User talk:BruceSwanson

DYK for Inventing the AIDS Virus

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Thanks for this one Victuallers (talk) 18:02, 21 April 2010 (UTC)

Userfied from Talk:AIDS denialism

Wikipedia is not a web forum. If you dispute the scientific consensus on anything, this is not the place to debate that. Wikipedia reports the scientific consensus, it is not the place to promote a fringe theory or attempt to convince other editors of your unscientific viewpoint. WLU (t) (c) Wikipedia's rules:^simple/_complex 12:00, 25 February 2011 (UTC)

I don't deny the existence of Hepatitis C. The clinical condition itself is real enough -- just like AIDS is. But I do find Duesberg's argument against their infectiousness and viral origin, and his description of the financial incentives for their viral-origin theories all to be compelling and credible.

If you want to provide the references that show HAART is just as toxic as AZT alone (Bingo #053), I'd certainly be open-minded about it, as such references would, no doubt, center on the degree of HAART's toxicity to the human liver. To start, you might go here (the full text for PMID 15090806), and do a search for During 1997-1999, mortality fell sharply in HIV-infected individuals. I certainly never meant to imply that AZT alone isn't toxic to the human liver.

I was definitely under the impression that AZT was the sole "antiretroviral" drug at least initially (Bingo #54), although I know other drugs were approved quickly enough. A host of them were in the money by 1996. Let me revise my initial statement above, as follows:

I read the studies. They do not indicate whether the HIV+ hemophiliacs were or weren't taking AZT or any other antiretroviral drug between 1987 and 1996.

What PMID 15090806 does say is This paper updates that evidence and reports on mortality rates since the introduction of effective treatment for HIV with highly active antiretroviral therapy (HAART) in mid-1996. Did you get that "effective treatment for HIV"? What does that say about the treatments before mid-1996? And again, were the HIV+ hemophiliacs studied taking those apparently less-than-effective treatments before 1996?

So, to business. Let's go through my argument one step at a time, to make it easier and possibly to provide additional bingo-points for the orthodox brethren: Was I right when I wrote that the studies don't indicate whether the HIV+ hemophiliacs were or weren't taking AZT or any other antiretroviral drug between 1987 and 1996?

Extra credit question: If I was right, is it important? BruceSwanson (talk) 20:12, 24 February 2011 (UTC)

I'm sorry, but I don't see how I can explain this to you. How could a biologist could explain evolution to someone who denied the existence of genes? How could a physicist explain an eclipse to someone who refused to accept heliocentrism? We don't speak the same language. Your beliefs are irrationally based, so it seems futile to try to combat them with reason. If I cite a study, you will ignore 99% of its content in order to mine one factoid which can be massaged into consistence with your pre-existing convictions about HIV/AIDS.

Worse, I don't believe that you've actually read the studies. You say things like "As for your scenario above, the mortality rate for HIV- hemophiliacs rose too." No. Here's what PMID 15090806 actually says: "During 1977–1984, mortality in individuals with severe haemophilia remained constant at 0.9%. Among HIV-uninfected individuals, mortality remained at this level during 1985–1999. In contrast, among HIV-infected individuals, mortality increased progressively in the years 1985–1986, 1987–1988, 1989–1990, 1991–1992, and 1993–1994." Do you understand what this study is saying? The mortality for HIV-negative hemophiliacs remained constant from 1985-1999. The mortality rate for HIV-positive hemophiliacs rose, and that rise began years before AZT was introduced. Whether or not you believe this to be true, can we agree that this is at least what the study actually says? MastCell ^Talk 06:49, 25 February 2011 (UTC)

Oh, if your colleagues could only see you now. BruceSwanson (talk) 20:10, 1 March 2011 (UTC)

Perhaps some of them can. If so, I'm sure they'd question my decision to invest in this discussion. Does that non-sequitur mean that you've (re?)read the study and internalized what it has to say about hemophiliacs and HIV/AIDS? MastCell ^Talk 06:04, 2 March 2011 (UTC)

What it doesn't have to say. BruceSwanson (talk) 19:39, 2 March 2011 (UTC)

Hmmm. If this is how you respond when you're caught misrepresenting a study, I don't think there's much to be gained by continuing this discussion. MastCell ^Talk 05:30, 4 March 2011 (UTC)

You should definitely not continue this discussion. BruceSwanson (talk) 17:45, 4 March 2011 (UTC)

On a Leash joins Discussion

Bruce you have completely missed the point of ADB #053 and ADB #054. Antiretroviral standard of care 1981-86 was "none" - there weren't any. Between 1987 and 1991 it was high dose AZT, usually 1000 mg/day, but not infrequently doses of 1200 or even 1500 mg per day. From 1992 to 1995 the standard was low dose AZT monotherapy: 500-600 mg per day. From 1996 to 1998 the standard was the same dose of AZT (500-600 mg per day) with two or more additional antiretrovirals.

AIDS denialists often claim that the changes in total US AIDS death numbers from year to year between 1985 and 2007 are proof that those deaths were caused by AZT. There are two problems with such a claim: AIDS deaths were highest from 1992-95 (highest in 1995) when the standard of care was low dose monotherapy, not high dose. Deaths plummeted in 1996 - 98 with the introduction of HAART, which consisted of exactly the same doses of AZT that were used as monotherapy in the previous four years, only with two or more additional antiretrovirals.

If you want to claim that AIDS deaths were caused by AZT, based on total death numbers, you have to explain firstly why death numbers were higher in the low dose monotherapy era than the high dose era, and secondly, why giving AZT 500-600 mg per day in combination with two other antiretrovirals suddenly makes it less toxic than giving exactly the same dose of AZT by itself. Now why does wikipedia ask you to sign posts by typing tildes when there is no tilde key on many computer keyboards? On A Leash (talk) 08:27, 9 March 2011 (UTC)

The point of this discussion is whether the HIV+ hemophiliacs participating in PMID 15090806 (full text here) and PMID 7659168 were taking antiretrovirals between 1987 and 1996. The question is whether hemophiliacs are indeed the best test for the orthodox HIV/AIDS hypothesis, as both Duesberg and his opponents declare, and as discussed in the Science article that is currently footnote 2 in the AIDS Denialism lede paragraph.

I defy you to produce the study showing a higher death rate for lower-dose AZT, or a reliable source summarizing those results. I'm curious who those people were whose mortality was higher at lower doses, and who they were being compared to -- HIV-negative controls, perhaps? BruceSwanson (talk) 22:33, 9 March 2011 (UTC)

You may be missing the point, or choosing to ignore it. On A Leash is pointing out a glaring flaw in your argument. If AZT in fact "caused" AIDS, then one would expect the mortality rate to be highest in 1987–1991, when AZT doses were highest. Instead, mortality from HIV/AIDS peaked in the years 1992-1995, when the standard of care was low-dose AZT. Mortality then dropped off precipitously from 1996 on, despite a constant dose of AZT (due to the introduction of protease inhibitors). These rates are not "compared" to HIV-negative controls - they are mortality rates among HIV-positive patients over time. MastCell ^Talk 23:45, 9 March 2011 (UTC)

"AIDS denialists" believe "antiretroviral" drugs to be one of the causes of AIDS, as the lede paragraph in AIDS Denialism plainly states. Before I continue below, I'm going to assume that you agree with On a Leash's statements below that It is very likely that many if not most of the HIV positive haemophiliacs in the study took antiretrovirals at some stage and you are correct that the study doesn't specify exactly how many subjects were taking AZT or when. BruceSwanson (talk) 01:49, 11 March 2011 (UTC)

Of course I'm not claiming that lower dose AZT is associated with a higher risk of death per individual compared to higher dose AZT monotherapy. However total AIDS death numbers were highest during the low dose monotherapy era, significantly higher than during the high dose era. The fallacy, of course, is to take total death numbers without considering the size of the population (the prevalence of AIDS) into account. This is the first error in the argument #053 and #054 address. In fact, median survival with AIDS was slightly better in the low dose era than it was in the high dose era. But it was better in the high dose era than the no antiretroviral era. And it was dramatically better in the low dose AZT-plus-two-or-more-other-antiretrovirals-era than it was in the low dose AZT monotherapy era.

The second error is to claim that the drop in death numbers between the two periods 1992-5 and 1996-8 could be attributed to "toxic" AZT being replaced by "less toxic" HAART, unless you want to provide a plausible explanation of why adding say 3TC plus a protease inhibitor or 3TC plus nevirapine to 600 mg of AZT makes it less toxic than taking 600 mg of AZT by itself. And in fact, the improvement in survival was far more dramatic than than the plunging total deaths curve would suggest, because those reduced deaths occurred despite an increasing PWA population.

The hypothesis that AIDS deaths in the monotherapy era were predominantly caused by AZT toxicity does not stand up to scrutiny when you compare survival in the pre-monotherapy, high dose monotherapy, low dose monotherapy and HAART eras. It is very likely that many if not most of the HIV positive haemophiliacs in the study took antiretrovirals at some stage: between 1987 and 1990 the standard of care was high dose AZT monotherapy after a diagnosis of AIDS/ARC; between 1990 and 1991 high dose AZT (typically 1000 mg if tolerated and sometimes more) was used in both symptomatic and asymptomatic individuals, and from 1992-5 low dose AZT was used. Yes, you are correct that the study doesn't specify exactly how many subjects were taking AZT or when. Why do you think this is important to whatever you are trying to argue? On A Leash (talk) 00:06, 10 March 2011 (UTC)

So at least some and possibly all of the HIV+ hemophiliacs in PMID 15090806 (full text here) were probably taking variable amounts of AZT and/or other "antiretroviral" drugs while participating in the study.

