WHY UNAIDS SHOULD BE DISBANDED

James Chin, formerly epidemiologist at the World Health Organization and currently clinical professor of epidemiology at the School of Public Health, University of California at Berkeley, adds further weight to the call (A SMALL HITCH IN THE BANDWAGON?) to end the UN’s HIV program. In the China Post (Taiwan), Chin wrote (“Myths behind AIDS might lead to billions in misspending”, 18 May 2008):

“UNAIDS — the U.N.’s specialist AIDS advocacy body — has raised some US$110 billion for the next five years: . . . AIDS will shortly become the biggest single item in foreign aid. . . . UNAIDS has systematically exaggerated the size and trend of the pandemic, in addition to hyping the potential for HIV epidemics in ‘general’ populations. . . .  But UNAIDS’s claims are not supported by the epidemiologic data.
. . .
UNAIDS has ignored this and promoted a range of myths that have more to do with political correctness than science.
For instance, UNAIDS claims that poverty and discrimination are major determinants of high HIV prevalence. In 1987, John Mann, the first head of AIDS at the World Health Organization, claimed that being ‘excluded from the mainstream of society or being discriminated on grounds of race, religion or sexual preference, led to an increase of HIV infection,’ a litany uncritically accepted by UNAIDS.
All available data suggests the opposite. In Africa, AIDS is a disease associated with wealth. The richest people in Kenya, Tanzania and Ethiopia have HIV rates several times higher than the poorest, probably because wealthy men and women in these countries have more sex partners. [[More likely, the reason is that it’s among the wealthy that drug abuse is more common, and the illnesses that are caused directly by overindulgence in drugs]]
Poverty and discrimination present barriers to gaining access to prevention and treatment but are not primary determinants of sexual behavior . . . .

UNAIDS has consistently claimed that the world is on the brink of generalized heterosexual HIV epidemics. . . . [To the contrary, a] recent report by an independent commission on AIDS in Asia has acknowledged that epidemic sexual HIV transmission has not spread in Asia beyond the highest HIV-risk groups, such as gay men, injecting drug users, and sex workers, into any general population. However, UNAIDS’s perpetuation of the myth that everyone is at risk of AIDS has led to billions wasted on HIV prevention programs directed at general populations and especially youth, who, outside of sub-Saharan Africa, are at minimal risk of any exposure to HIV.
. . . .
At least US$5 billion has been wasted in this way in the last five years. Meanwhile, to the shame of the global health bureaucracy, a handful of diseases that are relatively inexpensive to prevent or treat — several vaccine-preventable diseases, diarrheal diseases, malaria and some acute respiratory infections — continue to account for about four million annual child deaths globally.
. . . . HIV is incapable of epidemic spread in the vast majority of heterosexual populations.
Continued denial of these realities will further erode whatever credibility UNAIDS and other mainstream AIDS agencies and experts may still have, and will seriously damage the future fight against this disease: let’s face the data and put the money where the real problems really are” [emphases added].

Chin is author of The AIDS Pandemic. The China Post story reports also that his The Myth of a ‘General’ AIDS Pandemic is to be published this month by the Campaign for Fighting Diseases. The latter is described in Wikipedia as funded by pharmaceutical companies. The Campaign’s own website is inscrutable as to its funding and governance.

A SMALL HITCH IN THE BANDWAGON?

“Health expert calls for end to UN HIV programme” (InTheNews.co.uk, 9 May 2008 )

