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JAMA confirms HIV load doesn’t govern CD4 loss


Lynchpin falls out of paradigm

No explanation yet from Dr Fauci, and we think we know why

Interesting JAMA story moving on the UPI ticker just now: HIV measurement is questioned. Seems viral load has little to do with CD4 loss in untreated HIV + patients.

Dr. Benigno Rodríguez of Case Western Reserve University and colleagues conducted a study to estimate the extent to which presenting blood levels of HIV can account for the rate at which CD4 cells are depleted among an untreated HIV-infected population of patients.

The researchers found only a small proportion of the rate at which CD4 cells are lost could be explained by plasma HIV RNA level, suggesting more than 90 percent of the determinants of CD4 cell decline are not reflected in the amount of virus in blood.

So don’t hurry to take HAART just because your HIV count is high. Is that right?

If so, where does that leave the paradigm and Anthony Fauci’s assurance that HIV causes depletion of CD4 cells, directly, indirectly and some other mysterious way as yet undefined but characterised by the paradigm defense team’s head man, Zvi Grossman, as a “conundrum”.

Seems we don’t even have to work out what the conundrum is. HIV doesn’t correlate with CD4 loss, period. Not in untreated patients. Not before HAART messes with your constitution.

Ah well, it’s late, maybe we got it all wrong. But looks to us as if the paradigm is failing on every front. Viral load doesn’t govern CD4 loss. That’s a problem to explain, unless you are a dissenter, ie someone with a few working brain cells left in this field.

Is it time for Gallo et al to pack for Rio? He should buy his ticket, the way things are crumbling.

Still, since Fauci presumably has been forewarned, he probably has an answer for us tomorrow, and Larry will let us know at the Times.

UPDATE: here is an AMA rundown of the paper:

“These findings represent a major departure from the notion that plasma HIV RNA level is a reliable predictor of rate of CD4 cell loss in HIV infection and challenge the concept that the magnitude of viral replication (at least as reflected by plasma levels) is the main determinant of the speed of CD4 cell loss at the individual level. The clinical implications are that in the majority of cases, an individual patient’s plasma HIV RNA level at the time of presentation for clinical care cannot predict, to a significant extent, the rate of CD4 cell decline that he or she will experience over the subsequent years and is therefore of limited clinical value in shaping the decision to initiate antiretroviral therapy,” the researchers write.

(JAMA. 2006;296:1498-1506.)….

“The second and potentially more exciting implication of the findings of Rodriguez et al is that future improvements in the treatment of HIV infection and AIDS may result from improved understanding of the 90 percent of CD4 cell depletion that remains enigmatic,” they write. “A better understanding of the immunologic and genetic factors that drive HIV-associated CD4 cell loss may translate to novel therapeutic approaches that could favorably shift the pathogen-host balance.

So 90 per cent of CD 4 depletion is not driven by HIV? But… but… Dr. Fauci, come to our rescue here. We were under the impression that HIV caused AIDS by depleting CD4 cells. You told the audience that when you appeared in New York with Mathilde Krim and Larry Kramer at the New School to celebrate “AIDS after 25 Years”. Help us here.

Did Dr Fauci censor himself on HIV∫AIDS flaws?

Why was this paper not flagged at NIAID before it could be published? The answer to that question also seems enigmatic. Maybe it was because Dr Fauci thought there might be something in our previous nomination on his behalf for recognition from Stockholm (Dr Fauci finds solution to AIDS – it’s HIV; NAR nominates him for Nobel) on the grounds that he had discovered that HIV actually increased CD4+8 proliferation, and therefore was an antidote to itself.

Readers may note that at the bottom of that post is a Comment by Robert Houston which points out that Dr Fauci himself in a review of HIV∫AIDS quoted from a paper he himself forwarded to the National Academy of Sciences that showed that a huge rise in HIV load of 5,560% resulted in a negligible change in CD4 count of -6%, at the same time as boosting CD8 count 20%.

Is it possible that Dr Fauci is aware of the fact that HIV load has no great influence on CD4 count, and even wrote about it for the information of the medical community, on the basis of a paper he forwarded to the National Academy, and somehow forgot to tell government officials, health workers and the public?

Surely it would be too cynical to imagine that the director of NIAID would censor himself in this way, after censoring the media for twenty two years?

Surely a public servant of the well paid and important kind that Dr Fauci is would never withhold information from members of the public who pay his salary who might then be misled into taking drugs with horrendous side effects for no good reason?

Surely a public servant of the stature of Dr Fauci would not freely acknowledge a flaw in the paradigm which has brought so much funding to his institution among colleagues, and yet somehow neglect to tell the public?

If he did, then it behooves us to wonder just how flawed does Dr Fauci think the HIV∫AIDS paradigm really is. Are there other flaws which he has quietly recognized in chats and talks to his peers in the medical policy fraternity, but has omitted to acknowledge in public?

It already seems clear that his answer to Robert Houston at the “AIDS after 25 Years” panel on how HIV killed CD4 cells was misleading. He repeated the same old claims that there was direct killing and indirect killing which have not only been revealed as specious by mainstream papers which he must have read himself, but he knew himself from his own review and paper that HIV load has very little to do with CD4 count changes.

So today’s revelation in JAMA is nothing new to him, and we don’t really expect him to help us to understand it. Dr Fauci’s policy on informing the public seems to be this: however many reasons there are to doubt that HIV is “the virus that causes AIDS”, it is important not to undermine public confidence by acknowledging them in public.

But it is fine to talk and write about them among colleagues.

We wonder what all the haplessly gullible gays now staggering about with wrecked and ugly bodies, and the ghosts of their dead, will have to say about it when they finally come to their senses?

Maybe they will take up Larry Kramer on his suggestion for a latter day Nuremburg Trial, and put Dr Anthony Fauci in the dock.

AMA rundown:

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Libraries

Medical News

Keywords

HIV, CD4 CELLS, IMMUNE RESPONSE

Contact Information

Available for logged-in reporters only

Description

Preliminary research indicates that the initial HIV RNA level in untreated HIV-infected patients appears to have little value in predicting the rate of CD4 cell count decrease, potentially limiting its clinical value concerning the decision of when to begin antiretroviral therapy for an individual, according to a study in the September 27 issue of JAMA.

Newswise — Preliminary research indicates that the initial HIV RNA level in untreated HIV-infected patients appears to have little value in predicting the rate of CD4 cell count decrease, potentially limiting its clinical value concerning the decision of when to begin antiretroviral therapy for an individual, according to a study in the September 27 issue of JAMA.

Depletion of CD4 cells is a characteristic of progressive human immunodeficiency virus (HIV) disease and a powerful predictor of the short-term risk of progression to AIDS, according to background information in the article. Blood levels of HIV are also thought to predict HIV disease progression risk. In addition to their role as predictors of the clinical outcomes of HIV infection, CD4 cell count and plasma HIV RNA level are commonly used as markers of the success of highly active antiretroviral therapy (HAART). Until this study was completed, however, the degree to which blood levels of HIV could predict the rate of CD4 cell loss in HIV-infected individuals with similar demographic characteristics to those seen in clinical practice was unclear.

To address this question, Benigno Rodríguez, M.D., of Case Western Reserve University, Cleveland, and colleagues conducted a study to estimate the extent to which presenting blood levels of HIV can account for or “explain” the rate at which CD4 cells are depleted among an untreated HIV-infected population of patients including women and ethnic minorities. The study included repeated analyses of 2 multicenter groups, with observations beginning in May 1984 and ending in August 2004. Analyses were conducted between August 2004 and March 2006. The participants included antiretroviral treatment–naïve, chronically HIV-infected persons (n = 1,289 and n = 1,512 for each of the 2 groups) who were untreated during the observation period (6 months or greater) and with at least 1 HIV RNA level and 2 CD4 cell counts available. Approximately 35 percent were nonwhite, and 35 percent had risk factors other than male-to-male sexual contact.

The researchers found that only a small proportion of the rate at which CD4 cells are lost (only 4 percent – 6 percent) in a given individual patient could be explained by presenting plasma HIV RNA level, suggesting that in chronic untreated HIV infection over 90 percent of the determinants of CD4 cell decline are not reflected in the amount of virus in blood at the time of initial medical evaluation.

“Our findings confirm previous observations that the magnitude of HIV viremia [the presence of a virus in the blood stream], as defined by broad categories of presenting HIV RNA level, is associated with the rate of CD4 cell loss and extend this observation to patient populations comprising both men and women. Despite this association, however, only a small proportion of the interindividual variability in the rate of CD4 cell decline can be explained by plasma HIV RNA level, even after accounting for the effect of measurement error,” the authors write.

“These findings represent a major departure from the notion that plasma HIV RNA level is a reliable predictor of rate of CD4 cell loss in HIV infection and challenge the concept that the magnitude of viral replication (at least as reflected by plasma levels) is the main determinant of the speed of CD4 cell loss at the individual level. The clinical implications are that in the majority of cases, an individual patient’s plasma HIV RNA level at the time of presentation for clinical care cannot predict, to a significant extent, the rate of CD4 cell decline that he or she will experience over the subsequent years and is therefore of limited clinical value in shaping the decision to initiate antiretroviral therapy,” the researchers write.

(JAMA. 2006;296:1498-1506. Available pre-embargo to the media at http://www.jamamedia.org.)

“The second and potentially more exciting implication of the findings of Rodriguez et al is that future improvements in the treatment of HIV infection and AIDS may result from improved understanding of the 90 percent of CD4 cell depletion that remains enigmatic,” they write. “A better understanding of the immunologic and genetic factors that drive HIV-associated CD4 cell loss may translate to novel therapeutic approaches that could favorably shift the pathogen-host balance.

Editor’s Note: This work was supported in part by the Case Western Reserve University Center for AIDS Research and NIH grants. Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc.

Editorial: Explaining, Predicting, and Treating HIV-Associated CD4 Loss – After 25 Years Still a Puzzle

In an accompanying editorial, W. Keith Henry, M.D., of the University of Minnesota, Minneapolis; Pablo Tebas, M.D., of the University of Pennsylvania, Philadelphia; and H. Clifford Lane, M.D., of the National Institute of Allergy and Infectious Diseases, Bethesda, Md., discuss the findings concerning HIV RNA levels and CD4 cell loss.

“The study by Rodriguez et al may have several important clinical implications. The first and more straightforward is that baseline measurements of viral load alone should have less of a role in driving decisions on when to start antiretroviral therapy for an individual patient; these initial viral load levels cannot predict how rapidly the disease will progress. … The seemingly useful practice of combining a CD4 cell count and plasma HIV RNA levels to assess an individual patient’s prognosis for AIDS progression or response to highly active antiretroviral therapy needs reexamination.”

“The second and potentially more exciting implication of the findings of Rodriguez et al is that future improvements in the treatment of HIV infection and AIDS may result from improved understanding of the 90 percent of CD4 cell depletion that remains enigmatic,” they write. “A better understanding of the immunologic and genetic factors that drive HIV-associated CD4 cell loss may translate to novel therapeutic approaches that could favorably shift the pathogen-host balance. … Discovering and developing therapies that target key nonviral factors has the potential over the decades ahead to build on the success of antiretroviral therapy and expand access to sustainable effective therapy.”

(JAMA. 2006;296:1523-1525. Available pre-embargo to the media at http://www.jamamedia.org.)

Editor’s Note: Please see the editorial for financial disclosures, funding and support, etc.

HIV measurement is questioned

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CLEVELAND`, Ohio, Sept. 26 (UPI) — Preliminary U.S. research indicates the HIV RNA level in untreated HIV-infected patients has little value in predicting the rate of CD4 cell count decrease.

Researchers say that potentially limits HIV RNA’s clinical value concerning the decision of when to begin antiretroviral therapy.

Until the new study was completed, the degree to which HIV blood levels could predict the rate of CD4 cell loss was unclear.

To address the question, Dr. Benigno Rodríguez of Case Western Reserve University and colleagues conducted a study to estimate the extent to which presenting blood levels of HIV can account for the rate at which CD4 cells are depleted among an untreated HIV-infected population of patients.

The researchers found only a small proportion of the rate at which CD4 cells are lost could be explained by plasma HIV RNA level, suggesting more than 90 percent of the determinants of CD4 cell decline are not reflected in the amount of virus in blood.

The research appears in the current issue of the Journal of the American Medical Association.

UPDATE: Nick Bennett Replies on his site Viral load paradigm shift? Not really.

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Wednesday, September 27, 2006

Viral load paradigm shift? Not really.

An interesting study came out recently (I managed to get a copy of the article from one of the authors) on the predictive value of viral load. It’s well known (at least among those who bother to read and understand the literature) that those people with higher viral loads tend to progress faster, as was shown by John Mellors back in the mid 1990s using the large Multicenter AIDS cohort study (MACS).

