HIV/AIDS Skepticism

Pointing to evidence that HIV is not the necessary and sufficient cause of AIDS


Posted by Henry Bauer on 2008/02/26

The rates at which people in the United States test HIV-positive have remained at about the same level, and have remained distributed geographically in the same manner, for two decades. The rates also vary with age, sex, and race in the same manner in all social groups. Those demographics are characteristic of something endemic, not of something contagious that causes epidemics; thus “HIV” is not something that’s sexually transmitted (see also WHAT “HIV” IS NOT: IT’S NOT SEXUALLY TRANSMITTED, 6 January 2008).

That demographics-based argument, detailed in The Origins, Persistence and Failings of HIV/AIDS Theory (McFarland 2007), is strongly confirmed by finding similar demographic characteristics in Africa as in the United States.


Consider how testing HIV-positive varies with age and sex:


Sexually transmitted diseases tend to strike adolescents and young adults more than others; by contrast, rates of HIV-positive are highest in newborns and in middle-aged people.

Resistance to infections and illnesses is greatest among adults in the prime and middle years of life; old people are at particular risk for flu, pneumonia, etc. The very opposite applies with HIV: the risk of testing HIV-positive is greatest in middle age.

The above diagram describes general trends. As noted in the source (The Origins, Persistence and Failings of HIV/AIDS Theory, there are some variations: “The only major variation between groups is in the precise ‘middle’ age at which F(HIV) peaks, anywhere from 30s to 50s; and that precise age is not always the same for males and females. . . . There are also hints . . . that the peak ages and the male-to-female ratios may be somewhat different in the various racial categories” (pp. 26-7); “black women test positive relatively frequently under some sort of not-necessarily-serious physiological stress, such as pregnancy or childbirth” (p. 247).

Those very same trends can be seen in the Demographic and Health Survey for Rwanda (2005 edition, published July 2006; available at



The data from the United States contained hints that black women are particularly prone to test HIV-positive; the Rwanda data confirm that strongly—women there test HIV-positive more often than men up to age 40, whereas in the United States women test positive more often than men only up to the later teens.

Then there’s the variation with marital status (from Table 15.6, Rwanda Demographic and Health Survey, 2005):


As earlier remarked (TO AVOID HIV INFECTION, DON’T GET MARRIED, 18 November 2007), this illustrates the usual variation with age: the widowed are likely to be on average older than the divorced, who are likely to be on average older than those currently married or in a stable relationship, who are likely to be older than those who never had sex. Note, too, that 2 per 1000 men, and 8 per 1000 women, have contracted this supposed STD without ever having had sex.

Yet another confirmation of this variation of HIV-positive with age is reported by Brewer et al., Annals of Epidemiology, 17 (2007) 217-26. The following rates of testing HIV-positive (as percentages) are extracted from their Table 5:


All show the increase with age from teens into “middle age” (which is in the 30s except with Tanzanian males and uncircumcised Kenyan males). Only 1 cell out of 32 (18-24-year-old circumcised Kenyan males) does not fit the pattern, a remarkably consistent, reproducible result for such a demographic variable.

In the Kenya data, note that uncircumcised females test positive more often than males only up to the late teens, which is more like the US data than the Rwandan; whereas in the circumcised group, females test positive more often than males into the thirties, which is more like the Rwandan data than the US data.

Note too how irreproducible is the variation of HIV-positive rate with circumcision status; in 6 cases, circumcised corresponds to a greater HIV-positive rate, in the other 10 cases it is the opposite.


Among the surprises in the US demographic data was the consistent increase of HIV-positive rates with increasing population density (which is again not characteristic of sexually transmitted diseases). Such a correlation is, however, consistent with an explanation of HIV-positive as a non-specific physiological response to a variety of minor and major insults such as environmental pollution (see p. 89 in The Origins, Persistence and Failings of HIV/AIDS Theory).

Remarkably, the same trend with population density is found in Rwanda:
“in 1986 . . . [rates of HIV-positive] were 17.8 percent in urban areas and 1.3 percent in rural areas. . . . In . . . 1991 . . . 27 percent in urban areas, 8.5 percent in semi-urban areas, and 2.2 percent in rural areas. . . . in 1996 . . . 27 percent among urban residents, 13 percent among semi-urban residents, and 6.9 percent among rural residents”; in 2002, 7.0-8.5% in urban areas and 2.6-3.6% in rural areas; in 2003, 6.9-8.3% urban, 2.7-3.6% rural.

The overall rates in 2005 were reported as 2.6 rural and 8.6 urban for women, and 1.6 rural and 5.8 urban for women. This makes the urban-to-rural ratio 3.3 for women and 3.6 for men, so similar that it speaks against any interpretation in terms of different sexual behavior by men and women. Moreover, these ratios are uncannily similar to the approximate ratio of 4 found in the United States (p. 67 in The Origins, Persistence and Failings of HIV/AIDS Theory).


