View Full Version : Pro-circ myths 5: STIs
If you repeat a nonsense often enough, with sufficient conviction, even sensible people will begin to believe it. There is no clearer example of this principle at work than the assertion that routine infant circumcision (but illogically only of boys) will prevent or protect against sexual diseases. This has become the equivalent of the moral panic over masturbation which gave rise to RIC in the first place.
Now it is true that on the “disease” front, removal of the labia or the foreskin will likely reduce the incidence of thrush (genital candidiasis), but just about every other claim about sexually transmitted infections in a developed world setting will not survive serious scrutiny. This is a big topic, and will take a number of posts. I have already dealt with the HIV bogeyman some months ago in this thread (http://www.bubhub.com.au/community/forums/showthread.php?t=242912), so time for the scary set of other STIs.
Summary
Every well-constructed study of the relationship between circumcision and STIs in a developed world setting validates the null hypothesis. That is, circumcision will not protect a boy from any STI they are likely to encounter later in life in contemporary Australia. Therefore using disease “protection” as an excuse to circumcise is simply invalid.
The history of the disease defence of RIC is an ignominious embarrassment to the medical profession, particularly in the US, which keeps trying to cover its tracks by burying the real history of this discussion under ever more complex but no less improbable “studies”. It is important to understand why many of these studies are either deeply flawed or irrelevant to the Australian (and European) context.
No one has actually presented a proper analysis of STI epidemiology in Australia as part of this debate. This is long overdue, but will take several posts since it is important to actually understand the infections we are talking about rather than simply gesturing at “disease”.
The best, indeed only, defence we can give our children against STIs is accurate information about sexual health and responsible sexual practices. Chopping off part of their genitals shortly after birth in the perverse hope we can avoid this task, or somehow relieve them of their responsibilities when they become adults is both cowardly and doomed.
I should have the next post for this thread by tomorrow morning. Please chime in if you want something in particular covered, or indeed have any thoughts at all :idea:
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Hmm... Teaching safe sex is important. ALL children need to be taught safe sex. STIs are a risk for everyone who participates in sexual intercourse.
Fellow Traveler
24-10-2009, 07:58
Well, lets cover as many as we can. HSV, HPV, ect...
Well, lets cover as many as we can. HSV, HPV, ect...
I'm intending to do the lot, including GUDs that have been totally eradicated in Australia, such as chancroid and donavonosis, as well as outline disease reservoirs in largely circumcised populations of Aboriginals. Just will take me a while to write it up, but I'm in no special hurry ;)
Fellow Traveler
24-10-2009, 10:19
I'm intending to do the lot, including GUDs that have been totally eradicated in Australia, such as chancroid and donavonosis, as well as outline disease reservoirs in largely circumcised populations of Aboriginals. Just will take me a while to write it up, but I'm in no special hurry ;)
I am looking forward to it.
The problem with studying STIs is that by definition they are contracted as a result of sexual activity, yet the levels and nature of this activity vary radically according to a wide range of parameters, including race, ethnicity, age, education and socio-economic status.
But circumcision status in populations where this is relevant (the developed Anglophone countries) is also non-randomly distributed via the same parameters, so unless a study controls for all the variables, one can never know whether a causal association actually exists. A 25-year-old poor Hispanic is much less likely to be circumcised than a white Boston millionaire, but the nature of their sexual activity is also likely to be world's apart, so even in principle any found association between circumcision status and STIs in a sample that includes both will be invalid unless all variables can be controlled for in the data analysis.
The only studies that can be relied on to collect all of the required information in sufficient volume to make meaningful judgments are large-scale population-based studies, which also establish behavioural variables such as number of life-time sexual partners, sexuality, marital status, and type of sexual activity. Fortunately, three such large datasets exist. None has found any association between the foreskin and the likelihood of contracting an STI.
