"The will to believe or disbelieve is neither data nor argument. At this point in the debate, there is a price of admission: one must either give an account of the composition of Q that is more cogent than those proffered hitherto, or explain clearly why such an account does not matter."

I'll add that claiming that an issue is "settled" because a "majority of experts" agree (even though only a small number of them has actually studied the issue in detail) is roughly equivalent to slapping a proverbial fig leaf on the reality that only the "will to believe" is present, and as stated by J.S. Kloppenborg Verbin, this "is neither data nor argument.

Source: the book, "The Sayings Source Q and the Historical Jesus" by Andreas Lindemann (ed.), 2001, page 164.

I found it somewhat amusing that a scholar of the New Testament would make a point that is certainly at least as applicable to those who assert that nobody should even consider questioning "HIV/AIDS." The problem with "HIV/AIDS" is that advocates will not accept its possible refutation, no matter what facts one presents to them (assuming they could even agree about what the "HIV/AIDS" claim actually is). For example, if the "viral load" test is as accurate as is claimed, then one could test "HIV negative" people who are afflicted with an acute bout of the flu. Obviously, such people should test "negative," but what if many test "positive?" Would the "HIV/AIDS" advocates then admit that something is terribly wrong?

February 17, 2007.

When I say "AIDS," I don't mean women who "test positive for HIV" and die of cervical cancer, which is classified as an "AIDS death" in the USA. Instead, I am interesting in those who die young of what are called "opportunistic infections." Of course, there is no way to know all of the things a person who is said to have "died of AIDS" in the USA did to his/her body, or endured for some other reason (such as work-related toxic exposures), but it is possible to examine the evidence and determine whether there is an underlying mechanism that is consistent with the experimental data, such that it is. My sense is that one reason this has yet to be done involves the way almost all scientists seem to view the phenomena they study. They seem to feel the need to argue that there is one cause for "syndromes" that should have only been created in the first place as a first step, but instead ossified into an entity that is viewed as more important than the underlying "disease" mechanism itself. With "HIV/AIDS," a press conference, not a scientific paper containing experimental data, announced to the world that the "probable cause" of "AIDS" had been found. After that, the mainstream media and the "AIDS experts" gradually made stronger and stronger claims about "HIV" causing "AIDS." One can go back and read coverage of this in the major newspapers of the time, such as the New York Times, to see exactly how this transition occurred. Also, a book entitled "Impure Science," by Steven Epstein, documents this phenomenon. Within a couple of years, few scientists were interested in considering whether the "probable cause," according to a small number of scientists, actually was the cause. Rather, most saw that there was a great deal of funding and career advancement opportunities in simply "going with the flow," and were content to force the square pegs of their experimental data into the round holes of "HIV/AIDS" ideology in the studies they were able to get published. My understanding the "immune system" problems often encountered in those said to have "AIDS" is based upon reading a great deal of health, nutritional, and medical literature over the course of several years. Moreover, I decided not to take any ideological notions for granted, but to allow the evidence to lead wherever it did. And this approach has "paid off," as it's now clear that there is indeed a clear underlying mechanism, though there are several factors that can greatly enhance it (or inhibit it), and as I said above, most scientists seem to have great difficulty thinking in a "flexible" way that allows for this. I, on the contrary, was trained as a historian, and I came to understand that it would be ridiculous, for example, to argue that Julius Caesar "caused" the downfall of the Roman Republic.

I will start with the best explanation put forth by scientists to date. The "Perth Group" has an "oxidative stress hypothesis," but they don't talk about what the body does when there are a great deal of oxidized molecules in the body (from what I've read of their work). Instead, most if not all who propose this kind of explanation talk about how it would affect the CD4 T "helper" cells. However, there is another model that is worthy of consideration, because it has a similar effect, and that is the heart disease/oxidized cholesterol one. Basically, the body attacks oxidized cholesterol as if it were "foreign" and potentially dangerous. If there is too much oxidized cholesterol, it causes macrophages to become dysfunctional, and they can accumulate in arteries, causing narrowing in an ongoing chronic inflammtory process. Clearly, if one does things like takes certain drugs, there will be plenty of oxidized molecules, and they could cause the lymphadenopathy characteristic of early stages of "AIDS," as most US doctors encounter it. At some point, the "immune system" loses the ability to tell the difference between "self" and "foreign" because there are so many kinds of similar molecules - when molecules get oxidized, they do so in diffferent ways. There are at least several different kinds of "oxidized cholesterol" molecules, for example. At some point this element of the "immune system" ("Th1") must be "shut down" in order to avoid an "all out attack" on all molecules that resemble the oxidized ones, and that includes molecules crucial for basic life functions. The CD4 T helper cells do this, and the "experts" have mistaken this phenomenon as a sign of "retroviral infection," apparently due largely to a lack of scientific imagination and a ideological belief in the "germ theory."

