By Angela Nitzke-Martin

I have no doubt that at some point after having my blood drawn, I have likened the experience to torture. Those minutes spent prospecting for gold in my evidently intractable veins is certainly unpleasant, and on occasion painful, but torturous — no. It is an attempt to add drama to a pretty boring story, and absurd to suggest that a medical professional would support suffering that wasn’t ultimately in the patient’s best interest. After all, they do have to take an oath.

Maybe that is why “Medical Complicity in Torture,” the title of a lecture given by New York University’s Allen Keller was a bit shocking. CIA physicians and psychologists seem out of place in military prisons, but they do play a role in interrogations and were present at Guantanamo Bay. Should medical professionals participate in torture or enhanced interrogation? “Moral and scientific reasons ultimately lead to the same conclusion: That, no, we shouldn’t be doing this,” said Keller, an associate professor of medicine and director of the Bellevue/NYU Program for Survivors of Torture.

Keller spoke at the University of Chicago on Wednesday as part of the MacLean Center for Clinical Medical Ethics seminar series. In his lecture, Keller drew from vast experience dealing with torture victims and the report he coauthored for Physicians for Human Rights titled, “Aiding Torture.” The paper cites the CIA Inspector General’s report released in 2004 that said psychologists not only monitored enhanced interrogation techniques like waterboarding, but also kept data on the prisoners’ reactions.

It is impossible to separate the physical, psychological and social dimensions of health, said Keller. “The consequences of torture are all interrelated.” Prisoners who are not mortally wounded may still experience intense psychiatric trauma with long lasting effects. Preventing death or severe injury does not preclude inflicting harm.

Although not as mind-boggling as what the definition of “is” is, there is still debate about what constitutes torture. We have the UN’s definition and the American Medical Association’s definition, but it boils down to something much simpler for Keller. “If it looks like torture, smells like torture, it’s probably torture,” said Keller.

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Disease screening is often a delicate balance. Catching a disease in its early stages almost always makes it more treatable, and can prevent permanent damage or even death. But it’s also cost-prohibitive to screen every person for every disease - even if you could convince everyone to show up for their regular doctor’s appointments - and so difficult decisions about benefit vs. cost and risk must be made.

Who actually makes those decisions is one of the key features of the U.S. health care debate. It’s nice to think that they are made by clinicians looking at the latest in medical research, but choices about what screens are affordable enough to be useful often boil down to which are considered acceptable for coverage by health insurance. In theory, insurance companies will follow the recommendations of scientific societies and expert task forces entrusted to analyze available data and make a decision. But what if those experts disagree?

That’s the battle being fought this week as new recommendations about mammograms for breast cancer screening are released by the U.S. Preventive Services Task Force. Published Tuesday in the Annals of Internal Medicine, the recommendations go against the grain of recent practice advising all women to start receiving mammograms at the age of 40, with yearly screening after the age of 50. Now, the task force says women who are not high-risk due to genetic factors or family history don’t need routine mammograms until age 50. Even then, screening every other year is sufficient until the age of 75, the task force concluded.

These new recommendations were not received quietly, as you may have discerned from the media covearge. University of Chicago professor of radiology Robert Schmidt told the Chicago Tribune that the recommendations were “arrogant and irresponsible.” My wife reports that one of the ladies of The View called the decision “gender genocide.”  Some medical societies have come out in favor of the new practice, while others said they will stick to the old guidelines. Ultimately, the decision on whether to be screened (if not the decision on how much screens will cost) lies with patients themselves. So here’s a quick primer on the support and opposition to the new recommendations.

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A sleeping zebra finch (courtesy of Margoliash lab)

One of the repeated themes of the Darwin/Chicago 2009 meeting two weeks ago was the history of the anti-evolution movement, a resistance that has actually changed form, even *cough* evolved, quite a bit since The Origin of the Species. At the opening night event in Rockefeller Chapel, science historian Ronald Numbers talked about differences between the anti-Darwinists led by William Jennings Bryan in the 1920’s (immortalized in the Scopes Monkey Trial and Inherit the Wind) and today’s intelligent design supporters and creationists. Surprisingly, Bryan and his followers were considerably less extreme than today’s anti-evolutionists, as Numbers explained that most who railed against Darwinism in the early 20th century were fine with the evolution of animals over billions of years, they merely could not abide that humans also evolved.

The evolution vs. creation debate has obviously become a lot more complicated since then, but Bryan’s primary objection has lingered - the core of most people’s opposition to evolution is the idea that humans must be somehow separate and different from the rest of the natural world. One “proof” of this uniqueness is the complexity of human language, a form of communication that, to the casual observer, appears in an entirely different league from the songs, gestures, or simple noises that animals use to share information. The assumption that the more complex forms of human language are unique is even held by some in the field of linguistics and psychology, including the legendary Noam Chomsky, who argued as much in a 2002 Science paper with cognitive psychologist (and Darwin/Chicago speaker) Marc Hauser.

