HIV/AIDS Skepticism

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

Living with HIV; Dying from What?

Posted by Henry Bauer on 2008/12/10

Recent comments by “Köpek Burun” (= “dog nose”?? “snout”? Menganito?!),  about “Poison in South Africa” [26 October 2008]  inevitably referred back to “HAART saves lives — but doesn’t prolong them!?” [17 September 2008]. In my response, I referred to calculations that I’ve been working on, of the age distributions of PWAs (“People living With AIDS”), and the age distribution of death rates. Since it’s so pertinent to that discussion, I need to post the calculations even though my full analysis isn’t finished yet.

Age distributions of PWAs can be calculated from the data in Table 2 of “HAART saves lives”.  The (average) number of PWAs during a given year results from adding new diagnoses in that year to survivors at the end of the previous year. Those survivors can be calculated from the total number of diagnoses minus deaths up to and including that year.  For calculating total numbers of PWAs for each year, that is straightforward, and the results were given in Table 3 of “HAART saves lives”.   However, for the age distribution of PWAs in each year, one must take into account that survivors from a given year will be a year older, on average, in the following year. For example, some of the survivors from the age range 20-29 in 1990 will be in the range 30-39 in 1991. I made the assumption of symmetrical distribution within each age range — in other words, represented the data by histograms defined by the age ranges in which the data were reported. A number of trial calculations using more elaborate curve fitting showed that this did not make a significant difference to the results, presumably because the chief variable of interest is the median age and most of the cases fall in the middle age ranges (where the cases-vs.-age curves are steepest, there numbers of cases are so much smaller than in the middle age ranges that small errors there hardly affect the calculation of median age).

Another complication is that the age ranges for which deaths and diagnoses, respectively, are reported were not the same in the years 1993-98. For those years, the age ranges for the deaths were converted to those for the diagnoses, again using a histogram model; that this did not introduce drastic errors was verified by the fact that the re-calculated median ages remained within 1% of the initial ones.
The reason for dual death reports for 1998, for comparison with earlier and later years, was given in the notes to Table 2 in “HAART saves lives”.  For purposes of comparison over the whole period 1982 to 2004, the most appropriate values for 1998 are presumably the average of those dual numbers, namely, 39.4 for median age of PWAs, 41.2 for median age of deaths, 1.8 for the interval between them, and 4.5% for the death rate. All of those fall smoothly into the progressions from 1982 to 2004.

Table I

pwaagedistributions1

I had begun this work to probe the effect of HAART, but I realized eventually that these death statistics speak directly to the issue of whether HIV causes AIDS, well beyond merely demonstrating that HAART doesn’t extend life. From 1982 to 2004, the death rate (last column in the Table) declined from 65% to 2.8%; yet the difference between the median age of the population of PWAs and their median age of death increased only from about 7 months (0.6 years)  to about 22 months (1.8 years). That’s a stark contradiction. The median age of death in any population is the average life-span. If the median age of the existing population is within a couple of years of the life span, then the death rate must be enormous; but here the mortality in recent years is small while the life span is a mere 22 months greater than the median age of the population.

The contradiction means that the basis for classifying as “PWA” is not the same as what determines death; those who are dying are in some manner atypical within the PWA population. What typifies PWAs, though, is being HIV-positive. Therefore something other than being HIV-positive distinguishes those who are dying from those who are not dying.

At least for the most recent decade, HAART seems the obvious “missing link”. Let’s assume that those few percent of PWAs who are dying have not been getting HAART. Then PWAs who survive, who are benefiting from HAART, would be getting older, and the median age of the PWA population would be steadily increasing IN CONTRAST to the median age of those dying, which would continue to be that typical for untreated PWAs. The data show no such thing. During the HAART era, the median ages of death and of PWAs drift upwards in tandem, with no discernible change in the magnitude of the difference, 1.7-1.9 years. Most striking, the median age of surviving PWAs remains below, not above, the median age of death.
In any case, the same contradiction between median-age differences and mortality rates applies in the years 1982 to 1996. The only resolution for this conundrum is to recognize that what determines PWA status — namely, being HIV-positive — isn’t what determines death among PWAs. In other words, HIV doesn’t cause death.

*******************************

There’s another, independent, aspect of “HIV disease” deaths that speaks against HIV as a cause of death. Several times [for example, “How ‘AIDS Deaths’ and ‘HIV Infections’ vary with age — and WHY”, 15 September 2008]  I’ve remarked on the peculiarity that the death rate for “HIV disease” is at a maximum roughly at ages 35-45, something like the prime years of adulthood.

All other diseases show the very opposite, death rates at their lowest among young-to-middle-aged adults and high among very young children and increasing progressively at ages beyond middle age. For instance, in “’HIV Disease’ is not an illness” [19 March 2008], Table B shows all-cause mortality lowest among young teens and increasing with age (very roughly, doubling in each higher decade); Table C  shows a similar variation for cerebrovascular diseases; the “Health, United States” (HUS) reports from the National Center for Health Statistics display this type of variation with age for every type of illness. For influenza, here’s a graphical representation:

Figure I
from a poster presentation, “Death and Aging in the Time of Influenza: United States, 1960-2002” by Nobuko Mizoguchi, MPH/MPP  Department of Demography, University of California at Berkeley]
http://www.popassoc.org/files/public/MizoguchiPoster.pdf
flumortality

“HIV disease” is entirely different, see for instance Figures 2a,b in “No HIV ‘latent period’: dotting i’s and crossing t’s” [21 September 2008] , or any of the tables for deaths from HIV disease in HUS reports, e.g. reproduced as Table D in “’HIV Disease’ is not an illness”, 19 March 2008 ; see also Table 2 in “HAART saves lives — but doesn’t prolong them!?”, 17 September 2008. “AIDS” deaths, be it in absolute numbers or in rates, are at a maximum around age 40 ± 5.

In my view, this alone already gives the lie to claims that HIV is fatally pathogenic. No matter what the origin may be of an attack on the living human organism, the tendency to succumb and die increases steadily with age. What could it be about “HIV” to allow older people to resist its ravages better than people in their prime middle years?

The data can’t be explained away speculatively as something about ages at which people most likely get “infected”, because EVERY age distribution having to do with HIV or with AIDS peaks in those same years: positive HIV tests, new AIDS diagnoses, deaths from “HIV disease”, median age of all PWAs (see Table I above). Age distributions for deaths and for positive HIV tests superpose, as illustrated graphically in “How ‘AIDS Deaths’ and ‘HIV Infections’ Vary with Age — and WHY”, 15 September 2008 , and in “No HIV ‘latent period’: dotting i’s and crossing t’s”, 21 September 2008 .

Yet another way to illustrate this is to calculate age-specific PWA-specific death rates, see Table II below. The usual way of reporting death rates (as in the HUS reports) is per 1000 or 100,000 for the population as a whole in the given age-group. But one might try to gain further insight into why HIV is so peculiar by looking at what proportion of PWAs in each age group die each year (deaths in that year in that age range divided by the number of PWAs in that age range in the same year). I haven’t yet done the calculation for every year, because the salient overall conclusion seems obvious enough:

Table II

pawdeathratesagespecific

These numbers are much more sensitive than the median ages are, to the various assumptions made in calculating age distributions of PWAs, so the variations are less smooth and only clear major differences should be regarded as reliable. The crucial point is quite clear, though: how little variation there is between the death rates in the various age ranges in any given year. In 1999, for example, about the same proportion of PWAs aged 35-44 died as among those aged ≥65 or among those of intermediate age. In the years 2002-2004, a smaller proportion those PWAs aged ≥55 died than of those younger PWAs aged 35-54.

This makes no sense, if PWA, “living with AIDS”, means suffering from a fatal illness that is only temporarily staved off by continual antiretroviral treatment. Older people should succumb more readily than younger people.

The only death statistics that show maximum rates among younger adults are accidents, homicide, suicide: what one might call lifestyle hazards, not biological health challenges. That accords with the hypothesis — for which there is much supporting evidence — that AIDS in the early 1980s was an epiphenomenon of the fast-lane lifestyle practiced by small groups of gay men; look back at Tony Lance’s essay on intestinal dysbiosis.

I offer another speculation as to a possible cause of death that would not discriminate much by age. A highly toxic chemical poison that’s likely to kill within a few years would probably kill old and young people at comparable rates. AZT and other antiretroviral drugs would fit that bill.

But I don’t want to conclude on so speculative a note. The fact that deaths from HIV or AIDS are maximum at ages 35-45 shows that those deaths are not the result of an infectious disease, or for that matter of any natural illness. The fact that the median age of the PWA population has been steadily lower (within about two years) than the median age of death among those people, while the mortality has declined enormously over two decades, proves that whatever caused the deaths is not what defines the category “PWA” — i.e., HIV doesn’t cause death, HIV doesn’t cause AIDS. A fortiori, the data show that HAART doesn’t extend life: the interval between median age of the PWA population of deaths among them has held steady at 1.7-1.9 years throughout the HAART era, and surviving PWAs are not living longer than those who die.

The only explanation that satisfies all the data is that testing HIV-positive is an artefact as regards illness or death. Testing HIV-positive is just a marker of some sort of physiological response to a variety of challenges.

60 Responses to “Living with HIV; Dying from What?”

  1. Michael said

    The most laughable quotation from the remarks of Kopek Burun/snout/Menganito, were:

    “It is clear, then, that something happened around 1996-7 to significantly improve the survival of people with AIDS. Whether this was attributable to the introduction of HAART or not, I cannot say on these figures alone, but they are at least consistent with that hypothesis”.

    Yes, indeed something quite major happened, Mr. Kopek. And simply looking at the facts clearly shows us exactly what had happened:

    The years of highest death, from 1987 to 1995, are the EXACT YEARS of high dosage AZT monotherapy given to every person who was diagnosed as HIV positive. Those who took AZT lived an average of 8 months to 1-1/2 years.

    Comparing the results of the years of high dosage AZT monotherapy to the results of the years of HAART drugs, and using the results to make the claim that HAART drugs are “life extending” or “life saving”, is an identical comparison to that of comparing executing victims with a quick bullet to the head from which the victims died quickly, versus executing the victims by multiple stab wounds from which the victim still expired, but more slowly, and then claiming that multiple stab wounds are “life extending”.

    It is simply mind boggling to anyone other than a psychologist studying psychopathic behaviors that those who promote HAART drugs would ever dare to compare the years of AZT to HAART as a way of claiming that HAART drugs are somehow beneficial. Such behavior is a unique form of denialism that allows them to escape the fact that they are responsible for the deaths of HIV positives. Out of egoic denial and self protection, the promoters of AZT and HAART drugs will likely go to their own graves disowning the fact that they themselves were fully responsible and culpable for the deaths of HIV positives who took AZT, and that they are still fully responsible and fully culpable for the deaths of HIV positives who now take HAART drugs.
    Period.

  2. Great analogy, Michael! I don’t think this point can be emphasized strongly enough, namely that ALL of these epidemiological studies alleging benefits of HAART are based on the assumption that AZT monotherapy is superior to true placebo. And the only direct clinical studies we have concerning that comparison were done 20 or so years ago, and continue to be cited, despite evidence that they were improper or fraudulent.

    That’s a lot of interesting new material you’ve put up recently, Henry. I don’t have time to digest it all at the moment and comment, but I’ll try to do so in time.

