“Persistent crack users were over three times as likely as non-users to die from AIDS-related causes, controlling for use of HAART self-reported at 95% or higher adherence, problem drinking, age, race, income, education, illness duration, study site, and baseline virologic and immunologic indicators. Persistent crack users and intermittent users in active and abstinent phases showed greater CD4 cell loss and higher HIV-1 RNA levels controlling for the same covariates. Persistent and intermittent crack users were more likely than non-users to develop new AIDS-defining illnesses controlling for identical confounds. These results persisted when controlling for heroin use, tobacco smoking, depressive symptoms, hepatitis C virus coinfection, and injection drug use. CONCLUSION: Use of crack cocaine independently predicts AIDS-related mortality, immunologic and virologic markers of HIV-1 disease progression, and development of AIDS-defining illnesses among women” (Cook et al., “Crack cocaine, disease progression, and mortality in a multicenter cohort of HIV-1 positive women”, AIDS 22 [2008] 1355-63 ).

Of course the authors of this study don’t admit that it is the cocaine that causes the “HIV-1 disease progression” and “AIDS-related mortality”; they interpret the results as signifying that crack cocaine somehow enhances the evil effects of HIV.

Cook et al. controlled, commendably, for many conceivably confounding variables: heroin use, tobacco smoking, depressive symptoms, hepatitis C virus co-infection, injection drug use (crack cocaine is smoked, not injected). But they failed to control for the single most centrally relevant variable: “HIV-positive”. What would have been the findings had the comparison been between crack users who are HIV-negative and others who are “HIV-positive”?

But, of course, such controls might be very difficult to find, especially with comparable levels of drug intake, because drug abusers test “HIV-positive” as frequently as do TB patients and fast-lane gay men:

Whatever it is that stimulates an “HIV-positive” response--or rather, whatever “they” are, whatever range of molecular species it is that can produce an “HIV-positive” response--, evidently most or all “recreational” drugs are capable of doing so, as well as of causing illnesses that could be called “AIDS”.

Everything in this article by Cook et al., and in other literature cited there, is readily explained on the basis that crack cocaine and other drugs produce an “HIV-positive” response, ill health in general, and specific damage to the immune system. Cocaine has been shown to cause “immune alterations”, “decreasing operation of important immune responses”. It causes “membrane permeability” permitting passage across the “blood-brain barrier”---recall Tony Lance's report (gay-related-intestinal-dysbiosis.pdf) that “leaky gut syndrome” seems able to produce an “HIV-positive” response as well as illness [WHAT REALLY CAUSED AIDS: SLICING THROUGH THE GORDIAN KNOT, 20 February 2008]. Cocaine has been shown to interfere specifically with the Th1-Th2 balance that seems involved in “HIV-positive” and in AIDS [Culshaw, Journal of American Physicians and Surgeons 11 (#4, Winter 2006) 101-5; Sacher, AIDS AS INTESTINAL DYSBIOSIS, 23 February 2008, and ALTERNATIVE TREATMENTS FOR AIDS, 25 February 2008]. One cited study had already reported crack use as stimulating progression to AIDS. Another study had found “the risk of AIDS-related opportunistic conditions was greater for persistent users  and intermittent  users  during periods of active use, with no difference during periods of abstinence” [emphasis added], consistent with reports that HIV-positive drug abusers revert to HIV-negative when they abstain (Moss et al., AIDS 8 (1994) 223–31). The cited finding that “hard drug use (i.e., cocaine, heroin, methadone, or injection drugs) was significantly associated with AIDS-defining illnesses, but not with change in CD4 cell count, HIV- RNA, or mortality” is consistent with the finding that CD4 counts, viral load, and clinical progression are not directly correlated (Rodriguez et al., JAMA 296 [2006] 1498-1506). The cited fact from another study that “cocaine in combination with alcohol places individuals at increased risk of infection with a number of pathogens, due to additive or synergistic effects resulting in impaired immune function” will seem surprising only to people unaware that alcohol and cocaine are both bad for health.

Despite all the previous work referred to, despite the sheer common-sense knowledge that drugs are bad for you [COCAINE AND HEROIN AREN’T GOOD FOR YOU! — a Golden Fleece Award, 13 June 2008], the authors congratulate themselves on the ground-breaking nature of their work: “Ours is the first study to show that use of crack cocaine in a  large,  national  cohort  of  HIV-positive  women  is longitudinally associated with subsequent deterioration in immune status, failure of virologic suppression, development of AIDS-defining conditions, and mortality due to AIDS-related causes, even among those who reported adhering to HAART regimens 95% of the time or more”.

Ample grounds for seeking research grants to take this knowledge even further.

That TB patients test HIV-positive at a very high rate has been known for a long time, from data gathered in the United States:

Are TB patients particularly promiscuous sexually, or incessantly sharing infected needles for drug abuse? [IS TUBERCULOSIS AN APHRODISIAC?, 4 January 2008] Or is it that HIV tests, which react “positive” on a wide range of conditions, are particularly prone to test positive in the presence of TB? Surely the latter interpretation is much the more plausible.

As to the benefits of nevirapine and its utility in pregnant women, read Celia Farber’s “Out of Control” [Harper’s magazine, March 2006]: a pregnant woman taking nevirapine in a clinical trial died thereby; and the main initial trial of the drug in Africa had been so flawed that the claims based on it should have been disregarded.

Nevirapine is a known cause of liver disease, sometimes fatal, as well as of other potentially fatal “side”-effects. The following quotes are taken from the January 2008 revision of the official HIV/AIDS treatment guidelines:

“Nevirapine may be used as an alternative to efavirenz for the initial NNRTI-based regimen in women with pretreatment CD4 counts <250 cells/mm3 or in men with pretreatment CD4 counts <400 cells/mm3 (BII). Symptomatic and sometimes serious or life-threatening hepatic events have been observed with much greater frequency in women with pretreatment CD4 counts >250/mm3 and in men with pretreatment CD4 counts >400/mm3. Nevirapine thus should be initiated in these patients only if the benefit clearly outweighs the risk. Close monitoring for elevated liver enzymes and skin rash should be undertaken for all patients during the first 18 weeks of nevirapine therapy. . . . nevirapine was associated with greater toxicity (see below) and did not meet criteria for non-inferiority compared with efavirenz. . . . Two deaths were attributed to nevirapine use. One resulted from fulminant hepatitis and one from staphylococcal sepsis as a complication of Stevens-Johnson syndrome (pp. 18-19).”
“Serious hepatic events have been observed when nevirapine was initiated in treatment-naïve patients. These events generally occur within the first few weeks of treatment. In addition to experiencing elevated serum transaminases, approximately half of the patients also develop skin rash, with or without fever or flu-like symptoms. . . . A 12-fold higher incidence of symptomatic hepatic events was seen in women (including pregnant women) with CD4 counts >250 cells/mm3 at the time of nevirapine initiation . . . . Most of these patients had no identifiable underlying hepatic abnormalities. In some cases, hepatic injuries continued to progress despite discontinuation of nevirapine [129, 131]. . . . More detailed recommendations on the management of nevirapine-associated hepatic events can be found in Table 18a [whose heading is, ‘Potentially Life-Threatening and Serious Adverse Events’] (p. 19).”
“female patients seem to have a higher propensity of developing Stevens-Johnson syndrome and symptomatic hepatic events from nevirapine (p.29).”
“Because nevirapine is an inducer of the drug-metabolizing hepatic enzymes, administration of full therapeutic doses of nevirapine without a 2-week, low-dose escalation phase will result in excess plasma drug levels and potentially increase the risk for toxicity (p. 41).”
“. . . . Hepatic failure and death have been reported among a small number of pregnant patients (p. 48).”
“DISADVANTAGES (Table 9):
• Higher incidence of rash than with other NNRTIs, including rare but serious hypersensitivity reactions (Stevens-Johnson syndrome or toxic epidermal necrolysis)
• Higher incidence of hepatotoxicity than with other NNRTIs, including serious and even fatal cases of hepatic necrosis”

There is also a “Black Box Warning” for nevirapine (Table 20, p. 86):
“• Severe, life-threatening, and in some cases fatal hepatotoxicity, including fulminant and cholestatic hepatitis, hepatic necrosis, and hepatic failure, has been reported. Patients may present with nonspecific prodromes of hepatitis and progress to hepatic failure.
• Women with CD4 counts >250 cells/mm3, including pregnant women receiving chronic treatment for HIV infection, are at considerably higher risk of hepatotoxicities.
• Severe, life-threatening, and even fatal skin reactions, including Stevens-Johnson syndrome, toxic epidermal necrolysis, and hypersensitivity reactions characterized by rash, constitutional findings, and organ dysfunction have occurred with nevirapine treatment.
• Patients should be monitored intensively during the first 18 weeks of nevirapine therapy to detect potentially life-threatening hepatotoxicity or skin reactions.
• A 14-day lead-in period with nevirapine 200 mg daily must be followed strictly.
• Nevirapine should not be restarted after severe hepatic, skin, or hypersensitivity reactions”

“Nevirapine has also been shown in animal studies to cause cancer: “hepatocellular adenomas and carcinomas in mice and rats” (Table 26).”

