Tuesday, November 11, 2008

42 nd page of the old MSN site.

A unified "AIDS" hypothsis without "HIV." Part II.

Whatever “HIV/AIDS” is now (apologists have refused repeatedly to provide a hypothesis for it), one point is crucial; the way it is presented to the general public makes it an impossibility to “cure.” That is, there will never be a way to demonstrate scientifically (down to the molecular level) how a few “retroviral” particles cause an “HIV infected” woman to die of cervical cancer, for example. Instead, there will likely be more “models” presented (such as David Ho’s impossible scenario about how the “virus” destroys the T cells in question) that are little more than a child’s fanciful wishes. Thus, funding for “HIV experts” will continue, as will profits for pharmaceutical companies that produce “medicine” designed to “fight HIV.” What’s interesting, sociologically, is that this is how many “conspiracy theories” likely start out, that is, in retrospect, it appears to nicely fit together to help a few people at the expense of millions, and so some conclude that the few who benefit greatly planned it all out from the beginning. My sense is that the appeal of the “germ theory” for those in charge of the “biomedical establishment” came to dovetail with what major pharmaceutical companies had to offer, and politicians wanted to be able to reassure an anxious public. The irony, of course, is that a sense of certainty was bought at a very high price, because almost all resources have been devoted to various aspects of the ludicrous “HIV/AIDS” notion, which is now impossible to cure due to the way it is perceived.

A recent report makes the same point about "IBS" that I'm making for "HIV/AIDS:" QUOTE: Irritable bowel syndrome (IBS) is a common gastrointestinal disorder in the developed world. It is characterized by altered bowel function, abdominal discomfort, and pain. However, there are few effective treatments for IBS, in part because the molecular mechanisms underlying the disease symptoms have not been well defined. UNQUOTE.

Source: http://www.sciencedaily.com/releases/2007/02/070215181503.htmp

In any case, what I am interested in doing involves trying to understand what the molecules in question are doing and what can be done to restore normal physiology and biochemistry. Most “HIV experts,” of course, think that they need to devise a way to “kill the germs,” not realizing that germs are almost always a problem due to conditions, and not because of some inherently malevolent quality. And they are basically repeating the many of the same mistakes made in the “war on cancer,” particularly in terms of using highly toxic “medicines” or “therapies,” which will often result in killing the patient anyway (though he or she may live a few more months). After teaching the scientific method to college students for many years, and after researching “HIV/AIDS” and related issues for several years, it is obvious to me that controlled experiments should be conducted in which those said to be “HIV infected” change their lifestyles so that they are subject to very little stress (especially oxidative), rather than taking very toxic “medicines” aimed at destroying particles that are just effects of the stress that led to the “positive” “HIV” test in the first place. Instead, such people are sometimes told to avoid “doing drugs” that may lead them to becoming “uninhibited,” leading to “unprotected sex” and exposure to a “deadly retrovirus.” When they “test positive for HIV” or “develop AIDS,” the sex is blamed rather than the drugs (as there is almost always one episode of “unprotected sex” that has occurred), even though the drugs many young people use generate a lot of oxidative stress, particularly in the context of being “overloaded” with arachidonic acid. Since we can all probably agree that such an experiment will not be undertaken any time soon, one must rely upon the evidence that now exists, and fortunately, as the studies I cited in Part I demonstrate, there are many studies that are highly suggestive of one underlying mechanism, though with several “co-factors” that can enhance this mechanism. Moroever, as I have seen in the nutrition field, even if the right experiments were conducted, those in charge could simply dismiss them for some reason, and most of the "mainstream media" seem all too willing to just assume that whatever this small number of people claims is correct, for whatever reason.

One interesting point about the “HIV/AIDS” story is that it “makes sense” to most people (in terms of their “germ theory” preconceptions), and most can’t imagine that the claim (s) is based upon indirect and non-specific “markers” that correlate to some degree with what is conceived as the clinical syndrome, “AIDS,” though this syndrome (basically, a list of symptoms, some of which are considered “diseases”) has changed over time, for reasons that make little sense to me. I encountered a very similar situation when I began my research in the nutrition field, and was disappointed to see the same kinds of mistakes made in a field that I thought would be more scientifically rigorous. As with “HIV/AIDS,” the nutritional “story” is easier for almost everyone to think that they understand compared to trying to think about what is actually occurring biochemistry. The incoherent nature of the nutritional story is not problematic, as nutritionists themselves don’t seem to realize how silly some of their claims and organizing principles are, and so the “average” person just “goes along with the program,” no matter how unsatisfactory the results. What’s even more disappointing is how some biochemists actually “step aside” and accept nutritional claims that violate a basic understanding of biochemistry. An example of this can be found in a book like "The Cookbook Decoder" (1981), written by chemistry professor Arthur E. Grosser. In this book, the chemist tells people not to be "haunted by morbid thoughts of sagging stomachs or fatty deposits clogging our arteries..." in the context of making a sauce, because corn starch can be used, presumably instead of something like cream (page 141). Though it may not have been clear that only oxidized cholesterol was dangerous when this book was published in 1981, it is obvious that this chemistry professor simply assumed that whatever the nutritionists say about the health benefits (or hazards) of certain foods is accurate. Instead, biochemists should take every opportunity to point out that when nutritionists advise people to do things like “be sure to use heart-healthy unsaturated fats” they are actually telling people to expose themselves to incredibly toxic molecules (in terms of the way most Westerners prepare their food).