    I would point out, however, that your data confirm my earlier observation that the severity of the “epidemic” peaked around the years 1984-1986, and has been declining ever since. Why people continue to look at absolute number of deaths rather than death rates is a mystery to me.

    darin

    • Henry Bauer said

      Darin:

      Lots of things about HIV/AIDS proponents are something of a mystery 8)

      Yes, the “epidemic” was dropping off in the late 1980s already, though the CDC revised its earlier reported numbers to mask that fact, pp. 220-221 in The Origin, Persistence and Failings of HIV/AIDS Theory (McFarland 2007), http://failingsofhivaidstheory.homestead.com/

  3. Macdonald said

    Whoever Burun is, he is attempting a serious critique, keeping to the actual issues. That is laudable.

    • Henry Bauer said

      Macdonald:

      Yes, it’s laudable when defenders of the HIV/AIDS faith attempt substantive critiques. All the more remarkable that they do so anonymously, isn’t it?

      I accept your implication that I was being a bit sarcastic by suggesting translations of KB’s pseudonym. I’m not particularly happy that I get more impatient, maybe bristly, as I get older, and I certainly don’t like the fact that I now automatically distrust anonymous commentators instead of, as only a year or so ago, automatically trusting them until further notice. But once bitten, twice shy. At least one started with apparently serious critiques and then slowly morphed into time-wasting nit-picking; and another turned out to be fishing for inside info about Rethinkers; and then there’s the ghost who created the Wikipedia entry that does a great job of misrepresenting my views and writings. So, I now have very little time for these HIV/AIDS dogmatists in disguise.

      However, as you see, I do post any of their comments that may have actual substance.

  4. umber said

    Why don’t they refer to the study of Ruengpung Sutthend, which really compares AZT to placebo, and which shows that AZT leads 3 times faster to AIDS :

    “CONCLUSION: Our results preliminary suggested that infected infants who were perinatally exposed to ZDV may have a more rapid early disease progression with unfavorable viral manifestations than those without exposure to antiretroviral drug.”

    I think that these guys don’t know how to read.

  5. Sadun Kal said

    It was a tough job to persuade these people to offer their critique over here instead of the “Denialism blog”. But it paid off, I guess? Should I do it more often?🙂 I’m pretty good at dealing with all their insults, so I don’t mind. They recently blocked my comments though…

    • Henry Bauer said

      Sadun Kal:

      We all need to decide these things for ourselves, and do what seems right for us. For example, decisions that seem right for a long-retired former professor whose work and reputation were fairly well fixed quite some time ago is in an entirely different situation from someone who is beginning a career.

      I’m a firm believer in learning from experience, not from others’ opinions. You may be more right about “them”, or SOME of “them”, than I am.

  6. Köpek Burun said

    I thank Professor Emeritus Bauer for his kind praise in describing my poor attempt at critique as “substantive”, despite his later implication I might be a “dogmatist”. I appreciate his concerns about pseudonymnity, but say in my defence that such identifiers almost a norm these days for casual posters such as myself on the electric interwebs, and indeed are not unknown in the world of literature, employed by the writers of poetry, novels and even memoir.

    Like Associate Professor Brown I am still digesting the results of your labours, and I look forward to his future comments. For now, though I would like to make a small correction to Mr Michael’s history of zidovudine monotherapy to treat HIV infection from 1987 until 1995.

    Mr Michael says:

    The years of highest death, from 1987 to 1995, are the EXACT YEARS of high dosage AZT monotherapy given to every person who was diagnosed as HIV positive.

    It is true that daily doses of 1000 mg and even 1500 mg were common at the beginning of that period, however such doses were unusual in clinical practice by 1993 at the latest. By the years of highest numbers of deaths, 1994 and 1995, the standard dose of zidovudine was 500 to 600 mg daily, either as monotherapy or increasingly as part of a dual combination .

    Early HAART regimens c1996-7 typically consisted of these same doses of zidovudine (500-600 mg daily) together with a second nRTI (often lamivudine) and either the nnRTI nevirapine or one or two of the early protease inhibitors saquinavir and ritonavir. In patients previously treated with zidovudine who were likely to have developed resistance this was often substituted with another nRTI such as stavudine.

    In other words, the principal change in therapy between 1993-5 and 1996-7 was not the abandonment of zidovudine or the reduction of its dose, but the addition of two other antiretrovirals to the previous standard treatment.

    Furthermore, it is not substantiated by evidence to attribute AIDS mortality to zidovudine, whether taken as monotherapy, dual, or triple therapy. While the early placebo controlled trials of monotherapy had their limitations, comparison of the available data comparing no treatment with mono- dual- and triple- therapies shows a stepwise improvement in mortality and AIDS defining illnesses, as is demonstrated by this systematic review and meta-analysis of 54 RCTs:

    http://www.bmj.com/cgi/content/full/324/7340/757

    If AIDS deaths were caused by taking one antiretroviral, why are they reduced when another is added to the first, and then further reduced when taking three or more?

    Further, as your Table II above shows, death rates among PWAs were highest in the years before the introduction of zidovudine rather than afterward. This does not appear to support the hypothesis that zidovudine was the cause of such deaths.

    • Henry Bauer said

      Köpek Burun:

      One of the difficulties in discussing these things is the number of variables about which too little is known. I think Michael’s comment would be quite appropriate, had he omitted the over-emphatic “EXACT”. I doubt that you or he or anyone else could know, with any degree of assurance, how many AIDS patients were getting how much AZT/ZDV daily in the years for which you question his assertion.

      Apart from Umber’s citation re toxicity of ZDV, there’s also the Concorde study, of course. But I doubt that anyone would seriously suggest that AZT/ZDV isn’t HIGHLY toxic, would they? Was Sigma Chemical being needlessly over-careful when they labeled their 100 mg bottles of AZT, “TOXIC: toxic by inhalation, in contact with skin and if swallowed. Target organs(s): Blood Bone marrow. If you feel unwell, seek medical advice (show the label where possible). Wear suitable protective clothing.”

      As noted in an earlier post, Walensky et al. (Journal of Infectious Diseases 2006; 194:11–9) in their claims for benefit from ARVs included none for AZT up to 1993. And it’s not as though HAART were without toxicity; I’ve cited several times the NIH Treatment Guidelines: “In the era of combination antiretroviral therapy, . . . the risk of several non-AIDS-defining conditions, including cardiovascular diseases, liver-related events, renal disease, and certain non-AIDS malignancies [97-102] is greater than the risk for AIDS”. ARVs are more toxic than HIV, in other words.

      The assertion that triple therapy is better than dual which is better than mono is, like all these claims, based on mortality data, which don’t translate into life extension, that’s what my post is about. The “elephant in the room” is the changing nature of the population of “PWAs”. Before AZT, before “HIV”, PWAs were diagnosed clinically and were already quite ill with KS, PCP, yeast — that’s why the mortality was so high in those years, mortality that was matched by an appropriate average interval of ~7 months between diagnosis and death . After PWAs began to be diagnosed on the basis of lab tests, and an increasing range of much less serious conditions were included as “AIDS-defining”, naturally enough the mortality dropped, despite the toxicity of AZT; after all, healthy people die less quickly than ill people do, when exposed to similar amounts of poison. Since 1992/93, about 2/3 of all “PWAs” have been asymptomatic individuals, and that’s why the mortality took another nose dive at that time.

  7. Köpek Burun said

    [Editorial preamble: For convenience, I have here combined 3 comments that were in my in-box at the same time. Also for convenience, I have inserted numbers at points to which I make specific responses — HHB]

    Submitted on 2008/12/11 at 1:30am

    1. M. Umber will of course be aware that short course perinatal use of zidovudine is not for the treatment of established HIV infection (what we are discussing here) but rather to prevent its transmission, something it is moderately successful at, as Sutthendt and colleagues acknowledge in the first line of their paper: “…perinatal short-course zidovudine (ZDV) chemoprophylaxis that can reduce HIV-1 vertical transmission by 51%..”.

    However, they found in this very small study that among HIV infected infants, those infants for whom this intervention was unsuccessful did worse than those infected infants in whom no attempt was made to prevent transmission. No progression to symptoms was noted among uninfected infants, including those exposed to zidovudine.

    One likely reason for the worse outcome in treated infants subsequently found to be infected compared to the untreated group later found infected is that short course ZDV at 36 weeks selected for those infants already infected prior to 36 weeks, i.e. the infected infants who did worst overall were those infected at the earliest stage.

    The significance of Sutthendt’s findings (bearing in mind the extremely small numbers) is that infants born with HIV infection despite short course perinatal zidovudine may have particularly aggressive disease, not that the “toxicity” of zidovudine causes that disease (and certainly not in the absence of HIV infection).
    [see response *1a*]

    2. No one is claiming that zidovudine or any other pharmaceutical is free of toxic effects. The question, answered in detail in the literature [see response *2*], is whether the benefits outweigh the risks in particular circumstances.

    In the case of AIDS, the benefits of HAART in reducing mortality from AIDS conditions far outweighs the risk of ARV related toxicity, even though the latter is not negligible.[see response *1b*]

    “In the era of combination antiretroviral therapy, . . . the risk of several non-AIDS-defining conditions, including cardiovascular diseases, liver-related events, renal disease, and certain non-AIDS malignancies [97-102] is greater than the risk for AIDS” does not mean that “ARVs are more toxic than HIV, in other words.”

    It means that with the reductions in AIDS events, non-AIDS events become relatively more common, whether they are complications of ART or not. The risk/benefit decision about ART cannot be made simply by comparing the relative risk of one set of causes of mortality versus another, but by comparing all mortality with and without ART. Untreated HIV is vastly more toxic than ARVs, at least once infection has significantly progressed toward AIDS.[see response *1c*]

    3. Your assertion that PWAs have reduced mortality only because the CDC definition of AIDS was changed in 1993 to include those with HIV and <200 CD4 cells but no AIDS defining illnesses applies only to that period,
    [see response *3*]
    and does not apply at all in most parts of the world: similar reductions in mortality have been noted in Australia and Western Europe where that criterion does not apply.
    Nor does the addition of other AIDS defining illnesses to the original two select a healthier population: most occur at more advanced stages of immunosuppression than is typical for the first appearance of PJP and KS.
    [see response *1d,4*]

    ————-

    Submitted on 2008/12/11 at 12:39am

    One further point to add to the last: if anything, where AIDS is defined solely by the appearance of opportunistic disease (as it is virtually everywhere except the US) the introduction of prophylaxis for PCP and toxoplasmosis and the decline in seroprevalence for HHV8 may
    [see responses *1e,5*]
    mean that AIDS is typically diagnosed at a more profound degree of immunosuppression than in the early days.

    ————–

    Submitted on 2008/12/11 at 1:30am

    I apologise for the multiple posts, Professor, as I realise this is a tiresome habit, and I promise to do my best to avoid it in the future. However I think it’s important to address your doubts about zidovudine doses in the 1990s:

    “I doubt that you or he or anyone else could know, with any degree of assurance, how many AIDS patients were getting how much AZT/ZDV daily in the years for which you question his assertion.”

    Indeed I did have personal knowledge of zidovudine doses in common clinical use in Australia from about 1991 on, and the standard monthly supply available through the Highly Specialised Drugs Program was 60 x 250 mg capsules. While there may have been occasional cases of prescriptions deviating from that 500 mg per day standard, they were rare to my knowledge.
    [see response *6*]

    The efficacy and superior tolerability
    [see response *7*]
    of the lower dose was established by 1990. (1,2) Perhaps we were ahead of the rest of the world down here in the Antipodes, but I doubt it.