THAT’s the drug that HIV/AIDS experts describe as “can be used in women of child-bearing age”.
THAT’s the drug widely used in Africa to supposedly protect newborn babies from their “HIV-positive” mothers.

It occurs to me that this mode of arguing AGAINST something has disadvantages both substantive and rhetorical.

A major substantive disadvantage is that it typically requires much more effort to debunk a claim than to make the claim in the first place. For instance, articles asserting benefits for antiretroviral treatments incorporate a large number of assumptions, a variety of mathematical techniques and elaborate models, and many inadequacies in the data. Explaining what’s questionable in all of those is an Herculean labor---at the end of which one has only shown that the particular article is not convincing. That doesn’t do much to shake HIV/AIDS dogma.

A major rhetorical disadvantage of arguing AGAINST something is that one adopts an essentially defensive posture. Thereby rethinkers allow the mainstream to choose the battlegrounds, the specific topics, and these also determine to a certain extent the weapons that come to be used. Bystanders and observers surely note (at least subliminally) that rethinkers are REACTING, and will assume, naturally enough, that the mainstream has posited a case that seems able to withstand assaults.

As I continue to look for the potentially most convincing case that HIV/AIDS theory is wrong, I suggest that there are a number of other possible modes of arguing that might be more effective than the debunking of detailed aspects of mainstream claims.

1. Make a positive case about HIV and AIDS.

Rather than argue what HIV is not, and what AIDS is not, expound what AIDS  IS, and what “HIV” IS. I don’t mean to say, of course, that rethinkers have not done those things. They have, in many ways and in many places, but typically late in the discussion and in the context of debunking mainstream assertions and presenting alternatives. What I have in mind now is an ab initio story about the several different types of “AIDS” and about what “HIV” is.

2. Enlist the power of laughter.

Emphasize the range of unbelievable things that HIV/AIDS theorists require people to believe: more breast-feeding leads to less transmission of “HIV”; married women are more at risk of incurring a sexually transmitted infection than are single women, even prostitutes; “HIV” is spread by quite different mechanisms in different regions of the world; those who share needles are less frequently HIV-positive than those who do not share needles; and so on.

There will always be room, of course, for criticizing mainstream claims that are not obviously and absurdly unbelievable, but I suggest that here too one can distinguish more than one mode (points 3 and 4 below):

3. Point to essential things that are absent from the mainstream case.

We have no electron micrographs of authentic virions of “HIV” extracted direct from AIDS victims or HIV-positive people.

We don’t know how “HIV” destroys the immune system.

We have been unable to discover what  properties an anti-HIV vaccine would need to have.

4. Flaws in mainstream claims.

This category includes the mass of material that I described as the outset, and that---it now seems to me--- is a less potentially convincing mode of arguing than the first three. One need only read some of the to-and-fro on those blogs in which rethinkers and mainstreamers have at one another, or the lengthy exchange in the on-line British Medical Journal, to recognize that arguing over those particular points cannot bring resolution, because the evidence on those particular matters permits of opposing interpretations---not equally plausible ones, admittedly, but we need final and conclusive evidence, not high or low plausibility.

I chose to moderate this blog in hopes of keeping strictly to substantive issues, and the occasional interventions from mainstreamers illustrate the point I’m trying to make. The questions, whether HAART benefits or doesn’t, and if it does benefit then to what extent, and how to factor in toxic “side”-effects, are sufficiently complex that no agreement is going to be possible when people approach the questions with fundamentally opposed preconceptions; see, for example, More HIV/AIDS GIGO (garbage in and out): “HIV” and risk of death, 12 July 2008.  “Fulano/Mengano de Tal” (a. k. a. John/What’sis-name Doe) and I had some further private exchanges about claimed HAART benefits and the particular article that I had originally criticized, until I suggested that we should rather discuss first the more basic issue: Does/do he/she/they agree that the cumulative record of HIV tests in the United States, surveyed and analyzed in my book, demonstrates that what is being detected is not a contagious or infectious thing? If he/she/they does/do not agree, why not?

I have heard no more.

An ad hominem review of my book by one of the AIDStruth vigilantes was soon withdrawn again from amazon.com.

The only mainstream journal to review the book noted that it “can be used as a mirror for some of the major failings of HIV epidemiology during the first quarter century of its existence . . . HIV/ AIDS researchers and health workers . . . should take a hard look at the weak quality of evidence supporting the views of HIV propagation appearing in their pages . . . richly documented . . . asking good questions and . . . detailing how ‘competent and qualified people who questioned the orthodoxy have been largely excluded from the leading journals’ . . . and, consequently, the media . . . Readers should ask the HIV/AIDS establishment, especially the health agencies entrusted with monitoring and intervening in HIV epidemics, why they have settled for evidence from a lesser god when the stakes for getting the picture right are so high. Bauer, Epstein and Chin ought to be thanked for providing us with such a (regretfully unflattering) mirror. Our task ought to be to recognize the serious weaknesses in the available evidence and to insist on rigorous studies that can supply the strong, direct evidence needed for epidemiologic validity”. (The review also had some criticisms, of course, to which I responded in a letter published by the journal).

The mainstream’s strategy evidently is to ignore wherever possible any positive cases made for rethinking. Where they cannot ignore, as with Celia Farber’s article in Harper’s, they respond with character assassination  and undocumented counter-arguments. They simply cannot answer such positive cases as those raised by the death of Joyce Ann Hafford or the epidemiology of “HIV” tests in the United States.

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The four points set out above represent scientific or intellectual cases against HIV. There are also cases to be made against HIV on grounds of human costs, both individual and social ones. These human costs might be called “collateral damage” from the mainstream’s paradigmatic war against HIV/AIDS.

5. The individual human case against HIV/AIDS is what an “HIV-positive” diagnosis does to the person concerned---psychologically via the nocebo effect as well as physically if the individual accepts antiretroviral treatment.

6. The social case against HIV/AIDS has two parts:
(a) What the individual’s plight does to others: family, friends, groups.
(b) The enormous amounts of mis-spent money, which dwarf expenditures on much more widespread health-care deficiencies in both the developed and the developing  regions of the world---things like cancer or heart disease in the former, malnutrition or malaria or TB (and more) in the latter.

There is yet another human cost which, just like most of the claimed benefits of antiretroviral treatment [HIV/AIDS SCAM: Have antiretroviral drugs saved 3 million life-years?, 6 July 2008], has not yet accrued and is yet to be experienced:

7. The frightful burdens of guilt and remorse that will be the lot of “AIDS activists” and AIDS organizations and HIV/AIDS researchers when finally they have to cope with the realization that they have horribly hurt innumerable people. That the mainstreamers and their groupies have done harm unwittingly, unknowingly, sometimes only indirectly, will be no source of comfort to them.

A just-published article seemed to promise delivery from this dilemma (“Duffy antigen receptor . . . mediates trans-infection of HIV-1 . . . and affects HIV-AIDS susceptibility”, Weijuing He et al., Cell Host & Microbe 4 [2008] 52-62). The significance and authoritativeness of this revelation was underscored by the fact that one of the members of the “international team” is “renowned virologist Robin Weiss” [Sabin Russell, San Francisco Chronicle, 16 July 2008]:

“An international team of AIDS scientists has discovered a gene variant common in blacks that protects against certain types of malaria but increases susceptibility to HIV infection by 40 percent. Researchers, keen to find some biological clues to explain why people of African descent are bearing a disproportionate share of the world's AIDS cases, suspect this subtle genetic trait --- found in 60 percent of American blacks and 90 percent of Africans --- might partly explain the difference. Ten percent of the world's population lives in Sub-Saharan Africa, but that region accounts for 70 percent of the men, women and children living with HIV infection today. In the United States, African Americans make up 12 percent of the population, but account for half of newly diagnosed HIV infections. ‘The cause of this imbalance is not necessarily driven by behavior,’ said Phill Wilson, founder of the Black AIDS Institute in Los Angeles. ‘Gay black men do not engage in riskier behavior than gay white men, for example. African people with this gene may have a higher vulnerability’. . . .
The researchers compared 814 African American military personal who were HIV negative with 470 who were infected with HIV. Out of this comparison popped the surprising number: A 40 percent higher risk of HIV among those whose genes suppressed the Duffy protein.”

At first sight, I was less than overwhelmed. A 40% increased risk doesn’t seem all that much help in explaining why African-American men are about 7 times more often “HIV-positive” than white American men, and African-American women about 21 times more often “HIV-positive” than white American women; nor that certain countries in sub-Saharan Africa report an “HIV-positive” rate of between 5 and 35% whereas no other region in the world, with the exception of the Caribbean, reports anything as high even as 1%. Still, HIV/AIDS dogmatists have proven their ability to explain anything, forget about plausibility; one could easily enough conjure some amplification effect.