That assumption is a handicap to the study of language, argue University of Chicago’s Daniel Margoliash and Howard Nusbaum in a recent issue of the journal Trends in Cognitive Science. The idea that human language is biologically unique, and thus the kind of “hopeful monster” geneticist Richard Goldschmidt coined to describe the sudden appearance of a new feature in evolutionary history, walls off language from the world of biology. Perceiving human language in its proper evolutionary context, and thus exposing it to the tools of comparative biology, will allow scientists to fully understand how language works and where it originated, Margoliash and Nusbaum conclude.

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Studies of human disease often work from the patient backwards - doctors and scientists take the common symptoms of a particular disorder and use them as clues to figure out what first went awry to spur the disease. For neurological diseases like Parkinson’s or amytrophic lateral sclerosis (aka Lou Gehrig’s Disease), symptoms and brain images have pointed the research at particular parts of the brain, which are then studied in animal models and on the genetic or cellular level. But disease research can also work from the other direction, where a particular cellular process is identified as a potential culprit in the disorder before a patient with that defect is even found.

That’s the case with a paper published this month by a team of University of Chicago researchers studying the cellular mechanisms that underlie diabetes. There are many types of diabetes mellitus, but all can be traced back to the hormone insulin - the body’s signal that cells should soak up sugar from the blood. Most cases of juvenile, or Type 1, diabetes result from the immune system erroneously attacking and killing the Beta-cells of the pancreas, which release insulin. Type 2 diabetes, which often develops in adulthood, results from a reduced sensitivity to insulin and/or a decreased release of the hormone.

But diabetes can also have a genetic origin, in some rare cases, when one of the genes involved in the secretion of insulin is disrupted. Previously on the blog, we’ve talked about the story of Lilly Jaffe, whose diabetes was found to be caused by a rare genetic mutation in a protein called a potassium channel, critical for the release of insulin. The mutated potassium channel seen in Lilly’s case interferes with the trigger of insulin release, causing lower amounts of the hormone to circulate through her blood. Thus, Lilly was treated by daily injections of insulin, until doctors at the University of Chicago detected the mutation and prescribed her a drug that directly targeted the potassium channel.

Now researchers at the University of Chicago have found another ion channel that must function properly for the right amount of insulin to be released. Only problem: there’s no patient.

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And so Neuroscience 2009 comes to an end, and it’s time to put away my badge, rest my weary feet and note-taking hand and think about biology below the neck again. Here’s the final installment of our live coverage, but come back tomorrow for a roundup of the conference with highlights, loose observations and links to other people’s thoughts on the conference. Thanks for reading!

2:30 PM - The Final Talk

The schedule may say that Neuroscience 2009 runs through the end of the day today, but judging by how many suitcase-toting scientists were jumping in airport cabs this afternoon, a small portion of the 30,000+ attendance makes it to the very end. Indeed, even the main stage ends its conference early, shutting down after a talk by Mt. Sinai School of Medicine’s Eric Nestler, an expert in the field of molecular psychiatry.

Nestler’s research focuses on the gritty details of how drugs of abuse change the expression of a person’s genes - yes, it was another addiction talk, and the former addiction researcher that I am, it was great to see the topic getting so much attention this year. In the addiction press conference I attended yesterday, Nestler hinted at a bombshell idea - frequent users of addictive drugs such as cocaine, heroin or alcohol may change the mechanics of their genes so permanently, the modifications could be passed on to their children. This “inheritable addiction” has already been observed in lab rats, Nestler said, mirroring similar results seen with the offspring of obese rats (which I talked about on Monday).

But that data must be too fresh for mass consumption, despite Nestler telling a roomful of reporters about it the day before. His talk today focused on the steps leading up to that discovery, carefully examining how repeated cocaine increases or decreases the activity of hundreds of genes in the reward pathway of the brain. Those long-lasting changes, which can cause cells of the reward pathway to actually grow and change shape, help explain why addiction is such a difficult condition to treat - it may require a complete re-re-structuring of the brain.

Much of the addiction research I’ve talked about this week has taken place in animals, but before Nestler’s talk, I came across a rare experiment that looks at the behavioral effects of a commonly-used drug in humans. It might seem strange that we know a ton about the specific genes that are up or down-regulated by cocaine, but not so much about its effects upon humans, but that’s due to procedural reasons - it’s quite hard to get approval for a study that gives illegal drugs to humans.