    1.Volberding PA, Lagakos SW, Koch MA, et al. Zidovudine in asymptomatic human immunodeficiency virus infection: a controlled trial in persons with fewer than 500 CD4-positive cells per cubic millimeter. N Engl J Med 1990;322:941-949
    2.Fischl MA, Parker CB, Pettinelli C, et al. A randomized controlled trial of reduced daily dose of zidovudine in patients with the acquired immunodeficiency syndrome. N Engl J Med 1990;323:1009-1014
    [see response *8*]

    • Henry Bauer said

      Köpek Burun:

      I merged into one the 3 comments received here on 11 December, and inserted some markers to indicate what I’m responding to.

      Above all, though, I fear we are in danger of lapsing into what happens on so many blogs: going over the same ground again and again without any way of resolving differences of OPINION, each side “cherry picking” the literature for supporting references.

      I await your promised reaction to what I posted in specific response to your qualitative scenario that suggests lowered mortality not matched by commensurate increase in life span might be compatible with HIV/AIDS theory. The mortality among PWAs declined from 65% to 2.8% from 1982 to 2004. The difference has remained at only about 2 years or less, between the median age of death and the median age of the population of PWAs from which the deaths are drawn. I assert that this shows that the deaths and the definition of PWA are not congruent, and since the latter are defined by HIV-positive, the deaths cannot be. Note too that the conundrum persists throughout the HAART era; though, of course, if HIV doesn’t cause death (or AIDS), then antiretroviral drugs are irrelevant a priori.

      Response 1: indicates some of the places where you make unsupported assertions that are matters of opinion and to which one can only respond, “Sez who?”:
      a “…may…”
      b “…far outweighs…”
      c “…vastly more toxic than…”
      d “… most … than… PJP and KS…”
      e “… may … “

      Response 2: I’m sorry to see this standard “answered in detail in the literature”; quite useless without specific citations. As Darin Brown remarked, there is copious literature on both sides of this issue, and observers, onlookers, bystanders should read up in it for themselves and reach their own conclusions. They should not neglect John Lauritsen, “Poison by Prescription”, or two books that describe how AZT came to be adopted in the first place: Bruce Nussbaum, “Good Intentions” and Stephen Epstein, “Impure science”.

      Response 3: The re-definition of 1992/93 applies to every year from 1993 on. Whether or not it applies only in the USA is beside the point, since all the data I present are from and about the USA; but if HIV doesn’t cause AIDS in the USA, presumably it doesn’t cause it anywhere else either.

      Response 4: Look at the list of “AIDS defining” diseases in Table 12 of the CDC Surveillance report for 1997 (the last year such a breakdown was published). Where is your source for the information that these represent such advanced stages of immunosuppression?

      Response 5: “where AIDS is defined solely by the appearance of opportunistic disease (as it is virtually everywhere except the US)” is an extraordinary assertion. What about the Bangui definition for Africa? Where outside Africa is “HIV-positive” not a criterion, “solely” opportunistic infections? In Australia, why was Parenzee prescribed antiretroviral drugs?

      Response 6: Here, you see, is one of the problems with attempted anonymity. Why should anyone accept your assertion that you “have personal knowledge” of so technical a matter? That your knowledge of matters in the whole country is so extensive that “rare to my knowledge” should carry any weight?
      In an earlier comment, you implied that you are a “casual” occasional participant in discussions of these matters. Now you’re claiming insider knowledge.
      Onlookers, bystanders, observers have a right to know whether participants in a controversy have conflicts of interest. If you have inside knowledge of AIDS treatment, it raises the suspicion that you have a conflict of interest.

      Response 7: It doesn’t require any studies at all to establish that low doses of poison are tolerated better than high doses. Speculation as to what might or might not have been the case elsewhere doesn’t get us anywhere.

      Response 8: MA Fischl would be a very good person to look at lower dosages, since she was the one who treated Kim Bergalis. Observers should Google “Kim Bergalis” and read all sides of that sad story.

      Again:
      I fear we are in danger of lapsing into what happens on so many blogs: going over the same ground again and again without any way of resolving differences of OPINION, each side “cherry picking” the literature for supporting references.

      I await your promised reaction to what I posted in specific response to your qualitative scenario that suggests lowered mortality not matched by commensurate increase in life span might be compatible with HIV/AIDS theory.

  8. Michael said

    Mr. Burun.

    The majority of those who yet died in 1995 and 1996 had indeed been on AZT monotherapy in the years prior to their deaths. There were still many who were taking AZT only in 1994 and 1995! The “cocktails” were still just being “phased in” during 1995!

    Simply looking at who was taking what prior to their deaths gives the entire story.

    You say that 500 to 600 mg of AZT was “typical” in years 1996/97? No sir! It was not. What was far more typical by 1996 was 200 mg of AZT daily in combination with 2 other drugs.

    A daily dose of 200 mg was a substantial drop from the 1200 to 1500 mg average dosage during 1987 to 1993.

    There is one other factor that is also paid little attention to by those who are consumed by “scientific evidence”, and that is the placebo effect and the role of emotion in affecting human health.

    Prior to 1995, patients were given a sentence of imminent hopelessness and sure death and were told unequivocally that they would die. So they did.

    Surely, such a diagnosis being given to patients by trusted doctors put them in states of intense emotional stress followed by utter apathetic hopelessness and helplessness to the point that many would not even eat.

    Post 1995, patients were beginning to be told they could live longer. So they did.

    Ever since Rene Descartes, the mind and thoughts and emotions of a human being have essentially been cut off at the neck from any connection to their effects on the rest of the body and on human health. Even today, the average doctor, and certainly most “scientists”, fail to see the obvious and intimate connections to health and well-being of the patients’ state of mind, inner beliefs, and emotions.

    Many studies have been done, including several on HIV positives, and then fully ignored by overly left-brained logic-entrenched scientists, that clearly show highly stressed patients being the most likely to be ill or to die on or off any medications, but still the majority-consensus rulers of science and medicine cling to beliefs that it is all and only about the mechanics of viruses, CD4 cells, and magic-bullet drugs.

    One would have thought that the placebo effect alone, which became apparent so long ago, would have fully alerted scientists and doctors, and would have led them to their obvious error in thinking in ignoring emotions and beliefs, but some seem to need to be smacked in the head with a reality stick before they “get it”.

    • Henry Bauer said

      Michael, re placebo:

      The mainstream is beginning to take placebo seriously. There was even a conference on it at NIH, http://www.nih.gov/news/pr/nov2000/nccam-14.htm
      Excellent books include “The powerful placebo–from ancient priest to modern physician” by Shapiro & Shapiro; “The placebo effect–an interdisciplinary exploration”, ed. Anne Harrington; “The placebo response: how you can release body’s inner pharmacy” by Howard Brody (not at all new-agey wishy-washy as the subtitle might suggest, Brody is a respected doctor and philosopher; Brody’s blog is well worth visiting for an insider’s jaundiced but informed and factual view of the drug industry: http://brodyhooked.blogspot.com/).

  9. Köpek,

    Your civil tone and absence of ad hominems are appreciated.

    “While the early placebo controlled trials of monotherapy had their limitations, comparison of the available data comparing no treatment with mono- dual- and triple- therapies shows a stepwise improvement in mortality and AIDS defining illnesses, as is demonstrated by this systematic review and meta-analysis of 54 RCTs”

    Yes, we’re all familiar with that paper. Your phrase “comparison of the available data comparing no treatment with mono- dual- and triple- therapies” slyly skirts my previous point, namely that there has never been a direct “[comparison of] no treatment with … dual- and triple- therapies”. As I wrote in a previous article:

    “…the claim that a combination therapy of 3 drugs is better than true placebo is dependent upon a chain of clinical comparisons, just as the proof of a mathematical theorem is dependent upon a chain of logical implications. So if even a single clinical comparison is invalid, the entire chain falls apart, as a mathematical proof falls apart if even a single logical implication is invalid. What this means for HIV therapy is that we must look very closely at the original studies comparing AZT monotherapy to true placebo. If we find these original studies to be unsound or fraudulent, then we have no basis for claiming combination therapy is better than true placebo.”

    You admit the “early placebo controlled trials of monotherapy had their limitations”. If that’s how you choose to characterize Fischl/Volberding, ACTG 016, ACTG 019 (to mention several cited in the meta-analysis), I suppose that’s your prerogative. I personally find that characterization to be a euphemism, to say the least. I would suggest anyone interested should actually read the papers and everything they can get their hands on discussing the trials, from BOTH sides, and then see if they think the characterization “limitations” is a euphemism.

    Here’s my favorite graph from the paper you cite:

    http://www.bmj.com/cgi/content/full/324/7340/757/F5

    The graph clearly suggests that when the clinical trials are carried out to their intended duration, the early “benefits” of AZT evaporate.

    “If AIDS deaths were caused by taking one antiretroviral, why are they reduced when another is added to the first, and then further reduced when taking three or more?”

    Now this is starting to sound like AIDSTruth talking points, as this has been addressed numerous times previously on blogs and discussion boards. The answers are not hard to find.

    “Further, as your Table II above shows, death rates among PWAs were highest in the years before the introduction of zidovudine rather than afterward. This does not appear to support the hypothesis that zidovudine was the cause of such deaths.”

    But neither does it provide evidence against that hypothesis. The point is that the death rates began to fall before the introduction of AZT, so falling death rates after such introduction cannot be taken as positive evidence of AZT’s alleged benefits.

    darin

  10. Martin said

    Hi Dr. Bauer, You don’t have to publish this response — this guy (I think it’s a guy) Burun, in spite of his affected politeness, comes over as either a dolt or an establishment mole — you pick. I think you’re being too kind. As John Lauritsen has said to me in the past, people who don’t see that AIDS really isn’t an infectious disease are stupid (he doesn’t mince words). Maybe it’s a convention or something the average reader relates to better, but the use of the terms “infected” or “HIV positive” keep irking me. Neither are true. But repeating them even by dissident writers appears to affirm them. Even the term AIDS isn’t really true anymore. How people really get sick (and the appropriate treatment) is obscured by the inaccurate and unfortunate diagnosis of AIDS or HIV infection.

    I believe though that you are doing a great service with your blog — it’s really one of the most informative ones on the web along with David Crowe’s Reappraising AIDS website.

    • Henry Bauer said

      Martin: Thanks! As I responded to Macdonald a little while ago, I used to presume people were genuine unless there was proof to the contrary, but my experience with blogs and anonymity has made me rather suspicious. Still, when comments appear to be directed toward an unresolved issue, I approve them. If they were “bait”, as in “bait-and-switch”, that becomes clear enough pretty soon — as when Fulano/Menganito dropped out when (s)he was challenged to address a central self-contradiction in HIV/AIDS theory.

      I regret the need to use terms like “infection”; and I can understand that it can feel like twisting the knife to people who have been victims — but I just don’t know how to write about these things without using the commonly understood terms. I’m trying to reach people who don’t yet understand what’s going on.

  11. Dr. Bauer,

    You wrote to KB: “If you have inside knowledge of AIDS treatment, it raises the suspicion that you have a conflict of interest.”

