Why do gay men test “HIV-positive” more frequently than others?

AIDS was first noticed and described among gay men.

In 1984, it was concluded, officially but mistakenly, that AIDS was caused by HIV.

That AIDS is not caused by HIV follows from innumerable pieces of evidence (The Case against HIV http://thecaseagainsthiv.net), for example that the incidence of AIDS does not correlate with instances of “HIV-positive” (1).
Why then do gay men test “HIV-positive” more often than others?

That is of more than academic interest. If there is some inherent connection between HIV and gay men, and since AIDS is inextricably connected historically to gay men, the two connections reinforce the mistaken conventional wisdom that HIV causes AIDS.

Well: Do gay men really test “HIV-positive” more often than others?

According to the Centers for Disease Control & Prevention, “Gay and bisexual men are more severely affected by HIV than any other group in the United States. From 2005 to 2014, HIV diagnoses decreased in the United States by 19% overall, but increased 6% among all gay and bisexual men … . Gay, bisexual, and other men who have sex with men made up an estimated 2% of the population but 55% of people living with HIV in the United States in 2013. If current diagnosis rates continue, 1 in 6 gay and bisexual men will be diagnosed with HIV in their lifetime, including 1 in 2 black/African American gay and bisexual men, 1 in 4 Hispanic/Latino gay and bisexual men, and 1 in 11 white gay and bisexual men” (“HIV Among Gay and Bisexual Men” [Page last updated: September 30, 2016] ).

In New Zealand, it is claimed that 1 in 15 gay and bisexual men are “HIV-positive” (New Zealand AIDS Foundation, “Three reasons gay guys are more likely to get HIV”) — the three reasons given include anal sex and the statistical likelihood of having sex with “HIV-positive” men.

A survey of global data for the years 2007-2011 reported (2) relative rates of “HIV-positive” for gay men as compared to all adults, in different regions of the world, showing consistently higher prevalence among gay men; once again the authors suggest that the greater likelihood of transmitting HIV by anal sex is the reason.

But since we know that HIV is not sexually transmitted (see section 3 in The Case against HIV), what could be the real reason for this disparity?

When greater incidence of “HIV-positive” among gay men is cited in terms of numbers found to be positive, one can suspect that it is because gay men are more likely to be tested in the first place; but no such explanation in terms of sampling bias can be invoked when the disparity appears to be in relative rates.

We know also that positive “HIV” tests are not proof of the presence of the purported retrovirus HIV; and we know that innumerable physiological circumstances may produce a “positive” result on an HIV test, see sub-section 3.2.2 in The Case against HIV). Those circumstances include many types of infections and ailments, as well as some conditions that are not ill health , say pregnancy or vaccinations, or some quite non-specific indications of perhaps quite minor threat to health, say oxidative stress.

It is not easy to see, however, why any or all of those “false positives” should be more common among gay men across cultures and regions. Perhaps anal sex, with possible tissue damage and transfer of semen, could induce release of substances reflective of physiological stress. Where antibody “HIV” tests yield an indeterminate result, it is known that heterosexual men and women tend to be reported as negative but gay men as positive. Perhaps too there is a nocebo effect: gay men have been indoctrinated to worry about “getting HIV”, and such worry is likely to be greatly exacerbated when anticipating or undergoing testing. Perhaps social persecution has also brought on average a higher rate of anxiety and somehow unhealthy living among gay men.

No combination of those possibilities seems adequate to explain the reported variations in rates, however. Moreover, as to anal sex, it is unlikely in the extreme that this is in itself notably dangerous to health: humans have been practicing anal sex for millennia, and if it were a significant risk to health, that would surely have been noticed very long ago.

Could it be that there is a biological, genetic basis for a tendency toward homosexuality? That suggestion has been ventured at times, albeit without convincing proof coming to hand as yet (3).

