HIV/AIDS Skepticism

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

Posts Tagged ‘Jeckoniah O. Ndinya-Achola’

Spontaneous generation of “HIV”

Posted by Henry Bauer on 2009/10/25

In places where claimed outbreaks of “HIV” have had “infected needles” as the only possible source of the supposedly infecting agent, the large but unaddressed question is, how did those needles become infected in the first place? And then remain infected long enough to pass on that infection when the purported contagious agent is supposed to survive for only a brief time outside bodily fluids? [HIV/AIDS in Italy — and “NEEDLE ZERO”, 11 October 2008; “Needle ZERO” again; or, HIV pops up magically out of nowhere, 15 November 2008].
It’s as though this “HIV” were spontaneously generating itself. That would not have seemed absurd a couple of centuries ago, when spontaneous generation of living organisms was an acceptable theory, but HIV/AIDS theory is supposed to be scientifically up-to-date.

An even more direct instance of “HIV-positive” in absence of “HIV” is that of certain elite controllers who have no detectable “viral load” (Compounding HIV/AIDS absurdities, 11 October 2009).

There are at least two other situations where “HIV-positive” pops up without any sign that “HIV” was present in the first place: In clinical trials of circumcision as a means of preventing “HIV-positive” status, and in a prospective study of acquisition of “HIV” by pregnant women.

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Two clinical trials of circumcision both reported that participants in both control and intervention groups acquired “HIV-positive” status during the trial even while abstaining from intercourse:

“there were seven early seroconverters . . . : four in the circumcision group and three in the control group. Three of the four in the circumcision group reported no sexual activity in the month after circumcision. We cannot exclude the possibility that any of these individuals were actually HIV positive at baseline, and that their infection was not detected. Two of the three early seroconverters in the control group also denied sexual activity in the period before seroconversion” [emphases added; Bailey et al., “Male circumcision for HIV prevention in young men in Kisumu, Kenya: a randomised controlled trial”, Lancet, 369 (2007) 643-56].

circumcision  was not protective against HIV acquisition in the few men  who  reported  no  sexual  activity in  a  given  follow-up  interval. There were six incident cases (three in each group)  during periods of reported abstinence. None of these six  participants reported receipt of injections or transfusions  during the follow-up interval of HIV seroconversion; these  participants probably under-reported their sexual activity” [emphases added; Gray et al., “Male circumcision for HIV prevention in men in Rakai, Uganda: a randomised trial”, Lancet, 369 (2007) 657-66].

The mainstream explanation, then, is that the individuals concerned lied, or that they had been “HIV-positive” at enrolment but failed to be detected by those highly specific “HIV” tests. Sherlock Homes might have agreed in general that when all the likely possibilities have been excluded, one must accept those of high improbability — but Holmes would never have come to believe HIV/AIDS theory in the first place. What a coincidence, that about the same number of men in all four groups became “HIV-positive” in absence of sexual activity. Or, alternatively, what a coincidence that the number who not only lied about sexual activity but also became “HIV-positive” should be the same in all four groups.

HIV Skeptics and AIDS Rethinkers, however, understand that “HIV-positive” does not necessarily bespeak an infection transmitted sexually or by other means. These facts are perfectly compatible with the copious data that show “HIV-positive” to be a condition inducible by any number of stimulating influences. Moreover, the tendency to test “HIV-positive” increases with age from the teens into middle age:

agevariations

Therefore it is only to be expected that in any group of young men observed for any substantial length of time, a few will become “HIV-positive” — perhaps as a result of flu, or malaria, or a vaccination, etc.

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Consistent with these occasional real-time observations of “HIV-positive” incidence among people who have had no sexual activity, no blood transfusions, and no injections is the finding in a large clinical trial carried out over many years that pregnant women become “HIV-positive” at a greater rate than do those who have already given birth and are lactating or those who are neither pregnant nor breastfeeding:

