HIV/AIDS Non-Thinkers

An important credential for HIV/AIDS researchers is that they should not think about the wider implications of data or observations, because all too often those conflict with HIV/AIDS theorizing. Two recent examples:

“Swaziland to test entire population for HIV
Published on : 26 July 2011 – 11:24am | By Klaas den Tek
Authorities in Swaziland want to subject the entire Swazi population to an HIV/AIDS screening test. Those eventually found to be HIV positive would then receive antiretroviral drugs (ARVs). It is an ambitious project involving various donors including the Dutch organization, Stop Aids Now! But is it possible to test an entire population? . . .
Nearly 200,000 of Swaziland’s 1.2 million inhabitants are HIV positive, which makes the southern African country the world record holder for HIV prevalence. Moreover, many Swazis have never been tested for HIV before. The number of people living with the virus that causes AIDS could thus be much higher.
HIV/ AIDS expert, Joep de Lange, from the University of Amsterdam, is among the supporters of the project.
According to him, the screening test could lower the prevalence of the pandemic to one percent of the Swazi population” [emphases added].
Commentary:
The CIA Fact Book has the HIV prevalence as 25.9% (estimated, of course). A couple of years earlier it had been estimated to be 38.8% (Deconstructing HIV/AIDS in “Sub-Saharan Africs” and “The Caribbean”, 2008/04/21) . According to the UNAIDS 2008 Global Report, in “Swaziland — HIV prevalence appears to have stabilized at extraordinarily high levels” [my emphasis], namely “the 26%  . . . found in adults . . . in 2006 [which] is the highest prevalence  ever documented in a national population-based survey anywhere in the world (Central Statistical Office [Swaziland] & Macro  International Inc., 2007)” — although among pregnant women, Swaziland had recorded  >40% HIV prevalence in 2004.
So much for official statistics. 200,000 of 1.2 million is 17%; CIA says 26% as does UNAIDS, but CIA had nearly 39% just a few years earlier. Believe what you choose and whatever suits the immediate purpose. But furthermore:
Up to 2004, less than 10% of the “HIV-positive” population was getting the benefit of antiretroviral drugs. “In Swaziland, the Global Fund is financing care and support services for 100 000 children orphaned as a result of HIV (Global Fund, 2008)”.
The CIA Fact Book estimates for 2009, 180,000 Swazis living with HIV/AIDS but only 7000 HIV/AIDS deaths.
The death rate should have been much higher, if HIV/AIDS is as deadly as claimed in absence of life-saving antiretroviral drugs.
The Golden Fleece Award for Outstanding Non-Thinking, though, ought to go to expert Joep de Lange for suggesting that universal testing and antiretroviral treatment could bring the prevalence from ~16% down to ~1%. No one has yet suggested that antiretroviral drugs are a cure, that they convert “HIV-positive” to “HIV-negative”. For prevalence to decrease from 16% to 1%, 15% of the population would have to die — that is, 15 of the 16% “HIV-positive” people, i.e. 94% of those “living with HIV/AIDS” — even as they are all being treated with antiretroviral drugs!? And that’s assuming no new infections in the meantime, of course; taking those into account would require an even higher death rate.
This is far from the first time that HIV/AIDS gurus have made such ridiculous claims about projected or even achieved decreases in HIV prevalence in various African regions, for example, Uganda, decreases that simply do not jibe with birth and death rates let alone claimed new-infection rates.
Joep de Lange is one of the most prominent HIV/AIDS gurus. He is Professor of Internal Medicine at Amsterdam, has been engaged in HIV/AIDS matters for more than 15 years, and has been President of the International AIDS Society. Perhaps he was misquoted in suggesting that Swaziland could reduce its HIV prevalence from ~16% to ~1%? Or then again perhaps not, since he apparently swallowed the claim that Uganda had reduced its rate from 30% to 11% (“De eerlijke aidsbestrijder” — The honest anti-AIDS warrior).
The interview was given to a Dutch reporter, so perhaps de Lange was not misreported.