It is quite certain, though, that the tendency to test “HIV-positive” is strongly determined by genetics: the relative rates of testing “HIV-positive” are universally race-associated (chs. 5 & 6 in [1]), and substances taken to be characteristic of HIV are characteristic of commonly occurring human endogenous retroviruses, HERVs (4).

I find it amazing that mainstream researchers venture hand-waving non-explanations (5) for the much greater incidence of “HIV-positive” among African Americans than among white Americans, even though “risky” behavior is less among African Americans, and national rates of “HIV-positive” are highest in countries with a large proportion of people of African ancestry, namely Africa and the Caribbean. The Centers for Disease Control & Prevention has published innumerable data showing persistent and consistent variations by race, for instance (above) the rates of 1 in 11 for white Americans, 1 in 4 for Hispanics, and 1 in 2 for black Americans.

But the most likely reason why gay men test “positive” is also a major reason for the “AIDS” illnesses and deaths in the early years: INTESTINAL DYSBIOSIS; search this blog for all the posts describing this condition and confirming the plausibility of this hypothesis.

Why all this matters so much

The continuing refrain in the media about the prevalence of “HIV-positive” among gay men reinforces the mistaken notion that “HIV-positive” is dangerous to health, in particular that it presages overt illness, AIDS, and death. At the very least this strengthens the force of the mainstream dogma and makes it more difficult to present the Rethinking case. Very likely it exerts a nocebo effect that itself contributes to poor health.

It needs to be said, shouted, over and over again:

“HIV-positive” does not mean definitely ill, it does not mean infected by HIV, and anyway HIV doesn’t cause AIDS. Anyone, gay or not, who is told they are “HIV-positive”, should consult a physician who is not indoctrinated into HIV=AIDS, see Rethinking AIDS Medical Professional List.

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1. Henry H. Bauer, The Origin, Persistence and Failings of HIV/AIDS Theory, McFarland 2007.
2. Chris Beyrer, Stefan D. Baral, Frits van Griensven, Steven M. Goodreau, Suwat Chariyalertsak, Andrea L. Wirtz & Ron Brookmeyer (2012). “Global epidemiology of HIV infection in men who have sex with men”, The Lancet,  380 (9839) 367-77.
3. Brian P. Hanley (2011). “Dual-gender macrochimeric tissue discordance is predicted to be a significant cause of human homosexuality and transgenderism”, Hypotheses in the Life Sciences, 1 #: 63-70.
4. Etienne de Harven (2010). “Human endogenous retroviruses and AIDS research: Confusion, consensus, or science?”, Journal of American Physicians and Surgeons, 15: 69-74.
5. Gregorio A. Millett, John L. Peterson, Stephen A. Flores, Trevor A. Hart, William L. Jeffries 4th, Patrick A. Wilson, Sean B. Rourke, Charles M. Heilig, Jonathan Elford, Kevin A. Fenton & Robert S Remis (2012). “Comparisons of disparities and risks of HIV infection in black and other men who have sex with men in Canada, UK, and USA: a meta-analysis”, The Lancet, 380 (9839): 341-8.

HIV infectivity: high, low, or non-existent?

Analysis of essentially all published results of HIV tests in the USA reveals properties unlike those of an infectious agent (The Origin, Persistence and Failings of HIV/AIDS Theory, McFarland 2007).  In every social sector, the same regularities are seen: rates of testing positive vary by US official “racial” and ethnic classification (black >> native American > Caucasian > Asian); rates of testing positive decrease drastically from birth into the teens and increase from the late teens into middle age and then decline again; in early teens, females are more likely to be HIV+ than are males but by the 20s that is reversed (see references cited in section 3.3.5 in The Case against HIV).

In cloned HIV virions, only between 1 in 10,000 and 1 in 10 million were infectious (Layne et al., “Factors underlying spontaneous inactivation and susceptibility to neutralization of human immunodeficiency virus”, Virology, 189 (1992) 695-714).

The instructions that come with HIV test kits warn that a positive test is not proof of infection.