CondomsPregnantGray

Lest one attempt to explain this away by postulating, counter to common sense, that pregnant women have more sex or more unsafe sex than do non-pregnant women, Gray et al. note that
“The  mean  monthly  frequency  of  intercourse  was  lower  during  pregnancy  (6·7  acts  per month) than during breastfeeding (7·5 acts per month) and  during  non-pregnant  and  non-lactating  intervals (8·0 per month; p<0·05). Therefore, we also estimated the  rate  of  HIV  acquisition  per  coital  act,  which  was higher during pregnancy than in the non-pregnant and non-lactating group (incidence rate ratio 1·42, 95% CI 0·37-3·82). . . . [P]regnant women were  significantly  less  likely  to  report  multiple  sexual partners  than  were  non-pregnant  and  non-lactating women,  and   in   married   couples   the   husbands   of pregnant  women  reported  significantly  fewer  sexual partners  than  husbands  of  non-pregnant  and  non- lactating women. Although there could be misreporting of  sexual  behaviours,  the  results  are  unlikely  to  differ between the three exposure groups, so both female and male  sexual  behaviours  are  unlikely  to  account  for  the excess risk of HIV during pregnancy. . . . [W]e  conclude  that  behavioural  factors  are unlikely  to  explain  why  the  HIV  incidence  rate  is increased  during  pregnancy,  and  we  speculate  that biological factors might have a role. . . . . Hormonal  contraception  has  been  associated  with  increased  risks  of  HIV acquisition   in   some   but   not   all   epidemiological studies” [emphases added].
In overall summary, Gray et al. state:
“Interpretation The risk of HIV acquisition rises during pregnancy. This change is unlikely to be due to sexual risk behaviours, but might be attributable to hormonal changes affecting the genital tract mucosa or immune responses. HIV prevention efforts are needed during pregnancy to protect mothers and their infants.”

How close they come to recognizing the fact of the matter, that “HIV-positive” signifies any one or more of a wide range of physiological conditions, of which pregnancy has long been known to be one. They even cite a study from Malawi that reported higher incidence of “HIV-positive” in pregnancy than post-partum, by a factor of 2.19, and another from Rwanda that reported higher incidence of “HIV-positive” early post-partum compared to later. In South Africa, “HIV-positive” prevalence is persistently higher among pregnant women than among women as a whole [HIV demographics are predictable; HIV is not a contagious infection, 27 August 2008].

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But perhaps most remarkable of all is the quite direct evidence in the Gray article that “HIV” can be “caught” in absence of “HIV”. During the study, 338 seroconversions were observed: 23 among pregnant women, 40 among lactating women, and 275 among the others. The article also reports on discordant couples — male partner “HIV-positive”, wife “HIV”-negative — and in those cases there were 77 seroconversions: 6 among pregnant women, 11 among lactating women, and 60 among the rest. The inference is clear that 261 (338-77) seroconversions occurred among couples not known to be discordant — in other words, one partner “caught” “HIV” though the other partner didn’t have it.

Of course, “partners not known to be ‘HIV-positive’” is not the same as “partners known not to be ‘HIV-positive’”. But since the investigators explicitly sought to ascertain the “HIV” status of partners, and were confident enough of their data that they reported separately on “transmission” among discordant couples, it seems unlikely that they would have missed a large enough number to explain all the seroconversions observed in the study; therefore it does seem that as many as 77% (261/338) of the women in the study who became “HIV-positive” did so without any evidence of sexual intercourse with an “HIV-positive” male, indeed, with implicit evidence of LACK of such contact.

Lest this line of inference not be convincing, consider this clear statement in the article’s Summary:
“In married pregnant women who had a sexual relationship with their male spouses, the HIV incidence rate ratio was 1·36  (0·63-2·93).  In  married  pregnant  women  in  HIV-discordant  relationships  (ie,  with  HIV-positive  men)  the incidence rate ratio was 1·76 (0·62-4·03).”
Thus the rate of seroconversions in discordant relationships was very little higher than overall; evidently the rate of seroconversion in non-discordant relationships was appreciable. “HIV” was appearing in absence of “HIV”.

AGAIN: The obvious inference, consistent with large amounts of other data, is that pregnancy per se is a condition that conduces to testing “HIV-positive”. Pregnancy is one of many conditions that conduce to testing “HIV-positive” (see Why pregnant women tend to test “HIV-positive”, 5 October 2009).

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Under mainstream HIV/AIDS theory, then,

“HIV” is sometimes SPONTANEOUSLY GENERATED.

