HIV/AIDS Skepticism

Pointing to evidence that HIV is not the necessary and sufficient cause of AIDS

Defenders of the HIV/AIDS Faith: Why Anonymous?

Posted by Henry Bauer on 2008/11/06

I’ve used the Internet pretty much from its inception, at first chiefly for e-mail, of course. I tried a few on-line lists, groups, discussions on various topics pertinent to my academic interests — for example, fraud in science — or on my hobbies — Loch Ness monsters, say. These were open to all who wanted to participate, and participants were open about their identity; electronic communication was just adding some speed and convenience to exchanges that we’d been engaged in via letters, conferences, phone calls.

Some of the discussion groups touched on fairly controversial matters, like political correctness and associated sensitive topics like race, IQ, affirmative action. Still, we knew who everyone was, where they worked, what their professional credentials were; and — possibly for that reason — lack of civility was rare, even as disagreements could be stark and forcefully expressed; ad hominem innuendo or direct attacks didn’t feature. I didn’t stay long with any list or discussion, though, because I so rarely learned anything new.

I came late to the ranks of HIV/AIDS Rethinkers and Skeptics. It was around 1995 that I first discovered, through reading Ellison & Duesberg, “Why we will NEVER win the war on AIDS”, that some people question whether HIV is the cause of AIDS — people with impressive and relevant credentials. I was sufficiently intrigued to read more. Bialy’s scientific biography of Duesberg caused me to consult primary sources about HIV tests, and thereby to discover that “HIV” is not infectious and doesn’t correlate with “AIDS”. Astonished, bemused, I looked for people with whom I could discuss the matter, and that caused me to visit, and sometimes to send comments and questions to, a number of web-sites and blogs. In too many cases, I was appalled at the level of “flaming” as well as the lack of substantive discussion, indeed the prevalence of violently asserted claims on factual matters without the benefit of supporting citations to reliable publications.

Those experiences informed my decisions when I set up this present blog as a means of furthering substantive discussion:

“All comments are moderated, and may be edited.
I have a  great preference for comments that are concise, substantive, and not ad hominem.
Giving a fake e-mail address makes it less likely that your comment will be accepted.
. . .  please understand that I can only respond if the e-mail address you give is a valid one. For example, e-mails cannot be delivered to ‘anonymous@anonymous.com’.”

Because of the blog, I’ve learned a great deal from commentators and correspondents, and I’ve been stimulated to look into an increasing range of HIV/AIDS-related matters. Tony Lance provided to the salient question, “So what did cause AIDS?”, a highly plausible suggestion supported by a large variety of published evidence [“What really caused AIDS: Slicing through the Gordian Knot”, 20 February 2008]. Invitations to comment on various “news” items led me to look, for the first time, into statistics about deaths from “HIV disease”, and to discover another clear disproof, or set of disproofs, of HIV/AIDS theory [“’HIV Disease’ is not an illness”, 19 March 2008;  “HAART saves lives — but doesn’t prolong them!?”, 17 September 2008]. I’ve heard from a number of individuals who have experienced at first hand the psychological and physical damages wrought on healthy people by diagnoses of “HIV-positive” followed by antiretroviral “therapy”; and those interactions in particular keep me constantly aware of how important it is that HIV/AIDS theory be publicly discarded.

But I’ve also learned quite a lot about the deplorable behavior of fanatical HIV/AIDS true-believers, groupies, and vigilantes [“Dissenting from HIV/AIDS theory”, 8 December 2007]. It’s not only the disgustingly ad hominem nature and sadly lacking-in-intellectual-substance content of so many of the “mainstream” HIV/AIDS blogs, I’ve also been taken aback at underhanded approaches, via comments sent to my blog as well as e-mails to me direct, from individuals (I suppose individuals, but of course it could be groups) whose purpose is not to discuss substantive issues but to find ways to discredit and undermine AIDS Rethinking. For example, a graduate student evidently took the trouble to read my memoir about academic deaning and at least some  issues of a newsletter that I had edited for a number of years in order to mis-interpret as homophobic and racist a few out-of-context quotes in a “review” of my book on amazon.com (that review is no longer there, at one time there was a note that it had been withdrawn by the author, but even that note is no longer there). Another vigilante posed as a graduate student in personal e-mails to me, fishing for information about Rethinker doings. Several comments have been submitted anonymously to my blog — for example by “Fulano de Tal” [“John Doe and his ilk: pitfalls of pseudonymity”, 28 August 2008], alleging mistakes in factual matters, yet when I requested citation of sources for those facts, I never heard more.

