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Medical Forum / Diseases and Disorders / AIDS / October 2006Viral Blood Levels Don't Indicate Course of HIV Infection
from drdach: Dr Rodriguez in the Sept. 27 issue of JAMA: HIV levels in the blood aren't a good indicator of how fast CD4 T-cells will decline. This study suggests that viral load levels shouldn't be used as a deciding factor in initiating treatment. The researchers found that "the viral load for the individual has very little predictive value in terms of how rapidly a person is going to progress to AIDS," In fact, he added, "In our study, we had about 10 percent of patients with low viral loads that had extra rapid disease progression, so people should know that having a low load doesn't mean you're OK." regards from www.drdach.com Which is why over recent years the emphasis on how high a viral load may be has had less influence on decisions as to when to start therapy. In the UK, CD4 counts are the primary marker used for this purpose, and have been for many years. The value of using viral load as a marker for effectiveness of therapy or for viral breakthrough with development of resistance remains undisputed. > Which is why over recent years the emphasis on how high a viral load > may be has had less influence on decisions as to when to start therapy. [quoted text clipped - 3 lines] > or for viral breakthrough with development of resistance remains > undisputed. reply from drdach: Have you discussed this with DR. Rodgriguez? He disagrees with you, and has published a paper in JAMA to prove it. Where is yours? www.drdach.com > Have you discussed this with DR. Rodgriguez? He disagrees with you, > and has published a paper in JAMA to prove it. Where is yours? He doesn't disagree. You are implying he stated something on the topic of the utility of VL in monitoring the outcome of therapy. Give his words in quotes please if you think he has said anything which contradicts what I have stated above. The UK guidelines 2003 (http://www.bhiva.org/pdf/2003/guides/BHIVA_2003_Guidelines.pdf#search=%22bhiva%2 0treatment%20guidelines%22 ) have this to say about when to start treatment: "In asymptomatic patients this decision should be driven primarily by the CD4 count." Exactly what I said. I don't have my own "paper" saying this, but there are dozens referenced within the guidelines if you would care to look. > > Have you discussed this with DR. Rodgriguez? He disagrees with you, > > and has published a paper in JAMA to prove it. Where is yours? [quoted text clipped - 11 lines] > I don't have my own "paper" saying this, but there are dozens > referenced within the guidelines if you would care to look. reply from drdach: Here is a quote from the JAMA article Sept 27 page 1505 under conclusions (Predictive Value of Plasma HIV RNA Level on Rate of CD4 T-Cell Decline in Untreated HIV Infection): "The results of our study challenge the concept that CD4 depletion in chronic HIV infection is mostly attributable to the direct effects of HIV replication." "Presenting HIV RNA level predicts the rate of CD4 decline only minimally in untreated persons. These findings have implications for treatment decisions in HIV." In other words, the results his study challenge one of the basic concepts that HIV replication causes CD4 cells decline and causes immune-suppression. The is a major pradigm shift in thinking similar to the discovery that gastric ulcers were caused by a microbe H. Pylori, or that Vitamin C deficiency causes scurvy, or that that simple lumpectomy could replace radical mastectomies for breast cancer treatment. regards from www.drdach.com >Here is a quote from the JAMA article Sept 27 page 1505 under >conclusions (Predictive Value of Plasma HIV RNA Level on Rate of CD4 [quoted text clipped - 3 lines] >chronic HIV infection is mostly attributable to the direct effects of >HIV replication." This is actually not news. We have known that most CD4 cells are undergoing apoptosis are NOT HIV-infected. This has been known for years. This is NOT an argument for claiming that HIV is not the cause of AIDS. Yet again--your vast ignorance is revealed. George M. Carter > >Here is a quote from the JAMA article Sept 27 page 1505 under > >conclusions (Predictive Value of Plasma HIV RNA Level on Rate of CD4 [quoted text clipped - 14 lines] > > George M. Carter reply from drdach: I suggest you learn how to read. Or perhaps this JAMA article threatens your belief system so that you do not allow yourself to read it. "The results of our study challenge the concept that CD4 depletion in chronic HIV infection is mostly attributable to the direct effects of HIV replication." quote from JAMA study Sept 27 2006. This is big news and creates a major change in thinking about HIV/AIDS. regards from www.drdach.com I am still waiting for Dr Dach to quote the text from the Rodrigues study which he implied contradicted my statement that CD4 counts are the primary parameter used to determine when it is appropriate to start therapy. Rodrigues has published a study. The authors say "The results of our study challenge the concept that CD4 depletion in chronic HIV infection is mostly attributable to the direct effects of HIV replication." 2 comments. Firstly, as George has pointed out, there are a number of ways in which HIV causes CD4 depletion. DIRECT effects are felt by most authorities to be less important than other mechanisms, a concept that this Rodrigues study seems to support. Certainly the results of his study challenge the concept that it is "mostly" attributable to HIV replication directly. Secondly, it is a study which CHALLENGES one part of current thinking on HIV pathogenesis. Scientists enjoy challenges, it makes them discover more. No doubt theories on HIV pathogenesis will be looked at again in the light of this study, but to assume paradigm shifts is rather premature. And, as I said and as Dr Drach has not disputed, HIV levels will remain the cardinal parameter for assessing response to and failur of therapy. > I am still waiting for Dr Dach to quote the text from the Rodrigues > study which he implied contradicted my statement that CD4 counts are [quoted text clipped - 22 lines] > And, as I said and as Dr Drach has not disputed, HIV levels will remain > the cardinal parameter for assessing response to and failur of therapy. drdach reply: I would dispute, as would most health care practitioners, your last statement that HIV levels (or any laboratory marker for that matter) is a cardinal parameter for assessing response to or failure of therapy. Clinical outcome is the important parameter. Laboratory values may be low, normal or high- it doesnt matter if there is a failed clinical outcome, and death is the ultimate failed clinical outcome. I would also restate the importance of the Sept 27 2006 JAMA article in which a major shift in thinking about HIV/AIDS has occurred. for those who wish to continue this discussion, please reply to the contact page on my web site www.drdach.com regards from www.drdach.com snip >I would dispute, as would most health care practitioners, your last >statement that HIV levels (or any laboratory marker for that matter) is >a cardinal parameter for assessing response to or failure of therapy. Wow. What planet do you live on? And you claim to have treated people with HIV for 25 years? You're deluded. > Clinical outcome is the important parameter. Laboratory values may be >low, normal or high- it doesnt matter if there is a failed clinical >outcome, and death is the ultimate failed clinical outcome. Viral load ain't everything but when it appears in a way more than a blip during ARV therapy, it usually means resistance has developed. And it's time to think about a change in medications. THAT is common among genuine clinicians who treat people with HIV. >I would also restate the importance of the Sept 27 2006 JAMA article in >which a major shift in thinking about HIV/AIDS has occurred. No major shift--but an important contribution and reminder to many who need to realize there is more to managing HIV disease than ARV. To leap to the other end of a polemic and claim that ARV are not needed or that elite controllers are everywhere is just deranged whistleblowing. George M. Carter "jdach" <drdach@drdach.com> wrote in message > I suggest you learn how to read. Or perhaps this JAMA article > threatens your belief system so that you do not allow yourself to read [quoted text clipped - 3 lines] > chronic HIV infection is mostly attributable to the direct effects of > HIV replication." quote from JAMA study Sept 27 2006. The Local6.com Health Encyclopedia Online Science Journals Challenge Peer-Reviewed Counterparts October 2, 2006 LOS ANGELES -- Scientists frustrated by the iron grip that academic journals hold over their research can now pursue another path to fame by taking their research straight to the public online. Instead of having a group of hand-picked scholars review research in secret before publication, a growing number of Internet-based journals are publishing studies with little or no scrutiny by the authors' peers. It's then up to rank-and-file researchers to debate the value of the work in cyberspace. The Web journals are threatening to turn on its head the traditional peer-review system that for decades has been the established way to pick apart research before it's made public. Next month, the San Francisco-based nonprofit Public Library