I was impressed, however---though still not quite overwhelmed---by another aspect of this study:
“The researchers also made another remarkable finding --- once a person with the African gene became infected, the same genetic trait appears to prolong survival. One of the Duffy protein's natural roles appears to be to ramp up the immune system. It attracts a number of chemical signals that promote inflammation --- a defensive mechanism that normally protects the body, but lays out a banquet of white blood cells for HIV to infect and destroy. So the same genetic mutation that raises the risk of HIV infection provides some protection to those who become infected. Similarly, those who carry the normal Duffy protein may be somewhat shielded from HIV infection, but once infected may sicken and die sooner without treatment.”

This counter-intuitive claim struck me hard because I had suggested elsewhere on the incongruity that blacks do in fact survive “HIV disease” to greater ages than members of other races, even as they are also “infected” by “HIV” to a far greater extent than are members of other races [HOW TO TEST THEORIES (HIV/AIDS THEORY FLUNKS), 7 January 2008]. I had taken this as further confirmation of my view that testing “HIV-positive” is an entirely non-specific indication of an immune-system response and that racial disparities reflect differences in genetic patterns relevant to immune-system function; now here was a generic explanation that was consistent with the data AND with the mainstream HIV/AIDS theory!

Admittedly, this explanation of how the Duffy protein could both increase and decrease susceptibility to “HIV” made my head swim. It ramps up the immune system, that should be good. But those extra cells whose job it is to defend the body are thereby exposed to the predations of “HIV”! That fits with the Ho view of frantic rapid turnover, but Ho’s math was discredited as soon as it was published. The explanation is also reminiscent of attempts to invoke immune (hyper)- activation or auto-immune reactions to explain how HIV destroys the immune system---but those had also been found wanting. Just too technically sophisticated for a lay person to understand. Anyway, wouldn’t this mean that anything that ramps up the immune system also makes it easier for HIV to destroy it? Beware vaccination! No wonder all attempts to make an anti-HIV vaccine have failed, indeed have sometimes increased susceptibility!

I was totally confused, so it was some comfort to find that technically sophisticated people could also find this explanation difficult: “The researchers offer an explanation that they concede is far from straightforward. ‘If you found the paper plain sailing, most of my students didn’t,’ Dr. Weiss said.”

Still, that didn’t erase my concern that here was a shred of evidence to support a mainstream explanation. Fortunately, alleviation came from several sources. Nick Wade in the New York Times cited certain reservations [17 July 2008; Gene variation may raise risk of H.I.V., study finds]: “David B. Goldstein, geneticist who studies H.I.V. at Duke University, said that the new result ‘would be pretty exciting if it holds up’” [emphasis added]; and he remarked that the techniques used to avoid effects of chance correlation “might not have been adequate”.

The crucial point seems to be that the Duffy gene in question is characteristic of---closely associated with---African ancestry. The tendency to test “HIV-positive” is also strongly associated with African ancestry. Therefore the Duffy gene and testing “HIV-positive” will inevitably show an association, a correlation, whether or not the gene has any causative role as to “HIV”. It’s the same old correlation-doesn’t-prove-causation fallacy that HIV/AIDS researchers---and innumerable others too, of course---often commit (for example, about “HIV” and excess deaths in Africa, see p.194 in The Origin, Persistence and Failings of HIV/AIDS Theory).

Two blogs concerned with genetics give a full explanation of why the attempts by this “international team of AIDS scientists” to rule out chance correlation were flawed. Some of the gene bits (SNPs) used as “tests” were not independent of the Duffy gene; others were poor discriminators between European and African ancestry, and therefore unsatisfactory for gauging the proportional ancestry of African Americans; and the choice of SNPs raised the suspicion that they had initially been looked at for possible correlations with “HIV” and only later for ancestry-indicating tests; see “DARC and HIV: a false positive due to population structure?” and “Duffy-HIV association: an odd choice of ancestry markers”.

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An HIV-gene claim analogous to the Duffy one was made some years ago about the supposedly protective properties of CCR5 genes with a particular deletion (Δ32), because that is found in European but not in African populations. But it’s present in only a small proportion of Europeans, and moreover its distribution varies enormously from north to south. It’s also present to a negligible extent in North Africa, whereas HIV is as uncommon in North Africa as it is in Europe.

Novembre J, Galvani AP, Slatkin M (2005) The Geographic Spread of the CCR5 Δ32 HIV-Resistance Allele. PLoS Biology 3(11): e339 doi:10.1371/journal.pbio.0030339

For comparison, “HIV” rates, with North African countries in bold; "HIV" should increase from red to pale yellow regions if CCR5delta32 protects against it:
Albania, Algeria, Bosnia/Herzegovina, Bulgaria, Croatia, Cyprus, Czech Republic, Egypt, Libya, Romania, Slovakia, Slovenia, Turkey <0.2%; Finland, Germany, Hungary, Malta, Morocco, Norway, Poland, Tunisia 0.1; Denmark, Greece, Iceland, Ireland, Netherlands, Serbia/Montenegro, Sweden, United Kingdom 0.2; Austria, Belgium 0.3; France, Portugal, Switzerland 0.4; Italy 0.5, Spain 0.6 (UNAIDS 2006 report on the global AIDS epidemic)

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These quite typical episodes illustrate something that science writers and journalists do not usually know but should know---indeed, that it would be good for everyone to know:

REAL SCIENCE ISN’T NEWS

“Real science”, the stuff that is almost universally regarded as reliable, trustworthy, in fact true, is not and cannot be the latest, newest “breakthrough”, because it takes time and the critiquing and testing by other investigators to determine how much validity any new claim has. The real, reliable science is what’s been around long enough to have been thoroughly tested. Science is made trustworthy not by any formulaic “scientific method” but by a knowledge filter of the criticisms and repetitions and modifications and disproofs rendered by other researchers and peer reviewers.

Those who cover science for the media should learn to be as cautiously suspicious of “scientists” and “scientific” institutions as they mostly are of politicians, political institutions, business executives, and corporations. Scientists are no less human than other people, and they are no less capable of being corrupted by career ambitions and pressures, by “the system”, by taking goodies “because it doesn’t hurt anyone” “because everybody does it” and “If I didn’t do it, someone else would”.

Modern-day “Big Science” does not fit the traditional view of a quasi-religious vocation attracting disinterested truth-seekers who form an intellectual free market in which an invisible hand safeguards against error; modern-day “Big Science” is an array of bureaucracies that produce knowledge monopolies and research cartels.

Nevertheless, the epithet “pseudo-science” continues to be bandied about in controversies over such matters as human-caused global warming, psychic phenomena, HIV/AIDS, Loch Ness monsters---wherever dogmatists are 100% sure of their beliefs, they like to describe the opposing position as pseudo-science.

The history of such arguments teaches that they are finally settled only by evidence specific to the particular claims, not by application of abstract notions like scientific method or falsifiability (2); for no matter how plausible some abstract criterion may seem at first sight, in practice illustrations of it can be found on both sides of the imagined divide between science and pseudo-science.

Take the matter of burden of proof (3). Defenders of mainstream paradigms like to portray those who put forward unorthodox claims as saying, “Prove me wrong”, when actually the onus is on the dissenters to prove their claims right; but in practice, one can find mainstreamers themselves setting the challenge, “Prove us wrong”, instead of providing the necessary proof that the mainstream view is sound.

Immanuel Velikovsky’s “Worlds in Collision” had received great public acclaim in the 1950s, and the Velikovskian cult gained widespread support even among prominent humanists and social scientists (4), despite the huge implausibility of his claims: that a comet ejected from Jupiter had nearly collided with Earth and Mars, producing such Biblical events as the parting of the Red Sea and the fall of Jericho’s walls before settling eventually into its present position as the planet Venus.
“Throughout Velikovsky’s writing runs the subtly misleading attitude that the onus is on his critics to prove him wrong. Whenever he states --- as he often does --- that his case is unshaken and has not been disproved, the unwary listener or reader is led to expect that some clear disproof is called for, and that in its absence Velikovsky’s reconstruction stands as plausible or even valid. But in all fields of knowledge the onus of proof rests on the new proposition” (5).

Yet when it comes to HIV/AIDS, it is the orthodoxy that states, “Prove us wrong”, and that refuses to accept the onus of proof. Mainstream discourse is salted and peppered with statements to the effect that “the evidence that HIV causes AIDS is overwhelming” (6), yet the mainstream has never established, for example:
1. That a positive HIV-test marks the presence of active infection (7).
Whole virions of HIV have never been isolated direct from an HIV-positive individual. Indeed, a prize of $50,000 awaits anyone who uncovers a scientific publication in which such isolation has been demonstrated (8).
2. That HIV-positive portends progress to AIDS, and all AIDS patients are HIV-positive.
To the contrary: It has long been known that there are thousands (at least) of “long-term non-progressors” or “elite controllers”, HIV-positive individuals who have not become ill, some of them “positive” since the early 1980s. It has also been known since the early 1990s that there are many clinically diagnosed AIDS patients who have never tested HIV-positive, causing the mainstream to invent the new condition of “ICL” (9).
3. What mechanism it is by which HIV destroys the immune system (11).
4. What properties a vaccine needs to have to protect against infection (12).

