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.

Larry Kramer in Love and Anger

Larry Kramer in Love and Anger is a 2015 HBO documentary. It recounts most of the history of AIDS through Kramer’s personal involvement and it is largely accurate in what it discusses, though omitting and ignoring some crucial points.

Watching it brought home to me once again what an enormous tragedy this has been and still is and will continue to be because the ultimate crux remains unaccepted: namely, that “science” including medical science can go wrong, and that there are no systemic safeguards against that, no checks or balances, because minority voices within the scientific community are not attended to, instead are castigated and persecuted.

This film gives a good account of the fear that spread among gay men as a mysterious syndrome of illnesses was bringing deaths, several hundred thousand in about half-a-dozen years. But the film also misses the opportunity to make the case against HIV, despite some significant clues. Thus Kramer’s 1978 novel, Faggots, is correctly described as his jeremiad against the fast-lane lifestyle that included much health-damaging use of “recreational” drugs. The film might well have been pointed out that this preceded the appearance of AIDS and could indeed explain why so many people became very ill — as some of them recognized, for instance Michael Callen and his physician Sonnabend. Again, Kaposi’s sarcoma (KS) is mentioned as a characteristic AIDS disease, but the film neglects to point out that KS virtually dropped out of the picture after some years as insightful gay men abandoned the use of the nitrite inhalants (“poppers”) that cause this damage to blood vessels (“AIDS KS” is probably different from the classic KS.)

Completely missing is the tragic story of how HIV came to be the accepted cause of AIDS, essentially by declaration at a press conference before any scientific publication.

Kramer’s initiatives are properly credited for revision of the FDA’s procedures for approving drugs — but missing is a discussion of the damaging consequences, not only because of the toxicity of AZT and later “anti-retroviral” drugs but because the fast-track approval system is now abused routinely by Big Pharma to bring to market avalanches of new drugs that reveal their toxicity within a short time after marketing: note the TV and print announcements by lawyers about class-action suits against such medications as Pradaxa, Xeralto, Invokana, and others at the very same time as the drug companies continue to advertise those drugs with dishonest descriptions of potential benefits (“remission is possible”, for example) and down-playing of “side” effects, for instance in TV ads showing healthy actors instead of actual patients actually on the drugs.

The film applauds the introduction of protease inhibitors, but fails to describe their toxicities, again despite obvious clues. Thus the film opens and closes with Kramer in hospital after a liver transplant; and there is a short clip of Kramer warning earlier about the side effects of his medications. The New York Times review of the film of course says, misleadingly, “liver transplant necessitated by his H.I.V. infection” instead of “made necessary by the anti-retroviral medication including protease inhibitors”: “Drug-induced hepatitis and hepatic decompensation (and rare cases of fatalities) have been reported with all PIs” (Table 14, Guidelines for the Use of Antiretroviral Agents in HIV-1-Infected Adults and Adolescents, 8/8/2014).

And of course nothing is said about dissent from HIV/AIDS theory.

So this documentary can serve only as a reminder of the tragic history of AIDS. I realized also how the nature of the tragedy has changed. Initially it was the mis-identification of the cause as HIV and the subsequent hundreds of thousands of deaths from AZT. But nowadays this has been compounded by the abuse of HIV tests as proof of infection, whereby no sector of society is free from the danger of mis-diagnosis and subsequent mistreatment. Since pregnancy seems to stimulate positive “HIV” tests, especially with women of African ancestry, women and their fetuses and babies are being harmed in significant numbers and will continue to be until the HIV/AIDS blunder is corrected.

For the facts about HIV and AIDS, see The Case against HIV. For why HIV cannot be the cause of AIDS, and the story of how the error was made and entrenched, read The Origin, Persistence and Failings of HIV/AIDS Theory [Jefferson (NC): McFarland 2007].

About money, and HIV in Estonia

A correspondent from Estonia shared this recent news:

“Unique HIV is spreading in Estonia
Research has shown that recombined (?) [recombinant = hybrids of the known “strains”] form of HIV spreads in Estonia. People get infected locally and it is not brought in from abroad.
‘We have done more than 10 years of research and we do not have exporters [?importers?] of HIV, we do not get it from Russia or Western Europe’, says Irja Lutsar, professor of medical microbiology and virology. She added that people get infected with HIV locally and a recombined [recombinant] form of HIV is spreading here.
‘Our virus is unique but if you ask where it came from then I do not know answer to that.’”