To answer your question, Why do you think this is important to whatever you are trying to argue? What I am trying to argue is that the study should have pointed out that HIV- hemophiliacs were definitely not taking the drugs and HIV+ hemophiliacs either may have taken them, probably did or did take them, or that nothing is specifically known about their use of such drugs for the duration of the study. And this is important because the effect of such drugs at specific dosages is obviously clinically relevant, and therefore readers should be apprised of their use or non-use by participants in the study. In other words, the use or non-use of the drugs is an experimental parameter. Surely you agree.

You admit I'm not claiming that lower dose AZT is associated with a higher risk of death per individual compared to higher dose AZT monotherapy and In fact, median survival with AIDS was slightly better in the low dose era than it was in the high dose era. And then you add But it was better in the high dose era than the no antiretroviral era. And it was dramatically better in the low dose AZT-plus-two-or-more-other-antiretrovirals-era than it was in the low dose AZT monotherapy era.

I suspect that one clue to the mystery is can be found in your own rather salesman-quick use of the phrase if tolerated. Think of the host of variables implicit in that qualifier. With that in mind, and since this is my own Talk page, I will add my own interpretation of your stats, which at least sound true (although feel free to cite the published sources).

Duesberg pointed out in his Inventing the AIDS Virus that AZT was initially shelved because it was both ineffective and toxic -- at would-be therapeutic dosages it killed its test-animals before it could attack their cancers. At lower dosages, it did nothing at all, at least in the short term.

But suppose HIV doesn't cause AIDS. An "antiretroviral" drug would need only be tolerable to give the appearance of effectiveness -- provided the patient hasn't passed the point of no return. That's exactly what the earliest AIDS patients had done. They had clinical AIDS all right, but 10-15 years of living a life based on poppers, multiple anal-sex partners, and drug-use that some of them admitted could be found nowhere in the straight world -- no parallel at all -- doomed them.

By 1987 reports indicated that things had changed. The gays, we are told, had been warned about poppers, and begun to use condoms and moderate their drug use. Now at this point something interesting happens: the higher the dose of AZT, the better the therapeutic result. Why? Because hardly anyone could tolerate that dose so they quit altogether or cut the dose on their own. But they admit neither to their doctors (who perhaps wouldn't have wanted to hear it anyway). Later, the official dosage falls to a more marketable level. More people can take the stuff and do. So the lower the dose the better too: either extreme reduces the level of the drugs in their bodies. To summarize, there was collective behavior modification in conjunction with reduced drug use -- recreational and "antiretroviral".

Finally, as to the apparent contradiction of the multiple-drug HAART being just as tolerated as single dose AZT. I'm not sure of the point you are trying to make. If adding two drugs to AZT without changing AZT's dose makes no immediate difference in a patient's tolerance level, then the added drugs are making no immediate difference at all. A placebo would be equally inert. But no one argues that the added drugs make no long term difference. I'm not aware that AZT gives its customers a buffalo hump. In any case, neither approach is actually tolerated -- it simply take much longer now for the effects of such drugs to be felt. Premature aging (and buffalo humps) are two of those effects (the former discussed here). In a sense, the old high-dose AZT was preferable because it couldn't be tolerated at commercially exploitable levels.

You wrote the improvement in survival [under HAART] was far more dramatic than than the plunging total deaths curve would suggest, because those reduced deaths occurred despite an increasing PWA population. But after 1990 the population of consumers of "antiretroviral" drugs vastly increased when, by your own account, asymptomatic patients began to take them (or at least buy them for awhile). Isn’t it at least reasonable at this point to ask whether claims of reduced mortality among AIDS patients after 1990 might be based at least partially on this specific artificially increased number of possibly redefined PWAs?

I suggest that if you or MastCell want to pursue this discussion on a more detailed basis you should cite your sources so that other readers here (if any) may also read them and comment. BruceSwanson (talk) 01:49, 11 March 2011 (UTC)

Bruce, although I am aware that certain dissidents have claimed, as you are doing now that "AZT was initially shelved because it was both ineffective and toxic -- at would-be therapeutic dosages it killed its test-animals before it could attack their cancers", citing Duesberg's book. There Duesberg says "However, when he tested the compound on cancer ridden mice, it failed to cure the cancer. Horowitz was so disappointed he never bothered publishing the experiment and eventually abandoned that line of research. The drug must have killed the tumors, which contain dividing cells, but it so effectively destroyed healthy growing tissues that the mice died of the extreme toxicity." Must have? Really? Duesberg provides no citation supporting his claim there was ever any experiment in which AZT actually did kill tumors but killed experimental mice through "extreme toxicity". If no such experiment can be found, then I think given his track record on similar claims in his book it would be reasonable to conclude that he just made it up, as is suggested by his couching his claim in terms of must have. Somehow, it seems, Duesberg's speculative "must have" has turned into an actual fact.

As far as I am aware, AZT was shelved as a potential anti-cancer drug in the 1960s because it was found ineffective against cancer in the initial test models which included in vitro studies of its activity against Jensen sarcoma cells and various animal cancers. If you know of any toxicity studies prior to its being abandoned as a potential anti-cancer drug, then do tell. Duesberg only tells us they "must have" done them, and he reports what the results "must have" been, The basis for claim seems to me to be simply his own preconceived beliefs. Not very convincing to me, but this hasn't stopped the claim that "AZT was shelved because it was too toxic for human use" being endlessly copy-pasted over the internet. Do a Google search for: AZT "too toxic for human use" and you'll see what I mean.

The LD50 of AZT in mice, by the way, is greater than 3000 mg/kg, which is roughly the LD50 of common table salt. http://www.medscape.com/druginfo/monograph?cid=med&drugid=4666&drugname=Lamivudine-Zidovudine+Oral&monotype=monograph&monographid=387007&secid=6

You ask "But after 1990 the population of consumers of "antiretroviral" drugs vastly increased when, by your own account, asymptomatic patients began to take them... Isn’t it at least reasonable at this point to ask whether claims of reduced mortality among AIDS patients after 1990 might be based at least partially on this specific artificially increased number of possibly redefined PWAs?" Short answer is no, it's not reasonable. Survival improved (modestly) among AIDS patients. An AIDS patient is defined as a person diagnosed with AIDS, not a person taking AZT, and prior to 1993 does not include any asymptomatic persons, whether taking AZT or not.

You still seem to be struggling to rationalise why mortality fell dramatically from 1996-8 among people with AIDS compared to the years immediately prior - 1993, 1994 and 1995, when both the diagnostic criteria for AIDS and the standard AZT dose of 500-600 mg daily were identical. Your suggestion that the high death numbers among people with AIDS in 1993, 1994 and 1995 were caused by AZT, but it suddenly stopped causing these levels of deaths in 1996, 1997 and 1998 lacks any plausible basis as far as I can see.On A Leash (talk) 07:29, 11 March 2011 (UTC)

Conclusion thus far

That at least some of the HIV+ hemophiliacs participating in PMID 15090806 (full text here) had taken AZT either before or during the study.

You may also want to read PMID 7659168 (Nature 1995), which looks at the same general population of hemophiliacs. The Nature paper confirms that zidovudine treatment became the norm around 1989 for these patients, but that the increased mortality in HIV-seropositive hemophiliacs was in evidence well before the introduction of zidovudine. Thus, even if one looks at this study in isolation (a bad practice, but let's go with it), it does not support the idea that zidovudine a) causes AIDS, or b) was responsible for the increased mortality among HIV-positive hemophiliacs over HIV-negative hemophiliacs. MastCell ^Talk 20:49, 24 March 2011 (UTC)

Putting aside the contaminated Factor VIII that initially killed both HIV+ and HIV- hemophiliacs, Duesberg explains here (currently footnote 2 in the AIDS Denialism lede paragraph) that HIV was (and is) rare, thus only those hemophiliacs who received the most blood transfusions at the time (before HIV screening) were likely to become infected by it. So HIV was simply a marker for severe hemophiliacs. What killed them was their need for transfusions -- either their underlying injury or disease, or the massive and repeated influx of foreign protein, or both.

As for PMID 7659168, it seems to be available for free only in abstract form, as follows:

During 1977-91, 6,278 males diagnosed with haemophilia were living in the UK. During 1979-86, 1,227 were infected with the human immunodeficiency virus (HIV-1) as a result of transfusion therapy (median estimated seroconversion date, October 1982). Among 2,448 with severe haemophilia, the annual death rate was stable at 8 per 1,000 during 1977-84; during 1985-92 death rates remained at 8 per 1,000 among HIV-seronegative patients but rose steeply in seropositive patients, reaching 81 per 1,000 in 1991-92. Among 3,830 with mild or moderate haemophilia, the pattern was similar, with an initial death rate of 4 per 1,000 in 1977-84, rising to 85 per 1,000 in 1991-92 in seropositive patients. During 1985-92, there were 403 deaths in HIV seropositive patients, whereas 60 would have been predicted from rates in seronegatives, suggesting that 85% of the deaths in seropositive patients were due to HIV infection. Most of the excess deaths were certified as due to AIDS or to conditions recognized as being associated with AIDS.