As noted before [Science Studies 101: Why is HIV/AIDS “science” so unreliable?, 18 July 2008], the repeated publication of mainstream HIV/AIDS claims without adequate proof represents a failure of peer review that began in the late 1980s when Duesberg’s critiques were ignored. The initial claim that Gallo had discovered the “probable” viral cause of AIDS became accepted by default, it was never followed by definitive published proof; a prize of ₤50,000 awaits whoever produces proof of isolation of virions from AIDS patients (13).

By contrast, HIV/AIDS rethinkers and skeptics have accepted the onus of proof by publishing positive evidence to the effect that
1. A retrovirus cannot do what HIV is charged with doing (14).
2. Illnesses developing in “AIDS” patients who abuse drugs are specific to the particular drug; signifying that it is the drug that produces the illness and the frequently positive HIV-test in drug abusers (15).
3. Kaposi’s sarcoma in gay men in the United States results predominantly from persistent inhalation of nitrite “poppers” (16).
4. Official data show that the tendency to test HIV-positive has the characteristics of an endemic physiological property, not of a spreading infection (10).
5. Officially reported deaths from “HIV disease” since 1987 demonstrate that antiretroviral drugs have had no life-extending effect (17). AIDS patients treated by alternative modalities have lower mortality than those treated with antiretroviral drugs (18).
6. Officially reported death statistics together with officially reported data on HIV “infection” demonstrate that the 10-year latent period supposed to intervene between “infection” and illness does not exist (17).

References

1. Larry Laudan, “The demise of the demarcation problem”, pp. 111-27 in Physics, Philosophy and Psychoanalysis, ed. R. S. Cohen & L. Laudan, Dordrecht: D. Reidel, 1983

2. Henry H. Bauer, Science or Pseudoscience: Magnetic Healing, Psychic Phenomena, and Other Heterodoxies, University of Illinois Press, 2001

3.  pp. 220-1 in reference 2

4. Henry H. Bauer, Beyond Velikovsky, University of Illinois Press, 1984

5. P. 171 in reference 4

6. For instance, read the testimonies of the expert witnesses in the Parenzee case.

7. “The birth of antibodies equal infection”, Appendix II (pp. 333-40) in Celia Farber, Serious Adverse Events, Melville House, 2006

8. May 2007: Alive & Well $50,000 Fact Finder Award---Find one study, save countless lives

9. See “ICL” in index of reference 10 for details and sources

10. Henry H. Bauer, The Origin, Persistence and Failings of HIV/AIDS Theory, McFarland, 2007

11. Chapter 7 of Principles of Molecular Virology

12. “Is it time to give up the search for an Aids vaccine? After 25 years and billions of pounds, leading scientists are now forced to ask this question”, 24 April 2008, by Steve Connor and Chris Green, Independent.co.uk

13. The Michael Verney-Elliott Memorial Prize: £50,000 reward for the existence of 'HIV'; letter of 29 March 2008

14. Peter H. Duesberg, Retroviruses as carcinogens and pathogens: expectations and reality, Cancer Research 47 (1987) 1199–220; Human immunodeficiency virus and acquired immunodeficiency syndrome: correlation but not causation, Proceedings of the National Academy of Sciences, 86 (1989) 755–64.

15. Duesberg, P., Koehnlein, C. and Rasnick, D. The Chemical Bases of the Various AIDS Epidemics: Recreational Drugs, Anti-viral Chemotherapy and Malnutrition, Journal of Bioscience 28 (2003) 383-412

16. John Lauritsen and Hank Wilson, Death Rush: Poppers & AIDS, Pagan Press, 1986

17. “HIV DISEASE” IS NOT AN ILLNESS, 19 March 2008; “Disproof of HIV/AIDS theory” [Society for Scientific Exploration, Annual Meeting, Boulder CO, June 2008]; http://aras.ab.ca/index.php at News for June 30; “Incongruous age distributions of HIV infections and deaths from HIV disease: Where is the latent period between HIV infection and AIDS?” in press, Journal of American Physicians and Surgeons

18. Only 3 of 36 (12%) of Dr. Köhnlein’s AIDS patients died under alternative treatment compared to about 63% of all AIDS patients in Germany, most of whom were treated with antiretroviral drugs; pp. 401-2, Table 8, in reference 15

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.

“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.

That conclusion is contrary to what’s nowadays well known about the independence of behavior and genotype, and it is blatantly racist. Point 3., what the syllogism presents as demonstrated, being ignorant as well as racist (but then racism is in any case a sub-category of ignorance) means that at least one of points 1. and 2. is wrong. Which one?

The evidence for 1. is, as already stated, undisputed. Many illustrative sources are cited in The Origin, Persistence and Failings of HIV/AIDS Theory. Others have been added in many earlier posts (HIV AND SEXUALLY TRANSMITTED DISEASE: IT JUST ISN’T SO, 28 November; “HIV DISEASE” IS NOT AN ILLNESS, 19 March 2008; REGULAR AS CLOCKWORK: HIV, THE TRULY UNIQUE “INFECTION”, 1 April 2008; HIV: THE VIRUS THAT DISCRIMINATES BY RACE, 11 April 2008; HIV: A RACE-DISCRIMINATING SEXUALLY TRANSMITTED VIRUS!, 16 April 2008; DECONSTRUCTING HIV/AIDS in “SUB-SAHARAN AFRICA” and “THE CARIBBEAN”, 21 April 2008 ). Perhaps the most striking demonstrations that it is biological, physical, race that determines rates of testing “HIV-positive” are the difference between Hispanics on the East and West coasts in the United States, and that in South Africa the “coloreds”, of mixed racial ancestry, test positive at rates intermediate between those seen with blacks and with whites.

Since point 1. is correct, and point 3. is wrong, therefore point 2. must also be wrong.

Indeed, the evidence against point 2. is just as solid as the evidence for point 1.; for sources and discussion, see WHAT “HIV” IS NOT: IT’S NOT SEXUALLY TRANSMITTED, 6 January 2008 and Chapter 4 in The Origin, Persistence and Failings of HIV/AIDS Theory.

What’s so difficult to accept, to comprehend, to explain, is that the conventional wisdom has ignored this evidence for so long and with such passionate determination.

In order not to admit that point 2. --- that “HIV” is sexually transmitted --- is in error , it is necessary to recast point 3. in a manner that masks its erroneous and racist nature. How to do this?

“The promiscuity, blind sexual trust and intravenous drug use that gave life to this incurable disease is just as prevalent today as when former NBA great Magic Johnson gave HIV/AIDS a recognizable face. Black people in Mississippi make up 70 percent of the new HIV/AIDS cases; black women make up 49 percent. No major study exists to tell us why, so we're left with theories that have no scientific foundation” (Ronnie Agnew, “HIV's new target: Black women”, Clarion-Ledger [Jackson, MS], 23 April 2006).

Political correctness offers a working model for obfuscating the matter: Accept that undesirable behavior is linked to race, but assert that this is only because race has meant discrimination and its after-effects of deprivation, poverty, lack of health care, etc. In other words, “their” behavior is admittedly despicable, but it’s not really their fault.

Thus, as Potterat pointed out recently, there has been “evidence and speculation that epidemic trajectories are shaped by demographic, social, economic and network configurations” (“Blind spots in the epidemiology of HIV in black Americans”, Int J STD & AIDS 19 [2008] 1-3).

The currently fashionable parlance among HIV/AIDS experts is “multiple concurrent relationships”. That abstract mouthful fails to reveal the magnitude of sexual activity required to explain the spread of HIV: 20-40% of the population must be having sex with several people during the same short period of time and all the people involved must be changing partners every weeks (B***S*** about HIV from ACADEME via THE PRESS, 4 March 2008). A colloquial description of such behavior allegedly found among Africans and African Americans might be, “Those macacas screw around in ways that us civilized folks don’t”.

(For the expression “macaca” I am indebted to Republican Senator and former Governor of Virginia, George Allen, whose use of it on a public occasion is widely thought to have spelled the demise of his campaign for the presidential nomination of his party.)

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

In any case, no one attempts to deny the statistical facts. Under HIV/AIDS theory, those facts must be interpreted in racist fashion, relying on racist stereotypes as to sexual behavior. The mainstream attempt to hide that inescapable fact, to obfuscate it, harnesses nice-sounding, politically correct, words like “cultural differences” and references to “minorities” in relation to “poverty”, “discrimination”, lack of access to health case, and the like. What that amounts to is admitting that “they”, the macacas, do behave that way, but it isn’t really their individual or collective fault. Here are some actual examples of this rhetoric:

“The marked racial and ethnic differences in HIV prevalence, even among persons treated in the same clinic, suggests that both behavioral norms and complex social mixing patterns within racial and ethnic groups are important determinants of HIV transmission risk” (emphasis added; Centers for Disease Control and Prevention, HIV/AIDS surveillance report for 1992, p. 37).
Translating from jargon: “behavioral norms” = regarded as acceptable behavior; “complex social mixing patterns” = those who behave improperly are not sexually segregated from others “within racial and ethnic groups”.

