COCAINE AND HEROIN AREN’T GOOD FOR YOU! — a Golden Fleece Award

My generation of scientists was familiar with the Golden Fleece Awards bestowed by Senator William Proxmire on federally funded research to find answers that were already known or on topics of no importance. Proxmire would certainly have given an award for the work described by the headline,

HIV-positive illicit drug users have increased risk for opportunistic infections, death, study says (Kaiser Daily HIV/AIDS Report, 8 March 2006)

When Google Alerts delivered me this headline, I naturally inferred that the study had found that “HIV”-positive drug users had a poorer prognosis than HIV-negative drug users. That would have made this just another study showing that if you were “HIV”-positive you were more likely to be ill than if you were HIV-negative, given that testing “HIV”-positive is a sign of physiological stress, albeit not necessarily serious enough to worry about unless your physician decided that you needed to take antiretroviral drugs. Moreover it would have been consistent with several reports that “HIV”-positive drug addicts reverted to HIV-negative, as well as to better health, upon conquering the addiction.

Imagine my delight, not to say surprise, on finding that my inference was dead wrong:

“HIV-positive users of cocaine and heroine have an increased risk for opportunistic infections and death compared with HIV-positive nonusers, according to a study published in the January 4 on-line edition of the American Journal of Epidemiology, Reuters reports. Gregory Lucas of the Johns Hopkins University School of Medicine and colleagues surveyed a total of 1,851 HIV-positive individuals every six months starting in 1998. Researchers grouped the participants into different categories: 1,028 ‘nonusers’; 588 ‘intermittent users,’ who had used illicit drugs an average of 14 days in the last six months; and 235 ‘persistent users,’ who had used illicit drugs an average of 27 days in the last six months. After three years, researchers found that the approximate survival rates were 87% for nonusers, 80% for intermittent users and 68% for persistent users. After adjusting for various factors — including age, race, gender and CD4+ T-cell counts — researchers found that the risk of death was almost double in intermittent users and almost triple in persistent users. During periods when users abstained from illicit drug use, the risk of opportunistic infections decreased to the level associated with nonusers, according to the study.”

Imagine that!

Congress, The National Drug Enforcement Agency, indeed all law enforcement entities, as well as the NGOs that preach “Just say NO to drugs”, will be greatly relieved at this proof that their work has actually had a genuinely substantive basis. No longer need they worry, whether they have an objective basis for their animus against cocaine, crack, crystal, heroin, etc., etc.—now it’s been scientifically proven at last that those substances are health-threatening.

“The observed increase in risk might be attributed to the effect illicit drugs have on the immune system…”
Well. Yes, that seems plausible enough.

But let us not overlook that this whole study involved “HIV”-positive people. So the really major question is, how do cocaine and heroin interfere with treating HIV? So, as Jon Stewart of the Daily Show would say, “Here’s your moment of Zen”:

“The observed increase in risk might be attributed to … failure to adhere to antiretroviral therapy”.

So therefore:

“Effectively targeting and treating active substance abuse in HIV treatment settings may provide a mechanism to improve clinical outcomes”.

Would anyone disagree?

Would anyone have disagreed before this study was ever done??

RACE and SEXUAL BEHAVIOR: STEREOTYPE vs. FACT

Racial disparities in testing “HIV-positive” are explained — by proponents of HIV/AIDS theory, that is — as stemming from the harmful effects of racial discrimination, which mire the discriminated-against in circumstances rife with drug abuse and sexual promiscuity. That runs counter to a goodly body of actual evidence that undercuts this type of explanation; and it also draws on stereotypes not readily distinguishable from racist beliefs (see 19 May, HIV/AIDS THEORY IS INESCAPABLY RACIST).

Some of the evidence confounding the stereotypes is cited in my book (p. 77):

“As a matter of actual fact, research in the context of HIV/AIDS has not revealed any racial differences in sexual behavior. Among drug users, no significant differences in behavior by race were found as to numbers of sexual partners, frequency of intercourse, numbers of sexual partners who were IDUs, numbers of non-IDU sexual partners, prostitution, or intercourse with people then or later diagnosed with AIDS (Friedman et al. 1987). Samuel and Winkelstein (1987) found no significant racial differences in behavior among gay men in San Francisco, and they concluded that the black-to-white ratio of . . . [“HIV-positive”] could not be explained by differences in major risk factors. The San Francisco Department of Health (1986) found no differences between races as to anal intercourse . . . . Bausell et al. (1986) found white Americans less likely than black Americans to take protective measures during sex. Historical data from Zimbabwe records a higher incidence of venereal disease among the white South Africa Police and the British Armed Services than among the Native Police or among Africans in general (McCulloch 1999, 205, 207). Contemporaneous surveys have found that levels of sexual activity in general populations in Africa are comparable to those in North America and Europe (Brewer et al. 2003; Gisselquist 2002).”