    Of course it does! I suspected Prof. Dr. KB as being one of the many employees of AIDS Inc. from his very first comment on this blog. However, I’m also grateful that he survives without engaging in this extremely ugly and disgusting uncivilized behavior, which seems to be mandatory for his colleagues, and which is by far worse than the manners of some construction-site personnel or truck drivers.

    But I think suspecting him as having “conflicts of interest” is a kind of a misnomer. In fact he combines all possible interests amazingly nicely: his own conscious and unconscious private interests, his financial and career-wise interests, and the interests of his sponsors. That’s why he is promoting their creed as widely as possible. Supporting their assertions by solid, non-fraudulent scientific references doesn’t seem necessary, because it’s just a creed.

    “Dying from What?” was the second part of the title of this article. “Everybody knows” that lung cancer is not caused by a virus; very much unlike Kaposi, which is caused by the “Kaposi-virus”, or cervical cancer, which is caused by the “cervical-cancer-virus”. Instead it is widely accepted, that lung cancer is a lifestyle-malignancy caused by decades of smoking.

    Why do people want us to believe that lung cancer is the only behavioral disease? Of course it is not.

    But scapegoating is convenient. If you suffer from a lack of money, the Jews have taken it all. If you suffer from unconscious homophobia, you have to blame homosexuals for their “destruction of whole families” and for “spreading a deadly virus” upon you brave heterosexual. If you suffer from too small an ego and are therefore afraid of the Black man, you have to blame the Black man for his “irresponsible promiscuous sexual behavior”, and you must assure, that he will not reproduce himself to later confront you with even more Black men. The second-best means to achieve this aim obviously is to destroy their reproductive functions by not giving them enough to eat and by letting them drink contaminated water. And the very best is to destroy these functions in their offspring from the very beginning of their lives by feeding them so-called “antiretrovirals” to let the “side-effects” do their destructive job.

    The smaller your ego and purse, the bigger your greed and your angst, the more you have to obey your superiors, to follow their orders, and to stop thinking for yourself. Once and for all.

  12. Photonaut said

    It’s good to see, as Darin Brown says, a courteous debate around these issues without ad hominems or personal superfluities flying. What a wonderful medium is the internet: while the mainstream press has suppressed the debate, it is nonetheless happening here, everywhere and nowhere. Still, what yet needs to be recorded in the electric æther is a discussion like this one where a proponent of the Orthodoxy duly recognizes their defeat based on presented facts, and openly and honourably says so. I don’t believe I’ve yet witnessed that.

    Dr Bauer, I think Köpek has a point that anonymity in contentious debates is nothing new, and stretches back centuries; I would say, let people remain anonymous: what counts is their dynamic integrity in the debate itself. I am stimulated so far by Köpek’s contribution, and am excited to see what he will say next.

    • Henry Bauer said

      Photonaut:

      I too am rather excited to see what “Köpek Burun” has to say about the data in “Living with HIV, dying of what?!”

      My feelings and thoughts about anonymity are quite various. Whistle blowers neeed to remain anonymous: EXCEPT to those who are in a position to take corrective actions, unless the whistle blower can provide actual documents that prove the wrong-doing. Writers may use several pen-names to distinguish their writings in different genres, but the their actual identity is an open secret. I’ve used pen-names myself a few times, when I was writing critically about waht’s wrong with university administration in general and didn’t want my critiques to be misconstrued as applying only to the place where I happened to be at the time, so I remained “anonymous” to people elsewhere even though those on my own campus knew I was the writer. But anonymity has the possible drawback that it can cause readers to question the writer’s credibility; it raises the question, whether personal scores are being settled or conflicts of interest hidden.

  13. Sadun Kal said

    I think many people like “Burun” are as sincere as any Rethinker is. What’s different is just the perception, the point of view. It depends on how strong the emotional bonds with the mainstream community is, for whatever reason. Otherwise the fraud, deception, censorship, non-science etc. are so obvious that no objective person can defend the mainstream community so passionately. I haven’t seen a single one of those passionate HIV/AIDS defenders admit even the most obvious un-science by the mainstream scientific community… They need to hold on to that belief in its purity.

    • Henry Bauer said

      Sadun Kal:

      One aspect of the human tragedy is the damage that can be caused by perfectly “sincere” people.

  14. Marcel said

    Let me insert this irrelevant comment (I haven’t had time to read the latest posts here yet.) We have made a breakthrough with an article in the anti-globalization media, which has long ignored this issue. I have long felt that we will get nowhere until we get this much larger movement to take notice of the AIDS fraud. I urge everyone to visit this site and post comments.

    http://www.prisonplanet.com/top-scientists-ask-medical-journal-science-to-retract-original-aids-papers.html#comment-102140

    • Henry Bauer said

      Marcel, thanks! According to one of our Rethinkers, the prisonplanet site is one of the most visited alternative news web-sites, with about 1 million hits per day

  15. Köpek Burun said

    [I’ve removed extraneous material in order to concentrate on the main issue — HHB]

    ….

    On to your argument:

    I have to admit not following some of your logical jumps, so feel free to add further clarification if there is something I have missed.RESPONSE 1

    From 1982 to 2004, the death rate (last column in the Table) declined from 65% to 2.8%; yet the difference between the median age of the population of PWAs and their median age of death increased only from about 7 months (0.6 years) to about 22 months (1.8 years). (italics added)

    Not quite. The median age of deaths that actually occurred among PWAs in 2003, say, is not the median age of death of the whole cohort of PWAs RESPONSE 2alive at the start of that year, for the simple reason that most of them didn’t die that year: most deaths in the cohort will occur in years later than 2003.
    Each passing year increases the average age of deaths-so-far in that cohort in proportion to the numbers that die in that year, until all of them have died, at which point the actual average age of death and its median can be established.

    That’s a stark contradiction. The median age of death in any population is the average life-span.

    Well, it’s the median lifespan of those who died, but as I note above, the median age of deaths occurring in a given year in a cohort is not the median age of death (or lifespan) of members of that population as a whole. For that you need the ages of deaths among the cohort for all years in which members of that particular cohort die.

    If the median age of the existing population is within a couple of years of the life span, then the death rate must be enormous; but here the mortality in recent years is small while the life span is a mere 22 months greater than the median age of the population.

    See above.

    The contradiction means that the basis for classifying as “PWA” is not the same as what determines death; those who are dying are in some manner atypical within the PWA population.

    Why not? I don’t follow the logical jump.RESPONSE 1

    What typifies PWAs, though, is being HIV-positive.

    Not quite: what typifies PWAs is having a particular disease of the immune system, in addition to being HIV-positive. Not all HIV-positive people are PWAs, but all PWAs have HIV.RESPONSE 3

    Therefore something other than being HIV-positive distinguishes those who are dying from those who are not dying.

    Again, I don’t understand your point. What distinguishes PWAs who die in a given year from those that survive is not to any extent their HIV status. All PWAs are HIV positive. But the fact that most HIV-positive people don’t die in a given year doesn’t mean that HIV isn’t a cause in those that do. What distinguishes those PWAs who die from those who don’t is the degree and rate of progression of HIV disease, and increasingly the incidence of concomitant disorders such as end stage hepatitis C disease. Prior to HAART and its precursor antiretroviral treatments, few PWAs survived AIDS long enough to get those concomitant conditions.RESPONSE 4

    At least for the most recent decade, HAART seems the obvious “missing link”.

    No, I don’t think that whether people get HAART is not the only qualitative determinant distinguishing the subgroup of PWAs who die from the subgroup that doesn’t in a given year in the US. Most PWAs, and particularly those at most imminent risk of death, will use HAART. The use or non use of HAART and perhaps the degree to which it is used optimally determines the size of the group that dies relative to that of the survivors rather than providing a clear qualitative distinction between the two.

    Let’s assume that those few percent of PWAs who are dying have not been getting HAART. Then PWAs who survive, who are benefiting from HAART, would be getting older, and the median age of the PWA population would be steadily increasing IN CONTRAST to the median age of those dying, which would continue to be that typical for untreated PWAs. The data show no such thing. During the HAART era, the median ages of death and of PWAs drift upwards in tandem, with no discernible change in the magnitude of the difference, 1.7-1.9 years. Most striking, the median age of surviving PWAs remains below, not above, the median age of death.

    The median age of death of those who are dying is increasing because use or non-use of HAART is not the only factor distinguishing those who die from those who survive.

    However, median life expectancy in the group as a whole is increasing faster than the median age of deaths that occur from year to year, RESPONSE 5because the proportion of survivors from previous years is increasing from year cohort to year cohort. Again, and I am probably flogging a dead horse here, the median age of deaths occurring within a year is not the ultimate median age of death within the population if an increasing proportion from year to year are not dying.RESPONSE 6

    In any case, the same contradiction between median-age differences and mortality rates applies in the years 1982 to 1996. The only resolution for this conundrum is to recognize that what determines PWA status — namely, being HIV-positive — isn’t what determines death among PWAs. In other words, HIV doesn’t cause death.

    No, the solution to “conundrum” is to recognise that the median age-of-death figures apply only to a diminishing proportion of the PWA population each year from whom you derive the overall median age figures. This is because the mortality rates are currently falling — due to a recent major advance in treatment and a number of smaller ongoing advances.

    If I get time, I’d like to address the second part of your post about whether or not an infectious aetiology of a disease can be derived from its peak age of death.RESPONSE 7 For now, though, all I can suggest is that those interested in the question might like to look up the relative untreated disease progression and mortality rates of those infected with HIV perinatally, in young adulthood and in old age respectively.RESPONSE 8

    ———————

    A/Prof Darin, I’d particularly like to take up your points because I think they highlight some interesting distinctions between the epistemological frameworks and methods applicable respectively to mathematics and applied sciences, particularly medical science. However, despite your assurance that a plausible and well evidenced answer to my one and only question on this thread (post number 8, in bold toward the end) was easy to find by searching the net, I have been unable to do.

    • Henry Bauer said

      “Köpek Burun”:

      RESPONSE 1:
      The main point that you apparently miss is this: One thing (X) has not changed appreciably over the years; another (Y) has changed drastically; therefore X and Y are governed by different determinants, causes, definitions, whatever — something affects X that doesn’t affect Y, or vice versa.
      X has to do with age of death, whether it is the ABSOLUTE median age of death, or the difference between median ages of death and of those newly diagnosed, or the difference between the median ages of death and of the population from which those deaths come, or the difference between the median ages of death and of the survivors of that year. In ALL those variants of measures of age of death, there are only very gradual changes over the years, with no major discontinuities. Nothing to do with age of death supposedly from “HIV disease” has changed dramatically in more than two decades, and whatever has changed has done so very gradually with no sudden leaps.
      Y is the RATE of death, the mortality, among PWAs who are by definition suffering from “HIV disease”. Y has changed by a huge factor (25 fold) during those same two decades, and there have been at least two significant discontinuities (1992/93, 1996/97) as well as a period of rapid change (1987 to 1992).
      Therefore something determines age of death that does not determine PWA status, or vice versa.

      Under HIV/AIDS theory, the population of PWAs is supposedly at risk of dying because of HIV/AIDS, and actual deaths are also ascribed to HIV/AIDS: inclusion in the category X and inclusion in the category Y are governed by the same determinant, cause, definition, whatever; call it HIV-positive, call it HIV-positive plus advanced immunedeficiency, call it anything you like. PWAs are people “infected”, deaths come because of the “infection”. Under HIV/AIDS theory, X and Y should go in tandem. But they don’t.