The National Health and Social Life Survey in the United States (n=1,410, with an oversample of Blacks and Hispanics, and conducted with 90-minute face-to-face interviews) concluded: “...circumcision status does not appear to lower the likelihood of contracting an STD. Rather, the opposite pattern holds. Circumcised men were slightly more likely to have had both a bacterial and a viral STD in their lifetime.”
The British National Survey of Sexual Attitudes and Lifestyles (n=4,762, also with racial and ethnic oversamples): “We did not find any significant differences in the proportion of circumcised and uncircumcised British men reporting ever being diagnosed with any STI (11.1% compared with 10.8%, p =0.815), bacterial STIs (6.4% cf 5.9%, p =0.628), or viral STIs (4.7% cf 4.5%, p =0.786). We also found no significant associations between circumcision and being diagnosed with any one of the seven specific STIs.”
The Australian Study of Health and Relationships (n=10,173, with racial, ethnic and homosexual oversamples) found: “No significant protective effect of circumcision is discernible for genital warts, chlamydia, genital herpes, gonorrhoea, non-specific urethritis or pubic lice.”
To summarise: The most extensive and rigorous examination on three continents shows no association between circumcision status and the likelihood of contracting an STI in a developed world context once all the relevant variables are controlled for. Nothing. Nada. Zip.
So the question becomes how did this idea arise and why is it still being propagated, including by health professionals who should know better? That will the subject of my next post in this thread.
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The Australian historian Robert Darby has tracked the origins of the "circumcision prevents disease" meme in a compelling article on Jonathan Hutchinson (http://www.historyofcircumcision.net/index.php?option=com_content&task=view&id=25&Itemid=51)that I highly recommend.
Hutchinson first proposed the view that removing the foreskin would prevent syphilis. Now while it is perhaps unfair to judge the medical ignorance, quackery and moral totalitarianism of Victorian England by today's understanding, Hutchinson was pretty whacky even by the standards of his own day.
Among his many other gifts to medical understanding were the convictions that Jews were immune to syphilis; circumcision of male infants was necessary to discourage masturbation and promote continence; contraception was morally objectionable and physically harmful; and leprosy was a form of tuberculosis, caused by eating bad fish.
However, his firm conviction that removal of the foreskin would somehow cure disease (and a host of other ills) is still with us today. Indeed Hutchinson's 1855 work is cited by Australia's arch circumcision advocate Brian Morris, whose website is again being promoted this very day in this forum.
How and why this idea survived will be the next part of the story.
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In the 100 years that followed Hutchinson's assertion that circumcision protected against syphilis, the foreskin debate was dominated by the medicalised moral panic over masturbation. By the time this started to subside, conventional medical wisdom, particularly in the US, had fully accepted that the foreskin was the only inherently pathogenic part of the human body and therefore its removal would protect against diseases and infections of all sorts. And more than 90 per cent of white hospital-born babies were now being neonatally circumcised, often without parental consent.
All of this happened without any empirical studies that would be regarded as even vaguely credible today, and with a disproportionate input from Jewish doctors, who were naturally enthusiastic that one of their previously reviled cultural practices was becoming a social norm, justified by medical “science”.
But as the dust settled on the embers of WWII, and masturbation hysteria lost its force, the American medical establishment also felt the need to justify this massive surgical intervention with some actual evidence beyond vague appeals to hygiene. Most attention was paid to cancers of various sorts – cervical, prostate, penile, though not vulva, which would raise some uncomfortable questions – with the leading hypothesis being the bizarre notion that smegma, uniquely among all human bodily secretions, was carcinogenic.
But the post-war moral climate was also deeply concerned about sexual disease, and this was a great opportunity for doctors. The most effective interventions – sex education and condom usage – were severely restricted by social puritanism, which left newly discovered antibiotics, of which doctors were the gatekeepers, and (drumroll) circumcision.
A medical monopoly on a key social issue of the day was formed.
