Circumcision and condom idiocies

When children are taught to use calculators, the importance is well recognized of teaching them to THINK about what the result should be, by doing a rough mental or manual calculation, so that they don’t accept a silly order of magnitude through mistaking an exponential or use a stupid number of decimal places as “significant figures”. So too, people who use statistical analyses of possible correlations should THINK about the implied meaning of suspected associations. That could hardly have been the case with those who wrote

“The protective effect of MC [male circumcision] on HIV infection was unchanged when controlling for sexual behaviour, including condom use” [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].

THINK about it, please. Circumcision supposedly protects against “HIV” whether or not the male is wearing a condom?!  How could that possibly be?
The claimed protective effect of circumcision can only have something to do with the foreskin. Indeed, it is hypothesized to result from the high density of “HIV”-susceptible cells in the foreskin or from the foreskin’s greater tendency to tear during intercourse. But condoms prevent contact of the foreskin with anything except the condom. How could the foreskin be relevant when condoms are used?

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Those 3 flawed clinical trials of circumcision against “HIV”, with results at best inconclusive and at worst unbelievable, have nevertheless formed the basis for projections, under the auspices of UNAIDS, of how many “HIV infections” could be prevented, and at what minimal cost. Those projections are based, as usual, on elaborate models incorporating innumerable assumptions as well as unwarranted reliance on the clinical studies whose faults are legion.

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Everyone knows, of course, that condom use decreases the risk of contracting “HIV”. But, as so often with HIV/AIDS shibboleths, the facts don’t bear that out [for example, Condoms and HIV: What everyone knows is once again wrong, 10 February 2008; HIV and sexually transmitted disease: it just isn’t so, 28 November 2007].

For instance, during a clinical trial of the influence of pregnancy in which the actual incidence of “HIV” was being observed in real time, the rate of becoming “HIV-positive” was greater among those using condoms than among those not using them, in all 3 studied cohorts [as I noted already in Spontaneous generation of “HIV”, 25 October 2009]:

At what straws might the investigators grasp to explain this away?
“HIV incidence rates were lower in non-condom users than condom users, but interpretation was constrained by small sample sizes in the pregnant and breastfeeding groups, and by the fact that female condom use in this population is strongly correlated with multiple sexual partners.”

So condoms don’t protect you if you have multiple partners, and not using them protects you if you don’t have multiple partners. By all means, sign me up for the next time a Brooklyn Bridge goes on sale.

As to sample sizes:
Those never using condoms irregularly or always totaled 2763, of whom 49 became “HIV-positive”, a rate of 1.77%. Those not using condoms totaled 25,440, of whom only 289 became “HIV-positive”, a rate of 1.14%.
It’s not immediately obvious why the samples 49/2473 and 289/25,440 are too small to permit significance whereas 23/997 (pregnant women becoming “HIV-positive”), 40/3,043 (lactating women becoming “HIV-positive”), and 275/24,161 (women neither pregnant nor lactating becoming “HIV-positive”) were sufficiently large to establish that pregnancy is significantly associated with becoming “HIV-positive”, as the study concluded.

I suppose it’s really that when the facts don’t jibe with HIV/AIDS theory, the facts must be wrong, and if the only conceivable reasons are small sample sizes and an association between condom use and multiple partners, so be it, that’s the best explanations there are, and there’s no need to worry about their plausibility because the theory is right and the facts are therefore wrong.

The conclusion that pregnancy is significantly associated with becoming “HIV-positive” is in itself mind-boggling. The researchers “explain” it by postulating hormonal and other physiological changes in pregnancy that enhance the virus’s infective powers! Because, of course, they must not admit that “HIV+” might be a direct consequence of pregnancy, the so-called “HIV” test actually reacting directly to precisely something associated with those physiological changes. That’s why pregnant women everywhere, always, test “HIV+” more often than non-pregnant women.

Laugh, cry, or summon up pity for those caught in this “research” mess, who have to swallow absurdities in ever-increasing amounts in order to maintain their belief in HIV/AIDS theory.

Spontaneous generation of “HIV”

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:

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:

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.

Why pregnant women tend to test “HIV-positive”

Sabine Kalitzkus drew to my attention this plausible explanation for the tendency of pregnant women to test “HIV-positive”:
1. Pregnancy brings a Th1→Th2 shift in the immune system.
2. “HIV-positive” is associated with a Th1→Th2 shift.

