HIV/AIDS Skepticism

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

Posts Tagged ‘James Chin’

Double-talk about multiple concurrent sexual relationships

Posted by Henry Bauer on 2010/02/10

It has become a shibboleth that the HIV/AIDS epidemic resulted from large networks, or overlapping sets of networks, of people engaged in multiple concurrent sexual partnerships. The basic reasons are that (1) the rate of observed apparent transmission of “HIV” is only a fraction of a percent per act of unprotected intercourse, hundreds of times lower than for common sexually transmitted infections like gonorrhea or syphilis or chlamydia or herpes (p. 46 in The Origin, Persistence and Failings of HIV/AIDS Theory), and (2) an epidemic means spreading to ever-increasing numbers of individuals, the inescapable criterion being that every person who gets infected must infect on average more than one other person within a rather short time.

James Chin, former epidemiologist for the World Health Organization and earlier for the State of California, has published calculations showing that the extent and rapid spread of the sub-Saharan epidemic can be explained only by postulating that 20-40% of the adult population there have been and are engaged in multiple concurrent sexual relationships with changes of partners weekly or monthly to the tune of as many as 100 in a given year (Table 5-1, pp. 64-5, The AIDS Pandemic).

The latest issue of AIDS and Behavior has 9 articles about this central issue of concurrent sexual relationships as a factor in spreading “HIV”, and a healthy diversity of views is represented. From the most outspoken skeptics:

“We would like to thank the authors for their comments on our article that questioned the amount and quality of the evidence to support the hypothesis that concurrent partnerships are a key driver of the HIV epidemics in Africa [8]. All three letters agree with us that we “raise some valid concerns” that the “evidence for this link is still somewhat limited” [10] and that further research is needed [3, 11]. We note further that the three letters were from the most vocal concurrency advocates, and do not necessarily represent mainstream opinion about the current state of knowledge on this important topic [7]. . . . In the end, the burden is on the advocates of concurrency to use empirical data to prove that concurrency is a driving force of the African HIV epidemics; thus far they have been unable to do so. Association and causation are very different levels of evidence, and our colleagues provide no convincing empirical evidence of causation” — Mark N. Lurie and Samantha Rosenthal “The concurrency hypothesis in Sub-Saharan Africa: Convincing empirical evidence is still lacking. Response to Mah and Halperin, Epstein, and Morris”, AIDS and Behavior, 14 #1 (2010) 34-7.

Another article reports that in Zambia “Thirteen percent of rural and 8% of urban men reported more than one ongoing relationship in 1998, and these proportions declined to 8% and 6%, respectively in 2003. The proportion of women reporting concurrent relationships was 0-2%” — Ingvild F. Sandøy, Kumbutso Dzekedzeke1, and Knut Fylkesnes “Prevalence and correlates of concurrent sexual partnerships in Zambia”, ibid.,  pp 59-71.

“HIV” prevalence in Zambia, at 16.5% a few years ago, is about midway between the lowest in sub-Saharan Africa (SSA) and the highest, the range being ~5% to >35% — “Deconstructing HIV/AIDS in ‘Sub-Saharan Africa’ and ‘The Caribbean’”, 21 April 2008.  That 16.5%  rate requires the sort of “fast-lane” multiple concurrency postulated by Chin, 20-40% of the adult population with up to 100 partners in any given year; yet the actual rate of multiple concurrency is far below that; <13% of men and <2% of women reported any concurrent relationship, let alone dozens or scores.

Altogether, the articles that postulate high rates of “concurrency” offer evidence only that people have had more than one sexual partner during a given period (which could mean serially, not necessarily concurrently) or at a given time; but even if half of a population had two partners simultaneously all the time, that would not begin to satisfy the criteria established by Chin’s calculations, which call for weekly or monthly exchange of partners to the tune of dozens or scores per year.

Again, the assertion that Africans do it differently than others is supported only by such weak claims as that, for example, “55% of men and 39% of women in Lesotho . . . reported having more than one regular partner in the previous year, as compared to 3 and 2% of men and 0.2 and 1% of women in Thailand and Sri Lanka, respectively” (Timothy L. Mah and Daniel T. Halperin, “The evidence for the role of concurrent partnerships in Africa’s HIV epidemics: A response to Lurie and Rosenthal”, pp. 25-8) — more than one in year, not excluding serially, is negligible in terms of Chin’s criteria; scores per year would be needed, not “more than one”.