      RESPONSE 2:
      You need to define what you mean by “cohort”, and you need to keep to the same definition throughout. I simply can’t understand what you are trying to say in this paragraph and the next one.
      You are trying to argue a case qualitatively, without rigorous definition of terms (what in science we call “hand waving” talk). As I mentioned earlier, to visualize how people becoming PWA would fare over the years by age group and survivorship, actual calculations can clarify matters. You now have available the results of those calculations, the age distributions of PWA survivors at the end of each year, and of cumulative survivors in each year, as well as the earlier data on age distributions of newly diagnosed PWAs and of annual deaths. Pick any definition of “cohort” that you wish, choose any starting year that you wish, and then try to explain how it is possible for the mortality to plunge as it did, by a factor of 25, while the median ages have remained so close to one another for two decades, and the age distributions have remained overlapping, and in any given year the mortality in each age group is about the same. You’ve got to make your case QUANTITATIVELY if you wish to argue against the case I’ve made quantitatively.
      The implication of what you say is that people who die in future years in some “cohort” will be dying at higher ages than those who die now in that cohort. That requires that there’s a bias toward earlier death among younger members of the “cohort”; why should that be? It’s contrary to any normal experience — for any illnesses or diseases, mortality is higher among older and not younger people.
      But your approach is basically wrong. The way to phrase what you apparently are driving at is, “Are the PWAs dying in any given year a representative sample, in terms of age distribution?” It’s a matter of statistical inference, sampling theory, probability. What we know is that at least a few percent of PWAs die in a given year (in the most recent years, larger in earlier years). Mutatis mutandis, that’s a very large sample, and one would expect it to be representative in absence of any variable that might bias the sample. I suggested HAART — or, in general, treatment as opposed to non-treatment — as such a possible variable, but the data disproved that possibility, as I pointed out. In any case, if there is such a biasing variable that affects deaths but not inclusion as PWA, it simply underscores the logic I set out under “X” and “Y”. Beyond that, there are excellent grounds within the data to support the view that deaths in a given year are a representative sample: namely, year after year the same age distribution shows up.
      Life expectancy = median age of death. Deaths in any given year are a representative sample of all deaths that will occur in that “cohort”. Thus life expectancy of PWAs is far shorter than demanded by HIV/AIDS theory and its treatment corollaries, and is self-contradicted by the incongruous 25-fold decline in mortality rate.

      RESPONSE 3:
      Note in RESPONSE 1 & 2: It’s immaterial, how you choose to define what you see as the difference between those who die and those who don’t — the point is, the data show that there is a difference, but there’s nothing in the definition of PWA that provides for such a difference. People are supposed to be dying of AIDS because they are PWAs. That’s why I mentioned HAART as a possible way around this, TREATING some PWAs differently from others; but that doesn’t work, as I pointed out.

      RESPONSE 4:
      You are simply wrong to say that “Prior to HAART and its precursor antiretroviral treatments, few PWAs survived AIDS long enough to get those concomitant conditions”. In the early 1980s, AIDS was recognized precisely because of opportunistic infections. All PWAs were surviving long enough to get those conditions!

      RESPONSE 5: The median life expectancy isn’t increasing faster than the median age of deaths. The data show that the difference between median ages of the PWA population and of those dying has remained the same throughout the HAART era, and it didn’t change much from the late 1980s on either, for that matter.
      Look at the numbers: Yes, an increasing proportion are surviving as the years go by; but the age distribution of those surviving is remaining the same; and their median age is NOT overtaking the median age of those dying (which is the life expectancy).

      RESPONSE 6: “an increasing proportion from year to year are not dying” but the age distribution of the survivors is not changing; the median ages of new diagnoses, of survivors, and of deaths all change in tandem. There’s no indication of an accumulating proportion of older and older survivors to bring the median death age below that of the survivors.
      If some “cohort” is getting older each year without dying so that “ultimately” their median age of death will be much higher than that of those who are now dying, it means that those dying earlier must be younger compared to those who are surviving! But median death ages are consistently higher than those of the population from which the deaths are drawn, which is also what one would normally expect.

      RESPONSE 7: That’s not what I said. I said that mortality for any and all diseases increases with age from about the twenties on. There isn’t an infectious disease where mortality declines after middle age, or where the proportion of those dying is about the same in every age range.
      But “the second part” of my post isn’t a separate entity, it throws further light on the whole self-consistent argument. That mortality is about the same across age groups is another reflection of what’s odd and wrong about HIV/AIDS theory.

      RESPONSE 8: You should definitely give citations for where one might find data on “the relative untreated disease progression and mortality rates of those infected with HIV perinatally, in young adulthood and in old age respectively”. After all, a common complaint from AIDS Rethinkers and HIV Skeptics is that the mainstream has singularly failed to do controlled trials of antiretroviral drugs against placebo, i.e. “untreated”; and PWAs are incessantly urged to remain on their medication, and parents are forced to have their children medicated.

      To sum up:
      You go astray by not recognizing that you are discussing an issue of sampling. My guess is that you started with the presumption that HAART is effective and that you must find some way to square that with the data. But when you approach the matter empirically, from the side of the data, and apply sampling theory to the data, it turns out that such a presumption is disproved.

      If you want to verify that by calculations based on the data, you will need first to define “cohort” and stick to a single definition throughout.

      You didn’t respond, however, to the central point: mortality and median age of death do not vary in tandem, yet both are supposed to reflect “HIV/AIDS” or “HIV disease”.

  16. Marcel said

    Maybe I spoke too soon. My comment to Prison Planet was “awaiting moderation” when I submitted it there yesterday. Today, 24 hours later, it still has not appeared, though posts made after it have appeared.

    There was nothing in my comment that should have gotten it rejected. It was very intelligent and had links to good information.

    I must admit that I have often wondered whether Prison Planet and similar sites are really agent-provocateur operations, mainly because they excluded the AIDS controversy, but also because the elite have a long history of creating their own opposition in order to control it (this is known as “controlled opposition”). Good examples are the “left gatekeepers” who define and limit the spectrum of opinion that is available to left-oriented readers.

    This development is rather confusing to me, because PP ran a story about the controversy, and yet are possibly censoring the most compelling posts.

    Has anyone else here made comments to this story that passed or didn’t pass moderation?

    • Henry Bauer said

      Marcel:

      I haven’t yet tried to post a comment on Prison Planet, but the first time I tried to follow the link you had given, I was unable to connect, and it took several more tries at intervals before I could get through. Maybe their server sometimes gets overloaded. I would try again with the same comment and see what happens. It might also be that the moderator sometimes “approves” the straightforward comments immediately, and takes longer over comments that deserve a response, I do that occasionally when short on time. For example, I’ve approved several that came in later than a couple from “Köpek Burun”, that are difficult to understand.

  17. Marcel said

    Of course, that may be the idea; run a story to acknowledge that a lot of people have heard rumblings that Aids is a fraud…then only print the dumb replies, along with lots of defenders of the official view, in order to discredit the story that you ran.

    I have read various “reader comments” on these prison planet stories and they are mostly really dumb, hysterical rants, often anti-semitic (which passes moderation!)

  18. Marcel said

    Henry, perhaps your problem connecting was due to the fact that I inadvertently posted my comment link instead of the story link, and my comment has not yet been approved.

    Try this link: http://www.prisonplanet.com/top-scientists-ask-medical-journal-science-to-retract-original-aids-papers.html

    • Henry Bauer said

      Marcel:

      The “comment” link may have been the problem, as I recall, I got through eventually by deleting the last part of the link

  19. Just my 2 cents:

    A website with 1 million hits per day cannot be an “alternative” news website.

    The first paragraph ends: “An online posting of the letter can be found here.”

    Great. But where is “here”? “Here” must be somewhere in the orbit, because neither here nor there nor somewhere else can something be detected that resembles a link.

    But I really like this comment by somebody called “8-P” (“Köpek Burun” sounds better):

    “bloody hell, as Im reading through here, are you saying AIDS doesnt exist or what? what about the millions in Africa? True, never been there myself, BUT… !”

    But?…!

  20. CathyVM said

    Somebody called “Alex (not Jones)” has posted some fairly sensible stuff there. Some sites moderate the first 10-20 comments when you are new to them so that may possibly explain why Marcel’s comment was held up.

  21. Marcel said

    My two posts have still failed to appear. Has anyone else here tried to post and succeeded?

    This fails the smell test…something’s fishy.

    I just tried to post a third time. After I posted, I guess the cookie let me see my other two earlier posts, which are still labeled as “awaiting moderation” 2 days later.

  22. Marcel said

    Okay. I did some experimentation and think I figured out what’s happening with my posts at Prison Planet.

    I had posted the following 3 times over 3 days, with some small variations each time, to the PP article:

    “At long last, Prison Planet publishes an article about the biggest fraud of the last millennium. The fact is that there are thousands of doctors, scientists and other accomplished people who have studied the evidence and concluded that there is very little evidence that HIV causes AIDS, and in fact the evidence that HIV even exists at all is highly disputed.

    And the tests are an outright con, judged differently depending on which country you reside in. Positive in South Africa? Move to Australia, where the same test might be deemed not positive. Have Aids in the US? Move to Canada, where the Aids definition is different, and suddenly you might no longer have Aids.

    This information has been suppressed too long not only by the mainstream media, but by the left and the anti-globalization websites. I salute Prison Planet for finally bringing this to the attention of readers.

    More information designed to give you a concise presentation of the tremendous dissent:

    See the many doctors and scientists who dispute that HIV causes AIDS. Why isn’t this information in your newspaper?
    http://www.rethinkingaids.com/quotes/rethinkers.htm

    Read quotes from these scientists and others:
    http://www.rethinkingaids.com/quotes/aidsquotes.htm

    *******

    Each time my post was labeled as “awaiting moderation.” Three days later, none of my posts has appeared.

    So I did an experiment. I posted in favor of Aids, Inc. as “Doctor Jay.” The post appeared immediately, without moderation.

    It read:

    Doctor Jay Says:

    December 15th, 2008 at 6:50 am
    I think that these people are just conspiracy theorists. We know that HIV causes AIDS, as surely as we know that apples fall to earth due to gravity and the moon orbits the earth. These people saying otherwise are dangerous quacks and they belong in the lunatic asylum.

    *****

    Then I posted my original post again…for a 4th time. The result? My post is “awaiting moderation.” Then I deleted the cookies from the browser and tried to post again with a different name and email than “Marcel.” The post was again labeled as “awaiting moderation.” So whatever censorship mechanism is at work here was not just keyed to the name “Marcel.”

    But just 10 minutes ago, I finally succeeded in posting that post. How? I deleted the links!

    But other posts have links…why are these two URLs censored?

    Then I tried to post a different, very brief post giving just those 2 URLs. Result? “Awaiting moderation.”

    Then I tried to post the same brief post, but instead of the List of 2700 Credentialed Rethinkers and Aids Quotes URLs, I just gave the link to the Rethinking Aids home page, to see if maybe that entire site was perhaps being censored.

    Result? The post appeared immediately without moderation.

    In another post, I also succeeded in posting the following links:

    http://www.aliveandwell.org
    http://www.virusmyth.com
    http://www.duesberg.com
    http://www.theperthgroup.com/

    What can we conclude but that those two Rethinking Aids links, the List of 2700 credentialed dissidents, and the huge Aids Quotes page, which was designed to give a concise education in the major dissident points, are being censored and the PP blog system is programmed to reject any post that contains them.