It has become fashionable to assert that black women in the United States are at particular risk because of black men “on the down low” (indulging secretly in male-with-male sex), becoming “HIV-positive”, then transmitting that to their female partners. But here again, the evidence doesn’t sustain the speculation:

“The lifestyle referenced by the term the DL is neither new nor limited to blacks, and sufficient data linking it to HIV/AIDS disparities currently are lacking. Common perceptions about the DL reflect social constructions of black sexuality as generally excessive, deviant, diseased, and predatory. [“social construction” means stemming from human interpretation rather than from the objective reality] Research targeting black sexual behavior that ignores these constructions may unwittingly reinforce them” (Ford et al., Ann Epidemiol 17 [2007] 209-16).

An illustration of such unwitting reinforcement is one of the CDC’s statements:
“The phenomenon of men on the down low has gained much attention in recent years; however, there are no data to confirm or refute publicized accounts of HIV risk behavior associated with these men. What is clear is that women, men, and children of minority races and ethnicities are disproportionately affected by HIV and AIDS” (emphasis added; unchanged since at least March 2006; www.cdc.gov/hiv/topics/aa/resources/qa/downlow.htm, accessed 11 May 2008).

Another common and politically correct gambit (attempting to explain away that blacks always test “HIV-positive” more often than others) seizes on the high incarceration rate of young black men, particularly from inner-city regions, and combines that with the shibboleth that prisons are a hotbed of “HIV” transmission (for example, Johnson & Rafael 2006). But once again the speculation goes contrary to fact, because “actual observations in prisons have failed to reveal transmission of HIV there (Brown 2006; Horsburgh et al. 1990; Kelley et al. 1986)” (p. 79 in The Origin, Persistence and Failings of HIV/AIDS Theory).

In South Africa, blood from black donors was, for some time, being destroyed as “unsafe” because it tested “HIV-positive” so much more often than blood from people of mixed race or from South-East Indians or whites (p. 75 in The Origin, Persistence and Failings of HIV/AIDS Theory). However, since testing was available for the blood, this blanket rule surely owed something to underlying and pre-existing racist beliefs. Racist preconceptions in the 1980s among HIV/AIDS workers in Africa — some of whom are still prominent in HIV/AIDS research nowadays — were described, long ago and in detail, by the Chirimuutas (AIDS, Africa and Racism, Free Association Books, London [UK] 1987/89). Konotey-Ahulu, a distinguished Ghanaian physician and medical researcher, also exposed the lack of evidence for an African origin of HIV/AIDS in a book (What is AIDS? 1989/96, ISBN 0-9515442-3-3) I described in a review as “flavored by a traditional attitude toward what constitutes acceptable behavior” and displaying “what used to be called good breeding and proper upbringing”, exploding by personal example all sorts of notions about “those Africans” (Journal of Scientific Exploration 21 [2007] 206-9).

That blacks always test “HIV-positive” more often than others simply cannot be explained by differences in behavior:

“AIDS researchers don’t have a solid explanation for why black women in America have such a shockingly high prevalence of HIV infection. . . . injection drug use, a particularly effective way to spread HIV, is actually lower in black women than in white women” — Jon Cohen, “A silent epidemic”, 27 October 2004, www.slate.com/id/2108724/.

“Black young adults . . . are at high risk even when their behaviors are normative. Factors other than individual risk behaviors and covariates appear to account for racial disparities” — Halfors et al., Sexual and drug behavior patterns and HIV and STD racial disparities: the need for new directions, Am J Public Health 97 [2007] 125-32.

“HIV-positive gay men are more likely than HIV-positive black African heterosexual men and women to engage in sexual behaviour that presents a risk of HIV transmission. . . . There were no significant differences between white gay men and those from other ethnic background in terms of sexual behaviour” (Rod Dawson, 5 January 2007. AIDSmap news, summarizing Elford et al., “Sexual behaviour of people living with HIV in London: implications for HIV transmission”, AIDS 21 [suppl. 1, 2007] S63-70).