But there were some problems on the horizon, the most obvious of which were that STI rates were higher in the US than developed countries with lower circumcision rates (and still are) and that there was a distinct lack of evidence, let alone a plausible biological model, for why the foreskin should make transmission of sexual infections more common.
Thus we entered the modern era of American STI “studies”, whose value and validity were measured by how decisively they supported the self-interest of the medical establishment.
This will be the subject of the next post.
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Opinionated
25-10-2009, 20:28
This is great John, a very interesting read.
Fellow Traveler
26-10-2009, 08:59
So far so good John. I've seen those papers. I am wondering, it might have been better to start this post in the 'discussing it' section. There may be those who won't discuss this in the 'anti' section.
So far so good John. I've seen those papers. I am wondering, it might have been better to start this post in the 'discussing it' section. There may be those who won't discuss this in the 'anti' section.
This is turning into a bigger beast than I originally anticipated -- I'm still two posts away from starting the analysis of the current Australian data! Trying to boil down 150 years of peer-reviewed literature into something intelligible for the non-specialist reader, in my spare time, is an interesting challenge. :rolleyes:
While I'm all for debate (that's the point of a forum, after all), I would prefer to complete the project and then start a a more polemical thread in the Discuss It section which references this thread.
The problem post-war researchers faced was that to date different studies had come to radically different conclusions. An influential British study (http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=2444120&blobtype=pdf&tool=pmcentrez)in 1934 found: “The absence of the prepuce is not the important preventive factor in the acquisition of syphilis that is commonly believed”, while an equally influential North American study (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1583341/pdf/canmedaj00604-0056.pdf/?tool=pmcentrez)found: “From these figures it will be seen that 76.7% of the V.D. Group were uncircumcised whereas in the control group, 52% were uncircumcised. The most striking difference is in syphilis where 90% of the cases were uncircumcised.”
What was going on? To understand the issue, we need to consider how such studies work.
Unless one is doing a population-based survey (see post #6 (http://www.bubhub.com.au/community/forums/showthread.php?p=4183770#post4183770)), then researchers could only study those attending treatment centres (clinics, hospitals, etc). Such patients are of course not representative of the general population, but that doesn't matter as long as circumcision status is genuinely randomly distributed among the subgroups that make up the study population.
That of course never happens. So in reality the likely validity of a study is determined by the degree of homogeneity of the study population and/or the use of a control group that mirrors as closely as possible the demographic characteristics of the study group.
Even then, if circumcision status is more strongly associated with a key demographic variable, such as ethnicity, than the found association with an STI, then statistical control becomes impossible. This is why the 19th and early 20th century studies comparing Jews and Gentiles are invalid, because there is no way of knowing whether one is seeing a correlation with circumcision status or with different sexual practices associated with cultural identity.
For cost reasons, most studies are retrospective, which means inevitably the relevant demographic information has never been collected in the first place. Indeed, it has been found that circumcision status itself is unlikely to be recorded correctly in 10-20% of retrospective studies!
Until the invention and widespread availability of computers, regression analysis that would allow for the control of variables even if the study were properly constructed was not an viable option for researchers.
Adding all this up and looking over the studies that meet a minimum standard of statistical validity, a definite trend emerges: the more homogenous the study population (and hence the more circumcision status is truly random), the weaker the association between circumcision and STI incidence. This in fact explains the difference between the first two studies cited, exacerbated by the fact that the second study's control group was not even drawn from the same population.
This problem is particularly acute in the US, where circumcision status has for a hundred years been radically stratified by age, race, ethnicity and locality – all likely markers of differential sexual behaviour. This is still the case today. An interesting little study of indigent youth (http://aje.oxfordjournals.org/cgi/content/full/159/11/1095) in Houston, Texas, found 22% of Hispanics, 58% of African Americans and 82% of whites were circumcised – a huge variation between demographic groups likely to have very different sexual practices. To make matters worse “23 percent of fully circumcised and 31 percent of uncircumcised youth did not know their status”.
