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I thought I'd devote this thread to studies (or their abstracts) or reports that support a comprehensive understanding of "disease," meaning that the connection between phenomena like "inflammation," "autoimmune disease," immune system failure (such as "AIDS") and things like dietary PUFAs, is addressed:
http://www.pasteur.fr/applications/euroconf/nutrition/3_Strandvik_abstract.pdf
Also, see some of the abstracts at:
http://www.issfal.org.uk/index.php?option=com_content&task=view&id=81&Itemid=113%20
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This new report demonstrates that some scientists have "the right idea" about the role of inflammation in chronic disease, but of course they don't mention (are likely have no idea) that the kinds of fatty acids in your cells (which can be manipulated with diet) make a huge difference in this context, as I've tried to explain on this site in various essays and posts:
QUOTE: Drugs that have helped treat millions of rheumatoid arthritis sufferers may hold the key to many more medical conditions, including atherosclerosis -- a leading cause of heart disease -- says the researcher who jointly invented and developed them...
The drugs target proteins called cytokines, which are protein messaging molecules released by immune cells to alert the immune and other systems that the body is under attack from a pathogen and to initiate a protective counter-response against the infection.
"In autoimmune diseases, such as arthritis, we discovered that cytokines are over-produced causing the immune system to fight itself, resulting in inflammation and tissue destruction," said Professor Feldmann, from Imperial College London, who is speaking at the EPHAR 2008 conference at The University of Manchester the week of July 18.
"We further found that by blocking just one cytokine -- Tumor Necrosis Factor (TNF) alpha -- we were able to block all the cytokines involved in the inflammation, with remarkable clinical results..." UNQUOTE.
Source: http://www.sciencedaily.com/releases/2008/07/080717193027.htm |
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Here is what I'd call a "smoking gun," and not just for "HIV/AIDS," but for the arachidonic acid/"chronic inflammation" view of "disease:"
QUOTE: "...During both HIV infection in humans and SIV infection in macaques, the host immune system becomes highly activated, experiences increased destruction and decreased production of key immune effector cells and progressively fails as a result. In contrast, natural hosts for SIV infection, like sooty mangabeys, do not exhibit aberrant immune activation and do not develop AIDS despite high levels of ongoing SIV replication. Our studies sought to understand the basis for the very different responses to AIDS virus infections in different species," says Mark Feinberg, MD, PhD, the paper's senior author. Feinberg is a former investigator at the Emory Vaccine Center and the Yerkes Research Center and a professor of medicine at the Emory University School of Medicine. He currently serves as vice president of medical affairs and policy for vaccines and infectious diseases at Merck & Co., Inc.
The reasons are found in significant differences in immune signaling in a specific type of dendritic cells in AIDS-susceptible or resistant host species. Dendritic cells are part of the immune system that play a key role in alerting the body to the presence of invading viruses or bacteria, and in initiating immune responses that enable clearance of these infections. They detect the invaders using molecules called Toll-like receptors.
Feinberg's team found that in sooty mangabeys, dendritic cells produce much less interferon alpha--an alarm signal to the rest of the immune system--in response to SIV. As a result, the dendritic cells are not activated during the initial or chronic stages of SIV infection, and mangabeys fail to mount a significant immune response to the virus. In contrast to mangabeys, dendritic cells from humans and macaques that are susceptible to developing AIDS are readily activated by HIV and SIV.
The difference in whether or not dendritic cells become activated upon AIDS virus exposure in specific primate hosts appears to result from species-specific differences in patterns of Toll-like-receptor signaling. Because host immune responses are unable to clear AIDS virus infections, ongoing virus replication leads to unrelenting activation of the immune system in humans and macaques.
Unfortunately, rather than promoting clearance of the infection, chronic dendritic cell stimulation may result in chronic immune activation and significant unintended damage to the immune system in AIDS-susceptible species. Such chronic immune activation is now recognized to be a major driving force for the development of AIDS.
The observation that mangabey dendritic cells are less susceptible to activation by SIV may explain why mangabeys do not exhibit abnormal immune activation and do not develop AIDS. Thus, in mangabeys, the generation of a less vigorous immune response to SIV may represent an effective evolutionary response to a virus that is so resistant to clearance by antiviral immune responses... UNQUOTE.
Source: http://www.sciencedaily.com/releases/2008/09/080916143900.htm
Of course, it's crucial to determine if the more resistant animals have no AA or less AA in their cells than the ones that die of "AIDS," but these "scientists" are not pursuing their investigation objectively, nor with full knowledge of how chronic inflammatory issues can be controlled or lessened significantly. Instead, as is often the case today, very useful findings are filtered through lenses that don't allow the light of truth to come through. Rather, they see what they want to see, and this results in ridiculous explanations about what "HIV" does, in this particular case
The kind of problem they describe here is not uncommon, and can be replicated by doing things to organisms that do not involve "infectious disease," such as drug abuse. And in science, one needs to control all possible variables before one posits a formal hypothesis. Moreover, a virus can't do what they are arguing here, unless the conditions that allow it are present, such as a great deal of "oxidative stress" (which can occur with drug abuse). Thus, even if one believes "HIV" exists and can cause some amount of cell death, it could be controlled by altering the conditions that make it so active that it causes dangerous cell death and/or chronic inflammation. The claims often made by these folks, such as that "HIV" is "wiley," "mysterious," or possesses some sort of incredible cunning, are beyond ludicrous, and makes one think that such people have been watching too many science fiction movies. |
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And, coincidentally, on the same day the report from the post above appeared, so did this one:
QUOTE: ...In battles against chronic infections, the body's key immune cells often become exhausted and ineffective. Researchers at The Wistar Institute have found a way to restore vigor to these killer T cells by blocking a key receptor on their surface, findings that may advance the development of new therapies for diseases such as HIV, hepatitis B and C, and cancer...
Researchers have known that T cells �?white blood cells capable of inducing the death of infected or cancerous cells �?become progressively less functional over time. In earlier studies, Wherry and his colleagues found that, during the course of a chronic infection, gene expression in killer T cells changed dramatically as the cells became exhausted and immune response to a pathogen slowed down... UNQUOTE.
Source: http://www.sciencedaily.com/releases/2008/09/080915174546.htm
The key point here is they are talking of this cause of immune system failure or dysfunction, but when it comes to "HIV/AIDS," they don't even question the possibility that this might have been what the original "AIDS" deaths were due to, most likely in conjunction with drug abuse (legal or otherwise) or other things known to suppress the immune system.
Of course, if you read the post above, you should realize that it's not a straightforward issue. Certain kinds of stressors cause certain cells to produce and secrete dangerous molecules, such as IFNs and TNFs. It is the combination of too much of these substances and less activity among certain cells (specific T cells) that can lead to "AIDS," without "HIV" or any real virus. Looking at the evidence comprehensively, it appears that when a person has arachidonic acid in his/her cells, the kind of very dangerous chronic inflammation that can cause "AIDS"-like conditions (among other things) is to be expected, if certain stressors are present.
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