HIV DEMOGRAPHICS FURTHER CONFIRMED: HIV IS NOT SEXUALLY TRANSMITTED

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.

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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 Theoryhttp://failingsofhivaidstheory.homestead.com/), 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 http://www.measuredhs.com/pubs/pub_details.cfm?ID=594&srchTp=).

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.

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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).http://failingsofhivaidstheory.homestead.com/

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).

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Religion:
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]

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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.

ALTERNATIVE TREATMENTS FOR AIDS

In AIDS AS INTESTINAL DYSBIOSIS (23 February 2008), I mentioned that the clinical experience of Dr. Juliane Sacher in Frankfurt, Germany, is entirely consistent with Tony Lance’s identification of intestinal dysbiosis as a likely cause of testing HIV+ and also of suffering AIDS, especially among gay men who indulge in certain practices.I’ve been asked for English versions of the German articles that Dr. Sacher had sent me. Here is a free translation of them, abbreviated where material could be omitted without changing the meaning.

sacher2006english.pdf

AIDS AS INTESTINAL DYSBIOSIS

The article by Tony Lance posted in WHAT REALLY CAUSED AIDS . . . [20 February 2008] is powerfully persuasive that the outbreaks of “AIDS” in the 1980s were really outbreaks of intestinal dysbiosis among people whose lifestyle was conducive to such dysbiosis. It is further support for Lance’s thesis that some doctors have been successfully treating “AIDS” patients for intestinal dysbiosis, or something very like it, from the very beginning of the “epidemic”.

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Dissenters from orthodox HIV/AIDS theory differ among themselves over what really caused AIDS. John Scythes, for example, believes that undiagnosed syphilis played and perhaps continues to play a significant role (for details, see the website maintained by his colleague Colman Jones ). But Scythes doesn’t claim to have all the answers, and he was an outstandingly objective and helpful reader of drafts of my book. He has met a number of people in various parts of the world who are involved in HIV/AIDS in one way or another, and recently he mentioned to me Dr. Juliane Sacher in Germany as someone who has successfully treated “AIDS” patients without resort to antiretrovirals. I asked Dr. Sacher for published accounts of her work, and she sent me 3 articles published in 2006 in the German periodical Raum & Zeit (141: 34-38: AIDS—Chronology of the mistakes; 142: 18-23: II. AIDS—The virus that doesn’t exist; III. 143: 60-62: “AIDS”—How alternative therapies can help [titles translated by Henry Bauer]). It turns out that Dr. Sacher’s practical clinical experience with AIDS patients and with HIV-positive people affords convincing support for Tony Lance’s hypothesis of intestinal dysbiosis.

Sacher had served as a physician with Lufthansa and had noted already in the 1970s that male flight-crews often had reduced lymphocyte counts, were often homosexual, and indeed were among the first AIDS cases in Germany. In the 1980s, Sacher was in a medical group in Frankfurt that treated many AIDS patients, and she noted their high, sometimes extreme levels of immunoglobulins and antibodies: from 35 to 40 or 45% as against the normal 18%. But T4-cells, which HIV supposedly destroys, are instrumental in the production by B-cells of these globulins; so how could patients supposedly low in T4-cells be producing excess globulins? The answer, shown by research in the early 1990s, is that the low counts of T4-cells in the blood, characteristic of AIDS, does not mark destruction of those cells but rather reflects that they move elsewhere—in particular, into the lymph system. They act against inflammation of the lymph nodes, and return into the blood once the inflammation subsides.

Sacher also notes that the balance between two types of T4 cells is shifted in AIDS patients: typically they display a relative dearth of Th1 and an excess of Th2 cells.
In 1987, Germany funded research to asses the efficacy of antiretroviral treatment of AIDS patients. Dr. Sacher had the largest or second-largest group of HIV/AIDS patients in Germany enrolled in the study. Results after one year showed that in patients treated with AZT the T4-cell counts had decreased by 70%, whereas in those treated by Sacher using alternative treatments–80-90% of all her patients–the decrease had been an average of only 7.5%! Most of these patients had had full-blown AIDS, though a few were HIV-positive but asymptomatic. This result was described in the Ärzte-Zeitung (Physicians Newsletter), 6/7 October 1989, #189, page 15: some 50 patients treated by alternative means did better than 56 patients treated with AZT (Sacher’s Raum & Zeit article no. I includes a photocopy of that publication in the Ärzte-Zeitung).

Sacher’s “alternative” approach to treatment of AIDS patients is informed by the views of Dr. Heinrich Kremer; his 2005 book, “Die stille Revolution von Krebs- und AIDS-Medizin” (The quiet revolution in cancer and AIDS medicine), Ehlers Verlag, Wolfratshausen, is to appear in English translation in the near future. The key is recognition that glutathione is a most important antioxidant which also regulates the Th1/Th2 balance: deficiency of glutathione shifts the balance in the direction of Th2. HIV-positive patients invariably have a glutathione deficiency, and their health improves when this is rectified. In addition, Dr. Sacher monitors carefully and corrects deficiencies in vitamins and minerals; she encourages a healthy lifestyle—exercise, minimizing stress—and uses a number of dietary supplements as indicated in individual cases.