Those communications led me to ponder the apparently common practice of participating anonymously in Internet discussions. Why would one do that? (I would be interested to learn of any scholarly discussions of Internet anonymity, how the practice started, what justifications there might be for it, and so on.)

I can’t bring myself to engage in discussion with people who are unwilling to tell me who they are. It throws immediate doubt on their bona fides. Signing one’s name to one’s opinions seems to me the natural as well as proper thing to do, and I’m one of those who always signed manuscript reviews even when the journal policy did not require it. I think it’s a useful form of self-discipline, to ensure that one is being as honest and unbiased as humanly possible.

I can understand why whistle blowers must practice anonymity — except with the appropriate investigating authority to whom they bring grievance; and I understand why HIV/AIDS Skeptics are sometimes forced to remain anonymous in view of the career-threatening activities boasted of by people of the ilk of Wainberg and Moore (“AIDS and the dangers of denial”, Globe and Mail, 4 July 4 2007). But why would AIDStruth groupies and other supporters of mainstream views be unwilling to communicate openly and honestly? What are they afraid of? Do they sense subconsciously that they have no substantive grounds to stand on and that they must fight by innuendo and attempted character assassination? Why are they ashamed to let others know who they are?

14 Responses to “Defenders of the HIV/AIDS Faith: Why Anonymous?”

  1. Tom Saville said

    Hi Dr Bauer

    Following up the reference to intestinal dysbiosis, I forwarded Tony Lance’s paper to a senior biologist with experience in the field who is also skeptical of the HIV = Aids hypothesis. I am copying the reply with permission for your consideration here.

    With best wishes, Tom

    REPLY:

    I don’t think dysbiosis could cause a deficiency in lymphocytes, but just the opposite; it triggers the proliferation of lymphocytes and other kind of antibodies which lead to a hyper-reaction of the immune system. This is an allergic condition, not an immunological deficiency. I concede that the clinical tests give false positives because many diseases and biochemical conditions could give false positives, but it is not AIDS, by no means.

    If we continue stumbling from one cause to another we won’t be taken seriously by the scientific community. The same thing is happening today with respect to AGW; each academic throw his own hypothesis about global warming into the ring without centering in on one obvious cause, the Sun. For example, there are about 1400 new hypotheses on the cause of global warming as if it existed; the last compels external censors not to take real science seriously and for those promoting AGW to laugh at us. I think we should stop emitting weird hypotheses on something which is not real.

    The same management must be applied to AIDS. If HIV doesn’t exist, we must concentrate our batteries on the real target, which is the antiretroviral medicine. The HIV-positive condition can be given by many factors other than an exotic virus which has not been individually detected nor isolated. On the other hand, leaky gut is historically a very wide-ranging disease produced by imbalance of symbiotic microorganisms in the intestine, i.e. dysbiosis. However, dysbiosis produces lymphocytosis, which is an increase in the number or proportion of lymphocytes in the blood, while AIDS is the opposed condition, that is to say, collapse in the number or proportion of lymphocytes in the blood.

  2. Henry Bauer said

    Tom:

    Many thanks. I’ve drawn Tony Lance’s attention to this and I hope he will respond.

    My own impression, definitely subject to correction by Tony, is that dysbiosis, destruction of necessary microflora, destroys the bugs that keep endemic fungi in check, and can induce “leaky gut syndrome” whereby stuff can get into the bloodstream to produce a false-positive HIV result. In other words, intestinal dysbiosis can produce AIDS (PCP, Candida) and “HIV+”. Lymphocyte (CD4) counts may be irrelevant.

    I certainly accept the point that lack of consensus among HIV/AIDS skeptics serves as yet another opening for the defenders of the faith to castigate us. I believe that the basic initiative must be to demonstrate that published data disprove the HIV/AIDS hypothesis. But we’ve done that. The data in my book show that “HIV” isn’t infectious and that “HIV” doesn’t correlate with “AIDS”; moreover, that “HIV+” signifies a very non-specific immune-system response or presence of proteins, RNA, maybe other stuff generated under physiological stress. A blog post has shown that HAART doesn’t in fact lengthen lives: “HAART saves lives — but doesn’t prolong them!?”, 17 September 2008.
    https://hivskeptic.wordpress.com/2008/09/17/haart-saves-lives-but-doesn’t-prolong-them/

    Having proved that HIV didn’t cause AIDS, though, opens the question, so what DID cause AIDS? What were people dying of? So skeptics are really obliged to present suggestions, and since the research was never done, naturally there’s no consensus.