An irreverent observer might express this as

“HIV” is IMMACULATELY CONCEIVED

or as Axel put it,

the virgin birth of “HIV”

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P.S. re condoms:
Alert and wary consumers of data will have noted in the Table above not only that pregnant women become “HIV”-positive more often than others, but also that women who used condoms (regularly or irregularly) became “HIV”-positive more often than those who never used condoms.
Just another unacknowledged self-contradiction in HIV/AIDS theory.

Posted in clinical trials, experts, HIV absurdities, HIV as stress, HIV does not cause AIDS, HIV risk groups, HIV skepticism, HIV tests, HIV transmission, HIV varies with age, HIV/AIDS numbers, sexual transmission | Tagged: , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , | 11 Comments »

Clinical trials of circumcision against “HIV” “infection”

Posted by Henry Bauer on 2009/09/10

An earlier post [“Circumcision pseudo-science”, 2 September 2009] pointed out that the well-known immune-suppressing effect of surgery is a highly plausible explanation for the quantitatively concordant results of the 3 clinical trials of circumcision to prevent acquisition of “HIV-positive” status. But dubious interpretation is not by far the only flaw in these studies.

Auvert et al., “Randomized, controlled intervention trial of male circumcision for reduction of HIV infection risk: The ANRS 1265 trial”, PLoS Medicine 2(11) (2005) e298.
Other mainstream researchers have criticized this study on a number of grounds:
— questions of randomization [Siegfried, “Does male circumcision prevent HIV infection?” PLoS Med 2(11): e393; Winkel, “Rush to judgment”, PLoS Med 3(1): e71];
— that the intervention and control groups were treated unequally in terms of instructions regarding intercourse [Young, “Two groups not on all fours”, PLoS Med 3(1): e75];
— that “the authors did not control for other sources of HIV transmission, such as exposure through blood transfusions or infected needles” [Vines, “Major potential confounder not addressed”, PLoS Med 3(1): e63].
— Others might question whether a study stopped after 12 months should be given much credence. Among 1582 controls, 49 new “HIV-positive” cases were observed whereas there were only 20 among the circumcised group of 1546; but 234 of the control group and 154 of the intervention group had been lost before the 12-month visits.
— The claimed incidence of 49 in the control group within a year bespeaks an incredibly high rate of intercourse, given that all estimates of “HIV” transmission report no more than a few per 1000 acts of unprotected intercourse with an infected partner.
— That claimed incidence (2.1% per year) also seems far too high when the overall prevalence of “HIV-positive” at baseline was only 4-5%; the prevalence would be reached after only 2 years!
— “In light of the anomalies and lacunae in Auvert and colleagues’ study, the protective effect of male circumcision they observed amounts to a faith lift for the empirically beleaguered paradigm of heterosexual HIV transmission in sub-Saharan Africa” [Potterat et al., “The protective effect of male circumcision as a faith lift for the troubled paradigm of HIV epidemiology in Sub-Saharan Africa”, PLoS Med 3(1): e64].
— Glass [“Rubbery figures?”, PLoS Med 3(1): e70] asked why 4 separate reports by Auvert et al. had given different numbers: “If we just look at the official figures — 15 to 45 at the International AIDS Conference and 20 to 49 in PLoS Medicine — between 1 August 2005 and 23 October 2005, it appears that there have been four seroconversions among the uncircumcised and five seroconversions among the circumcised. In less than three months, a 3:1 difference has shrunk to a 2.45:1 difference. Why are the numbers of seroconversions so much at variance in reports published by reputable journals?”
— This studied group of 18-24-year-old males was surely uncharacteristic in some fashion, since 596 of the 2236 participants observed during 21 months “received blood transfusions, were hospitalized, or received injections” [Auvert et al., “Authors’ reply”, PLoS Med 3(1): e67].

So there are ample reasons for not taking the Auvert study as definitive, yet its claim of 60% risk reduction through circumcision has become a shibboleth in the HIV/AIDS literature.
It is intriguing that other studies have found an increased risk of male-to-female “HIV” “transmission” when the male is circumcised [Sykes, “Male circumcision increases risk for females”, PLoS Med 3(1): e72; Chao et al., “Risk factors associated with prevalent HIV-1 infection among pregnant women in Rwanda”, Int J Epidemiology 23(#2, 1994) 371-80: “partner circumcision . . . remained strongly associated with HIV-1 infection even when simultaneously controlling for other covariates”].