In Part III of her articles in Raum & Zeit, Sacher offers more details of how she treats specific conditions that AIDS patients often experience—diarrhea, bronchitis, bladder and kidney problems. She also recommends preventive measures including specific laboratory tests. A brief professional biography of Dr. Sacher is included in these articles:
Dr. Sacher has been in private medical practice since 1983. She worked with the German Federal HIV Study between 1987 and 1993; served in 1988 on the Parliamentary HIV/AIDS Commission; and was co-recipient in 1990 of a prize of 100,000 Deutschmark for her work with HIV/AIDS patients. Between 1975 and 1993 she served under contract with Lufthansa. From 2000 to 2002 she worked part-time in the biostatistics unit of Wuppertal University. She takes a special interest in all aspects of chronic illnesses, and in complementary as well as mainstream medicine.

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I’ve often been struck by how frequently I come across, “by chance” or from unexpected quarters, material relevant to what I’m thinking about at some given moment. Here it is again. Dr. Sacher’s clinical experience with “AIDS” patients is fully in line with Tony Lance’s intestinal-dysbiosis theory, in particular the role of glutathione and of Th1-Th2 shifts. Dr. Sacher’s work shows the salience of those factors; Lance’s theory explains why so notable a proportion of gay men display glutathione deficiency and Th1/Th2 imbalance and therefore benefit from Dr. Sacher’s approach to medical care.

WHAT REALLY CAUSED AIDS: SLICING THROUGH THE GORDIAN KNOT

The hypothesis that HIV causes AIDS fails to explain the demographic characteristics of HIV-positive tests (The Origins, Persistence and Failings of HIV/AIDS Theory); it has generated a large number of conundrums and claims that cannot be reproduced (for example, as to herpes, circumcision, vaccines—see HERPES AND HIV, 8 February 2008). Virions of HIV have never been isolated from HIV-positive people. Nor has the hypothesis led to satisfactory answers to salient questions:
1. Why did AIDS appear first among gay men in the United States?
2. Why in the late 1970s to early 1980s?
3. Why did it manifest in the specific forms of Pneumocystis carinii pneumonia, candidiasis, lymphadenopathy, and Kaposi’s sarcoma?

Dissent from HIV/AIDS theory has persisted for some two decades, but the dissidents agree only over the inadequacy of that theory; no consensus has formed over a possible alternative among a number of suggestions: drug abuse; multifactorial—a combination of many insults including a variety of infections and antibiotic treatments; undiagnosed syphilis. None of those offer convincing answers to those three questions. And dissidents have an additional question to answer:
4. If HIV doesn’t cause AIDS, why do antiretroviral drugs sometimes make people feel much better, quite quickly? (even if that benefit doesn’t last, and the drugs themselves cause harm in the longer run).

Drug abuse evidently has something to do with AIDS.
John Lauritsen was first to point out that all the early AIDS patients had a history of using “recreational” drugs and that the Centers for Disease Control and Prevention obscured the fact through its misguided “hierarchical” classification of AIDS cases. Lauritsen also argued cogently for nitrites, “poppers”, as the specific cause of Kaposi’s sarcoma (http://paganpressbooks.com/jpl/POPPERS.HTM).
Peter Duesberg has gathered considerable supporting evidence for the role of drug abuse, including different manifest infections associated with different drugs .
Still, acknowledging an association with drug abuse leaves unanswered those same three questions. After all, there had been an epidemic of drug abuse, not restricted to gay men, in the 1960s to 1970s. Then, and also in more recent times with cocaine, crack, and meth, certain consequences deleterious to health are well known—but they did and do not prominently feature Pneumocystis carinii pneumonia or candidiasis.

The multifactorial hypothesis, too, lacks convincing answers for the specificity of the affected group, when it was affected, and what the manifest infections were.

The inability to offer good explanations for these specifics may well be a major reason why the dissidents’ sound arguments against HIV/AIDS theory have been so little attended to. It’s one thing to show that some theory is inadequate, but it’s a well known aspect of science that an unsatisfactory theory is not abandoned until a better alternative becomes available. Non-scientists, too, can only shrug helplessly when they are shown how obvious the evidence is that HIV doesn’t cause AIDS; they need, quite reasonably, to be given at least plausible answers for what caused AIDS and what “HIV” is.