On the other hand, a thoroughgoing survey of 59 countries had found “that the number of lifetime partners is lower in Africa than in industrialized countries, and that the prevalence of multiple partnerships is generally higher in industrialized countries. In addition, more men and women in Africa are sexually abstinent, with two-thirds of the population reporting recent sexual activity compared to three-quarters of the population in industrialized countries. . . . on average, African adults are less sexually active and have fewer lifetime partners than their counterparts in industrialized countries” —  Mark N. Lurie and Samantha Rosenthal, “Concurrent partnerships as a driver of the HIV epidemic in Sub-Saharan Africa? The evidence is limited”, pp. 17-24, citing Wellings et al., “Sexual behavior in context: A global perspective”, Lancet 368 [2006] 1706-28; 369 [2007] 557. Several more references to that same effect are
Brewer et al., “Mounting anomalies in the epidemiology of HIV in Africa: cry the beloved paradigm”, International Journal of STD & AIDS 14 [2003] 144-7;
Gisselquist et al., “HIV infections in sub–Saharan Africa not explained by sexual or vertical transmission”, International Journal of STD & AIDS 13 [2002] 657-66;
McCulloch, “The management of venereal disease in a settler society: colonial Zimbabwe, 1900-30”, Chapter 9, 195-216 in Histories of Sexually Transmitted Diseases and HIV/AIDS in Sub–Saharan Africa, ed. Setel et al., Greenwood 1999.

The mere fact that there is such a healthy to-and-fro between these articles demonstrates that, after more than two decades of intensive study, it remains controversial whether multiple concurrent sexual relationships can account for the purported level of HIV/AIDS in Africa — or elsewhere, because the shibboleth has been used also to rationalize the higher rate of “HIV-positive” among African Americans.

It is interesting to note that none of the 9 articles arguing over concurrency and published in 2010 so much as mention Chin’s book, which had been published 3 years earlier and which quantifies the level of concurrency and multiplicity required to account for an epidemic of African proportions. That omission makes it possible to overlook that all the asserted evidence for concurrency falls very far short of what would be necessary to explain the prevalence of “HIV” in Africa and among African Americans.

Not having to deal with numbers makes it easier also to offer hand-waving “explanations” whose plausibility rests on subterranean racist stereotypes about African sexual behavior — “Racist stereotypes are inherent in HIV/AIDS theory”, 2010/02/08.

AIDS and Behavior, like other mainstream journals, is of course peer-reviewed. How well peer review can work is illustrated by this total ignoring of perhaps the most central publication on this topic, written by an experienced epidemiologist who has held high office in HIV/AIDS-related organizations.

Posted in clinical trials, experts, HIV and race, HIV risk groups, HIV transmission, HIV/AIDS numbers, prejudice, sexual transmission | Tagged: , , , , | 2 Comments »

Racist stereotypes are inherent in HIV/AIDS theory

Posted by Henry Bauer on 2010/02/08

“HIV” is spread primarily through sexual intercourse, according to official dogma. Particularly as a result of promiscuity, carelessness, irresponsibility in sexual behavior.
Africans and African Americans test “HIV-positive” at rates far exceeding those of any other identifiable racial group, and they do so in every social and economic sector: among repeat blood donors, pregnant women, gay men, newborns, military cohorts, applicants for marriage licenses, in prisons, in hospitals . . . . (see, for example, Tables 6-8, 10, 21, 22, 28 in The Origin, Persistence and Failings of HIV/AIDS Theory). Caribbean “Hispanics”, who have on average much African ancestry, test “HIV-positive” at a higher rate than Mexican “Hispanics” who have on average little African ancestry (pp. 71-3, ibid.).

A natural inference, a straightforward syllogism, leads to the conclusion that people of relatively recent African ancestry are, anywhere and everywhere, genetically predisposed to be carelessly and irresponsibly sexually promiscuous to a greater extent than other human beings. (“Relatively recent” means in the last couple of hundred thousand years, because ALL human beings are of African ancestry before that relatively recent diaspora of Homo out of Africa. So one has to postulate that such a purported genetic predisposition evolved during this recent period.)

If that conclusion seems obviously and absurdly wrong, as it does to me, then there’s something wrong with one or both of the first two parts of the syllogism: Either blacks do NOT always test “HIV-positive” significantly more often than others, or “HIV” is not spread primarily through sexual intercourse.

But the truth of one part of the syllogism is not controversial: Blacks do always test “HIV-positive” significantly more often than others. That’s mentioned frequently in publications of the Centers for Disease Control and Prevention (CDC) and elsewhere, for example:
“In 2006, blacks made up 12% of the population aged >13  years but accounted for 46% of the number of persons  estimated to be living with HIV (1). Both the estimated  HIV  prevalence  and  incidence  rates  for  black  men  and  women were higher than those for any other racial/ethnic  population (1,2). Among black males, male-to-male sexual  contact accounted for 63% of new infections; among black  females, high-risk heterosexual contact accounted for 83%  of new infections (3) . . . .
during  2004–2007,  85% of diagnoses of perinatal HIV infection were in blacks or  African Americans (69%) or Hispanics or Latinos (16%). The  average  annual  rate  of  diagnoses  of  perinatal  HIV  infection  during 2004-2007 was 12.3 per 100,000 among blacks, 2.1 per  100,000 among Hispanics, and 0.5 per 100,000 among whites” (Morbidity and Mortality Weekly Report 59[4], 5 February 2010).