There is a "disease" that is similar to the "early stages of AIDS," and that is MAS. I will now quote an abstract of a study about this disease: QUOTE:"OBJECTIVE: To review and analyze the clinical features, treatment, and outcome of macrophage activation syndrome (MAS) in children with systemic onset juvennil rheumatoid arthritis (SOJRA). METHOD: Retrospective review and analysis were performed on cases with MAS from a prospectively collected database of children with SOJRA from the year of 2003 to 2006 in the Hospital. RESULTS: Twenty four patients (21 boys, 3 girls) were diagnosed as having MAS with SOJRA. Mean age of the patients with MAS at diagnosis was 7 years, and the duration prior to diagnosis of MAS was 12 months. No trigger factors were found except in one case whose MAS was triggered by use of methotrexate and in another by parvovirus B19 infection. High grade fever, new onset hepatosplenomegaly and lymphadenopathy, pancytopenia, liver dysfunction were common clinical features in all the 24 cases (100%). Bleeding from skin, mucous membrane and gastrointestinal tract were noted in 9 cases (38%). Twelve (50%) cases had CNS dysfunction (high intracranial pressure, seizure and coma). Six cases (25%) developed ARDS. One patient suffered from renal damage. The laboratory test revealed elevated live enzymes and ferritin, decreased value of ESR, albumin, complete blood count and fibrinogen in all the 24 cases. Bone marrow examination supported the diagnosis of definite hemophagocytosis in the 24 cases. Lymph node biopsy was done for one case and histopathological examination showed that the node was full of activated macrophage. As to treatment, five cases only received high dose steroids (three of them died), 14 cases were treated with high dose steroids plus cyclosporine (one died), two were treated with steroids plus cyclosporine and etoposide (none died). The causes of deaths were ARDS and CNS involvement. In three of the cases who died, treatment was given up by their parents. CONCLUSIONS: MAS is a rare and potentially fatal complication of SOJRA. Most of our patients were male. Bone marrow studies support the diagnosis. CNS involvement and ARDS were poor prognostic signs. Early diagnosis and aggressive therapy are essential." UNQUOTE.

Source: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17274865&query_hl=1&itool=pubmed_docsum

The "opportunistic infections" of "AIDS" occur when the body puts a halt to a "MAS"-like condition, thereby preventing serious damage from taking place. When one examines literature of cholesterol oxidiation, there is an obvious connection to this MAS-like phenomenon: QUOTE: Atherosclerosis. 1994 Nov;111(1):65-78.

Iron induces lipid peroxidation in cultured macrophages, increases their ability to oxidatively modify LDL, and affects their secretory properties."

Fuhrman B, Oiknine J, Aviram M.

The present study demonstrates for the first time that iron ions can induce lipid peroxidation in intact macrophages without causing cell death. Macrophage lipid peroxidation increases cell-mediated oxidation of LDL, enhances the release of interleukin 1... UNQUOTE.

Interleukin 1 (IL-1) is considered a "pro-inflammatory" cytokine and the following is characteristic of how "HIV/AIDS experts" view it: QUOTE: While some cytokines may promote or restore immunity, some can accelerate HIV replication and are associated with disease progression. Cytokines associated with inflammation, such as IL-1, IL-6 and TNF-alpha, have been associated with increased viral replication, wasting syndrome and progression of Kaposi’s Sarcoma... UNQUOTE.

