Reading HIV/AIDS numbers

A Top Story at AIDSMEDS this week was:  “Tenofovir HIV prevention gel to be fast-tracked for FDA approval”. The success of the gel had been one of the most publicized highlights of the XVIIIth International AIDS Conference in July in Vienna: male-to-female HIV transmission had been cut by 39 percent.
Biased as I am to disbelief, I looked for reasons to cast doubts, and did not have far to look.
In the first place, of course, there is the question of what testing “HIV-positive” even means. Since the demography of “HIV” demonstrates that it isn’t infectious (see my book and many subsequent blog posts), any changes in apparent transmission need to be explained in other ways; however and unfortunately, the mainstream rarely reports the variables needed to construct such alternative explanations. One can then only deconstruct mainstream claims on their own terms. In the present instance, even the researchers acknowledge that their trial (CAPRISA 004) — a “proof of concept” study, not a full-fledged clinical trial of effectiveness — was too small, conducted in too few places, and had too low adherence (Quarraisha Abdool Karim et al., Science 329 [2010] 1168-74).
The gel was tested on 445 women while another 444 received a placebo gel. The total study cumulated to 1341 women-years, so an average of only about 18 months per woman. The “HIV infection” rates were 5.6/100 women-years using the tenofovir gel and 9.1/100 women-years using placebo. In other words, incidence rates of 5.6% and 9.1% respectively!
Even the study’s authors remark that this is extraordinarily high. Their only explanation, however, is that the study was carried out in the epicenter of the HIV/AIDS epidemic where prevalence rates are around 30%. But this entails absurd improbabilities: it would have taken only a bit over 3 years to reach that prevalence (9.1% being the normal rate, the control no-prevention rate in the study). Why is the prevalence then as low as 30%? These sexually active women had a median age of about 24 and a median age of “sexual debut” of 17.5; at 9% annual infection rate, why is the prevalence only 30%? And furthermore, why is there any population left alive, since this epidemic has been raging for more than a decade in absence of effective prevention or widespread antiretroviral treatment?
These numbers are simply not compatible with the theory that testing “HIV-positive” means the active presence of a deadly infectious agent.
The study also displays a “too good to be true” aspect in its details. The 889 enrolled women were randomized into treatment and control groups. Miraculously, those in the two groups behaved indistinguishably (dashed and continuous lines in the Figure below) as to use of condoms, adherence to use of gel, and even the number of sex acts per month and the rate at which this declined — from about 7.2 to about 3.1 — during the two years of observation:

That two groups of women should behave so similarly in 4 distinct respects seems most unlikely, doesn’t it? Would they also have such similar smoking and shopping habits, say?
And what about that marked decline in frequency of intercourse within a couple of years? The authors don’t discuss it. The pregnancy rate was 4%, far too low to explain such a drastic decrease in frequency of intercourse. The most obvious possible explanation, then, is that the women or their spouses found use of the gel — be it tenofovir-laced or placebo — so displeasing that they had sex less frequently. That would not augur well for the prospects of bringing something like this gel into general use.

Quite a few aspects of this study, then, do not inspire confidence, and seem at considerable variance from the ballyhoo that greeted the announcement of this preliminary and flawed little study. Though the plaudits and ballyhoo are substantively unwarranted, they are of course understandable from a psychological and sociological viewpoint, given that more than two decades have brought no success to mainstream ventures as to vaccines, microbicides, or effective and tolerable (non-toxic) treatment. Any slight sign of success is naturally welcomed with profuse and unrestrained overstatements.

