HIV/AIDS Skepticism

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

Posts Tagged ‘Bertran Auvert’

What do CD4 counts mean?

Posted by Henry Bauer on 2010/01/29

The level of CD4 cells in peripheral blood is a prime criterion for diagnosing AIDS (in the United States in particular) and for monitoring antiretroviral treatment. However, these applications of CD4 counts stem from the initial and unhappy coincidence that when “AIDS” appeared around 1980, the counting of immune-system cells was in its infancy. By now it is known that CD4 levels are extremely variable in healthy individuals, and that a variety of physiological conditions other than “HIV” may profoundly influence CD4 counts. There seems to be no fundamental evidential warrant for the manner in which HIV/AIDS diagnosis and treatment rely on CD4 counts. Juliane Sacher among others has pointed out that the levels of CD4 cells in peripheral blood are not a meaningful measure of immune-system status, since these cells move around the body according to where they seem to be needed [Alternative treatments for AIDS, 25 February 2008].

An obvious question: what is the range of CD4 counts in healthy individuals and in a variety of illnesses? (I’m grateful to Tony Lance for alerting me to some of the intriguing sources mentioned in the following).

One of the striking aspects of CD4 counts is how enormously they vary among individuals, including healthy individuals. Here, for example, are data from HIV-negative Senegalese:

C. Mair, S. E. Hawes, H. D. Agne, P. S. Sow, I. N’doye, L. E. Manhart, P. L. Fu, G. S. Gottlieb and N. B. Kiviat. Factors associated with CD4 lymphocyte counts in HIV-negative Senegalese individuals. Clinical and Experimental Immunology 151 (2007) 432-440

In any normal distribution, the standard deviation (s.d. or σ) describes the degree of scatter around the average (or mean) value. Only about 2/3 of a sample are within (±) 1 σ; in other words, about 1/6 are further from the mean on both the higher and the lower sides. In the Table above, among the men with mean CD4 count of 712, σ = 333, about 1 in every 6 men have CD4 counts below 379 or above 1045; and about 2% have counts more than 2σ above and below 712 , that is >1378) and <50. CD4 = 200 is about 1.5σ below the mean, which corresponds to about 6-7% (~1/15) of the sample. In other words, about 1 in every 15 healthy HIV-negative Senegalese men has CD4 counts below the 200 that, in HIV-positive people, is taken to be a sign of AIDS.

Of course, CD4 counts may not follow a normal distribution, especially at upper and lower levels; but since this article reports means and standard deviations without specifying a different distribution, the authors themselves are presuming it is normal. Moreover, a similarly wide range of CD4 counts and an approximation to normal distribution is shown in other data sets as well. For example, healthy North Indians were reported to have a mean CD4 count of 720 with σ = 273 and an actually observed range of 304-1864 among 200 individuals; 10% were below 400, consistent with a normal distribution which would have about 16% below 450 (Ritu Amatya, Madhu Vajpayee, Shweta Kaushik, Sunita Kanswal, R.M. Pandey, and Pradeep Seth. “Lymphocyte immunophenotype reference ranges in healthy Indian adults: implications for management of HIV/AIDS in India”. Clinical Immunology 112 [2004] 290-5). Actual distributions for several African populations, however, show a skewing toward higher CD4 counts, which indeed seems highly plausible a priori — one might expect to see a definite lower bound to CD4 counts in healthy individuals (Williams et al., “HIV infection, antiretroviral therapy, and CD4+ cell count distributions in African populations”, J Inf. Dis. 194 [2006] 1450-8).

Worth particular note is the comment in Amatya et al. that “These low counts could be due to physiological lymphopenia potentially caused by protein energy malnutrition, aging, antigenic polymorphism of the CD4 molecule, prolonged sun exposure, circadian rhythm, and circannual variation [9,10]”. The use of contraceptive pills by women has also been reported to influence CD4 counts (M. K. Maini, R. J. Gilson, N. Chavda, S. Gill, A. Fakoya, E. J. Ross, A. N. Phillips and I. V. Weller. “Reference ranges and sources of variability of CD4 counts in HIV-seronegative women and men”. Genitourin Med 72 [1996) 27-31]. Most of those circumstances do not represent illness. So CD4 counts can be low for a variety of fairly normal, not seriously health-threatening conditions. It follows that reliance on CD4 counts as diagnostic of “HIV disease” increases the danger that some unknown number of “HIV-positive” individuals are being told on the basis of laboratory tests — sometimes SOLELY on the basis of laboratory tests — that they are actually sick even though they feel and actually are healthy; and these people are then at risk of being consigned to toxic “treatment” for this imaginary illness. The risk is greatest if the blood tested for CD4 counts happens to have been drawn in the morning, or in the wrong season of the year, because CD4 counts vary appreciably with both those variables: T. G. Pagleironi et al., “Circannual variation in lymphocyte subsets, revisited”, Transfusion 34 [1994] 512-6; F. Hulstaert et al., “Age-related changes in human blood lymphocyte subpopulations”, Clin. Immunol. Immunopathol. 70 [1994] 152-8. Maini et al. (above) report a 60% variation during the day with lowest counts at 11 am. Yet another report describes a similarly large diurnal variation, from 820 at 8 am to 1320 at 10 pm (Bofill et al., “Laboratory control values for CD4 and CD8 T lymphocytes. Implications for HIV-1 diagnosis”, Clin. Exp. Immunol. 88 [1992] 243-52).