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The other two trials of circumcision are reported in Lancet, 369 (2007): Bailey et al., “Male circumcision for HIV prevention in young men in Kisumu, Kenya: a randomised controlled trial”, 643-56; Gray et al., “Male circumcision for HIV prevention in men in Rakai, Uganda: a randomised trial”, 657-66.
These articles are honored by several commentaries in the same issue of Lancet, including a respectful bio sketch of Ronald Gray, who has been pursuing proof of circumcision as preventive for two decades: “His careful analyses of the data from that trial [an unsuccessful one to prevent “HIV” by treating women for sexually transmitted diseases] identified the importance of HIV viral load, lack of male circumcision, and genital ulcer disease on HIV transmission” (“Profile — Ronald Gray: collaborating with Ugandan researchers on HIV trials”, p. 635).
An editorial, “Newer approaches to HIV prevention” (p. 615) unblushingly states that they “show that male circumcision halves the risk of adult males contracting HIV through heterosexual intercourse. . . . a solid evidence-base to inform health policy. . . . Male circumcision might also directly protect against male-to-female transmission of HIV. A trial to test this hypothesis is under way in Uganda, with results expected in 2008” [emphases added].
Note the direct contradiction with the cited Chao study re male-to-female transmission.

Newell and Bärnighausen (pp. 617-9) are also enthusiastic: “We now have proof” that circumcision, “a permanent intervention . . . can reduce the risk of HIV infection in men, which is positive news about prevention after past and current disappointments.”

But there are similar problems with the Bailey and Gray articles as with the Auvert study, for instance that the incidence of new “HIV-positive” cases was extraordinarily high, respectively 2.1% and 1.33% “infections” per year, difficult to reconcile with the low transmissibility of “HIV-positive” — a few per thousand with unprotected sex with an “HIV-positive” partner — as well as with the overall prevalence of “HIV-positive”. In the Bailey study the prevalence was 8%, which would be reached within 4 short years at an incidence of 2.1%, so unlikely a situation as to call the study into question on that ground alone. (The Gray study did not cite a baseline prevalence.)

The Bailey study was halted prematurely after a year, on the basis of 1232 and 1234 results for the initial 1391 and 1393 enrollees. Again as with the Auvert study, a high proportion (751 of 2778) had received injections in the 6 months before the study. During the study, “10,154 unrelated adverse events were recorded among 1979 (71%) participants. The most frequent unrelated adverse events were upper respiratory tract infections (3189 events, 1184 participants, 43%), malaria (2271 events, 1076 participants, 39%), skin or mucous membrane infections (1011 events, 682 participants, 24%), and gastroenteritis (456 events, 327 participants, 12%). Study groups did not differ with respect to these common illnesses”.
With all due respect: It seems unbelievable that the incidence of each one of these was similar in the two study groups. Skeptics remain free to suggest that those adverse events most likely to stimulate a positive “HIV” test might have been more frequent in the control group, since the treated (circumcised) group had rather intensive post-operative medical attention that the control group did not, including “free medical care, were counselled about safe sexual practices, had unrestricted access to condoms, were tested for sexually transmitted infections, and were treated for bacterial infections.”
A definite difference in the two groups was that “sexual abstinence in the circumcision group . . . returned to baseline level at month 24”. Presumably sexual abstinence — lack of it — had remained at baseline in the control group, which was therefore exposed more frequently to all sorts of contagious infection, not only sexually transmitted ones.
It was also reported that herpes infection correlated with “HIV-positive”; the skeptical explanation is, of course, that herpes is one of the many conditions that can yield a positive “HIV” test.