On the other hand, the study’s introductory literature review is unexceptionable:
“The search for new technologies to prevent sexually transmitted HIV infection over the past three decades has had limited success. Only five of 37 randomized controlled trials, which tested 39 HIV prevention strategies, have demonstrated protection against sexual transmission of HIV infection . . . . The successful trials tested medical male circumcision . . . , sexually transmitted infection (STI) treatment in Tanzania . . . , and a HIV vaccine combination in Thailand . . . . Hence, HIV prevention technologies that women can use and control remain a pressing priority . . . . Over the last 20 years of microbicide research, none of the 11 effectiveness trials of six candidate products have demonstrated meaningful protection against HIV infection”.
Unexceptionable, that is, except for:
1. “Limited success” is euphemistic for “no success”.
2. The cited successes have not been replicated, and perhaps for that reason they have not been adopted, as any proven effective prevention surely would be.
3. Five successes out of 37 trials might well mean no actual successes. The criterion typically used, 95% confidence intervals or p ≤ 0.05, means that at least 1 in 20 apparent successes will be artefacts, occurring by chance; 2 successes in 37 trials would certainly be no better than chance. A Bayesian statistical approach, however, reveals that p ≤ 0.003 rather than p ≤ 0.05 is required to make the odds of being wrong only 1 in 20 (Matthews, “Significance levels for the assessment of anomalous phenomena”, Journal of Scientific Exploration, 13 [1999] 1-7).  So in 37 trials, one would reasonably expect significantly more than 2, perhaps something like 5 or even more, to be successful purely by chance, if the studies used the typical frequentist statistical analysis as a criterion rather than a Bayesian analysis. For a discussion of the flaws underlying frequentist p-value analyses that is accessible for non-specialists, I recommend very highly Robert A. J. Matthews, “Facts versus Factions: The use and abuse of subjectivity in scientific research”, European Science and Environment Forum Working Paper (1998), reprinted (pp. 247–282) in J. Morris (ed.), Rethinking Risk and the Precautionary Principle, Butterworth, 2000.

Avoiding life-saving treatment

Jonathan alerted me to the New York Times story, “Trying to follow the trail of missing AIDS patients” by David Tuller:
“More recently, however, studies have found that 15 to 40 percent of those who start treatment are lost to follow-up within one to three years. This unsettling trend has emerged at a difficult time; financing for treatment from the United States and other donors is not keeping pace with the rate of new infections, which has generated waiting lists for the lifesaving medications in some parts of Africa.”
The “more recent studies” are a 3-year-old article by Rosen, Fox, & Gill, “Patient retention in antiretroviral therapy programs in Sub-Saharan Africa: A systematic review”, PLoS Med 4(#10, 2007): e298
“Since the inception of large-scale ART access early in this decade, ART programs in Africa have retained about 60% of their patients at the end of 2 y. Loss to follow-up is the major cause of attrition, followed by death. Better patient tracing procedures, better understanding of loss to follow-up, and earlier initiation of ART to reduce mortality are needed if retention is to be improved. Retention varies widely across programs, and programs that have achieved higher retention rates can serve as models for future improvements.”

Evidently those models for attaining higher retention rates have had no effect during the intervening 3 years. Hardly the first time that expert predictions have failed, thereby providing welcome opportunities for more research.

I’ve often been struck by the extraordinary regularities in HIV/AIDS demography. “HIV-positive” rates vary by age, race, sex, and population density in the same manner in all tested groups in the USA, and the same regularities show up in other parts of the world, mutatis mutandis (e.g. the particularly high tendency for black women to test poz); see my book and many subsequent blog posts here. Not only has the rate of non-compliance with these “life-saving” drugs remained apparently the same in Africa for at least 3 years, it is about the same as the rate in Washington DC and other parts of the USA:
“In any given month, about 40 percent of the approximately 1,900 clients actively enrolled in the D.C. AIDS Drug Assistance Program (ADAP) are not utilizing antiretroviral medications. . . . [although] almost all of these ‘nonutilizers’ have active prescriptions for antiretroviral drugs written by their physicians, nurse practitioners or physician’s assistants. . . . ADAP programs across the country report similar rates of ‘nonutilizers’ (about 40 percent)” (Drug non-adherence, imaginary epidemics, and sexual nonsense, 2009/08/30).

Question:
Why would so many people reject life-saving treatment?
Especially given that it is free or nearly so?

