HIV/AIDS Skepticism

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

Posts Tagged ‘latent period’

More HIV/AIDS GIGO (garbage in and out): “HIV” and risk of death

Posted by Henry Bauer on 2008/07/12

HAART had supposedly saved at least 3 million years of life by 2003, thereby supposedly justifying the expenditure of $21 billion in 2006 from federal US government funds alone—how much more was disbursed or used by charities and other NGOs is not known. On examination, that claimed 3 million turned out to be 1.2 million: and since these are not lives but life-years, they represent the lives of perhaps 6% of AIDS victims [Antiretroviral therapy has SAVED 3 MILLION life-years, 1 July 2008;
HIV/AIDS SCAM: Have antiretroviral drugs saved 3 million life-years?, 6 July 2008]. Not so impressive after a quarter century of research costing >$100 billion.

Another more recently trumpeted claim of benefits from antiretroviral therapy is that the “excess mortality” ascribed to “HIV” has decreased substantially in the era of HAART (Bhaskaran et al. for the CASCADE collaboration, “Changes in the risk of death after HIV seroconversion compared with mortality in the general population”, JAMA 300 [2008]51-59). This article resembles the older one in its reliance on computer modeling to produce desired results; in addition, it displays astonishing ignorance of such HIV/AIDS basics as the latent period of 10 years between “infection” and illness; and it deserves a Proxmire Golden Fleece Award for discovering what was already known.

The methodology is described in laudable detail, which reminded me of the V-P who always got his requested budget because he submitted it as a computer print-out [Antiretroviral therapy has SAVED 3 MILLION life-years, 1 July 2008]; how many unqualified fools like me would rush in when Bhaskaran et al. talk of “the familiar Cox hazard ratio”, “Kaplan-Meier methods”, “Poisson-based model”, and use of Stata version 10 for the statistical analysis? Yet the weakness of the whole approach is separate from any possible technical flaws: assertions and assumptions are made that are demonstrably wrong. [Which is not to deny that specialists might well also question the applicability of any one or all of those mentioned techniques to this particular task. Specialists might also want more information than the statement that “The median duration of follow-up was 6.3 years (range, 1 day to 23.8 years), with 16 344 individuals (99%) having more than 1 month of follow-up” — what exactly does “follow-up” mean here? Were not all of these patients monitored throughout the study?]

Bhaskaran et al. ascribe to antiretroviral drugs the lower mortality in the HAART era compared to the pre-HAART era. It is at least equally plausible that this reduction in “excess mortality” was owing to the abandonment of high-dose AZT monotherapy. After all, deaths from AIDS in the United States about doubled from 1987 to 1990, and increased by more than another 50% from 1990 to 1995, dropping back then to 1987 levels (National Center for Health Statistics, Table 42, p. 236, in “Health, United States, 2007”; “HIV DISEASE” IS NOT AN ILLNESS, 19 March 2008; http://aras.ab.ca/news.html, June 30, “Disproof of HIV/AIDS Theory”).

Bhaskaran et al. themselves admit—albeit only in by-the-way fashion in concluding comments—that their analysis is rotten at the core: “it is likely that HIV-infected individuals in our study differ from the general population in other ways”. Yes indeed! Or rather, it’s not that the studied group (HIV-positives) is “likely” to differ in multiple ways from the “control” group (HIV-negative general population), it’s a certainty that they do. On the mainstream view of HIV/AIDS, HIV-positive people have been exposed to health risks that others have not, bespeaking significant behavioral differences. On my view and that of many others, “HIV-positive” is—like a fever—an indication that the immune system has reacted against something or other, that HIV-positive people have been exposed to health challenges that HIV-negative people have not. So differences in mortality between these two groups may have nothing at all to do with “HIV”.

The gross ignorance of HIV/AIDS matters displayed in this article is illustrated by the statement, also by-the-way in the concluding comments, that “race/ethnicity are also likely to differ among HIV-infected persons”. How could these authors not know that “HIV” is found disproportionately among people of African ancestry?

Here is a further illustration of incredible ignorance of HIV/AIDS matters: “Interestingly, we found that by 2004-2006, the risk of death in the first 5 years following seroconversion was similar to that of the general population . . . further research will be needed before our finding of no excess mortality in the first 5 years of infection in 2004-2006 can be generalized beyond those diagnosed early in infection”.
Almost from the very beginning, one of the salient mysteries about the lentivirus (slow virus) HIV has been the “latent period” between presumed infection by HIV and the appearance of any symptoms of illness. That latent period is nowadays agreed to be about 10 years. Therefore there should be no excess mortality at all for an average of 10 years after infection among people not being treated with HAART, and of course for much longer if HAART staves off AIDS. Unless, of course, “HIV” is causing death in symptom-less people, so that deaths from “HIV disease” during the latent period are deaths without apparent cause. It seems unlikely that such a phenomenon would long have gone unnoticed. Here is a typical representation of the supposed progression from infection to illness and death:

The death rate shown during the putative latent period is flat and runs along the baseline.