The Gray study in Rakai began with 2474 and 2522 in the intervention and control groups respectively, of whom only 2253 and 2250 were available to the 12-month follow-up when the trial was suspended. About 400 in each group reported symptoms of a sexually transmitted disease within the previous year. During the follow-up period, the control group reported more than twice as many different sexual partners than the intervention group and 3 times as many non-marital partners, with the actual numbers comparable to the numbers of seroconversions. Again, the controls were exposed much more often to all sorts of contagious conditions.
The variation of “HIV” incidence with age was the familiar one: highest at an intermediate age, lower at both lower and higher ages, in this case a maximum in the range 25-29, which is earlier than in American cohorts but not so different from 25-34 reported from Kenya and Lesotho [HIV demographics further confirmed: HIV is not sexually transmitted, 26 February 2008]  or South Africa (25-29 among females, ~35 among males — HIV demographics are predictable; HIV is not a contagious infection, 27 August 2008].
Despite the flaws in the study, the authors claim that “circumcision must now be deemed to be a proven intervention for reducing the risk of heterosexually acquired HIV infection in adult men” [emphasis added] even as it is admitted that “trials that are stopped early could overestimate efficacy”. It is also admitted that circumcision has significant risks, especially in rural areas: “the rate of moderate and severe adverse events related to surgery was almost 4%, which is comparable with rates in the South African and Kenyan trials.6,9 One should note that there were cases in which appropriate follow-up management was required to prevent more serious sequelae. Furthermore, substantially higher complication rates have been reported when surgery is done in rural clinics or by traditional circumcisers.24” [emphasis added].

Risks from circumcision are far from negligible, in other words.

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The numerous flaws in these trials demonstrate that they cannot be regarded as definitive, to put it as mildly as possible. Yet the HIV/AIDS Establishment has treated as gospel the “HIV”-preventive effect of male circumcision, and the Centers for Disease Control and Prevention is even contemplating recommending universal circumcision of male babies in the United States even though these flawed trials were done in Africa and data from the United States show no association between circumcision and “HIV-positive” status.

Posted in clinical trials, HIV absurdities, HIV risk groups, HIV skepticism, HIV transmission, HIV varies with age, HIV/AIDS numbers, sexual transmission | Tagged: , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , | 4 Comments »

Circumcision pseudo-science

Posted by Henry Bauer on 2009/09/02

The possible benefits and drawbacks of male circumcision have been argued over for decades, centuries, probably millennia. The coincidence that a procedure originating as a religious ritual should turn out to have beneficial, health-protective side-effects is by no means impossible, though no one argues that case for the religious ritual of female circumcision. What’s clear is that medical opinion has been and continues to be divided [David L. Gollaher, “From ritual to science: the medical transformation of circumcision in America”, Journal of Social History, 28 #1 (1994) 5-36]:
“Ironically, but predictably in the context of the history of medical arguments for circumcision, some doctors have conjectured that removing the foreskin may protect men from the most dreaded epidemic of the post-modern world: the human immunodeficiency virus (HIV). Using retrospective data (the epidemiological equivalent of empiricism) from a venereal disease clinic in Kenya, for example, researchers observed that there were higher rates of HIV infection in the home communities of uncircumcised than circumcised men. Ignoring racial, ethnic, and sociocultural variables — the chief factors dictating whether or not an African boy is circumcised in the first place — they hypothesized that circumcision might serve to inhibit the transmission of the AIDS virus. One wonders whether this theory will endure. But within a medical community desperate to find some weapon against AIDS, its appeal is understandable. Even a physician who is a sober skeptic of the methodologies behind such studies allows that they ‘do suggest that HIV may be more infective during heterosexual intercourse if the male partner is uncircumcised and has a mucosal or cutaneous ulcer.’ [77] AIDS, the nemesis of modern science and medicine, remains a mystery. By some equally mysterious process, it is surmised, circumcision may help”.
[77: Simonsen et al., “Human Immunodeficiency Virus infection among men with Sexually Transmitted Diseases: Experience from a Center in Africa,” NEJM 319 (1988) 274-8; Cameron et al., “Female to male transmission of Human Immunodeficiency Virus Type I: Risk factors for seroconversion in men,” Lancet 2 (1989) 403-7; Marx, “Circumcision may protect against the AIDS virus,” Science, 245 (1989) 470-1; Poland, “The question of routine neonatal circumcision,” NEJM, 322 (1990) 1312-5”]

It is worth noting that circumcision as a way of avoiding becoming “HIV-positive” was mooted already in the late 1980s, and enthusiasts have continued to pursue definitive evidence for that for some two decades, despite contraindications no less probative than the pro-indications: a number of studies have found circumcision to be NOT associated with a lower rate of “HIV-positive”; see, for example, those cited in “Rwanda: Circumcise all men — even if it means more ‘HIV’ ‘infection’” [3 February 2008].

