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The Best Australian Science Writing 2014

Page 20

by Ashley Hay


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  If one accepts that women may have preferences for penises of a certain size, one is left with the not-inconsiderable challenge of how to measure such preferences. Asking people doesn’t always work. Women – and men – have all sorts of reasons to prevaricate, or to grow indignant that the question has even been asked.

  In earlier work, my UNSW Australia colleague Barnaby Dixson used a series of five line drawings, manipulated to have different sized flaccid penises, to study women’s preferences in Cameroon, China, New Zealand and the USA. He found that slightly larger than average penises tend to be favoured by women. Important as this study was, it cannot illuminate how important penis preferences are relative to other preferences – such as for muscular torsos or for taller men. If the only thing that varies among stimuli in an experiment is the trait of interest, then we shouldn’t be surprised to find it has an effect.

  And subjects quickly cottoned on to what the experiment was about. Also, the smallest and largest penises may have just looked strange, relative to the body on which they had been drawn.

  In this new work, Mautz and his colleagues used a higher tech method, building three-dimensional computer models – 343 models in all – that varied in torso shape, height and flaccid penis size. They then showed each female subject a subset of 53 bodies, one at a time, projected life-size on a wall, and asked them to rate the attractiveness of each on a seven-point scale.

  According to Mautz, the life-size projection of the images was important:

  While using small figures can provide important insights into how mate-choice might affect particular traits, I think responses will be affected by the size of the pictures (or stimuli if you will). Ever wondered why they do so many close-ups in pornographic videos?

  Well, no. But moving right along.

  For me, the stroke of genius was the independent manipulation of three traits, two of which (height and torso shape) are already well known to influence attractiveness. This allowed Mautz and his colleagues to calculate that penis size affects attractiveness – of CGI models at least – about as much as height does.

  It also allowed them to test for interactions between penis size and the other traits. While well-endowed models tended to get the best ratings, they did so especially in taller men who had more masculine bodies.

  That is to say the effects of all three traits – height, torso shape and penis size – were not independent; rather, models who were tall, broad-shouldered and with large members did particularly well.

  Critics of this type of study love to point out that women usually decide if they will have sex with a man well before ever sighting his genitals. And, if so, then how can penis size influence choice?

  Well, let’s just stress the importance of repeat business. A first-time disappointment can rapidly become a one-time-only thing. And an unsatisfied customer can talk to other potential customers, ruining a reputation.

  Not becoming physically acquainted before making a lifetime commitment has its perils, including in the genital department. In March 2013, the world’s media got to rehash its stock ‘small-penis-as-grounds-for-divorce’ stories, when a Taiwanese woman’s wedding night was marred by the disappointing discovery that her groom’s member measured a mere 5 centimetres long.

  In Mautz’s experiment, women certainly chose among the models presented. They took an average of three seconds before scoring each video clip – and were mercilessly faster than that with the least attractive figures. According to Mautz, ‘that’s so quick that you can’t really, in that short space of time, consciously go through the pros and cons of each character; that rating is an overall impression of attractiveness, not focused on any particular body part.’

  The reflex to disbelieve that women can and do discriminate about penis size echoes 150 years in which evolutionists and the public alike have often doubted that female sexual agency has the power to shape the evolution of male traits. And yet female choice – across the animal world – represents one of the most potent forces driving the evolution of male traits.

  Showing that women choose among large numbers of CGI models isn’t quite the same as showing their in-the-flesh mating decisions are biased in quite the same ways. Eye-tracking technology confirms that while men tend to look at the faces and chests of pictures of nude women, women tend to look at the faces and crotches of nude men.

  For now, Mautz’s study suggests that female choice may well be responsible for the prodigious size of the human male penis. Even if not everyone feels comfortable admitting it.