After my book was published, I learned a great deal more from people who got in touch with me, and yet more after I began writing this blog. The most striking discussion that was new to me, something that gave me a “Eureka” moment, came from Tony Lance, whose explanations offer satisfactory answers to all four of those central questions. What we now know as “AIDS” had been described at first as “GRID”: Gay-Related Immune Deficiency. It turns out that it should have been named Gay-Related Intestinal Dysbiosis:

gay-relatedintestinaldysbiosis.pdf

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HIV-POSITIVE BABIES ARE NOT VIRUS-INFECTED

MacDonald reminded me that the Perth Group have documented in devastating fashion that “HIV-positive” data on mothers and babies proves that testing HIV-positive does not signify an infection.

I really should have emphasized that when commenting on the self-contradictions regarding “HIV” and breastfeeding (HIV and BREASTFEEDING AGAIN, 13 February 2008; FIRST: DO NO HARM!, 19 December 2007; MORE HIV, LESS INFECTION: THE BREASTFEEDING CONUNDRUM, 21 November 2007) and claims of mother-to-child transmission generally (for instance, TWINS ATTRACT THEIR MOTHER’S HIV, 12 January 2008; HIV-POSITIVE CHILDREN, HIV-NEGATIVE MOTHERS, 25 November 2007).

The Perth Group’s website has two comprehensive discussions available as links: “Monograph on mother-to-child transmission”, and “BMJ Online Debate”.

MacDonald cited (from the latter) this concise yet fully documented argument by the Perth Group in response to orthodox viewpoints pressed by a certain Peter Flegg:

“In regard to ‘HIV’ seropositive mothers, their infants and antibody specificity, we would be grateful for Peter Flegg’s view on the following:

In 1987 the CDC advised: ‘Most of the [CDC] consultants believed that passively transferred maternal HIV antibody could sometimes persist for up to 15 months’. (18 ) In 1991 the CDC extended the time to 18 months 13 and by 1995 ‘…the range of WB seroconversions might eventually extend beyond 30 months’, (14) that is, at double the age ‘believed’ eight years earlier. Before the AIDS era the evidence was that transplacental maternal antibody in offspring did not persist beyond nine months.(15) In 1993, Parekh from the CDC developed ‘a human immunodeficiency virus type 1 (HIV-1)-specific 1gG-Fc capture enzyme immunoassay (1gG-CEIA) to elucidate the dynamics of HIV-1 maternal antibody decay and de novo synthesis of HIV-1 antibodies in infants’. He and his colleagues demonstrated a rapid decay of maternal ‘HIV’ antibody ‘with decline to background levels by 6 months’. (16 ) In other words, if the ‘HIV’ antibody test is specific, any child who has a positive ‘HIV’ antibody test beyond 9 months should remain positive for the remainder of his or her life. In the only study providing a detailed analysis of post partum loss of infant HIV seropositivity, the European Collaborative Study, (17) approximately 23% of the children became seronegative between birth and 9 months. However, 59% became seronegative between 9 and 22 months. Since the latter cannot be due to loss of maternal antibodies, the only explanation is that either: (i) the antibody test is non-specific or; (ii) the children managed to clear ‘HIV’ infection without treatment. If 23% of children test positive because of maternal antibodies and in 59% the test is non-specific, how certain can Peter Flegg be that in the remaining 18% of children the test will not also serorevert after 22 months? Or if the test remains positive, is it a true positive? May we ask, what does Peter Flegg tell the mother of a child who tests positive between 9 and 30 months and what is his approach to the clinical management of this child?”

The cited references are

14. Chantry CJ, Cooper ER, Pelton SI, Zorilla C, Hillyer GV, Diaz C. Seroreversion in human immunodeficiency virus-exposed but uninfected infants. Pediatr Infect Dis J 1995;14(5):382-7.

15. Stiehm ER. Immunologic diseases in infants and children. 3rd ed. Philadelphia: WB Saunders Company, 1973.

16. Parekh BS, Shaffer N, Coughlin R, Hung CH, Krasinski K, Abrams E, et al. Dynamics of maternal IgG antibody decay and HIV-specific antibody synthesis in infants born to seropositive mothers. The NYC Perinatal HIV Transmission Study Group. AIDS Res Hum Retroviruses 1993;9:907-12.

17. Epidemiology, clinical features, and prognostic factors of paediatric HIV infection. Italian Multicentre Study. Lancet 1988;ii:1043-6.

18. CDC. Current Trends Classification System for Human Immunodeficiency Virus (HIV) Infection in Children Under 13 Years of Age. Morb Mortal Wkly Rep 1987;36:225-30, 235-6.

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One can hardly ask for better grounded reasons for recognizing that “HIV-positive” does not signify permanent infection; and that consequently all the claims of mother-to-child transmission of a virus — be it perinatally or as a result of breastfeeding — cannot be taken as valid, based as they are on the most dubious grounds.

Given these facts, how could anyone recommend the administering of toxic antiretroviral drugs to pregnant women and babies? Yet now we have studies exploring how longer exposure to these drugs might influence the spurious indications of the presence of “HIV” (HIV and BREASTFEEDING AGAIN, 13 February 2008).