    I have long felt that those were perhaps the two single most powerful web pages in the entire dissident universe, and this suggests that the other side feels the same way.

    And either Prison Planet is a sham “anti-globalisation” provocateur site, or the CIA or similar covert agency is remotely interfering with the operation of the PP website. At least on THIS powderkeg story which has the potential to be quite destabilizing to Established Power.

    Also, let us take note that the article on PP contained NO links to rethinking aids or any other dissident site.

    I welcome any thoughts on this and comments on my experimentation methods and conclusions. And want to apologize, once again, for hijacking this thread.

    • Henry Bauer said

      Marcel:

      Your post was labeled as “SPAM” and I had to rescue it. I think WordPress automatically labels some things as SPAM because there are too many included links. Apparently prisonplanet has a similar automat.

  23. “Dying from What?” was the question. In comment #12 for the Prison Planet story “Alex (not Jones)” gives us the sad answer:

    “I know a man who tested HIV+. He was not in any of the risk groups and had no symptoms. He avoided the drugs for 3 years and had no symptoms. His doctor threatened him saying he was being irresponsible and said he would talk to CPS to have his children taken away — yes this is true. He was one of my employees. I offered to pay his legal defense but he relented and started AZT. His ‘AIDS’ symptoms started within a week. I begged him to flush the drugs.

    A month later he drive out to a secluded lake and put a .38 special to his head.

    He was so afraid of wasting away with AIDS he shot himself.

    In my opinion his physician is guilty of manslaughter at the very least.”

  24. Köpek Burun said

    Reply to Response 1:

    “Under HIV/AIDS theory, X and Y should go in tandem. But they don’t”

    Let’s stick to defining X as the median age at which incident deaths occur during a given year. X has been rising at roughly 0.67 years each year since the introduction of HAART, compared to an average rise of 0.30 years per year prior to that.

    Y is the annual mortality expressed as a percentage of the whole population of PWAs. This has been falling by varying percentages every year since 1987, with the most marked yearly fall (by more than half) in 1996-7.

    You seem puzzled that marked falls in Y aren’t paralleled by sudden surges in X. (Or more properly rises in 1-Y by commensurate rises in X since we’re talking “parallels”). The short answer is that a marked one year change in Y, even the halving of rate of deaths in a year cannot result in a comparable one year increase in X: even if Y suddenly goes from almost everyone dying to almost no-one, the median age of incident deaths cannot increase faster than the median age in the population in which those deaths occur, unless the age distribution of those deaths changes suddenly, and there is no reason to expect that the fall in Y should disproportionately affect one age group rather than another. This is also borne out by the fact that median age of incident deaths parallels that of living PWAs.

    Leaving aside new diagnoses of AIDS, the maximum possible increase in median age of incident deaths from one year to the next can only approach but not exceed 1.0 (the exact age increase in age of all survivors from one year to the next) assuming the distribution of deaths by age remains fairly constant, the median creeping forward year by year basically in parallel to the forward creep of age of PWAs. The current annual increase (0.67) reflects the fact that the median age of deaths is a little higher than the overall median age of PWAs, and new diagnoses occur at a lesser median age, resulting in the median of the group as a whole ageing by less than 1 year.

    An especially marked fall in Y during year A is reflected by an increase in X not only in year A, but also further increases distributed in years B, C, D, E etc until the survival advantage is expended and all its beneficiaries have died. This is why increases in median age of death don’t occur all at once in the year a new improved treatment is introduced (assuming it is introduced uniformly in one year). They are spread out over following years according to the distribution of the survival advantage. What you do see though with a significant treatment improvement is that the rate of increase in median age of PWAs changes – for example more than doubling from an average 0.3 years per year pre 1996-7 to 0.67 years per year afterward. But it can never increase above 1.0 years per year without a change in the age distribution of incident deaths.

    Reply to Response 2:

    “You need to define what you mean by “cohort”, and you need to keep to the same definition throughout. I simply can’t understand what you are trying to say in this paragraph and the next one. You are trying to argue a case qualitatively, without rigorous definition of terms (what in science we call “hand waving” talk).”

    A cohort is a group of subjects defined by experiencing an event in a particular time span. From the beginning I defined a PWA cohort as those experiencing being alive with AIDS in a specific year (as distinct from the total PWA populations alive in any subsequent year which consists not only of the survivors of our original cohort, but also the survivors among those diagnosed subsequently), and I have been consistent in that definition throughout.

    The distinction is important, because survival and mortality cannot be calculated simply by looking at deaths in a cohort during the first year, nor by examining deaths in the PWA population as a whole for subsequent years, because they are not the same as the cohort as you were originally looking at.

    “Deaths in any given year are a representative sample of all deaths that will occur in that “cohort”. Thus life expectancy of PWAs is far shorter than demanded by HIV/AIDS theory and its treatment corollaries, and is self-contradicted by the incongruous 25-fold decline in mortality rate.”

    No they are not. They are representative only of deaths that occur during the first year following the definition of that cohort: if the mortality for that year is 5% then they are representative only of the earliest 5% of deaths. A cohort defined at the start of 2003 will have deaths in 2003, 2004, 2005… The median life expectancy from 2003 of the “start of 2003 PWA cohort” can only be established once half of that cohort has died, whatever year that might be.

    Reply to Response 3:

    “Note in RESPONSE 1 & 2: It’s immaterial, how you choose to define what you see as the difference between those who die and those who don’t — the point is, the data show that there is a difference, but there’s nothing in the definition of PWA that provides for such a difference.”

    PWAs are people who have a specific serious disease of the cell mediated immune system. Some people with that disease survive a given year, and some die, mostly from conditions aetiologically associated with the immune system disease that defines the PWA group.

    Reply to Response 4:

    By “concomitant conditions” I meant condition occurring in PWAs that are not AIDS defining conditions, for example end stage hepatitis C disease and non-AIDS defining malignancies. Although these conditions are not AIDS defining, the immune system dysfunction characteristic of AIDS is often part of their aetiology. Prior to HAART these conditions were less common because people died from AIDS defining conditions before they had a chance to develop.

    Reply to Response 5:

    The median life expectancy isn’t increasing faster than the median age of deaths. The data show that the difference between median ages of the PWA population and of those dying has remained the same throughout the HAART era, and it didn’t change much from the late 1980s on either, for that matter.

    Look at the numbers: Yes, an increasing proportion are surviving as the years go by; but the age distribution of those surviving is remaining the same; and their median age is NOT overtaking the median age of those dying (which is the life expectancy).

    No. The median age of those PWAs dying in a given year is not the life expectancy for those PWAs alive in that year. Nor is the difference between the median age of the population and that of incident deaths in the same year a measure of how much longer people alive in that year can expect to live.

    The median survival is however long it takes for 50% of your cohort to die. If we take our “PWAs alive at the start of 2003” cohort and 5% of this original group die in each of the following years then it will take till the start of 2013 for half to have died, in other words the median survival of PWAs at start-2003 is 10 years, not 2 years (the difference in median age of PWAs and that of incident deaths that year).

    All the survivors (50% of our original start-2003 cohort) will be 10 years older in 2013, although on current trends the PWA population as a whole will be only 6.7 years older because it consists not only of the survivors of those PWAs alive at the start of 2003 (our original cohort) but also the survivors among everyone diagnosed in the intervening ten years.

    There is no reason for the difference between the median age of PWAs and the median age of death to change as survival improves. The difference measures the distribution of deaths among the population, not their life expectancy.

    Reply to Response 6:

    “An increasing proportion from year to year are not dying” but the age distribution of the survivors is not changing; the median ages of new diagnoses, of survivors, and of deaths all change in tandem. There’s no indication of an accumulating proportion of older and older survivors to bring the median death age below that of the survivors.
    If some “cohort” is getting older each year without dying so that “ultimately” their median age of death will be much higher than that of those who are now dying, it means that those dying earlier must be younger compared to those who are surviving! But median death ages are consistently higher than those of the population from which the deaths are drawn, which is also what one would normally expect.

    An increasing proportion of the PWA population as a whole in a given year are not dying. Cumulative deaths among any given cohort can only increase over time.

    You are confusing survivors from year to year of a given cohort (say our “alive at start-2003 cohort”) with the total PWA population in a given year, which consists not only of those survivors but also any survivors of those diagnosed subsequently to start-2003. With each passing year the start-2003 cohort is a diminishing proportion of the total PWA population because some die each year and none are added, while the “others” are being added faster than they are dying.

    Reply to Response 7:

    It is a common pattern for survival to decrease and mortality to increase from adolescence to old age for a given condition, but not an invariable rule, including in infectious diseases. The 1918 influenza outbreak is a good counterexample: mortality was highest among infected young adults than among young children and the elderly.

    However, this is immaterial: mortality and survival rates for untreated HIV infection do, in fact, follow the general rule of worse mortality with age at infection (see reply to Response 8, refs 1,2,3)

    Nor is increasing mortality with age a particular characteristic of infectious versus other causes: most diseases have worse mortality with age including those caused by toxic assaults including medication side effects. Interestingly, though, older adults get a relatively greater survival benefit from HAART than younger adults do. I don’t know why, but it runs counter to the general rule that severe toxic side effects from medications tend to be more common in the elderly than the young (4).

    Reply to Response 8:

    Increasing mortality with age of infection in adults has been observed in haemophiliacs:

    “Survival was strongly related to age at seroconversion (86% [82-90], 72% [68-76], 45% [39-51], and 12% [5-21] at 10 years among those patients who seroconverted at ages less than 15, 15-34, 35-54, and greater than or = 55). This steep age-gradient in survival was not explained by deaths expected in the absence of HIV infection or by confounding with other factors such as haemophilia type or severity. The age-gradient was steeper for survival (ie, time from HIV-1 infection to death) than for time to diagnosis of AIDS, partly because survival after an AIDS diagnosis was poorer in older patients, and there was also a substantial increase in mortality among HIV-infected patients who did not satisfy the formal AIDS definition and this increase was greater in older patients.”(1)

    And among untreated Westerners:

    “Before widespread use of highly-active antiretroviral therapy (before 1996), time since seroconversion and age at seroconversion were the major determinants of survival and development of AIDS in Europe, North America, and Australia.”(2)

    And among untreated Africans:

    “The median survival time was 8.7 years (95% CI 8.1-9.3), and did not differ by sex, place of residence or time period of seroconversion. Survival time decreased significantly with older age at infection (P = 0.01).”(3)

    However, HAART may be more effective in improving survival in older adults than younger, removing that survival disadvantage:

    “Predicted survival for people with HIV-1 has continued to increase, since the introduction of HAART; however, the importance of age and exposure category as determinants of progression seems to have changed “(4)

    (1) http://www.ncbi.nlm.nih.gov/pubmed/8667864
    (2) http://www.ncbi.nlm.nih.gov/pubmed/10791375
    (3) http://www.ncbi.nlm.nih.gov/pubmed/18032934
    (4) http://www.ncbi.nlm.nih.gov/pubmed/14575971

    • Henry Bauer said

      To KP reply to Response 1:

      If you choose to regard the changes in the last column of Table I as being in any way correlated with those in the second-last column (or the third-last, for that matter), then there’s nothing more I can usefully say to you. I invite observers to choose which of our views seems to them to be faithful to the data.
      Moreover, you have ignored my point about sampling, and you continue to imagine, apparently, that median age of survivors can remain below that of those dying while the average PWA’s survival is supposed to increase steadily, in the HAART era by a decade or more.