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It is vital to bear in mind — always, not only in this connection! — that testing “HIV-positive” does not signify the presence of a specific agent, still less the presence of an human immunodeficiency virus. There are several lines of proof for that:
First: a great variety of conditions can bring about an “HIV-positive” test-result. For empirical proof, see Christine Johnson, “Factors known to cause false positive HIV antibody test results”, Continuum 4 #3, Sept/Oct 1996, www.healtoronto.com/testcross.html or www.virsumyth.com/aids/hiv/cjtestfp.htm); or The Origin, Persistence and Failings of HIV/AIDS Theory; or a large number of posts on this blog in the category “HIV tests”. (Quite recently, a correspondent told me of testing “HIV-positive” after having abused steroids, which I have not seen mentioned elsewhere as inducing “HIV-positive”. After changing his lifestyle, he now tests negative again. Was Magic Johnson perhaps one of the many athletes who [ab]used steroids?)
Second: For a priori proof, note that the ELISA and Western Blot tests respond to many combinations and magnitudes of 2 or more among 10 separate proteins, none of which has been proven to be unique to the hypothesized “HIV” — virions of which have never been isolated directly from “HIV-positive” people or from AIDS patients, even though the latter are postulated to experience overwhelming viremia in the later stages of their illnesses [HIV tests: Danger to life and liberty, 16 November 2007].
Third: Again empirical and entirely consistent with and illustrative of the first two: Surveys of “HIV” “prevalence” show a continuum of rates of “HIV-positive” test-results among different groups. The progression from low to high rates appears to correlate with the likelihood that some sort of health challenge is present. Note in particular that pregnant women (pre-natal clinics) test positive at a higher rate than the general average of the population (National Health and Nutrition Survey), and quite significantly more often than women at family planning clinics:

Not only do surveys of “HIV” prevalence find it higher among pregnant women, a full-scale prospective clinical trial in Africa actually found a higher incidence of “HIV-positive” during pregnancy [Gray et al., “Increased risk of incident HIV during pregnancy in Rakai, Uganda: a prospective study”, Lancet 366 (2005) 1182-8].

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Among the variety of circumstances that can stimulate an “HIV-positive” response is “AIDS”, and in AIDS, “A gradual shift from Th1- to Th2-dominance is observed. . . . This Th1-to-Th2 shift perfectly explains some of the major conundrums of the AIDS clinical syndrome. . . . Furthermore, elevated levels of antibodies, including autoantibodies, are characteristic of all AIDS patients — a finding consistent with a decrease in the Th1 subset coincident with an increase in the Th2 subset. . . . HIV is expressed primarily in Th0 and Th2 cells, and is scarcely to be found in the Th1 subset. 38-40 This is curious indeed, since it is the Th1 cells that decline, whereas the cells in which HIV prefers to reside do not decrease” [Culshaw, “Mathematical Modeling of AIDS Progression: Limitations, Expectations, and Future Directions”, Journal of American Physicians and Surgeons 11 (#4, Winter 2006) 101-5].

Notoriously, gay men are more likely than others to suffer an “AIDS” condition, and — independently — they are more likely to test “HIV-positive” without necessarily becoming ill: many “HIV-positive” gay men have remained healthy for upwards of two decades. As Tony Lance has pointed out, much evidence indicates that gut dysbiosis can induce gut leakage, testing “HIV-positive”, and in severe cases the most characteristic of the AIDS illnesses, namely, the fungal infections Pneumocystis carinii pneumonia and candidiasis; and gut dysbiosis is also associated with a shift in the Th1-Th2 balance:
“T-cell abnormalities — There appears to be a connection to be elucidated between gut dysbiosis, glutathione deficiency, and T-cell anomalies thought to be characteristic of HIV/AIDS. . . . A direct connection between the composition of gut microflora and the balance of Th-type cells has been reported by several authors: . . . ‘What typically happens in a person with gut dysbiosis is that two major arms of their immune system, Th1 and Th2, get out of balance with underactive Th1 and overactive Th2. . . ’ (35)” [emphases added; Tony Lance, “GRID = Gay Related Intestinal Dysbiosis?
Explaining HIV/AIDS Paradoxes in Terms of Intestinal Dysbiosis”, pdf at “What really caused AIDS: Slicing through the Gordian Knot”, 20 February 2008].

Testing “HIV-positive”, then, correlates with a Th1→Th2 shift, under some circumstances at least.
The immune system is of course much more complicated than just these two categories of cells. There are a variety of Th1 cells and of Th2 cells, so a shift in the overall balance might mask more specific differences; in other words, a given Th1/Th2 ratio in healthy gay men may bespeak functionally different circumstances than the same numerical ratio in AIDS patients, or in TB patients, or in pregnant women. The mere fact of a Th1→Th2 shift does not necessarily signify a dangerous health condition, any more than an “HIV-positive” test necessarily signifies a dangerous health condition or that an “HIV-positive” test always signifies the presence of the same combination of two or more of those ten proteins.