of Science will launch its first open peer-reviewed journal called PLoS ONE, focusing on science and medicine. Like its sister publications, it will make research articles available for free online by charging authors to publish. But unlike articles in other PLoS journals that undergo rigorous peer review, manuscripts in PLoS ONE are posted for the world to dissect after an editor gives them just a cursory look. "If we publish a vast number of papers, some of which are mediocre and some of which are stellar, Nobel Prize-winning work -- I will be happy," said Chris Surridge, the journal's managing editor. It's too early to tell how useful this open airing will be. Some open peer-reviewed journals launched in the past year haven't been big draws. Still, there appears to be enough interest that even some mainstream journals like the prestigious British publication Nature are experimenting. Democratizing the peer-review process raises sticky questions. Not all studies are useful and flooding the Web with essentially unfiltered research could create a deluge of junk science. There's also the potential for online abuse as rogue researchers could unfairly ridicule a rival's work. Supporters point out that rushing research to the public could accelerate scientific discovery, while online critiques may help detect mistakes or fraud more quickly. The open peer review movement stems from dissatisfaction with the status quo, which gives reviewers great power and can cause long publication delays. In traditional peer review, an editor sends a manuscript to two or three experts -- referees who are unpaid and not publicly named, yet they hold tremendous sway. Careers can be at stake. In the cutthroat world of research, publishing establishes a pedigree, which can help scientists gain tenure at a university or obtain lucrative federal grants. Researchers whose work appear in traditional journals are often more highly regarded. That attitude appears to be slowly changing. In 2002, the reclusive Russian mathematician Grigori Perelman created a buzz when he bypassed the peer-review system and posted a landmark paper to the online repository, arXiv. Perelman later won the Fields Medal this year for his contribution to the Poincare conjecture, one of mathematics' oldest and puzzling problems. Editors of traditional, subscription-based journals say the peer-review system weeds out sloppy science. The traditional process isn't designed to detect fraud (referees rarely look at a researcher's raw data), and prestigious journals have unwittingly published bogus work. Last year, for example, Science retracted papers on embryonic stem cell research by a South Korean cloning scientist who admitted falsifying his results. Work submitted to PLoS ONE, for instance, is debated after publication by colleagues who rate the research based on quality, originality and other factors. Commenters cannot alter the paper, which becomes part of the public record and is archived in databases. If there is disagreement, authors can respond to comments. To prevent abuse, the site is monitored for inflammatory language and the postings can't be anonymous. "The fact that you get published in PLoS ONE isn't going to tell you whether it's a brilliant paper. What it's going to say is that this is something worth being in the scientific literature, but you need to look at it more closely," Surridge said. Another open peer-reviewed journal, Philica, launched earlier this year takes a more radical approach. Authors are responsible for uploading their research to the Web site at no cost and without any peer review. Comments are anonymous, but users whose identities have not been verified by site administrators are flagged with a question mark next to their comments. The journal, still in the trial stage, has published about 35 papers so far. About a third still needs to be critiqued. Philica co-founder and University of Bath psychology professor Ian Walker said the system discourages authors from publishing fake studies because others can rat them out. "Imagine if somebody puts up absolute garbage, you will have plenty of reviews that will say, 'This is terrible, terrible, terrible,"' he said. Academics are eyeing the open peer-review experiment with interest. Andrew Odlyzko, a mathematician who heads the University of Minnesota's Digital Technology Center, is encouraged by the growing number of online journals. Whether they will work -- he's not sure. Some researchers might only post unhelpful one-liners for fear of reprisal. Granting anonymity may boost participation, but could lead to "malicious postings from cracks," Odlyzko said. Even some mainstream journals are toying with a tame form of open peer review. This summer, Nature allowed authors whose papers were selected for traditional peer review to have their manuscripts judged by the public at the same time. Editors weigh both sides when deciding whether to publish a paper, and rejected research can be submitted elsewhere. Linda Miller, the journal's U.S. executive editor, said she was encouraged by the participation. More than 60 papers have been posted on Nature's site for open peer review as of mid-September including one that has been accepted for publication. Several others are on the path to being published. Miller said Nature's experimentation with the Internet is just another way the journal is trying to reach out to the public. Two of its specialized journals on neuroscience and genetics already offer a blog-like forum for researchers to post their thoughts on published articles, though they have attracted little attention, she said. "If we don't serve the community well, we will become irrelevant," she said. Death wrote... > "jdach" <drdach@drdach.com> wrote in message > [quoted text clipped - 27 lines] > publications, it will make research articles available for free online by charging authors to > publish. And it degrades science, because it allows any quack to compose a manifesto, put it on some website, and have it used as "a study" to back up the claims of some magic weight loss or penis enlargement pill in an infomercial. The whole point of peer review is to vet the quackery so that only studies that can be duplicated and have their results verified by professional scientists and accepted as valid science. "crack baby" <crack@backdoho.net> wrote in message > And it degrades science, because it allows any quack to compose a manifesto, > put it on some website, and have it used as "a study" to back up the claims > of some magic weight loss or penis enlargement pill in an infomercial. The > whole point of peer review is to vet the quackery so that only studies that > can be duplicated and have their results verified by professional scientists > and accepted as valid science. Supporters point out that rushing research to the public could accelerate scientific discovery, while online critiques may help detect mistakes or fraud more quickly. "The fact that you get published in PLoS ONE isn't going to tell you whether it's a brilliant paper. What it's going to say is that this is something worth being in the scientific literature, but you need to look at it more closely," Surridge said. Another open peer-reviewed journal, Philica, launched earlier this year takes a more radical approach. "Imagine if somebody puts up absolute garbage, you will have plenty of reviews that will say, 'This is terrible, terrible, terrible,"' he said. Academics are eyeing the open peer-review experiment with interest. "If we don't serve the community well, we will become irrelevant," she said. snip >And it degrades science, because it allows any quack to compose a manifesto, >put it on some website, and have it used as "a study" to back up the claims >of some magic weight loss or penis enlargement pill in an infomercial. The >whole point of peer review is to vet the quackery so that only studies that >can be duplicated and have their results verified by professional scientists >and accepted as valid science. Clearly, you haven't even looked at the PlOS website. You oughta. > "jdach" <drdach@drdach.com> wrote in message > > [quoted text clipped - 18 lines] > Democratizing the peer-review process raises sticky questions. Not all studies are useful and > flooding the Web with essentially unfiltered research could create a deluge of junk science. We don't have to worry. In fact, it's exactly the peer review practice that has turned science into junk. Peer review=Friends judge friends, then friends publish friends ==> quickest way to junk science. "js" <me@nospamplease> wrote in message > We don't have to worry. In fact, it's exactly the peer review practice that has turned > science into junk. > > Peer review=Friends judge friends, then friends publish friends ==> quickest way to junk > science. You credited me with the statement you replied to. My opinion is the same as yours in this matter. The kickbacks from grubment grants will soon be stopped. Papers will no longer be held back due to some petty grudge someone carried over from college. No doubt there is a list of reasons I haven't thought of. > >Here is a quote from the JAMA article Sept 27 page 1505 under > >conclusions (Predictive Value of Plasma HIV RNA Level on Rate of CD4 [quoted text clipped - 14 lines] > > George M. Carter reply from drdach: It seems that you have been hiding a few pieces of baggage from your readers Mr Carter: (see