Ask anyone in the street whether HIV causes AIDS and whether AIDS kills, and you won’t find many who disagree. Ask anyone in southern Africa whether HIV causes AIDS and whether AIDS kills, and you won’t find many who disagree. So this huge degree of non-compliance is not because of any lack of the “awareness” of the danger of HIV/AIDS that official propaganda has been spreading for these many years.

So, again, why do so many who believe that the drugs are life-saving refuse them?

Lies, Damned Lies, and Medical Science

That’s the title of an article by David H. Freedman in the November issue of  The Atlantic. Described is the work of John Ioannidis, who was very prominent in the news media in 2005 as a result of articles in PLoS Medicine and in JAMA that pointed out how frequently even highly cited claims and universally held beliefs about medical facts and practices turn out to be wrong.

In “Antiretroviral treatment benefits? from 3 MILLION to 1.2 million to …!?!”, posted  on 2008/07/18, I had cited a 1996 article by Ioannidis et al. that found prophylaxis against PCP had not increased lifespan: “no statistically significant reduction in the overall mortality of patients who received prophylaxis”.

The article by Freedman is well worth reading, if only to reassure AIDS Rethinkers that our claims, of basic mistakes by the orthodoxy, are highly plausible given how often such mistakes occur.

 

Testing and race

The good news:
“More than 70% of people getting care at a major Midwest clinical center had never been tested for HIV despite numerous encounters with the healthcare system”

How to make matters worse?
“The low numbers persisted despite 2006 CDC recommendations for universal HIV testing . . . . ‘there are no teeth in the recommendations and, in fact, in some states in the U.S. it’s still illegal to follow them, because you need informed written consent.’”
How long before a reason is found not to require informed consent? In the interests of public health, perhaps?
In the meantime, “a solution might be to make patient knowledge of HIV status a measure of quality of care”.

The orthodoxy has achieved something, though, if not yet universal testing. The incessant propaganda that minorities (blacks and Latinos) are especially at risk seems to be paying off:
“Black and Hispanic men were more likely to have been tested than white men, with odds ratios of 1.34 in 2008 and 1.41 in 2009. . . .
Black and Hispanic women were also more likely to have been tested than white women, with odds ratios of 1.46 in 2008 and 1.56 in 2009.”
So the absolute numbers of blacks and Hispanics testing “HIV-positive” will rise far more than those of white Americans, confirming the propaganda. And so the predictable results will be used for another twirl of the vicious cycle by which blacks and Hispanics will be subjected to toxic “medications” in ever-increasing numbers.
Yet that “HIV” tests are racially biased is known to anyone who has looked at the literature. No matter what the condition may be that produces a positive “HIV”-test-result — pregnancy, TB, whatever — blacks are 5-to-≥20 times more likely to test poz than are whites.
There will come a time when historians of medicine rank this episode with the Tuskegee and Guatemalan syphilis trials.

Worms are as smart as HIV!?

HIV possesses wondrous powers. Antibodies specific to it don’t neutralize it. Innumerable ingenious approaches to generating a vaccine have turned up no clue as to what might be effective against it. HIV exists as and mutates into an endless variety of clades, strains, sub-strains, and recombinant hybrid strains that evade immune responses and which, unlike other mutated pathogens, remain fully pathogenic. HIV kills the immune system by mechanisms so subtle that they have remained secret despite 25 years of investigation, and by mechanisms equally unknown it causes chronic inflammation, cause cancers of all sorts, and damages such organs as heart, kidney, liver. This is surely the cleverest pathogen evolution has produced — leaving us with a final puzzle of why it has not spread beyond the groups initially affected and why any human beings still remain alive.

But wondrous as HIV may be, in terms of resisting immune responses it is at least equaled by the worms that cause elephantiasis, which use human-made vaccines as a stimulus to ever greater spread:

“Parasitic worms can adjust their survival strategy based on their host’s immune response. This means potential vaccines against elephantiasis might make the infection spread more easily through communities.”

This should serve as a grave warning to the International AIDS Vaccine Initiative.  If they do ever come up with a vaccine that shows the slightest promise of guarding against “HIV infection”, you may be sure that “HIV” will capitalize on it to spread even further and faster.