Nor has the Centers for Disease Control and Prevention changed its belief since then, as they informed me in 2005: “The ‘characteristic differentiation by race’ that you note is compatible with a behavioral explanation” (emphasis in original, Shari Steinberg [Divisions of HIV/AIDS Prevention, CDC], letter to Henry Bauer, 19 May 2005).

“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 … .
What steps is CDC taking to address the down low?
CDC and its many research partners have several projects in the field that are exploring the HIV-related sexual risks of men, including men who use the term down low to refer to themselves. The results of these studies will be published in medical journals and circulated through press releases in the next few years as each study is concluded and the data analyzed. CDC has also funded several projects that provide HIV education, counseling, and testing in minority racial and ethnic communities. CDC’s research and on-the-ground HIV prevention efforts will continue as more information about the demographics and HIV risk behaviors of men who do and men who do not identify with the down low becomes available” (emphasis added; unchanged since at least March 2006, accessed 11 May 2008).

Note the weasel-word “minority” used here, as so often in similar contexts. It doesn’t mean minority, it’s a euphemism for “black”. Asian-Americans are less affected by “HIV” than are whites, and at 4.5% of the population they surely qualify as a “minority”, certainly by comparison with about 13% African Americans. Perhaps the smallest recognized minority group in the United States is comprised of Native Americans, who are affected by “HIV” almost as little as are white Americans. The persistent usage of “minority” is intended to mask the fact that it is blacks who are so disproportionately affected, and simultaneously to suggest --- in condescending and demeaning terms --- that it isn’t their fault, because it’s so well known that “minorities” are devastatingly discriminated against.

It’s hard to believe that this usage of "minority" is other than deliberate. Its use implies quite clearly that the user accepts that “black” is the determining factor. The only way to explain that under HIV/AIDS theory is by differences in sexual behavior. But one mustn’t say that, even though it is evidently believed by those who resort to these euphemisms. In other words, these statements are made by people who harbor stereotypically racist beliefs --- albeit they would likely be horrified if made aware of that subconscious or suppressed belief.

A large part of the problem is that the rethinkers’ case is not readily made in a convincing way via self-evident sound-bites. “The ‘HIV’ tests don’t detect a virus”, or “ ‘HIV’ tests have never been proven to be specific for ‘HIV’”, while perfectly true, are based on evidence that is too technical for most people to feel comfortable with; to appreciate the strength of the case against HIV/AIDS theory, to appreciate that those mainstream-contradicting sound-bites are really true, requires prolonged immersion in much data. Even the most concise as well as documented overview, say, Christine Maggiore’s excellent What If Everything You Thought You Knew About AIDS Was Wrong?, or Rebecca Culshaw’s similarly concise yet also comprehensive Science Sold Out: Does HIV Really Cause AIDS?, are hardly bed-time reading. A promising alternative approach is through “fiction”.

There’s a long and respectable history of literary fiction that aims to acquaint readers with important facts. (Most good literature teaches at least indirectly about people and about human life, of course, but I’m now referring to deliberately didactic treatments of specific issues.) Sinclair Lewis in Martin Arrowsmith conveyed important truths about medical practice and medical research and commercial conflicts of interest. Upton Sinclair revealed through novels some ugly truths about the meat-packing industry (The Jungle), the oil industry (Oil), and others, and his Lanny Budd series can serve as a descriptive political history of the era of Nazism, the Second World War, and its aftermath. Most recently, Michael Crichton exposed the lacunae and fault lines in the current obsession with man-caused global warming in State of Fear.

HIV/AIDS seems a natural candidate for this sort of treatment, and Stephen Davis has put his hand, head, and heart into the endeavor. His first novel, Wrongful Death: The AIDS Trial, was published in 2006; the second, Are You Positive?, appeared this year.

Both books feature legal trials, and are thereby consistent with my growing suspicion that HIV/AIDS theory will only be overturned when the mainstream is forced, in a court of law, to reveal the extent to which the theory is like an Emperor wearing no clothes at all.

Wrongful Death tells the story of a class-action suit brought by relatives of those who died needlessly because “HIV-positive” people were treated with AZT. The novel was exceptionally timely, given that the Centers for Disease Control and Prevention was just then recommending that “HIV”-testing should become routine. If that were to happen, then a few perfectly healthy people in every thousand would be misguidedly told that they harbor a deadly virus and should begin taking drugs whose “side” effects make the rate of “adherence to treatment” quite low and which ultimately reward compliant adherence with serious illness and often death.

Davis follows, for legal reasons, the convention of claiming fictional character for the protagonists (except for a few well-known public figures), but readers at all familiar with HIV/AIDS matters will recognize many of the characters, most of whose names are faithful to the initials of their real-life models. The story is told in quite a straightforward manner, an appropriate vehicle for acquainting readers with the facts in a steady succession of digestible pieces. Though the story is straightforwardly told, there are also a couple of ingenious twists in the plot.

Are You Positive? features a trial that has, unfortunately, some real-life precedents: an HIV-positive man on trial for transmitting the virus to a sexual partner. As in the earlier book, the real-life models of some protagonists are recognizable, including by their initials. The evidence is unfolded at digestible pace: the lack of validity of “HIV” tests, the racial bias of the tests, the particular likelihood that TB patients and pregnant women will test “HIV-positive”. The recommendation that everyone be tested is mentioned, and the gruesome story of the orphans used as guinea pigs in clinical trials. The Padian study revealing lack of sexual transmission is dissected expertly. Gallo’s scientific failings are described accurately, as well as his self-incriminating testimony in the Parenzee trial in Adelaide (Australia). The role of conflicts of interest in the HIV/AIDS industry is brought out. An Appendix has a recommended “Informed Consent” form that people should require their doctors to sign if they are being asked to take an HIV test.

The story is told very accurately indeed in this novel. Because I already knew that every detail is correct, I found it emotionally difficult reading--I know of a dozen people languishing in jail for the crime of making love while testing “positive” for a supposedly active infection that the tests cannot actually establish, and there are surely many more in jail of whom I am not aware. HIV/AIDS-naïve readers, however, may not experience that emotional burden as they are led slowly to doubt what the conventional wisdom insists on.

My respect for these books and their author was only increased when, toward the end, I found cited one of my favorite epigrams, one I had used myself for years as the motto of a newsletter I once edited:

All that is necessary for the triumph of evil is for good men to do nothing

Both these books are paperbacks published via automated “on demand” printing. Their material quality is comparable with such productions from large publishers, but in their lack of typographical errors they are far superior to most contemporary works, including in hard covers from long-established and respected presses.

Rethinkers ought to consider giving these books to their friends and acquaintances who scoff at the possibility that the mainstream could be wrong about HIV/AIDS. Leading HIV/AIDS-naïve people through salient details of the evidence in measured and linear succession is likely to make it easier for them to begin to shake off unthinking acceptance of the conventional wisdom than trying to argue all the scientific issues in concentrated form. Wrongful Death cites hundreds of supporting published sources; Are You Positive? relegates them to the website. In both cases, you can assure those to whom you give these books that the cited evidence is solidly supported in the mainstream literature and that the cited sources represent fairly the totality of what has been published and what is known.

The overall rate of “HIV-positive” in prisons, 2004-2006, was 1.7-1.8%; most of the cited sources in my book reported 2-3%. More strikingly, the geographic distribution is once again the same: Northeast (3.9%) > South (2.2%) > Midwest (0.9%) and West (0.7%).

The same geographic distribution is seen among prisoners as among military cohorts including applicants, new mothers, blood donors, members of the Job Corps, and the totality of public testing sites. The geographic distribution of “HIV-positive”, in other words, is not a function of social status or circumstances, and it is not a function of time, having remained without significant change for more than twenty years.

Moreover, the geographic distribution can be calculated simply from the racial disparities in testing “HIV-positive” and the racial composition of the population in each region (DECONSTRUCTING HIV/AIDS in “SUB-SAHARAN AFRICA” and “THE CARIBBEAN”, 21 April 2008).

“HIV-positive” is not the mark of an infectious agent.

This is so incredible, and the matter is so centrally important, that no amount of supporting evidence could be redundant. To de-throne HIV/AIDS theory calls for overkill. So to the data presented in an earlier post (HIV: THE VIRUS THAT DISCRIMINATES BY RACE, 11 April 2008 ), I add some more.

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

The UNAIDS statistics for the global distribution of “HIV-infection” rates in 1997 and 2007 are, respectively:
Sub-Saharan Africa, 7.4% and 5.0%
Caribbean, 1.9% and 1.0%
Everywhere else, ≤ 1% in both years
(The decreases from 1997 to 2007 are officially ascribed to recent data being more accurate, not to any actual decline; after all, any decline might raise questions about the incessant propaganda alleging an uncontrollably spreading epidemic)

That unchanging global distribution parallels the proportions of people of African ancestry in those regions: a larger proportion of the Caribbean population is of African ancestry than elsewhere outside Africa.