I didn’t come across reports in the United States for how HIV-positive rates vary with religion, but the Rwanda report does include this information:


HIV/AIDS dogma explains rates of testing HIV-positive by sexual and drug-abusing behavior. That provides a dubious basis, to say the least, for understanding how these rates vary with religious affiliation in Rwanda: are we to infer that Muslim women are particularly prone to unsafe promiscuity or drug injecting, while Muslim men are least likely to indulge?

Under the alternative explanation of what HIV-positive means, however—namely, non-specific physiological stress* —, this wouldn’t be at all puzzling if the proportion of Muslim women who are black—of Negroid racial type—is greater than in the other religious groups, since black women are particularly prone to test HIV-positive.
[* see posts of 12 & 25 November 2007, 22 & 29 December, 4, 7, 8 & 12 January 2008]


It’s often said that scientific theories can be disproved by data that contradict them whereas theories are confirmed when they make successful predictions. Sexually transmitted diseases do not infect middle-aged people more than others in all social groups on disparate continents.
HIV/AIDS theory is disproved because “HIV” is not sexually transmitted.

The theory that HIV-positive reflects a non-specific physiological response was based (in part) on demographic data for the United States, see The Origins, Persistence and Failings of HIV/AIDS Theory. The trends published there and taken as universal constitute effectively predictions that the same trends as to age, sex, and population density would be found elsewhere. They have been found in Africa. The theory is thereby confirmed.


  1. heja said

    you wrote

    “Under the alternative explanation of what HIV-positive means, however—namely, non-specific physiological stress* —, this wouldn’t be at all puzzling if the proportion of Muslim women who are black—of Negroid racial type—is greater than in the other religious groups, since black women are particularly prone to test HIV-positive.”

    I am not an expert in races, demographics and religion in Africa but given that both Islam and Christianity are religions “imported” to Africa from other, ethnically different, regions, it is not unimaginable that actually Muslim women may be less of Negroid racial type in Rwanda…

    Can someone confirm that this is actually a fact?

  2. hhbauer said


    I don’t know how one would get such information. My point is that under the orthodox view of a sexually transmitted virus, these religion-related differences make no sense, cannot be explained . The alternative view at least offers a possible expanation. My book cites support for race-related differences in how immune systems react to stress, and specifically that African ancestry seems to correlate with particularly strong responses; that doesn’t exclude that some other racial groups might also have such strong responses.

  3. heja said

    Yes, you are right; they make no sense however we look at them’ though the way we look at them is very much affected by the stereotypes about religions we have in our heads.

    The alternative view and especially the evidence on racial differences described in your work offers an explanation, especially if, as you yourself pointed out, Muslim women are indeed more of Negroid racial type in Rwanda. If they are not (say Muslims there are people with Arabic roots going far back which makes them, say, racially closer to whites) then the alternative explanation does not fit the data in the table so much better. It can only be considered better because it offers a more open explanation—something along the lines: everyone (or every race) is different in this respect, which is intuitively very persuasive but not helpful in interpreting the incidence-by-religion table.

    Let me put it this way: The racial differences documented in your work are a very strong evidence against the orthodox paradigm but (remembering that good science requires a good balance of both healthy scepticism and open-mindedness/enthusiasm) I think you are being too enthusiastic about the ability of the alternative view to explain the incidence-by-religion table. In any case, I suspect tables like this are flawed because e.g. they do not control for the intensity of testing in different subgroups (e.g. are Catholics more likely to test because of their guilt-based background?)

    Sorry for a long post.

  4. hhbauer said


    Last point first: The data are rates of testing positive, not numbers, so it is irrelevant whether more Catholics (say) are tested.

    On your main point I agree. Perhaps I should put it this way:
    The orthodox HIV = AIDS theory cannot explain these differences.
    The alternative, “stress”, theory can potentially explain it because it holds that the tendency to test HIV+ is an individual physiological response that varies characteristically with certain genetic groupings; for example, among racial groups the tendency is Asian < Caucasian < Native American < African. If Muslim women in Rwanda include a high proportion of people whose immune-system genes make for a strong response to challenges—as for example in Africans—then what seems an insoluble puzzle may have a simple solution.

  5. CathyVM said

    According to the Joshua Project there are only 9,000 people in Rwanda classified as “Arab”. The only other group identified with Islam listed as religion is Swahili with only 13,000 people. Of the other groups identified (apart from Gujerati Indians) all were identified as Christian. How accurate this information is I don’t know.

  6. hhbauer said


    That is fascinating. I didn’t know of the Joshua Project. If those data are accurate, then 13,000 out of 22,000 Rwandan Muslims are Swahili-speaking and classed as Sub-Saharan African, Bantu, which is one of the population groups that appears to be particularly prone to generate an “HIV+” response. The alternative, “stress”, theory seems to work here!

  7. CathyVM said

    Stress would be the word all right. Yesterday I heard from an African social scientist (fully within the HIV-AIDS paradigm and not happy with me at all) who talked of a young girl, a Rwandan refugee, who hid for days under dead bodies while her village was slaughtered. She is now HIV positive, purportedly from the dead bodies bleeding on her. It hurts my heart to think this girl has survived such a dreadful, traumatic experience only to be “sentenced to death” by an equally powerful and oppressive regime.

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