“According to Robert Janssen, director of CDC’s Division of HIV/AIDS Prevention, blacks do not engage in riskier sexual behavior compared with other groups, but the population’s HIV/AIDS infection rates mean that blacks who have sex with other blacks are more likely to get HIV than people in other ethnic groups” — (emphasis added; Kaiser Daily HIV/AIDS Report, 9 March 2007).
Perhaps Janssen has never heard of the chicken-&-egg conundrum? How did the infection rate in the black community become higher than in others in the first place, given that the first affected groups in the USA were predominantly white gay men?

That ill-founded grasping-at-straws argument is not unique with Janssen:
“racial disparities in seroprevalence were . . . not attributable to disparities in risk factors such as STD, bisexuality, or acceptance of HIV testing. This finding suggests that the observed differences may reflect racial differences in the background seroprevalences” — Torian et al., Sex Transm Dis. 29 [2002] 73-8.
I suppose one must sympathize with people trying desperately to explain the unexplainable. This “explanation” is a tautology: blacks test “HIV-positive” more often than others because blacks already test “HIV-positive” more often than others.

“Paradoxically, potentially risky sex and drug-using behaviors were generally reported most frequently by whites and least frequently by blacks. . . . Understanding racial/ethnic disparities in HIV risk requires information beyond the traditional risk behavior and partnership type distinctions” — Harawa et al., “Associations of race/ethnicity with HIV prevalence and HIV-related behaviors among young men who have sex with men in 7 urban centers in the United States”, JAIDS 35 [2004] 526-36.

The Centers for Disease Control and Prevention found, in one study, that “Black gay and bisexual men . . . [were] more likely to engage in safe-sex practices than their white counterparts. . . . ‘Across all studies, there were no overall differences [by race] in reported unprotected receptive sex or any unprotected anal intercourse . . . among young MSM — those ages 15 to 29 — African-Americans were one third less likely than whites to report in engaging in unprotected anal intercourse’ . . . . Black gay or bisexual men were also ‘36 percent less likely than whites to report having as many sex partners as white MSM’ . . . . Blacks in the study were also less likely to use recreational drugs, such as methamphetamine or cocaine, compared to whites” (“One-third of HIV-infected gay men have unsafe sex: CDC”, HealthDay News, 3 December 2007).

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Black people always test “HIV-positive” more often than others.

Black people do not differ greatly from others in their sexual behavior. Where they do, it is through behaving somewhat more responsibly than white people.

The racial disparities in testing “HIV-positive” cannot be explained by differential behavior: blacks always test positive much more often, but their sexual behavior does not constitute a corresponding risk.

THEREFORE: Testing “HIV-positive” must indicate something other than a sexually acquired condition. Testing “HIV-positive” does not mark infection by a sexually transmitted agent. Rather, testing “HIV-positive” is a very non-specific indication of some sort of physiological stress; see, for example, REGULAR AS CLOCKWORK: HIV, THE TRULY UNIQUE “INFECTION”, 1 April 2008; “HIV DISEASE” IS NOT AN ILLNESS, 19 March 2008; UNRAVELING HIV/AIDS, 8 March 2008; HIV DEMOGRAPHICS FURTHER CONFIRMED: HIV IS NOT SEXUALLY TRANSMITTED, 26 February 2008; TWINS ATTRACT THEIR MOTHER’S HIV, 12 January 2008; HOW TO TEST THEORIES (HIV/AIDS THEORY FLUNKS), 7 January 2008.

UPDATE: MORE SPONTANEOUS SEROREVERSION

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

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

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

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

And here’s more detail about Andrew Stimpson:

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

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

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

REGULAR AS CLOCKWORK: HIV, THE TRULY UNIQUE “INFECTION”

Astonishment, disbelief, incredulity would merely begin to describe my feelings when I began collecting published data about HIV a few years ago.

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.

“HIV DISEASE” IS NOT AN ILLNESS

This post is longer than I prefer, but I saw no good way to split it into parts. It explains that the way “HIV infections” and deaths from “HIV disease” vary with age and with race and over time constitutes a resounding disproof of HIV/AIDS theory.

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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).

TABLE A (click in table for full size)

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 “HIV”-positive. As Rebecca Culshaw noted, this led to the extraordinary situation that the death from any cause of a person known to be “HIV”-positive would be reported as a death from “HIV disease”—even when the immediate cause of death was heart attack, liver failure, CMV infection, or even suicide, a car accident, or drowning (“Science Sold Out”, 2007, p. 30, citing Massachusetts Department of Health, 2002). (There may be a financial incentive to do this: federal funds to “fight HIV/AIDS” are apportioned to states and cities according to the perceived relative impacts of HIV/AIDS.)