below) http://www.pahealthsystems.com/archive253-2005-6-444458.html from :redrum1@alltel.net 2005-06-12, 11:46 am Carter actually isn't allowed to "think"... pharma wouldn't stand for it. Not for one second, as evidenced by Pharma Ilk Carter, Stein, Canzi, Mailman and others operating from their public relations internet damage control boiler rooms. However, Carter's lies are intended to distance himself and his previous ACT UP co-conspirators from their sordid pasts, when they were paid to solicit victims for the pharma poison squads. The only exception to the ACT UP = PHARMA DEATH rule was, of course, ACT UP San Francisco (see the pharma gang's attacks on AUSF's Pasquarelli, especially after his death to get the true flavor of the compassion professed by Carter et al). Carter says "no, I didn't take pharma money", but the facts remain otherwise. Unfortunately for Carter, he can't go back and destroy every copy of POZ Magazine in which his columns and SPV-30 ads appeared. Would anyone care to guess which industry funded POZ? Carter also refuses to disclose his seemingly endless other financial conflicts of interests involving his Pharma money and his internet "nutriceutical" schemes (NAC, SPV-30, etc., etc.). Then there were all those drug company-paid trips here and there; and various other pharma-funded-and-sponsored opportunites for self-promotion and profit. Some call those "International AIDS Conferences", but by now we know better, don't we? Carter and his "friends" were there. Always. And they NEVER paid their own way. NEVER! The drug companies paid them and the drug companies even orchestrated their "protests", (e.g. the parade of actor-protesters demanding their latest cures in front of the news media - ALL of it was phony). The term "Quizzling" comes to mind. And then there was Carter's crowned jewel - Arkopharma France's SPV-30 and his true one chance to be a hero! Carter admits taking their money, but now brushes it off as if a pittance. He'll only admit that much because he was caught in the act ... again. But Carter lies when he claims that he didn't write the ads for SPV-30. He did. Carter admits "helping" with the distribution of this immune system killer, a confession that Carter refuses to reconcile with all the goodies he received along the way. Carter also downplays the deadly nature of the SPV-30 boxwood extract's high volume of steroidal drug compounds (nearly 70) which were even classified at the time as good candidates for cancer therapy. Similar to tamoxifen, they were highly immunosuppressive, if only by inference understood by even the most casual observer. Yet there Carter was - making money by killing those whose HIV-positive tests left them desperate, lonely and vulnerable to psychopathic predators of Carter's sad ilk - a seemingly endless stream of opportunists who, like roaches, scamper off when light is shed on their handiwork ... and conflicts of interest. That's why Carter's desperation is so obvious - as evidenced by his recent "child molester" ploy and the various other smear campaigns he regularly orchestrates against his tormentors (anyone with common sense and/or science). That's what Carter and his co-workers here are paid to do. That's the job for the Pharma PR boiler rooms who plague Usenet for the purpose of obscuring the truth that is so embarassing and risky to their employers. (Hence the demise of sci.med.aids - the group which was "moderated" by the Pharma PR boiler rooms ... into oblivion). redrumtza > >Here is a quote from the JAMA article Sept 27 page 1505 under > >conclusions (Predictive Value of Plasma HIV RNA Level on Rate of CD4 [quoted text clipped - 14 lines] > > George M. Carter reply from drdach: It seems Mr. Carter, that you have been hiding some past baggage from your readers: (see below) http://www.pahealthsystems.com/archive253-2005-6-444458.html redrum1@alltel.net 2005-06-12, 11:46 am Carter actually isn't allowed to "think"... pharma wouldn't stand for it. Not for one second, as evidenced by Pharma Ilk Carter, Stein, Canzi, Mailman and others operating from their public relations internet damage control boiler rooms. However, Carter's lies are intended to distance himself and his previous ACT UP co-conspirators from their sordid pasts, when they were paid to solicit victims for the pharma poison squads. The only exception to the ACT UP = PHARMA DEATH rule was, of course, ACT UP San Francisco (see the pharma gang's attacks on AUSF's Pasquarelli, especially after his death to get the true flavor of the compassion professed by Carter et al). Carter says "no, I didn't take pharma money", but the facts remain otherwise. Unfortunately for Carter, he can't go back and destroy every copy of POZ Magazine in which his columns and SPV-30 ads appeared. Would anyone care to guess which industry funded POZ? Carter also refuses to disclose his seemingly endless other financial conflicts of interests involving his Pharma money and his internet "nutriceutical" schemes (NAC, SPV-30, etc., etc.). Then there were all those drug company-paid trips here and there; and various other pharma-funded-and-sponsored opportunites for self-promotion and profit. Some call those "International AIDS Conferences", but by now we know better, don't we? Carter and his "friends" were there. Always. And they NEVER paid their own way. NEVER! The drug companies paid them and the drug companies even orchestrated their "protests", (e.g. the parade of actor-protesters demanding their latest cures in front of the news media - ALL of it was phony). The term "Quizzling" comes to mind. And then there was Carter's crowned jewel - Arkopharma France's SPV-30 and his true one chance to be a hero! Carter admits taking their money, but now brushes it off as if a pittance. He'll only admit that much because he was caught in the act ... again. But Carter lies when he claims that he didn't write the ads for SPV-30. He did. Carter admits "helping" with the distribution of this immune system killer, a confession that Carter refuses to reconcile with all the goodies he received along the way. Carter also downplays the deadly nature of the SPV-30 boxwood extract's high volume of steroidal drug compounds (nearly 70) which were even classified at the time as good candidates for cancer therapy. Similar to tamoxifen, they were highly immunosuppressive, if only by inference understood by even the most casual observer. Yet there Carter was - making money by killing those whose HIV-positive tests left them desperate, lonely and vulnerable to psychopathic predators of Carter's sad ilk - a seemingly endless stream of opportunists who, like roaches, scamper off when light is shed on their handiwork ... and conflicts of interest. That's why Carter's desperation is so obvious - as evidenced by his recent "child molester" ploy and the various other smear campaigns he regularly orchestrates against his tormentors (anyone with common sense and/or science). That's what Carter and his co-workers here are paid to do. That's the job for the Pharma PR boiler rooms who plague Usenet for the purpose of obscuring the truth that is so embarassing and risky to their employers. (Hence the demise of sci.med.aids - the group which was "moderated" by the Pharma PR boiler rooms ... into oblivion). redrumtza >It seems Mr. Carter, that you have been hiding some past baggage from >your readers: >(see below) So this is the FOURTH time you've repeated the libelous comments of Fred Shaw? Or is it the fifth? That's spam, mr. dach. That's committing the libel. And I am proud of my days with ACT UP. I met some of the most intelligent, passionate, great-hearted people I have ever had the privilege to know in this life. Too many of them have long since died. So, go right ahead. You keep posting those libelous comments. I expect nothing more of you. George M. Carter > >It seems Mr. Carter, that you have been hiding some past baggage from > >your readers: [quoted text clipped - 17 lines] > > George M. Carter reply from drdach: So we can assume that you at least got as far as addition in grade school since you can count to four. Did you actually graduate high school? Have you ever studied biology or science in high school? Tell us about ACT UP. What is it that they do? regards from www.drdach.com snip... >reply from drdach: > >So we can assume that you at least got as far as addition in grade >school since you can count to four. Did you actually graduate high >school? Have you ever studied biology or science in high school? >Tell us about ACT UP. What is it that they do? We address bullshit wherever we see it. > Which is why over recent years the emphasis on how high a viral load > may be has had less influence on decisions as to when to start therapy. [quoted text clipped - 3 lines] > or for viral breakthrough with development of resistance remains > undisputed. It's fantastic to see how the AIDS apologists always think they can with it no matter how devastating research results. Once again a study should be an eye opener for all the silly people who still believe that something named HIV causes something named AIDS. But it's not an eye opener. I can only conclude that apologists are definately blind. Or, if they're not, they're tied to the HIV cause by emotional straps and/or financial interest that have nothing to do with scientific considerations. > It's fantastic to see how the AIDS apologists always think they can with it no matter how > devastating research