Innumerable conditions produce HIV+ results (see references cited in section 3.2 in The Case against HIV), so all claims to have measured infectivity or transmission are at best dubious and at worst — or more accurately — meaningless. There is no valid published evidence of transmission or infectivity (see references cited in section 3.3 in The Case against HIV). The Office of Medical and Scientific Justice successfully defended more than 50 individuals http://www.omsj.org/human-rights/52nd charged with transmitting HIV because the prosecution could not prove HIV to be transmissible.

Researching phantoms

It can take a long time before researchers realize that they have been on a wild-goose chase, pursuing phantoms (“Phantom phantoms”, pp. 110-116 in Fatal Attractions: The Troubles with Science, Paraview Press 2001); even “an unknown phenomenon [that] towered 6 standard deviations above the mundane background of known physics — enough to satisfy a 99.9999% confidence level that it wasn’t a fluke” and that had been reported in more than a dozen experiments turned out to be non-existent.

Given that HIV/AIDS theory is wrong (The Case against HIV), observations and experiments and clinical trials will continually throw up what seem to be conundrums, which serve as the basis for yet more research. To date, mainstream HIV/AIDS researchers have failed to recognize the accumulation of conundrums and absurdities  as being in reality the hard evidence that HIV/AIDS theory is simply wrong: HIV is not infectious, and “HIV” doesn’t cause AIDS.

Mainstream science sticks to theories that had once been accepted by ignoring anomalies, conundrums, absurdities for as long as possible (Thomas S. Kuhn, The Structure of Scientific Revolutions, University of Chicago Press 1970 [2nd ed., enlarged; 1st ed. was 1962]). Things that don’t fit an existing theory are accommodated by ad hoc adjustments (Imre Lakatos, “History of science and its rational reconstruction”, pp. 1-40 in Method and Appraisal in the Physical Sciences, ed. Colin Howson, Cambridge University Press 1976), just as Ptolemy long maintained belief in the circular perfection of heavenly motions by adding epicycles upon epicycles, wheels within wheels, to avoid acknowledging that the movements are not really circular after all.

So too HIV/AIDS researchers create new hypotheses to bolster their belief whenever they seem unable to explain what they observe. Since all the data point to HIV not being infective, or being apparently infective to so low a degree as to be incapable of producing an epidemic, auxiliary hypotheses were suggested which have become accepted as shibboleths:

1. The epidemic in Africa is said to have come about because of an incredible rate of promiscuity. Sexually active South Africans (black South Africans, that is) are postulated to have an average of 10 sexual partners at any give time and to change them about annually (pp. 63-65 in James Chin, The AIDS Pandemic, Radcliffe 2007).
2. Soon after initial infection, there is an “acute phase” where large amounts of HIV are present, and intercourse during that phase makes transmission much more likely: infectivity is very high during these short periods, so overall measurements of transmissibility are deceiving.

The first suggestion is absurd, since such behavior would be so visibly evident that it could not be overlooked; yet it is not observed.

The second suggestion has been undermined by a careful re-analysis of the single study on which it had been based: the “excess hazard-months attributable to the acute phase of infection” is about 5.3, not the previously estimated 31-to-141 (Bellan et al., “Reassessment of HIV-1 acute phase infectivity: accounting for heterogeneity and study design with simulated cohorts”, PLoS Medicine, 12(3):  e1001801).

HIV/AIDS research is chasing red herrings, phantoms, in a decades-long wild-goose change that has been enormously expensive in lives and in dollars. But the interests vested in this state of affairs — drug-company profits, research careers, administrative careers, honors and awards — are so widespread and powerful that the actual evidence is given little or no chance of speaking for itself. Try to imagine what it would take for Anthony Fauci to shed cognitive dissonance and admit that he has been so disastrously wrong.

 

Gay genes and HIV

Some 20 years ago, Dean Hamer reported an association between certain DNA markers and being gay [1]. The report was met with considerable skepticism. Now a new study [2] has reached much the same conclusion as Hamer. This may be relevant to the apparently greater frequency of “HIV-positive” among gay men.