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It’s long been well known that HIV is sexually transmitted, and that people who have contracted some other venereal disease (STD) such as gonorrhea or chlamydia are more prone to acquire HIV as well. It’s remained well known even as the data have shown negative correlations between HIV and STDs. It’s remained well known even as the rate of “HIV” among actors in pornographic films has been virtually zero despite the almost total absence of condom use among those performers. Nevertheless, HIV/AIDS gurus and activists have continued to declaim about the dangers of HIV spread among porn performers and that they should be forced to use condoms. For example, the recent article by Goldstein et al. (“High chlamydia and gonorrhea incidence and reinfection among performers in the adult film industry”, Sexually Transmitted Diseases, 38 [2011] 644-8):
“industry standards for protecting adult film performers lag far behind established worker health and safety standards. Adult film performers routinely engage in anal and vaginal sex without condoms, including prolonged and repeated sexual acts with multiple sexual partners over short periods. 3 These practices often lead to rectal and/or vaginal mucosal trauma with exposure to seminal and vaginal fluids, fecal material, and blood, a combination that is ideal for transmission of human immunodeficiency virus (HIV), other sexually transmitted diseases (STDs), and fecal pathogens. . . . ‘an average popular male in the industry, through partner-to-partner-to-partner transmission, reaches approximately 198 people in 3 days.’ 7 Although the total population of performers at any one time may appear small, they have a very large sexual network and
serve as a bridge population for STD transmission to and from the general population. 6
. . . .
We focused on repeat infections with CT [chlamydia] and GC [gonorrhea] in this analysis because they are generally indicators of (1) participation in higher sexual risk behaviors; (2) higher risk for HIV acquisition and transmission 15 . . . .” [emphases added].
Now here are the data reported by Goldstein et al.:
“Between 1998 and 2008, 17 HIV cases were reported among performers. 4”
For gonorrhea and chlamydia between 2004 and 2008,

Thus 1294 cases of gonorrhea and 2175 cases of chlamydia in the 5 years from 2004 to 2008, in other words ~260 cases per year of gonorrhea and ~ 435 cases per year of chlamydia.
With HIV, by contrast, there were less than 2 per year, under conditions “ideal for transmission of human immunodeficiency virus (HIV)”.

Go figure.

Go think.

We have to do it for ourselves because we obviously can’t rely on the researchers to do it for us.

SEX, RACE, and “HIV”

Proponents of HIV/AIDS theory claim that purported epidemics of “HIV” reflect primarily sexual behavior (except in Eastern Europe, where 85% of it is ascribed to drug abuse — see HIV/AIDS ILLUSTRATES COGNITIVE DISSONANCE, 29 April 2008 — implying a truly inconceivably prodigious sharing of infected needles).

Everywhere in the world, people test “HIV-positive” according to their race. People of African ancestry test positive far more often than others. Asians always test positive least frequently. Caucasians, Native Americans, and non-black Hispanics are in between, but much closer to Asians than to Africans.

Therefore, the orthodox view as to HIV/AIDS postulates, implicitly but inescapably, that members of different racial groups display characteristically different, race-determined sexual behavior.

So egregious is this assertion that I would have thought it sufficient, in and of itself, to disabuse anyone and everyone of the notion that “HIV” could possibly be a sexually transmitted agent. Consider and compare the furor over an oft-claimed association of IQ and race. The claim led to excruciatingly detailed dissection of what IQ tests actually measure. Even those who claim that there is an association between race and IQ also acknowledge that it is only probabilistic, not fully determinant (typically, heredity is said to be responsible for only about half of the variations in IQ). If there is indeed such an association of race and IQ, one could at least speculate about a possible physical or physiological and therefore genetic basis for it, by analogy with the folklore — favored by devotees of table tennis — that Asians tend to have faster reflexes, and that faster reflexes make for better IQ-test scores. But in the purported association of testing “HIV-positive” and race, no careful dissection of what the “HIV” tests measure has been carried through (except, of course, by HIV/AIDS rethinkers). In particular, it has never been shown that testing “HIV-positive” denotes active infection, as the orthodoxy maintains. Indeed, there’s a substantial prize ($25,000, plus a matching amount to charity) awaiting anyone who can produce a publication proving that “HIV-positive” means active infection (http://www.aliveandwell.org/, May 2007 under “News and Updates”). There is an even larger prize for proof of the very existence of “HIV”: the Michael Verney-Elliott Memorial Prize of £50,000 .

As to whether sexual behavior might be determined definitively by race-associated genetics, I am not aware that anyone has been so foolish as to suggest it explicitly. Behavior is determined by culture, learning, environment, within very wide limits set by human genetics. Sexual mores and sexual practices have changed dramatically over short periods of time in several individual cultures without any change in racial composition of the populations expressing those cultures. Monogamy and polygamy have been practiced at times within cultures whose members belong to different racial groups. The notion that any form of behavior is directly determined by race has been thoroughly undermined by understanding and knowledge accumulated in anthropology, sociology, developmental biology, psychology, and so on. Nevertheless, the orthodox view of HIV/AIDS implies such an association, for the racial disparities in testing “HIV-positive” are at least as firmly reproducible as anything else about HIV/AIDS.

