HIV/AIDS Skepticism

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

Posts Tagged ‘sex and race’

RACE and SEXUAL BEHAVIOR: STEREOTYPE vs. FACT

Posted by Henry Bauer on 2008/05/27

Racial disparities in testing “HIV-positive” are explained — by proponents of HIV/AIDS theory, that is — as stemming from the harmful effects of racial discrimination, which mire the discriminated-against in circumstances rife with drug abuse and sexual promiscuity. That runs counter to a goodly body of actual evidence that undercuts this type of explanation; and it also draws on stereotypes not readily distinguishable from racist beliefs (see 19 May, HIV/AIDS THEORY IS INESCAPABLY RACIST).

Some of the evidence confounding the stereotypes is cited in my book (p. 77):

“As a matter of actual fact, research in the context of HIV/AIDS has not revealed any racial differences in sexual behavior. Among drug users, no significant differences in behavior by race were found as to numbers of sexual partners, frequency of intercourse, numbers of sexual partners who were IDUs, numbers of non-IDU sexual partners, prostitution, or intercourse with people then or later diagnosed with AIDS (Friedman et al. 1987). Samuel and Winkelstein (1987) found no significant racial differences in behavior among gay men in San Francisco, and they concluded that the black-to-white ratio of . . . [“HIV-positive”] could not be explained by differences in major risk factors. The San Francisco Department of Health (1986) found no differences between races as to anal intercourse . . . . Bausell et al. (1986) found white Americans less likely than black Americans to take protective measures during sex. Historical data from Zimbabwe records a higher incidence of venereal disease among the white South Africa Police and the British Armed Services than among the Native Police or among Africans in general (McCulloch 1999, 205, 207). Contemporaneous surveys have found that levels of sexual activity in general populations in Africa are comparable to those in North America and Europe (Brewer et al. 2003; Gisselquist 2002).”

It has become fashionable to assert that black women in the United States are at particular risk because of black men “on the down low” (indulging secretly in male-with-male sex), becoming “HIV-positive”, then transmitting that to their female partners. But here again, the evidence doesn’t sustain the speculation:

“The lifestyle referenced by the term the DL is neither new nor limited to blacks, and sufficient data linking it to HIV/AIDS disparities currently are lacking. Common perceptions about the DL reflect social constructions of black sexuality as generally excessive, deviant, diseased, and predatory. [“social construction” means stemming from human interpretation rather than from the objective reality] Research targeting black sexual behavior that ignores these constructions may unwittingly reinforce them” (Ford et al., Ann Epidemiol 17 [2007] 209-16).

An illustration of such unwitting reinforcement is one of the CDC’s statements:
“The phenomenon of men on the down low has gained much attention in recent years; however, there are no data to confirm or refute publicized accounts of HIV risk behavior associated with these men. What is clear is that women, men, and children of minority races and ethnicities are disproportionately affected by HIV and AIDS” (emphasis added; unchanged since at least March 2006; www.cdc.gov/hiv/topics/aa/resources/qa/downlow.htm, accessed 11 May 2008).

Another common and politically correct gambit (attempting to explain away that blacks always test “HIV-positive” more often than others) seizes on the high incarceration rate of young black men, particularly from inner-city regions, and combines that with the shibboleth that prisons are a hotbed of “HIV” transmission (for example, Johnson & Rafael 2006). But once again the speculation goes contrary to fact, because “actual observations in prisons have failed to reveal transmission of HIV there (Brown 2006; Horsburgh et al. 1990; Kelley et al. 1986)” (p. 79 in The Origin, Persistence and Failings of HIV/AIDS Theory).

In South Africa, blood from black donors was, for some time, being destroyed as “unsafe” because it tested “HIV-positive” so much more often than blood from people of mixed race or from South-East Indians or whites (p. 75 in The Origin, Persistence and Failings of HIV/AIDS Theory). However, since testing was available for the blood, this blanket rule surely owed something to underlying and pre-existing racist beliefs. Racist preconceptions in the 1980s among HIV/AIDS workers in Africa — some of whom are still prominent in HIV/AIDS research nowadays — were described, long ago and in detail, by the Chirimuutas (AIDS, Africa and Racism, Free Association Books, London [UK] 1987/89). Konotey-Ahulu, a distinguished Ghanaian physician and medical researcher, also exposed the lack of evidence for an African origin of HIV/AIDS in a book (What is AIDS? 1989/96, ISBN 0-9515442-3-3) I described in a review as “flavored by a traditional attitude toward what constitutes acceptable behavior” and displaying “what used to be called good breeding and proper upbringing”, exploding by personal example all sorts of notions about “those Africans” (Journal of Scientific Exploration 21 [2007] 206-9).