That leaves only these possibilities: Either “HIV” isn’t spread primarily through sex, or blacks are, anywhere and everywhere, irresponsibly sexually promiscuous to a significantly greater extent than others — including among women and among gay men, and even among repeat blood donors, who are normally regarded as being the most tightly screened against all sorts of infections and thereby screened against unhealthy behavior. The incredible degree of postulated promiscuity is illustrated by the calculation performed by James Chin, former epidemiologist for the World Health Organization: To explain the asserted prevalence of “HIV” in sub-Saharan Africa, one has to accept that 20-40% of all sexually active adults have several sexual partners simultaneously and change them frequently enough that, in the course of a year, each has as many as 100 different partners (pp. 64-65 and elsewhere in The AIDS Pandemic).

When I first noted this conundrum, these inexplicable racial differences in testing “HIV-positive”, I had asked the CDC about it; and I had been flabbergasted at their response, that “The ‘characteristic differentiation by race’ that you note is compatible [emphasis in original] with a behavioral explanation” (p. 75 in The Origin, Persistence and Failings of HIV/AIDS Theory). CDC was apparently willing to accept as accurate the traditional racist stereotype of irresponsibly promiscuous sexual behavior by black people.

But it’s not just common sense or politically correct thinking that rejects that stereotype, the latter is demonstrably refuted by actual observations and studies that have found African Americans and Africans are if anything LESS likely than Caucasians to indulge in sexual excesses; I give a few references for that conclusion in chapter 7 of The Origin, Persistence and Failings of HIV/AIDS Theory.

Empirically speaking, then, one has the following:
Black people test “HIV-positive” much more often than others, irrespective of region or social or economic factors — irrespective, in other words, of cultural factors.
Black people are not significantly more sexually careless and promiscuous than others.

Therefore, testing “HIV-positive” is not in general the result of sexual behavior.

Why then do black people test “HIV-positive” much more often than others?

As Ruth Benedict pointed out long ago, there is nothing racist about acknowledging that there are physical and physiological differences associated with the generally recognized racial groups; that just reflects that some genes that influence physiology are often associated strongly with some genes that influence hair color, skin color, eye color. The racial disparities in testing “HIV-positive” simply reflect some racial difference in physiology [“Racial disparities in testing ‘HIV-positive’: Is there a non-racist explanation?”, 4 May 2008].

That conclusion entails, of course, that testing “HIV-positive” is not necessarily an indication of infection by the putative “HIV”. That’s well known to AIDS Rethinkers, though it is not part of the conventional wisdom. Still, it’s plain enough from the technical literature, which reports “false positives” from such events as vaccinations and a host of other conditions (Christine Johnson, “Whose antibodies are they anyway? Factors known to cause false  positive  HIV  antibody  test  results”, Continuum 4  [#3,  Sept./Oct. 1996]).

It remains to be explored, what precisely the race-associated physiological factors may be that conduce to testing “HIV-positive”. One was already cited in my book (p. 100), that blacks react more strongly than others to the antigen p24, p24 being one to which “HIV” tests are sensitive (for example, the 4th generation rapid HIV diagnostic test, Determine® HIV 1/2 Ag/Ab Combo, marketed by Inverness Medical for “separate detection of HIV p24 antigen . . . . During HIV infection, the p24 antigen is produced during the first few weeks . . . . excellent sensitivity of 100% for patients at chronic stage of infection and a specificity of . . . 99.66% for. . . HIV-1 p24 antigen”).
Tony Lance has gathered many references that illustrate the connection between intestinal dysbiosis and testing “HIV-positive”, and he has found a host of publications connecting disturbances of the vaginal microflora in women to both pregnancy and testing “HIV-positive” (for example, Shin & Kaul, “Stay It with Flora: Maintaining Vaginal Health as a Possible Avenue for Prevention of Human Immunodeficiency Virus Acquisition”, J. Infect. Dis. 197 [2008] 1355-7). Recently Tony drew to my attention a report of racial disparities in bacterial vaginosis (BV) that run parallel to racial disparities in testing “HIV-positive”:
“Curiously,  the  incidence  of  BV  varies markedly among racial and ethnic groups (Rajamanoharan  et  al.,  1999;  Royce  et  al.,  1999),  ranging from 6% in Asians and 9% in whites, to 16% in Hispanics  and  23%  in  African  Americans.  The reasons for differences in the incidence of BV among racial  groups  are  unknown,  but  they  cannot  be explained  by  differences  in  socio-demographics, sexual  activity,  health  behavior  or  hygiene alone (Goldenberg et al., 1996; Royce et al., 1999)” [emphasis added; Xia Zhou et al., “Differences in the composition of vaginal microbial communities found in healthy Caucasian and black women”, The ISME Journal, 1 [2007] 121-33).
Goldenberg  et al. (1996). “Bacterial colonization of the vagina during pregnancy in four ethnic groups. Vaginal infections and prematurity study group”. Am J Obstet Gynecol 174: 1618-21.
Rajamanoharan et al. (1999). “Bacterial vaginosis, ethnicity, and the use of genital cleaning agents: a case control study”, Sex Transm Dis 26: 404-9.
Royce et al. (1999). “Race/ethnicity, vaginal flora patterns, and pH during pregnancy”, Sex Transm Dis 26: 96-102.