Now: illness and death are in and of themselves often associated with positive “HIV”-tests (after all, they represent extreme challenges to health). Hospital patients (admitted for reasons not connected with HIV/AIDS) test “HIV”-positive at between 0.1 and 7.6% (The Origin, Persistence and Failings of HIV/AIDS Theory, Table 3 p. 25; Table 23 p. 81); and moreover the tests vary with age as in the diagram above (ibid., Table 26 p. 98); emergency-room patients tested at 5-6% (ibid., pp. 48, 85); “HIV”-positive rates in autopsies were reported in one instance as between 1.9 and 3.7% and increasing in proportion to the degree of death-causing trauma, and in another instance at 18% with no indications of AIDS (ibid., p. 85). Since even accident and trauma victims tend to test “HIV”-positive, as well as people ill for a wide variety of other reasons, there is then a definite probability that anyone who is seriously ill will test “HIV”-positive, and so anyone who dies for any reason may well have tested “HIV”-positive while in hospital, or may well do so in autopsy, with a probability of a few percent or more; that’s much higher than the “normal” rate in the US population as a whole, which is an order of magnitude lower at a few per thousand or less.

The maximum death-rates from “HIV disease” in 2004 (Table D) were 10.9 (per 100,000) at ages 35-44 and 10.6 at ages 45-54. The all-cause death-rates for those age groups were (Table B) 194 and 427 respectively. Thus deaths from “HIV disease” represented respectively 5.5% (10.9/194) and 2.5% (10.6/427) of all deaths in those age groups, quite comparable to the frequency of positive “HIV”-tests among non-AIDS hospital patients and emergency-room patients and in autopsies. Thus deaths from “HIV disease” are merely that fraction of all deaths in which the non-specific “HIV”-positive reaction happened to turn up in response to the health challenge that had caused the death.

So death rates from “HIV disease” parallel the age variation of “HIV” tests simply because all deaths of “HIV”-positives are called deaths from “HIV disease”, and because “HIV” tests are so highly non-specific as to react to many life-threatening conditions. And that is also why the age variation of death rates ascribed to “HIV disease” is (for chronic diseases) unlike or (for infectious diseases) opposite to the variation with age of death rates from every other malady.

Figure 1 is schematic, not quantitative. I had mentioned in connection with its first appearance (ibid., p. 26) that the actual “middle” age of the peak appears to vary somewhat with sex and with race. To compare the actual years of that peak on “HIV” tests with the peak years of “HIV” deaths, I wanted “HIV”-test data for the population as a whole, since the death-data in Table A are also for the population as a whole. The most appropriate data-sets are those, totaling nearly 10,000,000 tests, published in 1995-8 by CDC for all public testing-sites (clinics for TB, HIV, STD, drugs, family planning, prenatal care, and more, as well as prisons and colleges and some reports from private medical practices). Pooling the actual numbers for each of those four years and making the appropriate calculations delivers the following results:

TABLE E (click in table for full size)

The highlighted cells and the “XXX” overlap or straddle in 12 of 13 cases; there is a good quantitative correspondence between the ages of maximum probability of testing “HIV”-positive and the ages of maximum rate of dying from “HIV disease”. But under HIV/AIDS theory, infection by HIV is supposed to be followed by a “latent period” of about 10 years: the peak ages for deaths from “HIV disease” should be a decade or more later than the peak ages for “HIV” infection, rather than overlapping in the same age-ranges. Furthermore, the difference between age of “infection” and age of death should have increased during the years—from the mid-1990s on—when “life-saving” antiretroviral treatments supposedly extended the life spans of “HIV”-positive people by a significant amount. Yet in 2002-4 (Tables A and D), the peak ages for “HIV” infection and for deaths from “HIV disease” are virtually the same as the ages where infections were most common in 1995-8, even though most people “infected” in 1995-98 should have survived well beyond 2005-8!

All this is inexplicable under HIV/AIDS theory, whereas it comports perfectly with the alternative theory that testing “HIV”-positive denotes physiological stress.

HIV/AIDS theory lacks substantive legs to stand on. “HIV” is not any cause of illness. Testing “HIV”-positive signals the presence of some sort of challenge to health. The tendency to test “HIV”-positive depends on what the health challenge is, and on how strongly an individual tends to respond.