Overall data are clear, that “HIV-positive” does not behave like an infectious condition [3]. More specifically, if “HIV-positive” is ever transmitted sexually then it is with essentially negligible probability, according to the Centers for Disease Control & Prevention:

Heterosexual vaginal transmission is estimated as less than 1 per 1000, but receptive anal intercourse is estimated at 1.4%. This is still less by a large factor than the transmissibility of known venereal diseases like syphilis and gonorrhea. Where does the estimate originate?

It cannot be based on observations in prisons since several such studies reported much lower rates there (p. 47 in [3]). Rather, the estimate likely comes from data on “HIV-positive” among gay men who frequently practice receptive intercourse. In other words, there is a correlation between being gay, receptive anal practices, and testing “HIV-positive”. In prisons, there is a significant amount of anal intercourse by men who are not gay, yet this apparently does not correlate with becoming “HIV-positive”. Evidently it is being gay, more than anal intercourse, that correlates with being “HIV-positive”.

If there is a genetic pre-disposition to being gay, as the Hamer and Sanders studies indicate, then perhaps there is also a genetic pre-disposition among gay men to testing “HIV-positive”.

That some genetic characteristics do predispose to testing “HIV-positive” is demonstrated by racial differences. Men of sub-Saharan ancestry test “HIV-positive” at rates about 7 or 8 times greater than with Caucasian men and about 10 times greater than with Asian men. There are also racial differences in the sensitivity of “HIV” tests to the p24 protein which is one of the “HIV” markers (section 3.4 in The Case against HIV).

I’m not suggesting, of course, that genes could be the sole reason why gay men are more frequently “HIV-positive” than others. Genetic pre-dispositions are probabilistic. Not all gay men test “HIV-positive”. In the earliest days of AIDS, only a small proportion of gay men became ill. Many gay men are both “HIV-positive” and healthy and never contract “AIDS”-type diseases.
Moreover, “HIV-positive” reflects any number of possible conditions, most of which are experienced equally by gay men and everyone else (section 3.2.2 in The Case against HIV).

Similarly, the Hamer and Sanders studies do not suggest that genetics determines sexual orientation, merely that it can bring a heightened tendency; it is explicitly a small effect, to the degree that genetic studies on infants or embryos could not have any useful predictive value [2]. It is widely agreed that behavioral characteristics in general arise from some combination of hereditary and environmental factors. Moreover, it remains to compare the frequent correlation of certain genetic factors with being gay to the overall frequency of those particular factors among all men, which would indicate how strongly those factors may predispose toward a preferred sexual orientation.

So explanations for the greater incidence of “HIV-positives” among gay men are obviously and necessarily partial and multiple. I believe that some proportion of “HIV-positives” among gay men, correlated with also becoming ill, can be explained by the intestinal dysbiosis theory. Here I am suggesting that one possible and additional reason why some gay men are “HIV-positive” may be a genetic pre-disposition, particularly when “HIV-positive” does not correlate with a high probability of illness. Since the markers identified by Hamer and Sanders are not exclusive to gay men, a linkage between those markers and testing “HIV-positive” could also explain some of the incidence of “HIV-positive” among men who are not gay.
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[1] Dean H. Hamer et al., “A linkage between DNA markers on the X chromosome and male sexual orientation,” Science 261 (1993) 321-7
[2] A. R. Sanders et al., “Genome-wide scan demonstrates significant linkage for male sexual orientation”, Psychological Medicine 45 (2015) 1379-88
[3] Henry H. Bauer, The Origin, Persistence and Failings of HIV/AIDS Theory, McFarland 2007

 

Race, HIV, media pundits

People carrying black-African genes test “HIV-positive” at far greater rates than do people without that genetic ancestry. HIV/AIDS theory “explains” that by postulating greater rates of careless “not-safe-sex” promiscuity and infected-needle-sharing drug injection. Thereby HIV/AIDS theory postulates significant genetic determination of behavior, which in other contexts is dismissed as pseudo-science.