  Planet of the vines

  Eleven grams of trouble

  Eleven grams of trouble

  Frank Bowden

  In 2010 the Prostate Cancer Foundation of Australia produced a television advertisement called ‘It could happen to you,’ a masterly example of beautifully lit, tightly focused, talking-head communication. Fifteen famous Australian actors, celebrities, sportsmen and musicians construct a 30-second narrative about the threat that prostate cancer poses to Australian men and what they can do about it. In grabs of a few seconds each, the facts of prostate cancer are established in turn: ‘It kills more Australians every year than breast cancer. Or skin cancer. Or car accidents. Over 3000 men. One every three hours.’ (It must be an important topic – one of the speakers is a Wiggle.) Then three young heads: ‘Just like me.’ (That guy from Underbelly.) ‘Just like me.’ (Nathan Bracken: cricketer.) ‘Just like you.’ (Craig Bolton: AFL star.)

  If you thought prostate cancer was an old man’s disease, then the appearance of these three 30-somethings strongly suggests otherwise. Following the rules of good health promotion, the next step is reassurance and a plan of action: ‘Prostate cancer is treatable. And early detection is the key. So if you’re over 50 – or over 40 with a family history – talk to your GP.’ And what will my GP say? ‘It could be as easy as a blood test.’ And then, to reiterate the central message, ‘Because if you get to it early … surviving prostate cancer could happen to you.’ The closing words are spoken by Bert Newton.

  It’s all very simple, and persuasively done. So why, if prostate cancer is common and treatable, and if early detection will save my life, did I want to throw my mouse through the computer screen when I saw this advertisement recently on YouTube?

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  The prostate gland is the female God’s revenge for menstruation. The genitourinary tract of women is like a Mexican-built Volkswagen: beautifully designed but just a bit unreliable. Any woman of child-bearing age can suffer conditions with names that men neither pronounce nor comprehend: Mittelschmerz, dyspareunia, cystitis, menorrhagia and dysmenorrhea are just a few of the things that punctuate the life of even the healthiest woman. The male equipment, on the other hand, doesn’t need servicing until well into middle age. Most owners of a prostate have no idea what it does, but just as the curse of hormonal flux is receding from their female partner’s life, the tiny, walnut-shaped organ starts to exert its malign influence. Now it’s the man’s turn to suffer from conditions with Latin and Greek names – nocturia, strangury – and, worst of all, the one with Anglo-Saxon origins: cancer.

  A tumour of the prostate begins as a growth of abnormal cells within the gland itself. No one knows why the cancer cells develop but they appear to be an inevitable part of ageing. Postmortem studies have shown that if a man lives to 90 he is almost certain to have evidence of cancer in his prostate gland. The cancer sometimes reveals itself by compressing the urethra as it exits the bladder and impeding the passage of urine. But many cancers cause no symptoms until they have spread into the surrounding organs, or to bones, lungs, liver or brain.

  Prostate cancer is Australia’s number one cancer (18 560 diagnosed in 2012) and the third-highest killer (3235 in 2012). No other male cancer has shown the same rise in case numbers over the past 30 years. In 1982, one in 23 Australian men were diagnosed by the age of 75; by 2009 this had risen to one in seven. This rise has been associated with a striking f
all in the age of diagnosis: in 1982, the annual rate of diagnosis in men aged 45–49 years was only three per 100 000; by 2009 this had risen to 56 per 100 000. Rates in men in the 50–54 age group had risen from 12 per 100 000 to 164 per 100 000. Yet the overall death rate for prostate cancer hasn’t changed much: in fact, the age-standardised death rate in 2008 (31 per 100 000) was only slightly better than it was in 1970 (36 per 100 000). Similar trends are seen elsewhere in the developed world.

  What explains this late-20th-century epidemic? Agent Orange and dioxins in the environment? Trans fats in our food? Tight underwear and decreased sunlight exposure? Undiagnosed Lyme disease? The best answer, in fact, may be sociological rather than biological.

