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.

WHAT “HIV” IS NOT: IT’S NOT SEXUALLY TRANSMITTED

If one thing is certain about HIV/AIDS, it is that “HIV” is not a sexually transmitted agent.

I can be certain about that because I’ve examined the reported evidence for myself.

Not all of the evidence, of course, because no one could possibly do that; but I have gathered the published data about HIV tests in every HIV/AIDS Surveillance Report published by the Centers for Disease Control and Prevention (CDC); every pertinent article in the CDC’s Morbidity and Mortality Weekly Report; and hundreds of articles reporting HIV tests in JAMA, New England Journal of Medicine, and other medical-scientific journals. I used PubMed to find many relevant articles and to guide me from one article to related ones.

The data represent more than 50,000,000 tests. Several social groups have been tested routinely–applicants for military service, active-duty military personnel, blood donors, Job Corps members–and the results from those groups comprise an unparalleled resource for identifying trends: unparalleled because the tests were carried out on essentially all members of those groups, so that there are none of the uncertainties associated with sampling that often leave interpretation of statistical medical and social data less than certain.

The regular trends in those data are nothing less than astonishing. Whether “HIV” tests concerned newborns or their mothers, or military personnel, or blood donors, or gay men or people injecting illegal drugs, several things are always the same:
—The geographic distribution of positive HIV tests is the same. Even though the average rate of testing HIV-positive varies by a factor of 100 or more between drug users and blood donors, within each group the geographic distribution is the same: highest in the North-East and South-East, lowest in the North Central regions, higher in the South than in the West.
So unvarying a geographic distribution across social groups is not found with syphilis, gonorrhea, or other known sexually transmitted diseases (STDs).
—This geographic distribution of positive HIV tests has remained the same throughout the AIDS era: it was the same in the early 1980s as in the late 1990s. That’s certainly not like a contagious disease, and certainly not like an STD that spread across the country from New York, Los Angeles, and San Francisco since the 1970s.
—Among the low-risk groups–excluding gay men and drug injectors, in other words–, the frequency of positive HIV tests varies with age and sex in the same manner in every tested group:

With genuine STDs, it is typically adolescents who are at greatest risk, not middle-aged people; and newborns and young children are not infected with STDs at rates comparable to those among adults; yet “HIV-positive” is as common among newborns as among the most highly “infected” middle-aged adults in low-risk groups.

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If you have unprotected sex with someone who has gonorrhea or syphilis, your chance of catching that infection yourself is something like 50:50 (anywhere from 10% to 90%).

If you have unprotected sex with an HIV-positive person, what are the odds that you will become HIV-positive yourself?

About 1 in a 1000.

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Why believe what I’ve just written, when the media are full of official statements warning that everyone is at risk, that condoms should always be used, that sex is the main way that “HIV” is transmitted?

You shouldn’t believe anything just because I say so. And you shouldn’t believe anything just because others say so, either, even if they are a Director of the National Institute for Allergy and Infectious Diseases, or because they have won a Nobel Prize or other prizes, or because they have been acclaimed for discovering something. You should believe something only if you have the good reason of having seen for yourself that the evidence supports the statements made.

One of the things I learned through doing science is that anyone can be wrong; and I learned the more difficult lesson that I myself can be wrong. I’ve been wrong through accepting what others said, and through misinterpreting data, and because there were totally unknown and unsuspected factors involved, and I’ve been wrong through just plain making mistakes because of muddle-headedness or tiredness or ignorance. So I’m wary of saying I’m certain about something, and especially wary when “everyone” knows something different.

It took me months to come to terms with the data showing that “HIV” is not sexually transmitted, and I reached the conclusion simply because there is no other way to explain the data. If you want to make up your mind about this, you may have to look at all the data for yourself. Ideally you should start from scratch, gather whatever data you can find about HIV tests, and tabulate the results by age and geography and sex and date and anything else that you think might be relevant. Then look to see whether there are any regularities to be explained.

A second-best way would be to look at my collection of the data and discussion about them, and to check my sources: make sure I haven’t misquoted or omitted, and search the literature for things I overlooked and that might contradict my analysis.

A not-very-good way to make up your mind would be to judge that I’m sincere and to trust that I’ve done what I say I’ve done. But that would be no worse than believing what you read in the newspapers, or believing that gurus in white coats are always right. In fact, believing the white coats or the media may be the worst possible way of making up your mind about anything important.