This study took things one step further. They replicated the original findings of Mellors by showing again that viral load roughly predicted how fast AIDS occurred in another large cohort composed of people from 3 seperate study sites. For example, in this new paper people with viral loads less than 500 had an average loss of CD4 cells of 20 per year whereas those with viral loads over 40,000 had an average loss of 78 a year (with a smooth change for values inbetween). Basically this data proved that viral load was a reasonable predictor of rate of progression! They compared this analysis with the original MACS cohort and it looks practically identical!

But then they tried to look at the individual rate of progression of each member of the cohort. Unsurprisingly they found that the rough-and-ready estimates of progression rate within a subgroup varied from one individual to another. When they ran complex statistical analysis on the effects of viral load on THIS data they found that only about 5-6% of the inter-individual variation can be explained by the initial viral load. In another words, while viral load predicts that you WILL lose CD4 count, and you can give an AVERAGE loss of CD4 cells per year based on that count, you can’t say for sure what the ACTUAL loss will be for any one person very accurately.

Well, duh. Nothing amazing there.

Now, what’s sad about this whole thing is that is appears as if the dissident websites have jumped all over the mass-media coverage of this without bothering to read the paper. They are assuming that this somehow negates the usefullness of viral load measurements. Ironically if a paper showing that viral load predicted 100% of the CD4 T cell loss (an impossible thing) relied on complex statistical analysis I’m sure they wouldn’t accept it with anything like the same level of naivity!

This is nothing new – we’ve known for years that various other factors can play into AIDS progression, from nutritional status to immune makeup, depression, and viral genetics. We’ve known for years that overall T cell losses include uninfected as well as infected cells, that immune hyperactivation leads to apoptosis but a lack of renewal – both things that are only indirectly due to HIV infection, but not direct cell killing. What we haven’t done before is put a number on anything – to say roughly HOW much influence these things can have on an individual level.

It should also be noted that this should lay to rest any idea that mainstream science is simply laying back and accepting the current paradigm without question. If that were the case, why was this large, comprehensive, complex study performed? Is it because that when dissidents say that scientists ARE sitting back on the current paradigm they are…*gasp*…lying??! And, SHOCK HORROR, this was supported by an NIH grant, the very same NIH that the dissidents are trying to claim is horribly corrupt and under the thumb of pharmaceutical sponsors!

Ahh, is that the sound of cherries being picked?

Anyhow, I will quote from the paper:

“Our findings confirm previous observations that the magnitude of HIV viremia, as defined by broad categories of presenting HIV RNA level, is associated with the rate of CD4 cell loss and

extend this observation to patient populations comprising both men and women.”

In other words, viral load predicts rate of progression to AIDS.

If the dissidents are trying to twist this paper to say anything else, they are managing a feat of astonishing deception. Is there more to the story? Of course! No-one, except the dissidents, is saying anything else. They also state that “In humans, the predictive value of immune activation level on HIV disease course, independent of plasma HIV RNA levels, can be demonstrated even when measured during early infection”, which goes back to what I said above.

And I refer the reader to my older post on HIV pathogenesis.

It should also be mentioned that viral load isn’t used as a clinical criteria for starting treatment unless the load is very high and the CD4 counts are equivocal. Viral load is almost exclusively used for monitoring response to therapy on the individual level, so inter-individual variability isn’t an issue anyway.

This result is very important in that it highlights the need to investigate other factors important in triggering or controlling rate of progression to AIDS, but it won’t really change the current paradigm in terms of understanding AIDS pathogenesis, nor will it change current treatment guidelines, because neither depends on the idea that HIV viral load is the be-all and end-all of AIDS.

Except of course, that it is in the minds of the dissidents.

Which is (one reason) why they’re wrong.

posted by Bennett at 11:18 PM

0 Comments:

Comment: Bravo, Bennett, for defending the paradigm against what looked like a nasty finding judging from the first reports. Now we too have the actual paper in hand, we can see that the point Dr Bennett makes is perfectly correct, this was a paper dealing with variations between individual experiences, not with the overall correlation between the two measures of HIV and CD4 for all the patients in the study. Naturally there can be many other factors accounting for variations in individual experience, as there are many reasons for contracting AIDS symptoms, and reasons for vulnerability.

But he entirely overlooks the thrust of the paper, which demonstrates that the authors are unable to discern what those causes of variation might be. They explored the possibilities that sex, risk factor and/or presenting HIV RNA stratum might be the answer and found nothing that could predict the rate of CD4 loss. In fact, Bennett’s reassurance that everything is fine in HIV∫AIDS la la land is merely the same old reflex denial of the big black headline over the AMA comment by W. Keith Henry, which is that “Explaining, Predicting and Treating HIV-Associated CD4 Cell Loss (is) After 25 Years Still a Puzzle.

Henry et al note that the report “challenges the notion that, at the individual level, a limited number of HIV measurements over a short period of time provide meaningful prognostic information regarding the rate of CD4 cell decline and by extension the risk of opportunistic infections.” Of course, if the medical fraternity would take off their NIAID provided glasses with “HIV is behind everything” etched onto them they would have known this in the first place. If they bothered to read their own literature (or this blog) or even think clearly they would know that it is just as likely that CD4 counts are lower at rest and higher when activated, than vice versa, as Dr Fauci has recently touched on in his extensive review. Moreover, the level of active virus in the blood of patients without AIDS symptoms in the long “latent period” is utterly negligible. It is hard to conceive it has anything at all to do with changes in CD4 count, compared with myriad other influences on the immune system.

The result of the study is in fact utterly predictable, and the only surprise it holds is for those who imagine that the simple minded mechanism of HIV causing AIDS imagined in the first place over two decades ago – HIV killing CD4 cells dirctly – is still part of the paradigm. This includes Dr Fauci, it appears, who doesn’t read his own medical literature according to his public statement at the New School on the ways HIV kills CD4 cells, which repeated this now outmoded idea, as well as the cell suicide theory of “indirect killing”, when both are rejected by his top theoretical thinker Zvi Grossman, who has retreated to the conclusion that how it all happens is a “conundrum”.

What is really the study’s only novel usefulness is its demonstration yet again that no one has any idea how HIV can possibly govern the loss of CD4 cells that is held to be cause of AIDS, and that the obvious alternative – that HIV is merely an opportunistic infection, and rather than governing CD4 count, it is CD4 count that governs the rise and fall of HIV viral load, as CD4 numbers are affected by other factors – the poisons and other assaults that may bring on AIDS symptoms.

It puts yet another nail in the coffin of a paradigm that has never been able to demonstrate its central premise.

184 Responses to “JAMA confirms HIV load doesn’t govern CD4 loss”

  1. Chris Noble Says:

    You simply repeat back to us in your post above, and in the post above that, the four key points in what we told you ie that a) you are arguing against the authors of the study and b) you have not read the paper properly, c) if you disagree with the authors you should write to the authors or JAMA and d) you cannot see around your preconceived notion that the paradigm is inviolable.

    a) I am not arguing against the authors of the study. You are.

    b) Michael Lederman has made it clear “Clearly the people who are misrepresenting our work are not only incapable of clear thinking, they are also apparently unable to read.”

    c) You are the the one that is disagreeing with the authors.

    d) You are dreaming.

    I wish you well with your delusions of adequacy.

  2. Truthseeker Says:

    Chris, we have begged you not to be a parrot, and here you are doing it again, so all we can do is offer you a peanut and stroke the top of your head against the feathers, which is what parrots like, which we know on account of having our own grey parrot here, who sends his greetings in the form of a whistle.

  3. nohivmeds Says:

    I find the discussion with Noble somewhat ridiculous regarding interpretations of the JAMA paper. As I was trained, it was made quite clear to me that 5 of the best scientists in a particular area could sit down, look at a paper, and come out with 5 equally plausible interpretations. Mr. Noble – there is no “correct” way to interpret a paper — and the authors’ interpretations are not necessarily the “correct” interpretation either. The authors of any paper clearly always have biases in interpretation, and dislike it when others interpret their work in varying ways, but THAT IS HOW THINGS WORK IN SCIENCE. You can dislike someone’s interpretation, but I don’t see anything here in TS’s interpretation that you can invalidate, and the authors’ opinions make little difference in this.

    Might I suggest this: Mr. Noble only agrees with interpretations that are consistent with the AIDS meme. He allows for no possible interpretations that differ from that conception, yet this ignores one basic issue in science, which is that findings may be interpreted in any number of ways, all logical and coherent. That is simply a fact, Mr. Noble. And it has made for fascinating scientific debate for decades now, in every existing area of science. I’m afraid that it is you who really demonstrates a lack of understanding of the role of interpretation in science.

  4. YossariansGhostbuster Says:

    Well, while ya’all are whistling past the graveyard, Chris is as close to a clearer explanation of the JAMA article as anyone else. TS is still throwing hamburger helper to the puppies whilst he yet drives another rubber nail for some buddies paradigm.

    Yossarian has looked at this carefully and hath discover’d the following truth not quite ready for the history channel:

    It is not clear how much of the pathology of AIDS is directly due to the virus and how much is caused by the immune system itself, but the JAMA article people are actually going in the appropriate direction for which they ought not be driven into
    NAR’s bull dozer.

  5. Gene Semon Says:

    It’s interesting how the “comeback kid” consistently ignores any branching points in the discussion that may lead to a wider world, such as my previously-posted response to the concluding sentence of the JAMA RNA/CD4 paper.

    In the Bizarro World, it is simply understood that “future efforts” are necessary to consider “other mechanisms”, “non-virological”, since our esteemed JAMA authors’ seem totally oblivious to the efforts of others who have already proposed them in numerous peer-reviewed publications. Adding to Robert Houston’s excellent post is Roberto Giraldo’s thorough review, “NUTRITIONAL THERAPY FOR THE TREATMENT AND PREVENTION OF AIDS: SCIENTIFIC BASES”. (http://www.robertogiraldo.com/ => eng/papers/NutritionalTherapy_SADC_2003.html)

    Excerpt: “There is today a growing number of scientific publications indicating that oxidizing stress is an absolute requisite for both testing positive on the tests for HIV (201-207) and for developing the clinical manifestations of AIDS (208-230).

    “Free radical reactions of special significance to immunological phenomena are, for example, the many oxidizing agents that can abstract a hydrogen atom from thiol groups to form thiol radicals (231-233). Thiol groups are important for enzyme activities, receptor functions, disulphite links in immunoglobulins, and T cell activation and proliferation. The super oxide anion radical can react with nitric oxide, resulting in loss of endothelium-derived relaxing factor activity, which is important in the inflammation/disinflammation process. Methionine oxidation can cause protein damage with subsequent changes in immunogenicity. Proteolysis can be increased by free radical damage. The per oxidation of lipids by reactive free radicals produce many biological modulators such as, for example, the 4-hydroxy-alkelans, which produces strong chemotactic activity for phagocytes, alters the adenyl cyclasa system, increases capillary permeability, and alters lymphocyte activation. Lipid hydroperoxides, also from per oxidation of lipids, alter lymphocyte activation. Conditions favoring lipid per oxidation may result in chemo taxis of leukocytes, protein modification, immune complex injury, and cell death (231-233).

    “Free radicals are produced throughout the regular immune system network. Despite the beneficial effects of the inflammation responses, they can also aggravate existing tissue damage by releasing free radicals. When uncontrolled, initiated by an abnormal stimulus, or occurring for prolonged periods of time, inflammation may become a disease process (231-233). It is critical for optimal immune responses that there be a balance between free radical generation and antioxidant protection. During phagocytosis by polymorphonuclear leukocytes, for example, super oxide anion radicals are released. These oxygen free radicals can oxidize thiol groups to thiol radicals, and can stimulate lipid per oxidation with the formation of H2O2, which is highly significant in the mechanisms of cell injury. Oxygen free radicals produced during phagocytosis of immune complexes are associated with injury to immune complexes (231-233).

    “It has often been proposed that free radicals and specifically oxidizing species play important roles in the pathogenesis of AIDS (189-200,234-236).

    “The above are the scientific fundamentals for the use of antioxidants such as vitamin A and carotenoids, vitamin C, vitamin E, selenium, n-acetyl cisteine, l-gluthamin, zinc, cooper, manganese, alphalipoic acid, coenzyme Q10, and flavonoids or vitamin P, as supplementation for the prevention and treatment of AIDS (48,188-236).”

    Note the 49 references and number 230, “Staal FJT et al. Antioxidants inhibit stimulation of HIV transcription. AIDS Res Hum Retroviruses 1993; 9: 299-306”. Again, this makes clear to a literate person – meaning one doesn’t have to ask the authors that it confirms the Perth Group – what is cause and what is effect.

    The wider world also includes, “Mitochondria and Cancer, by Professor Serge Juragunas, Townsend Letter – August/September 2006”, which has relevance to AIDS and is “based on the notion that mitochondria can indeed regulate genomic activity”. Additionally, “mitochondria have been shown to play a crucial role in the regulation of apoptosis and the maintenance of cellular redox, which regulates growth … at the cell surface of specific signal transduction pathways, which in turn induce crucial transcription factors to regulate genes essential for cell growth.” The article continues the above discussion on the pathogenic effects of oxidative stress as they relate to the mitochondria and represents a neat synthesis with some of the new findings in regulatory genomics.