results. Once again a study should be an eye opener for all the silly [quoted text clipped - 3 lines] > if they're not, they're tied to the HIV cause by emotional straps and/or financial > interest that have nothing to do with scientific considerations. Are YOU blind? Have you even read the paper? Have you even read the original work that lead to the idea that viral load was predictive of rate of progression to AIDS? A hint. Read Mellors work from the 1990s. Read this paper. You'll discover that this paper DUPLICATED the original findings from Mellors work. They even copy one of Mellors graphs to highlight the similarity between his findings and theirs! In other words, it also showed that viral load, when analyzed as subsets, was predictive of rate of progression to AIDS. What this work did that Mellors work didn't was to try to calculate the mathematical effect that viral load has on the individual level, not on the large subset level. Not surprisingly they found that on the individual level the rate of progression was dependant on more than simply viral load. Well shucks, this is nothing new. But no-one had to date tried to put a number on it. If they had performed the same mathematical model and put the effect at 90% or more than no doubt the dissidents would be crying out at the fact we "had to use" complex math to prove our point. I repeat - this work REPEATS the original Mellors work that shows that VIRAL LOAD PREDICTS RATE OF PROGRESSION TO AIDS. But it also adds additional insight. Nothing more. http://aidsmyth.blogspot.com/2006/09/viral-load-paradigm-shift-not-really.html I have permission to quote from the paper's author, when he found out that the AIDS dissidents were hijacking his work. "The idea that our findings published today in JAMA can be taken to support the concept that HIV is not the cause of AIDS is ludicrous. The role of HIV as the cause of AIDS has been proven over and over again. Clearly the people who are misrepresenting our work are not only incapable of clear thinking, they are also apparently unable to read." Michael M. Lederman MD Cheers Bennett > > It's fantastic to see how the AIDS apologists always think they can with it no matter how > > devastating research results. Once again a study should be an eye opener for all the silly [quoted text clipped - 48 lines] > > Bennett Reply from drdach: I have read the JAMA article and noticed the 2 charts on page 1502 for the study cohort and the MACS cohort (Mellors) which were similar. However, Mellors work is mainly an affirmation of the idea that viral load predicts prognosis. The Sept 27 JAMA paper presents a major challenge to this idea, by stating that "Presenting HIV RNA level predicts the rate of CD4 decline only minimally in untreated persons." In other words, the results this study challenges one of the basic concepts that HIV replication causes AIDS. Some patients with low viral load went on to AIDS while some patients with high viral load did not proceed to AIDS. The is a major paradigm shift in thinking similar to the discovery that gastric ulcers were caused by a microbe H. Pylori, or that Vitamin C deficiency causes scurvy, or that that simple lumpectomy could replace radical mastectomies for breast cancer treatment. I would also like to add that laboratory measurements such as viral load and CD4 levels are useful, but the most important parameter of treatment evaluation is clinical outcome and the ultimate parameter of failed clinical outcome is death. Viral load measures or any other lab measurement should not replace assessment of clinical outcome in therapeutic trials. Regarding the quote (see above) from the last author of the paper Michael M. Lederman MD in which he laments that the people who misrepresent the work as being unable to think clearly or unable to read, I would only ask if he was involved in the actual writing or composition of the paper. It is well known that the last author may be uninvolved in the actual thought process of the paper. In addition, some papers published in medical literature may be ghost written by writers paid by the funding drug company and the authors may never see the data. (Actonel Paper) Since the work was funded by the NIH, I doubt that is the case. However, because of the NIH funding, the authors would be inclined to reach conclusions which are politically correct according to NIH guidelines, making his after the fact comments rather expected. Regards from www.drdach.com > > > It's fantastic to see how the AIDS apologists always think they can with it no matter how > > > devastating research results. Once again a study should be an eye opener for all the silly [quoted text clipped - 53 lines] > I have read the JAMA article and noticed the 2 charts on page 1502 for > the study cohort and the MACS cohort (Mellors) which were similar. Then you have absolutely no excuse for your blatant misrepresentation of the paper. Clearly despite the title you gave to this thread, on average, viral load levels do predict the course of HIV infection. There are also other factors independent of viral load such as immune activation that also predict the course of HIV infection. Chris Noble > Reply from drdach: > > I have read the JAMA article and noticed the 2 charts on page 1502 for > the study cohort and the MACS cohort (Mellors) which were similar. > However, Mellors work is mainly an affirmation of the idea that viral > load predicts prognosis. Oh deary me. Mellors work _started_ the idea that viral load predicts prognosis. The Sept 27 JAMA paper presents a major > challenge to this idea, by stating that "Presenting HIV RNA level > predicts the rate of CD4 decline only minimally in untreated > persons." In other words, the results this study challenges one of > the basic concepts that HIV replication causes AIDS. Some patients > with low viral load went on to AIDS while some patients with high viral > load did not proceed to AIDS. That isn't the case at all. But the RATE at which they progressed had a poorer relationship to viral load, at the individual level, than it did at the subgroup level. > The is a major paradigm shift in thinking similar to the discovery that > gastric ulcers were caused by a microbe H. Pylori, or that Vitamin C > deficiency causes scurvy, or that that simple > lumpectomy could replace radical mastectomies for breast cancer > treatment. I'm afraid that it's mostly only a paradigm shift to the dissidents, as frankly this study wasn't a huge surprise to me! > I would also like to add that laboratory measurements such as viral > load and CD4 levels are useful, but the most important parameter of > treatment evaluation is clinical outcome and the ultimate parameter of > failed clinical outcome is death. Viral load measures or any other lab > measurement should not replace assessment of clinical outcome in > therapeutic trials. A fair comment, but for the sake of getting effective therapies to market surrogate markers are needed. The facts are that suppression of viral load does correlate very well indeed with improved survival and less opportunistic infections. > Regarding the quote (see above) from the last author of the paper > Michael M. Lederman MD in which he laments that the people who > misrepresent the work as being unable to think clearly or unable to > read, I would only ask if he was involved in the actual writing or > composition of the paper. It is well known that the last author may be > uninvolved in the actual thought process of the paper. Ah,so the conspiracy starts. In addition, > some papers published in medical literature may be ghost written by > writers paid by the funding drug company and the authors may never see [quoted text clipped - 3 lines] > according to NIH guidelines, making his after the fact comments rather > expected. LOL! And yes, yet more cherry picking. You clearly aren't aware of the background to this group of researchers, or this work in particular. From the Nature website (subscription only I'm afraid): ", a group of scientists calling itself 'The Bad Boys of Cleveland' reports evidence that rebels against one of those principles. The findings cement a feeling that has been growing in the HIV research community: that the virus enlists patients' own defences to dismantle their immune systems." It's worht repeating "A FEELING THAT HAS BEEN GROWING IN THE HIV RESEARCH COMMUNITY" (i.e. nothing unexpected). "The Bad Boys were first convened by Michael Lederman, head of the Case Western Reserve University Center for AIDS Research and senior author of the recent paper. "The idea was to have a relaxed but intense forum where we could present our unpublished data, share ideas, then go back to our lives and work some more," Lederman says. "We've been doing this on a shoestring - people pay their own air fare. They come because they like the atmosphere in which we work." So Michael is hardly likely to have been outside of the loop, but the NIH almost certainly was ;-) With you being wrong on so many counts, could you be wrong on one more?! Cheers Bennett > > Reply from drdach: > > [quoted text clipped - 87 lines] > > Bennett reply from drdach: Thanks for the reply. I find it had to undersand how you can say that isnt the case at all, when it is a direct quote from the paper. It is as if you are saying the verbiage in the paper reads one way but really means something else. Perhaps in conversation the authors say one thing, but when you read the