  In the 1970s, the emerging women’s health movement urged women to take control of their own bodies and become more demanding of a medical profession still dominated by men. Around the same time, the belief that early detection of cancers would reduce mortality was taking hold. As a result, screening for two female cancers – breast and cervix – became popular in the 1980s, and coordinated screening programs were established across the developed world. The Pap smear and the mammogram became a normal, if annoying, part of most women’s routine, and an international consensus accepted that these screening programs save lives. Women’s cancers have received considerable media attention and generous public and private funding, adding up to about $320 million per year in Australia’s case.

  A kind of backlash was brewing among ageing male baby boomers. During the 1990s, advocacy groups emerged with the aim of redirecting some of the coverage and funding to what is now known as ‘men’s health’. They chose prostate cancer as one of their flagship diseases. If screening works to save lives for one cancer, they argued, then it will work for all of them. And so the idea that cancer screening is a universal good became an article of faith among many doctors and men’s groups – despite being repeatedly dashed on the rocks of experimentation and evidence. In fact, the evidence has been mounting for more than a decade that prostate cancer screening offers little or no overall benefit to the male population at any age. But, believe me, these are seen as fighting words among men’s health organisations.

  * * * * *

  Surely screening is screening, regardless of whether we’re talking about breast cancer or prostate cancer? Unfortunately, as simple as it might seem, that’s not the case. To understand why, we need to go back to the underlying principles.

  Put simply, screening tries to identify a disease in people who don’t have symptoms of that disease. If symptoms are present, we are diagnosing, not screening. You may, for example, perform a blood glucose test to screen for diabetes in a fit middle-aged man who presents to his GP for a check-up, but then perform the same test to diagnose diabetes in a young person who has lost weight, has an increased thirst and is passing large volumes of urine. The distinction is critical: patients with symptoms of a disease are far more likely to have the disease than those who don’t. This may sound self-evident but it fundamentally changes the way we should act on test results.

  No medical diagnostic test is perfect. Sometimes it will show a negative when the person actually has the disease (a false negative) and sometimes it will show a positive when the person doesn’t have the disease (a false positive). The degree to which these two unwanted (but unavoidable) attributes are present determines the test’s utility: the best tests return very few false negatives (these are called ‘highly sensitive’) and very few false positives (these are called ‘highly specific’). But no matter how good the test, it will indicate the presence of disease with less confidence when the chance of the person having the disease is low (when the patient comes in for a routine check-up, for instance) than when the chance of the person having the disease is high (in the case of the young patient with symptoms). Let’s examine this in more detail using the specific example of prostate cancer.

  In 1970 Richard Ablin, a New York immunologist, discovered an enzyme in the prostate that was subsequently shown to be present at a raised level in the blood of patients with prostate cancer. It became known as prostate specific antigen, or PSA. At a time when the only digital technology at a urologist’s disposal was his index finger, a blood test for cancer must have seemed like a godsend.

  It soon became clear that the PSA was neither highly sensitive nor highly specific. PSA levels were also raised in men with other conditions affecting the prostate, including simple agerelated prostate enlargement, infections, the effects of aspirin-like drugs, and fun things like ejaculation and riding a bicycle. In fact, it became apparent that as many as two-thirds of the men with elevated PSA results didn’t have cancer and the test was negative for as many as 15 per cent of those who did have cancer. Despite these recognised weaknesses, by the 1990s millions of men across the world were undergoing PSA screening.

  Although there is no government-sanctioned prostate cancer-screening program in Australia, Medicare data show that an extraordinary 1 688 370 PSA tests were performed in 2012 at a cost of just under $32 million to the taxpayer. (The estimated cost of testing in the United States is $3 billion per year.) While it isn’t possible to calculate the exact proportion of Australian men who are screened each year, the Medicare data suggest that around 66 per cent of men aged between 55 and 64 had a PSA test in 2012, which is a higher proportion than the 55 per cent of women who have a Pap smear every two years. Such is the power of simply suggesting to men that they should ‘talk to their GP’.