    Unfortunately, too many biomolecular scientists – especially those who directly perceived the ultimate truth of the JAMA RNA/CD4 article, as Chris has explained to us – are clueless when it comes to the above.

  6. YossariansGhostbuster Says:

    Wouldn’t you know it, Capt’n Crunch Gene Semon shows up with yet another oxidation theory on cluelessness.

  7. Robert Houston Says:

    Gene Semon has provided a valuable resource in highlighting the magnificent 2003 review by Roberto Giraldo, M.D., on “Nutritional Therapy for the Prevention and Treatment of AIDS”, which contains 315 references. Another very useful paper of his is “‘Co-factors’ cause AIDS”, which surveys the many oxidative and immunological stressor agents that can lead to immune deficiency.

    Snide remarks by “YosariansGhostbuster” (AKA McKiernan) are offbase and ill-informed (e.g., “oxidation theory on cluelessness”). As I documented in my previous Comment, even HIV discoverer Luc Montagnier agrees that oxidative stress is a major factor in AIDS and can be moderated by antioxidants, a view similar to the Oxidative Stress Theory of AIDS which was first proposed in the 1980s by biophysicist Eleni Papadopulos-Eleopulos, leader of the Perth group of dissenting scientists centered in Australia. In a new scientific publication, she discusses the similarity of Montagnier’s views and her original theory (click HERE).

    In his memoirs, Montagnier objected to the common practice of virologists to attribute all phenomena in AIDS to HIV. He termed this “a naive and simplistic conception” and pointed out that “all opportunistic agents can likewise contribute to oxidative stress…so can mycoplasmas” (Virus, W.W. Norton Co., 2000, pp. 183 and 185). The Perth Group has long pointed out that recreational drugs, dietary deficiencies and other lifestyle factors characteristic of AIDS risk groups can produce oxidative stress. Furthermore, the very low levels of actual HIV virus in AIDS patients, which NIAID director Fauci has estimated affect on average only 1 in 1000 T-cells, means that any effect of HIV “envelope proteins” (such as TAT) on oxidative stress would be miniscule compared to the onslaught of strong oxidizing agents such as nitrite drugs and corticosteroids common in HIV/AIDS risk groups.

    Glutathione, a peptide containing the amino acid cysteine, is a major antioxidant in the body and helps protect T-cells from oxidative damage. Its levels are known to fall in AIDS. A Stanford University study found that oral supplements of the glutathione precursor N-acetylcysteine (which is now available in every health food store) resulted in a doubling of the survival time of AIDS patients (L. Herzenberg et al. Glutathione deficiency is associated with impared survival in HIV disease. Proc. NAS 94:1967-72, 1997). Other antioxidants, such as selenium, are relevant to the glutathione defense (see the Giraldo review).

    Contrary to a typically misleading claim of Chris Noble on this thread, Herzenberg et al. did not attribute the drop in glutathione (GSH) in AIDS solely to HIV. On the contrary, they wrote that “multiple mechanisms may contribute to systemic GSH deficiency in HIV disease, including excessive production of inflammatory cytokines and excessive use of GSH-depleting drugs.” They advised that “the unnecessary or excessive use of acetaminophen [e.g. Excedrin], alcohol, or other drugs known to deplete GSH should be avoided by HIV-infected individuals” (see abstract).

    It’s also pertinent that while Herzenberg et al. in 1997 measured “total GSH”, additional research in Norway found that a variable more predictive of AIDS progression and CD4 decline was “”increased levels of oxidized glutathione and a decreased ratio of reduced [non-oxidized] to total glutathione” (F. Muller et al. Thiols to treat AIDS. In: Nutrition and AIDS, Ed.: R. Watson, 2nd Edition, CRC Press, 2001, p. 79).

  8. Chris Noble Says:

    I find the discussion with Noble somewhat ridiculous regarding interpretations of the JAMA paper. As I was trained, it was made quite clear to me that 5 of the best scientists in a particular area could sit down, look at a paper, and come out with 5 equally plausible interpretations. Mr. Noble – there is no “correct” way to interpret a paper — and the authors’ interpretations are not necessarily the “correct” interpretation either.

    There is indeed often room for a large amount of interpretation in any paper. This does not mean that any interpretation is as valid as any other. Postmodernism has not managed to take over science – so far. Some interpretations are better than others and some are just plain wrong where they specifically contradict results in the paper.

    TS’s interpretation was formed before he read the paper. He did not base his interpretation on the totality of the results in the paper. In particular his interpretation contradicts the results in figure 1. The idea that the paper falsifies the idea that HIV causes AIDS is frankly ridiculous. This interpretation is inconsistent with the results.

    Any valid interpreation needs to provide some explanation for the data in figure 1. Ignoring it is not good enough. Claiming that it is not statistically significant is also not good enough – it clearly is. When pushed some of you came up with alternative explanations for the relationship between HIV viral load in subgroups and the rate of depletion of CD4 cells. None of these alternatives were plausible.

    While the authors of an article do not have the final say on the interpretation of their results their opinion has much more credibility than that of an innumerate journalist who does not have access to the information that the researchers have. If you are going to stand up and claim that your interpretation is more valid than that of the authors you would be advised to actually learn a bit more mathematics and science. Resorting to political arguments is not valid. It might convince an audience prone to conspiracy theories but it won’t convince the majority of scientists.

    The authors have made a further clarification here.

    http://www.aidstruth.org/rodriguez-lederman.php

    TS has repeatedly claimed that I have contradicted the authors of the paper. This is clearly not so. This is simply a silly rhetorical trick and is frankly bizarre.

    TS’s rhetoric might work well in the small enclosed world of HIV “rethinkers” where everybody slaps each other on the back for their brilliant insights and laugh at the thousands of scientists that are stupid enough to believe that HIV causes AIDS but it just won’t wash in the real world

  9. Chris Noble Says:

    Contrary to a typically misleading claim of Chris Noble on this thread, Herzenberg et al. did not attribute the drop in glutathione (GSH) in AIDS solely to HIV.

    Is there a school that you have all attended where you can learn the art of misreading? I have never made that claim.

    In fact it is clear that a significant number of healthy HIV- controls also had low GSH levels.

    GSH levels on their own are not a good predictor of who is going develop AIDS. In HIV+ people there was an observed relation on average between GSH levels in CD4 cells and progression to AIDS.

    The “interpretation” that the Herzenberg paper is evidence against the role of HIV in AIDS is also ludicrous.

  10. Truthseeker Says:

    There is indeed often room for a large amount of interpretation in any paper. This does not mean that any interpretation is as valid as any other. Postmodernism has not managed to take over science – so far. Some interpretations are better than others and some are just plain wrong where they specifically contradict results in the paper.

    At last, a correct statement from Chris. This is a cause for celebration. We agree with every word, and shudder to think what “I’m OK, you’re OK” science would lead to, if unleashed.

    As to the rest of your comments, however, we can only say, Chris, you are repeating yourself yet again, without any greater effect than before. Same old inability to understand Fig 1 as anything but a contradiction of what the authors say. The problem, however, is that what you are repeating is wrong. It is, as another distinguished poster characterized it, “typically misleading”. Your denialist (of reason and evidence) mode has lost its regulator, and now you apply it even to a study you believe supports your religion.

    Chris, you cannot at one and the same time support and deny the quoted conclusions of the authors, claim that a figure in the study supports your denial, and say that our agreement with their conclusion is ludicrous. You are chasing your own tail, and will soon spin ever faster into a blur that will deliver you into another universe altogether, an alternate reality where HIV causes AIDS. But then, that is the one you believe in so steafastly, it appears, so you will be happy there, we imagine.

    Anyway we welcome this self-exposure of yours, this parade of repeated “same to you” schoolboy denial of what is obvious to everyone else. It illuminates your determinedly denialist (of reason and evidence against HIV) mode, your refusal to take in new information, or to understand repeated explanations of material which baffles you. Your piteous repeated cries of “please explain Fig 1” are very moving. We wish we could help. But apparently words are not enough.

    So these are our last on the subject and we hope, yours too. There comes a point where repetition is redundant to the point of migraine.

  11. nohivmeds Says:

    One does not need postmodern thought to recognize the fact that data can be validly interpreted in a number of ways. Postmodernism had absolutely nothing to do with the argument I made — science did.

    The authors of an article are, contrary to what CN would like to think, often the worst authorities on their own work — that is an inescapable fact. Researchers set out to do a study with particular assumptions (many unknown to them) guiding their choices of method and interpretation. If authors were the best representatives of their work, there would be no need for peer review, or science journalism, for that matter. But human subjectivity does inevitably interfere with all interpretations — especially those of the original researchers, as they have more invested in the correctness of their interpretations than do other readers. Simple, really. Basic psychology, nothing more.

    CN raises one interesting point that was raised during the EJ Scovill catastrophe — TS, would you, as Christine Maggiore insisted she was, be ready to reject your current frame and accept HIV as causal in AIDS if you were presented with the proper evidence? If not, then CN is correct in asserting that you are likely as biased as he is. All good scientists leave a great amount of room for the possibility that they are utterly wrong. All good commentators on science should do the same.

  12. Dave Says:

    This is a great question by nohivmeds:

    would you, as Christine Maggiore insisted she was, be ready to reject your current frame and accept HIV as causal in AIDS if you were presented with the proper evidence?

    It shouldn’t be limited to TS, though, it should be propounded to all folks who are skeptical of the virus theory.

    The converse question should also be propounded to viral proponents as well:

    would you be ready to reject your current frame and reject HIV as causal in AIDS if you were presented with the proper evidence?

    And, of course, then follow up questions, ie, What would be “proper evidence?” etc, etc would ensue, and then, holy smokes, there’d be intelligent back and forth on this critical issue.

  13. Truthseeker Says:

    If authors were the best representatives of their work, there would be no need for peer review, or science journalism, for that matter. But human subjectivity does inevitably interfere with all interpretations — especially those of the original researchers, as they have more invested in the correctness of their interpretations than do other readers. Simple, really. Basic psychology, nothing more.

    Well said. Interpretation is typically subjective to some extent, humans beings being what they are, emotional enough to keep psychologists in business for another few decades at least. You are quite right to point this out, especially since it is a major factor in keeping the HIV∫AIDS fantasy rolling. This doesn’t mean that all interpretations must be allowed equal credibility, however, in a sort of scientific democracy, where everyone has one equal vote. Interpretations must reviewed critically, as you also state. But are authors “often the worst interpreters of their work”? Interesting to hear a psychologist say that, since you must be talking mostly about psychology, we assume.

    Anyhow, in this case, the authors of the JAMA paper seem to be clear headed about the significance of their data, and about the awkward politics of it. It is only CN that seems muddled, and to think that their disclaimer is purely scientific. Our own interpretation, of course, is purely objective. We are the single exception among all commentators in that respect. We are surprised you haven’t noticed this.

    CN raises one interesting point that was raised during the EJ Scovill catastrophe — TS, would you, as Christine Maggiore insisted she was, be ready to reject your current frame and accept HIV as causal in AIDS if you were presented with the proper evidence? If not, then CN is correct in asserting that you are likely as biased as he is. All good scientists leave a great amount of room for the possibility that they are utterly wrong. All good commentators on science should do the same.

    If that means we are rated a “good commentator”, we hurry to get out the green border for your comment. But to answer your query, the answer is tautological, isn’t it? “Accept HIV as causal in AIDS if you were presented with the proper evidence”? By definition, we would have to, no? What you may mean is, do we argue from a bias, as CN does, and always pick out what we conceive to be in line with our overall conclusion – in his case, that HIV causes immune deficiency which causes AIDS, in our case, there is no evidence for that yet, and every evidence that AIDS is caused by familiar factors such as drugs, malnourishment, and disease itself? Do we pick out these data, and ignore the rest?

    The answer is no, in fact, we are not particularly invested in toppling the paradigm, if anyone would care to present a single good theoretical pillar of support for it. In many ways, it would be convenient if someone did that, and we could all pick up our marbles and find some less obvious issue to discuss. Convenient in the practical sense of use of time, energy and money, and avoidance of repetition. The fact that grown men sit around nitpicking the dung of an elephant and discussing whether it exists or not when it is standing right behind them is the real interest in this topic, as you, a psychologist, obviously see. So it has to be acknowledged there would be that loss – of the greatest example of human foolishness extant in the present age.

    There would be other disappointments associated with that ending, too, of course. It is always a boost to one’s vanity to see more clearly than other people, and recognize the elephant they cannot see behind them. But that sort of self satisfaction wears off fairly rapidly, we find, especially since a know-it-all is liable to get punched on the nose even if he is right. It would be much better if everyone saw the elephant, lives could be saved, and money and time devoted to something more constructive.

    Besides which, as CN shows, the same secure feeling of being right and knowing better is shared by everyone in this discussion, no matter which side people are on.