“The joint United Nations programme on HIV and Aids should be ‘closed down rapidly’, according to . . . Roger England, chairman of Health Systems Workshop — an independent advisory group on health management in poor countries — . . . [because] its mandate is “wrong and harmful”. . . . Writing in the British Medical Journal (BMJ), Mr England says the agency was set up on the argument that HIV and its impact are exceptional.  But he writes that this argument is no longer valid and says the claims HIV needs its own body as it can tip households into poverty would also apply to all serious diseases and disasters. ‘HIV is a major disease in southern Africa, but it is not a global catastrophe, and language from a top UNAids official that describes it as ‘one of the make-or-break forces of this century’ and a ‘potential threat to the survival and well-being of people worldwide’ is sensationalist . . . . Worldwide the number of deaths from HIV each year is about the same as that among children aged under five years in India. . . . far too much is spent on HIV relative to other needs and . . . this is damaging health systems . . . . HIV causes 3.7 per cent of mortality but receives a quarter of international healthcare aid and a “big chunk” of domestic expenditure. ‘HIV exceptionalism is dead — and the writing is on the wall for UNAIDS. . . .  Why a UN agency for HIV and not for pneumonia or diabetes, which both kill more people? . . . UNAids should be closed down rapidly, not because it has performed badly given its mandate, which it has not, but because its mandate is wrong and harmful. Its technical functions should be refitted into [the World Health Organisation], to be balanced with those for other diseases.’”

Similarly, in the United States the expenditure on HIV/AIDS research dwarfs that on major killers like cancer or cardiovascular disease: 20 times as much per “HIV” death than per cancer death, 100 times as much per “HIV patient” as per cardiovascular patient (STOPPING THE HIV/AIDS BANDWAGON—-Part II, 1 February 2008).

Perhaps free-market economics can slow the bandwagon?

After all, if funds start to dry up, then the propaganda will also begin to ebb. So long as UNAIDS exists, it will seek to justify its existence by putting out the scary pseudo-statistics that James Chin, for example, has debunked (CONDOMS AND HIV: WHAT EVERYONE KNOWS IS ONCE AGAIN WRONG, 10 February 2008;  B***S*** about HIV from ACADEME via THE PRESS, 4 March 2008).

But I am not holding my breath. Too many careers and livelihoods depend on the disproportionate attention paid to HIV/AIDS. And what happens to drug sales and profits if TB, malaria, intestinal worms, malnutrition, become the focus? All those can be handled at far less expense than the provision of toxic antiretroviral drugs.

RACE and SEXUAL BEHAVIOR: STEREOTYPE vs. FACT

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).

*******************

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.

UPDATE: MORE SPONTANEOUS SEROREVERSION

According to HIV/AIDS dogma, testing “HIV-positive” denotes infection by “HIV” which is permanent and ineradicable. One of several independent proofs that HIV/AIDS theory is wrong is the fact that people do spontaneously revert from “HIV-positive” to “HIV”-negative, perhaps most notably and frequently, babies born “HIV-positive” and reformed drug abusers (p. 96 ff. in The Origin, Persistence and Failings of HIV/AIDS Theory). But whenever spontaneous reversion happens to be noticed, it’s treated as the secular equivalent of a miracle (HIV “INFECTION” DISAPPEARS SPONTANEOUSLY, 22 January 2008). Here are a couple more instances:

“BEIJING, Dec. 3 (Xinhua) — A farmer in northeast China’s Jilin Province has tested HIV negative, six years after being diagnosed as HIV-positive, according to the provincial Center of Disease Control (CDC).
Wen Congcheng . . . first tested HIV positive in 2001 [during testing of blood donors]. . . . Late in 2003, he was re-confirmed to have HIV/AIDS as a result of another test . . . . However, in July this year [2007], Wen received a negative test result at the No. 1 Clinical Hospital of Beihua University in Jilin. Wen decided to seek another opinion and went to the First Hospital of the China Medical University and another three hospitals for HIV tests, which all proved to be negative. The Jilin municipal CDC carried out a follow-up test which confirmed the negative result, and later the provincial CDC also confirmed the result.”

But, of course, the white-coated gurus refuse to accept this, and have questioned the original positive result, while the lab that made the diagnosis sticks by it.