So: the fact that pregnant women are more likely to test “HIV-positive” does not necessarily signify a health challenge more serious than normal pregnancy.
As to a Th1→Th2 shift in pregnancy, Sabine Kalitzkus sent a link to impfreport, Zeitschrift für unabhängige Impfaufklärung, 56/57, July/August 2009 [vaccination report, magazine for independent vaccination education; editor, Hans U. P. Tolzin]. Pages 4-5 report information for doctors and pharmacists that was issued by the Paul Ehrlich Institute on 4 September 2009. What follows is free translation from German:

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Vaccinating pregnant women during the swine-flu pandemic
The immune system has broadly speaking two arms. Cellular immunity is mediated largely by Th1 “killer” cells which attack “foreign” cells, i.e. those not recognized by their protein coating as belonging to the host. The other arm is mediated by Th2 cells which are responsible for generating antibodies to foreign proteins.
A fetus is at least partly “foreign” to the mother since its genes, and consequently the generated proteins, come partly from the father. To prevent aborting of the fetus, pregnancy causes a partial Th1→Th2 switch. [In other words, such a shift is perfectly normal in healthy pregnancies, but it will also tend to be associated with an “HIV-positive” test]
The [European] swine-flu vaccine contains adjuvants to stimulate the Th1 arm, which may increase the risk of spontaneous abortion. Indeed, it is known that spontaneous abortion is associated with a shift towards Th1.
The Paul Ehrlich Institute’s release minimizes this risk in bureaucratic weasel-word fashion:
Altogether, a harmful effect on pregnancy of adjuvant-containing vaccines seems rather unlikely. But since data from clinical trials are lacking, such an effect is not impossible.
[Insgesamt erscheint ein negativer Effekt von squalenhaltigen Influenzaimpfstoffen auf die Schwangerschaft eher unwahrscheinlich. Da jedoch umfangreiche Daten bei Schwangeren in klinischen Studien fehlen, kann ein Effekt auch nicht vollständig ausgeschlossen werden.]

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To paraphrase this “conclusion”: We have no relevant data, hence no evidence. What we know about the immune system and pregnancy would incline one to be concerned. However, in our opinion the risk is negligible, though we can offer no evidentiary basis for that judgment.

That evidence is totally lacking for this Micawber-ish, Panglossian or Pollyanna-ish failure to be concerned is obvious, since pregnant women are (at least in developed countries) not eligible for enrolment in clinical trials — except, of course, in the case of HIV/AIDS and the attempt to find out how high a dose of antiretroviral drugs can be tolerated by “HIV-positive” pregnant women [Celia Farber, “Out of control: AIDS and the corruption of medical science”, HARPER’S MAGAZINE, March 2006, 37-52].

To recapitulate:
Empirical fact: Pregnant women test “HIV-positive” more frequently than others.
Empirical fact: In several groups, Th1→Th2 shift is associated with a tendency to test “HIV-positive”.
Empirical fact: Normal, healthy pregnancy induces a Th1→Th2 shift.

The higher frequency of “HIV-positive” tests among pregnant women
may be nothing more than a natural consequence of pregnancy

Abuses of statistics in HIV/AIDS research

There are many ways of lying under the cover of statistics. One that I’ve not previously emphasized is to imply a correlation where none exists; for example, “the declining incidence in the control group in Rakai — which, although not statistically significant, reduces the difference between the groups” [emphasis added; Gray et al., “Male circumcision for HIV prevention in men in Rakai, Uganda: a randomised trial”, Lancet, 369 (2007) 657-66].

The whole point of this type of statistical analysis is to determine whether or not an association plausibly exists. If there is no statistically significant association, then no association has been found.
The proper statement would be significantly different:
“The declining incidence apparently had nothing to do with the difference between groups”.

Here’s another example: “The odds of being HIV-positive were nonsignificantly lower among MSM who were circumcised than uncircumcised (odds ratio, 0.86; 95% confidence interval, 0.65-1.13; number of independent effect sizes [k]=15)” (emphasis added; 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).
The enumeration of odds ratio, confidence interval, and effect sizes conveys a sense of technical correctness which, whether intended or not, lends rhetorical weight to the assertion of “lower” when, in actual technical fact, no significance has been established at the 95% probability level.
It is unwarranted, irresponsible, pseudo-scientific to say “nonsignificantly lower”, because that suggests that it is actually lower, though perhaps for purely technical statistical reasons not statistically significantly so.