  Because of its poor specificity, PSA testing is just the first step on the cancer-screening pathway. It would be wrong (unscientific, costly and unethical, that is) to treat 100 men with a raised PSA to reach the 34 with cancer. So a more specific test – a test that returns fewer false positive results – must be performed. This is where things start to get a bit medieval.

  When I was a medical student in the early 1980s one of my female colleagues argued that if men had to undergo screening for testicular cancer in the same way that mammograms were performed for breast screening, the male engineers responsible for the development of the technology would invent an X-ray machine that didn’t squash the relevant body part between two cold metal plates while the patient remained motionless for several minutes. She also pointed to the indignity of the Pap smear, implying that the speculum examination was part of a male conspiracy to subject women to needless discomfort and indignity. If there was any truth to this polemic, it was demolished in 1987 when a male urologist introduced the trans-rectal ultrasound guided biopsy – innocently referred to as the TRUS biopsy.

  The prostate gland sits at the base of the bladder and is adjacent to the rectum, the last part of the large bowel before it opens to the world through the anus. To perform a TRUS biopsy, an ultrasound probe the thickness of a modest-sized Lebanese cucumber is inserted into the rectum of a patient who is wide awake and, after the location of the prostate is identified by ultrasound, a needle is passed down a channel in the probe, through the wall of the rectum and into the prostate. Multiple biopsies are taken and examined by a pathologist for the presence of cancer.

  Male readers who haven’t fainted by this point may already have calculated that, on average, only a third of men with raised PSAs will have a cancer diagnosed using the TRUS biopsy. In 2012, just over 29 000 TRUS biopsies were performed in Australia, so approximately 19 000 men had an unnecessary procedure. Not too bad a price to pay if 10 000 men have had their life saved because the cancer was picked up early?

  Again, the commonsense view takes a hit from the complex biology of prostate cancer. It has been known for over 100 years that the majority of men with prostate cancer die with the disease, not of it. Because it is mainly an older man’s disease, most will succumb to cardiovascular disease or another malignancy before the prostate cancer has a chance to kill them. That might sound like cold comfort, but there are two more subtle concepts to consider here, the first of which is known as ‘lead-time bias’. All prostate cancers start off as small tumours, conf
ined to the gland, which can be detected by PSA and biopsy many years before they cause symptoms. The increase in prostate cancer in men in their 40s and 50s over the past 20 years doesn’t mean that more men are developing prostate cancer, it just means that screening has lowered the age that men are diagnosed. This conclusion is supported by the observation that in the same period there has been a mild decline in the rate of diagnosis among men in their 70s and 80s because they have already been diagnosed in middle age.

  The second concept is that screening for prostate cancer will identify people with small tumours that are never going to cause any harm regardless of how long they live. This is known as ‘over-diagnosis’, and most people (including, surprisingly, many doctors) have difficulty believing in it. Between 30 to 50 per cent of all prostate cancers are ‘what you don’t know about won’t hurt you’ cancers that will never grow outside the prostate or spread to distant organs. But no currently available test can distinguish between the cancers that will progress and those that won’t. If we apply the low estimate of over-diagnosis, 30 per cent, to our 10 000 men with biopsy-diagnosed cancer, we are left with 7000, out of our original 29 000, who have a disease that needs to be treated.

  Both of the potentially curative options for prostate cancer – radical prostatectomy and radiotherapy – are complicated, expensive and time-consuming. Both are associated with significant side effects, the most common being impotence, urinary incontinence and radiation-associated inflammation of the bowel. Men who receive a diagnosis of prostate cancer in their 40s and 50s will usually be prepared to risk a permanent loss of erections or decades of incontinence if it means that they will be cured of cancer. But this ‘if ’ is as big as the Ritz: despite a widely held perception to the contrary, by the time most men have had their cancer identified through screening it will be too late to cure it.

 

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