At any rate, there is nothing implausible about racial differences in physiology, and there are reports that connect such racial differences to a greater tendency for testing “HIV-positive” among Africans and African Americans.

That racial differences in testing “HIV-positive” are not the result of differences in behavior is indicated independently and more directly by the manner in which “HIV” tests are calibrated: the calibration itself builds in a racial bias. The “null” reading — “HIV-negative” — is based on “normal controls” who are presumed to be uninfected; and the population from which such controls are drawn are repeat blood donors, since those are routinely screened for a variety of infections and represent people least likely to be “HIV-infected” (Weiss & Cowan, see “HIV” tests are demonstrably invalid, 19 May 2009). But with tests calibrated in this manner — initially in the United States, and all subsequent tests are based on those — it turns out that repeat blood-donors of different racial groups test “positive” at significantly different rates: African-American blood donors tested “HIV-positive” 14 times more often than white American blood donors, and in Africa the ratio was 23 (pp. 51 and 76 in The Origin, Persistence and Failings of HIV/AIDS Theory).
Now, blood donated by repeat blood-donors of every race is screened in the same fashion. There is no basis for rejecting repeat blood-donors who are black as inherently more likely to harbor undetected infections. The obvious conclusion to be drawn is that “HIV” tests ought to be calibrated separately for every identifiable group in which, using the presently available tests, repeat blood-donors react at a significantly different rate than the overall average. As it stands, however,

“HIV” tests are racially biased
and
overestimate “HIV infection” among blacks
by a large factor

If tests were calibrated separately for each racial group, the prevalence of “HIV-positive” in sub-Saharan Africa might well turn out to be little if at all different from the prevalence elsewhere. A hint in that direction is that in many countries the rate of “HIV” prevalence among blood donors parallels the overall rate in the country (Sedyaningsih-Marnahil et al., “The use of blood donor data for HIV surveillance purposes. A global perspective”, Int Conf AIDS, 7-12 July 2002; 14: abstract no. WeOrC1268).

The present willingness on the part of HIV/AIDS theorists and the media — thereby inscribed into the conventional wisdom — to accept a behavioral explanation for racial disparities in testing “HIV-positive” illustrates that racist stereotypes about sexual behavior remain deeply albeit subconsciously ingrained, and that such subterranean ideological racism influences interpretations and activities by such agencies as the Centers for Disease Control and Prevention.

Posted in experts, HIV absurdities, HIV and race, HIV risk groups, HIV skepticism, HIV tests, HIV transmission, HIV/AIDS numbers, prejudice, sexual transmission, uncritical media | Tagged: , , , , , | 24 Comments »

Not with a bang but a whimper

Posted by Henry Bauer on 2009/12/27

This is the way the world ends
Not with a bang but a whimper.

That’s the conclusion of one of T. S. Eliot’s best known poems, “The Hollow Men”, which begins,

We are the hollow men
We are the stuffed men
Leaning together

End and beginning seem very appropriate respectively to HIV/AIDS theory and to its creators. Those creators and their camp followers lean together, excluding any evidence that doesn’t fit their theory; they are empty of any wider perspective than their little bailiwick, and their failure to respond to substantive criticism makes all their statements hollow; and they are certainly stuffed: with self-importance and with dollars from drug companies and research agencies.

There’s been much speculation over the years as to when and how this house-of-cards theory will implode: Will it be with a bang when a Congressional Committee asks what we’re getting for $20 billion a year? Or why HIV tests are used to diagnose HIV infection despite the fact that  those tests are not able to do so and are not officially approved to do so? Or why a greater number of serious adverse non-AIDS events than “AIDS” events strike and kill people who are given the benefit of “life-saving” antiretroviral drugs?
Or will it end with a whimper, as HIV/AIDS fades even further into public indifference? — as it already has begun to do in the developed world, where not many besides grant-receiving researchers and politicians take it seriously.