      To my mind, the data clearly show several distinct periods:
      1982 to 1986/87; high mortality, commensurately short survival after diagnosis; diagnosis based on clinical condition, chiefly KS, PCP, candidiasis. (PJP may be the technically used name nowadays, but PCP continues to be used in most of the HIV/AIDS literature.)
      1986/87 to 1992: Mortality approximately halved, but average life-span (median age of death) of those dying increasing only from about half a year to about 2 years.
      1992/93: Mortality declines by more than a third — because retroactively included as “PWAs” are asymptomatic HIV-positive people with low CD4 counts. Nevertheless, those PWAs who do die continue to do so at about the same median age: those who die are evidently not representative of PWAs, as I pointed out previously. What makes them unrepresentative?
      1993 to 1996: Mortality about halved, no evident change in survival time.
      1996/97: Mortality about halved again, but — if anything — a decrease in average survival.

      In other words, there are 5 opportunities to compare mortality and life-span. The relationship between them is different in each of the 5 cases. Therefore something is determining one of them that isn’t determining the other one. PWA is defined as “at risk of dying from HIV/AIDS”; therefore something else is determining deaths among PWAs.

      “the median age of incident deaths cannot increase faster than the median age in the population in which those deaths occur”
      “the maximum possible increase in median age of incident deaths from one year to the next can only approach but not exceed 1.0 (the exact age increase in age of all survivors from one year to the next)”
      are both wrong.
      Any increase in median age of death depends first and foremost on what may have changed about the conditions that produce death, not just that everyone gets a year older each year.
      Imagine that, rather than HAART, there had been introduced in 1996 a “magic bullet” that reconstituted the immune function very quickly rather than slowly, making it also possible to treat successfully the manifest opportunistic infections that actually cause death. Then no one from the 1996 PWA population would have died of AIDS in 1997, they would be dying only from “natural causes”, and the median age of those dying in 1997 would have been comparable to the normal life expectancy, on the order of 75 years in the USA.
      HIV/AIDS enthusiasts don’t go quite so far as to describe HAART as a “magic bullet”, though you do see it credited with making HIV/AIDS a chronic but manageable disease that offers almost a normal life-span. HAART’s efficacy has supposedly been improving year by year since 1996, and survival time has supposedly increased year by year. So if HAART were as effective as claimed, extending life by decades, then the median age of death would have increased progressively by more than a year per year. {“According to the Antiretroviral Therapy Collaboration (Lancet 372 [2008] 293-99), life expectancy for 20-year-old HIV-positives had increased by 13 years between 1996 and 2005 to an additional 49 years; for 35-year-olds, the life expectancy in 1996-99 was said to be another 25 years. According to Walensky et al. (Journal of Infectious Diseases 194 [2006] 11-19), survival after an AIDS diagnosis now averages more than 14 years.”}

      You are still missing the point about sampling: The median age of deaths in any given year is a sample of all the deaths that will ever occur in the cohort from which those deaths were drawn. A few percent or more is an amply large sample to be representative, so long as there are no confounding variables. I already explained why treatment can’t be such a confounding variable.

      KP reply to Response 2:
      (Nitpicking quibble: “Cohort” doesn’t need to be defined by a time period. It’s just a group, sometimes a generational group, sometimes a group recruited for a clinical trial, etc. That’s why you always need to say at the outset exactly how you’re using the term. Re AIDS, a common usage is, diagnosed in a given year; or seroconverted in a given year.)

      “survival and mortality cannot be calculated simply by looking at deaths in a cohort during the first year”
      “The median life expectancy from 2003 of the ‘start of 2003 PWA cohort’ can only be established once half of that cohort has died, whatever year that might be.”

      In other words, you are rejecting the whole centuries-in-the-making edifice of statistical inference, probability theory, and sampling theory. You are denying the validity of what statisticians do routinely all the time in all sorts of connections. In the present context, HAART enthusiasts have not hesitated to project life-spans decades into the future on the basis of mortalities experienced within a few years of the introduction of HAART; they used the sample of mortalities in these years as being representative of mortality and life-spans to be experienced in the future.

      KP reply to Response 3:
      “PWAs are people who have a specific serious disease of the cell mediated immune system”.

      That may be your definition, but it isn’t that of the Centers for Disease Control and Prevention. And you re-assert that what defines PWA also causes death, when the data show that is not the case.
      You concentrate on 1996 and later. But what caused the 5-fold drop in mortality from 1982 to 1996 (much greater than the 1996/97 one) if it wasn’t the definitional changes in classifying PWAs? Death, however, has not been re-defined since 1982, even among PWAs.

      KP reply to Response 4:
      I wish you hadn’t repeated this after I explained why it isn’t pertinent.
      “Concomitant conditions” are the ONLY things from which PWAs die. “HIV” itself is alleged only to kill critical cells of the immune system, “HIV” isn’t even alleged to cause death directly.

      KP reply to Response 5:
      “The median age of those PWAs dying in a given year is not the life expectancy for those PWAs alive in that year.”
      Please consult a statistician about sampling and statistical inference.
      Your confusion may be owing in part to taking on trust the conclusions of those who claimed to calculate increased life-span from the decrease in mortality; they assumed that the two change in tandem. That isn’t the case, however: the data show that mortality and life-span have not gone in tandem, see above, 5 distinct periods.
      There is some confounding variable at work. It isn’t treatment, as I explained before. The only other obvious one is the re-definition of “AIDS”, from clinically based diagnosis to lab-test-based diagnosis. The latter explains every change in mortality up to 1996; and the change in 1996/97 reflects lower toxicity of HAART compared to earlier treatment. (Is there a mainstream source that denies that HAART is less toxic than its predecessors?)
      Please also ask a statistician or demographer to comment on “There is no reason for the difference between the median age of PWAs and the median age of death to change as survival improves. The difference measures the distribution of deaths among the population, not their life expectancy.” I simply don’t understand what you’re trying to say.

      KP reply to Response 5 & 6:
      Once more: SAMPLING!

      KP reply to Response 7:
      The 1918 flu epidemic is universally recognized as an oddity that remains to be fully explained and that continues to be researched. One of its unusual features was a very rapid onset and decline. That has led some investigators to suggest that EXPOSURE to the infection was very age-dependent: people (particularly of soldier age, this was the time of World War I) who traveled or were in contact with those who traveled were exposed to a great extent while “stay-at-homes” were not; and the epidemic was over before it could spread into the general population. The very young and the very old were relatively unlikely to get into contact with infected people. But where exposure is not age-dependent, mortality for all illnesses increases very rapidly with age. (Other people had mentioned the 1918 flu to me when I pointed to the oddity of HIV/AIDS picking out people aged 35-45, so I had read up on it before.)

      “mortality and survival rates for untreated HIV infection do, in fact, follow the general rule of worse mortality with age at infection”
      is contradicted by the actual PWA death rates, see Table II. The changes with age in Table II are nothing like the doubling every 7 or 10 years (Gompertz’s law) that applies generally in diseases and illnesses in the age range we’re concerned with (up to about 70 or 80).

      “including those caused by toxic assaults including medication side effects”
      I don’t know what source you rely on for this, but it’s obviously wrong. A sufficiently toxic chemical kills people of all ages with equal speed. Cyanide, say; or the stuff used in execution by lethal injection; or any number of things featured in mystery novels, including medication over-dosages.

      KP reply to Response 8:
      I resist being drawn into distractions, KP, and cherry-picking citations that aren’t directly pertinent to the central questions. “Time since seroconversion” can only be estimated retroactively using a variety of assumptions, so the basis for all those papers is questionable.

      ——————

      Unless we can reach agreement on the issue of what the median age of death means, we won’t be able to get any further. So:

      Do you deny that the median age of the deaths in any given year can be a reasonable estimate of the life-span of the whole population or cohort from which those deaths are drawn? Especially when the sample is as large as several percent or more? Unless there is a confounding variable that distinguishes those who died from the others in that population?

      Or put it this way: Do you deny that the life expectancy of a population can be estimated validly, by normal statistical procedures (sample size, type of distribution, etc.), on the basis of deaths in any given year?

  25. Marcel:

    Things are getting funny now. On December 15th, 2008 at 7:08 pm somebody called “Taraffal” said there( http://www.prisonplanet.com/top-scientists-ask-medical-journal-science-to-retract-original-aids-papers.html ):

    “I just found some interesting news about actual censorship here:

    https://hivskeptic.wordpress.com/2008/12/10/living-with-hiv-dying-from-what/#comment-2032

    That is your comment #36 here.

    I accessed the page on December 16th, at 7:15 GMT, and the comment has still not been deleted.

    Censorship there doesn’t work properly.

    Re your pen name “Doctor Jay”:

    Perhaps that would be the best strategy: Dissidents masking themselves as quacks to control the quackery.

    I’m really enjoying your experiment.

    And I finally found the letter the story is all about:

    http://www.rethinkingaids.com/Home/tabid/146/Default.aspx

    The story PP published is just a copy of the press release of Rethinking AIDS. The only creative work of PP consisted in deleting the links to “here” and to “Rethinking AIDS”.

    Henry:

    Marcel’s original comment had only two links. Later he published a comment with four links and they accepted it. I think he’s right in suspecting that they censor precisely the Rethinking AIDS website. They did it twice in their copy of the press release.

    • Henry Bauer said

      Sabine:

      I trust that I put the right link in re there?

      Sabine & Marcel:

      You may well be right about actual substantive censorship, I just don’t know. I DO know that automated SPAM filters can’t think, and no matter how cleverly they are programmed and re-programmed, they will stop things they shouldn’t and let through others that they should stop. I don’t know what rules WordPress uses (and it wouldn’t help me if I did!). I’ve had only one comment come through that should have been filtered out as spam, but I’ve had quite a few legitimate comments that I had to rescue from the SPAM pile. So I infer that the rules are constructed to filter more rather than less, “when in doubt, mark as spam”. I also don’t know whether PrisonPlanet uses the same SPAM software as WordPress.

      Marcel, your last long comment to me wasn’t really awaiting moderation, it was in the SPAM pile. I also don’t know whether WordPress sends an automated response, “awaiting moderation”, only when I get to see it in “Comments” or also if I see it only in “SPAM”.

      At any rate, all this uncertainty makes me doubly reluctant to draw firm conclusions from a few cases.

  26. Marcel said

    I noticed that when I posted it to your site, Henry, I did not get the usual “awaiting moderation” feedback. I was just taken back to the thread and my post was not there. So I submitted it again, and got the “duplicate post detected” message. That has never happened to me before on your site.

    Your theory that it was rejected at PP because it had more than one link is contradicted by the fact that one of my test posts contained 4 links, yet was accepted by the forum, I assume because those four links did not include the List and Quotes pages. My rejected posts only had 2 links.

    Also, and not surprisingly, this story has now disappeared from the Prison Planet site.

    Even doing a search on the site now, the article is nowhere to be found.

    • Henry Bauer said

      Marcel:

      I suppose you didn’t get the “awaiting moderation” because it was classed as SPAM.

      The PP stuff is strange, after all they posted lots of “dissident” material from “Alex (not Jones)”

      As I responded to Sabine, I don’t understand automated filters.

  27. Marcel said

    Sabine,

    I did point that out to Henry, the fact that a post with 4 links was accepted. For some reason, that latest post of mine has not yet appeared here.