    By the way, connoisseurs of foolishness should hurry over to trrll’s comment, just up over at the “In Europe, fish oil after heart attacks – but not here” post (Click HERE). In his view he has completely demolished Peter Duesberg’s set of HIV∫AIDS’ failed predictions, and single handedly rescued the paradigm from its most damaging challenge. Foolish, foolish Duesberg! Clever, clever trrll!

  14. Robert Houston Says:

    Having been exposed in his attempt to misrepresent a study, Mr. Noble compounds his error by now claiming that he made no such statements. Here’s our recent exchange:

    Houston (10-12-06, 11:56 pm): Contrary to a typically misleading claim of Chris Noble on this thread, Herzenberg et al. did not attribute the drop in glutathione (GSH) in AIDS solely to HIV. .

    Noble (10-13-06, 12:28 am): Is there a school that you have all attended where you can learn the art of misreading? I have never made that claim.

    Now here are Mr. Noble’s actual words in making “that claim”:

    Noble (10-9-06, 2:27 am): People can read the Herzenberg paper here… In fact the authors make it clear that GSB [a measure of glutathione] is lost progressively in HIV disease. It is a result of the HIV infection and not vice versa.

    And this is what the authors of the study actually wrote:

    Herzenberg et al. (Proc NAS 94:1967-72, 1997): Multiple mechanisms may contribute to systemic GSH deficiency in HIV disease, including excessive production of inflammatory cytokines and excessive use of GSH-depleting drugs.

    The authors also stated that “lower levels of GSB (a…measure of GSH in CD4 T cells) predict decreased survival…the probability of surviving 2-3 years increases dramatically as GSB levels approach normal range.” Contrast that with Mr. Noble’s latest misstatement in suggesting that the study indicates that glutathione (GSH) levels are “not a good predictor.”

    The doubling of survival with higher glutathione apparently means nothing to an HIV true believer, but that 4-6% predictive value of HIV viral load is really something to trumpet!

    For a sound analysis by a real mathematician regarding the recent JAMA study on the poor predictive value of HIV measures, see the new article at Barnesworld by Darin Brown, Ph.D. on “Correlation coefficients, viral loads and T-cell dynamics” (click HERE). Dr. Brown points out that “there is no correlation between viral load and CD4 cell loss to speak of. Almost none of the loss of CD4 counts can be explained by viral load levels. The rest of the paper is nothing more than an attempt to obscure this central fact.”

  15. Chris Noble Says:

    The doubling of survival with higher glutathione apparently means nothing to an HIV true believer, but that 4-6% predictive value of HIV viral load is really something to trumpet!

    On average survival rate increased with glutathione levels. At the individual there was a large variation even in the healthy control group with a significant number of healthy individuals having low glutathione levels.

    On average subjects with HIV viral load measurements above 40,000 copies/ml had almost a fourfold higher CD4 cell depletion rate than those with a viral load below 500 copies/ml. Despite all the waffling by Darin Brown the difference is mathematically significant and won’t go away.

    If Darin Brown has a valid criticism of the paper then he should send it to JAMA for publication.

  16. Truthseeker Says:

    On average subjects with HIV viral load measurements above 40,000 copies/ml had almost a fourfold higher CD4 cell depletion rate than those with a viral load below 500 copies/ml. Despite all the waffling by Darin Brown the difference is mathematically significant and won’t go away.

    Chris, we strongly advise you not to try driving in the UK, since you apparently have no concept of direction.

    If Darin Brown has a valid criticism of the paper then he should send it to JAMA for publication.

    Brown is merely pointing out what the paper actually says, not that it is wrong. Are you even aware of the difference? For example, in connection with your favorite peg to hang your hat on:

    At first I was perplexed trying to reconcile Figures 1 and 2. Each gives the median random-effect model estimate of CD4 cell loss/mm^3/year. However, the two data sets are quite different. The data in Figure 1, quoted in the abstract, are 20.2, 39.3, 47.7, 55.9, and 77.7 cells/mm^3/year for the 5 subgroups of increasing HIV RNA level. However, Figure 2 gives the data 37.3, 42,8, 45,8, 48.9, and 52.2 and there is significant overlap between the cell loss rates in different subgroups, which would indicate that the “simple relationship on average between viral load and rate of CD4+ cell depletion” is not supported. The difference between the two data sets is that the data for Figure 2 were computed using the same model for the entire data set, while for Figure 1, each subgroup was studied in isolation and different random-effects models were used for each subgroup.

  17. Chris Noble Says:

    Chris, we strongly advise you not to try driving in the UK, since you apparently have no concept of direction.

    Are you denying that the results showed that people with a high viral load (>40,000 copies/ml) showed a much larger CD4 depletion rate than those with a low viral load (
    This difference is statistically significant.

    Brown is merely pointing out what the paper actually says, not that it is wrong.

    Compare the paper :

    Our findings confirm previous observations that the magnitude of HIV viremia, as defined by broad categories of presenting HIV RNA level, is associated with the rate of CD4 cell loss…

    with Brown’s comment:

    the “simple relationship on average between viral load and rate of CD4+ cell depletion” is not supported

    Despite your crazy hallucinogenic rhetorical contortions it is Brown that is contradicting the paper and it’s authors. Any assertion to the contrary is evidence of a psychological disorder.

  18. nohivmeds Says:

    CN wrote:

    “Despite your crazy hallucinogenic rhetorical contortions it is Brown that is contradicting the paper and it’s authors. Any assertion to the contrary is evidence of a psychological disorder.”

    Now, Dearest CN, I know you’re not a psychologist or psychiatrist, so that was simply a cheap shot at another commentator at the expense of an entire field of study — which only goes to illustrate your desperation and inability to be open to alterntative interpretations. That, in itself, does not constitute evidence of a psychological disorder, but keep making statements like the one above, and you just might get there. And I’d be sure to let you know, of course, if you had provided me enough evidence to saddle you with a diagnosis.

  19. nohivmeds Says:

    And to TS: I agree entirely that not all interpretations are equally valid — if I had made that argument (which I was accused of making), then I would have been making the postmodern argument which deconstructs science to nothing more than a series of interpretations. Again, I am not making that argument.

    As for whether or not the authors are the worst representatives of their own work — this is only more obvious in psychology, but permeates every scientific field, to be sure. Think about cold fusion, for example.

  20. Robert Houston Says:

    Isn’t monomania a psychiatric disorder? Could the whole field of HIV/AIDS be suffering from it? How else to explain a monolithic fixation that is obliged to interpret all phenomena in terms of a single virus and that excludes from consideration any and all other potential influences on the illness, even well-known factors (such as drug abuse, corticosteroid exposure, and nutrient deficiencies) which have been demonstrated to be rampant in the risk groups and fully capable of causing profound immunodeficiency in their own right?

    As a case in point, when confronted by the doubling of patient survival with the enhancement of a natural antioxidant (glutathione), HIV devotee Noble dismissed this as unimportant compared with an association of HIV viral load with a surrogate marker ! He also steadfastly ignored Figure 2 of the new JAMA report, which shows that a 1000-fold increase in viral load is associated with only a 15 cell decrease in CD4 count, i.e., only 3% of the average total count. (Dr. Darin Brown, a mathematician, pointed out in his recent article that valid subgroup comparisons require that the same mathematical model be applied to all, as was the case in Figure 2 but not Figure 1, which involved “separate models to produce estimates [of] CD4 decline for each HIV RNA stratum,” according to the authors.)

    Be this as it may, the authors of the Sept. 27 JAMA report on the (non) “predictive value of plasma HIV…” have opened the locked door a tiny crack. In their stirring reaffirmation of the faith at Aidstruth, Drs. Benigno Rodriquez and Michael Lederman, sing paeans of tribute to the sacred doctrine in terms bordering on religious fanaticism (e.g., “There is absolutely no doubt that HIV is the cause of AIDS”). But heretofore the tacit or even explicit corollary has been to the effect that “there are no other causes or influences worth mentioning,” i.e., “thou shalt worship no other gods.” At the very end, however, the authors append a summary that seems like a plea to let a thousand flowers bloom. They conclude:

    “Levels of HIV in blood explain only a small portion of the variability in the rate at which CD4 T cells are lost. Therefore… Expanded efforts to identify the other elements that drive CD4 cell losses in chronic HIV infection are needed.”

  21. james Says:

    http://www.altheal.org
    taken from above and below
    http://www.aidsmythexposed.com general section thread titled viral-load doesnt predict cd4

    You might want to read this statement by Rodriguez (JAMA: viral load) and Lederman:

    http://www.aidstruth.org/rodriguez-lederman.php

    “There is absolutely no doubt that HIV is the cause of AIDS.”

    “Our results imply that although HIV infection drives the progressive immune deficiency of AIDS (as evidenced by the response to successful treatment with anti-HIV medicines, which decrease the viral load, increase CD4 cell numbers, and prevent or help resolve opportunistic infections, reflecting an improvement in immune function), there must be other intervening elements that cause progressive CD4 cell losses in HIV infection.”

    “The next obvious question is, “What are the other elements in the fuel mixture that are driving the engine?” We think that this will soon be illuminated. Stay tuned.”

    XXXXXXXXXXXXXXXXX

    The elemant is oxidative enviromental level coupled with low antioxidant levels, either through Eleni’s theory, reduction of apoptosis, shifts rebalancing of th1 th2 balances modulated by oxidation and GSH, cell migration , thymus gland atrophy due to oxidation Or a cobination of all of these or possibly others , but the element behing all of these is low antioxidants particulary GSH, selenium and ongoing increased oxidative, lipid peroxidation levels.

    So the answer is the same what ever you care to think .stop oxidative exposures and address the antioxidant defiencies, the cd4 goes up regardless of viral load , diseases are inhibited, patients put on more weight, have fewer infections and less hospitalisations.

    I just wanted to ram this point home and add a little more data and a reference for that selenium study. Please note the “viral-loads” went down in the combo group and the combo plus selenium group at the SAME rate, so the “viral-loads” in both groups where the SAME and the auther states “Our finding that selenium did not have an effect on viral load levels” however the CD4 rise in the selenium plus combo group was approx 2 and half times that of combo alone, thus the rise in CD4 has nothing to do with “viral-load”, thus this plus al the other studies proves that rises in levels are not related to or caused by the “viral-load” levels but rather high levels of oxidation and low levels of antioxidants like GSH and selenium among others.

    The study examined the impact of selenium supplementation in Nigerians with advanced disease who are on HAART. One hundred and seventy one people with HIV on ART were randomized to receive 200micrograms of selenium daily and 170 people with HIV to receive antiretroviral therapy alone. All patients received an antiretroviral regimen of d4T/3TC and nevirapine.

    HIV viral load, CD4 counts, hematological and biochemical indices were measured at the start of the study (baseline) and then every three months. At each visit, adherence and nutritional counseling were given. Patients were followed for 72 weeks.

    Among the 340 subjects recruited with advanced disease, CD4 cell counts were < 50 cells/mm3.

    Although the median time for undetectable viral load was similar in the two groups (p = 0.2), PLWA on HAART + selenium showed the following distinct advantages over those on HAART alone:

    The rate of CD4 cell recovery was significantly higher; median CD4 count increment from baseline to 72 weeks was almost twofold higher in patients on supplementation (+120 cells/mm3 versus +50 cells/mm3).

    The incidence of opportunistic infections were lower resulting in fewer hospital visits.

    Weight gain was significantly higher (p = 0.004).

    Haemoglobin increment from baseline to 64 weeks was 3-fold higher (+30 g/l versus +10g/l).

    Selenium supplementation resulted in a higher CD4 count response and had a significant impact on the quality of life as evident by weight gain, hemoglobin increment, and fewer hospital visits.

    The study suggests that selenium might be a useful complement to HAART in the management of people with HIV with severe immunosuppression, said Dr N Odunukwe, presenting the study.

    She cautioned that selenium should not be considered as an alternative to antiretroviral therapy: “Our finding that selenium did not have an effect on viral load levels does not suggest that it can be given instead of ART,” she emphasised.
    (ADDED BY JAME :-) selenium has no impact on “viral-load” but it doubles the cd4 ? Oh really is that dissociated non corralation between cd4 and “viral-load” yet again LOL funny how antioxidants often seem to that )

    This subject was debated in the censored and banned BMJ debate, By eleni, Mr Christopher, others and myself and in the altheal paper by John kirkham.

    In the following threaad you will find papers that show 1.Diseases get better before “cd4” goes up and before “viral-load” go down or “undectable”, you will find papers that show that “cd4” rises strt before “viral-load” drops and that drugs like “hiv” protease inhibitors despite “viral-failure/resistance” keep on inhibiting apoptosis thus preserving or even increasing “CD$4” despite “viral-failure/rebound/resistance”.

    In the KS thread there apers that show they work on non “hiv” type KS.