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From where did I get that “1 chance in 1000” for sexual transmission of HIV? I looked hard into the literature but found no study that claimed more than a few per 1000. Chapter 4 of my book, The Origins, Persistence and Failings of HIV/AIDS Theory, http://www.failingsofhivaidstheory.homestead.com/ cites a score of publications that all arrive at about the same 1-per-1000 odds, and it cites the doctors and biostatisticians who concluded that “the transmission probabilities presented are so low that it becomes difficult to understand the magnitude of the HIV-1 pandemic” (Chakraborty et al. AIDS 15 [2001] 621-6).

I found in Robert Gallo’s memoirs an acknowledgment that HIV is “distinctively difficult to transmit” (p. 131, “Virus Hunting”, 1991).

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Gonorrhea and syphilis, transmitted quite efficiently at about 1 chance in 2, cause local outbreaks periodically, but they don’t bring about worldwide epidemics. With HIV/AIDS, we are being asked to believe that something transmitted 100 times less efficiently than gonorrhea or syphilis is producing epidemics all over the world. Seems like a good time to offer some more Brooklyn Bridges for sale.
Gisselquist and colleagues have published a number of articles arguing, on the basis of observed sexual behavior as well as lack of transmission efficiency, that sexual transmission cannot explain the African epidemic of “AIDS” (“Not investigating HIV riddles puts lives at risk”, Business Day [Johannesburg], 4 October 2007; “How much do blood exposures contribute to HIV prevalence in female sex workers in sub-Saharan Africa, Thailand and India?” International Journal of STD & AIDS 18 [2007] 581-588; Gisselquist et al., “HIV infections in sub-Saharan Africa not explained by sexual or vertical transmission”, 13 [2002] 657-666; “Running on empty: sexual co-factors are insufficient to fuel Africa’s turbocharged HIV epidemic” ibid. 15 [2004] 442-452; Brewer et al., “Mounting anomalies in the epidemiology of HIV in Africa: cry the beloved paradigm”, ibid. 14 [2003] 144-147).

Pillars of the orthodoxy have offered specious arguments running about like this: “Sure, on average it’s only 1 per 1000, but there may be special circumstances when it’s much higher, say just after infection when the virus is replicating madly”. The sufficient but not only basis for calling that suggestion specious is that epidemics require an average, overall “reproduction ratio” appreciably greater than 1. You cannot have an epidemic unless, on the whole, on average, every infected person infects more than one other person within a rather short space of time. A score or more of specific studies, in Africa and Haiti as well as the United States, tells us that with “HIV” this does not happen.

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This was known long ago. Already in 1988, Anderson & May (Nature, 333: 514-9) guessed that there might be some special period of high infectiousness because the average apparent transmission rate is too low to bring about an epidemic. Reporters for the Wall Street Journal recognized in 1996, from CDC sources, that “for most heterosexuals, the risk from a single act of sex was smaller than the risk of ever getting hit by lightning” (Bennett and Sharpe, “AIDS fight is skewed by federal campaign exaggerating risks”, 1 May, pp. A1, 6). Fumento (“The Myth of Heterosexual AIDS”, 1990) among others pointed out that AIDS never spread into the general population outside Africa and the Caribbean. But the white-coated gurus who uphold the mistaken HIV/AIDS theory continue to do their best to obfuscate these facts. Take what Anthony Fauci said on the Diane Rehm show (“HIV/AIDS”, 17 August 2006, PBS Radio, transcript by Soft Scribe LLC).

Fauci admitted that “it is not a one to one ratio by any means. It’s not you have one sexual contact, and therefore you’ll get infected. It’s a relatively low efficiency”–but he failed to acknowledge that it’s about 1 per 1000, a vast and misleading difference from “not one to one”. And Fauci went on to venture this: “since there is so much sexual activity . . . , when you compound all of the sexual contacts among people, . . . , then you get the infection rates that we just spoke about where you windup getting five million new infections per year. There has to be a lot of sexual contact for that to occur. But, in fact, there is a lot of sexual contact going on everyday in the world”.

But that probability of 1 per 1000 applies only when one of the sex partners is already HIV-positive. UNAIDS puts the average global infection rate at about 1%: on average, if you choose your sexual partner at random, you have 1 chance in 100 of getting an HIV-positive one. So your overall risk is 1 in 100 multiplied by 1 in 1000, in other words 1 in 100,000. That, Fauci would have us believe, is capable of producing 5,000,000 new infections in the world each year.

And all that sexual activity Fauci conjures up somehow fails to spread gonorrhea or syphilis while disseminating something that is 100 times less infective.

So, I suggest, don’t believe everything that Dr. Anthony Fauci says, even about matters on which he is supposed to be expert.

But, of course, as I said, don’t believe what I say, either.

Just look at the evidence for yourself. That’s the smart thing to do.