvelous control network I could ever imagine, is badly out of adjustment and causing all kinds of problems. The net result is our sorry selves, overachieving heroes who collapse at the gates of Moscow or Troy or whatever metaphor suits you.

Every facet of PD that I know of can be explained by this model. For example-
1) PD is common at the community level but rare at the individual level. That is, you aren't likely to have it but are very likely to know someone who does. This is an odd pattern if there is a single cause, but if seen as the end result of a chain of variables it makes sense. Prenatal immune problems won't do it, nor will maternal stress, nor will the two together. Otherwise PD would be more common. But if the timing for both is perfect synchronized with times of fetal vulnerability then the child is vulnerable to further insults and PD exists as a potential. At some point the potential is realized as the scales are tipped by the sum of environmental toxins, stress, pathogens, hyperglycemia, etc etc

Lord, I do go on. But it isn't a simple matter. But, then, we've all noticed that.

Interesting concept. I just had my thyroid gland removed. Should I be on the lookout for anything, before they start me on the replacement therapy?

Do you remember the threads on antihypertension drugs slowing PD and AD?
Gary Smith says,
"If we could halt AT1 with an existing type of drug known as an angiotensin receptor blocker, we can not only switch off the inflammation, but also allow the body to recognise the disease".
Anti hypertension (high blood pressure) drugs such as Angiotensin receptor blockers have already been shown to have a very beneficial effect.
on PD and AD
See http://www.sciencedaily.com/releases...0901185313.htm

See also
http://www.answers.com/topic/angiote...tor-antagonist
Angiotensin II receptor antagonists, also known as angiotensin receptor blockers (ARBs), AT1-receptor antagonists or sartans, are a group of pharmaceuticals which modulate the renin-angiotensin-aldosterone system. Their main use is in hypertension (high blood pressure), diabetic nephropathy (kidney damage due to diabetes) and congestive heart failure.

In 2008 they were reported to have a remarkable negative association with Alzheimer's Disease. A retrospective analysis of five million patient records with the US Department of Veterans Affairs system found that different types of commonly used anti-hypertensive medications had very different AD outcomes. Those patients taking angiotensin receptor blockers (ARBs) were 35—40% less likely to develop AD than those using other anti-hypertensives. (Preliminary unpublished data)[1][2]
Ron

This thread is too technical for me to weigh in but I wanted to mention that back in January 2003 MJFF launched a program (~$2 million) to fund efforts to better understand the role of inflammation in PD. I remember extensive discussions at the time that we really didn't even know if inflammation was cause or effect...I remember thinking in 2005 (or 2006?) at the SFN conference that so many posters were being presented on the topic--basically from our program--and it really got people talking since almost no work had ever been done in that field for PD. You can go to the michaeljfox.org and search on inflamation to see more about the grants we funded (you can choose to search our whole site or merely our grants database). This was one of the more basic science programs we funded (along with protein degradation) to open up new areas of inquiry...I believe these early grants provided data and insights that lead to more funding at NIH on the topic.

Debi

Debbie, it is getting too technical for me too!!
Before I studied PD, I thought of inflammation as a bad thing, like a sore red, inflammed wound. It must have been a bad thing I thought, since we take anti-inflammatory drugs and use anti-inflammatory creams.

Then when I got PD and studied disease, I learned that inflammation that occurs around the infected area helps it to heal. So it is a good thing.
A definition is given as
"Inflammation is a process by which the body’s white blood cells and chemicals protect us from infection and foreign substances such as bacteria and viruses."
http://my.clevelandclinic.org/sympto...d_To_Know.aspx
Yet we still used anti-inflammatories!!!

Now this new theory says, no, it is a bad thing again, inflammation prevents the body recognising a foreign substance and therefore serves as a "hiding place" for "invaders". Gary states,
"The inflammation is not the body trying to fight the infection; it is actually the virus or bacteria deliberately causing inflammation in order to hide from the immune system"
When research makes no progress, (nothing major since sinemet in the last 40+ years), then one or more of your assumptions is wrong. You need to recheck your "facts". By this time, we should know the true nature of inflammation.
Ron