Getting back to "AIDS;" while, as the Perth Group argue, potent oxidative stress (probably much more problematic in cells containing arachidonic acid) can cause the T cell dysfunction/Th1 to Th2 shift that leads to the "opportunistic infections," and probably some of the other "AIDS"-related disorders, there is the "heart disease" model as well. Applying this to "AIDS," the following sequence of events likely occurs in many who have "progressed top AIDS:" a great deal of oxidized molecules are present, which can be due to a number of things, and then lymphadenopathy often occurs. The "inflammation" that accompanies having too many oxidized molecules in the body can then cause the T cell dysfunction and Th1/Th2 shift. Below are some studies that are supportive of this possibility:

1. Eur J Immunol. 2003 Aug;33(8):2178-85.

Title: Oxidative-stress-induced T lymphocyte hyporesponsiveness is caused by structural modification rather than proteasomal degradation of crucial TCR signaling molecules.

Cemerski S, van Meerwijk JP, Romagnoli P.

Tolerance and Autoimmunity section, INSERM U563, Toulouse, France.

QUOTE: In several human pathologies (e.g. cancer, rheumatoid arthritis, AIDS and leprosy) oxidative stress induces T cell hyporesponsiveness... UNQUOTE.

2.

QUOTE: ...deficient allergen-specific Treg cell responses have been associated with a number of allergic and autoimmune disorders. Tolerization to allergens and autoantigens is associated with augmentation of Treg cell numbers and suppressive function... UNQUOTE.
Source: Journal of allergy and clinical immunology, 2005, vol. 116, no5, pp. 949-959 [11 page(s) (article)] (121 ref.).

3.

QUOTE: Microparticles are membrane-derived vesicles that are released from cells during activation or cell death. These particles can serve as mediators of intercellular cross-talk and induce a variety of cellular responses. Previous studies have shown that macrophages undergo apoptosis after phagocytosing microparticles. Here, we have addressed the hypothesis that microparticles trigger this process via lipid pathways. In these experiments, microparticles induced apoptosis in primary macrophage cells or cell lines (RAW 264.7 or U937) with up to a 5-fold increase... To evaluate further signaling pathways induced by microparticles, the extracellular signal regulated kinase (ERK-) 1 was investigated. This kinase plays a role in activating phospholipases A2 which cleaves membrane phospholipids into arachidonic acid; microparticles have been suggested to be a preferred substrate for phospholipases A2. As shown in our experiments, microparticles strongly increased the amount of phosphorylated ERK1/2 in RAW 264.7 macrophages in a time-dependent manner, peaking 15 min after co-incubation. Addition of PD98059, a specific inhibitor of ERK1, prevented the increase in apoptosis of RAW 264.7 macrophages. Together, these data suggest that microparticles perturb lipid homeostasis of macrophages and thereby induce apoptosis. These results emphasize the importance of biolipids in the cellular cross-talk of immune cells. Based on the fact that in clinical situations with excessive cell death such as malignancies, autoimmune diseases and following chemotherapies high levels of circulating microparticles might modulate phagocytosing cells, a suppression of the immune response might occur due to loss of macrophages. UNQUOTE.
TITLE: The role of membrane lipids in the induction of macrophage apoptosis by microparticles.
SOURCE: Apoptosis. 2006 Dec 26.
4. QUOTE FROM THE ABSTRACT: C57B16 mice were fed for 6 weeks on a low-fat diet or on high-fat diets containing coconut oil (rich in saturated fatty acids), safflower oil [rich in n-6 polyunsaturated fatty acids (PUFAs)], or fish oil (rich in n-3 PUFAs) as the main fat sources. The fatty acid composition of the spleen lymphocytes was influenced by that of the diet fed... The ratio of production of Th1- to Th2-type cytokines (determined as the IFN-gamma/IL-4 ratio) was lower for lymphocytes from mice fed the safflower oil or fish oil diets... It is concluded that saturated fatty acids have minimal effects on cytokine production. In contrast, PUFAs act to inhibit production of Th1-type cytokines with little effect on Th2-type cytokines; n-3 PUFAs are particularly potent. The effects of fatty acids on cytokine production appear to be exerted at the level of gene expression. UNQUOTE.
Source: J Leukoc Biol. 2001 Mar;69(3):449-57. "Dietary fatty acids influence the production of Th1- but not Th2-type cytokines," by Wallace, FA, et al.
5. TITLE: Programmed Cell Death Protects Against Infections.

QUOTE: ...For more than hundred years it was known that neutrophil granulocytes kill bacteria very efficiently by devouring them. After eating the germs neutrophils kill tehm with antimicrobial proteins...

...scientists...discovered a second killing mechanism: neutrophil granulocytes can form web-like structures outside the cells composed of nucleic acid and enzymes which catch bacteria and kill them...

...Only after lengthy live cell imaging and biochemical studies it became clear how neutrophils make NETs. The cells get activated by bacteria and modify the structure of their nuclei and granules, small enzyme deposits in the cytoplasm.

"The nuclear membrane disintegrates, the granules dissolve, and thus the NET components can mingle inside the cells", explains Volker Brinkmann, head of the microscopy group. At the end of this process, the cell contracts until the cell membrane bursts open and quickly releases the highly active melange. Once outside the cell, it unfolds and forms the NETs which then can trap bacteria.

Surprisingly, this process is as effective as devouring bacteria... UNQUOTE.

Source of the quoted material: http://www.sciencedaily.com/releases/2007/01/070110124142.htm

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