    They also some how reduce/buffer oxidative stimuli of chemicle, radiological origin.I.E. they are some how sometimes having antioxidant increasing effects.
    xxxxxxxxxxxxxx

    ceramide,apoptosis,antioxidants,”cd4″,Atrophy,combo?

    “Eleven, asymptomatic, HIV-1-infected subjects, who refused any antiretroviral treatment despite experiencing a progressive decline of CD4 counts, were treated with daily infusions of L-carnitine (6 g) for 4 months.” (57) “L-carnitine therapy resulted in an increase of absolute CD4 counts, which was statistically significant on day 90 and 150 (P = .010 and P = .019, respectively). A positive, not significant trend was also observed even in the change in absolute counts of CD8 lymphocytes. L-carnitine therapy also led to a drop in the frequency of apoptotic CD4 and CD8 lymphocytes. This reduction occurred gradually, but changes in actual values between each time point and baseline were strongly significant (P = .001 at the end of the study compared with the baseline). A strong reduction (P = .001) in cell-associated ceramide levels was found at the end of the study. In general, HIV-1 viremia increased slightly. No toxicity related to L-carnitine therapy was observed and dose reductions were not necessary. In HIV-1-infected subjects, long-term infusions of L-carnitine produced substantial increases in the rate and absolute counts of CD4 and, to a lesser degree, of CD8 lymphocytes. This was paralleled by a reduced frequency of apoptotic cells of both subgroups and a decline in the levels of ceramide. No clinically relevant change of HIV-1 viremia was observed.”(57).

    “Lymphocytes from subjects infected with the human immunodeficiency virus type 1 (HIV-1) undergo an inappropriate programmed cell death (apoptosis), a major mechanism for the decline of CD4 and CD8 cells that is crucial to the progression towards the overt acquired immunodeficiency syndrome (AIDS).1-8 Indeed, lymphocyte apoptosis correlates with disease progression and lower CD4 counts: a high degree of apoptosis has been detected in patients with AIDS in comparison with long-term nonprogressors.1-8.”(57).

    “Patients with AIDS have significantly higher lymphocyte-associated ceramide levels than healthy individuals and HIV-1-infected long-term nonprogressors have less elevated lymphocyte-associated ceramide levels than subjects with evolving disease.8,20,21 Remarkably, this is paralleled by a lower frequency of apoptotic CD4 and CD8 cells in long-term nonprogressors than in patients with AIDS.8,21”.(57)

    “All of the subjects reported, with no exception, a sense of improved well-being by the second week of L-carnitine treatment.” (57).

    “The analyzed individuals represent a unique population of infected subjects, all of whom were living in the Community of San Patrignano, being exposed to the same environmental influences and with comparable nutritional regimens. Remarkably, in the majority of individuals, there was a past history of HBV or HCV infection and no opportunistic infection was detected during the trial period.”

    “Taken together, our data suggest that long-term L-carnitine administration may have a substantial impact on the chief immunologic abnormality associated with HIV-1 infection, the loss of CD4 T cells, through downmodulating the generation of ceramide and reducing the rate of apoptotic lymphocyte death, without affecting the HIV-1 viremia levels, thus suggesting that a dissociation exists between changes in viremia and CD4 depletion.” (57)

    Evidence has existed since 1997 and before that the “viral-load” is or can be dissociated from the CD4 depletion, in the study sited above which has been deliberatley ignored by “aids” “science” because it blows a massive indesputable hole in there stupid over simplified religious “hiv” theory. All these 100% patients had declining CD4’s for months before L carnitine/antioxidant infusion, in all 100% of patients they had significant increases in CD4 with either no change no decline in “viral-load” or even increases in “viral-load” with NO SIDE EFFECTS accept all patients had fewer infections, fewer hospital admissions and 100% reported feeling better, “aids” “sciences” and medicines answer to this syudy was either to ignore it or even censore it. In the link to the ceramide thread you will find studies that show that the CD4 increases in people on P.I. based combo start long before the “viral-load” load decreases and that when “drug-failure” /”viral-resistance-rebound-increase” takes place the P.I. based combo’s continue to reduce/inhibit apoptosis-cell death sustaining the cd4 level regardless of the increase in “viral-load”.

    If “aids” science was science and not a greedy ,corrupt, religion , real scientist would of done larger in vivo human research into antioxidants like l carnitine study which would of provided us with very clear cut answers, they didnt because they didnt want to know that the cd4 is dissociated from “viral-load”, there wouldnt of been any risk either because there was NO toxicity reported, no side effects and its cheaper than the toxic expensive “arv’s”.

    So we have tunnle vision and religion running medicine and “aids” “science” afraid of questions, afraid of debate and afraid of been proven how wrong they are.

    Antivir Ther. 1999;4 Suppl 3:7-11.

    Sustained CD4 responses after virological failure of protease inhibitor-containing therapy.

    Deeks SG, Grant RM.

    University of California and San Francisco General Hospital, San Francisco, California, USA. sdeeks@php.ucsf.edu

    This article explores current controversies related to ‘discordant’ responses to antiviral therapy, that is to say, patients with a sustained CD4 cell response despite virological failure. Observational clinical data of patients receiving protease inhibitor-based therapy who had a sustained CD4 cell count even with incomplete viral suppression will be presented, as well as possible mechanisms and clinical implications.

    Publication Types:
    xxxxxxxxxxxxxxxxxx

    The Journal of Immunology, 2003, 170: 6006-6015.
    Copyright © 2003 by The American Association of Immunologists

    Mitochondrial Membrane Hyperpolarization Hijacks Activated T Lymphocytes Toward the Apoptotic-Prone Phenotype: Homeostatic Mechanisms of HIV Protease Inhibitors

    “A decrease of mitochondrial membrane potential has been hypothesized to be a marker of apoptotic cells, including activated T lymphocytes. It was recently demonstrated that HIV protease inhibitors, independently from any viral infection, can hinder lymphocyte apoptosis by influencing mitochondrial homeostasis”

    “They also suggest that HIV protease inhibitors, by interfering with induction of the mitochondrial hyperpolarization state, can result in cell survival even independent of any viral infection”

    ” In contrast, some in vitro and ex vivo studies suggested that PIs, independent from any viral infection, were able to inhibit PBMC loss and to restore impaired T cell proliferative response (16). Accordingly, apoptotic cell death of both HIV-infected and uninfected cells was apparently inhibited. ”

    xxxxxxxxxxxxxxxxxxxx

    Clinical &Experimental Immunology
    Volume 118 Issue 3 Page 412 – December 1999
    doi:10.1046/j.1365-2249.1999.01076.x

    “HAART may increase CD4+ T cell counts despite a persistently detectable HIV load. The impact of HAART on apoptosis, which may play a role in the disease process in HIV-infected patients, has not been extensively studied”

    “We did not observe any correlation between the HIV viraemia and the level of apoptosis of T cell subsets. patients with HAART showed a lower percentage of apoptotic CD4+ T cells only: 16% (range 261%) versus 25% (range 573%) for patients receiving two nucleoside analogues (P = 0.02). T”

    “In conclusion, HAART, without any relation to plasma viraemia, is able to reduce apoptosis of CD4+ T cells. ”

    xxxxxxxxxxxxxxxxxxxxxxxx

    Decreased HIV-associated T cell apoptosis by HIV protease inhibitors.

    Phenix BN, Angel JB, Mandy F, Kravcik S, Parato K, Chambers KA, Gallicano K, Hawley-Foss N, Cassol S, Cameron DW, Badley AD.

    Department of Biochemistry, Microbiology, and Immunology, University of Ottawa, Ontario, Canada.

    “Emerging evidence suggests that some of the improvements in CD4+ T cell number that occur in response to protease inhibitor (PI) therapy may not be accounted for solely by enhanced viral suppression, implying that PI may directly affect T cell survival”

    “8 days of PI therapy in HIV-infected patients does not significantly alter plasma viremia, yet results in significant inhibition of CD4+ and CD8+ T cell apoptosis. The inhibitory effects of PI on apoptosis have implications concerning the treatment of HIV and its pathogenesis.”

    xxxxxxxxxxxxxxxxxxxx

    Front Biosci. 2004 Jan 1;9:338-41.

    Antiretroviral therapy influences cellular susceptibility to apoptosis in vivo.

    Cooper CL, Phenix B, Mbisa G, Lum JJ, Parato K, Hawley N, Angel JB, Badley AD.

    Division of Infectious Diseases, The Ottawa Hospital-General Campus, Ottawa, ON, Canada. ccooper@ottawahospital.on.ca

    It has been proposed that antiretroviral therapies (ART) possess both antiviral and immunomodulatory activities when used in HIV infected patients.Few studies have addressed whether these putative immunomodulatory effects are also seen in HIV negative patients, for example, when used for post exposure prophylaxis (PEP). We chose to evaluate immunologic function in HIV negative patients who received Nelfinavir and Combivir (AZT and 3TC) as PEP. Lymphocytes from patients taken immediately before, during, and after PEP were analyzed. No changes were seen in absolute or percent CD4 or CD8 T lymphocyte numbers, nor in markers of activation, memory, or co-stimulatory molecules. Surface expression of apoptosis-related ligands and receptors were unaltered, but apoptosis susceptibility was significantly inhibited by PEP (P less than 0.05). These data confirm in vitro that apoptosis susceptibility is altered by ART, including in HIV-negative patients who take PEP.”
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    http://www.bloodjournal.org/

    Human Immunodeficiency Virus Type 1 Protease Inhibitor Modulates Activation of Peripheral Blood CD4+ T Cells and Decreases Their Susceptibility to Apoptosis In Vitro and In Vivo
    By Elaine M. Sloand, Princy N. Kumar, Sonnie Kim, Aniruddho Chaudhuri, Frank F. Weichold, and Neal S. Young

    .” In this study, we examined the effect of protease inhibitors on Fas-R (CD95), ICE (caspase 1) expression, apoptosis, and cell death in CD4+ T cells of (1) HIV-infected patients who were receiving protease inhibitors, and (2) normal and patient CD4+ T cells cultured with a protease inhibitor in vitro. Fifteen patients with advanced HIV disease on treatment showed dramatically decreased CD4+ T-cell ICE expression, diminished apoptosis, and increased numbers of CD4+ cells within 6 weeks of institution of protease inhibitor therapy, and before down-modulation of Fas-R (CD95) expression was evident. To determine the role of HIV infection, we studied the effect of ritonavir, a protease inhibitor, on normal and patient cells in vitro. Stimulated and unstimulated normal CD4+ T cells, cultured with protease inhibitor, demonstrated markedly decreased apoptosis and ICE expression (P = .01). While Fas-R expression was not significantly altered during short-term culture by such treatment, Fas-Ligand (Fas-L) membrane expression of phytohemagglutinin (PHA)-stimulated blood lymphocytes was decreased by protease inhibitor. In the presence of ritonavir, CD4+ T cells from HIV-infected patients showed similar changes in ICE intracellular levels without alteration of Fas expression. In conclusion, protease inhibitors appear to decrease CD4+ T-cell ICE expression and apoptosis before they affect Fas-R expression in HIV-infected patients. This action was independent of HIV infection, as similar effects were seen in CD4+ T cells from normal controls. ”

    Some of the benefit of protease inhibitors may be related to modification of programmed cell death, which increases CD4+ T-cell number.

    ” However, clinical data suggest that the beneficial consequences of protease inhibitors persist even after viral resistance to the drug has developed,20 and these drugs may thus affect the immune system, independent of their inhibition of retroviral replication. ”

    “In vitro experiments, using CD4+ T cells from normal uninfected controls, showed similar significant declines in ICE expression, apoptosis, and cell death when lymphocytes exposed to Fas agonist or cultured in the absence of IL-2. Protease inhibitors may thus exert effects on apoptosis, independent of their effects on HIV, by affecting directly or indirectly the generation of active ICE protein in the apoptotic pathway. ”

    “One implication of our findings is that inhibitors of ICE or CD4 apoptosis, without antiviral activity, may have potential therapeutic utility in the treatment of HIV infection, even in patients with low viral loads.”

    Antivir Ther. 2005;10 Suppl 2:M29-45.

    HIV protease inhibitors prevent mitochondrial hyperpolarization and redox imbalance and decrease endogenous uncoupler protein-2 expression in gp 120-activated human T lymphocytes.

    Matarrese P, Tinari A, Gambardella L, Mormone E, Narilli P, Pierdominici M, Cauda R, Malorni W.

    Department of Drug Research and Evaluation, Istituto Superiore di Sanita, viale Regina Elena 299-00161 Rome, Italy.