    To my mind, Lance’s hypothesis of intestinal dysbiosis is a very plausible partial answer; together with poppers as the cause specifically of KS. I think Duesberg’s drug-AIDS hypothesis is an additional partial answer for the early 1980s, and assumes increasing importance after the introduction of AZT and the expanding definitions of “AIDS”.

    Your correspondent seems to accept, in the third paragraph, the definition of AIDS as decreased CD4 counts. But those don’t correlate with clinical condition (Rodriguez et al., JAMA, 2006, 296: 1498).

  3. Macdonald said

    Let us not forget that part of the proposed mechanism of cell depletion is precisely a hyperstimulation of the immune system, rapid turnover of CD4 cells etc. On some accounts, an initial and/or periodic CD4 cell boost is part of “HIV disease” progression.

    The drop in CD4 cells is real, even if the virus is not, and it is important for Rethinkers to attempt to figure out what is going on when the CD4 cell count drops, and what it means in each case.

    As with all other aspects of this, we are probably not going to find a single mechanism or condition to account for the various kinds of AIDS — or even the various kinds of CD4 cell loss, and most of us are not medically qualified, but until medically qualified peope do join the debate in earnest, informed layman’s speculation will have to do.

  4. Tom Saville said

    Henry:

    Thank you for informing Tony Lance of my post and for responding so promptly. I will forward your reply to my friend and report back in due course. Perhaps I can persuade him to join the discussion.

    With best wishes, Tom

  5. Henry Bauer said

    Macdonald:

    Lowered CD4 counts in the peripheral blood doesn’t mean depletion, those cells move around the body according to where they’re needed, according to Dr. Juliane Sacher. She mentions studies but doesn’t cite them, but I’ve since seen the same statement elsewhere, I’ll give citations next time I come across something like that again.

    Still, as you say, in each instance it would be good to enquire why the cells are needed somewhere else!

  6. MacDonald said

    Prof Bauer,

    By “depletion” I didn’t mean the CD4 cells were necessarily killed off, although I do think it’s quite possible they are in some cases. The Perth Group brings more aspects to our attention, notably the hypothesized (by mainstream) phenotype change:

    “In 1984 both Montagnier and Gallo knew that a decrease in the number of T4 cells (measured by antibody binding) is not proof the cells are dead. The decrease is “probably due to either modulation of T4 molecules at the cell membrane or sterile hindrance of antibody-binding sites”. (The “HIV” experts including Baltimore, now call it CD4 down-modulation (Chen et al J Virol, Vol 70 1996; 6044- Cohen et al, J Biol Chem, 2000, 275: 23097-) and can be induced by numerous agents including PHA, as well as many agents to which the AIDS patients are exposed.

    They also knew that this was due to a change in phenotype of lymphocytes from T4 to T8. That is a decrease in T4 is accompanied by an increase in T8 which is the case in AIDS patients. So what made Gallo and Montagnier claim that the decrease in T4 cells is due to their killing by “HIV” or any other agent?

    As far back as 1986, Robert Gallo himself conducted experiments and showed that:

    “HIV” + PHA leads to a decline in T4 cells (as measured by binding of CD4 antibodies to the cells)

    “HIV” by itself has no effect on T4 cell numbers

    HA by itself causes a decline in T4 cells.

    In other words they had A and B, A by itself had no effect on T4 cells, B caused a decline, yet for so many years, contrary to any scientific rule or even common sense, the world has been told that the cause of the T4 decline is A and billions of dollars are spent to prove the unprovable, that is the mechanism by which A (“HIV”) kills the T4 cells. Why?

    In our scientific publications from the beginning of the “HIV” era, we have shown that no evidence exists that the T4 cells in AIDS patients are killed by “HIV” or any other agents and gave plausible scientific explanations for their decline, at present accepted even by at least some “HIV” experts.”

  7. Tony Lance said

    Tom,

    Thank you for passing my writing along to your colleague and then sharing his comments. He wrote:

    “I don’t think dysbiosis could cause a deficiency in lymphocytes, but just the opposite; it triggers the proliferation of lymphocytes and other kind of antibodies which lead to a hyper-reaction of the immune system.”