All this makes the authors’ modest admission that “Our study has some limitations” more than a little inadequate. The many obvious deficiencies in this article, notably the ignorance of latent period, reflect unkindly not only on the authors but also on the journal, its editorial procedures, and the lack of competence or diligence of the “peer reviewers” who presumably were engaged to comment expertly on whether this deserved to be published. What on earth has happened to medical “science”? Or was it always so defective in such obvious ways?

As to Golden Fleece Awards, there is the finding that “those exposed through IDU at significantly higher risk than those exposed through sex between males”. Yes indeed, drugs are not good for you! But then it has been routine among HIV/AIDS experts to discount the risks of illegal drugs by comparison to those of “HIV”, to the extent that there are continuing campaigns to provide drug addicts with fresh, clean, needles; and occasional surprise is expressed that injecting drug users typically have health problems [COCAINE AND HEROIN AREN’T GOOD FOR YOU! — a Golden Fleece Award, 13 June 2008]. In the end, do seem to be aware of this: “It is unlikely that HIV infection is the only factor leading to increased mortality rates among those exposed through IDU” because of, among other things, “the direct risks of substance abuse”.

No less surprising (to Bhaskaran et al., that is) than the poorer health of drug addicts is the finding that older people are less able than younger people to stave off health challenges: “Older age at seroconversion was associated with a higher risk of excess mortality . . . there was a clear gradient of increasing risk of excess mortality with increasing age at seroconversion”.
In other words, the older you are when you “seroconvert”—become infected, according to mainstream views, or encounter some sort of health challenge, according to Perth-Group-type views—the more likely you are to succumb, compared to people of the same age who have not encountered the same challenge. Who would have thought it?

Yet another finding worthy of attention was that “Females were at consistently lower risk [of dying] than males”. On the one hand, even most lay people are aware that women have a greater life expectancy than men (in most countries and in all developed ones). On the other hand, might not this finding with respect specifically to “HIV-positive” have stimulated some thought among the authors, whether this means anything specifically with respect to “HIV-positive” as signifying infection by a virus?

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Here, as so often, some of what I’ve written might appear to accept that HIV is infectious and causes illness. That is not so; I am merely pointing out that even on its own terms, the HIV/AIDS view would still be wrong about the claimed benefits of antiretroviral drugs: there is no evidence that they prolong life. At best, as Dr. Juliane Sacher has pointed out, they might bring a temporary benefit by acting as antibiotics, for they certainly are inimical to life.

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ACKNOWLEDGMENT: I am grateful to Fulano de Tal (a commonly used pseudonym, compare “John Doe”) who pointed out that an earlier version of this post included speculations based on US data that are irrelevant here since the CASCADE study includes only European cohorts. I also added the graph in response to one of “Tal”‘s comments, because I was not able to put the graph into my response.

Posted in antiretroviral drugs, experts, Funds for HIV/AIDS, HIV absurdities, HIV and race, HIV as stress, HIV does not cause AIDS, HIV varies with age, HIV/AIDS numbers, M/F ratios | Tagged: , , , , , , , , , , , , , | 20 Comments »

ANTIRETROVIRAL DRUGS: HISTORY AND RHETORIC

Posted by Henry Bauer on 2007/12/12

The previous post (BEST TREATMENT…, 10 December) mentioned these aspects of the official Treatment Guidelines:
—They change incessantly.
—The recommendations are based more on opinion than on scientific evidence.
—The available evidence is overwhelmingly about surrogate markers rather than patient health.
—The recommendations are so complex and change so often that physicians must suffer constant dilemmas over how to advise their patients.
Several further posts will examine aspects of these Guidelines in more detail, in particular, “side” effects of the drugs and conflicts of interest among those who draw up the Guidelines. First, however, a quick look back at how and why antiretroviral treatment began.

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Wainberg, in his single-minded lauding of “lifesaving” antiretrovirals (WAINBERG’S HAMMER, 5 December), suggested that “Many people had forgotten” what went on in the early days of AIDS. Wainberg himself seems to have forgotten the genesis and rationale of antiretroviral treatment.

In the early 1980s, small clusters of people were coming down, it seemed suddenly, with otherwise rare opportunistic infections, predominantly fungal ones; and death was following within months. There were two obvious possibilities as to cause: either some shared environmental exposure, activity, or lifestyle; or perhaps a previously unknown infectious agent.

The question was effectively settled by fiat rather than freely attained scientific consensus with the official announcement by the Secretary of Health and Human Services that HIV (then called HTLV-III) was the probable cause. Since that came from the prime source of research funds, those seeking grant support naturally framed their proposals in that vein. The immediate goal became to find an HIV-killer. A desperate rummage among all conceivable chemicals turned up AZT, a twenty-year old candidate for cancer chemotherapy that had never been used because it is too toxic. AZT seemed effective against HIV in the test-tube and, in brief trials, AIDS patients appeared to survive for several months on AZT treatment. Given that the prognosis for a person newly diagnosed with AIDS was death within months, an apparent extension of a few months was regarded as worthwhile. Moreover, activists were clamoring for rapid approval of anything that offered some hope, so AZT was approved without the evidence of “safety and efficacy” that was normally demanded before drugs were allowed into general use.