Not only does HIV/AIDS theory incorporate by clear implication the extraordinary claim that sexual behavior is characteristic of race, the sexual behavior it ascribes to Africans is implausible in the extreme.

Since the average probability of apparently transmitting “HIV” is about 1 per 1000, to produce an epidemic would seem to call for extensive and incessant orgies, a high rate of intercourse among continually changing sexual partners. In order to save the hypothesis of sexual transmission in the face of this implausible scenario, the speculation was ventured long ago (Anderson & May, Nature 333 [1988] 514-9) — and has since become generally accepted without proof — that when a person is first infected, there might ensue a short period of weeks, at most months, during which the infectivity must be much higher than 1 per 1000.

However, the highest estimates for this putative initial infectivity allowed by actual data on apparent transmission are only 1/50 to 1/250 (Cohen & Pilcher, Journal of Infectious Diseases 191 [2005] 1391-3). Such a rate still requires prodigious feats of sexual promiscuity to explain the levels of “HIV infection” reported for sub-Saharan Africa, which are greater than 20%, remember, sometimes even above 35%, in Botswana, Lesotho, Namibia, South Africa, Swaziland, and Zimbabwe (21 April 2008, DECONSTRUCTING HIV/AIDS in “SUB-SAHARAN AFRICA” and “THE CARIBBEAN”).

James Chin, former epidemiologist for California and later for the World Health Organization, has carried out the requisite calculations (The AIDS Pandemic: The collision of epidemiology with political correctness, Radcliffe 2007): “epidemic HIV transmission requires a very high level of HIV risk behaviors” (pp. 44, 45). To achieve an epidemic spread over a period of “many years”, 20-40% of adults must have “multiple concurrent relationships” — several sexual partners at the same time, changing to new partners weekly or monthly, totaling to tens of different partners over the course of each year (p. 64, Table 5.1). (Chin does not seem specifically to consider the postulated short periods of higher infectivity. However, doing so would then require even more rapid change of partners to produce an epidemic since the window of opportunity for transmission is so brief.)

That, then — according to the official view — is what must have been going on in “sub-Saharan Africa” for many years. Also on the official view, as one travels from south to north one would observe the level of sexual activity steadily decreasing, until in North Africa promiscuity is at quite a low level, comparable to that in the civilized regions of the developed world; see the maps in DECONSTRUCTING HIV/AIDS in “SUB-SAHARAN AFRICA” and “THE CARIBBEAN”, 21 April 2008.

These staggering estimates, 20-40% of adults in multiple concurrent partner-changing relationships, are not usually cited, perhaps because they are so truly not worthy of belief. Instead, what HIV/AIDS theory implies — actually demands — is masked by abstract jargon not translated into concrete quantitative scenarios: it’s just said typically that the HIV/AIDS epidemic in sub-Saharan Africa results primarily from multiple concurrent relationships among heterosexuals in overlapping networks of partners. That sort of longwinded discourse in sociological jargon allows lay people’s eyes to glaze over and to defer to the experts who surely must know what they’re talking about. But the concrete fact behind that abstract jargon remains what Chin calculated: between 20% and 40% of adults having sex with several partners during the same period of time, all of them changing those partners every few weeks. It boggles the mind. Try to imagine that in your neighborhood: between 20% and 40% of men would have several mistresses, changing them every few weeks or months for new ones, and the women would be no less promiscuous. Just about everyone would have to be doing it, and certainly everyone would know about it.

Moreover, that degree of sexual activity would surely be causing to spread also the commonly known sexually transmitted infections (STIs or STDs) — gonorrhea, syphilis, chlamydia, etc. Those are transmitted with probabilities that are far greater, ten times higher or more, than that of 1 per 50, the highest short-period rate postulated for HIV. Wherever “HIV” is spreading, therefore, the population should have been absolutely swamped by the common STDs. They are not. This in itself offers direct observational proof that HIV is not sexually transmitted, proof available to anyone who looks even cursorily at the evidence.

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Now that HIV/AIDS in the United States is acknowledged to have become a disease of black communities, similar feats of sexual activity as postulated for Africa have to be imagined there as well. A high rate of “multiple concurrent relationships” has indeed been offered explicitly as partial explanation for the purported epidemics now said to be endangering, in particular, young black women, notably in the Southeast and in Washington city, DC; see, among many available examples, Kulik et al., American Journal of Public Health 85 (1995) 1119-22; Hammett et al., Sexually Transmitted Diseases 33 (2006, July suppl.) 817-22; Adimora et al., Annals of Epidemiology 14 (#3, 2004) 155-60.