paper , the words are placed into string which imply something else. How do you read the statement :"Presenting RNA levels predicts the CD4 decline only minimally in untreated persons" which is a direct quote from the paper? I'd like to know who pays all these other guys who are repeatedly replying up to 10 to 20 times a day to this newsgroup like monkeys banging at a typewriter ? Their job is to spread insults and nonsense over any post which presents an opinion which they dont like. That kind of effort by a bunch of political activists has to be financed from someplace. Are these guys a bunch of HIV positive gays with othing else to do? I smell something fishy going on here. Having all these distracting and insulting posts from your associates (who are not very highhly educated) doesn't make for a pleasant exchange of ideas which is what the internet is intended (at least I thought so). LOL. We will agree to disagree. regards from www.drdach.com snip >I'd like to know who pays all these other guys who are repeatedly >replying up to 10 to 20 times a day to this newsgroup like monkeys [quoted text clipped - 6 lines] >very highhly educated) doesn't make for a pleasant exchange of ideas >which is what the internet is intended (at least I thought so). Wow. You smell something fishy? Probably coming from your nether regions. A homophobe to boot! Who knew? Me? I don't get paid to post here. It takes about a half hour a day to deal with your crap--the group is pretty moribund. It used to be more interesting when there was more discussion of issues of pathogenesis and the like--though sometimes as heated. But you're too deeply insulted to carry on, I suppose. A good, nice, innocent fellow like you has nothing but his own best interests at heart, after all, I'm sure. George M. Carter > > > Reply from drdach: > > > [quoted text clipped - 100 lines] > decline only minimally in untreated persons" which is a direct quote > from the paper? The sentence is easily understood by the vast majority of people. On average viral load correlates well with the rate of CD4+ cell depletion. This is clearly demonstrated in figure 1 in the paper. The paper far from being support for Duesberg's nonsense is in fact very good evidence against it. Anyone that claims otherwise has serious cognitive problems. However although on average the relationship between viral load and progression rate is clear on an individual basis viral load is not a good predictor of progreesion rate. There is no mystery and no contradiction. Chris Noble > > > > Reply from drdach: > > > > [quoted text clipped - 115 lines] > > Chris Noble reply from drdach: The Sept 27, 2006 JAMA article (Figure 3 page 1504) contradicts an important part of the HIV AIDS explanation: Here is the accepted explanation of HIV and AIDS: http://encarta.msn.com/encyclopedia_761579757/Human_Immunodeficiency_Virus.html When HIV enters the body, it infects lymphocytes, which are a type of white blood cell in the immune system. HIV uses its glycoproteins to attach itself to receptors on the surface of a lymphocyte. The outer envelope of HIV then fuses with the lymphocyte, enabling the HIV capsid to enter the lymphocyte itself. HIV commandeers the genetic material of the lymphocyte, instructing the cell to replicate more viruses. The newly formed viruses break free from the host, destroying the cell in the process. The new viruses go on to infect and destroy other lymphocytes. Over a period that may last from a few months to up to 15 years, HIV may destroy enough lymphocytes that the immune system becomes unable to function properly. An infected person develops multiple life-threatening illnesses from infections that normally do not cause illnesses in people with a healthy immune system. Some people who have HIV infection may not develop any of the clinical illnesses that define the full-blown disease of AIDS for ten years or more. Doctors prefer to use the term AIDS for cases where a person has reached the final, life-threatening stage of HIV infection. The recent JAMA article contradicts the above idea destruction of lymphocytes and AIDS progession (on an individual basis) is caused by replicating virus. In this study, on an individual basis, there was no correlation (or very poor correlation) between viral replication measured by viral load levels and lymphocyte count. I would direct your attention to Figure 3 page 1504 of the Sept 27 2006 JAMA article by Rodriguez which shows scatter plots of CD4 T cell change on the vertical axis and HIV Viral Load on the horizontal axis. Notice how all the dots are placed like shotgun pellets and don't form a definite meaningful line. There should be a straight line here ( or dots which are trying to make a line). This scattered scattergram is the finding which indicates that HIV plasma RNA level (Viral Load) is not a reliable predictor of CD4 cell loss in HIV infection and challenges the concept that the magnitude of viral replication is the main determinant of the speed of CD4 cell loss at the individual level. regards from www.drdach.com snip >I would direct your attention to Figure 3 page 1504 of the Sept 27 2006 >JAMA [quoted text clipped - 10 lines] >magnitude of viral replication is the main determinant of the speed of >CD4 cell loss at the individual level. I haven't had a chance to read the JAMA article but would like to if anyone could email me a copy. I do not trust Dach's interpretations. However, presuming he is representing the data accurately--which I concede here is possible--I think it is not so surprising. Most of the CD4+ lymphocytes that die are not infected. This has long been known. Mechanisms for the destruction of uninfected CD4 cells include oxidative stress, immunological aberrations, effects of HIV proteins (env, tat, nef, etc.) and so forth. We know that the blood compartment, easier to access and test, is not the real site of the activity, which is in lymphoid tissue. And we know that people do NOT see a steady decline of CD4 counts to zero except in extraordinary circumstances. Like infection with HIV. HIV causes AIDS. How it does so is an extremely important question for which data are emerging based on sensible hypotheses. That's science. Maybe dach will get it eventually. But I doubt it. George M. Carter > snip > >I would direct your attention to Figure 3 page 1504 of the Sept 27 2006 [quoted text clipped - 37 lines] > > George M. Carter reply from drdach: For all members of the AMA: you can read the article online. full text of the JAMA article is available on the AMA web site http://pubs.ama-assn.org/ https://subs.ama-assn.org/ama/exec/guest?url=http%3A%2F%2Fjama.ama-assn.org%2F If you are not a member, then you have to wait 6 months for it to be free : Registering as a Guest is FREE. Registered Guests access to JAMA - Full text and PDF access to original research articles, review articles, special communications, and editorials 6 months after publication. regards from drdach.com snip >For all members of the AMA: you can read the article online. >full text of the JAMA article is available on the AMA web site Thanks for the worthless information! George, look at Orac's blog. http://scienceblogs.com/insolence/2006/10/more_distortion_of_peerreviewed_data_b y.php#more >George, look at Orac's blog. >http://scienceblogs.com/insolence/2006/10/more_distortion_of_peerreviewed_data_b y.php#more Thanks, DavidT, for the USEFUL information. What a delight to learn of all these terrific blogs! Is there a Blog Resource list? I'd like to make it available along with links to relevant URLs to counter the denialist horseshit. Before it kills to many more people. George M. Carter Draw a line over the scattershot. Cut out the graph. Weigh the paper. See also http://en.wikipedia.org/wiki/Monte_Carlo_method http://en.wikipedia.org/wiki/Calculus > Thanks for the reply. I find it had to undersand how you can say that > isnt the case at all, when it is a direct quote from the paper. It is [quoted text clipped - 6 lines] > decline only minimally in untreated persons" which is a direct quote > from the paper? Here is another direct 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." Which is exactly what I said, and what Mellors said. The existing paradigm is not wrong, merely incomplete. That's how science works - it's called progress. If you read my AIDSMYTH blog (I assume you have, if you have taken the time to research me a little) you will find the points you raise discussed and put into their proper context - as indeed the paper's authors have done. You've shown that you can cut and paste from an internet forum (Deansworld). If you can make any sense from Harvey Baily's ramblings from that 'debate' you're welcome to try. Duesberg incidentally stopped writing to me once I gave him several references dismantling his ideas: my emails to him are all posted on DW. Dean credits me because he thought I was lying about Duesberg not replying to me (hence the disingenuous comment), when in fact he is merely unable to read the posting date and time of various posts made to his website. Dean sadly falls into the same category of people like those who follow "intelligent design" (such an ironic name...) as an excuse for failing to understand what it is they're trying to discuss. God of the Gaps... http://www.don-lindsay-archive.org/creation/god_of_gaps.html http://en.wikipedia.org/wiki/God_of_the_gaps http://en.wikipedia.org/wiki/Argument_from_ignorance