I’ve commented before on the remarkable similarities between HIV/AIDS and topics often labeled pseudo-science [“Science Studies 102: Burden of proof, HIV/AIDS ‘science’, pseudo-science”, 22 July 2008;  “HIV/AIDS and parapsychology: science or pseudo-science?”, 30 December 2008;  “Mainstream pseudo-science good, alternative pseudo-science bad”, 25 February 2009]. The failure after two decades of effort to find conclusive proof that circumcision prevents “HIV-positive” is somewhat reminiscent of decades of enthusiastic seeking of evidence for the reality of UFOs or the existence of Nessies; though one might have imagined, perhaps naïvely, that it might be easier to observe circumcision and frequency of “HIV-positive” than to investigate objects like UFOs or Nessies that cannot be brought under observation on command. Still, as Scientific Explorers like to say, “absence of evidence is not evidence of absence”.

At any rate, two decades of observational studies have been inconclusive as to whether there is an association between circumcision and “HIV-positive” status. A recognized problem is the number of potentially confounding factors in these observational studies, primarily cultural and religious characteristics that are often correlated with genetic characteristics.

A powerful argument that CIRCUMCISION DOES NOT PROTECT against “HIV-positive” status comes from solid and consistent observational data on cohorts of gay men. Universally, the groups most frequently testing “HIV-positive” are drug abusers and gay men; in the official jargon, injecting drug users (IDU) and men who have sex with men (MSM). Since IDU are supposedly infected via needles that do not normally make contact with the foreskin, MSM are the group most at risk for acquiring “HIV-positive” status via the foreskin; therefore this would be the ideal group for detecting any preventive effect of circumcision. But a review of 18 such studies found no preventive effect of circumcision against “HIV-positive” among MSM: Millett et al., “Circumcision status and risk of HIV and sexually transmitted infections among men who have sex with men”, JAMA, 300 [2008] 1674-84.

How then does it come about that the HIV/AIDS Establishment has accepted as an article of faith that circumcision reduces by half the risk of becoming “HIV-positive”? For example,

“CDC mulls routine circumcision of infants to reduce spread of HIV” (Tracy Miller, 25 August 2009)
“In an effort to reduce the spread of the AIDS-causing HIV virus, the Centers for Disease Control are currently mulling routine circumcision for all baby boys born in the United States . . . . The controversial recommendations, scheduled for a formal release by the end of the year, come on the heels of research that shows circumcised men in African countries hit hard by AIDS had half the risk of getting infected as those who were uncircumcised.
Critics say that focusing on newborns in the United States would only have an effect years down the road, and that circumcising infants subjects them to medically unnecessary surgery without their consent.
But CDC experts maintain that any step to reduce the spread of HIV is worthy of serious consideration.
‘We have a significant H.I.V. epidemic in this country, and we really need to look carefully at any potential intervention that could be another tool in the toolbox we use to address the epidemic,’ Dr. Peter Kilmarx, chief of epidemiology for the CDC’s division of HIV/AIDS prevention, told the Times. ‘What we’ve heard from our consultants is that there would be a benefit for infants from infant circumcision, and that the benefits outweigh the risks.’
Experts acknowledge that a new circumcision policy is unlikely to have a dramatic effect in HIV infection rates, as most adult men are already circumcised. Additionally, scant evidence exists to prove circumcision protects homosexual men from getting HIV.
79 percent of adult American men are already circumcised, according to public health statistics, though circumcision of newborns has dropped to about 65 percent in recent decades” [emphases added].

Note the usual bureaucratic prevarications:
— Unnamed “experts” and “consultants” are cited in the attempt to outweigh the actual scientific evidence;
— “a significant H.I.V. epidemic” is asserted to exist in the USA, contrary to fact;
— however, insofar as there may be an appreciable frequency of  “HIV-positive” instances in the USA, a large proportion is among MSM, who have been found NOT to benefit in this respect from circumcision;
— and that fact is euphemized or obfuscated by saying “scant evidence exists” instead of that the evidence speaks clearly against any benefit from circumcision.

Note too, “on the heels of research”: It is elementary that new research is not to be relied on until it has been confirmed over time by independent investigators and in a variety of circumstances. This rush to judgment is junk science. REAL SCIENCE ISN’T NEWS [Scientific illiteracy, the media, science pundits, governments, and HIV/AIDS, 15 January 2009].