Moreover, actual observations and studies have repeatedly shown that the facts vitiate that proposed “explanation”: Africans and African-Americans indulge in risky behavior at lower rates than do white Americans (pp. 77-9 in The Origin, Persistence and Failings of HIV/AIDS Theory).
The conclusion is inescapable: HIV/AIDS theory is radically wrong about how “HIV-positive” is transmitted.

But that inescapable conclusion continues to escape mainstream practitioners and researchers and such media pundits as Donald G. McNeil Jr. of the New York Times (Poor Black and Hispanic men are the face of H.I.V.):

“The AIDS epidemic in America is rapidly becoming concentrated among poor, young black and Hispanic men who have sex with men”
NO. There’s nothing recent or rapid about it. The racial disparities have always been there (Chapters 5 & 6 in The Origin, Persistence and Failings of HIV/AIDS Theory).
Furthermore, it is black WOMEN who are most affected compared to others, 20 times more likely to be “HIV-positive” than white women, whereas for males the ratio is (“only”) 7.

“Nationally, 25 percent of new infections are in black and Hispanic men, and in New York City it is 45 percent”
Yes, of course, because it’s blackness that contributes overwhelmingly to testing “HIV-positive”. Hispanics in New York are primarily of black Caribbean-African stock, whereas West-Coast Hispanics are largely non-black, of Latin-American stock. Therefore national-average rates of “HIV-positive” among Hispanics are lower than East-Coast Hispanic rates of “HIV-positive” (pp. 57-8, 71-2 in The Origin, Persistence and Failings of HIV/AIDS Theory).

“Nationally, when only men under 25 infected through gay sex are counted, 80 percent are black or Hispanic — even though they engage in less high-risk behavior than their white peers” [emphasis added]; “a male-male sex act for a young black American is eight times as likely to end in H.I.V. infection as it is for his white peers. That is true even though, on average, black youths in the study took fewer risks than their white peers: they had fewer partners, engaged in fewer acts of sex while drunk or high, and used condoms more often”.
So McNeil is even aware of this conundrum which falsifies the central axiom of HIV/AIDS theory, namely, that HIV is transmitted as a result of risky behavior. Yet he does not follow this statement of fact with any explanation of this paradox which contradicts and falsifies mainstream views.
Instead, McNeil passes on without comment the usual meaningless weasel-words about some unspecified “intervention”:
“Critics say little is being done to save this group, and none of it with any great urgency. ‘There wasn’t even an ad campaign aimed at young black men until last year — what’s that about?’. Phill Wilson, president of the Black AIDS Institute in Los Angeles, said there were ‘no models out there right now for reaching these men’”.
What conceivable use could any models be, when it’s acknowledged that these supposedly at-high-risk people already practice less risky behavior than the no-high-risk white folk?
Still, of course there’s no harm in asking for more money even in absence of any clue what to do with it:
“With more resources, we could make bigger strides”.

What the mainstream says about the high rates of black “HIV-positives” is pitifully, woefully inadequate; it misses the whole point. It suggests that although their behavior is less risky, black folk have “other risk factors. Lacking health insurance, they were less likely to have seen doctors regularly and more likely to have syphilis, which creates a path for H.I.V.”
But it’s yet another counterfactual canard that syphilis and other STDs make it more likely that someone will “contract” “HIV”, i.e. become “HIV-positive”: there is simply no correlation between incidence of STDs and of “HIV” (pp. 31-5, 109 in The Origin, Persistence and Failings of HIV/AIDS Theory).
As to insurance, what is the evidence that having health insurance makes for lower rates of being or becoming “HIV-positive”? This is simply hand-waving bullshit* emitted because no sensible explanation can be offered.
As to seeing doctors regularly, what is the evidence that seeing doctors regularly makes for lower rates of being or becoming “HIV-positive”? Quite the opposite, in fact: The largely white gay men who first contracted “AIDS” had mostly been seeing doctors very often because of their constant need for treatment after suffering all sorts of illnesses. Dr. Joseph Sonnabend, with a practice of largely gay clients in New York in the 1970s, had in fact warned his regular customers that if they did not change their lifestyle something drastic and awful would befall them.