If, as you say, AZT was standard for HIV+ hemophiliacs by 1989, I see nothing in the abstract that contradicts Duesberg's thinking. BruceSwanson (talk) 19:40, 25 March 2011 (UTC)

You're correct - there's nothing in the abstract that contradicts Duesberg's claims. However, if you're serious about overthrowing the HIV/AIDS paradigm, you might want to read the entire paper. Like most of the medical literature, it is freely available from any reasonably sized public library.

Moreover, HIV was not simply a marker for severe hemophilia in these studies. The analyses controlled for hemophilia severity. Even if you restrict your analysis to severe (or moderate, or mild) hemophilia, HIV+ hemophiliacs have much higher mortality than HIV- hemophiliacs at all given levels of transfusion dependence. This is, again, all in the cited papers. MastCell ^Talk 22:52, 25 March 2011 (UTC)

Well, my conclusions thus far are:

(1) that Duesberg just makes stuff up - like his claim that initial tests of AZT for cancer resulted in the deaths of the experimental animals from "extreme toxicity", and that this claim has been amplified on the internet by people who are too lazy to check whether it is true. And that when you challenge self-described "dissidents" on this they simply change the subject.

(2) that you have no answer to why mortality among people with AIDS plummeted in 1996-8 compared with 1992-5, when the AZT doses used in both periods were identical.On A Leash (talk) 08:08, 31 March 2011 (UTC)

To be Discussed

Where does the above conclusion leave us regarding the idea that hemophiliacs provide the best test of the HIV/AIDS hypothesis or the Duesberg hypothesis?

See immediately above. MastCell ^Talk 20:50, 24 March 2011 (UTC)

The standard HIV/AIDS hypothesis is not validated by the example of HIV+ hemophiliacs. First, contaminated Factor VIII killed both HIV pos- and neg- hemophiliacs. HIV's rarity meant that only the least healthy patients were infected. Thereafter, they received long-term chemo (AZT) as high-dose monotherapy. The result: HIV+ patients died in greater numbers. BruceSwanson (talk) 19:40, 25 March 2011 (UTC)

Wow. Why don't you explain (ideally with reference to actual data rather than Duesberg's book) what you mean by "contaminated" Factor VIII? and what percentage of hemophiliacs you think were "least healthy" and thus infected with HIV? and why you think that "high-dose AZT monotherapy" was responsible when mortality trends clearly fail to support such a claim? MastCell ^Talk 22:55, 25 March 2011 (UTC)

Consolidation

On a Leash: First you say that Duesberg made up or assumed that AZT's initial testing in 1964 "must have" killed tumors in mice and rats and that any therapeutic dose must also have exceeded the toxic dose. However, Duesberg's claim in the book does come with a couple of relevant footnotes, which you somehow missed.

Then you quite helpfully provided, above, a link that for a while (it doesn't anymore) reported the official results of someone's work establishing that, as you say, AZT's lethal dose for 50% of mice is greater than 3000 mg/kg, which, you add, is "roughly the LD50 of common table salt" (for rats).

So, AZT has a lethal dose for mice and rats. We know that the drug failed to have any therapeutic effect. Why make a point of discussing Duesberg's particular claim regarding this matter? Are you claiming that it was inert until lethal? That it failed to terminate DNA replication? Perhaps in vitro it didn't. As a non-clinician I will ignorantly wonder aloud whether or for how long such cells were able to continue dividing, or whether phosphorylation of AZT could take place long enough or at all. As for changing the subject, the subject is supposed to be about whether hemophiliacs provide the best test of the conventional HIV/AIDS hypothesis. Both you and MastCell seemed determined to expand it to the general population of AIDS patients.

We can now be reasonably certain that in all tests comparing HIV+ and HIV- hemophiliacs that either some, most, or all of the latter were on AZT during the course of the studies. And we know that in PMID 15090806 (full text here) no mention is made of such usage. (MastCell: I'm frankly skeptical that Web-unavailable 7659168 cites AZT usage by participants. Can you cite the page number and provide a quote? And why make a point of specifically mandating 7659168, published in 1995, when its follow-up 15090806, published in 2004 and sharing three authors with 7659168, is available on the Web?)

Omitting AZT use by HIV+ hemophiliacs must cast doubt on the credibility of such studies as well as the honesty of their authors. AZT is, to say the least, a critical parameter in any such endeavor.

And now to generalize the subject myself, conclusions drawn from any study involving AZT are dubious anyway because AZT use in would-be therapeutic dosages is always identifiable. The studies cannot be blinded unless the dosages are so low that effects would not be felt for years, which obviously hinders close monitoring. My question is: double-blind studies involving critically ill patients are conducted all the time. Some patients may benefit, others may die. Those are the ethics. Society accepts the trade-off, as do the participants themselves. So why can't a study be done deliberately withholding "antiretroviral" drugs from (non-hemophiliac) HIV+ AIDS patients and then comparing their progress with HIV+ AIDS patients given such drugs in a controlled setting? Has such a study ever been done? If not, why not? Is it because the results would be politically incorrect? "AIDS Denialists" would say Yes, that is exactly the reason. BruceSwanson (talk) 20:31, 1 April 2011 (UTC)

Trying to respond to this is sort of like trying to deal with the Gish Gallop. To take only your last paragraph: why do you assume that AZT use is "always identifiable"? Using what parameters? And how important is blinding if the endpoint is all-cause mortality? Why would low doses of a drug hinder close monitoring?

There are two issues you need to understand about clinical trials, one ethical and one logistical. First, the ethical issue: in order to ethically randomize patients, you need equipoise. In other words, you have to be genuinely uncertain that either arm of the trial is superior. If you are convinced that one arm is superior, you cannot ethically randomize patients. Existing data make a convincing case (convincing, at least, to people who actually treat patients with HIV/AIDS) that antiretrovirals are superior to placebo, so you're unlikely to find anyone who can pretend to have the necessary equipoise to randomly withhold these treatments from people with a lethal disease. It would be fundamentally unethical.

Second, the logistical issue: clinical trials need to enroll patients if they're to tell us anything. Even if such a study could be approved, how many HIV/AIDS patients, in 2011, would consent to a study which might (randomly) withhold proven, lifesaving treatment from them in order to test a hypothesis that is unanimously considered implausible? To obtain truly informed consent, patients would have to be made aware that the hypothesis being tested is rejected as deeply ignorant by the worldwide scientific community. Very few people would sign up for such a trial, even if it existed, and those who signed such a consent hardly be representative of the HIV+ population as a whole, limiting the study's generalisability.

Finally, there's the question of what such a study would prove. Everyone who actually treats HIV/AIDS understands the causative role of HIV, and the potentially lifesaving role of antiretroviral treatment. For the scientific community, this isn't an open question anymore, so such a study would prove nothing to them. On the other hand, AIDS denialists have demonstrated repeatedly that they cannot be convinced by scientific evidence or appeals to rationality. So even if such a study were completed, its results would be rejected (on the sorts of ignorant, facile grounds you've evidenced above) and the goalposts moved again, because the results would contradict your deeply held belief. If you don't accept, for instance, that Christine Maggiore and her daughter died of untreated AIDS, then you will never be convinced by the study you propose. One cannot address an irrational belief by rational means - that's always a waste of time.

And finally, if you want access to a paper that's not online, I cannot emphasize this enough: go to a library. I'm not citing obscure journals; this is Nature. Your friendly local librarian will either hand you a copy, or get one for you. I'm not going to discuss articles with someone who can't be bothered to take the most basic, free steps to confirm or refute their own assumptions. MastCell ^Talk 21:35, 1 April 2011 (UTC)

I think MastCell has explained it better than I could, Bruce, but to put it simply, where on earth do you think you might find participants for a randomised double blind trial of HAART versus placebo? No sensible person in need of HAART would agree to participate in a trial in which they might be randomised to placebo. And not even the most HAART-hating "dissident" would agree, either - once they realise that randomisation means they don't have a choice about whether or not to be on HAART. On A Leash (talk) 01:52, 2 April 2011 (UTC)

MastCell, If you'll recall, my point about Web-unavailable PMID 7659168 was that it is unlikely to be necessary to read at all, given that its follow-up study, PMID 15090806 is available online, here. Nevertheless, the next time I'm at the library I'll track it down and report what it says, if anything, about AZT use among its HIV+ hemophiliacs.

Regarding equipoise, it can of course be restated as follows: when investigators become convinced that treatment A is worse than treatment B (which might be no treatment), then they are ethically obligated to discontinue treatment A and offer treatment B. From the start, testing of AZT on advanced AIDS patients was unblinded because at dosages offered it was obvious who was taking it and who wasn't, and patients actively sought to evade the controls. Plenty of investigators and patients regarded the first tests as a travesty and were not convinced of AZT's efficacy. But today HAART could ethically be tested on non-pregnant HIV+ asymptomatic patients because you could easily find at least one patient participant convinced of the drugs' toxicity for every investigator and patient convinced of their efficacy. On a Leash, the study would be ethical because it needn't be blinded. And it would be doable. Just find committed Christian Scientists (or their various 'natural therapy' equivalents) who are HIV+ and otherwise healthy for the moment and not taking HAART on principle. Compare those profiles to those who take HAART following their beliefs. In this scenario, equipoise would amount to a kind of agreed-upon standoff. As for the results, well, we technically don't really know what they would be because apparently no such controlled test has ever been conducted, but note that both camps would be confident of the outcome and so committed to staying the course. Right?