    This is exactly what I argue early on in my paper. You see, it has been known for quite some time that it’s inaccurate to look at AIDS simply as a condition of immunodeficiency. This early view has been augmented with the observation that AIDS patients characteristically exhibit B-cell hyperactivation, hypergammaglobulinemia and other conditions indicative of severely over-stimulated immune systems. And until recently this was considered by mainstream researchers to be something of a mystery.

    Now, conventional thinking has moved toward the idea that gut-derived microbial translocation is the driving force behind the systemic immune activation seen in AIDS—with HIV said to be causing the damage to the gut mucosa, of course. In 2006 Brenchley et al. wrote “Chronic activation of the immune system is a hallmark of progressive HIV infection and better predicts disease outcome than plasma viral load, yet its etiology remains obscure. Here we show that circulating microbial products, probably derived from the gastrointestinal tract, are a cause of HIV-related systemic immune activation.” They go on to say “These data establish a mechanism for chronic immune activation in the context of a compromised gastrointestinal mucosal surface…”

    I argue that there are lifestyle-related factors common to the subset of gay men at risk for AIDS which are per se capable of causing the damage to the gut that is otherwise blamed on HIV. Perhaps you can persuade your colleague to take another look at my article.

    Regards,

    Tony

  8. Tom Saville said

    Henry, Tony

    My apologies for the delay. It was only last night that I received the reply which I have copied below for your consideration.

    Regards, Tom

    My dear friend, as you know I don’t like to assume something unless I am able to see a bit of evidence; thus, I have a couple of volunteers with AIDS under study. One of them is beginning to show AIDS phase symptoms after six months. I should clarify that neither had been put under any kind of therapy and that both were exempted for awhile from taking antiretroviral therapy by metropolitan and state health authorities. It is difficult at the moment for me to join the discussion directly due to pressure of work, however please forward this assessment as my answer to Tony’s message.

    The CD4 T-cells titles decrease upon the course of the infection. There are three categories or phases of the disease: Acute phase or Category A, Chronic phase or Category B, and AIDS phase or Category C.

    The count of CD4 T-cells during the Category A phase is above 800 molecules per cubic mm, which is the normal count of CD4 T-cells.

    About three to six months after the inception of the disease, the number of CD4 T-cells drops to around 500 cells per cubic mm.

    Several months to three years after the initiation of the disease, the Chronic Phase starts and the number of CD4 T-lymphocytes decreases gradually, but persistently. The CD4 T-cells decreases to less than 400 per cubic mm; however, the titles stay above 200 per cubic mm.

    About seven months after the commencing of the disease, in AIDS Phase, the CD4 T-cells count falls below 200 per cubic mm and the symptoms of the disease become evident. The question is what is causing the CD4 T-cells to die? Another question is why is there no possibility, in Category C, of the CD4 T-cells rising to normal levels?

    I have examined lymphoid tissues of people with AIDS and have not found the main indicators of apoptosis, or programmed cell death, so we are unable to conclude that the problem has been generated by a toxic substance or an imperfect protein or a damaged DNA sequence.

  9. I’m very confused. This guy is supposedly “skeptical of the HIV = AIDS hypothesis”, yet he seems to buy into the whole CD4-killing mechanism hypothesis, and all the excruciating delineations of definition of “HIV disease” or various “AIDS categories (sic)”, as well as the apocryphal story of “progression” handed down via Haseltine and Fauci. (??)

    Moreover, he thinks HIV “has not been individually detected nor isolated”, yet he still believes in that mythical being, the “false-positive”, which may be caused by “many diseases… and conditions”, but “not AIDS, by no means.”

    Has this guy actually read ANYTHING written by dissidents??

  10. Henry Bauer said

    Tom Saville:

    I’m not only confused like Darin, I even sense a “bait and switch”.

    Mainstream publications have reported a lack of correlation between CD4, viral load, and clinical progression. Changing CD4 counts in peripheral blood denote re-distribution to a much greater extent than loss or re-generation. There is no “normal” count of 800, the counts vary across a range of at least a factor of 3 in healthy individuals, with major variations during even a day. The Category A, B, C are based on a tentative hypothesis first suggested by Anderson and May two decades ago, that has gradually morpheed into dogma without the benefit of intervening evidence.

    Your friend’s last paragraph is non sequitur at best.

    The tone of his introductory paragraph, and the unlikely claim that he has a couple of AIDS patients under observation, prompts me to ask, is his name perhaps “Fulano/Mengano de Tal”?