Presaging a whimpery implosion may be this recent piece in the British Independent newspaper:

“Aids: the pandemic is officially in decline . . . . UN and World Health Organisation hail steep fall in number of new HIV infections” (2009/11/25, by Health Editor Jeremy Laurance)

The failure of the media to trumpet this article’s obvious implications is of a piece with the media’s failure to ask how HIV/AIDS theory could be compatible with a 25-90% “HIV infection” rate in African armies (South Africa needs Donald Rumsfeld, 15 December 2009):

“The HIV pandemic which started 28 years ago is officially in decline . . . . The number of new HIV infections peaked in the mid-1990s and has since declined by almost a third, according to the annual update on the pandemic for 2009, published yesterday by the Joint United Nations programme on HIV/Aids (UNAids) and the World Health Organisation.
It is the first time that UNAids and the WHO have confirmed that the pandemic is on a downward trend and represents a landmark in the history of the disease. In their 2008 report, they said suggestions the epidemic had peaked were ‘speculation’ and that it was ‘difficult to predict the epidemic’s future course’” [emphasis added].
The number of new infections peaked about 13 years ago, yet by last year the official gurus had not yet admitted it?! That certainly inspires confidence in anything that those official gurus have to say on the subject.

“‘The latest epidemiological data indicate that globally the spread of HIV appears to have peaked in 1996 when 3.5 million new infections occurred. In 2008 the estimated number of new HIV infections was approximately 30 per cent lower than at the epidemic’s peak 12 years earlier.’”
OK, in 2008 there were 30% fewer than in 1996. How many fewer than in 1996 were there in 2007? Was the difference not statistically significant, so that the gurus did not need to admit it? In which case the drop would have had to be nearly 30% in the single year from 2007 to 2008; the likelihood of that is easily equal to that of all the other extreme absurdities that HIV/AIDS aficionados seem able to swallow without even a grain of salt. Why were the gurus still calling it “speculation” a year ago, that the pandemic had peaked a dozen years earlier? Is a dozen years the latent period required to overcome cognitive dissonance on the part of HIV/AIDS believers?

“in sub-Saharan Africa — the worst-affected region — new infections in 2008 were ‘approximately 25 per cent lower than at the epidemic’s peak in the region in 1995’.”
In the meantime, since 1995, the population had grown appreciably and the supply of antiretroviral drugs has been far below what was needed to decrease the infection rate, according to the (ir)responsible officials. What on Earth can then explain this decline in heterosexual transmission of a sexual infection in a region where 20-40% of the adult population is used to having several partners at the same time and changing them frequently? (James Chin, “The AIDS Pandemic”, calculated that this level of promiscuity is needed to explain the numbers — the estimated numbers — disseminated by UNAIDS over the years; James Chin, former epidemiologist for the World Health Organization, that is.)

“Despite the fall in new infections, the number living with HIV increased last year to 33.4 million as people are surviving longer with the roll-out of antiretroviral drug treatment. Greater access to drugs has helped cut the death toll by 10 per cent over the past five years.”
Of course one must not forget the continuing need for more resources, so the overall increase in “HIV-positive” persons must be reiterated. But one should also bear in mind that all these numbers come out of computers, not from data “on the ground”. The increase to 33.4 million is a computerized guess, just like the guess of 33 million a couple of years ago, reduced at that time from an earlier computerized guess of 40 million; all these guesses are just as reliable as you would expect from gurus who can recognize a 30% decline after 13 years but not a decline of 25% or more after 12.
Not only that, these gurus are somehow able to discern that the “roll-out” of antiretroviral drugs is the reason for the purported — guessed, believed, held on faith — increase in survival and lower death rate. I’ve noted before that HIV/AIDS theory satisfies the criteria for pseudo-science usually directed at parapsychology; so perhaps the gurus discerned these reasons by extrasensory perception? But they didn’t really need that. Like the number of infections, that death toll is not a count, it’s a computer output; and THE COMPUTER COULD NOT HAVE SPAT THAT OUT UNLESS IT WAS PROGRAMMED IN A WAY THAT WOULD SPIT OUT SUCH A PURPORTED INCREASE IN SURVIVAL; and of course the computer model includes the assumption of benefit from antiretroviral treatment.
Any computer model is captive to the assumptions built into it. In South Africa, the registration of deaths is better than 50% complete; the official count of annual AIDS deaths has been on the order of 10,000-15,000 for the last half-a-dozen years; but UNAIDS’ computers have been estimating on the order of 300,000 AIDS deaths annually, a factor of 20 greater than the actual count; see — from the Statistician General of South Africa — Lehohla P.: (2005) Difficulties in attributing deaths to HIV/AIDS.
There’s not even need for the Statistician General of South Africa to point out that UNAIDS numbers are unbelievable, UNAIDS does it by and for itself. Its report for 2009 states, “Greater access to drugs has helped cut the death toll by 10 per cent over the past five years”; yet in the 2008 report, AIDS deaths in sub-Saharan Africa were given as 1.3 million for 2001 and 1.5 million for 2007, an INCREASE of 15% in 6 quite recent years. Did the number shoot up rapidly from 1.3 million in 2001 to 1.56 million in 2003 so that “in the last five years”, by 2008, it could decline by 10% to 1.4 million?