Overall, I find the equipoise angle in need of further discussion: what it presumes is that an investigator's personal perception, informed by inductive reasoning and intuition, can and should end a study involving people. Well, I can see how that could be appropriate. In the kind of test I proposed above, I can definitely imagine terminating the AZT arm of it after too many of its participants died at 50 of diseases common to those at 70 or 80 (see this). But of course that choice can only apply to certain kinds of studies. Where that kind of cessation occurs, the active arm involved -- prescribing a drug or surgical procedure (as opposed to the passive arm) -- should be classified as being untested and thus experimental by definition. It's a bit like the problem of HIV and Koch's Postulates. HIV/AIDS orthodoxists claim that HIV satisfies the postulates because uncontrolled accidental needle-jabs have supposedly induced a few cases of AIDS in labs workers, etc. But by definition such data can't conform to Koch, which, being essentially an algorithm based on deductive logic, is necessarily limited to strict laboratory-based procedures. The postulates may not cover all infectious agents and their diseases, but if so those agents would still fail the postulates, which are what they are and nothing more.

By this same reasoning, where clinical equipoise halts a double-blinded study, then by definition that drug or procedure has not been tested using double-blind protocols. They will have to be tested, if at all, by other means. And until they are, they are experimental. I think that by this reasoning, HAART remains experimental. By its very nature it can't be blinded at would-be therapeutic doses, and apparently no long-term comparison testing has been done on willing volunteers in the way I (and no doubt many others) have suggested.

So, do you first do no harm, or do you give HAART to pregnant patients and hope for the best? Maybe we should ask Frances. I for one would be curious to know her answer.

Am I the only reader who views MastCell's reference to Christine Maggiore as a Gish Gallop of his own? BruceSwanson (talk) 17:37, 2 April 2011 (UTC)

Scray joins in

Parallels to thalidomide are misguided - the problem there was a lack of safety data, whereas antiretroviral drugs are among the most-studied (and most effective) agents in medicine. Regarding that same (penultimate) paragraph of your comment, the benefits of antiretroviral therapy during pregnancy were clearly demonstrated in ACTG 076 (PMID 7935654) and confirmed in studies using combination therapy showing benefits to mother and baby. Regarding your final paragraph, your comment indicates a misunderstanding of the Maggiore case, the term Gish Gallop, or both. I wish you the best, but I find your edits to be misinformed. -- Scray (talk) 18:12, 2 April 2011 (UTC)

Bruce, I don't think you've thought this through. If you seek out Christian Scientists for your control arm, then of course randomization is impossible, since they would presumably refuse the possibility of receiving treatment. (As a side matter, exactly how many HIV+ Christian Scientists do you think there are in the U.S. at present? And of these, how many do you anticipate would be open to participating in an HIV clinical trial?)

You seem to believe that no hypothesis can be accepted as true unless it is proven in a randomized, controlled trial. By way of analogy, no one has proven in a randomized, controlled fashion that parachute use prevents death related to gravitational challenge, yet it seems to be accepted as fact on the basis of compelling observational and inferential findings, and it would certainly be unethical to test in a randomized fashion. That's what equipoise means. You're essentially asking people to jump out of a plane, and to be randomly assigned a parachute or not.

I will refrain from addressing your misconceptions about Koch's postulates, since it seems like a poor use of time. MastCell ^Talk 19:51, 2 April 2011 (UTC)

Scray, the Orwellian phrase safety data is a euphemism. It’s toxicity data. An example is the "efficacy and safety" trial PACTG 1022. Whatever you call it, the data on thalidomide and AZT was obviously insufficient for a number of its initial users. So, was the testing process technically flawed or morally flawed, or both? I think Jane Jacobs would have regarded the whole process as a monstrous moral hybrid. In the case of thalidomide, there was a Guardian in the US, Frances Kelsey. But by the 1980s the Guardians had become corrupted through syndrome mixing. (This is of interest regarding thalidomide. Here is Harper’s article on PACTG 1022). No wonder books like The Constant Gardner find readers.

The “benefits to mother and baby” depend on HIV causing AIDS. You’ll recall that this discussion was originally about how both sides on this issue agreed that hemophiliacs provided the best test for the HIV=AIDS hypothesis. We now know that the HIV+ hemophiliacs under study were probably on AZT, and that in at least one major study, PMID 15090806 (full text here) no mention was made of the AZT use, destroying the study's credibility to anyone with an open mind on the subject. Furthermore, at would-be therapeutic dosages “antiretroviral” drugs weren't randomized and blinded, either because their effects were obvious or because the patients themselves (and possibly equipoise-minded clinicians) actively circumvented the controls. Thus, the drugs remain experimental by definition and their use amounts to an ongoing uncontrolled experiment. So in a sense you are right: they are “among the most studied” in medicine. As for being “among the most effective agents” in medicine, you can't be serious.

(Regarding Christine_Maggiore my point is that she has no place in this discussion. MastCell’s bringing her up is merely a distraction. For the record, I don’t believe for a moment that either she or her daughter had “AIDS”. They’d both be alive today if Maggiore had kept mum about her “condition” and simply lived a normal life.)

MastCell, I’m not sure you’ve thought this through. I wrote: the study would be ethical because it needn't be blinded. I’m saying that randomized double-blinding isn’t necessary because committed volunteers from both camps could be recruited. As for professing Christian Scientists and their 'natural therapy' ilk, there may even be more former recreational drug-users among them then among the general population, since many of them (surely) are converts fleeing messier lifestyles. If HIV is, as orthodoxists claim, an infectious sex- and needle-transmitted agent, then there are going to be HIV+ volunteers among the 'natural' crowd willing to test (at least confidentially). And there would be no moral problem even with pregnant volunteers. After all, if it is ethical to let a pregnant woman take AZT to test its toxicities on herself and her fetus as part of a study, surely it is ethical to monitor a pregnant HIV+ Christian Scientist as part of a study. Such studies could go on for years at relatively low cost.

As for the parachute-paper, you apparently forgot that I wrote But of course that choice [granted by the ethics of equipoise] can only apply to certain kinds of studies. In other words, there are studies where equipoise would apply, and those where it wouldn’t. Having 300+ skydives myself, I am satisfied that the act of parachuting versus the situational alternative does not require randomized testing, although some kinds of equipment, such as computerized automatic-activation devices, may be subject to it. The paper was amusing, but I suspect it was cooked up to be used in just the circumstances in which you employed it – as rhetorical misdirection, like mentioning Christine Maggiore.

Finally, as for your refraining from commenting on my “misconceptions” regarding Koch’s Postulates, I agree that trying would be a poor use of your time. BruceSwanson (talk) 22:57, 4 April 2011 (UTC)

Bruce, books like The Constant Gardener find readers because conspiracy theories make entertaining fiction. The Twilight series also enjoys wide readership - does that make the existence vampires and werewolves more plausible? I get that your belief system views HIV as harmless and antiretrovirals as deadly concoctions foisted upon a healthy public by multinational drug companies. I just don't think you should couch your belief system in a fig leaf of science - it's not a good fit. It's obvious that you'll go to the ends of the earth to quote-mine a snippet supporting your belief system, but you won't even stop by the library in the interest of fully informing yourself. Those aren't promising conditions for rational discussion. MastCell ^Talk 23:55, 4 April 2011 (UTC)

Books like The Constant Gardener find readers because conspiracy theories make entertaining fiction. No, that book unfortunately makes plausible fiction. The Twilight series is merely entertaining.

Courtesy ProQust I have visited the library from home and found the study in question, PMID 7659168. It confirms that AZT was indeed in use by 1989 for HIV+ hemophiliacs (Duesberg says 1987). So it's official. The credibility of the conclusions is necessarily suspect: imagine giving severe hemophiliacs AZT and expecting them to live! I was amused by this gem: However, the steady increase in the death rate from 1985 to 1992 suggests that in this population [HIV+ hemophiliacs] the increasing impact of HIV-associated mortality has not been halted by these treatments [of AZT].

But that, of course, is quote-mining. — Preceding unsigned comment added by BruceSwanson (talk • contribs)

Hmmm. So you agree that the paper indicates that AZT use became widespread for HIV+ hemophiliacs in 1989. Yet the paper also makes clear that the mortality rate among HIV+ hemophiliacs began rising well before 1989, and continued its "steady rise" after 1989. So the logical conclusion is that AZT had nothing to do with the high mortality rate among HIV+ hemophiliacs. I'm not clear how you square this with your apparent belief that AZT (rather than HIV/AIDS) was responsible for the high mortality in this group. MastCell ^Talk 03:11, 11 April 2011 (UTC)

A study for consideration

Around and around we go. Now it's my turn to supply a paper by way of response: Foreign-Protein--Mediated Immunodeficiency in Hemophiliacs With and Without HIV, by Peter Duesberg. It is Appendix A in his book Inventing the AIDS Virus and is viewable almost in its entirety at its Amazon listing. Enter the title as the search criteria. This should also answer your earlier question, above: Why don't you explain (ideally with reference to actual data rather than Duesberg's book) what you mean by "contaminated" Factor VIII? I think the paper should satisfy your need for "actual data", as it was initially published in Genetica. BruceSwanson (talk) 03:56, 12 April 2011 (UTC)

Let's suppose that of the 7 assertions made by Duesberg in the abstract, all (or a majority) can be shown to be false or incorrect with reference to existing medical literature. Would that convince you of anything? MastCell ^Talk 19:43, 12 April 2011 (UTC)

It sure would, but there is no need to invalidate all of them or even a majority. Defeating any one of the seven assertions should be sufficient, as all of them are based on the same assumption: AIDS isn't infectious. Choose your poison. BruceSwanson (talk) 01:50, 15 April 2011 (UTC)

Fine. Let's start with #1: Duesberg's claim that "after 1987 the life span of hemophiliacs appears to have decreased again, probably because of widespread treatment with the cytotoxic anti-HIV drug AZT." As we've already discussed at length with reference to the medical literature, mortality among HIV+ hemophiliacs began increasing before 1987, and thus before the introduction of AZT. That's strong evidence against Duesberg's claim that AZT was responsible.