The situation nowadays is entirely different. Although HIV is still regarded as the agent causing AIDS, the official belief holds that there is an average period of about 10 years between infection with HIV and the first appearance of symptoms of illness. This is very different than expected death within months, and should–but apparently has not–set a very different basis for weighing possible benefits of treatment against the known risks from drug toxicity.

In point of fact, the official treatment guidelines of October 2006, introduced in the previous post (10 December), make abundantly clear the high risk of serious, indeed often fatal “side” effects of antiretroviral treatment. The risks and possible benefits are summarized in this way in the Introduction to those Guidelines (p. 10):

Potential Benefits of Deferred Therapy include:
—avoidance of treatment-related negative effects on quality of life and drug-related toxicities;
—preservation of treatment options;
—delay in development of drug resistance if there is incomplete viral suppression;
—more time for the patient to have a greater understanding of treatment demands;
—decreased total time on medication with reduced chance of treatment fatigue; and
—more time for the development of more potent, less toxic, and better studied combinations of antiretrovirals.
Potential Risks of Deferred Therapy include:
— the possibility that damage to the immune system, which might otherwise be salvaged by earlier therapy, is irreversible;
—the increased possibility of progression to AIDS; and
—the increased risk for HIV transmission to others during a longer untreated period.

A conspiracy theorist might wonder why this useful summary has been shifted in the December 2007 revision of the Guidelines to an inconspicuous place following Table 5 at the bottom of p. 58. Was it perhaps realized that having it up front is too unintentionally revealing of the grave and common risks associated with these drugs?

An analyst of rhetoric might point to a choice of words designed to play down the risks. Since the drugs supposedly do something good, the only reason not to use them is because of their harmful “side” effects; so “Potential benefits of deferred therapy” is a euphemism for “Treatment-associated risks”. Furthermore, those risks are spoken of in a rather masked way–“negative effects” on quality of life, “drug-related toxicities” instead of simply “drug toxicities”. The revealing need for “less toxic” drugs is inserted between the two hoped-for benefits of “more potent” and “better studied”. “Treatment demands” and “treatment fatigue” are euphemisms for the fact that a large proportion of patients find the “side” effects of antiretroviral treatment intolerable.

(Another common euphemism in mainstream discourse about antiretroviral drugs is “HIV lipodystrophy” or “HIV-associated lipodystrophy” for the dysfunctional distribution of body fat occasioned particularly by protease inhibitors. The drugs, not the HIV, are responsible for the lipodystrophy, but the terms in quotes are designed to give the opposite impression.)

In any case, the question nowadays is–or should be–whether the acknowledged, well known toxicity of all antiretroviral drugs calls for their use when people are not yet ill. It is highly pertinent here that the consensus in the United States asserts that “illness” warranting antiretroviral drugs can be diagnosed purely on the basis of laboratory tests, for example, CD4 cell counts below 200 (not to mention the HIV test itself!–see HIV TESTS: DANGER TO LIFE AND LIBERTY, 16 Nov ), whereas the consensus elsewhere, for instance in Canada, does not accept this as a conclusive marker of AIDS-illness.

A further, important datum not mentioned in these Treatment Guidelines is the fact that large numbers of HIV-positive people have lived healthy lives for a couple of decades or more without antiretroviral treatment. That was not known in the early days when an AIDS diagnosis presaged early death, and when HIV was first suggested as the culprit.

We cannot know, of course, how many HIV-positive people are quietly living healthy lives. People are rarely tested for HIV unless they are in high-risk groups or need medical attention for some reason. Official estimates that about one quarter or one third of HIV-positives don’t know their status implies that many of them suffer no ill effects from that condition–after all, about 1 million Americans have supposedly been HIV-positive steadily since the mid-1980s. The “long-term non-progressors” or “elite controllers” acknowledged in mainstream discourse have been estimated to number in the thousands, but this is surely an under-estimate because, again, only people with known risks tend to be tested; so these thousands represent chiefly high-risk non-progressors or controllers; there are likely to be a larger proportion of such people in low-risk groups. In addition and not usually acknowledged in mainstream discourse are those HIV-positive people who have eschewed treatment by their own decision; though many of them have joined in support groups, there is no reliable way to estimate their numbers, but it is certainly in the thousands.
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Drugs too toxic for cancer chemotherapy were approved for use at a time when a few months of extra life seemed a worthy objective. Infection by HIV is believed to produce no serious symptoms for an average of 10 years. Where is the rationale for feeding highly toxic medications to asymptomatic people? When moreover the mechanism by which HIV is supposed slowly or eventually to destroy the immune system is unknown? When it turns out that people being treated with these drugs are experiencing typical drug toxicities, and cancers, within the 10-year period during which it is officially acknowledged that HIV by itself on average does no harm?

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