“There are now 4 million people on the drugs worldwide, a 10-fold increase in five years. The report says 2.9 million lives have been saved since effective treatment became available in 1996 but less than half the patients who need them are currently getting them.”
Again: Doesn’t anyone THINK about these numbers?
Since 4 million are now getting the lifesaving drugs, why have not 4 million lives been saved? (Clue: the 2.9 million is a computerized guess based on innumerable assumptions and extrapolations to decades in the future.)

Parenthetically, note that “effective treatment became available in 1996”, which acknowledges that before 1996 the treatments were NOT effective. Yet when AIDS Rethinkers state directly that for a decade AZT was killing rather than curing, the AIDS apologists and the AIDS vigilantes will insist that AZT and its ilk were quite appropriate treatments; at best they may say, like Daniel Kuritzkes, “in retrospect the dose we started with, with AZT, was a dangerous and poorly tolerated dose”. Nothing wrong with AZT so long as the right dose is used, according to Kuritzkes. Same with arsenic, of course, or any other poison.

“The reasons for the decline in new infections are disputed.”
And well they might be. Any claim to have effected behavioral change among adults, 20%-40% of whom have an established tradition of high promiscuity with continually changing partners, ought to be based on some rather concrete evidence; for a priori, one might be inclined to doubt the efficacy of “sex education, HIV awareness campaigns and distributing condoms”, given, for instance, the failure of such programs to curb pregnancies among unwed teenagers in the United States. What we’re offered instead of substance is a pabulum of unsupported self-serving assertions:
“We have evidence [not revealed, however] that the declines we are seeing are due, at least in part, to HIV prevention. However, the findings also show that prevention programming is often off the mark and that, if we do a better job of getting resources and programmes to where they will make most impact quicker, progress can be made and more lives saved.”
But one might hesitate to provide more funds given that “Ties Boerma, a WHO statistics expert, said countries whose HIV prevalence declined dramatically, like Zimbabwe, were not always those that got the most HIV cash”, which would indicate that the interventions have not done any good. But don’t let facts get in the way of self-interested propaganda.

Perhaps the whimpering fade into neglect of HIV/AIDS theory will be hastened by those who have long been asking why more aid is not being directed into Africa’s more salient ills:
“Philip Stevens of International Policy Network . . . said with HIV declining it was time to rethink global spending priorities . . . . Globally, HIV causes about 4 per cent of all deaths, but gets [23% of what is] spent on development aid for health  . . . . In most countries HIV is a relatively minor problem compared with other conditions such as malaria and diarrhoeal disease” [emphasis added].

Those vested in HIV/AIDS careers will not retrench willingly, of course:
“Dr Karen Stanecki, senior adviser to UNAids, said repeated studies in different parts of the world, comparing the reduction in new infections with what happened where there was no intervention, had demonstrated the effectiveness of prevention programmes. ‘The decline was over and above the natural decline in the epidemic. They showed it could only have been explained by behavioural change.’”
So there was already a natural decline of the epidemic?
Connoisseurs of statistical legerdemain will recognize “could only have been explained by behavioural change” as a rather desperate and wishful assertion that could not possibly be based on concrete observational evidence and competent statistical analysis. Since there was already a natural decline, cause unknown and therefore unpredictable in future magnitude, how could it then be calculated that the rate of this natural decline had been substantially augmented by “intervention”?

Posted in antiretroviral drugs, experts, Funds for HIV/AIDS, HIV absurdities, HIV does not cause AIDS, HIV skepticism, HIV transmission, HIV/AIDS numbers, sexual transmission, uncritical media | Tagged: , , , , , , , , , , , , | 10 Comments »

Outsourced testing by the Centers for Disease Control and Prevention?

Posted by Henry Bauer on 2009/10/23

The Centers for Disease Control and Prevention have been lobbying for universal “HIV” testing; they appear to have outsourced successfully to India and UNAIDS:

Soon, mandatory for pregnant women in India to undergo HIV test
NEW DELHI: Passing AIDS from mother to child is a human rights violation and soon all pregnant women in India will have to undergo a mandatory HIV test, the parliamentary forum on HIV and AIDS said on Friday. . . . [T]he forum met UNAIDS executive director Michel Sidibe Thursday and discussed the issue with him. . . . Sidibe, on his first visit to India, has held a series of meetings with government authorities. He has emphasised the role of the political leadership in ensuring that the country’s universal access goals to HIV prevention, care and treatment are achieved” [emphasis added].

Note that Sidibe heads the institution, UNAIDS, which has persistently overestimated HIV/AIDS numbers, as attested by the former epidemiologist for the World Health Organization, James Chin (The AIDS Pandemic). A few years ago, UNAIDS had implicitly acknowledged this when it reduced its estimates for India by more than 50%.