As a secondary point, the increased mortality was limited to HIV+ hemophiliacs, even before the introduction of AZT. Taken together, these data are consistent with the HIV/AIDS paradigm and inconsistent with Duesberg's claims. So we're done here? MastCell ^Talk 04:31, 15 April 2011 (UTC)

We certainly should be done. Readers should be reminded that, per PMID 7659168, use of AZT among HIV+ hemophiliacs was standard from "about 1989" (this statement is not in the abstract but is in the full study). MastCell, you've helpfully reminded us that, per PMID 15090806, AZT obviously did not stop the rise in HIV+ hemophiliac mortality that began before the drug was approved for use and that continued until 1997 and HAART (the "effective treatment" referred to), upon which AIDS deaths fell but liver-disease deaths for HIV+ hemophiliacs remained as high as ever.

For Duesberg's explanation of PMID 15090806's statement that Survival was strongly related to age at HIV infection go here and do a search for age bias. That explanation touches on why the death rate for the HIV+ was higher than for the HIV-negative. HIV was simply a marker for quantity of transfusions. Duesberg specifically makes the point on p.483 of his book (search term: marker) that the longer you were a hemophiliac, the greater the chances of acquiring HIV, which was even then rare in the blood supply available to hemophiliacs.

So now the critical point to be addressed is AZT's failure to halt the documented rise in HIV+ hemophiliac mortality. Could that rise actually have had two causes: first, years of exposure to foreign proteins in Factor VIII; and second, the approval of AZT as a therapeutic drug for HIV+ individuals, many of whom were hemophiliacs already beginning to die anyway? BruceSwanson (talk) 18:27, 17 April 2011 (UTC)

Who's full of what

Hmmm. It's becoming harder for me to avoid the conclusion that you're full of it. You said that falsifying just one of Duesberg's 7 points, with reference to the existing medical literature, would lead you to re-examine your beliefs. I falsified the first of Duesberg's claims - he was wrong about the timing of the increase in mortality, which cuts the bottom out from under his claims about AZT.

You've responded with muddled nonsense about AZT and patient age, and completely failed to engage the actual content of my previous post. (As an aside, it is generally understood that AZT as monotherapy does not increase survival, so you can cease your vicious attack on that strawman). Do you see why people call this "denialism"? You not only disagree with findings that conflict with your belief system; you don't even acknowledge their existence. MastCell ^Talk 00:06, 18 April 2011 (UTC)

We are now going to find out who's full of what. You wrote above that it is generally understood that AZT as monotherapy does not increase survival. Is that general understanding reflected in the following AZT lede sentence: AZT use was a major breakthrough in AIDS therapy in the 1990s that significantly altered the course of the illness and helped destroy the notion that HIV/AIDS was a death sentence.? BruceSwanson (talk) 21:17, 18 April 2011 (UTC)

You really are desperate to avoid thinking critically about what I've said, aren't you? You asked me to falsify any one of Duesberg's pronouncements. I did so, and I can tell I succeeded by the amount of effort you're expending on evasive action.

Look: Duesberg based his claims on a purported increase in mortality among HIV+ hemophiliacs dating to 1987 and the introduction of AZT. In fact, he got the dates wrong - the increase started before 1987 and before AZT, and its tempo was not perceptibly affected by the introduction of AZT. That knocks the bottom out from under his very first point. You said that the invalidation of any one of Duesberg's claims would lead you to "rethink" your beliefs. I took you at your word, which is beginning to look like an error on my part. I'd like you to respond to this, directly.

Regarding your effort to change the subject: we can discuss the ins and outs of AZT monotherapy, but it's a somewhat academic exercise since it is not the current standard of care and has not been for at least 15 years. It's typically more of an idee fixe for AIDS denialists than a topic of current relevance, but as you like. PMID 3299089 showed a benefit - in terms of decreased mortality - to AZT over placebo in patients with advanced AIDS. On the other hand, PMID 7908356 (Concorde) and PMID 7616988 (ACTG 019) showed no mortality benefit from AZT treatment in asymptomatic HIV+ individuals. (Notably, AZT did not increase mortality as compared to placebo, demolishing in passing another AIDS-denialist assumption about the toxicity of AZT).

One could say that AZT "significantly altered the course of the illness" (in that it had a benefit in advanced AIDS, and slowed the decline of CD4+ count in early HIV). The more significant aspect of AZT is that a) it was the first compound to show any HIV-specific clinical benefit, and b) it formed the backbone of truly active combination antiretroviral therapy introduced in the mid-1990s. The wording of our article on zidovudine could be altered to reflect this, if you feel strongly about it.

Next? MastCell ^Talk 21:56, 18 April 2011 (UTC)

I entirely agree with what MastCell has said here (more importantly, reliable sources support MastCell's statements). During the 1990s we saw a series of new antiretroviral drugs licensed and the first of these was AZT. By the end of that decade we had combinations (including AZT) that halted and reversed AIDS. -- Scray (talk) 21:37, 18 April 2011 (UTC)

I encourage readers to re-read MastCell's "falsification" and my alleged failure to address the "wrong date" problem in Duesberg's paper.

Re the fine print: the "wording" (meaning) can't be "altered" (changed) using those three references, as per WLU's stern dictate. For the same reason, we can't use PMID 7659168 and PMID 15090806. I mean, open your eyes. Do you see any primary sources in the AZT article? We need to adhere to WLU's learned guardianship.

Re Scray's comment: Duesberg's paper was first published in Genetica. The drugs didn't halt and reverse AIDS. Most of their long-time consumers never had AIDS to begin with and will die of premature aging. The ones who really had AIDS died of AIDS and/or liver failure. BruceSwanson (talk) 22:21, 19 April 2011 (UTC)

OrangeMarlin's turn

MastCell...why do you persist? Bruce has a denialist answer for each comment you make. For example, Christine Maggiore and her daughter would be alive today if they weren't denialists themselves. Bruce is incapable of, unwilling to, or ignorant of real science and research. Let us recall the conditions that make a pseudoscience belief: everything from ad hominem arguments to confirmation rather than refutation to the use of vague claims. Bruce is like AGW denialists, vaccine denialists, evolution denialists, and birthers–no matter what evidence you bring to the discussion, they ignore it, dispute it, and deny it, while relying on some fringe theory that supports their denialism. It's not worth the effort. OrangeMarlin ^{Talk• Contributions} 15:01, 6 April 2011 (UTC)

Christine Maggiore and her daughter would be alive today if they weren't denialists themselves. Not quite. Maggiore and her daughter (who was too young to be called a "denialist") would be alive if Maggiore had kept mum about her (supposed) HIV+ status and simply lived a normal life. That means vaccinations, no "holistic" healing, no media pressure. Her daughter wasn't vaccinated and died as children commonly did before vaccinations became standard. Maggiore herself underwent severe "cleansing" treatment that probably hastened her demise.

What "ad hominem" arguments? What "vague" claims?

As for the global warming-, vaccine-, evolution-, Obama citizenship-denialism, you got one out of four right. Want to take a guess as to which one it is? BruceSwanson (talk) 18:15, 8 April 2011 (UTC)

So it's your belief that Maggiore's daughter died of a vaccine-preventable disease? Which one? MastCell ^Talk 03:04, 11 April 2011 (UTC)

Eliza Scovill

I have no objection to discussing the Maggiore case in greater detail.

The coroner's report begins with the cause of death being "pneumocystis carinii pneumonia due to AIDS" -- meaning that it was PCP in the presence of HIV. The HIV comes from a further statement that This immunohistochemical study confirms the presence of HIV core protein in the brain sections confirming a diagnosis of HIV encephalitis. In the absence of HIV, PCP alone would have been cited as the cause of death, however multinucleated giant cells were also found in the brain. A comment from Neuropathology is instructive: HIV envelope glycoproteins cause the membranes of HIV-infected macrophages to fuse, forming multinucleated giant cells (MGC) which are the hallmark of HIV encephalitis.

But aren’t MGC’s the hallmark of many kinds of infection?

Now I have to be careful not to go too far, lest I be accused of a Gish Gallop, so I’m going to stop here and await an answer before continuing. BruceSwanson (talk) 03:56, 12 April 2011 (UTC)

That would be relevant if the diagnosis of HIV encephalitis were based solely on the presence of multinucleated giant cells, which are characteristic but not completely specific for HIV encephalitis. MNC in combination with the detection of p24 antigen is specific for HIV.