Professor Lutsar might find some clues in de Harven’s article in Journal of the American Physicians and Surgeons  as well as in The Case against HIV.

“Also, US, British and Finnish embassies here recently wrote a public letter to Estonian parliament about HIV”.

Part of that letter reads;
“The U.S. President’s Emergency Plan for AIDS Relief (PEPFAR) is the largest commitment by any nation to combat a single disease. Through PEPFAR, the U.S. government works with vulnerable, developing nations on a framework to combat HIV/AIDS. Since 2009, the U.S. government has committed nearly $65 billion to support PEPFAR and its global HIV/AIDS response. While gains have been real, progress against this disease, even in the United States, has been uneven.”

That inevitably brought to mind the quote attributed to the late Republican fiscal conservative, Senator Everett Dirksen:

“A billion here, a billion there, pretty soon, you’re talking real money”.

(As commonly with the most delightful quotes, this may be a mis-attribution)

At any rate, the United States has apparently disbursed $65 billion without anyone getting any benefit and some undoubtedly being harmed as a result of being fed toxic drugs while not only healthy but even HIV-negative.
I shouldn’t have said, of course, that no one benefited. The drug companies and their shareholders and executives have certainly benefited.

 

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

 

Antiretrovirals kill: Official data, peer-reviewed journal

(updated with full article)

HIV+ people in hospital who were on anti-retrovirals were more likely to die of non-AIDS conditions than HIV+ people NOT being treated with ARVs. The deaths were owing to known “side” effects of ARVs: cardiovascular, liver, various infections.

That is reported in the paper drawn to my attention by a comment from lukas. Note that the data covers a period of 16 years beginning with the introduction of “life-saving HAART cocktails” in the mid-1990s:

Cowell et al., TRENDS IN HOSPITAL DEATHS AMONG HUMAN IMMUNODEFICIENCY VIRUS-INFECTED PATIENTS DURING THE ANTIRETROVIRAL THERAPY ERA, 1995 TO 2011,
Journal of Hospital Medicine, 30 June 2015 doi: 10.1002/jhm.2409. [Epub ahead of print]

Here is the full paper, courtesy of David Rasnick:

Cowell 2015 copy

And here is just the abstract:

RESULTS:
In-hospital deaths declined significantly from 1995 to 2011 (P < 0.0001); those attributable to non-AIDS increased (43% to 70.5%, P < 0.0001). Non-AIDS deaths were most commonly caused by non-AIDS infection (20.3%), cardiovascular (11.3%) and liver disease (8.5%), and non-AIDS malignancy (7.8%). Patients with non-AIDS compared to AIDS-related deaths were older (median age 48 vs 40 years, P < 0.0001), more likely to be on ART (74.1% vs 55.8%, P = 0.0001), less likely to have a CD4 count of <200 cells/mm3 (47.2% vs 97.1%, P < 0.0001), and more likely to have an HIV viral load of ≤400 copies/mL (38.1% vs 4.1%, P < 0.0001). Non-AIDS deaths were associated with 4.5 and 4.2 times greater likelihood of comorbid underlying liver and cardiovascular disease, respectively.
CONCLUSIONS:
Non-AIDS deaths increased significantly during the ART era and are now the most common cause of in-hospital deaths; non-AIDS infection, cardiovascular and liver disease, and malignancies were major contributors to mortality. Higher CD4 cell count, liver, and cardiovascular comorbidities were most strongly associated with non-AIDS deaths. Interventions targeting non-AIDS-associated conditions are needed to reduce inpatient mortality among HIV-infected patients. Journal of Hospital Medicine 2015. © 2015 Society of Hospital Medicine.
© 2015 Society of Hospital Medicine.

This journal is not held by our library, and I’m waiting for Interlibrary Loan to get me a copy. IN the meantime, the abstract’s details given above seem to tell the story clearly enough.