HIV/AIDS Skepticism

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

Posts Tagged ‘racist sexual stereotypes’

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
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 »

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