Since HIV/AIDS theorists do not hesitate to swallow absurdities wholesale, they do not blink at the suggestion that “While circumcision may help protect heterosexual men in Africa from contracting HIV, . . .  it does not appear effective in doing so for American gay men, according to the largest study yet on the issue. . . . Circumcision ‘is not considered beneficial’ for gay men concerned about lowering their risk of becoming infected with HIV, Dr. Peter Kilmarx of the CDC told the Associated Press. He released the study findings at a conference on Tuesday. . . . But circumcision may not offer the same protection when it comes to anal sex, Kilmarx said.” [“Circumcision won’t shield gay men from HIV: Study” ].
Here once more the HIV/AIDS gurus would like to swing both ways, or perhaps every way. On the one hand, it is an hoary shibboleth that gay men are particularly at risk because anal sex is more conducive to “HIV transmission” than is vaginal sex, because of a greater likelihood of skin breakage and blood contact. But in order to justify a program of universal circumcision, it becomes expedient to take somehow the opposite view.

Why would circumcision be preventive?
“Scientists think circumcision can protect against HIV because the tissue of the foreskin has a high number of target cells for HIV infection and is susceptible to tearing during intercourse, providing an entry point for the virus” [“Circumcision: Change in medical opinion possible”].
But, again, anal sex is supposed to pose a greater risk for tearing skin than does vaginal sex. “I also find it fascinating that the male prepuce has gone straight from being an inconsequential ‘flap of skin’ to being a complex immunological organ, just in time to be infected by a virus that targets immune cells” [Winkel, “Rush to judgment”, PLoS Medicine 3(1) (2006) e71].

So the official conclusion is not only highly implausible, it is contrary to the facts accumulated over some twenty years or so. Yet all that is jettisoned by reliance on 3 brand-new clinical trials in Africa, all of them stopped prematurely after a year, that have supposedly shown definitively that circumcision reduces by about 50% the risk of becoming “HIV-positive” — among African heterosexual men, that is, though not among American gay men [Gray et al., “Male circumcision for HIV prevention in men in Rakai, Uganda: a randomised trial”, Lancet, 369 (2007) 657-66; Bailey et al., “Male circumcision for HIV prevention in young men in Kisumu, Kenya: a randomised controlled trial”, ibid., 643-56; Auvert et al., “Randomized, controlled intervention trial of male circumcision for reduction of HIV infection risk: The ANRS 1265 trial”, PLoS Medicine 2(11) (2005) e298].
A detailed deconstruction of these reports has to be deferred to a later post, this one is already longer than I prefer, but at least one feature of them is readily cited and adds greatly to the implausibility of the conclusion drawn:
In all three trials — in South Africa, Uganda, and Kenya —, the purported effect of circumcision was essentially the same at 50-60%, and it was independent of all other observed variables, among them number of sexual partners, non-marital relationships, condom use, paying for sex, drinking alcohol before sex, age, marital status, education (so stated specifically in Gray et al.).
Think about that. The probability of acquiring any sexually transmitted infection must depend on the probability of intercourse with an already infected person, which itself depends on the prevalence of the infection in the population; also influential will be the number of acts of intercourse and the number of partners, and whether sex is “social” or paid for, because prostitutes are by shibboleth supposed to be a reservoir of HIV and STDs; important too must be the care taken to protect via condoms, which is supposedly influenced by the state of sobriety or lack of it. Yet in 3 different cultures, in 3 widely separated regions of Africa, with groups of different age ranges, and where the incidence of “HIV-positive” in the control groups differed  significantly, somehow all those variables turn out to balance one other so precisely that the overall effect of the studied treatment is almost exactly the same. This strikes me as about as likely as 2 blue moons in the same year, or as Nessie surfacing just as I’m greeted by an alien emerging from a landed UFO.

There is quite a good reason, actually, why all 3 studies should have delivered the same apparent effect of circumcision, but it has nothing to do with “HIV” or sexual transmission: Surgery is well known to suppress immune function. Now the standard test for “HIV” is actually a test for antibodies, and the evidence is ample that “HIV” tests are highly non-specific, reacting “positive” when large numbers of a variety of antibodies are present. Since post-operative antibody production is lower as a consequence of surgery, post-operative apparent “HIV” incidence will be lower.

These clinical trials have demonstrated only that surgery cuts by about half (50-60%) the production of non-specific antibodies.

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