    I see that the PP article is still available if you enter the URL, but it is no longer on the PP home page, and doesn’t appear when you search for it with PP’s search function.

    So I was wrong that it has disappeared, but it is impossible to find unless you have the URL.

  28. Köpek, you said,

    “However, despite your assurance that a plausible and well evidenced answer to my one and only question on this thread (post number 8, in bold toward the end) was easy to find by searching the net, I have been unable to do.”

    To remind readers, that question was,

    “If AIDS deaths were caused by taking one antiretroviral, why are they reduced when another is added to the first, and then further reduced when taking three or more?”

    First, we have to strip apart the hidden assumptions. The question assumes that the drugs ARE in fact, “antiretroviral”, i.e. that there is a retrovirus, and that the mechanism by which the drugs work is by acting against that virus. The implication seems to be that the AIDS deaths are due to AZT’s “antiretroviral” mechanisms. So, if you take more drugs with “antiretroviral” mechanisms, the deaths should increase, not decrease. The phrasing of the question removes the possibility that perhaps none of the drugs are “antiretroviral”, and that the observed effects are due to other mechanisms.

    However, I don’t know anyone who’s criticized ARVs who really thinks like this. Here’s an example of someone who definitely doesn’t think like this:

    Why did HAART improve the prognosis of AIDS?

    What if HIV was simply a natural signal of cellular death (apoptosis)?

    The fact is, we don’t fully understand the synergistic effect of all these powerful chemicals in patients. We do know that the protease inhibitors have general antimicrobial and antifungal effects, and we do know that many of the clinical trials lasted only 24 months, and many of them used CD4 counts or viral load as surrogate markers.

  29. Chris Noble said

    Life expectancy = median age of death

    No it doesn’t (except when life expectancy remains constant over time).
    A simple thought experiment is sufficient to show how wrong this is.
    Imagine a genetic condition X where people born with that condition almost invariably die before they are 5. Let’s say the median age at death for people born with this condition is 1 year – ie half of these people die before they reach 1 years of age.
    In 2000 they find a treatment Y that effectively cures condition X.
    In 2001 the median age at death will not magically jump to 70 because there aren’t any people with condition X over the age of 5.
    The median age at death for people born with condition X can only ever increase by less than 1 year per year as more people will continue to be born with condition X.
    So in 2001 the median age at death might have increased to 1.5 years.
    The median age at death dramatically underestimates the benefits of the treatment Y.
    The only way to measure the benefits of the treatment is to follow a cohort of people with condition X who are given treatment Y over a number of years and plot a survival curve.

    • Henry Bauer said

      Chris Noble:

      Statements should be taken in their proper context.

      You say, “except when life expectancy remains constant over time”: much of what I’ve been saying, in the original post and some earlier posts, and in response to “Köpek Burun”, is to take notice of how all the median ages have changed only ever so slightly and ever so gradually over the years. The median age of PWAs, and their median ages of death, have been changing about as slowly as the same variables have been changing for the population of the USA as a whole. (The median age of PWAs, in fact, is much the same as the median age of the population as a whole.)

      Your example, too, is hardly realistic in the context of what we’re talking about, median death-ages around 40. Moreover, I’ve discussed in detail why “treatment” cannot be the confounding variable in the disjunction between mortality and median death-age.

  30. Köpek Burun said

    You have argued that the median age of death and the mortality should go “in tandem” but you haven’t told us exactly what that relationship should be, only claimed that the reported median age and mortality are “inconsistent” with the relationship that should exist.

    Exactly what inconsistency? It’s pretty obvious that where the annual mortality is only a few per cent and the median age of death is rising at an average 0.67 years per year, then most of the deaths of people alive in a given year will ultimately occur at ages appreciably higher than those deaths which occur in that first year. So no, the first year deaths are not a representative sample of the age at which deaths will ultimately affect the cohort as a whole. Such a sample would only be representative if the median age of death were stable from year to year, and it is not, it’s rising.

    You claim that it is rising only “ever so slightly and ever so gradually over the years”. The stats show a 6.7 year increase over a decade.

    Exactly how quickly should it be rising to be consistent with the reported mortality? You haven’t said.

    Perhaps given that it is you making the claim of inconsistency you could calculate the expected change in the median age of death from the available mortality data (with a full error analysis) and compare it with the actual reports.

    Simply asserting that they are inconsistent is unconvincing.

    • Henry Bauer said

      Köpek Burun:

      Please don’t lapse from productive discussion into debating tricks. The data show that there’s no commensurability, no correlation, between mortality rates and death ages over the span of two decades. There are 5 distinct periods or discontinuities, as I pointed out. How exactly those two variables “should” change depends on what determines them; from my viewpoint, all that matters is that evidently different things determine each of them, which suffices to disprove HIV/AIDS theory.

      Observers will note that you have not attempted to answer my question, whether reasonable estimates of life span can be arrived at by normal methods of statistical inference from contemporaneously observed ages of death.

  31. Chris Noble said

    Your example, too, is hardly realistic in the context of what we’re talking about, median death-ages around 40.

    My example was deliberately created to highlight the differences in the median age of death in a population compared to the life expectancy of people alive in that population at the same time.

    The median age of death is only a good proxy for life expectancy of people alive in that year if the survival rates are constant over time.

    The survival rates of people with AIDS has not remained constant over the past two decades.

    You are simply wrong when you say that Life expectancy = median age of death

    The example I give completely destroys your argument.

    • Henry Bauer said

      Chris Noble:

      Your mere repetition of an unsound example does you no credit. I’m happy to let observers of these exchanges make up their own minds. I maintain that the slow changes over the years in median ages of death and of new diagnoses and of the whole PWA population satisfy even your ad hoc criterion that survival rates be “constant over time”. You would hardly insist that they must be ABSOLUTELY constant, would you?

      You have failed to respond to my point that those who calculate survival benefits from HAART have employed precisely the statistical approach that you state to be completely destroyed by your example.

      Like Köpek Burun, you appear to be starting with presumptions of HIV/AIDS theory instead of grappling with the actual data to see where they might lead. As with KP, this channels you off into polemics and attempted debating tricks that distract from the real issues.

  32. Martin said

    Hi Dr. Bauer, I just love the “debate” between you and Burun. Two observations, Burun is in a duel where he doesn’t know which side of the sword to hold, the other is that a debate is satisfying when both of the debaters agree on basic facts like 2+2=4.
    It’s kind of funny that Chris Noble came to Burun’s aid with his comment.
    Dr. Brown’s comment that the so-called ARV’s aren’t really ARV’s at all – they’re just called that in an Orwellian sort of way. Burun believes that when an “AIDS” patient “seroconverts” that means that a positive result on the “antibody tests” proves they are “infected”. Chris Noble believes the same.

    • Henry Bauer said

      Martin:

      I’m afraid your enjoyment of the “debate” has come to a dead end, note the last comments from KP and CN and my responses. Evidently they have been unable to counter my argument that mortality and death-ages have not gone in tandem; that therefore different determinants are relevant for each of them; i.e., being a PWA doesn’t entail risk of dying from “HIV disease”.

      I’m not sure that there’s anything incongruous about CN coming to KB’s aid. Both seem to start from absolute belief in HIV/AIDS orthodoxy instead of from empirical data — as of course many other defenders of the HIV/AIDS faith do. Both of them seem inclined to react instantly rather than after lengthier thought. Perhaps for that reason, both write with tone and style that varies wildly from communication to communication. I suspect they know one another quite well.

  33. Henry:

    Yes, it was the right link. I omitted it, because it was already there twice in Marcel’s comments and I didn’t want to produce SPAM.

    I do not even know, how to reach the SPAM comments on my blog, that AKISMET sorted out. Two months ago I sent an email to these folks asking for help. To date they didn’t reply.

    Henry & Marcel:

    It happened to me only once, that a comment on this blog was rejected because of “double submission”. But a minute later it was there “awaiting moderation”.

    Marcel:

    When I woke up this morning, the first thought that came to my mind, was “this PP page is gone”.

    I searched my computer, if by chance I had saved the page yesterday, but I didn’t. Then I read your first comment saying the page had really gone. Lazy me, I thought, why didn’t you…?

    Then I read your next comment and I rushed to the PP site to save this particular page with all the comments. I don’t trust them. Perhaps in a few days they completely delete the page.

    There’s overwhelming evidence for censorship on their part.

    Just remember the title of their website:

    “The truth will set you free!”

    Yes, it will. Unless you censor it.

    I’m just preparing an article for my German speaking readers about this event, where I’ll also include your two censored links. And a link to “here” (i.e. the letter to “Science”). And to here (i.e. “Living with HIV; Dying from What?”). And to there (i.e. the press release by Rethinking AIDS).

  34. Marcel said

    Sabine and whoever else is interested,

    I realized that maybe it wasn’t both of those two pages, the List page and the Quotes page, that triggered the censorship, it might have been only one of them. So today I just tried posting them individually. This time, they both were accepted.

    Either the previous behavior was an unexplained glitch, or whoever is controlling the PP website, realizing that he had been exposed on Henry’s blog (and realizing that now that the article had disappeared from the PP home page and its search engine, few people would be able to view it), decided to stop the censorship.

    But my previous posts, which are viewable to me when I login as Marcel, are still labeled “awaiting moderation.” And I saved the page in case anybody wants to see it.

  35. Marcel,

    The page did not only disappear from the PP homepage and their search engine – it disappeared from Google as well.

    Yesterday I googled for “Alex Jones” + “Top Scientists Ask Medical Journal Science To Retract Original AIDS Papers”.

    I got two results: a link to “infowars.com” and another one to “propagandamatrix.com”. Both sites seem to belong to the Alex Jones’ Empire. They offer similar content.

    “Infowars” gave no hint to the press release I was looking for. “Propagandamatrix” offered a teaser at the very bottom of their homepage with a link to the desired dokument.

    The I added “Prison Planet” to the mix and got only “infowars” as a result. Strange.

  36. Photonaut said

    Hi Dr Bauer –

    You had a comment up recently about the death of treatment activist Dan Dunable – have you removed it?? I can’t seem to find it anywhere.

    Thanks in advance,

    Jason

    • Henry Bauer said

      Jason, Photonaut:

      The piece about Dan Dunable was added as a comment, so it wouldn’t show up in a “Search” for Dunable. I’ve now inserted it at the end of that post itself so that it can be found via “Search”.

      Re the warning to Janine from Gos:

      Sure, the AIDStruth mob, whom I like also to describe as vigilantes, will pull any dirty trick they can to harm personally anyone who contradicts them. But there’s no point in anyone being anonymous in posting comments if they are already known to be Rethinkers. Then too their attempts at character assassination might bring side benefits, for example, Ken Witwer’s biased out-of-context insinuation that I’m a homophobe gave me the incentive to post prominently on my website what I’d earlier said only in a book review.

  37. Photonaut said

    More specifically, A poster at the change.org thread about HIV sent the message below to Janine Roberts, the author of Fear of the Invisible. Do you think it is founded? I wondered if any such consideration made you remove your notification of the death of Dan Dunable.

    “Janine,

    If you’d ever encountered “The Snout” and his buddies before, as I have, you wouldn’t be using your real name here.

    Especially not considering the fact that in this forum, we’re actually giving them their comeuppance for the Yahoo massacre — they’re not gonna sit still for it, and they are NOT a harmless bunch.

    — Gos

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