This demographic problem is compounded by the fact that the US medical establishment has a huge historical investment in proving a link between the foreskin and STI incidence and hence overlooking such confounding factors in their studies.
In the next post, I will analyse several influential modern studies in detail to see how the factors described here actually played out.
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In 1975 a study (http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1046564&blobtype=pdf&tool=pmcentrez) was published purporting to show an association between herpes and the foreskin, using a control group. It has been cited very often, and usefully tabulates most of its raw data, which permits re-analysis by modern statistical methods. The core finding can be seen in its Table I, and translates to OR 2.5 (95% CI 1.5 – 4.0), which means intact men in their study were significantly more likely to contract herpes (though there was no difference for any other STI).
[For those phobic about numbers: Don't be! I've recalculated all data in a uniform way for this post, and this is how it works. OR means odds ratio. It is the strength of association. If it is 1, then there is no association; any number larger than 1 means there is a correlation between having a foreskin and the infection in question; less than 1 means the foreskin is protective. The 95% CI is the confidence interval, and indicates among other things whether the association is statistically significant. If the upper and lower limits straddle 1, then the association is not significant, whatever the OR, and we should disregard the result. See? Simple!]
But problems arise the moment you look at Table II, which breaks down by “nationality” (which appears to be a euphemism for race/ethnicity). For white guys, it's OR 1.7 (95% CI 0.95 – 2.9), which means it's no longer statistically significant. And if we look at Table V and do the calculation for shop and office worker we get OR 1.5 (95% CI 0.7– 3.4), even less significance than for simply being white. But for the non-white folk it's OR 5 (95% CI 2.0 – 12.2), a strong and significant association.
This cannot be right. If the study is seeking an association between foreskins and the likelihood of contracting herpes, then any differences should be small and random between intact men in different demographic groups. A foreskin is a foreskin, if taken in sufficient number. So these results are invalidated by some confounding factors, most likely inexplicable differences in condom use and the effects of multiple STIs in lower class and non-Caucasian males, both of which are noted but neither investigated.
But it gets worse. If you look again at Table I, you'll see a significant number of patients did not have their circumcision status recorded. What happened to these people in Tables II and V? Those that were circumcised all grew foreskins! From the literature it would seem I'm the first person in the 34 years since this study was published to notice this glaring error, the effect of which is to distort the data even further in favour of an imaginary association.
Fast forward a couple of decades to probably the most influential STI study (http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1614986&blobtype=pdf&tool=pmcentrez) of the late 20th century, which purported to show an association between the foreskin and syphilis and gonorrhea, but no association with other STIs (including herpes), except genital warts, where circumcision was found to be a significant risk factor. (You may be starting to notice a pattern here – namely, that no two studies can agree on the infections for which the foreskin is an alleged risk.)
The heavy weaponry of statistical analysis (logistic regression) was rolled out in a retrospective chart review of thousands of patients passing through a Seattle clinic in the course of a full year, with relatively full recording of all demographic characteristics (though unhappily circumcision status was not recorded in 14% of cases, which had to be discarded from the analysis).
The basic story is told in Table 2 (they are calculating OR in the same way as in this post). But now look at Table 1 in the race/ethnicity section. Notice something deeply peculiar? I will pick up the plot in my next post.
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The data from Cook et al shows that the incidence of STIs is far more strongly associated with race than any other variable. In fact, the association between being non-white and syphilis is OR 15.6 (95% CI 4.7 – 51.6), with the huge spread in the confidence interval indicating a lack of statistical power due to the tiny number of white cases (3). On the other hand, being non-white is negatively associate with genital warts with OR 0.58 (95% CI 0.45 – 0.74).