And then, “Other risk factors include depression and fatalism” — What, pray, is the mechanism by which those conditions produce “HIV-positive”? Among people who are acknowledged to behave less riskily than those who are not at high risk of becoming “HIV-positive”?

Another popular non-explanation is that blacks become “HIV-positive” more often because “HIV-positive” is so much more common in the black community: It’s more common because it’s more common.

I cannot imagine a higher degree of hypocrisy, intellectual vapidity, sheer unwillingness to draw obvious conclusions from undisputed facts, than is demonstrated without fail and without end by mainstream researchers, doctors, and pundits when confronted with the plain fact that blackness makes for being “HIV-positive”.

Not that this perverse behavior is much different from behaving as though testing “HIV-positive” proved infection by “HIV” when standard authorities have long stated quite forthrightly that there is no gold standard “HIV” test, no test capable of demonstrating actual infection by “HIV”, and that the rates of false positives are inevitably high (Stanley H. Weiss & Elliot P. Cowan, “Laboratory detection of human retroviral infection”, chapter 8 in Gary P. Wormser (ed.), AIDS and Other Manifestations of HIV Infection, 2004 (4th ed.).

No technical expertise is needed to recognize the sheer unadulterated nonsense of talking about “risk factors” when the known end-result is less risky behavior. How can any number of purported risk factors be alleged to heighten risk when the facts show that the risk is lower of the only behavior that supposedly transmits “HIV”?

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* Words uttered without regard to their truth — Harry Frankfurt, On Bullshit, Princeton University Press, 2005.

Race, HIV/AIDS, peer review

Reading recently a critique of peer review reminded me of the experience I had with the DuBois Review: Social Science Research on Race [1], and it also reminded me that I continue to regard the race-associated epidemiology of “HIV” as a salient Achilles’ Heel of HIV/AIDS theory.

The mainstream has completely avoided, refused, to face an inescapable dilemma: If HIV/AIDS theory is correct, that “HIV” spreads primarily by sexual intercourse and secondarily via infected needles, then adults who become “HIV-positive” did so in one of those ways. If an identifiable social or ethnic or racial group is always “HIV-positive” more than other groups, then the members of that group are more carelessly sexually promiscuous or more addicted to drug-injecting than are other human beings.
People of African ancestry test “HIV-positive” at a higher rate than others, always and everywhere [2] — in Africa, in the Caribbean, in Europe, in the USA. In the latter, most noteworthy is that Hispanics on the East Coast, who are largely of African ancestry, test “HIV-positive” at rates comparable to those of African-Americans, whereas West-Coast Hispanics, who are predominantly Central and South American, test “HIV-positive” at the much lower rates found among Native Americans. So African ancestry determines being “HIV-positive” even within a socially defined cultural or ethnic or language group like American Hispanics.

Therefore, if HIV/AIDS theory were correct, then African ancestry would significantly determine behavior that includes a much higher rate of careless promiscuity or drug-injecting addiction than is seen in people of non-African ancestry. “Much higher” might better be “extraordinarily higher”: a factor of more than 20 in Africa [2], and in the USA a factor of 20 for black females compared to white females and 7 for black males compared to white males [3]. Furthermore, since the observed or calculated rate of sexual transmission of “HIV” is so low, a phenomenal rate of promiscuity would be called for: 20-40% of adults having something like a dozen sexual partners concurrently and changing them about annually [4].