  11. Nasif Nahle said

    Given that my response has risen some doubts on my posture about AIDS, I’ve decided to participate only for this time. As I have said in the message I sent to my friend, Tom Saville, I’m not able to attend a continuous dialogue in Internet.

    Darin… Indeed, I do not think the HIV causes AIDS; however, I’m a scientist and I prefer to test any assertion when I’m able for doing it, so I can get a feasible conclusion about the issue. The categories of AIDS have been fairly documented, and I have seen that actually the three phases occur in the same way I have described them. The point is if a virus (HIV)is causing the disease, not the evolution of the disease. The disease evolves in the way I have described.

    Darin… If you send a patient to the lab and use the enzyme-linked immunosorbent assay, you would find the patients are positive for reverse transcriptase, which are positives. It cannot be interpreted forcibly like the occurrence of the virus (HIV). There are other retrovirus and other pathogens which gives positive results, hence the false-positives I’ve mentioned.

    Darin… I’ve read a lot of “dissident” literature; however, I cannot give credit to all stuff that I read.

    Henry… I’m not correlating CD4 T-cells load with HIV load. You’ve done it. I described the course of the disease, and I have corroborated the occurrence of the three phases which I have described.

    Henry… I’ve mentioned that I have not found the signature of apoptosis in lymphoid tissues because some biologists, as Cooper, Campbell and other investigators, have suggested that the virus could induce the process of apoptosis in CD4 T-cells, B-cells and megakaryocytes. It’s not true.

    Henry, my name is not “fulano, mengano or zutano de tal”; my name is Nasif Nahle, I’m a biologist and my specialty is on Scientific ICA Medicine Research, by Harvard. I have also certifications on climatology and meteorology, antibiotic therapy, radiobiology, geology, physics, edafology, and paleobiology.

    Henry… If you don’t admit there is a normal label of AROUND 800 CD4 T-cells, then you cannot admit that there is any kind of homeostasis in humans. I have to admit that I didn’t expressed the fact in a proper way, for which I sincerely apologize.

    Cordially,

    Nasif Nahle

  12. We ARE the victims of a bait and switch:

    Nasif Nahle comments on HIV/AIDS

    Nahle is given as the author at the bottom of the page. It occurs at a website of “Biology Cabinet”, which was founded by Nahle.

    Case closed.

    darin

  13. Sadun Kal said

    I guess someone can have doubts on the inside but still repeat the same old claims made by the mainstream science for various reasons. Until the doubt is strong enough and the person is certain that he’s really supposed to have doubts, he might be keeping it relatively quiet, i.e. not express it in his professional career. Here’s a quote from Stefan Lanka:

    “…To my big surprise, I found that when they are speaking about HIV they are not speaking about a virus. They are speaking about cellular characteristics and activities of cells under very special conditions. I was so deeply shocked. I was thinking, “Well, I’m not experienced enough. I have overlooked something. On the other side, those people are absolutely sure.” Then I was afraid that speaking about this with my friends, or even my family, they would think is absolutely mad and crazy. So for a long time I studied virology, from the end to the beginning, from the beginning to the end, to be absolutely sure that there was no such thing as HIV.”

    So I wouldn’t jump on to conclusions about Nasif Nahle so easily…it can even be a simple case of lack of courage, which wouldn’t be that surprising when it comes to questioning HIV/AIDS.

  14. sadunkal said

    In regard to being able to publicly question HIV/AIDS, here’s a powerful story:
    http://www.howpositiveareyou.com/2008/11/27/hpay-010/

    “Sarah Breidenbach was a highly regarded social worker who specialized in assisting people diagnosed HIV positive or with AIDS. For Sarah, this position was far more than a job, it was an opportunity to make a real difference in the lives of her clients, and she approached her work with great dedication and conviction. She felt very strongly that by encouraging compliance with AIDS drug treatments and discouraging skepticism about the causal link between HIV and AIDS she was offering HIV positives their best possible chances for staying alive. But after more than half a decade of a professional and personal life that revolved around AIDS from the mainstream perspective, Sarah very reluctantly agreed to watch the documentary film, The Other Side of AIDS, and something remarkable happened as a result: she began to question the basis for her staunchly held views, and ultimately the direction and meaning of her life’s work. Listen in as David and Christine speak with Sarah about her journey from certainty into the unknown, an experience she recounts with intelligence, grace and unusual honesty.”

    Questioning HIV/AIDS is not an easy thing, especially for those who’re already too deep in it. Going public takes even more courage apparently.

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