And my personal favorite... http://en.wikipedia.org/wiki/Flying_Spaghetti_Monsterism Sadly, like HIV, there is no cure for stupidity. This is however a cure for ignorance - it's called "education". Hang around - these political activists, HIV positive gays, and other monkeys banging on typewriters (all financed by the great pharmaceutical cartels of the world of course - they do pay in banana's don't you know) might just teach you a thing or two. Heaven forbid these guys have been debating this topic for the last decade or more and might know something about it! Cheers Bennett > > Thanks for the reply. I find it had to undersand how you can say that > > isnt the case at all, when it is a direct quote from the paper. It is [quoted text clipped - 17 lines] > paradigm is not wrong, merely incomplete. That's how science works - > it's called progress. <snip> It is still amazing to me after several years of observing HIV "rethinkers" that they are so predictable and stupid. Figure 1 in the paper clearly shows that CD4+ cell depletion is directly correlated with HIV viral load. The paper demonstrates that this is a relatively minor factor but it is quite clearly reproducible. If HIV has absolutely nothing to do with CD4+ cell depletion then why should there be any relationship whatsoever? You would expect that "rethinkers" would at least attempt an ad hoc explanation - oxidative stress causes reshuffling of endogenous DNA etc - but no they just ignore it. I really have to question the integrity of these people. Chris Noble > It is still amazing to me after several years of observing HIV > "rethinkers" that they are so predictable and stupid. Less so for me these days - after debating with big guns like Duesberg, Bialy and the Perth Group it's not surprising at all that the sheep who follow them can't keep up either. > Figure 1 in the paper clearly shows that CD4+ cell depletion is > directly correlated with HIV viral load. The paper demonstrates that > this is a relatively minor factor but it is quite clearly reproducible. > If HIV has absolutely nothing to do with CD4+ cell depletion then why > should there be any relationship whatsoever? Bingo. > You would expect that "rethinkers" would at least attempt an ad hoc > explanation - oxidative stress causes reshuffling of endogenous DNA etc > - but no they just ignore it. To be fair some of the PG's work does try to vaguely hint at this, but mostly leaves it up to the reader to fill in the gaps. When confronted with the evidence against this theory they.....ignore it. All they say they're doing is poking holes in the existing theory, but they don't come up with a reliable, logical framework to replace it. Since they can't even do the first task with any accuracy or truthfullness it's a moot point. > I really have to question the integrity of these people. Bingo once again. Bennett > > Thanks for the reply. I find it had to undersand how you can say that > > isnt the case at all, when it is a direct quote from the paper. It is [quoted text clipped - 59 lines] > > Bennett reply from drdach: I would direct your attention to Figure 3 page 1504 of the Sept 27 JAMA article by Rodriguez which shows scatter plots of CD4 T cell change on the vertical axis and HIV Viral Load on the horizontal axis. Notice how all the dots are placed like shotgun pellets and don't form a definite meaningful line. This scattergram is the finding which indicates that HIV plasma RNA level (Viral Load) is not a reliable predictor of CD4 cell loss in HIV infection and challenges the concept that the magnitude of viral replication is the main determinant of the speed of CD4 cell loss at the individual level. as Dr Bennett would say: bingo I invite all readers to visit my web site and post your comment on my contact page. Where's your web site Dr Nick Bennett? Cheers from www.drdach.com > I would direct your attention to Figure 3 page 1504 of the Sept 27 JAMA > article by Rodriguez which shows scatter plots of CD4 T cell change on > the vertical axis and HIV Viral Load on the horizontal axis. Notice how > all the dots are placed like shotgun pellets and don't form a definite > meaningful line. But there is a trend, which is reflected in the subset relationship between high viral load being associated with more rapid progression of CD4 T cell loss. The trend allows them to say that approx 4-6% of the specific individual loss of CD4 T cells is directly related to the viral load value. A true "shotgun" scatter plot would give zero correlation and look like a circle. This scattergram is the finding which indicates that > HIV plasma RNA level (Viral Load) is not a reliable predictor of CD4 > cell loss in HIV infection No, wrong - it is not a reliable predictor of the EXACT RATE of CD4 T cell loss in any one individual. It is still a predictor of whether or not T cell loss will occur... and challenges the concept that the > magnitude of viral replication is the main determinant of the speed of > CD4 cell loss at the individual level. I'm not sure anyone is saying it's "the main" determinant any more since Hellerstein's and others work on T cell kinetics. People with higher viral loads _tend_ to progress faster, as do people with particular immune genetics, or people with super-infections with multiple HIV strains, or people who are depressed. Many factors play into it - we've known this for years. The authors of the paper state this explicitly. I find it astonishing that you somehow think yourself better qualified to analyse the results of a paper than the authors themselves or indeed anyone else with specialist qualifications in the relevant field > as Dr Bennett would say: bingo > > I invite all readers to visit my web site and post your comment on my > contact page. Where's your web site Dr Nick Bennett? http://aidsmyth.blogspot.com And, unlike you, I'm not trying to sell anything on my site :o) Now, my turn to ask a question - where's your research background in HIV (or even microbiology in general)? Why should I trust what you say versus what every microbiologist/epidemiologist/clinician and researcher I've ever met tells me about how to analyse a paper and judge and interpret the evidence? I ask because if I didn't know better I would say you had no relevant experience upon which to base your views and are incapable of correctly interpreting scientific evidence in context! ;-) Cheers Bennett jdach wrote: > I would direct your attention to Figure 3 page 1504 of the Sept 27 JAMA > article by Rodriguez which shows scatter plots of CD4 T cell change on > the vertical axis and HIV Viral Load on the horizontal axis. Notice how > all the dots are placed like shotgun pellets and don't form a definite > meaningful line. bennett wrote: >But there is a trend, which is reflected in the subset relationship >between high viral load being associated with more rapid progression of >CD4 T cell loss. The trend allows them to say that approx 4-6% of the >specific individual loss of CD4 T cells is directly related to the >viral load value. A true "shotgun" scatter plot would give zero >correlation and look like a circle. drdach replies: Look again at the scattergram Figure 3 on page 1504 of the Sept 27 JAMA. The R-squared (COEFFICIENT OF DETERMINATION) value is 0.04 for 1289 data points and the image looks like a swarm of bees or a shotgun blast on the wall. .04 is close to zero. The idea is that in order for the data to be predictive, we are looking for a number close to 1.0 here, not a number that is almost zero (indicating no predictive value). To require the R-squared to be exactly zero in order to conclude that the data has no predictive value is a red flag that means you need take out your Linear Regression book and read it. Are you sure you want to be quoted as making the statement that data with an R-Squared best fit value of close to zero ( 0.4 ) was still predictive data? Wouldn't you be more comfortable with study data which showed an R-Squared value near ( 1.0 ) to say that it has predictive value? R-squared is a ratio of the amount of variation in the data that is accounted for by the model over the total amount of variation in the data. An R-squared value of 1.0 means that all variability in the data is explained by the model (a perfect fit). A low value for R-squared indicates that very little of the variability in the data can be accounted for by the model (poor fit). High R-squared values (near 1.0) would support the hypothesis, while low R-squared values (near 0 ) would serve to reject it. My Dear Doctor Nick Bennett, it is difficult to believe that you did a PHD in molecular biology without ever understanding Linear Regression Analysis, but it probably happens more than we know. Since it is never too late to learn, I have given you a link to a Power Point slide presentation that will explain it to you. (see below) Power Point presentation on Linear Regression Analysis http://www.cba.hawaii.edu/remus/courses/zsimplereg.ppt Of course Linear Regression is a tool used by many researchers, and not preserved exclusivly for use only in HIV research papers. An R-Squared value of .04 (close to zero) is why the authors state: " HIV plasma RNA level (Viral Load) is not a reliable predictor of CD4 cell loss in HIV infection (at the individual level), and challenges the concept that the magnitude of viral replication is the main determinant of the speed of CD4 cell loss at the individual level. " You can