Never before has sexual behavior been ascribed by mainstream science to genetic determination in this fashion. Nor has any other behavioral characteristic ever been acknowledged to be so genetically determined and race-associated. Indeed, the very notion of behavior being significantly influenced by genetic factors (“sociobiology”, “evolutionary psychology”) remains highly controversial. HIV/AIDS theory is at odds with the mainstream consensus on the relationship between genes and behavior, moreover in a way that is consistent with now-largely-repudiated racial stereotypes.

I was taken aback, therefore, when the Centers for Disease Control & Prevention insisted to me that racial disparities in testing “HIV-positive” could be explained on behavioral grounds (p. 75 in 2]). In any case, the conundrum is quite plain, irrespective of theories about genetic determination of behavior:
Either African ancestry determines extraordinarily careless promiscuity of an extraordinarily high rate, possibly also an inconceivably high rate of sharing infected needles, or HIV/AIDS theory is plain wrong.

I continue to believe that this ought to be of prime significance to African-Americans. Official explanations try to skirt the issue and thereby make no sense, for example [3]:
“The greater number of people living with HIV in African American communities and the fact that African Americans tend to have sex with partners of the same race/ethnicity means that they face a greater risk of HIV infection with each new sexual encounter” — In other words, a classic tautology: there’s more HIV because there’s more HIV. But why are more African Americans “living with HIV” in the first place?
“African American communities have higher rates of other sexually transmitted infections (STIs) compared with other racial/ethnic communities in the United States. Having an STI can significantly increase the chance of getting or transmitting HIV” — First, it is simply not true that African Americans always and everywhere have higher rates of STIs. Second, it is simply not true that rates of STI incidence correlate with rates of “HIV-positive” (p. 31 ff. in [2]), and anyway the racial disparities in testing “HIV-positive” are seen even among people who have STIs (Figure 12, p. 42 in [2]). Third, even if STIs and “HIV” did correlate, the same conundrum would apply of apparent racial determination of carelessly promiscuous sexual behavior.
“The poverty rate is higher among African Americans — 28% — than for any other race. The socioeconomic issues associated with poverty — including limited access to high-quality health care, housing, and HIV prevention education — directly and indirectly increase the risk for HIV infection” — This is waffling, no real explanation, simply bullshit [5]. In Africa, “HIV-positive” rates are greater among the higher economic strata of Africans [6].

Current official statements and practices emphasize that “HIV/AIDS” has become largely a problem for African-Americans and their communities. That is damaging in several ways: increasing the pressure on black Americans to be tested and thereafter subjected to toxic antiretroviral drugs; causing untold harm to people and their families who happen to test “HIV-positive”, for which there are innumerable possible causes (see The Case against HIV); and providing apparent support for racist stereotypes;

Half-a-dozen years ago, such considerations led me to submit a manuscript posing this conundrum or dilemma to what would seem the most obviously appropriate journal, the DuBois Review: Social Science Research on Race. I’ve already described briefly the fate of that MS. [1]. I said there that the journal did not give me permission to reproduce the reviewers’ comments verbatim, but looking back on the e-mail correspondence, I see that they did not refuse permission, they simply did not respond to my query. Furthermore, the reviewers’ comments were not marked confidential, neither was my e-mail correspondence with the journal. So I’ve decided that the full story might interest some of my readers, and I post here copies of my manuscript, of the reviewers’ comments, and of my correspondence with the journal.

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[1] Pp. 49-50 in Dogmatism in Science and Medicine: How Dominant Theories Monopolize Research and Stifle the Search for Truth
[2] The Origin, Persistence and Failings of HIV/AIDS Theory
[3] Centers for Disease Control & Prevention, “HIV among African Americans”, February 2013, February 2014
[4] James Chin, The AIDS Pandemic, Radcliffe, 2007, p. 64
[5] Harry G. Frankfurt, On Bullshit, Princeton University Press, 2005
[6] Theo Smart, “Structural Factors — PEPFAR: Greater wealth, not poverty, associated with higher HIV prevalence in Africa, according to survey”, nam-aidsmap, 2 August 2006