It works like this: the pathologist sees MNC on an initial microscopic exam of the brain tissue. These are highly suggestive of HIV encephalitis. To confirm this suspicion, the pathologist requests special stains for p24 antigen by immunohistochemistry (a widely used and highly specific test in use for at least 20 years; see PMID 1907231). The combination of classic histologic findings (MNC) with immunohistochemical confirmation of the presence of HIV leads to the diagnosis of HIV encephalitis. This approach, which appears to have been used by the coroner's office, is entirely standard. MastCell ^Talk 19:25, 12 April 2011 (UTC)

Is it also standard to ignore an Otitis media infection in the presence of HIV? Amoxicillin is a standard treatment, but wouldn't have been effective against a virus. Eliza wasn't vaccinated, and Otitis media is known to be caused by viruses, and reported to potentially lead to meningitis, encephalitis or brain abscess. Finally, assuming HIV infection in the womb or through breastfeeding, Eliza would have long since have developed her own antibodies to p24, neutralizing the test. And why wasn't the standard HIV test performed on her body instead of relying on the p24? Its Wikipedia article states it is not useful for general diagnostics, as it has very low sensitivity and only works during a certain time period after infection before the body produces antibodies to the p24 protein. BruceSwanson (talk) 01:52, 15 April 2011 (UTC)

The autopsy report makes no mention of meningitis nor brain abscess, so I'm not sure why you bring those up. While bacterial otitis media can lead to intracranial infection, this is vanishingly rare in the post-antibiotic era. I'm not aware of any evidence that viral otitis media can lead to encephalitis, but perhaps you can enlighten me. In contrast, there is a vast literature on HIV as a cause of encephalitis, causing exactly the picture seen at Eliza Jane Scovill's autopsy.

Regarding HIV testing, you'd have to ask the L.A. County Coroner - I have no special knowledge of whether standard HIV tests were performed at autopsy. The statement on p24 antigen you mention is unsourced - certainly serum p24 antigen isn't used diagnostically, but it remains a widely accepted means of demonstrating HIV encephalitis, as supported by the literature I cited above. "Low sensitivity" means that the test is prone to missing infections (false negatives). Since the test was positive in Eliza Jane Scovill's case, its sensitivity has no bearing. MastCell ^Talk 04:44, 15 April 2011 (UTC)

Above I should have written Is it also standard to ignore an Otitis media infection in the presence of p24?, regarding which, see this. Remember that no conventional HIV test is mentioned in EJ's autopsy report, and we don't really know for sure that her mother even had HIV. The report makes no mention of meningitis nor brain abscess, but it does mention multinucleated giant cells. It does mention that she died of pneumonia (like her mother eventually did), of which this source has something pertinent to say. EJ had otitis media. She was unvaccinated. I certainly don't know if viral otitis media could lead to encephalitis -- this source doesn't specify as it lists facial nerve paralysis, meningitis, encephalitis or brain abscess as complications. But come on. Unvaccinated children died all the time from exactly that kind of preventable disease and still do.

I'm sure there is indeed a vast literature on HIV as a cause of encephalitis, all of it predicated on the apparently unfalsifiable (using the word in its philisophical sense) assumption that HIV causes AIDS.

That's a good debating point: under what conditions could the HIV=AIDS hypothesis be falsified? BruceSwanson (talk) 22:21, 19 April 2011 (UTC)

It might be helpful to run some of your reading past someone with some topical expertise, to help you filter it. The p24 information you linked describes serum p24 antigen testing, which is performed on serum samples using ELISA. The autopsy studies were performed on formalin-fixed tissue blocks, using immunohistochemistry. These are two very different methods, and it's an error to cite information about p24 ELISA when you're discussing p24 IHC, because the former has little or no bearing on the latter.

Unvaccinated children do sometimes die of specific vaccine-preventable illnesses such as measles or pertussis. There is no evidence at autopsy that any vaccine-preventable disease was present in the case in question, nor do the pathological findings support such a diagnosis. Instead, there was evidence of failure to thrive, suggesting a chronic illness, as well as severe thymic atrophy, which is a hallmark of late HIV infection (see [1]). There was evidence of Pneumocystis pneumonia, which is basically unheard-of in an 3-year-old child, vaccinated or not, except in the setting of advanced AIDS. There were large herpetic lip lesions, which while certainly not specific for HIV/AIDS, are consistent with advanced immunodeficiency. And, of course, HIV p24 antigen was demonstrated in the brain by immunohistochemistry.

If one is willing to completely discard Occam's razor and basic principles of reasoning, it may be theoretically possible to construct a series of outlandish alternative explanations for each of those findings. But such an unprecedented chain of coincidences is certainly implausible compared to the clear, consistent picture of advanced, untreated AIDS.

Falsifiability is an interesting angle. What criteria would falsify Duesberg's claims, in your mind? It seems that his claims remain unfalsifiable to an ever-shrinking but rather persistent group of people. But I digress. The hallmark of a good scientific hypothesis is that it makes testable predictions about objective reality. The HIV/AIDS model does this admirably. It predicts which hemophiliacs will go on to develop immunodeficiency and opportunistic infections (Duesberg's favored variables, like number of transfusions, have no predictive value in this regard). Even if one looks at Duesberg's favored risk groups (gay men, multiple sex partners, recreational drug use, etc), only the HIV/AIDS model accurately predicts which will show declining T-cell counts and ultimately opportunistic infections. The HIV/AIDS model predicts the risk of perinatal transmission and of iatrogenic infection, the latter of which has unfortunately been confirmed by various laboratory and clinical blood exposures.

Most impressively, the predictions of the HIV/AIDS model have led to tangible benefits. The blood supply has been rendered safe once again by HIV testing, fulfilling the predictions of the HIV/AIDS model. And HIV-specific therapies - namely, HAART - have led to dramatic improvements in health and life expectancy for HIV-positive people, which is the strongest confirmation of the HIV/AIDS model and the one that led the more intellectually honest "rethinkers", like Robert Root-Bernstein and Joseph Sonnabend, to see the light. This paper might be instructive; in it, a former "dissident" describes how the success of HAART converted him.

In the end, the HIV/AIDS model performs pretty impressively in terms of generating testable predictions which have been verified. That's pretty much what you want from a hypothesis. In contrast, the predictions of Duesberg's risk/AIDS hypothesis have proven incorrect at basically every turn. I suppose one could replace the HIV/AIDS model, but you'd have to come up with a model which better fits and predicts objective reality. I don't see a model like that on the horizon, and certainly the risk/AIDS model doesn't come close. MastCell ^Talk 23:32, 19 April 2011 (UTC)

Has the HIV/AIDS model made the testable prediction of when Magic Johnson's and Greg Louganis's T-cells will begin to fall? BruceSwanson (talk) 06:29, 27 April 2011 (UTC)

Magic Johnson and Greg Louganis

Wow. OK. Where to start?

• Are you seriously contesting a mountain of medical and epidemiological research with 2 anecdotes? Yes, of course you are, so let's move on.
• The HIV/AIDS model includes long-term non-progressors.
• Many valid pathogen/disease models don't predict 100% progression from infection to disease. These include tuberculosis and cholera (to use Kochian diseases) as well as hepatitis C.

  The HIV/AIDS model makes predictions about the proportion of HIV-infected individuals who will develop AIDS, and the timepoints at which they will do so, but those predictions are in aggregate and not designed to address individual cases. The "metastatic colon cancer" model predicts a median survival of about 2 years from diagnosis; if I show you one individual alive 5 years from diagnosis, does that invalidate the scientific understanding of colon cancer?

• You are, of course, aware that both Johnson and Louganis receive modern anti-retroviral therapy, almost certainly including an NRTI like AZT, and have for many years? So that their continued well-being is in fact a confirmation of the HIV/AIDS model, and a moving testament to the way in which the HIV/AIDS model has translated into concrete, lifesaving medical advances?
• Come to think of it, your "model", where antiretroviral drugs are dangerous and unnecessary toxins, would predict that Johnson and Louganis should fare poorly, and perhaps even develop opportunistic infections, as a result of their long-term treatment with HAART. So their current health status further undercuts the pernicious nonsense you've been putting forth about antiretroviral toxicity.
• It's really pretty shameless to use Johnson and Louganis, both of whom have done much to raise awareness of HIV/AIDS, to push an AIDS-denialist agenda.

But there you have it. MastCell ^Talk 19:26, 27 April 2011 (UTC)

Do Johnson and Louganis have the buffalo humps, sunken cheeks, and premature aging [that link may take a minute to load] typical of long-term consumers of HAART medication? Or are long-term non-progressors as immune from those as they are from HIV?

You said something about Occam's razor. BruceSwanson (talk) 21:22, 27 April 2011 (UTC)

Think rationally about the implications of your argument. The prevalence of lipodystrophy with HAART has been variously reported, but is probably no higher than 50% (e.g. PMID 11216932; for buffalo hump, it's about 6%). So then: if you look at two individuals on HAART (say, Johnson and Louganis), what are the odds that neither has lipodystrophy? (Answer to follow.) To put it another way: if you flip a coin twice and get heads both times, does that mean you have a two-headed nickel?

Moreover, I'm not even sure what you're arguing at this point. Are you implying that Johnson and Louganis aren't actually on HAART, despite reliable public reports to the contrary? Or... what? Even steeped as I've become in bizarro AIDS-denialist conspiracism, I'm having trouble following your logic in the last post. MastCell ^Talk 21:45, 27 April 2011 (UTC)

I take it you are saying that they indeed don't suffer from lipodystrophy. I didn't think they did, from their pictures and the apparent lack of Web chatter on the subject.

If you had been flipping a coin daily since 1997 and coming up heads every time, I would definitely think you had a double-headed coin. Are you arguing that the chances of lipodystrophy from HAART don't increase over time? The study you linked above states lipodystrophy was associated with older age (per year) and having ever used protease inhibitors.