Just as with the tendency to test “HIV-positive”, CD4 counts are influenced by demographic variables: “race, ethnic origin, age group, and gender” (Amatya et al.). Bofill et al. also report a steadily decreasing CD4 count with increasing age. The contrary has been reported, however, by Jiang et al. (“Normal values for CD4 and CD8 lymphocyte subsets in healthy Chinese adults from Shanghai”, Clinical and Diagnostic Laboratory Immunology, 11 [2004] 811-3). The discrepancy may be owing to differing attitudes toward statistical significance: the raw numbers in Jiang et al. do show an increase with age for men and a decrease with age for women but, as with the data of Bofill et al. and all others, the standard deviations are so large, on the order of one third of the mean values, that differences and trends would have to be very considerable if they are to be statistically meaningful.

Again, Jiang et al. report no difference between Chinese men and women, whereas several sources cite women as having higher CD4 counts than men: in Britain (Maini et al.) and in more than dozen other countries in Africa, Asia, and Europe (Mair et al.). Caucasians have higher CD4 counts than Asians or Africans, according to Amatya et al. and Jiang et al., but not according to Maini et al.

All these variations under the influence of several factors would make the diagnostic application of CD4 counts problematic even if “HIV” or “AIDS” had been shown to be the salient influence on CD4 levels. However, just as with the tendency to test “HIV-positive”, CD4 counts may be “low” in a wide range of conditions; perhaps most relevant to HIV/AIDS, in tuberculosis and general trauma, as well as with primary immunodeficiency, early acute phases of such viral infections as influenza, or Dengue fever (Bofill et al.) or recent respiratory infections (Maini et al.).

Not only are CD4 counts dubious for diagnosis or prognosis; just as with the tendency to test “HIV-positive”, CD4 counts generate a number of conundrums if interpreted according to HIV/AIDS theory: the counts are often HIGHER rather than lower in conditions generally regarded as associated with poor health. For example, smokers have higher CD4 counts than non-smokers (Maini et al., Mair et al.) and prostitutes have higher counts than other women (Mair et al.). Another “striking paradox” is in “co-infection” with “HIV” and herpes:
“We observed no effect of HSV-2 status on viral load. However, we did observe that treatment naïve, recently HIV-1 infected adults co-infected with HSV-2+ at the time of HIV-1 acquisition had higher CD4+ T cell counts over time. If verified in other cohorts, this result poses a striking paradox, and its public health implications are not immediately clear” (emphases added; Barbour et al., “HIV-1/HSV-2 co-infected adults in early HIV-1 infection have elevated CD4+ T-Cell counts”, PLoS ONE 2(10) [2007] e1080).

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There seems to be no clear warrant for diagnosing AIDS by means of CD4 counts, which may be why other countries have not followed the US example of taking <200 as a criterion. Similarly, there seems to be no clear warrant for assessing the progress of antiretroviral treatment by means of CD4 counts. Two practical illustrations of that are the fact that CD4 counts do not correlate with (or, changes in are not predicted by)  “viral load” (Rodriguez et al., JAMA, 296 [2006] 1498-1506), and that the NIH Treatment Guidelines distinguish immunologic failure (no increase in CD4 counts) from virologic failure (no decrease in viral load) and from clinical progression (does the patient’s health improve?).

A somewhat related illustration of the failure of HIV/AIDS theory is that “AIDS” patients with Kaposi’s sarcoma may have quite high CD4 counts: see for example Maurer T, Ponte M, Leslie K. “HIV-Associated Kaposi’s Sarcoma with a High CD4 Count and a Low Viral Load”. N Engl J Med 357 (2007) 1352-3; Krown SE, Lee JY, Dittmer DP, AIDS Malignancy Consortium. “More on HIV-Associated Kaposi’s Sarcoma” N Engl J Med 358 (2008) 535-6; D.G. Power, P. J. Mulholland K. J. O’Byrne. “AIDS-related Kaposi’s Sarcoma in a Patient with a Normal CD4 Count”. Clinical Oncology 20 (2008) 97; Stebbing J, Powles T, Bower M. AIDS-associated Kaposi’s sarcoma associated with a low viral load and a high CD4 cell count. AIDS 22 (2008) 551-2. Mani, D., Neil, N., Israel, R., Aboulafia, D. M. “A retrospective analysis of AIDS-associated Kaposi’s Sarcoma in patients with undetectable HIV viral loads and CD4 counts greater than 300 cells/mm3”. J Int Assoc Physicians AIDS Care (Chic Ill) 8 (2009) 279-85.

But then it has also long been known that “AIDS” Kaposi’s sarcoma is not caused by HIV, it’s now attributed to KSHV or HHV-8, which just happened — by the sort of extraordinary coincidence or oddity that is so common in HIV/AIDS matters — just happened to appear at the same time among the same risk groups as “AIDS” and “HIV” did; and then just as mysteriously went a separate path, so that KS declined from about 40% of all “AIDS” case in 1982 to well under 10% from 1987 onwards (Table 30, p. 128 in The Origin, Persistence and Failings of HIV/AIDS Theory).

More sales in the offing for snake oil and Brooklyn Bridges.

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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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