deny this all you want, but that is the data, that is the R-Squared value, and that is the authors conclusion which is merely stating the obvious. This finding is important it challenges a key part of the HIV/AIDS dogma, namely that HIV viral replication is killing off the CD4 cells in the individual. jdach wrote: > This scattergram is the finding which indicates that > HIV plasma RNA level (Viral Load) is not a reliable predictor of CD4 > cell loss in HIV infection bennett wrote: >No, wrong - it is not a reliable predictor of the EXACT RATE of CD4 T >cell loss in any one individual. It is still a predictor of whether or >not T cell loss will occur... bennett wrote: >I'm not sure anyone is saying it's "the main" determinant any more >since Hellerstein's and others work on T cell kinetics. People with [quoted text clipped - 8 lines] >My web site: http://aidsmyth.blogspot.com >And, unlike you, I'm not trying to sell anything on my site :o) drdach replies: There are no products for sale on my web site, there is no shopping cart and no mechanism to collect payment for products for that matter on my web site. I do mention various drugs and/or nutritional supplement products during discussions about various health topics (some of which I recommend from various independent sources). If and when I go commercial, you will be the first to know. Also, I would disagree with your statement that your web site : http://aidsmyth.blogspot.com is not trying to sell something. Obviously, your web site is selling the orthodox view of the HIV/AIDS hypothesis. Unlike your site, my web site does not sell any beliefs regarding HIV/AIDS, pro or con. >Now, my turn to ask a question - where's your research background in >HIV (or even microbiology in general)? Why should I trust what you say >versus what every microbiologist/epidemiologist/clinician and >researcher I've ever met tells me about how to analyse a paper and >judge and interpret the evidence? drdach replies: The reader is invited to review my CV which is posted on my web site. You did your PHD thesis on molecular biology of HIV and are now doing a pediatric residency in NY employed by the state of New York. I graduated from Medical School in 1976, and Internship and Residency 1976 - 1980. My fellow ship in CT/US and Interventional Radiology in 1980. I didn't have time for a PHD in molecular biology because I went right into clinical medicine. I am not employed by the government, so I have the liberty of engaging in discussion which may question government agency dogmas. . Of course, not even your friend, Chris Noble, the Australian MRI fellow, did a PHD in molecular biology or any training in HIV. This is true of most practicing physicans who go directly into clinical medicine. And of course your other friends, the ACT UP activists GM Carter (not sure what his job is), and David Thomson (computer programmer), have no formal education in medicine or biology yet they pontificate as if they had advanced degrees. Bennet wrote: >I ask because if I didn't know better I would say you had no relevant >experience upon which to base your views and are incapable of correctly >interpreting scientific evidence in context! ;-) drdach replies: Now it is my turn to be astonished that you would suggest that this Sept 27 2006 JAMA article was not written specifically for me to read and interpret. JAMA as you know is the Journal of the American Medical Association and is written specifically for the members of that organization. I have been a member of the American Medical Association and have been reading JAMA since 1976, which is before you were born. I was reading JAMA when you were in diapers, my youthful friend. I've had thirty years of experience reading and interpreting JAMA. How many years have you had? The reader is invited to post comments on my contact page at www.drdach.com Regards from www.drdach.com > jdach wrote: > [quoted text clipped - 26 lines] > data has no predictive value is a red flag that means you need take out > your Linear Regression book and read it. Which particular book is that? The same one where you can find Duesbergian statistics? If there is no relation between HIV viral load and the rate of CD4+ cell depletion then we would not expect to see figure 1. Take 176 people with HIV viral load <= 500 copies per m and 330 with > 40000 copies per ml. Is there a significant difference in the CD4+ depletion rate between the two groups? What is your conclusion? Chris Noblel > > jdach wrote: > > [quoted text clipped - 38 lines] > > Chris Noblel drdach replies: There are plenty of generic Linear Regression Anaysis learning resources on the web, none of which are in any way connected to the web sites you find offensive. Here is one for you Power Point presentation on Linear Regression Analysis http://www.cba.hawaii.edu/remus/courses/zsimplereg.ppt regarding the Sept 27 2006 JAMA article: Yes you are correct about Figure 1 on page 1502 which shows the Study Cohort data confirms the MACS Cohort data which looks at the data as a GROUP. The Figure 1 obviously shows a correlation between Viral Load and CD-4 count as anyone can see. However, when the data is evaluated on an INDIVIDUAL basis using linear regression (see Figure 3 page 1504), the coefficient of determination is only .04 which means that there was no (or very little) predictive value when Viral Load is plotted against CD4 count. This number R squared varies from a high of one (most predictve) to a low of zero (least predictive). They got .04 (point zero four) which is least predictive. I find it difficult to understand why this is so hard for you to accept. Obviously, the JAMA editorial board and peer review process accepted it and allowed publication. By the way, what's it like being an MRI fellow? The reader is invited to visit my web site and place a comment on the contact page. regards from www.drdach.com > > > jdach wrote: > > > [quoted text clipped - 64 lines] > you to accept. Obviously, the JAMA editorial board and peer review > process accepted it and allowed publication. You completely fail to understand the difference between the predictive value for an individual and that for an aggregate. Men are on average taller than women but height is not by itself a useful predictor of gender. The authors of the JAMA paper understand this. The JAMA editorial board understand this. The only people that appear to have trouble with this concept are people that haver the preconceived idea that HIV does not cause AIDS. If you really think that this paper supports the idea that HIV does not cause AIDS then write a letter to JAMA. > By the way, what's it like being an MRI fellow? I don't know. What about you? Chris Noble > > > > jdach wrote: > > > > [quoted text clipped - 84 lines] > > Chris Noble reply from drdach: I would think the letter to JAMA asking them to retract the paper would come from you since you are objecting to the authors conclusions. By the way, I noticed that my friend, Dr. Chris Noble has been busy making posts to this web site concernig the very same Sept 28 JAMA article. Your readers might be interested in what you had to say: http://www.newaidsreview.org/posts/1159330774.shtml#2307 regards from www.drdach.com > > > > > jdach wrote: > > > > > [quoted text clipped - 89 lines] > I would think the letter to JAMA asking them to retract the paper > would come from you since you are objecting to the authors conclusions. No you twit. I am not objecting to the authors conclusions. This is just a stupid rhetorical trick on your part. The PI has in fact made it very clear in his comment who is doing the misrepresentation. "The idea that our findings published today in JAMA can be taken to support the concept that HIV is not the cause of AIDS is ludicrous. The role of HIV as the cause of AIDS has been proven over and over again. Clearly the people who are misrepresenting our work are not only incapable of clear thinking, they are also apparently unable to read." If you really think that the paper shows that HIV does not cause AIDS then write a letter to JAMA and stop trying to tell other people what the authors really meant. > By the way, I noticed that my friend, Dr. Chris Noble has been busy > making posts to this web site concernig the very same Sept 28 JAMA > article. Your readers might be interested in what you had to say: Yes, the same people there have also misrepresented a number of other "orthodox" papers. This is the result of starting with the conclusion - that HIV does not cause AIDS - and trying to find something that you can twist into providing support for the unsupportable idea. > http://www.newaidsreview.org/posts/1159330774.shtml#2307 > > regards from www.drdach.com Chris Noble The Figure 1 obviously shows a correlation between Viral Load > and CD-4 count as anyone can see. Ahhh, so we agree. Case dismissed. But seriously, you're right, an R-squared of 0.04 is pretty damn shoddy - and no my PhD didn't use any linear regression because when you're doing PCR, viral cultures, Western blots and cell staining there isn't much need for statistics! But I do understand (at least) as much as you, with all your fine years of experience. My point, which you have failed repeatedly to grasp, is that (a) if viral load had NOTHING to do with predicting the rate of CD4 T cell loss then the statement you make above wouldn't be true and (b) at the individual level, it doesn't matter anyway because we're not basing