Source: http://www.projinf.org/pip/14/pip14i.html

This is also true for IL-8, but it's not just for "HIV/AIDS," but for "heart disease" as well. For example: QUOTE: Oxidized low-density lipoproteins play important roles in the development of atherosclerosis and contain several lipid-derived, bioactive molecules which are believed to contribute to atherogenesis. Of these, some cholesterol oxidation products, referred to as oxysterols, are suspected to favor the formation of atherosclerotic plaques involving cytotoxic, pro-oxidant and pro-inflammatory processes. Ten commonly occurring oxysterols (7alpha-, 7beta-hydroxycholesterol, 7-ketocholesterol, 19-hydroxycholesterol, cholesterol-5alpha,6alpha-epoxide, cholesterol-5beta,6beta-epoxide, 22R-, 22S-, 25-, and 27-hydroxycholesterol) were studied for both their cytotoxicity and their ability to induce superoxide anion production (O2*-) and IL-8 secretion in U937 human promonocytic leukemia cells. Cytotoxic effects (phosphatidylserine externalization, loss of mitochondrial potential, increased permeability to propidium iodide, and occurrence of cells with swollen, fragmented and/or condensed nuclei) were only identified with 7beta-hydroxycholesterol, 7-ketocholesterol and cholesterol-5beta,6beta-epoxide, which also induce lysosomal destabilization associated or not associated with the formation of monodansylcadaverine-positive cytoplasmic structures. No relationship between oxysterol-induced cytotoxicity and HMG-CoA reductase activity was found. In addition, the highest O2*- overproduction quantified with hydroethidine was identified with 7beta-hydroxycholesterol, 7-ketocholesterol and cholesterol-5beta,6beta-epoxide, with cholesterol-5alpha, 6alpha-epoxide and 25-hydroxycholesterol. The highest capacity to simultaneously stimulate IL-8 secretion (quantified by ELISA and by using a multiplexed, particle-based flow cytometric assay) and enhance IL-8 mRNA levels (determined by RT-PCR) was observed with 7beta-hydroxycholesterol and 25-hydroxycholesterol. None of the effects observed for the oxysterols were detected for cholesterol. Therefore, oxysterols may have cytotoxic, oxidative, and/or inflammatory effects, or none whatsoever.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=16142584

Now, if you read the following study abstract about findings concerning "HIV/AIDS," you should be able to see that it is very likely that the same mechanism is at work, though the tissue involved is different (and accounts for the different symptoms): QUOTE: An important role for selenium in human immunodeficiency virus (HIV) disease has been proposed. Decreased selenium levels, as found in persons with HIV infection or AIDS, are sensitive markers of disease progression. Selenium deficiency, an independent predictor of mortality in both HIV-1 infected adults and children, is an essential micronutrient that is associated with an improvement of T cell function and reduced apoptosis in animal models. In addition, adequate selenium may enhance resistance to infections through modulation of interleukin (IL) production and subsequently the Th1/Th2 response. Selenium supplementation up-regulates IL-2 and increases activation, proliferation, differentiation, and programmed cell death of T helper cells. Moreover, selenium supplementation may down-regulate the abnormally high levels of IL-8 and tumor necrosis factor-alpha observed in HIV disease, which has been associated with neurologic damage, Kaposi's sarcoma, wasting syndrome, and increased viral replication. Together, these findings suggest a new mechanism through which selenium may affect HIV-1 disease progression.

http://www.journals.uchicago.edu/cgi-bin/resolve?id=doi:10.1086/315911&erFrom=-5611785506958785470Guest

I can't emphasize strongly enough that as far as I'm concerned, there is no one "AIDS," except as a socio-political entity perhaps. Instead, it makes much more sense to investigate "from the inside out," that is, to carefully observe how the patient is living (and has lived) in order to understand how that lifestyle is causing certain molecular-level phenonema to occur. There is no technological barrier to this endeavor, but the "medical establishment" demands a sense of certainty (as does the general public), and the textbook categorizations supply this (and the drug companies need to craft their "medicines" to specific "diseases"). Even on the fictional TV show "Dr. House," though a thorough investigation is often performed (sometimes including actually going to the patient's residence for "evidence"), the resolution invariably involves matching up the patient's problems to a textbook entity (often a "rare" one). I was taught to look beyond what is considered the "standard," and while I understand why doctors are reluctant to do this, in light of all the promises of "cures" that have never occurred as well as the dire predictions of all kinds of health "epidemics" (along with ones that are supposed to be in full force already), it is an affront to basic common sense to brush aside alternative approaches. Some of you may be saying to yourselves, "this sounds like evidence-based medicine, so what is new about your idea?" Evidence with an improper interpretation of it can be worse than no evidence at all. Moreover, there can be a huge difference in the kind of "evidence" used (and much evidence is ignored). For example, the mainstream media often reports on epidemiological studies, but epidemiologists can only be as good as the underlying assumptions, which, if flawed, can produce results that lead to horrendous advice. Instead, molecular-level evidence should be taken much more seriously than it presently is.