Again: If the statistics delivers a verdict of “not significant”, then nothing has been established, not lower and not higher. Once more the proper statement would be significantly different:
“No association was found between circumcision and ‘HIV’ status”.

The silver lining in these instances, such as it is, is that I have stimulated many belly laughs — though also some very puzzled expressions — by inviting statistically literate friends to explain to me what “nonsignificantly lower” means.

The dark clouds, however, are that these people — who work at the Centers for Disease Control and Prevention, no less — are capable of writing such a phrase. They are either statistically illiterate or seeking deliberately to deceive. I don’t know which of those two would be the more depressing.

It is also worth noting and regretting that these statistical illiteracies passed the editorial- and peer-review processes of the Lancet and the Journal of the American Medical Association. “Peer review” is no better than the reviewers and the editors make it.

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Oxymoronic jargon like “nonsignificantly lower” surely comes about because of an unshakeable belief that there is — must be — a lowering, in the face of data that do not support the belief. There exists a persistent unwillingness among HIV/AIDS mainstreamers to accept facts that contradict their belief — they suffer cognitive dissonance, as I’ve had occasion to remark all too often [Cognitive dissonance: a human condition, 26 December 2008; The debilitating distraction of “HIV”, 21 December 2008; State of HIV/AIDS denial: carcinogenic HAART, 21 November 2008; True Believers of HIV/AIDS: Why do they believe despite the evidence?, 30 October 2008; “SMART” Study begets more cognitive dissonance, 11 June 2008; Death, antiretroviral drugs, and cognitive dissonance, 9 May 2008; HIV/AIDS illustrates cognitive dissonance, 29 April 2008].

Of course, one might try to argue that “95%” is just an arbitrary criterion: one could choose 85%, or 70%, or any other value; or one might say that “lower” is simply expressing the raw numbers in words without attempting statistical analysis to attach a particular probability. But that would mean jettisoning any pretence of being scientific by using statistics to guide judgment as to whether an effect is plausibly real or not. If one offers statistical details then one should also abide by what the statistical analysis concludes and not try to fudge it.

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Another abuse of statistical analysis that also may not be obvious until made explicit:

Upon finding  no correlation, divide the data into sub-groups in the hopes that one or other might show an apparently significant effect. This is statistically improper, a prelude to lying with statistics, because if you look at enough sub-groups the probability becomes appreciable that there will be found one or a few that appear to have a statistically significant association. Recall that if one uses a criterion as weak as “95% probability”, one apparently but not actually significant association will show up on average at least once in every twenty times — more often if the looked-for association is inherently unlikely [R. A. J. Matthews, “Significance levels for the assessment of anomalous phenomena”, Journal of Scientific Exploration 13 (1999) 1-7].

In the present instance, there was no association in the sub-group of insertive anal sex, nor between circumcision and sexually transmitted infections, two sub-groups where an association would not be implausible. On the other hand, highly implausible apparent associations were noted in studies conducted before the introduction of HAART, and between “HIV”-preventive circumcision and study quality. It is not easy to conceive why an association between circumcision and “HIV” acquisition would have anything at all to do with what treatment is provided people who have AIDS, long after acquiring “HIV”; and “study quality” is a highly subjective variable.

No. The Millett article leads to only one legitimate conclusion: No association found between circumcision and “HIV” status among MSM.

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The problem for HIV/AIDS dogmatists is that they have failed to find any way of preventing people from becoming “HIV-positive”. The mistaken view that it has to do with infection and with sex keeps them searching for data to support that view, rather as rats or guinea pigs are doomed to try eternally to scale the turning wheels in their cages. Study after study gives the same result, no association. At the 4th International AIDS Society Conference, Sydney 2007:
Guanira et al., “How willing are gay men to ‘cut off’ the epidemic? Circumcision among MSM in the Andean region”)
— “No association between circumcision and HIV infection when all the sample is included. A trend to a significant protective effect is seen when only ‘insertive’ are analyzed.”
Note again the unwarranted, illegitimate attempt to assert something despite the lack of evidence: a “trend” toward a significant effect, when the statistical analysis simply says “nothing”, no correlation.
Then there was Templeton et al., “Circumcision status and risk of HIV seroconversion in the HIM cohort of homosexual men in Sydney”)
— “Circumcision status was not associated with HIV seroconversion . . . . However, further research in populations where there is more separation into exclusively receptive or insertive sexual roles by homosexually active men is warranted” [emphasis added].
More research is always warranted, of course, that’s what pays the researchers’ bills [Inventing more epidemics; the Research Trough; and “peer review”, 2 August 2009; The Research Trough — where lack of progress brings more grants, 10 September 2008].

Clinical trials of circumcision against “HIV” “infection”

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.