the vast majority of our treatment decisions on the QUANTITATIVE value of viral load. For example, if two people with HIV on therapy have counts of under 50, and one climbs to 10000 and another to 100,000 then we don't consider one a "bigger" failure than the other. Each person is individual. For the person with 100,000, getting his count down to 10,000 might be considered a "success" because it would appear as if some degree of control (albeit probably inadequate) was being put upon viral replication. You're using the same kind of logic that is put into the "viral load doesn't measure 100% infections virions, therefore it's useless" argument. It's irrelevant - if there's viral load, it's coming from replicating virus. Nuff said. It's true that for people with "do we/don't we treat" levels of CD4 cells (say 300-350 or so), but with whopping viral loads, we might feel our hand tipped towards treating more than someone with a CD4 count of 300 and very low viral load. But that's only common sense. Even with the individual R-squared values being so shoddy, the cohort data ought to push you in that direction. All this paper tells us is that there's more to the story (which we already knew, but we didn't fully appreciate how much more). You can't logically conclude more than that. Anyhow, for poops and giggles I did some linear regression on the group data. For each group I picked a number that was the mean of the two outlying values (i.e. for the 501-1000 group I used the number 750). I plotted a scatter graph of the mean annual CD4 T cell loss for each group. For those over 40,000 I used 40,000 to underestimate the viral loads. Back of the envelope math for sure, but based on the data I had it seemed reasonable. Do you want to know the R-squared value you prize so highly? R-squared = 0.8166. But it was clear from the graph that those with very low viral loads (500 and under) were a dog-leg from the trend. So I reanalysed the graph using only the results for viral loads 500 and above. R-squared = 0.9776 I think that bears repeating in plain English. For viral loads over 500 the R-squared value for the relationship between subgroup viral load and the average rate of CD4 T cell loss is 0.9776 - or nearly 98% predictive value. Is that close enough to 1.0 for you? :-D I will try to post the results on my website. Cheers Bennett P.S. A PhD doesn't necessarily mean you will do linear regression, but it does mean you should be smart enough to figure out how to get an answer to a question real quick. Keep 'em coming. > For each group I picked a number that was the mean of the two outlying > values (i.e. for the 501-1000 group I used the number 750). I plotted [quoted text clipped - 5 lines] > > R-squared = 0.8166. In fact, to keep things comparable to the graphs in this paper I performed the linear regression using the same base units - i.e. log base 10 of the viral loads and the estimated T cell loss. R-squared for all groups = 0.9351, actually slightly better than when one ignores the lowest group. Bennett > > For each group I picked a number that was the mean of the two outlying > > values (i.e. for the 501-1000 group I used the number 750). I plotted [quoted text clipped - 14 lines] > > Bennett reply will be forthcoming on Monday > > For each group I picked a number that was the mean of the two outlying > > values (i.e. for the 501-1000 group I used the number 750). I plotted [quoted text clipped - 14 lines] > > Bennett from drdach: Complete reply can be found here: http://barnesworld.blogs.com/barnes_world/ please feel free to visit my web site and post comments on my contact page. regards from www.drdach.com > > > For each group I picked a number that was the mean of the two outlying > > > values (i.e. for the 501-1000 group I used the number 750). I plotted [quoted text clipped - 20 lines] > > http://barnesworld.blogs.com/barnes_world/ When can we read your reply in JAMA? Chris Noble > > > > For each group I picked a number that was the mean of the two outlying > > > > values (i.e. for the 501-1000 group I used the number 750). I plotted [quoted text clipped - 24 lines] > > Chris Noble reply from drdach: My JAMA publication can be found here: http://jama.ama-assn.org/cgi/content/abstract/250/19/2663 where's yours? regards from www.drdach.com > > > > > For each group I picked a number that was the mean of the two outlying > > > > > values (i.e. for the 501-1000 group I used the number 750). I plotted [quoted text clipped - 32 lines] > > where's yours? Never published in JAMA. My point that you apparently cannot understand or do not want to understand is that if you are really trying to convince the scientific community that HIV does not cause AIDS and that the Rodriguez paper somehow supports your claim then you should direct your attention to scientific journals and not weblogs. It is a hallmark of pseudoscience that it targets a lay-audience. Chris Noble I await the good doctor's response to the Rodriguez paper in JAMA. Should I hold my breath? Or will he be using the hank barnes blog entry on his CV as a scientific publication? Interesting that the entry is closed to comments (as most of them are - strange to find that in a blog...), so nobody has a chance to respond to his view. At least it has been "peer reviewed" by fellow denialists though! > Never published in JAMA. > [quoted text clipped - 7 lines] > > Chris Noble > > > > > > For each group I picked a number that was the mean of the two outlying > > > > > > values (i.e. for the 501-1000 group I used the number 750). I plotted [quoted text clipped - 44 lines] > > Chris Noble A hallmark of pseudo-science? I don't think so. It's a good thing to keep the public informed. And Internet is a must because you my friend, are a hallmark of the ferocious german shepherd trying to keep the sheep from where they should not graze for your good health and interests. > > > > > > > For each group I picked a number that was the mean of the two outlying > > > > > > > values (i.e. for the 501-1000 group I used the number 750). I plotted [quoted text clipped - 47 lines] > A hallmark of pseudo-science? I don't think so. It's a good thing to keep the public > informed. Yeah sure. Einstein succeeded by selling his book "What if everything you knew about gravity was wrong?" . It might not be 100% specific but it is fairly accurate. Take Hamer's so called New Medicine. Internet 100%. Scientific journals 0%. Chris Noble > > > > For each group I picked a number that was the mean of the two outlying > > > > values (i.e. for the 501-1000 group I used the number 750). I plotted [quoted text clipped - 24 lines] > > Chris Noble Chris cannot judge for himself. He need to read it in JAMA to know something holds. > Complete reply can be found here: > > http://barnesworld.blogs.com/barnes_world/ Thanks for all the free hits to http://aidsmyth.blogspot.com I already addressed and acknowledged the point you are trying to overemphasise in my own piece. The points you have missed are that (a) a relationship does exist, even if the predictive value of paired points is poor (b) the variance is also taken into account using the error bars in the original figure 1 of the Rodriguez paper and in Mellors' original MACS study. If the individual values in the subgroups really were randomly distributed, as you are implying, there would be a larger degree of overlap. Pontificate and handwave all you like - the evidence is there in black and white. The R-squared value is NOT a direct measure of _whether_or_not_ viral load is predictive of CD4 count decline, but it IS a simple measure of _how_well_ the quantitative value of one predicts the quantitative value of the other in paired samples. The model that the absolute viral load should accurately predict the paired absolute CD4 loss isn't accepted in any case - as we've all been pointing out to you all this time - but it was tested by Rodriguez et al in an attempt to quantify the magnitude of effect, as that was the only way to get the R-squared value. Variables such as mode of transmission, patient age, co-infections etc were not taken into account in this simple model, and since they've all been shown to affect rate of progression it's hardly surprising that the relative contribution of viral load is small. Viral load provides a measure of risk of CD4 T cell decline - and that's about as far as it's been taken. Anyone reading the original literature would (should) have concluded the same. Cheers Bennett > > Complete reply can be found here: > > [quoted text clipped - 33 lines] > > Bennett I don't think anyone ever expected a linear relationship between HIV viral load and the rate of CD4+ loss (except "rethinker" strawmen). The real question is do people with high HIV viral load have significantly greater CD4+ depletion rates than people with low HIV viral load. Duesberg's theory (and other flavours of rethinking) would predict no difference. The answer from figure 1 is a definite yes and is a blow against rethinkers. So far all "rethinking" of the Rodriguez paper avoids the issue. http://barnesworld.blogs.com/barnes_world/2006/10/darin_c_brown_f_1.html Darin Brown seems to completely misunderstand what subgroup analysis and what it isn't. If Darin Brown or Dr Quach have any valid criticism of the statistics in the Rodrigueaz paper then they should write a letter to JAMA. Chris Noble > The Figure 1 |
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