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The racial disparities in testing “HIV-positive” are clearly, obviously, inescapably incompatible with HIV/AIDS theory. If “HIV” were sexually transmitted, then the racial disparities in “HIV-positive” would mean that human racial groups differ characteristically and drastically in their sexual behavior and mores. Furthermore, if “HIV” were sexually transmitted, then wherever there is “HIV”, there would be vastly greater incidence of gonorrhea, syphilis, chlamydia, herpes, etc.

The notion that “HIV” is a sexually transmitted infection is simply unsustainable in light of the actual data.

HIV AND SEXUALLY TRANSMITTED DISEASE: IT JUST ISN’T SO

Everyone knows that HIV is a sexually transmitted disease (STD), and that the chances of contracting it are much greater if you have another STD, like gonorrhea, syphilis, or chlamydia.

Everyone knows those things even though the facts contradict them.

An Australian correspondent alerted me to this recent and typical story (by Tory Shepherd, Health Reporter, November 28, 2007 (http://www.news.com.au/adelaidenow/story/0,22606,22832996-5006301,00.htm):

“A surge in the rate of sexually transmitted diseases has hit South Australia. . . . chlamydia infections have trebled to more than 3000 a year in the past decade, while gonorrhea infections have increased from about 190 to about 500. The number of HIV/AIDS infections has fluctuated, from 46 HIV and 39 AIDS infections in 1996 to 23 HIV and five AIDS in 2000, then up to 61 HIV and 14 AIDS cases in 2006. . . . the increase in other STDs could herald a rise in HIV/AIDS infections, as it showed safe sex messages were being ignored. ‘If these trends continue, an increase in HIV infections can be predicted to follow,’ it said.
….
‘chlamydia is largely an infection of heterosexual adolescents and young adults while HIV remains largely associated with male-to-male sex, injecting drug use and heterosexual sex overseas,’ …. ‘Syphilis and gonorrhea in metropolitan Adelaide has also been predominantly associated with men who have sex with men, but recently a few heterosexual transmissions have occurred. A major concern for the future would be if these epidemics intersect with a rise in gonorrhea and syphilis among the heterosexual community, which could herald an increase in the heterosexual transmission of HIV.’”

The cited numbers and generalizations present these facts: In the quarter century of the claimed epidemic of HIV/AIDS, STDs in South Australia have gone up but HIV and AIDS have fluctuated at a much lower level: 50 times lower than chlamydia, 4 to 10 times lower than gonorrhea, and not increasing in tandem with them. Moreover HIV/AIDS has remained within the original risk groups and has not spread into the general population.

Yet the same story that presents these facts warns against what the experience of 25 years teaches will not happen.

That is typical of reporting and of official press releases about HIV/AIDS: dire warnings in the face of the facts. The primary medical-scientific literature, cited in The Origins, Persistence and Failings of HIV/AIDS Theory, demonstrates that

“HIV” is “transmitted” via unprotected sexual intercourse about 1 in 1000 times–whereas gonorrhea or syphilis are transmitted 200-800 times per 1000 acts (pp. 44-45 in the book).
The epidemiology of “HIV” is not like that of an STD (especially p. 31 ff, p. 44 ff. in the book).
Use of condoms has not been shown to decrease the “transmission” of “HIV” (pp. 44, 109 in the book).
Rates of STDs and of “HIV” have moved in opposite directions in South-East Asia (p. 109 in the book).

How could beliefs contrary to fact persist for a couple of decades? Parts II and III of the cited book suggest these answers:
1. Medicine and clinical science, like all of science, are liable to go wrong before they eventually go less wrong, if not necessarily quite right .
2. Initial reporting, speculating, and activism about AIDS sent things on a wrong track from which we have not yet recovered.

The idea that AIDS is sexually transmitted came about because the first cases were in clusters. Then the story of the airline steward, “Patient Zero”, seemed to confirm the idea because AIDS appeared within a few weeks or months of his visits around the country. However, now that the average lag between HIV infection and AIDS symptoms is estimated at about 10 years, those bits of evidence speak AGAINST sexual transmission and for a lifestyle explanation.

Another mistaken inference has to do with Africa. In the United States, AIDS in the early 1980s was virtually restricted to gay men and to drug abusers. When in Africa about equal numbers of men and women were said to have AIDS, this was trumpeted as showing that in Africa HIV was being spread via heterosexual intercourse. The basis for this inference is wrong: genuinely heterosexually transmitted diseases–chlamydia, gonorrhea, syphilis–do not strike men and women in equal numbers. The illnesses that do strike men and women equally are those transmitted though the air like flu, or via insects like malaria, or via the environment as with unsafe drinking water or malnutrition, say.