The assertion that something is a human rights violation is becoming so common that it will soon lose its force, if it hasn’t already.

It’s a perpetual irritation for me that people high and low declaim with dogmatic assurance about things they don’t understand. Almost everyone who learns that I was a chemistry teacher conjures up memories of “hating” chemistry, not understanding it, finding it removed from anything relevant to daily life — even as these same people will carry on about proteins and minerals and vitamins needed in the diet. An increasingly common expression is “carbon footprint”: how many of those who utter it, I wonder, could explain exactly what it means? Not so long ago, the heads of umpteen governments warned of disasters ahead if we did not curb carbon emissions: how many of them, I wonder, could state even approximately the relative contributions to global warming exerted by water vapor, methane, and carbon dioxide?

The proliferation of ignorant assertions about HIV/AIDS is far from a unique phenomenon. Nevertheless it remains deplorable that the executive director of UNAIDS should not know that pregnancy carries the risk of testing “HIV-positive” in absence of contact with any conceivable source of “HIV infection” (Why pregnant women tend to test “HIV-positive”, 5 October 2009).

Posted in experts, HIV in children, HIV risk groups, HIV tests, HIV transmission, uncritical media | Tagged: , , | 12 Comments »

Science Studies 103: Science, Truth, Public Policy — What the CDC should know but doesn’t

Posted by Henry Bauer on 2008/09/04

For decades, politicians have increasingly taken expert scientific advice as a guide to public policy. That’s wonderful in principle, but not necessarily in practice, because outsiders don’t understand that the experts’ advice is based on scientific knowledge, which is always tentative and temporary; scientific theories have a limited lifetime. It’s a widespread illusion, with seriously debilitating consequences, that “science” is synonymous with “truth”.

Not that anyone would, if asked, admit that they believe that science = truth; but observe how science is commonly talked about. If we want to emphasize that something really is so, we say it’s “scientific”. If we want to denigrate something as being untrue, we call it “unscientific”; or if we want to be nasty, we say it’s “pseudo-scientific”. “Tests have shown that …” somehow doesn’t seem convincing enough, so we say, “Scientific tests have shown …”, and then we need no longer fear any contradiction.

Policy makers ought to know that advice from scientific experts is fallible. Much public policy has to be based on judgments in situations where the facts are not certain, and decisions have to be made about possible benefits balanced by possible drawbacks. Therefore

the prime responsibility of technical experts
whose advice informs politicians
is to make as clear as possible
the uncertainties in what they think they know
.

Otherwise, policy is influenced by judgments made unconsciously by the technical experts, who may see the trees fairly well but who are usually ignorant about the forest.

For example, when the Centers for Disease Control and Prevention (CDC) publish estimates of something, their responsibility is to make plain, indeed to emphasize, the limits of uncertainty in those estimates. This the CDC singularly and repeatedly fails to do; for example, it issued a press release in 2005 that HIV infections has surpassed 1 million “for the first time”, when it had already released estimates of about 1 million throughout the previous twenty years (p. 1 in The Origin, Persistence and Failings of HIV/AIDS Theory).

This post was prompted by the brouhaha following CDC’s recent announcement that its earlier estimate of about 40,000 annual HIV infections had been too low, its new estimate being 56,000. CDC was hardly a shrinking violet with this revision: “The new data is [sic] scheduled for publication in the peer-reviewed Journal of the American Medical Association. The report’s release is meant to coincide with the opening Sunday of the biannual International AIDS Conference in Mexico City, Mexico.”
“Dr. Kevin Fenton, director of the CDC’s National Center for HIV/AIDS, Viral Hepatitis, STD and TB Prevention”, proclaimed that “‘The fact that 56,000 Americans each year are contracting HIV for the first time is a wake-up call for all of us in the U.S.’ . . . [CDC] is now using technology capable of determining when someone was infected. The new method can indicate whether someone has been infected with HIV during the previous five months, rather than relying on statistical models. Diagnosis of HIV can occur years after infection”.

News accounts do not always reflect accurately, of course, what a speaker or a press release says, but in this instance it was evidently something that could easily lead a listener or reader to believe that some “new method” had supplanted “statistical models” — which is entirely untrue. A few media accounts did mention that this new number is simply a revised estimate, not a claim that the rate of HIV infections has been on the increase. What none of the media accounts that I have seen has pointed out is how fraught with assumptions and uncertainties this new estimate is, and how wrong are the conclusions of this “new method” when tested against reported “HIV” numbers from earlier years. Figure A shows what the CDC’s “new method”, combined with its computer-statistical model, “predicts” new HIV infections to have been since before the beginning of the AIDS era (source: Hall et al., “Estimation of HIV incidence in the United States”, JAMA, 300 [2008] 520-529).