“ ‘I am pretty sure there are no problems with the blood samples and the tests,’ said Liu Baogui, former director of the HIV/AIDS and STD Section of the CDC of Jilin City. . . . Professor Wu Min, a member of the HIV/AIDS experts’ committee under the Ministry of Health, is sceptical about the validity of the original positive test result. ‘I can not believe that such miracle could have really happened,’ he said. ‘Some patients appear to be free of the virus after effective treatment, but the HIV anti-body is always there, so the test result will still be positive.’ Wu said the inaccuracy rate of tests by the provincial CDCs is lower than 0.01 percent. ‘But it is possible that the person’s name and blood sample was mixed up at the Chuanying District CDC where Wen tested HIV positive for the first time,’ he said.
. . .
In 2003, Andrew Stimpson, a 25-year-old Briton, tested HIV-negative 14 months after testing positive in May 2002. The case has never been scientifically explained.”

And here’s more detail about Andrew Stimpson:

“Doctors baffled as HIV man ‘cures’ himself” (Sophie Kirkham, Sunday Times, 13 November 2005)

“A MAN who tested positive for HIV, the virus that causes Aids [sic, British usage], has subsequently shown up negative for the disease in a case that has mystified doctors. It was claimed last night that Andrew Stimpson, 25, may have shaken off the virus with his own immune system after contracting HIV in 2002.
If proved, the NHS has said the case would be ‘medically remarkable’. … The Chelsea and Westminster Healthcare NHS trust, which treated Stimpson, has said he needs to undergo more tests before it can be established how he apparently conquered HIV. ‘These tests were accurate and they were his, but what we don’t know at the moment is why that has happened, and we want him to come back in for more tests… It is potentially a fantastic thing.’ Stimpson was tested three times in August 2002 … and the results showed he was producing HIV antibodies to fight the disease. Stimpson … contracted the virus from his boyfriend, Juan Gomez, 44. He began taking vitamins and other dietary supplements to keep his body healthy in the hopes that this might fend off the development of full-blown Aids. In October 2003, after impressing doctors with his good health, Stimpson was offered a new test, which came back negative. Further tests in December 2003 and March last year also proved negative. … ‘I couldn’t understand how anyone could cure themselves of HIV . . . I thought it had to be wrong because no one can recover from HIV, it just doesn’t happen.’ The tests were re-checked by the Chelsea and Westminster Healthcare NHS Trust when Stimpson threatened litigation believing there must be a mistake, but the results confirmed all the tests had been accurate. In a letter understood to be from the NHS Litigation Authority in October this year, Stimpson was told: ‘The fact you have recovered from a positive antibody result to a negative result is exceptional and medically remarkable.’ The trust said there had been several other cases of claimed ‘spontaneous clearance’ of the virus worldwide, although it is not believed any have been proved. A spokeswoman added that the trust had urged Stimpson to return for tests, but that so far he had not done so.”

If I were Stimpson, I too would decline further tests administered by people who would love to be able to tell me that I do, after all, have an incurable and fatal illness. Stimpson’s case is readily explicable by Tony Lance’s intestinal dysbiosis hypothesis [WHAT REALLY CAUSED AIDS: SLICING THROUGH THE GORDIAN KNOT, 20 February 2008] or by the Perth-Group view that testing HIV-positive merely denotes oxidative stress. It was not that Stimpson “contracted the virus from his boyfriend”, but that they shared a lifestyle conducive in some manner to oxidative stress or intestinal dysbiosis.

THE “GALILEO GAMBIT STRAWMAN”

Perhaps the most common reaction to dissident arguments is the argumentum ad populum, more commonly known as the “argument from consensus”. You know, “Fifty Million Frenchmen Can’t Be Wrong”. This is perfectly exemplified by a quote Robert Gallo gave to Anthony Liversidge in 1989:

“There is no organized body of science that thinks it is anything but comedy with Peter right now. That’s the fact. Why does the Institute of Medicine, WHO (World health Organization), CDC (Centers for Disease Control), National Academy of Sciences, NIH, Pasteur Institute and the whole body of science 100 percent agree that HIV is the cause of AIDS? If there was anything to what Peter is saying, wouldn’t it occur to you that there would be some other scientists that would agree with Peter? Can you tell me anyone?”