    It has been demonstrated that HIV protease inhibitors (Pls) are able to inhibit apoptosis of both infected and uninfected T cells
    xxxxxxxxxxxxxxxxxxxxxxx

    http://www.bloodjournal.org/

    Blood, 15 March 2001, Vol. 97, No. 6, pp. 1898-1901
    CORRESPONDENCE

    To the editor:
    T-cell apoptosis in HIV-1-infected individuals receiving highly active antiretroviral therapy

    Recently, Lu and Andrieu1 stated that the HIV-1 protease inhibitors (PIs) indinavir and saquinavir used in concentrations at least 30-fold lower than those needed for 90% viral inhibition apparently do not influence sensitivity of peripheral blood T cells from HIV-1-infected individuals toward apoptosis induced either by T-cell receptor/CD3 ligation or by direct triggering of the CD95 receptor in vitro.1 They conclude from their data that the beneficial effect of PI treatment on clinical and immunological parameters in HIV-1-infected patients, which can be encountered even in the absence of relevant virological effects, are not related to changes in T-cell apoptosis.

    In our own study in a cohort of HIV-1-infected children and adolescents, we had observed an increased sensitivity of freshly isolated T cells toward apoptosis,2 which was rapidly down-regulated following initiation of highly active antiretroviral therapy including PIs (HAART).3 Here we report that prolonged PI treatment in vivo reduced sensitivity of peripheral blood T cells toward apoptosis in vitro even when plasma viral load levels were not decreased and susceptibility for T-cell activation in these patients was not down-regulated.

    “Our observations suggest that the reduced T-cell sensitivity toward CD95-induced apoptosis in vitro might partly explain the observation that an increasing number of patients with virological rebound on PI therapy maintain stable CD4 counts and do not experience clinical deterioration as fast as one could expect from the increased viral load.

    xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx

    “http://www.thebody.com

    Treatment Action Group
    Antiretroviral Horizon: 35th Interscience Conference
    Unveils Results from Several
    Important Clinical Studies
    Protease and paradox

    November 1995

    Saquinavir (Invirase )
    Ann Collier of the University of Washington presented long-term follow-up data from ACTG 229, the 302-patient study which compared AZT+ddC to AZT+saquinavir to AZT+ddC+saquinavir. She showed that while throughout the first six months there were greater CD4 and viral load changes in the the triple-therapy arm compared to the two double-drug arms, clinically the three groups fared the same. [Yet another nail in the surrogate marker coffin.] ”
    “Jonathon Schapiro of Stanford presented an open-label study of two higher doses of saquinavir. Twenty patients each were randomized to receive 3,600 or 7,200 mg saquinavir daily for 24 weeks. Mild liver function test elevations, confusion and gastrointestinal upset were reported at the 7,200 mg dose. CD4 counts rose by an average of 72 cells/mm3 at 4 weeks and by 121 cells at 20 weeks. Thirteen of the forty patients developed either the 48 or 90 mutation over the course of the study; suggesting, but not proving, that the higher doses delay the emergence of resistance. (In a European study of regular dose saquinavir, 50% show low level resistance at week 25, and the rest develop it by week 52.) Curiously though, while the resistance-conferring mutations did not emerge until week 20, plasma HIV-RNA levels bottomed out and began to rebound after only 4 weeks of high-dose saquinavir therapy.”

    Caution !

    A higher CD$4 count does not always pridict increased survival.

    http://www.duesberg.com

    A Ray Of Hope
    Transcript UK BBC Documentary
    Panorama London, March 1996

    Retrovir, the drug better known as AZT, is a billion pound success for a British drug company. But can it do more harm than good? Tonight, Panorama reports on the controversial drug sold as a ray of hope.

    .

    Prof. Weller: “It was important therefore to at least run a trial for several years to get handle on whether it actually did any good in the long term in people that were well.”

    The company in line with some other experts also wanted to rely on a more immediate measure. AZT’s effect on patients’ blood. In particular their number of CD4 blood cells thought vital to the strength of the immune system. The study’s British Chairman rejected this, believing AZT might artificially raise this blood count, without bringing any real health benefit.

    Prof. David Warrell: “We were worried that the CD4 count might be a cosmetic measure.”

    Reporter: “Why then would the company want to include a CD4 count?”

    Prof. Warrell: “Well a CD4 count had the great advantage that the changes were seen early on. Clearly the longer the study the more expensive, the more delayed the results.”

    In fact it looked worse. The figures showed that more patients died among those who took AZT early. 96 died taking it early, 76 taking it late. But the investigators were cautious and anxious to avoid causing alarm. They calculated that given the size of their samples of patients the difference in death rates could be due to chance. It was not statistically significant.

    Dr. Tim Peto: “We were very concerned indeed to avoid scaremongering and statistically that 96 is the same as 76 even though mathematically they’re different.”

    Reporter: “But in fact the result was the wrong way?”

    Dr. Peto: “The result were certainly the wrong way mathematically yes.”

    There was also a paradox. While it did not improve survival, taking AZT early did raise the level of patients’ CD4 blood cells. So it should in theory give them longer life. But it didn’t.

    Prof. David Warrell: “It did seem to be a surrogate marker of potentially misleading index.”

    Reporter: “But this was one of the markers which the company had relied on in its own trial of AZT.”

    Prof. Warrell: “Exactly, so we felt vindicated in our reserve or scepticism about what one could infer from the CD4 count alone.”

    The Concorde doctors had agreed to publish a quick summary of their initial findings. But as Wellcome still maintained the value of CD4 counts this led to further disagreement still maintained the value of CD4 counts this led to further disagreement. The Committee Chairman tried to agree a form of words with the company to go as a letter in The Lancet.

    Prof. Warrell: “The company representatives wanted to tone down the wording of the letter. As the publication data approached the telephone communication was more and more frequent and more and more frenzied, and it really almost degenerated into a matter of considering individual adjectives. We wanted to say the results casts serious doubt on the value of using changes in CD4 counts. A serious doubt. The company were very keen that we should delete ‘serious’, so we deleted ‘serious’ under pressure from the company.”

    A week after the first Concorde results the letter appeared in The Lancet in April 1993.

    Newsman: “British drug company Wellcome has made millions selling AZT and today its shares fell over 15 pence or 7% of the company’s value.”

    AZT came under attack from patients in Britain whose hopes had been dashed.

    Pascal de Bock: “Initially I took the whole box of my tablets and put them in the bin and I mean well all the side effects disappeared. Somehow I wanted to make the wider public know that there was something, a very darker side into that marvellous treatment to help those people who suffer so much. Then suddenly the Concorde trial results just appeared and I felt really ecstatic. It was absolutely marvellous for me to realise that what the decision that I had made without somehow any medical advice had been the right one to make.”

    But the Wellcome Foundation seemed less ecstatic. Four days after the Concorde results at its London headquarters the company briefed the press and city analysts like Peter Cartwright about the trial’s findings.

    Peter Cartwright: “It wasn’t the sort of meeting where maybe its been laid on for months in advance and its well scripted and well rehearsed and comes across as a very slick and very professional affair. This one was damage limitation and called at short notice and the company were on the back foot a little bit.”

    Reporter: “Why do you call it damage limitation?”

    Cartwright: “Well because the share price was falling very rapidly.”

    The company told the press that an adequate analysis of Concorde would show it to fit their own shorter term studies suggesting that early treatment can improve survival. But this was the exact opposite of what Concorde had found. One of the company’s overhead slides shown to the press contradicted another Concorde finding, saying survival appears to be correlated with CD4 response.

    Prof. Ian Weller: “If anything Concorde showed that there wasn’t a correlation between CD4 and survival, so the whole exercise and its a personal view, was one of damage limitation.”

    Reporter: “Was it a distortion of your findings?”

    Prof. Weller: “I think you could interpret some of the overheads as a distortion of the conclusion, the main result, the bottom line of Concorde.”

    Prof. David Warrell: “Both the Chairmen of the co-ordinating committee were outraged by this behaviour of the Wellcome Foundation. I composed a letter and sent it to the Wellcome protesting the misleading information provided at the city meeting.”

    Reporter: “Did you get a response?”

    Prof. Warrell: “We didn’t.”

    Panorama wanted to ask Wellcome staff about their comments to analysts and the press. Dr. Trevor Jones, then Director of Research, and Dr. Paul Fiddian a member of the Concorde team – they both declined to be interviewed.

    Later that year, in December 1993, the whole Concorde team met in a hotel at Paris Airport to approve the wording of their full report. There were disagreements on points of scientifical detail, and one overriding problem.

    Prof. Weller: “Although there were lots of discussions about small points and indeed we did accommodate some of the suggestions, trying to work together on it, the real thing was the last sentence of the paper, and that was the result of this study do not encourage the early use of AZT.”

    In a compromise with the company this conclusion had been left out of the first letter in The Lancet. Now Wellcome wanted to delete it from the full report too.

    Prof. Warrell: “Really it was the conclusion, the main conclusion that they couldn’t swallow.”

    Reporter: “Why couldn’t they swallow it?”

    Prof. Warrel: “Well why means why scientifically or why commercially, I mean why commercially because this would decrease the market of one of their best selling drugs. Why scientifically we could never really understand.”

    Reporter: “There was deadlock. The Wellcome representatives continued to insist on deleting this sentence.”

    Prof. Warrell: “I must say we were a great deal more obstinate this time than we were over the letter because of our experience of the letter. There was no certainty at all that had we compromised the company would not have reneged again after publication.”

    Prof. Weller: “The company rehearsed its criticisms again and then late on in the meeting stated that they felt they couldn’t endorse the report.”

    Panorama wanted to ask why, but Dr. Thierry Nebout and Dr. Jane Yeo the two Wellcome scientists at the meeting have declined to be interviewed.

  22. james Says:

    I dont know if Mr Christopher Nobel is still reading this thread, but if you are I just wanted to thank you for your kind ,co operative , positive comments on another site , I wanted to reply but the “moderator” ended the discussion.

    Also please pass on my regards and thanks to Nicholas Bennett .

  23. james Says:

    “). In particular, it has been suggested that changes of mitochondrial membrane potential ()2 play a key role in apoptotic cascade. Given the important role of apoptosis in the pathogenesis and progression of HIV infection, several studies have specifically focused on apoptosis mechanisms in both HIV-infected and uninfected CD4+ cells (4, 5). In particular, a major role of the mitochondria in the process of CD4 T cell death has been suggested (6, 7). In fact, the reduction of CD4+ cell loss by apoptosis has been considered to be an important aspect of immune reconstitution under highly active antiretroviral therapy (HAART) (8, 9). This is a clinical approach that involves, among others, drugs of different nature, such as HIV reverse-transcriptase inhibitors, e.g., zidovudine (AZT), and HIV protease inhibitors (PIs). Those most commonly used are nelfinavir, indinavir (ind), saquinavir (saq), and, very recently, lopinavir (lop). Their “combined activity leads to viral load lowering as well as to reduced cell loss. Several lines of evidence have schematically indicated that AZT may be an apoptotic inducer (10), while PIs can be considered as apoptosis-hindering drugs (9, 11, 12). More specifically, the use of AZT, although of relevance in the control of the progression of the disease through direct activity on viral replication, was demonstrated to be per se cytotoxic to the immune system cells (13). In particular, some studies clearly indicated that AZT was irreversibly incorporated into mitochondrial DNA inducing
    mitochondrial dysfunction by acting on polymerase and inhibiting oxidative phosphorylation (14, 15). This resulted in apoptotic cell death process (10, 15). In contrast, some in vitro and ex vivo studies suggested that PIs, independent from any viral infection, were able to inhibit PBMC loss and to restore impaired T cell proliferative response (16). Accordingly, apoptotic cell death of both HIV-infected and uninfected cells was apparently inhibited”

    Activated cells

    In contrast, results obtained in activated human lymphocytes (Fig. 1B) were the following: 1) apoptotic proneness of activated lymphocytes was significantly higher compared with resting cells, and 2) receptor-mediated stimuli (TNF-, TRAIL, anti-Fas) were characterized by lower values of apoptosis (54, 22, and 34%, respectively) compared with radiation (>80%); more importantly, 3) a significant decrease in cell loss by apoptosis was found in activated human T lymphocytes pre-exposed to PIs before exposure to various apoptotic inducers (Fig. 1B). In particular: 1) the protection conferred by PIs (ind, saq, and lop, 100 nM) was, regardless of the stimulus used, significant in receptor-mediated (anti-Fas, TNF-, TRAIL) as well as in receptor-independent (UVB and UVB + anti-CD95/Fas-neutralizing Ab) apoptosis, and 2) no significant difference was found between various PIs in terms of antiapoptotic activity. Specifically, the mean values obtained from quantitative cytofluorometric analysis (conducted by pooling together the results obtained with ind, saq, and lop) indicated that PIs were capable of significantly reducing TNF—mediated apoptosis (-70.1 ± 7%), Fas-mediated apoptosis (-55.4 ± 8%), TRAIL-induced apoptosis (-49.0 ± 6%), and UVB-mediated apoptosis (-79.6 ± 8%) in activated T cells. In Fig. 1, only the results obtained with ind and saq have been reported.