That blacks always test “HIV-positive” more often than others simply cannot be explained by differences in behavior:

“AIDS researchers don’t have a solid explanation for why black women in America have such a shockingly high prevalence of HIV infection. . . . injection drug use, a particularly effective way to spread HIV, is actually lower in black women than in white women” — Jon Cohen, “A silent epidemic”, 27 October 2004, www.slate.com/id/2108724/.

“Black young adults . . . are at high risk even when their behaviors are normative. Factors other than individual risk behaviors and covariates appear to account for racial disparities” — Halfors et al., Sexual and drug behavior patterns and HIV and STD racial disparities: the need for new directions, Am J Public Health 97 [2007] 125-32.

“HIV-positive gay men are more likely than HIV-positive black African heterosexual men and women to engage in sexual behaviour that presents a risk of HIV transmission. . . . There were no significant differences between white gay men and those from other ethnic background in terms of sexual behaviour” (Rod Dawson, 5 January 2007. AIDSmap news, summarizing Elford et al., “Sexual behaviour of people living with HIV in London: implications for HIV transmission”, AIDS 21 [suppl. 1, 2007] S63-70).

“According to Robert Janssen, director of CDC’s Division of HIV/AIDS Prevention, blacks do not engage in riskier sexual behavior compared with other groups, but the population’s HIV/AIDS infection rates mean that blacks who have sex with other blacks are more likely to get HIV than people in other ethnic groups” — (emphasis added; Kaiser Daily HIV/AIDS Report, 9 March 2007).
Perhaps Janssen has never heard of the chicken-&-egg conundrum? How did the infection rate in the black community become higher than in others in the first place, given that the first affected groups in the USA were predominantly white gay men?

That ill-founded grasping-at-straws argument is not unique with Janssen:
“racial disparities in seroprevalence were . . . not attributable to disparities in risk factors such as STD, bisexuality, or acceptance of HIV testing. This finding suggests that the observed differences may reflect racial differences in the background seroprevalences” — Torian et al., Sex Transm Dis. 29 [2002] 73-8.
I suppose one must sympathize with people trying desperately to explain the unexplainable. This “explanation” is a tautology: blacks test “HIV-positive” more often than others because blacks already test “HIV-positive” more often than others.

“Paradoxically, potentially risky sex and drug-using behaviors were generally reported most frequently by whites and least frequently by blacks. . . . Understanding racial/ethnic disparities in HIV risk requires information beyond the traditional risk behavior and partnership type distinctions” — Harawa et al., “Associations of race/ethnicity with HIV prevalence and HIV-related behaviors among young men who have sex with men in 7 urban centers in the United States”, JAIDS 35 [2004] 526-36.

The Centers for Disease Control and Prevention found, in one study, that “Black gay and bisexual men . . . [were] more likely to engage in safe-sex practices than their white counterparts. . . . ‘Across all studies, there were no overall differences [by race] in reported unprotected receptive sex or any unprotected anal intercourse . . . among young MSM — those ages 15 to 29 — African-Americans were one third less likely than whites to report in engaging in unprotected anal intercourse’ . . . . Black gay or bisexual men were also ‘36 percent less likely than whites to report having as many sex partners as white MSM’ . . . . Blacks in the study were also less likely to use recreational drugs, such as methamphetamine or cocaine, compared to whites” (“One-third of HIV-infected gay men have unsafe sex: CDC”, HealthDay News, 3 December 2007).

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Black people always test “HIV-positive” more often than others.

Black people do not differ greatly from others in their sexual behavior. Where they do, it is through behaving somewhat more responsibly than white people.

The racial disparities in testing “HIV-positive” cannot be explained by differential behavior: blacks always test positive much more often, but their sexual behavior does not constitute a corresponding risk.

THEREFORE: Testing “HIV-positive” must indicate something other than a sexually acquired condition. Testing “HIV-positive” does not mark infection by a sexually transmitted agent. Rather, testing “HIV-positive” is a very non-specific indication of some sort of physiological stress; see, for example, REGULAR AS CLOCKWORK: HIV, THE TRULY UNIQUE “INFECTION”, 1 April 2008; “HIV DISEASE” IS NOT AN ILLNESS, 19 March 2008; UNRAVELING HIV/AIDS, 8 March 2008; HIV DEMOGRAPHICS FURTHER CONFIRMED: HIV IS NOT SEXUALLY TRANSMITTED, 26 February 2008; TWINS ATTRACT THEIR MOTHER’S HIV, 12 January 2008; HOW TO TEST THEORIES (HIV/AIDS THEORY FLUNKS), 7 January 2008.

Posted in HIV and race, HIV as stress, HIV risk groups, HIV tests, HIV transmission, prejudice, sexual transmission | Tagged: , , , , , , , | 3 Comments »

SEX, RACE, and “HIV”

Posted by Henry Bauer on 2008/05/14

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.

Posted in HIV absurdities, HIV and race, HIV risk groups, HIV transmission, HIV/AIDS numbers, sexual transmission | Tagged: , , , , , , , , , , | Leave a Comment »

 
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