No other sexually transmitted infection has managed to be quarantined geographically and racially in this way. North Africa, contiguous with sub-Saharan Africa, had a reported rate of 0.3% in 2007. Do people from sub-Saharan Africa not have sex with people in neighboring countries?

At various times and in various parts of the world, sex across racial lines has been taboo, even officially outlawed. The utter futility of such attempts to prevent miscegenation is demonstrated by the large numbers of people of mixed race living all over the world. Yet HIV somehow manages, more successfully than laws or taboos, to overcome sexual attraction across racial lines. HIV just doesn’t much care to be shared sexually with people of non-African (Negroid, sub-Saharan) ancestry.

You might ask, “What about all those gay men in the largely white communities where AIDS first appeared?”
True enough, there’s an apparent exception---though it implies that AIDS and HIV are synonymous whereas they are actually not correlated (chapter 9 in The Origin, Persistence and Failings of HIV/AIDS Theory). But leaving that aside, it would still be not so great an exception after all, because the same racial disparities as to HIV are found among gay men as in low-risk groups (and also among heterosexual clients at STD clinics). According to a CDC Fact Sheet (“HIV/AIDS among men who have sex with men”, revised June 2007), gay black men in large cities tested positive 46% of the time whereas gay white men in the same cities tested at the rate of only 21%. (See also Figures 11 & 12, p. 42, in The Origin, Persistence and Failings of HIV/AIDS Theory)

No interracial sex among gay men in large metropolitan areas?! Apparently, HIV-positive human beings display a sexual fastidiousness as to race that HIV-negative humans do not.

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

But it’s not just black and white (double entendre intended). Several anecdotes in the earlier post (HIV: THE VIRUS THAT DISCRIMINATES BY RACE, 11 April 2008 ) noted that people of mixed race test “HIV”-positive at rates that fall between those of their parents’ races; “HIV”-positive behaves, in other words, just like other physical attributes that are proportional to degrees of racial ancestry, skin color for example. Is the tendency to be infected by this sexually transmitted agent inherited in quantitative fashion?

Yet further evidence that “HIV” is race-linked comes from data on other human races; for instance, Asians always test “HIV”-positive much less frequently than whites: about 35% less often, in fact (sources cited at p. 54 in The Origin, Persistence and Failings of HIV/AIDS Theory, for data from the Job Corps, applicants for military service, public testing sites, and young gay men ). The death rates from “HIV disease” for 2000-2004 among Asians are also less than those of non-Hispanic whites, in that case by 70% or more (“HIV DISEASE” IS NOT AN ILLNESS, 19 March 2008).

“HIV” prefers whites over Asians by a substantial amount. I’ve come across no reports that contradict this generalization.

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

Data for Hispanics are routinely published in official US documents because Hispanics constitute a minority group eligible for affirmative action, but it is recognized that “Hispanic” is an ethnic and not a racial classification.

Here’s a most remarkable fact. Hispanics in the eastern USA test “HIV”-positive at far higher rates than do Hispanics in the western USA:

“In the Western states, HIV seroprevalence was similar among Hispanics and whites, while in states along the Atlantic Coast, seroprevalence was higher among Hispanics than among whites” (CDC Surveillance Report for 1992, p. 37). This difference, a large one, has been noted among military personnel and among new mothers, in the Job Corps and at various clinics, in low-risk groups as well as among drug abusers (sources cited at p. 71 ff. in The Origin, Persistence and Failings of HIV/AIDS Theory).

In what way could Hispanics in the East differ from Hispanics in the West?

Racially, of course.

In the Northeast, Hispanics are 40% Puerto Rican and 10% Mexican (3% Cuban, 47% “other”)
In the West, Hispanics are 75% Mexican and 2% Puerto Rican (≤1% Cuban, ≥20% “other”)
Puerto Ricans share a large proportion of relatively recent African ancestry, Mexicans do not.
(Numbers from US Census Bureau, “The Hispanic Population---Census 2000 Brief”)

Once again, people of African ancestry test HIV-positive much more frequently than do people of non-African ancestry.

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

US data recognize yet another racial classification, that of Native American. Compared to white Americans as 1.00, the frequency of positive “HIV”-tests among Native Americans averages 1.5 in four studies cited in my book (Table 14, p. 66; also 0.63 for Asians, 2.3 for Hispanics and 5.7 for blacks ). In a 2006 report from the Centers for Disease Control and Prevention, the ratios come out as 1.23 for Native Americans, 3.3 for Hispanics, 8.5 for blacks. Data for 2005 yield ratios of 1.2 for Native Americans, 0.85 for “Asians & Pacific Islanders”, 3.2 for Hispanics, 8.1 for blacks. Noteworthy perhaps in that latter report is that “Navajo-area American Indians” tested at 0.85 compared to white Americans.

Those data once again mirror racial ancestry since they place Native Americans quite close to Caucasians. The Americas were settled, according to the latest scenario, via four major migrations from Siberia and Asia, between about 10,000 and perhaps as much as 40,000 years ago; there is some evidence also of contacts across the Pacific or from Polynesia. So Native Americans (including Mexicans) are closely related genetically to Asians and Caucasians, with little if any vestiges of African ancestry (which was, however, shared by all Homo sapiens at about 200,000 years ago).

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The evidence is simply overwhelming: from every tested social group, high-risk as well as low-risk; from every part of the world; for both sexes and at all ages---wherever “HIV” tests are reported separately by race in any given sample, the tendency to test “HIV”-positive is paralleled by racial ancestry. Africans test positive most frequently, Asians least frequently, Caucasians in between but relatively close to Asians, and Native Americans quite close to Caucasians.

The geographic distribution of positive “HIV”-tests in the USA---which has not shown appreciable change during the two decades of the AIDS era---can even be calculated from the racial composition of the population in different parts of the country (p. 66 ff. in The Origin, Persistence and Failings of HIV/AIDS Theory). Try doing that with chlamydia, gonorrhea, herpes, or syphilis.

“HIV” discriminates by race just as though it were capable of recognizing the DNA sequences in the human genome. The tendency to test “HIV”-positive, for a given state of health, is determined primarily by race and significantly by age and sex. This is not how a sexually transmitted infection behaves.

Most people, too, would have to agree that there are some matters over which large chunks of humanity must be wrong. When it comes to God, say, there are a number of competing beliefs, none of which commands majority adherence even though no more than one of them can be correct. Most people would see matters of politics as another and similar illustration. Yet on those very same questions of politics and religion, each group of adherents is firmly convinced that their group---and only their group---has it right while all the others have it wrong. In other words, all manner of minorities believe that the others, who are in a majority, are wrong.

But in this age which is often (self-)described as a scientific age, there’s a widespread  belief that science is somehow exempt from the polarization of opinions that characterizes other spheres of intellectual life, that science possesses some magic ability---namely, the scientific method---to have it always right; and it’s blithely taken for granted that science is synonymous with the established institutions of science and with the views of those who happen to hold leading positions in those institutions.

That circumstance coexists with a general willingness to cite Thomas Kuhn (1962/70) on “paradigm shifts” and “scientific revolutions”, and to get the significance of Kuhn’s work entirely wrong. It’s not that science advances by periodic giant and revolutionary steps; “revolution” here means getting rid of the present order. Kuhn’s insight, buttressed by a pretty good knowledge of the history of science, is that periodically the accepted view of things is overturned, as it’s realized that what was previously believed to be right turns out to be wrong.

Very little known are the works of Bernard Barber (1961) and Gunther Stent (1978), lately revisited in an important, long-overdue discussion (Hook 2002): history of science reveals that corrections of mistaken scientific paradigms are always fiercely resisted up to the very moment that they succumb to a revolution. Just now I came across a discussion of this phenomenon that predates Barber’s classic and focuses in large part on matters of medicine (Stevenson 1958).

By and large, it’s only scientific pioneers who discover this truth of routine resistance to new scientific discoveries, when the pioneer’s peers refuse to consider even well-supported claims that don’t fit the mainstream consensus. Peter Duesberg illustrates the surprise that such pioneers experience when the approbation and high regard they have long enjoyed is suddenly switched off, indeed reversed, because they said something different.

Even when these insights of Barber and Kuhn and Stent and Stevenson are recalled and pointed out, it doesn’t shake the mainstream belief on any given topic; somehow, the conventional wisdom is able to sustain the illogical and intellectually unsustainable view that this time, on this particular issue, one can be absolutely sure that “science”---the mainstream, their own group, the Establishment---has it right beyond any doubt. Added to the certainty expressed by the insiders is that disseminated by the science groupies, herds of dogmatists who reveal themselves on blogs as utterly sure about matters of which they actually have little if any direct knowledge. All they know is that it’s what “science” says and so it must be right. Such dogmatists may be found in academe as elsewhere, and they populate such organizations as the Committee for Scientific Investigation of the Paranormal (CSICOP), which is comprised of more non-scientists than scientists, does no investigating, and is as one-sided in its approach to evidence as those blogs that style themselves as scientific.

