HIV/AIDS Skepticism

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

Posts Tagged ‘sexual behavior 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 »

RACIAL DISPARITIES IN TESTING “HIV-positive”: IS THERE A NON-RACIST EXPLANATION?

Posted by Henry Bauer on 2008/05/04

Whenever people in the United States have been tested for “HIV”, members of the officially recognized racial groups have yielded different results: blacks always test “HIV-positive” more often than others, Asians always test “HIV-positive” less often than others. Whites test “HIV-positive” significantly more often than Asians, Native Americans somewhat more often than whites, and Hispanics significantly more often than Native Americans.

The same racial bias in “HIV” tests is found in other parts of the world: within South Africa (pp. 75-6 in The Origin, Persistence and Failings of HIV/AIDS Theory); between sub-Saharan Africa and northern Africa; within the Caribbean; in Europe (HIV: THE VIRUS THAT DISCRIMINATES BY RACE, 11 April 2008; HIV: A RACE-DISCRIMINATING SEXUALLY TRANSMITTED VIRUS!, 16 April 2008; DECONSTRUCTING HIV/AIDS in “SUB-SAHARAN AFRICA” and “THE CARIBBEAN”, 21 April 2008).

A comprehensive recent review acknowledges the racial bias in testing “HIV-positive”:
“racial and ethnic minorities, especially African Americans and Hispanics, are disproportionately affected….
in Europe … many infections today are found among immigrants from sub-Saharan Africa” (Cohen et al., Journal of Clinical Investigation 118 [2008] 1244-54).

The racial disparities in testing “HIV-positive” are as firmly accepted in mainstream discourse as any aspect of HIV/AIDS is.

WHY? Why are “HIV” tests racially biased?

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For reasons that need no reiterating, deep and delicate sensitivities are aroused by any discussion of human differences associated genetically with the commonly used racial designations. One should therefore bear in mind that race is a matter of biology, not at all the same thing as perpetrating racism, which is a matter of social practices and public policy. The eminent anthropologist Ruth Benedict had wise things to say on this score (Race and Racism, first published 1942; page references from 1983 edition, Routledge & Kegan Paul):
—“a student may have at his tongue’s end a hundred racial differences and still be no racist” (p. vii)
—“Race is not ‘the modern superstition,’ as some amateur egalitarians have said. It is a fact. . . . Race . . . is not the modern superstition. But racism is.” (pp. 96, 97)

Benedict makes clear the distinction between race and culture. Race is a biological matter having to do with phenotypes, genotypes, DNA, physiology, colors of eye and hair and skin, and so on. Culture is a matter of learned behavior, and culture and behavior are not determined by race; innumerable cultures have maintained their distinguishing characteristics while the racial composition of the people expressing those cultures changed; and no race has always expressed some unique culture of its own everywhere.

“Race” is a very crude biological classification. There are only half-a-dozen or so human groups in the typical list of “races”, and there is enormous genetic variation among members of any one of these groups. Yet the classification has its uses, particularly perhaps in medicine, in view of significant statistical associations of race with predisposition to such conditions as Tay-Sachs disease or sickle-cell anemia.

But it is rather few predispositions that are significantly linked to this crude classification into half-a-dozen racial groups. That’s what makes the racial disparities in testing HIV-positive so extraordinarily difficult to explain on the basis of HIV/AIDS theory. Testing “HIV-positive” is unquestionably linked to biological race. HIV/AIDS theory ascribes testing “HIV-positive” to behavior. Thus HIV/AIDS theory appears to require that sexual and drug-abusing behavior be determined by biological race to an extent that is seen with rather few other characteristics and that has certainly not been found with any other form of behavior.

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If HIV is an infection transmitted predominantly via sex, then racial disparities in its distribution have to be explained in terms of racial disparities in sexual behavior. That is contrary to the evidence, and it is contrary to what anthropology and biology and psychology and sociology know. Is there any way in which racial disparities as to HIV could be explained in non-racist terms?

One would have to postulate that there are racially linked genes that influence how a person reacts when exposed to the virus. Perhaps people with certain genetic traits are more likely to be infected upon exposure? In that case, one would not have to ascribe racial disparities in rates of actual infection to differential rates of exposure, that is, differences in sexual behavior.

Much research has aimed to identify genetic factors that make for resistance to “HIV infection” or resistance to progression to AIDS after “infection” (or seroconversion), by studying so-called “long-term non-progressors” or “elite controllers” or individuals persistently exposed to HIV without seroconverting. These searches have remained unsuccessful. It has become something of a shibboleth that genetic variants of CCR5, a “co-receptor” of HIV, provide resistance, but this does not begin to accommodate the facts as to racial disparities: the pertinent allele is found “at high frequency in European Caucasians (5%-14%, with north-south and east-west clines) but is absent among African, Native American, and East Asian populations”; but non-CCR5-protected Asians resist “HIV” even more strongly than supposedly-CCR5-protected Caucasians, and Africans are affected by “HIV” far more than are Native Americans. Moreover, the CCR5 allele in question appears to have been the subject of neutral evolution over thousands of years and certainly was not selected for under the pressure of supposedly fatal infection by “HIV” (Sabeti et al., PLoS Biology 3 [(#11, 2005] e378.) http://biology.plosjournals.org/perlserv/?request=get-document&doi=10.1371%2Fjournal.pbio.0030378

The facts as to a putative resistance to infection also speak quite stubbornly against such a phenomenon. The probabilities of apparent transmission are the same for blacks, whites, and south-east Asians, always on the order of 1 per 1000 acts of unprotected intercourse (relatively more for male-to-female and less for female-to-male), according to (at least) three published reports from Africa, one each from Haiti and Thailand, and nine from the United States (individual sources cited at p. 44 ff. in The Origin, Persistence and Failings of HIV/AIDS Theory).

Since the apparent probability of transmitting “HIV-positive” displays this remarkably reproducible figure of about 1 per 1000, differences in prevalence of the “HIV-positive” condition can only be ascribed—under HIV/AIDS theory—to differences in frequency of exposure or type of sexual behavior.

There is no way around it. To accept HIV/AIDS theory means to accept that there are characteristic differences in sexual behavior between Asians, Caucasians, Native Americans, Hispanics, and blacks; and, among Hispanics in the United States, characteristic differences in sexual activity between the East and West coasts, differences that happen also to run parallel to differences in racial ancestry. That requires acceptance of a radically extreme version of sociobiology, namely, that sexual behavior is determined genetically and not culturally. Such acceptance also constitutes what Ruth Benedict correctly described as racism and as contrary to fact.

Posted in experts, HIV absurdities, HIV and race, HIV risk groups, HIV transmission, HIV/AIDS numbers, sexual transmission | Tagged: , , , , , | 6 Comments »

 
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