To treat such strong associations as confounders to be “corrected” because circumcision is the underlying causation is a nonsense, and it leads to preposterous conclusions. For instance, the study finds the foreskin significantly protective against genital warts with a corrected OR 0.7 (95% CI 0.5 – 0.9). So silly is this conclusion, that the authors tried to head criticism off at the pass by publishing another paper (http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1195083&blobtype=pdf&tool=pmcentrez) pre-emptively to “explain” what they admit is a “paradox”. In a masterpiece of Humpty Dumpty logic they speculate that intact penises had fewer warts because they are more susceptible to the virus!
The obvious answer to all these conundrums is that they are dealing with populations that are highly segregated, at least at a sexual level, and therefore have major differences in STI incidences. That poor urban blacks would have a higher incidence of syphilis is hardly a revelation. That they also have a somewhat lower rate of circumcision is not exactly news either. But to conclude that their circumcision status is the cause of the syphilis incidence would be blindness of the highest order.
To further cover their tracks the authors nowhere provide data on the circumcision status of different racial groups, or indeed any of their demographic groups, to allow independent researchers (or the peer-reviewers) to unravel this mess.
Compare with this New Zealand paper (http://www.doctorsopposingcircumcision.org/pdf/2008_Dickson.pdf), a prospective, longitudinal study of an entire year's birth cohort conducted over 32 years, which found no difference in STI incidence between intact and circumcised men. The authors are meticulous in providing the data linking their their variables and extremely conservative in applying any “corrections” via regression analysis. The study is convincing because of the homogeneity of their population, so little statistical correction is in fact required. Ditto for this Sydney study (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1195274/pdf/genitmed00023-0023.pdf/?tool=pmcentrez) of 300 consecutive patients to a leading clinic, which again found no differences in STI incidence between intact and circumcised men. The theme here is the absence of confounding factors.
At the opposite end of the spectrum, you have this study (http://content.nejm.org/cgi/reprint/346/15/1105.pdf) by Castellsagué et al, which alleges an improbable association between HPV and the foreskin. Their sample of circumcised men is drawn almost entirely from The Philippines while their intact sample comes from countries such as Colombia. It is a certainty that HPV incidence is different in different countries, and to propose that such differences are due to circumcision status rather than national variation is to stretch credulity to breaking point. (They also admitted problems in collecting samples from circumcised men.)
But enough of studies! Let's move on to actual STI incidences in Australia and the plausibility of various claims that have been made in relation to these. We'll start with HPV in the next post.
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In regard to the your last study.
http://content.nejm.org/cgi/content/full/346/15/1105
From JohnC:
Their sample of circumcised men is drawn almost entirely from The Philippines while their intact sample comes from countries such as Columbia. It is a certainty that HPV incidence is different in different countries, and to propose that such differences are due to circumcision status rather than national variation is to stretch credulity to breaking point.
They did highlight this in the study though. As per the statements below.
A potential concern with respect to our study was the fact that 65 percent of the circumcised men were from the Philippines. This result was not unexpected, since mass circumcision sessions are regularly conducted by many organizations in that country and most boys are circumcised before puberty. We performed a secondary analysis excluding men from this study site and found that results were virtually unchanged.
Thanks for the link, Father. I have now linked to the PDF in my post, which at least provides readable versions of the tables, since it is the data, rather what the authors claim about it, that is of interest.
I will also now make my next post a discussion of HPV, rather than chlamydia, so we can deal with this sooner rather than later.
And you know, somehow I wasn't surprised to see you rushing to Castellsagué's defence ;), but it's good to see someone's awake out there.
serendipity22
01-11-2009, 11:06
This thread is fun, its like reading a detective mystery.
This thread is fun, its like reading a detective mystery.
:) thanx. Unfortunately, there is a bit of a wait between episodes, since there's mountains of literature and data to review. But I can assure you the plot definitely thickens ;)
There are over 130 types of human papillomavirus of which about 35 infect the anogenital area more or less exclusively and can be considered STIs. Some can cause genital warts, some can cause cancers in the long term and some are probably completely asyptomatic. There is no cure for HPV but most infections are eventually cleared by the body's immune system either completely or to undetectable levels without the person being aware of it.