    “Because mitochondria hyperpolarization has been related to ROI hyperproduction (29), quantitative analysis of ROI generated during lymphocyte activation in the presence or absence of various PIs (saq, ind, and lop) was also performed by flow cytometry. In Fig. 3B, the increased ROI production detected using DHR 123 in activated T cells compared with resting cells can be observed (compare resting and IL-2/PHA dot plots and histograms). In particular, this increased ROI production was overall detected in a subset of lymphocytes that increased their physical parameters, i.e., their volume (dot plots, R2 region), as detected by fluorescence intensity histograms (green lines). Importantly, PI drugs, e.g., lop, were capable of significantly hindering both ROI production (green lines, see median values in the histograms) and changes in physical parameters described above and detectable in activated T lymphocytes (dot plots, R2 region). Hence, PIs (saq, ind, and lop) were able to significantly prevent either mitochondria hyperpolarization (Fig. 3A) or oxidative imbalance (Fig. 3B) associated with IL-2/PHA activation. Only data obtained with lop, considered as representative results, are shown in Fig. 3.”

    “Effects of PIs on AZT subcellular activity

    Previous reports suggested that one of the most important drugs in the management of AIDS, i.e., AZT, can be considered an apoptotic inducer in activated lymphocytes (10). More interestingly, it was also suggested that mitochondria could represent an important intracellular target of this drug (34, 35, 36, 37). We thus decided to evaluate whether mitochondrial toxicity and subsequent apoptosis induced by AZT could be counteracted by PI subcellular activity. We used AZT as mitochondriotropic drug and apoptotic inducer in untreated or PI-treated IL-2/PHA-activated lymphocytes. Results reported in Fig. 4, A and B (because no significant differences were detected among various PIs, only representative results obtained with ind are shown), clearly showed that: 1) PIs prevented AZT-induced apoptosis (Fig. 4A) and 2) this protection was mediated by a protective effect exerted on mitochondrial homeostasis (Fig. 4B, left panels, III quadrant). In addition, our results also show that: 3) AZT sensitized lymphocytes to receptor-mediated apoptotic triggering, e.g., by anti-Fas (Fig. 4A) and that 4) this sensitization was paralleled by an increase in the percentage of cells with depolarized mitochondria (Fig. 4B, right panels). Overall, these findings suggest that: 1) AZT-induced mitochondrial-mediated cell death of activated lymphocytes can be significantly prevented by PIs (the mean decrease of apoptosis exerted by PIs was 74 ± 12%, pooling results from saq, ind, and lop) (Fig. 4A); 2) the percentage of cells with depolarized mitochondria can be significantly lowered by pretreatment with PIs (data obtained by using saq, ind, and lop pooled together showed a mean decrease of 68 ± 8%) (Fig. 4B); 3) a significant correlation exists between the two events (r = 0.978, p < 0.001); and, finally, 4) cumulative synergic proapoptotic effects of AZT and various proapoptotic stimuli, e.g., by anti-Fas (Fig. 4A), can be counteracted by different PIs. In Fig. 4, A and B, considering the similar behavior exerted by PIs toward various apoptotic stimuli, only the more extensively studied physiologic stimulus, i.e., anti-Fas, is shown.

    Plus AZT depletes intracellular glutathione, induces cell death, mitochondrial damage, P.I.’s reduce this oxidative effect of AZT , P.I. based “haart” has been shown to increase intracellular GSH, plasma vitamin c and vit e levels as well as reduce apoptosis induced by oxidizers like radiation, AZT,Morphine,hydrogen peroxide.

    Like antioxidants do with the above plus other oxidizers like crystal meths which depletes/makes? cd4 dissapear/migrate after all we measure only the blood that has 2% of the t cell populaton in redicence temporily.

    Lancet Oncol. 2003 Sep;4(9):537-47.
    Use of HIV protease inhibitors to block Kaposi’s sarcoma and tumour growth.

    Sgadari C, Monini P, Barillari G, Ensoli B.

    Senior Investigators at the Laboratory of Virology, Istituto Superiore di Sanita, Rome, Italy.

    HIV protease inhibitors are antiretroviral drugs that block the enzyme required for production of infectious viral particles. Although these agents have been designed to selectively bind to the catalytic site of HIV protease, evidence indicates that other cellular and microbial enzymes and pathways are also affected. It has been reported that patients treated with highly active anti-retroviral therapy (HAART) containing a protease inhibitor may be at reduced risk of Kaposi’s sarcoma (KS) and some types of non-Hodgkin lymphomas; some disease regressions have also been described. Here we review recent data showing that several widely used protease inhibitors, including indinavir, saquinavir, ritonavir, and nelfinavir, can affect important cellular and tissue processes such as angiogenesis, tumour growth and invasion, inflammation, antigen processing and presentation, cell survival, and tissue remodelling. Most of these non-HIV-related effects of protease inhibitors are due to inhibition of cell invasion and matrix metalloprotease activity, or modulation of the cell proteasome and NFkappaB. These elements are required for development of most tumours. Thus, by direct and indirect activities, protease inhibitors can simultaneously block several pathways involved in tumour growth, invasion, and metastasis. These findings indicate that protease inhibitors can be exploited for the therapy of KS and other tumours that occur in both HIV-infected and non-infected individuals. A multicentre phase II clinical trial with indinavir in non-HIV-associated KS is about to start in Italy.

    Publication Types:
    Review

    PMID: 12965274 [PubMed – indexed for MEDLINE]

    xxxxxxxxxxx

    Drug Resist Updat. 2003 Aug;6(4):173-81.

    HIV protease inhibitors as new treatment options for Kaposi’s sarcoma.

    Barillari G, Sgadari C, Toschi E, Monini P, Ensoli B.

    Laboratory of Virology, Istituto Superiore di Sanita, V.le Regina Elena, 299, 00161 Rome, Italy.

    A reduced incidence and regression of Kaposi’s sarcoma (KS) and other tumours has been reported in Acquired Immune Deficiency Syndrome (AIDS) patients treated with antiretroviral combination therapies containing Human Immunodeficiency Virus (HIV) protease inhibitors (PIs) such as indinavir or saquinavir. Indeed, evidence indicates that although PIs were designed to selectively inhibit the HIV protease activity, they can interfere with several cellular pathways and can inhibit tumour growth. In particular, our recent results indicate that doses of indinavir or saquinavir similar to those employed to treat AIDS patients can induce regression of experimental KS by directly blocking two fundamental steps of KS initiation and progression: new blood vessel formation (angiogenesis) and KS tumour cell invasion. This is because indinavir or saquinavir inhibit the activation of matrix metalloproteinase-2 (MMP-2), a basement membrane-degrading enzyme, which is required for the progression of most tumours. Based on these results, a multicentre clinical trial is now starting in Italy, which will assess PI effects on the progression of KS in HIV-uninfected individuals (classical KS).

    Publication Types:
    Evaluation Studies

    PMID: 12962683 [PubMed – indexed for MEDLINE]
    xxxxxxxxxxxxxxxxxxxxxxxxxxxxxx

    Antioxidants NAC and GSH inhibits TB in vitro in humans with “hiv”, selenium defiency (involved in GSH production) in drug users predicts 13 fold liklyood of TB. crystal meths increases “fiv” 15 fold it oxidizers, it depletes GSH , it induces cell death/apoptosis and acetyl l carnitine (raises gsh amognst others things like mitochondria) and NAC a pro GSH agent block /reduce apoptosis induced by crystal meths, heroine and other recreational drugs /medical drugs “arv’s”/chemo’s.

    Also these agents could reduce and delay the need for more expensive and toxic “arv’s” which aslo have broad spectrum antimicrobial effects against many if not all the “O.Is” that are sometimes called “aids”.

    Antioxidants can also be used if “arv” treatment is need, they can be used along side and when they are there is very good evidence that negative/side effects/toxicity/ozidation can be reduced by combinations of antioxidants , micro nutrients ect and that these agents an also increase the positive effects of “arv’s”.

  24. james Says:

    Nac NIH/NCI 2001 study reverses established KS in vivo model and doubles the life span. Ks occurs in the absence of “aquired immune defiency” i is not caused by either hhv-8 or immune suppression low cd4.

    Whats really crazy about all in this artical this is that sadley the artical does not get the “hiv” protease inhibitors have there anti KS effects regardless of “viral” presence or non presence. Even with “viral” rebound “drug resistance” as already shown PI’s have the anti apoptosis effects independant of “viral” presence or non presence. And of course independant of “CD4” levels LOL.

    I hope you dont mind but I would like to repost the previouse two references about “hiv” specific LOL protease inhibitors treating non “hiv” kaposi Sarcoma in vitro and invivo and now trialed in humans. I would like to post them in the KS not aids post on here becusause they belong there as well, these two post are interlinked because others and I hypothesise the “hiv” P.I.’s act like antioxidants sometimes interefering with apoptosis/cell death INDEPENDANT of “viral” presence or not particulary so with activated t cells.

    PPPPPPSSSSSSSSSSSSTTTTTTTTT
    REMEMBER NAC INHIBITS?REVERSES KS IN VIVO< WELL P.I’S RAISE GSH AS WELL AS REDUCING OXIDATIVE STMULI JUST LIKE NAC DOES.

    xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx
    http://www.thebody.com/catie/switch_ks.html

    Canadian AIDS Treatment Information Exchange
    French Doctors Suggest That Therapy Switch May Cause KS Relapse

    By Sean R. Hosein

    July 8, 2003

    Kaposi’s sarcoma (KS) is a tumour that usually appears on the skin and most commonly affects gay and bisexual men with HIV/AIDS. KS was more common in North America and Western Europe at the beginning of the AIDS epidemic than it is now. Although KS most commonly affects the skin, over time, as immunity weakens, KS tumours can develop inside the body, particularly near lymph nodes and the digestive tract and in mucous membranes such as the mouth. As the tumours grow they can block lymph vessels, causing fluid to build up, which results in discomfort, further complications and even death. Treatments available for KS include radiation and chemotherapy, but these have seldom resulted in a cure for KS in people with HIV/AIDS (PHAs).
    In the mid-to-late 1990s, protease inhibitors (PIs) became widely available in high-income countries. When used as part of combination therapy, PIs helped put KS into remission. Researchers suspected that this occurred because PI combination therapy raised CD4+ cell counts and reduced levels of HIV in the blood. The changes in cell counts and viral load allowed the immune system a chance to begin repairing itself and perhaps to better fight KS tumours.

    However, this theory may now have to be reexamined, based on new findings from Paris, France. There, doctors reported that five PHAs who switched from a PI-based regimen to a regimen based on non-nukes (NNRTIs), such as efavirenz (Sustiva, Stocrin) or nevirapine (Viramune), had relapses in their KS.

    PI Therapy
    At the time the PHAs were originally diagnosed with KS, all five had “widespread” skin tumours. They received chemotherapy and/or radiation therapy. Eventually they took PI-based combination therapy for about 2½ years, and their KS went into remission and cleared up. However, three of the PHAs’ therapy was eventually unable to suppress HIV levels; the remaining two wanted simpler regimens. So doctors changed their combinations to ones based on non-nukes instead of PIs.

    After the Switch
    On average, the KS relapsed one year after the PHAs switched from PIs to a non-nuke. At the time the relapse occurred, in four of the five PHAs, CD4+ cell counts were relatively high — ranging between 350 and 1,300 cells. Also, in four of the five PHAs, viral loads were low — fewer than 20 copies.

    PIs and KS
    The doctors note that the recurrence of KS in their patients cannot be explained by low CD4+ counts or high viral loads. In seeking other explanations, the doctors report certain results of test-tube and animal experiments done by researchers. In these experiments, PIs seem to prevent the growth and development of KS tumours. The drugs appear to do this by blocking the production of growth factors (chemical messengers) needed by KS cells. Moreover, exposure to PIs caused KS cells to die.

    The report by the French doctors about KS relapse is interesting. However, much more study and analysis is needed to confirm these findings in other PHAs as well as to reconcile them with results from other clinical trials where combination therapy with either PIs or NNRTIs resulted in the regression of KS.

    In the meantime, the French doctors warn that other doctors should use caution when switching their patients who previously had KS from a PI to an NNRTI.

    References
    Sgadari C, Barillari G, Toschi E, et al. HIV protease inhibitors are potent anti-angiogenic molecules and promote regression of Kaposi sarcoma. Nature Medicine 2002; 8(3):225-232.
    Gaedicke S, Firat-Geier E, Constantiniu O, et al. Anti-tumor effect of the human immunodeficiency virus protease inhibitor ritonavir: induction of tumor-cell apoptosis associated with perturbation of proteasomal proteolysis. Cancer Research 2002; 62(23):6901-6908.
    Bani-Sadr F, Fournier S and Molina JM. Relapse of Kaposi’s sarcoma in HIV-infected patients switching from a protease inhibitor to a non-nucleoside reverse transcriptase inhibitor-based highly active antiretroviral therapy regimen. AIDS 2003;17(10):1580-1581.
    Gill J, Bourboulia D, Wilkinson J, et al. Prospective study of the effects of antiretroviral therapy on Kaposi’s sarcoma-associated herpes virus infection in patients with and without Kaposi’s sarcoma. Journal of Acquired Immune Deficiency Syndromes 2002;31(4):384-390.