Twenty years later, little has changed:

“Debating denialists dignifies their position in a way that is unjustified by the facts about HIV/AIDS. The appropriate way for dissenting scientists to try to persuade other scientists of their views on any scientific subject is by publishing research in the peer-reviewed scientific literature. For many years now, AIDS denialists have been unsuccessful in persuading credible peer-reviewed journals to accept their views on HIV/AIDS, because of their scientific implausibility and factual inaccuracies. That failure does not entitle those who disagree with the scientific consensus on a life-and-death public health issue to then attempt to confuse the general public by creating the impression that scientific controversy exists when it does not.” — “Answering AIDS Denialists”, AIDSTruth.org

The argument from consensus is a logical fallacy. The truth of a claim is not dependent on how many people hold the claim to be true. There are many counterexmaples from history, but a favorite is Galileo’s advocacy of Copernicanism. The response runs as follows: “Almost everyone thought Galileo was wrong, but he turned out to be right. Therefore, just because almost everyone thinks something is true, doesn’t make it so.”

The fallaciousness of the argument from consensus is a banal fact which is hardly in dispute. Therefore, people arguing from consensus are forced to either defend their claims with other valid arguments or to defend the argument from consensus with further logical fallacies. The clever try their hand at the former; the dim-witted almost invariably try their hand at the latter by using a logical fallacy I like to call the “Galileo Gambit Strawman”.

The idea behind the fallacy is to replace the above response to the argument from consensus with a strawman called the “Galileo Gambit”. The fallacy runs like this: “Yes, Galileo was right when almost everyone thought he was wrong. However, for every Galilieo, there are a thousand Bozo the Clowns who are wrong. Just because you compare yourself to Galileo, doesn’t mean you are right. You are far more likely to be wrong. Stop using the ‘Galileo Gambit’.”

The “Galileo Gambit” has become a favorite tactic of pseudo-skeptics, as it was recently popularized by one of our favorite surgeons-turned-blogger “Orac” (“Respectful Insolence”), certainly familiar to many readers of this blog. Unfortunately for dear Orac and his readers, it is a strawman argument.

When someone invokes Galileo as a counterexample against the argument from consensus, they are not asserting that because almost everyone disagrees with them, they are necessarily correct in their claims. Such an argument is patently absurd, and I have rarely, if ever, seen it advanced. When someone invokes Galileo, they are not claiming that such a comparison is sufficient to establish their claim, they are simply asserting that the example of Galileo provides evidence that consensus itself is insufficient reason to reject a claim.

The Galileo Gambit Strawman is committed in response to a perceived use of the Galileo Gambit, not the Galileo Gambit itself. It is ironic that such an elementary and obvious logical fallacy as this is perpetrated almost invariably by those who most claim to be “rational”, “skeptical”, and “scientific”.

APPENDIX

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For those wishing a more precise mathematical explication of the “Galileo Gambit Strawman” fallacy:

Let

D = “Everyone disagrees with me.”, and

R = “I am right.”

The skeptic is saying

“~(D ==> ~R),”

where “~” indicates logical negation, in words,

“It is not the case that because everyone disagrees with me, I am necessarily wrong.”

The defender counters

“~(D ==> R)”

in words,

“It is not the case that because everyone disagrees with you, you are necessarily right.”

The statement

“(D ==> R)”

in words,

“Everyone disagrees with me, therefore I am right.”

is called the “Galileo Gambit”, and it is correctly described as a fallacy.

But the skeptic did not say “(D ==> R)”, they said “~(D ==> ~R)”. So I call the strawman counter above from the defender the “Galileo Gambit Strawman”.

The Galileo Gambit Strawman then takes the precise form:

“~(D ==> ~R) <==> (D ==> R)”

The first statement is the correct argument against the argument from consensus. The second statement is the fallacious Galileo Gambit. Taking the two statements to be logically equivalent is the fallacious Galileo Gambit Strawman.