Genital HPV is ubiquitous among the sexually active, and with appropriate collection methods it is likely that most persons from their 20s on who have multiple sexual partners will have a detectable infection. With genital warts, 90% are caused by types 6 and 11, while 70% of cervical and other genital cancers are caused by types 16 and 18. The vaccine Gardasil protects against all four types and is currently recommended for all girls in Australia prior to the commencement of sexual activity. It has also been shown to be effective for boys, and it is hoped the immunisation program will be extended to include them. For the latest information on the Gardasil program, including side-effects, see the latest TGA report (http://www.tga.gov.au/alerts/medicines/gardasil.htm).
Until recently the only viable way of checking for HPV infection was by visual inspection for genital warts. However, researchers are now able to cost-effectively use a polymerase chain reaction-based (PCR) assay. (This is not available as a standard clinical test at STI clinics or pathology services.) It has recently been shown that collection method (http://www.ncbi.nlm.nih.gov/pubmed/14767822?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed _ResultsPanel.Pubmed_RVDocSum&ordinalpos=8) has a significant effect on the likelihood of positive results being obtained.
HPV is transmitted via skin-to-skin contact or via semen, vaginal secretions and urine (if you're into watersports). Since circumcised men do not possess a foreskin this is not a possible infection site. For intact men an infection of the inner foreskin is likely to also auto-inoculate the glans, so we would expect a slightly higher rate of HPV infection in that area. However, since the majority of HPV infections are detectable on the penile shaft and scrotum we would not expect a statistically significant difference in overall HPV infection rates between circumcised and intact men, just a slightly different distribution.
In fact, reviewing the literature on genital warts that is precisely what we do find: intact men with warts are more likely to have them in the prepuce and glans area, while the shaft is a more likely site in circumcised men. Because of the immunogenic properties of the foreskin it is also probable that the more common, and worrisome, types of HPV may have a lower overall incidence in intact men (a hypothesis I will return to in my next post). This may also explain why despite the larger skin surface area of intact men, no overall difference in genital wart incidence can be found in any well-conducted study. And this is likely to be the case with other HPVs as well.
On the other hand, it has frequently been speculated that the inner foreskin is more susceptible to HPV infection, but if that were so we would expect a higher frequency of genital warts in women, who have an equivalent and more extensive mucosal surface. But this is not the case, and again it is probable that immunogenic effects cancel out the surface area factor.
Now a note on the Castellsagué study (http://content.nejm.org/cgi/reprint/346/15/1105.pdf). This was in fact five separate studies, conducted across four continents, none of which found a significant association between HPV and circumcision. If one thing should have become clear from this thread by now, it is that you cannot put together different populations, even when they are in the same city, and expect a result that is anything other than a statistical artifact. Simply removing the Philippines from the set does not help at all, because you are still putting together Spain (a developed OECD country) with Colombia, Brazil and Thailand. Indeed, if you take out Spain and calculate the Fisher two-tailed probability, the whole thing fizzles into insignificance again (p > 0.3). But there are other issues as well that cripple this study's credibility:
Their collection method has been shown to be inadequate (see above) since no proper exfoliation was performed, which means about half of infections would have gone undetected, particularly from the more cornified glans of circumcised men.
They only sampled the glans and distal urethra, not the shaft or scrotum, which would seriously bias the study against intact men.
Their PCR assay used HPV probes that were not sufficiently specific for different types (no type result for the majority of samples), and there was no correlation of the relative incidence of types 16 and 18, which are the ones of interest in regard to cervical cancer, with the rest of the dataset.
Finally, they failed to find any significant association between cervical cancer and circumcision status in either any of the individual studies or the aggregated results, which was supposedly the point of the exercise.