  25. Gene Semon Says:

    From Robert Houston:

    Drs. Benigno Rodriquez and Michael Lederman, sing paeans of tribute to the sacred doctrine in terms bordering on religious fanaticism (e.g., “There is absolutely no doubt that HIV is the cause of AIDS”). But heretofore the tacit or even explicit corollary has been to the effect that “there are no other causes or influences worth mentioning,” i.e., “thou shalt worship no other gods.” At the very end, however, the authors append a summary that seems like a plea to let a thousand flowers bloom. They conclude:

    “Levels of HIV in blood explain only a small portion of the variability in the rate at which CD4 T cells are lost. Therefore… Expanded efforts to identify the other elements that drive CD4 cell losses in chronic HIV infection are needed.”

    Again, thanks for the clarity, Robert Houston. Here we see the JAMA RNA/CD4 authors exhibit the appropriate ritualistic behaviours to maintain their continued funding AND proceeding in a scientific manner with a comment that moves the discussion forward.

    Additionally, the comments by rethinker James display our non-monomania (!?) – and how much poor Chris is in over his head – , i.e. evaluating the use of pharma drugs when appropriate models indicate their efficacy.

    I feel sorry for Chris N because he doesn’t get what’s going on. At this point, any reasoning, literate person can see the unsatifactory performance of the surrogates pol or gag RNA that “explain only a small portion of the variability in the rate at which (surrogate for AIDS)* CD4 cells are lost” based on the single virus causing single disease epidemic model. *(parens added)

    When one decides, based on this poor performance, to revisit biological plausibility, strength of the association – i.e marker, not the agent itself – , etc. and concludes that reorderings of the identified risk factors/diseases/treatments (e.g. James above), in the collective phenomena known as AIDS, are necessary for progress; that person must have a psychiatric disorder. Of course.

    I am taking Chris’ advice and submitting to the DSM IV a new disease, “failure to take instructions from the established authorities in science: autocognitive-mania”. In a falsification process known as the Catch 22 Effect, if they respond, “you’re crazy”, I’ll know that I’m sane.

  26. nohivmeds Says:

    Just a quick note — while reading through some sites for HIV+ folk last night, I saw (yet again) the author of a “guide” to viral load say that it measures “viremia.” Disgusting, really, the lies that are told with such convincing sounding scientific language, to those who actually need to know the truth.

  27. CarefulObserver Says:

    Noble said,

    “Honestly the arrogance of people like you that think they can interpret papers better than the authors is astounding.”

    Yeah, kind of like you do with Duesberg, huh, Chris??

  28. james Says:

    http://www.altheal.org
    taken from above and below
    http://www.aidsmythexposed.com general section thread titled viral-load doesnt predict cd4

    You might want to read this statement by Rodriguez (JAMA: viral load) and Lederman:

    http://www.aidstruth.org/rodriguez-lederman.php

    “There is absolutely no doubt that HIV is the cause of AIDS.”

    “Our results imply that although HIV infection drives the progressive immune deficiency of AIDS (as evidenced by the response to successful treatment with anti-HIV medicines, which decrease the viral load, increase CD4 cell numbers, and prevent or help resolve opportunistic infections, reflecting an improvement in immune function), there must be other intervening elements that cause progressive CD4 cell losses in HIV infection.”

    Copy and paste url
    http://groups.msn.com/AIDSMythExposed/ general.msnw?

    action=get_message&mview=0&ID_ Message=25593&Last Modified= 4675595679954333234

    BHIVA: One-in-three UK HIV deaths ‘not directly related to HIV’
    http://www.aidsmap.com/en/news/ 8DB0098A-5707-4F4C-84FA-AE 9C854865F6.asp
    One-in-three UK HIV deaths ‘not directly related to HIV’

    From: MrChristopher (Original Message) Sent: 18/10/2006 18:16
    I saw this this morning.

    One-in-three UK HIV deaths ‘not directly related to HIV’

    “One-in-three deaths that occurred in HIV-positive individuals in the United Kingdom between 2004 and 2005 were not directly related to HIV”

    and;

    “CD4 and viral loads in the last six months of life were not uniformly poor. In fact, around half of all people who died had CD4 cell counts above 200 cells/mm3 and 30% had ‘undetectable’ viral loads. Consistent with these data is the finding that one-third of deaths were not considered to be directly linked to HIV infection.”

    Wow, they really try and squirm out of this uncomfortable information by saying ‘consistent with these data is the finding that one-third of deaths were not considered to be directly linked to HIV infection’.

    Unfortunately they didn’t tell us who did and did not have ‘poor’ stats ‘consistent’ with the ‘HIV’ paradigm. Meaning the article talks about this 1/3 of deaths in ‘HIV’ positive people whose deaths are not attributed to ‘HIV’. And then they say a big bunch of the total deaths in 2004-2005 had CD4 counts above 200 (though they didn’t give the range) or had ‘undetectable’ viral loads. They then try and imply these people with ‘non-standard’ surrogate markers were the ones that did NOT die from ‘HIV’. It’s squirmy language.

    It’s also funny how they say, ‘CD4 and viral loads in the last six months of life were not uniformly poor’

    What they COULD have said is, the surrogate markers for half the deaths didn’t fit the ‘HIV” paradigm.

    Chris
    Co-moderator

    First Previous 2-8 of 8 Next Last

    Reply
    Recommend (1 recommendation so far) Message 2 of 8 in Discussion

    From: HansSelyeWasCorrect Sent: 19/10/2006 17:56
    Also worthy of note:

    “4 due to accidental injection drug overdose (1.0%)”

    Now out of 133 adults in the general population of the UK, how many will die of this? Not even close to 1. Therefore, many of these “AIDS patients” are likely serious drug abusers, perhaps an overwhelming majority. Then there were the anal and penile cancer deaths. Again, what are the chances of someone dying of these, especially at the ages that these people likely were at the time? The “Hep B/C” deaths are also clearly related to this, because the liver is the “detox” organ. When will they ever remove the “HIV” colored glasses they are wearing?

    Reply
    Recommend Message 3 of 8 in Discussion

    From: HansSelyeWasCorrect Sent: 19/10/2006 20:48
    Looks like it was 389 adults, not 133. Still is an incredibly high incidence of these uncommon afflictions.

    Reply
    Recommend Message 4 of 8 in Discussion

    From: straightguyantiauthority Sent: 20/10/2006 13:42
    LOVE the “HIV colored glasses” expression

    A great metaphor for future use in getting people to reevaluate the data.

    Reply
    Recommend Message 5 of 8 in Discussion

    From: HansSelyeWasCorrect Sent: 20/10/2006 18:15
    I was thinking of the picture of Ho on the cover of Time (when he was “man of the year”). At least his glasses were pretty.

    :-)

    Reply
    Recommend Message 6 of 8 in Discussion

    From: GlutathioneSurvival1 Sent: 30/10/2006 01:20
    This “cd4” and “viral-load” is so so bollox, I cant see how doctors and “scientist” can have such tunnle vision and blinkers over there eyes, I had two friends in two weeks both with “undetectable” “viral-loads” and “cd4” around 700 with “PCP” an “aids” or rather in the west THE “aids” defining disease but theres no “virus” there and no “aquired immune defiency” -low “cd4” or anywhere near low “cd4” how can they just carry on ignoring, turning a blind eye, or not asking or thinking theres something very wrong with this theory. But no they stumble across these cases all the time, then just pick themselfs back up and forget, ignore these cases and carry on with the holy “hiv” “aquired immune defiency”=low “cd4” mantra of “aids” the new unquestionable “god” of “science” now run by religious zealots.

    Very interesting post Mr Christopher and guys thanks.

    Best wishes

    Hugs

    james

  29. Otis Says:

    The Final Nail in the Rodriguez/JAMA Coffin

  30. Chris Noble Says:

    The only thing that this “nail” proves is that Dr Dach can’t draw a line in the middle of a distribution.

    Rodriguez et al provide the median CD4+ depletion rate for each HIV viral load group on the figures.

    -37.3
    -42.8
    -45.8
    -48.9
    -52.2

    The “center bars” that Dr Dach hand draws on the figure do not correspond to these figures.

    Visual inspection of the figures also shows that the “center bars” are not in the centre of the distribution.

    In the top graph there is far more black ink to the right of the “center line” and in the bottom graph there is far more black ink to he left of the “center bar”.

    I have repeatedly asked Dr Dach to provide a description of the mathematical methods that he used to calculate his “center bars”. He hasn’t answered. Most people conclude that he simply used wishful thinking.

    HIV “rethinkers” are going to incredible lengths to avoid admitting that the study found that on average people with high HIV viral load had a faster CD4+ cell depletion rate than those with a low HIV viral load.

    Dr Dach’s “center bars” are only evidence of his own dishonesty.

    Why other HIV “rethinkers” with mathematical training tolerate this nonsense is bewildering.

  31. pat Says:

    Chris,

    I am having a very hard time believing anything you say and not because I think you are better at disseminating the medical literature but merely because of your style of argument. I find your style dismissive, arrogant and patronizing and I find myself wondering what it is that motivates you to appear day after day to engage the holders of opposite view points with such disdain. Ever since I started harbouring my own questions about the official story behind HIV and bumping into a rather well organized and vocal dissent, I have naturally been following it closely.
    From a purely presentational point of view, the “rethinkers” take the gold both for style and clarity. I hear them accused of peddling their “pseudo-science” to lay audiences by writing books and blogs, appearing on radio and God-knows-what else “cheap-shot”. How else would they do it to get their message out considering the very restrictive and venimous environment these people find themselves in, as is clearly demonstrated by yours and the “mainstream”s dismissive, arrogant and patronizing tone. For an example of the “either you are with us or you are against us” world
    visit some of the links posted to the right of this column. AidsTruth.org is the single most insulting message I have yet come across in this entire AIDS Info War. It is you and the likes of Moore that unabashedly peddle a theory by declaration and offering NOTHING by way of substance or information. My definition of peddling.

    You say:
    “Visual inspection of the figures also shows that the “center bars” are not in the centre of the distribution.

    In the top graph there is far more black ink to the right of the “center line” and in the bottom graph there is far more black ink to he left of the “center bar”.

    Are you having an artistic problem with the line or is there another meaning to this “more ink” thing but, true to style, you explain it away with a personal dismisal:
    “Dr Dach’s “center bars” are only evidence of his own dishonesty.”
    This doesn’t explain anything. AidsTruth doesn’t explain anything. Have I simply been convinced to believe in a fatamorgana because rethinkers are better manipulators?
    I have now seriously come to doubt the official relationship between HIV and AIDS because of the absurdity of the arguments and the scorch and burn tactics of the science. Duesberg was and is still correct on this point too. We are trying to kill a rabitt with a nuclear bomb. Observations, conclusions, “Overwhealming truths” and disclaimers and character assassinations in such obvious conflict I am surprised my screen isn’t in flames.

    “Dr Dach’s “center bars” are only evidence of his own dishonesty”.

    Dach is now just another of a long list of people who have been accused of dishonesty by you but have failed to convince anyone of it.What IS IT he is being dishonest about? The choice of black ink? What is it these people are being dishonest for anyway? What is the gain? WHO HAS MOST TO GAIN? What is YOUR gain?

    PS: try this, “Every statement accurate except where irony intended.” My grand father used to say “whatever you do, don’t panic”
    also meaning: “A gentleman doesn’t loose his shit”.
    What is YOUR gain out of slinging shit? My gain is zilch, nada.

  32. Chris Noble Says:

    Are you having an artistic problem with the line or is there another meaning to this “more ink” thing but, true to style, you explain it away with a personal dismisal:

    Dr Dach’s patented “center bars” are supposed to be in the centre of the distribution. I assume he means the median which has a strict meaning in statistics. The median is the value for which 50% of the distribution is below it and 50% is above. In a non-technical description there should be the same amount of black ink to the left and to the right of the median. This is clearly not true as anyone can see. In the top graph the value for the median is actually given as -37.3 yet Dr Dach has drawn his “center bar” at about -50.

    Dr Dach was obviously trying to prove something with his “center bars” so it was a natural question to ask what these “center bars” represented mathematically. Dr Dach has failed to respond. Perhaps initially Dr Dach’s statistical nonsense could be explained by ignorance.

    Now the only answer that I can think of is that Dr Dach is simply being dishonest.

  33. YossariansGhostbuster Says:

    To which one might add, Dr. Dach will not be answering as in

    “Comments to this post are closed.” cf Otis

  34. Truthseeker Says:

    This does not mean that Comments here are closed, of course. The policy of this blog is to expose all arguments for the supernatural qualities of HIV to daylight and reveal them as they are, and make them available for prolonged examination for those who cannot see their quality immediately.

    After all, the chief responsibility for the HIV∫AIDS debacle lies with those who have blatantly censored the review which would have otherwise have despatched the paradigm in short order, or about as fast as a direct hit with Combat despatches a group of roaches.

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