Figure A

I’ve highlighted several clues to how uncertain all this is, though the clues are not hard to recognize. What is not at all uncertain, though, is that the estimates given in this Figure are totally at odds with data-based estimates of HIV infections during at least the first decade of the AIDS era.

From the Y-axis scale, Figure A yields the numbers in Table A, column I. Column II lists the AIDS deaths during the relevant periods (from “Health, United States”  reports ). Column III is the net estimated prevalence, namely, the cumulation of annual new infections in Column I minus the deaths. Column IV lists earlier estimates from official reports and peer-reviewed articles. The CDC’s “new method” combined with their computer-statistical model constitutes a drastic re-writing of history. And just as the Soviet Union rewrote history all the time without mentioning the old version — let alone explaining what was wrong with it —, CDC fails to mention the numbers it and peer-reviewed articles had propagated during the 1980s and 1990s.

Those earlier estimates in Column IV had been made in a quite straightforward manner. The actually measured rate of testing “HIV-positive” in various groups was multiplied by the size of each group. Military cohorts, blood donors, and Job Corps members were routinely tested. Sentinel surveys had been carried out in hospitals and a range of clinics, and special attention had been paid to sampling homosexual men and injecting drug users. The only uncertainty was in estimating the sizes of the various groups, but good information was available about most of those, and moreover there was a National Household Survey that provided a good check on what is typical for the general population overall. Persistently over two decades, the result was an approximately constant prevalence of something like 1 million.

That fact is incompatible, however, with HIV/AIDS theory, which insists that “HIV” somehow entered the USA in the late 1970s. Naturally, the CDC’s model incorporates that assumption even though it remains unproven and is incompatible with surveillance of HIV infections since 1985. Now CDC continues its attempt to shape public policy with numbers derived from a model whose validity is not merely uncertain, it’s demonstrably invalid.

That seems incredible, but Science Studies once again offers insight. The modelers know they are “just” modeling, trying to establish the best possible algorithms to describe what’s happening. In their publication, they scrupulously set out all the assumptions made in this latest set of calculations; indeed, almost the whole text of the article describes one assumption after another. The failure to discuss how incompatible the model is with data from 1985 through the late 1990s is, plausibly, because the authors are not even aware of those earlier publications — they’re working on this particular model, that’s all. The blame, if any, should be directed at the administrators and supervisors, whose responsibility it is to know something about the forest, and most particularly about the CDC’s responsibility to the wider society: not to arouse panic without good cause, for example; to ensure that press releases are so clear to lay people that the media will not misrepresent them. But CDC big-shots, like bureaucrats in other agencies, suffer inevitable conflicts of interest: they want to attract the largest possible funding and to gain the highest possible public appreciation, esteem, prestige. That’s why, in the early days of AIDS, the CDC had hired a PR firm to convince everybody that AIDS was a threat to every last person, even as they knew that it wasn’t (Bennett & Sharpe, “AIDS fight is skewed by federal campaign exaggerating risks”, Wall Street Journal 1 May, 1996, A1, 6.)

At any rate, this latest misleading of the public, seemingly not unintentional, is far from unprecedented. The crimes and misdemeanors of CDC models are legion; see, for example, “Numbers”, “Getting the desired numbers”, and “Reporting and guesstimating”, respectively p. 135 ff., p. 203 ff., and p. 220 ff. in The Origin, Persistence and Failings of HIV/AIDS Theory). Consider the instance in Table B of CDC-model output that was wildly off the mark. The modelers had seen fit to publish this, as though it were somehow worthy of attention, when the calculated male-to-female ratios for “HIV-positive” are completely unlike anything encountered in actual HIV tests in any group for which such data had been reported for the previous dozen years.

Not that WHO or UNAIDS models are any better, as James Chin — who designed and used some of them — has pointed out cogently (“The AIDS Pandemic”).  Jonathan Mann was one of the first international HIV/AIDS gurus, responsible for authoritative edited collections like “AIDS in the World II: Global Dimensions, Social Roots, and Responses” (ed. Jonathan A. Mann & Daniel J. M. Tarantola, Oxford University Press, 1996) . In that volume, the cumulative number of HIV infections in the USA is confidently reported as in Table C below. On the one hand, I give Mann et al. high marks for restricting themselves to 4 significant figures and avoiding the now-standard HIV/AIDS-researchers’ penchant for giving all computer outputs to the nearest person. On the other hand, their estimates are in total disagreement with those based on actual data obtained during the relevant years.

The CDC’s 2008 model is a bit closer than WHO’s to the data-based estimates, but it’s still wildly off the mark, up at least to 1990.

The model is clearly invalid
and the numbers derived from it are WRONG

This post is already long enough. I’ve written more about science not being truth and related matters in Fatal Attractions: The Troubles with Science, New York: Paraview Press , 2001 . In another post I’ll write more specifically about this latest CDC publication, the array of unvalidated underlying assumptions as well as hints of troubling conflicts of interest.

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