I am indeed arguing that Johnson and Louganis are not on HAART, "reliable public reports" to the contrary. That's the simplest explanation. Johnson admitted in 1995 that he had quit AZT early on because it made him too ill. Such people don't have AIDS because they don't use Poppers and other recreational drugs. And it's not because being athletes they have super immune-systems. Rather, being athletes, they would have been unlikely to have taken up the drug lifestyle in the first place.

And don't forget the premature aging problem. (You may grow old waiting for it to load.) Looking at their pictures again, I see no signs of it. Do you? BruceSwanson (talk) 23:31, 27 April 2011 (UTC)

I have no idea whether Johnson and Louganis suffer from lipodystrophy, and I wouldn't confirm or reject such a diagnosis based on a Google Images search, for that matter. If you have better numbers for lipodystrophy prevalence, please share your source and enlighten me, but my reading of the literature suggests it's ~50% based on patient reporting, and substantially lower if more rigorous objective criteria are applied. You may be confusing prevalence with incidence, a common error suggested by your take on the coin-flipping analogy. In the study I linked, the likelihood of lipodystrophy increased with duration of stavudine use, but apparently not with duration of protease-inhibitor use. There may be other data out there; I'm open to hearing them.

I don't understand why you think Johnson and Louganis are putting it about that they take antiretrovirals while secretly not taking them. Are they part of teh HIV conspiracy? In bed with Big Pharma? It's not at all a "simple" explanation that they're systematically lying to the public - it's a much simpler explanation that they are taking HAART, and are among the 94% of HAART patients who don't develop buffalo humps.

I admire your propensity to toss out dubious assertions as if they were self-evident. For instance, you assert that professional athletes in the 1980s were particularly unlikely to use recreational drugs, which I find somewhat naive, to put it mildly. Certainly I'd need to see some substantiation of that assertion before I accepted your word, since athletic memoirs of the era paint a somewhat different picture.

As to premature aging, the piece you cite seems to discuss aging mostly in terms of non-visible items like increased risk of atherosclerotic cardiovascular disease, diabetes, bone fracture risk, etc. I'm not sure you can diagnose that sort of aging reliably by looking at online photos, but that's me. MastCell ^Talk 23:56, 27 April 2011 (UTC)

A birth date in the caption should clear up any confusion.

Johnson is indeed in bed with big pharma, or was. I wonder if GSK had an escape clause in the event that Johnson developed lipodystrophy. Or these. Louganis apparently doesn't suffer from them either. But perhaps my confusion of prevalence with incidence applies here as well. I don't even believe that manifestation of such effects would escape notice on the web. But that's me. BruceSwanson (talk) 02:28, 29 April 2011 (UTC)

Johnson is quite the business man. Gave up all those lucrative sponsorships from sports gear manufacturers, publicly claimed to have an incredibly stigmatizing disease that was believed at the time to be solely found in homosexuals, all so twelve years later he could swoop in and take advantage of those sweet, sweet Big Pharma dollars once they managed to fake enough deaths and research to create both a perceived need for, and appearance of effective treatments. I should talk to him about my retirement plan because he is one cunning mofo. To speculate that far in advance that an incredibly stigmatizing disease would turn out to be more lucrative than the notoriously profitable sporting goods endorsement deals - wow. Just wow. Though, of course, this is certainly more clear evidence of just how long-term the planning, and how deep the conspiracy behind AIDS runs - I mean, they somehow managed to convince Johnson to give up sports just with the promise that they would be able to maintain their foolproof, air-tight web of lies for twelve years and manufacture millions of research articles on a totally fake subject, all without a single person spilling the beans. Man, I wonder how their profit margins are doing when you account for all that hush-money paid to the millions of dishonest researchers (and former NBA players who must be guaranteed, for decades, earnings greater than anything they would make shilling for Big Shoe). Tsk, what line does that show up on in the annual financial statement!

By the way, John Holmes died of AIDS, if I can find at least two more famous people who died of AIDS, does that mean it's real and not a conspiracy theory? Or do they have to be athletes to count? Just wondering what sort of anecdotes count as proof. WLU (t) (c) Wikipedia's rules:^simple/_complex 03:22, 29 April 2011 (UTC)

Apropos of Johnson being a spokesman for GSK, here's a direct quote from Serious Adverse Effects by Celia Farber (2006), posted online. A longer excerpt is here. Correct me if I'm wrong, but I think Michael Weathers, Magic Johnson, and Greg Louganis are still around. Arthur Ashe, however, is not. After two heart surgeries and attendant blood-transfusions, his doctors gave him AZT, which, with deep misgivings, he took. Go here and do a search for Arthur Ashe. It starts on p. 356. BruceSwanson (talk) 21:03, 29 April 2011 (UTC)

So...he was in late-stage AIDS, suffering from multiple health problems and underwent major surgery, got AZT monotherapy, and died? Astonishing. When was he diagnosed with AIDS, 1988 after getting HIV in 1983? And Johnson was diagnosed in 1991, with an HIV-negative wife and daughter suggesting he had caught it only a short time before? That also doesn't really address the whole apparent motive for Magic Johnson to abandon a lucrative sports career with attendant multi-million dollar endorsement deals, and adopt a new identity as the celebrity face of an incredibly stigmatizing disease at a time when the most effective treatment was not very good. You kinda dodged that with your reference to two conspiracy theorists. Even for anecdotes, that's pretty poor. Here's an anecdote, Christine Maggoire died at 52 after not receiving adequate treatment for AIDS. What's the average life expectancy of a middle-class woman from California? No, keep it up though, you're doing great here. Will your next move be goalpost relocation, unrelated tangent, or jump to another AIDS denialist talking point? WLU (t) (c) Wikipedia's rules:^simple/_complex 23:05, 29 April 2011 (UTC)

The observation that Johnson and Louganis appear not to suffer from any of these is definitely anecdotal evidence for my hypothesis that they are not taking "antiretroviral" drugs. Want to try for an explanation of that observation? Feel free to offer your own anecdotal evidence. BruceSwanson (talk) 00:22, 30 April 2011 (UTC)

Ah, you went with ill-thought-out tangent. A solid choice.

Have you had the chance to ask them about their abdominal pain? Have you noted that Magic Johnson shaves is head and isn't particularly hirsute? Would blood loss be something you could note visually? How about muscle pain and weakness for these Olympic-level athletes? Not to mention most people don't tape their bowel movements, vomiting, or broadcast that they have gas or ingrown nails. Dizziness isn't a visible symptom either, nor is headache, hepatitis, high blood cholesterol, insomnia, mental confusion, mood swings, nausea, low white blood count, nightmares, oral ulcers, inflammation of the pancreas, parasthesia, neuropathy, drowsiness, changes to taste perception, or dry mouth. Dry skin and the few visible changes to skin tone are less visible in African Americans and possibly half-Samoans. Of all those symptoms, perhaps a half-dozen (gynecomastia, hyperpigmentation, abnormal fat deposition, rash and dry skin depending on its location) might be visible to someone intimately familiar with the person, or in constant contact. Those few visible adverse effects can be covered up by makeup, clothes, or simply waiting for them to heal. Or, Mr. Johnson might already have man-boobs. Not to mention these particular athletes might be chosen for public relations work because they appear to be in such good health. Most of those adverse effects are symptoms, and many that are not are signs that require lab work to complete. Plus, medications and dosing regimens are explicitly adjusted in order to maximize benefit while minimizing adverse effects. One of the reasons HIV is now more of an inconvenience in wealthy countries, rather than a death sentence, is because medications like AZT are far better at interfering with viral replication than bodily function.

I prefer analysis over anecdote, it plays to my strengths. In my analysis, Johnson and Louganis probably don't show signs of antiretroviral adverse effects because they are well-managed public figures who probably pay top-dollar to get the best medical care available, and were infected just as AIDS became treatable just after they finished careers that required bodies in peak physical fitness. I would guess that they gave up those careers because of HIV infection, not some sort of stupid idea that Big Pharma tricked them into losing all their endorsements in some sort of long-con conspiracy theory involving millions of researchers in nearly every country in the world. Big Pharma is rich, but as I said above, it wouldn't make sense to spend billions of dollars bribing researchers (and wealthy sports figures) in order to develop fake medications that they give away at cost or below in third-world countries. You cited Occam's razor above, do you not see how with every argument you're only adding more and more improbable explanations to an already wildly conjectural thesis? WLU (t) (c) Wikipedia's rules:^simple/_complex 01:47, 30 April 2011 (UTC)

Again, you have to understand that at least 50% of people on HAART do not develop lipodystrophy. That's not anecdote - that's data. One might fail to appreciate that fact if one's sole source of information about antiretrovirals is AIDS-denialist literature. It is likely that Johnson is simply in the fortunate 50% who don't develop lipodystrophy. It's far less likely that Johnson is part of a far-reaching, multilayered conspiracy to deceive the public into taking dangerously ineffective medication (which would have to exponentially dwarf literally every known conspiracy in human history in terms of scale - it wouldn't even fit on Glenn Beck's blackboard). The likelihood of the former is 50%. The likelihood of the latter is, well, substantially lower.