Over the years, I’ve come to prize more and more those rare individuals who are able to admit their own fallibility and who strive to mold their beliefs to the best available empirical evidence while remaining aware that what’s now the best available will not remain so. I’ve found such individuals everywhere, even in the ranks of CSICOP. The late Gordon Stein, for example, was active in CSICOP and intent on debunking what deserves to be debunked while refraining from the indiscriminate castigation of every unorthodox opinion in which most CSICOPpers indulge. Just as I know of no one who is always right, so too I’ve not been unfortunate enough to get personally into contact with anyone who is always wrong. (Well . . . maybe I can think of a couple.)

The state of affairs that I’ve described applies, of course, to HIV/AIDS as to many other and many less prominent topics. Dogmatists over HIV/AIDS will readily---or at least ultimately---admit that, of course, science and medicine have sometimes been quite wrong; it just happens, they maintain, that this time and on this issue, there’s just no doubt at all. The evidence, after all, is overwhelming, and the overwhelming majority of qualified and competent doctors and scientists are unanimous about it.

The trouble is, those dogmatists are committing the usual, the typical, the routine error of not applying to their one pet subject the lessons that history offers; and, as the saying goes, “Those who forget the past are doomed to repeat it”.

It’s not only the lessons from history of science that they forget; it’s also the substantive history of HIV/AIDS itself. “HIV” was never isolated by Gallo from all his AIDS patients, in fact he claimed to have found it in fewer AIDS patients than in association with what used to be called pre-AIDS. As Michelle Cochrane has documented, the shibboleth that the early AIDS victims were “young” and “previously healthy” is wrong on both those counts. As John Lauritsen pointed out long ago, the shibboleth that the early AIDS victims were young, previously healthy “gay men” is also misleading because the common factor was drug abuse, not gay sex. The Centers for Disease Control and Prevention seem to have forgotten that they have proclaimed year after year for about two decades that about 1 million Americans were “HIV”-positive, as they continue to talk of spreading infections. Some of the most careful and comprehensive studies are ignored whenever they conflict with the accepted view: the Concorde study which showed AZT to be useless at best and CD4 counts to be clinically irrelevant; the Rodriguez study that found no correlation between CD4 counts and “viral load”; the Antiretroviral Collaboration, with data from 22,000 patients, which found that HAART brings “adverse events” on sooner. The significance is ignored of huge masses of data: that HIV tests do not track an infectious agent; that deaths from HIV disease show no sign that the “lifesaving” antiretroviral drugs have extended life; that every bright idea for a vaccine against HIV fails to make good on its promise. And innumerable self-contradictions are swallowed whole, say, that HIV crossed in Africa from monkeys or chimps to humans, did no damage there but made its way to the Western Hemisphere where it produced the first epidemics, whose cause was then somehow transported back to Africa to spread like wildfire there even though it hasn’t in the developed countries where it first appeared. This infectious disease is unique, unprecedented, “everyone” is willing to accept: it discriminates by race, unlike every other infectious disease; it kills preferentially adults in the prime years of life, unlike every other infectious disease; the virus multiplies prodigiously without being detectable, and it mutates at an unprecedented rate while remaining fully pathogenic.

And so on. During these months where I’ve become increasingly irritated by the lack of intellectual integrity displayed by political partisans and pundits, I find myself sadly reminded that intellectual integrity is in short supply everywhere, by no means excluding academe, science, and medicine.

Citations:
Barber, Bernard (1961). Resistance by scientists to scientific discovery. Science, 134: 596-602.
Hook, Ernest B. (ed) (2002). Prematurity in Scientific Discovery: On Resistance and Neglect. Berkeley: University of California Press.
Kuhn, Thomas S. (1962/70). The Structure of Scientific Revolutions. Chicago: University of Chicago Press (1st ed. 1962, enlarged 2nd ed. 1970).
Stent, Gunther (1972). Prematurity and uniqueness in scientific discovery. Scientific American, December, 84-93.
Stevenson, Ian. (1958). Scientists with half-closed minds. Harper’s Magazine, 217: 64-71.

I got started because I couldn’t believe the assertion, in Harvey Bialy’s book about Peter Duesberg’s work, that (in the mid-1980s, no less) teenage females from every part of the United States were as likely as teenage males to be “HIV”-positive. But I verified the correctness of the assertion in the original source; whereupon I expected to find contradictions in other studies, and so I kept looking. I jotted notes on how rates of testing positive varied with all the factors mentioned in the various reports. And my head swam, or spun, or rebelled, because it made no sense: testing “HIV”-positive seemed to be as regular as clockwork, not at all like the incidence of something infectious or contagious, which sweeps back and forth, here and there, as the opportunity offers itself.

---“HIV”-positive was always greater among men than among women: except in the teenage years, where it was often higher among females.
---“HIV”-positive always increased with age from the teens into the 30s or 40s, and then declined again.
---Most extraordinary of all, so far as age was concerned: children below teenage tested “HIV”-positive more than teenagers did, and increasingly so, the younger they were! The rate of testing positive among newborns rivaled the highest rates among adults in their 30s and 40s!

I was looking at the wealth of data based on tests in the United States, but also came across some reports from elsewhere, published by the same reliable researchers. That strange variation with age, including young children, had been reported also from Africa!

US data of all sorts are typically reported by racial category. Regular as clockwork, rates of testing “HIV”-positive always increased from among Asians to among white Americans to among Hispanic Americans to among black Americans. Whether it was blood donors or gay men, injecting drug users or newborns or their mothers; whether it was military personnel or prisoners, people at STD clinics or women at pre-natal clinics---there were simply no reports that did not fit into that progression of testing “HIV”-positive according to racial category. What sort of infection is it that discriminates consistently and regularly by race?

Whenever there’s discussion of racial disparities between blacks and whites in the USA, the first resort is to explanations based on slavery, Jim Crow laws, racial discrimination in general and their lingering after-effects: high rates of poverty, unemployment, drug abuse, criminality, and so on. But analogous circumstances have been the lot of Native Americans, displaced from their homelands, traditional practices disrupted, never integrated into the American mainstream. So one would expect that Native Americans might test “HIV”-positive about as often as African Americans. But they don’t. Every published study finds that Native Americans test “HIV”-positive at rates closer to those of white Americans than to those of any other group; somewhere between the rates of whites and those for Hispanics, but generally closer to those of whites. HIV is very race-sensitive indeed, and it discriminates by broad racial genetic category as no other infection does.

In South Africa, the same racial disparities in testing “HIV”-positive were reported as in the United States. Whites always much lower than blacks, and coloreds---mulattos---tested in between. “HIV”-positive rates even reflect miscegenation!

Similarly, within the United States, the ethnic category of Hispanic delivers “HIV”-positive rates that are distinctly higher in the East than in the West---in the same manner as the racial proportions among Hispanics differ, higher proportion of Caribbean and African descent in the East than in the West. HIV is adept at recognizing human racial genetics.

HIV is regular as clockwork in other respects, too. The same number of Americans has been “HIV”-positive from when testing began in the mid-1980s right up to the present; about 1 million, give or take whatever uncertainty the Centers for Disease Control and Prevention (CDC) is prepared to admit at any give time.

Who dies of “HIV disease”, the latest obfuscating term devised by CDC? Always the highest rate is among adults in their 30s and 40s, steadily from 1987 to date; no sign of any change in the distribution of deaths by age, no sign that treatments have had any effect, that they have shifted deaths to later ages (“HIV DISEASE” IS NOT AN ILLNESS, 19 March 2008). HIV is regular as clockwork. You can bet on it.

HIV is distributed in the United States in a pattern that hasn’t changed in two decades. Just as the total number of “HIV”-positive Americans has remained the same, so their geographic location hasn’t changed. It’s highest in the Northeast, next highest in the Southeast, and lowest in the North Central and Midwest. That applies to military personnel, new mothers and their infants, members of the Job Corps, blood donors---every tested group shows that same geographic distribution. Like no other infectious agent, HIV knows its place and sticks to it. Regular as clockwork. You can bet on it.

I put one and one together. Constant geographic distribution, constant racial disparities---maybe the geographic distribution merely reflects the racial proportions of the American population in the different parts of the country?
Yes. Calculate what the geographic distribution of HIV would be if it depended only on the racial make-up of the population and the relative rates at which the different races test positive, and you get a very good fit with the maps of “HIV”-positive rates.

There was one regularity in the data I collected that was, if possible, even more puzzling than the others. Quite a few reports made a point of noting that “HIV”-positive rates were higher in urban areas than in rural regions; always that same progression, and always higher, too, in the large urban areas than in the smaller ones. So regular was this that it seemed quantitative: in the largest metropolitan areas, rates of testing “HIV”-positive were about 4 times as high as in rural areas, and in “semi-urban” regions the rates were about half those in the largest cities.
Leave aside “why”, I thought. Clearly, the calculation of geographic distribution should be modified by taking also this factor into account. Doing that, the fit between the calculated and the actual geographic distributions of HIV is even better.

