Now that LIPOSOMAL SERUM looks interesting but lets say I had what I was suggesting backwards...
that gene that encodes for catalase gets *attacked* by bacteria.
I asked a question of Amy Proal a Marshall Protocol advocate about how a healthy person might be able to use the Marshall Protocol to kill intracellular bacteria and slow their aging process.
http://bacteriality.com/about-the-mp/
Question is post 106 her answer is post number 108
Her whole website is full of really exciting articles like this one:
http://bacteriality....07/11/18/aging/
“I’m sixty going on sixteen.” “I think that at the moment my brain functions even better than it did when I graduated from college 50 years ago.” “I’m convinced that I will live longer because I’m doing the Marshall Protocol.” Comments like these - which were made by actual patients in the MP phase II study trial - are increasingly common as people reach the later stages of the treatment. In fact, many Marshall Protocol patients who have recovered from inflammatory conditions, such as sarcoidosis, rheumatoid arthritis, diabetes, and others report that recovery feels like “being 20 years younger.”
In a 2006 paper in the Journal of Immunity and Aging, Italian researcher Sergio Giunta argues that inflammation and aging are intricately connected, to the point where the term “Inflammaging” has been coined “to explain the now widely accepted phenomenon that ageing is accompanied by a low-grade chronic, systemic up-regulation of the inflammatory response and that the underlying inflammatory changes are also common to most age-associated diseases.”
Also the following article is fascinating:
http://bacteriality..../07/09/aging08/
Several talks also focused on what are referred to as “senescent” cells - cells that fail to undergo the usual process of cell death and instead enter a stable and essentially irreversible growth-arrest state. Senescent cells have been shown to accumulate with age and with age-related diseases, making it clear that the presence of these cells contributes to the aging process and disease in general. And while the reason behind the formation of senescent cells remains a mystery to the medical community at large, it’s quite probable, at least in my eyes, that senescent cells are simply infected cells.
As Judith Campisi of the Lawrence Berkeley National Library and Buck Institute made clear in a speech, cancerous stimuli often foster the development of senescent cells and, as discussed above, the Th1 pathogens are quite prolific during cancer. But the greatest giveaway that senescent cells are at the mercy of the Th1 pathogens stems from the fact that, as Campisi described, senescent cells are metabolically active and secrete myriad inflammatory cytokines. In my opinion, nothing screams infection more than the release of inflammatory cytokines, since the inflammatory molecules are released by the immune system in response to infection. Campisi also described how, although senescent cells are targeted for clearance by the innate immune system, they are able to defy the immune response by secreting high levels of enzymes called matrix metalloproteinases (MMPs). In my opinion, the creation of these enzymes probably marks yet another way the Th1 pathogens have evolved to alter cellular machinery in order to foster their survival.
Then there’s stem cells. If the rest of our cells can be infected by the Th1 pathogens, then why not our stem cells? Or, can our stem cells be damaged by the cytokines secreted by other infected cells? Indeed, Amy Wagers of Harvard University presented a talk in which she clarified that much of the aging process results when the stem cells can no longer repair the tissues. Wagers stated that her work points towards “a discrete set of metabolic regulators and inflammatory cytokines which may alter the signals that stem cells receive from their environment in aged animals.” Again, the fact that inflammatory cytokines seem to affect stem cell resiliency points to the involvement of chronic infection in stem cell decline.
and
Another doctor was so moved by Dr. Marshall’s speech that, during the dinner before the Sunday poster session, he cornered me in the salad line to let me know how excited he was about the MP’s implications. He said the MP reminded him of a particular Sherlock Holmes short story where Holmes figures out the killer’s identity by looking for a clue in the very place no one had considered. He was referring to an electron microscopy image Dr. Marshall showed during his talk, one of a cell infected by bacteria. The bacteria is inside the human cell– no one thinks to look there! I have seen few people so animated and I was so surprised by his exuberance that I dropped my tray (we were eating in a cafeteria) and my dish shattered on the floor. Whoops!
I'd love to find that picture and I'm hunting around the net trying to find it right now. For now how about an infected blood cell:
Here's the link to Dr Marshall's UCLA aging conference talk overview:
http://www.mfoundati...racts/marshall/
and video:
So there we go... i'm excited and feeling on top of the world... the deathists don't have a leg to stand on if much of aging is caused by chronic intracellular bacteria!
Edited by caston, 10 March 2009 - 04:27 AM.