The publication of this study was another example of the failure of the peer-review system, and it is no longer taken seriously by researchers in the area. But it does help to define, negatively, the sort of study we should be looking for to shed further light on these important issues. This will be the subject of the next post.
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Just to break up this very serious thread for a moment :rolleyes:
It is entirely biologically plausible that men with shorter erect penises are at reduced risk of contracting an oncogenic HPV from women whose cervix is infected, and are themselves a lower risk for infecting the cervixes of other women.
So penile reduction surgery may be effective in preventing cervical cancer. I don't see anyone rushing to investigate this hypothesis, however ;)
sockstealingpoltergeist
02-11-2009, 17:27
Just to break up this very serious thread for a moment :rolleyes:
It is entirely biologically plausible that men with shorter erect penises are at reduced risk of contracting an oncogenic HPV from women whose cervix is infected, and are themselves a lower risk for infecting the cervixes of other women.
So penile reduction surgery may be effective in preventing cervical cancer. I don't see anyone rushing to investigate this hypothesis, however ;):laughing:
I have never heard it suggested.
Opinionated
03-11-2009, 21:17
Just to break up this very serious thread for a moment :rolleyes:
It is entirely biologically plausible that men with shorter erect penises are at reduced risk of contracting an oncogenic HPV from women whose cervix is infected, and are themselves a lower risk for infecting the cervixes of other women.
So penile reduction surgery may be effective in preventing cervical cancer. I don't see anyone rushing to investigate this hypothesis, however ;)
:idea:Well that could be the circumcision link! Without enough skin left, erections are shorter. No wonder people keep banging on about circumcision reducing cancer. It's because it can make penis's shorter so they don't hit infected cervixes.
A short delay in proceedings. The focus of part 2 of the HPV section was to be a study that has an excellent design and is very recent, but has a number of problems in its data presentation that are currently under active discussion between myself and the authors. That discussion may last a few more days.
This may be an opportune time, however, to reflect on the fact that the majority of studies concerning circumcision have serious problems in design, statistical handling and/or interpretation. There are a number of possible reasons for this:
Straightforward authorial bias in a small minority of cases.
Cultural blindness, often race or class based, such that the investigator does not recognise their little corner of the universe is just that and not representative of the broader population or other cultural contexts.
Specialisation whereby the clinicians who conduct the study understand less about the statistical handling, and the statisticians very little about the clinical situation.
The pressure to find correlations in your study in order to make it interesting, and most important, publishable. Proving the null hypothesis is rarely an attention-grabber for journal editors.
This is all understandable, but once a study is published it is likely to be cited evermore, even though it has been effectively refuted or seriously challenged in the subsequent literature.
This is why multidisciplinary reviews, such as done by the RACP and other peak medical bodies are so important when formulating health policy, because it is only when a range of experts work over the entire body of studies that a balanced picture has a chance of emerging. And even then things can go seriously awry, as we have seen with the African AIDS experience.
This is why the notion that parents are going to “research” circumcision via Google or whatever is not a credible position. In the end, there is no consensus among “experts” on whether there is any medical benefit, potential or otherwise, to circumcision in a developed world setting, and it therefore seems an unimpeachable case that the best thing to do is leave it to the owner of the foreskin when he is old enough to make that decision.
sockstealingpoltergeist
10-11-2009, 21:57
This is why multidisciplinary reviews, such as done by the RACP and other peak medical bodies are so important when formulating health policy, because it is only when a range of experts work over the entire body of studies that a balanced picture has a chance of emerging. And even then things can go seriously awry, as we have seen with the African AIDS experience.
This is why the notion that parents are going to “research” circumcision via Google or whatever is not a credible position. In the end, there is no consensus among “experts” on whether there is any medical benefit, potential or otherwise, to circumcision in a developed world setting, and it therefore seems an unimpeachable case that the best thing to do is leave it to the owner of the foreskin when he is old enough to make that decision.
:yelclap::yes:
serendipity22
21-09-2010, 11:20
bump
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