So HIV is this unique, unprecedented, even magical infection that hides itself not only in human bodies (because none of it has never been isolated in live form from an “HIV”-positive person), it hides itself also in its demographic characteristics, by behaving just like something endemic! It doesn’t go up and down in incidence like other infections or contagions. It doesn’t skip, hop, and jump around regions and countries and the world like other viruses or bacteria. It’s just there. It mimics DNA, in fact, because it distributes itself according to racial category. It mimics physiology: it varies according to the age of its host--- regular as clockwork, it’s lowest in the teens and highest at birth and in middle age. You can bet on it.

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I’ve mentioned before, on this blog (for instance, HIV DEMOGRAPHICS FURTHER CONFIRMED…, 26 February 2008), how reassuring it has been to find that these regularities, described and documented in my 2007 book (The Origin, Persistence and Failings of HIV/AIDS Theory), continue to be reported in newer studies. Reassuring because it emphasizes that the regularities I had discerned were not artefacts of those particular samples---which was unlikely a priori, in any case, given that those “samples” included just about all the published data and represented upwards of 60 million tests; including some, like blood donors and military cohorts, in which all members of those groups were tested, not just sampled; and moreover tested regularly throughout the era of AIDS.

The present little essay was stimulated by finding confirmation of that most puzzling of the regularities, the variation of “HIV”-positive rates with population density. In gathering data for my book, I had not come across a piece in the Journal of Rural Health by Steinberg and Fleming of the CDC, “The geographic distribution of AIDS in the United States: Is there a rural epidemic?” (16 [2000] 11-19). Maybe I had missed it because I focused my searches on “HIV”, not “AIDS”.

Despite its title, that paper is about the distribution of “HIV”. CDC has added to its many sins by conflating, since the late 1990s, HIV and AIDS in such a manner as to make it difficult if not impossible to know what their statistics refer to. In this instance, “AIDS” is said to include “HIV-related severe immunodeficiency”---healthy, asymptomatic people who test “HIV”-positive and have low CD4 counts. So the numbers given in this publication represent “HIV”-positive rates. The article reports specifically on data for 1996; and it confirms rather strikingly the regular trends, including the variation with population density, that are published in my book, for data collated from the mid-1980s to the later 1990s.

Geographic distribution:
Northeast > South > West > Midwest  (49.4 to 34.2 to 28.6 to 13.5 per 100,000)

Black-to-white ratio, 7.2 (in my book, 5.5 ± 3.4)
Hispanic-to-white ratio, 3.4 (in my book, 2.7 ± 2.1)

Variation with population density:
Metropolitan statistical area (MSA) >500,000, 41.6;  50,000 - 500,000, 17.7; non-MSA, 10.1
In my book, 4 to 2 to 1

Regular as a clock that keeps good time.

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A couple of years ago, I had come to the conclusion that the demographics of positive “HIV”-tests, data published largely by the Centers for Disease Control and Prevention (CDC), represent definitive proof that “HIV” is not an infection. Icing on that cake is the fact that “HIV” and “AIDS” are not correlated---again, in officially published statistics---, as became clear to me while writing The Origin, Persistence and Failings of HIV/AIDS Theory (see chapter 9). Now I’ve found that a more direct line of proof lies in comparing the data on deaths from “HIV disease”---as the CDC has come to call it---with data from “HIV” tests.

In earlier blogs, I had argued that “HIV disease” is not an illness, citing among other things Table A below (see WORLD AIDS DAY . . ., 22 December 2007; “HIV DISEASE”, 28 December 2007; HOW TO TEST THEORIES . . ., 7 January 2008).

There I had waffled about how the racial disparities and sex differences in “HIV” deaths parallel those found on “HIV” tests, and how strange it is that blacks and Hispanics are more susceptible to “catching” HIV and yet survive to later ages than do whites or Asians or Native Americans equally suffering from “HIV disease”, and how all this supports the hypothesis that testing “HIV”-positive is a non-specific indication of some sort of physiological stress. But I had failed to grasp the significance of the fact that the age distribution of deaths from “HIV disease” reaches a maximum in people in the prime years of life, mid-thirties to early forties. That is the very opposite of how people react to infectious diseases, where everyone is about equally at risk of infection, but the young and the old are most at risk of succumbing to the infection, from pneumonia, say, or influenza; so the variation with age of “HIV” deaths is the very opposite of how death rates from infectious diseases vary with age; and for the same reason, it’s the very opposite of how all-cause death rates vary with age (Table B).

TABLE B (click in table for full size)

Even death rates from chronic diseases---diabetes, say---or “diseases of old age”---heart and cardiovascular, say, or cancer---show the same trend, though the death rates at very young ages are much less prominent:

TABLE C (click in table for full size)

The all-cause death rates of people in their thirties or forties are comparatively low, between ¼ and ½ of the age-adjusted overall death-rate (Table B, 193.5 or 427 compared to 800.8). Nowhere have I found mention of an illness that is most life-threatening for people aged 35-44 or 45-54---except, of course, “HIV disease”.

One might quibble that the numbers in Table A are not rates for each of the given age-groups; but adjusting for the age distribution in the population makes little difference, as shown by the age distribution of reported death-rates from “HIV disease” (Table D, which is Table 42, p. 236, in “National Center for Health Statistics: Health, United States, 2007 with Chartbook on Trends in the Health of Americans”, Hyattsville, MD, 2007) : for males as for females and in every calendar year, the highest rate of death from “HIV disease” comes at ages 35-44 with the single exception of females in 1987 when it came at 25-34.

TABLE D (click in table for full size)

 * in table D means rates based on fewer than 20 deaths, considered unreliable

The failure of HIV/AIDS theory is demonstrated not only by this incongruous age-dependence of death rates. Note how constant over the years is the shape of this age distribution. While the magnitudes of the rates go up from 1987 to 1995 and then down, they do so in similar fashion in each age group. By contrast, HIV/AIDS theory would have predicted high death-rates at relatively early ages in 1987 and before, when there were no treatments for AIDS and victims were dying within months, or at most a year or two, after diagnosis; then---HIV/AIDS theory would have it---the highest death-rates would have moved steadily to older ages as treatments were introduced, and particularly after the supposedly revolutionary introduction of “life-saving” HAART in the mid-1990s and the development of continually better individual drugs. But there is no such trend; the actual data show no change at all, over the years, in the age range within which people are most at risk of dying of “HIV disease”. For two decades, the greatest risk of dying from “HIV disease” has been experienced by people between 35 and 44years of age.

Also to be noted is that from 1987 into the mid-1990s, every age-group saw a great increase in death rates. That was the era of AZT monotherapy, initially deploying doses so high that even the mainstream acknowledged their toxicity by cutting them back drastically. Discontinuation of monotherapy in favor of “cocktails” then allowed the death rates to fall back again; but, as mentioned above, there is no indication at all that years of survival were increased by introduction of HAART as monotherapy was phased out.

(After writing this I was struck by a sinking feeling that, like increasing arrays of HIV/AIDS numbers issued by the CDC, Table D might have been drawn from computer models, which would explain their astonishing regularity. Then I noticed the phrase in fine print just below the Table’s header, “Data are based on death certificates”, and I was reassured ---at least provisionally.)

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That “HIV”-positive” is not an illness is, of course, the reason that African Americans survive “HIV disease” to later ages than do white, Asian, and Native Americans (Table A), one of the points to which I had drawn attention earlier (7 January). Black people test “HIV”-positive more often than others under all circumstances and in both sexes and at all ages (The Origin, Persistence and Failings of HIV/AIDS Theory, Figures 13-17, pp. 53-6), so when they die they still test positive more often at every age, even to an appreciable extent at ages where others test positive so rarely as not to show up in the statistics (above 55 for men and above 45 for women, Table A).

These variations with age of death rates from “HIV disease” run exactly as would be expected on the hypothesis that testing “HIV”-positive is a non-specific response by the immune system to some sort of physiological stress and that, for a given challenge to health, the strength of that immune response varies according to the capacity of the individual’s immune system (The Origin, Persistence and Failings of HIV/AIDS Theory).

From the teens into the “golden years”, external health challenges do not (on average, overall) vary systematically with age, so on average the variation with age of the tendency to test “HIV”-positive reflects the capabilities of the immune system, which tend to be at their best in the middle years of life:

FIGURE 1

Health challenges are considerably higher, though, at very early ages, because newborns experience the stress of birth and because young children meet many health challenges for the first time as their immune systems are just learning to cope with them. So the graph rises to the left not because the immune system is fully capable, as in the middle years, but because the stresses and health challenges encountered in those years are exceptionally great.

But why should deaths from “HIV disease” parallel the tendency to test “HIV”-positive in the middle years if that tendency represents a capable immune-system response?

Because of the manner in which the CDC defines “HIV disease”.

After “HIV” had become accepted as the cause of “AIDS”, an increasing number of diseases were included by the CDC as “AIDS-defining” just because a significant number of people with those diseases were reported as testing