You probably won't get anywhere citing Duesberg's or Farber's book to any scientifically literate person, since both are filled with factual errors, misstatements, and convenient omissions. As On A Leash (talk · contribs) noted above, the reader might well conclude that Duesberg simply makes up the basis for many of claims on AZT, while Farber's book evinces a lack of very basic knowledge that one might acquire in an early college-level microbiology course. Given their track record with basic, verifiable facts, I'm not personally willing to extend their books any credibility on Ashe et al. Let's stick with the reputable literature if we're going to have a serious discussion. MastCell ^Talk 16:14, 30 April 2011 (UTC)

Not to mention when AIDS advocacy organizations or Big Pharma pick their spokespeople, they either pick the ones who are doing well (if they're trying to sell hope) or really, really badly (if they're trying to raise money). Magic Johnson in particular was selected, out of the millions taking anti-AIDS medications, because he is famous and (more importantly) he looks healthy. This is why you don't use anecdote to support science - you can pick from all available choices the one that best supports your argument. That is why scientist are very, very careful to try to select well-matched control groups for interventions, and why pseudoscientists either don't bother with a control group, or select it in such a way that their results are inevitably favoured. It's easy to do sciency-looking stuff when you ignore the inconvenient. It's hard to do actual science because much of your time is spent very carefully making sure you're listening to, rather than dictating the data. Along with an unwillingness to change their minds in the face of contrary evidence, selecting what data to report is one of the hallmarks of a pseudoscientist. WLU (t) (c) Wikipedia's rules:^simple/_complex 16:46, 30 April 2011 (UTC)

MastCell, you wrote Farber's book evinces a lack of very basic knowledge that one might acquire in an early college-level microbiology course. Do you mean something on the order of this? I'm referring of course to my own ignorant question, not WLU's trenchant reply. However, I am having a problem with his Hirsute Hypothesis. BruceSwanson (talk) 17:57, 30 April 2011 (UTC)

So, your initial hypothesis is that Greg Louganis and Magic Johnson are not on HAART because they don't show signs of adverse effects, like hair loss. But both of them have very little body hair in the pictures linked here. Thus suggesting they are on HAART. So I'm not sure how you are making any case except "Greg Louganis and Magic Johnson lack body hair, a side effect of antiretroviral medications, suggesting they may be on HAART because they have AIDS". Are you now going to change your mind? Or admit that your arguments are baseless? Or just change the subject? I notice that in cases where it's quite obvious that you are wrong, you simply ignore this inconvenient fact. There is no harm admitting you are wrong and changing your mind - that shows maturity and the ability to learn from mistakes. Continuing to defend the same flawed claims puts you in the same group as creationists, flat-earthers, birthers, and yes, AIDS denialists. Most are merely curiosities and misfirings of the human intellect but the latter can kill people. WLU (t) (c) Wikipedia's rules:^simple/_complex 19:54, 30 April 2011 (UTC)

So Louganis is covered by the Hairpiece Hypothesis? BruceSwanson (talk) 22:39, 30 April 2011 (UTC)

Alopecia is hair loss in the head or body. Note the hairless chest in the pictures. Not to mention both might have any of the couple dozen symptoms that are not visible in the body, and you're still ignoring the many other reasons I cited above why neither may show evidence of being on HAART. You have seized on a single, flawed argument as if it invalidated all of them, rather than admitting you might simply be wrong. I can understand why you would not want to do so - humans are subject to cognitive dissonance and hate having to admit they were wrong, and will go through the most transparently illogical convulsions in the process. Ask any cult member who was told the Rapture was coming - then it doesn't happen. Most will double down rather than accept the fact that the were wrong about an incredibly obvious fact. You can double-down, fall deeper into the rabbit hole, or you can think that perhaps Peter Duesberg might be misguided. WLU (t) (c) Wikipedia's rules:^simple/_complex 22:52, 30 April 2011 (UTC)

So do you think Louganis is wearing a hairpiece or not? BruceSwanson (talk) 00:30, 1 May 2011 (UTC)

I don't really care since alopecia is only one of many potential side effects and there's no way of confirming any short of him disclosing it making the whole discussion pointless and your last point little more than a continued failure to address any of the substance of my points. Looks like this time you've chosen irrelevant tangent. Also - note the arrangement of your argument. If Johnson and Louganis look sick, then the ineffective medication is making them sick. If they look healthy, then they're not taking it because it's a conspiracy. I'm curious, what would it take for you to even consider the fact that HIV is a deadly virus and AZT along with other retrovirals are an effective treatment with side effects? WLU (t) (c) Wikipedia's rules:^simple/_complex 02:22, 1 May 2011 (UTC)

I will accept HIV as a deadly virus when AIDS-defining diseases are retroactively shown to have behaved epidemiologically like other viral diseases proven to be infectious by Koch's Postulates, instead of staying at all appearances for 30 years rigorously within their original risk groups: fast-track gay males; heavy drug-users in general; drug-addicted mothers and their infant children; hemophiliacs (before highly purified Factor VIII); consumers of "antiretroviral" drugs; and chronically malnourished populations living in unsanitary conditions. Want to start with why severe hemophiliacs never manifested a higher propensity for Kaposi's Sarcoma; and why heavy Popper-users (fast-track gay males again, who reportedly inhale the drug to relax their anal sphincter-muscles) show a definite propensity for pulmonary Kaposi's, a manifestation according to Duesberg never seen by Kaposi (d. 1902) himself?

As far as AZT et al. being effective treatment with side effects -- as well ask when their side effects will be seen as effective against something -- anything -- else. BruceSwanson (talk) 06:37, 1 May 2011 (UTC)

Ah, you went with spherical chicken in a vacuum. That's where you approach a real-world problem as if it were an idealized, and much simplified problem that can be dealt with using solely abstract principles. It's absurd to expect all groups to react the same way. AIDS is a syndrome, HIV undercuts the immune system and also comes in a variety of flavours - not to mention each group is exposed to different risk factors. Poppers may indeed increase the risk factor for certain syndromes, but that doesn't make it causative - correlation doesn't mean causation. The number of churches increases with the rates of crime in a city. Do churches cause crime? No. Both increase with larger populations. HIV infection and popper use are both associated with risky homosexual intercourse. Poppers don't cause HIV infection or AIDS. The immune system is destroyed by HIV infection. The chances of developing HIV-associated diseases is due to the diseases exposed to and other risk factors. But without HIV infection, the other diseases are rare, or not deadly. Kaposi's sarcoma was the canary in the coal mine for HIV infection because it is normally rare, and required very specific treatments whose requests were tracked by the CDC.

Anyway, theories describe reality. If your theory does not accurately reflect reality, that means there is something wrong with your theory because reality is what it is. As for your final comment - side effects is merely a term for medication effects we don't want. One man's side effect is another man's main effect. Does aspirin treat pain with a side effect of reduced clotting, or does aspirin reduce clotting with a side effect of unwanted analgesia? Depends on what you want. WLU (t) (c) Wikipedia's rules:^simple/_complex 13:26, 1 May 2011 (UTC)

Any real-name editors care to comment? BruceSwanson (talk) 01:27, 2 May 2011 (UTC)

Shouldn't you term it "any editors able to criticize WLU's points care to comment?" It's not like I'm basing any of my arguments on my own personal authority or experience. It's not like I'm saying "I'm an expert on HIV/AIDS, believe me". I'm using basic logic to point out the holes in your arguments. Why does my name matter? If I used my actual name, why would that make my points any better? Yours seem to consistently fail despite you apparently using your real name - and after all we have no idea if you are really named "Bruce Swanson". You could be a hermaphrodite midget named Leslie, editing from a sterile bubble in Brazil and it wouldn't make your arguments any better or worse because HIV causes AIDS and AIDS is deadly for most people who are infected. It's possible I'm wrong, why don't you try refuting my points through logic or research? You may have to go beyond the works of Peter Duesberg though, and that may in turn require you to reconsider whether HIV causes AIDS. If you're basing your beliefs on rational principles, they should be open to change. If you're not, then just admit your beliefs about AIDS are based on prejudice, irrationality or some other idea that is not open to change - and stay away from any page related to HIV/AIDS. WLU (t) (c) Wikipedia's rules:^simple/_complex 10:59, 2 May 2011 (UTC)

Any editors able to criticize WLU's points care to comment? MastCell? BruceSwanson (talk) 15:47, 2 May 2011 (UTC)

Two points. First, you have no idea who MastCell is, does this mean you have given up your "only named editors are reliable" stance? Second, isn't it more important that you either accept my conclusions or refute them? Because if you do neither and merely stick to your previous argument, you've essentially admitted that you are unable to come up with a substantive reply but are also unwilling to change your mind. You would have just demonstrated the belief that AIDS denialists are motivated by something other than rationality, putting you in the same camp as Birthers, "controlled demolitions" theorists, creationists, flat-earthers, perpetual motion proponents and faked moon landing zealots. If you are admitting this, then you can realize the implications of these associations, or dive deeper down the rabbit hole. Again, there is no harm in changing your mind, but to continue to argue a point long after it is refuted, irrespective the evidence, is both foolish and dangerous for yourself and society. WLU (t) (c) Wikipedia's rules:^simple/_complex 16:19, 2 May 2011 (UTC)

Adrian J. Hunter comments

Real-name editors commented long ago. Real-name editors no longer care to comment, as they know nothing they could ever say could possibly influence your views. Adrian J. Hunter^{(talk•contribs)} 16:35, 2 May 2011 (UTC)

So they see no reason to question whether Johnson and Louganis are on HAART? BruceSwanson (talk) 17:08, 2 May 2011 (UTC)