Michael Ballard, from the University of Chicago laboratory of Harriet DeWit, was trying to fill in at least one of those gaps in the research by testing the effects of THC (the active ingredient in marijuana) to presumably eager volunteers. Ballard then tested the subjects’ ability to judge facial expressions and determine the emotional content of pictures and personality trait words while they were under the influence of the drug. Interestingly, higher doses of THC caused the subjects to misjudge the facial expressions they were shown, suggesting an effect of the drug on social perception. The other tests were normal during the drug effect, but when brought back to the laboratory a week later, the subjects showed a decreased ability to remember neutral and negative personality traits, possibly indicating that their memories of the drug effect were biased toward happier stimuli. Ballard hopes to continue that research into other drug types - he’s currently testing amphetamine - to give the field of addiction research much-needed, laboratory-controlled human data to make sense of the flood of animal experiments.

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Laughter is almost universal. It’s an expression that is seen across all human cultures, babies begin to laugh within the first few months of life, and animals such as apes and even rats exhibit forms of laughter. The ubiquity of laughter suggests that it’s a behavior that dates far back in human cultural history and evolution – and that you might be able to trace laughter back to some of the most basic parts of our brains.

The neurobiological roots of laughter will be the focus of a lecture this Saturday by University of Chicago professor of neurology and psychology Steven Small built from the latest discoveries in brain imaging research. But Small’s lecture won’t be happening at the big Neuroscience meeting at McCormick Place, but as a special part of the Chicago Humanities Festival. Small, appearing from 10:00 – 11:00 Saturday, Oct. 17 at the Max Palevsky Cinema in Ida Noyes Hall, 1212 E. 59th St., said he will give a talk for non-scientists on the strange but primal act of laughing, including where it appears to be localized in the brain and what can happen to make this simple act go awry.

Small, whose own research focuses on the neurobiology of language, said he has not studied laughter himself, but found the behavior to be an intriguing example of the brain at work. Gathering material for his talk led him to discover popular 1920’s novelty records of people laughing, medical case studies of uncontrollable laughter caused by neurological diseases and tales of a contagious laughing epidemic in Tanzania that lasted as long as one week in some children.

For his lecture, “Humor Humours, Laughter and the Brain,” Small said he will focus on laughter itself and its relation to emotional expression, which is not always related to what people find funny – a distinction that actually makes neurobiological sense.

“Laughter as a response to humor is what we think of, but that’s not what laughter is. It’s a reflex.” Small said. “It’s a motor sequence and a sound sequence, and it can be produced by a mechanism that doesn’t even have to be controlled by the cerebral cortex. You don’t need to have a cognitive stimulus: I could tickle you, and you would laugh. It doesn’t have to have humor involved at all. Of course, its association with emotion, social exchange, and humor is what makes laughter in humans different from laughter in other animals.”
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The Nobel Prize Medal (from nobelprize.org)

The University hasn’t directly won any of the first two Nobel Prizes awarded this week, but one of today’s winners has a UChicago connection: George E. Smith, one of three scientists who will share the $1.4 million prize in physics, received his doctorate at the University of Chicago 50 years ago in 1959. And Monday’s prize has a much more tenuous connection to the proprietor of this very blog, which I’ll explain below.

First, today’s prize rewarded innovations that power technology integral to our daily lives: digital cameras and the Internet. Smith and Willard S. Boyle received the award for the invention of charge-coupled devices, CCDs, the technology put to work in the millions of digital cameras now in use. Charles K. Kao, the third recipient of today’s award, was responsible for improving the use of fiber optic cables, changing the material used in those cables to dramatically extend the distance that light can travel within. Thanks to Dr. Kao, I can quickly research this blog post and you can quickly read it, downloading the information through fiber optic cables that he helped create.

Monday, the award was given to three scientists who made crucial advances in the study of chromosomes, cancer and aging. No, it wasn’t Janet Rowley, but her friend Elizabeth Blackburn was one of the awardees alongside Jack Szostak and Carol Greider. The trio were honored for the discovery of telomeres, repeated sequences at the ends of DNA that prevent genetic material from being damaged and degraded every time a cell is replicated. There really is no better metaphor to explain the function of telomeres than the one used by the Associated Press all day yesterday: “It’s been compared to the way plastic tips on the ends of shoelaces keep the laces from fraying.”

In honor of their award, Scientific American republished an excellent article by Greider and Blackburn that explains why telomeres (and their enzyme partner telomerase, which preserves telomere length) are significant to the study of aging and cancer. As people and their cells age, telomerase works less efficiently, and telomeres and chromosomes shrink, making the cell replication process less accurate. The inability to create new cells could lead to conditions associated with old age, such as artherosclerosis and a weakened immune system. In cancer cells, on the other hand, telomerase is a bad thing, allowing tumor cells to replicate rapidly, grow, and spread around the body. Researchers have thus turned to telomerase inhibitors as a potential cancer treatment.

It is with tongue firmly in cheek that I note my nanoscale contribution to the field of telomere research, from my time at the National Institute of Child Health and Human Development in 2002. I worked in the laboratory of Jeffrey Baron, who studied mechanisms of bone growth in children. As humans grow, a strip of cartilage in the bones of arms and legs called the growth plate produces new cells that lengthen those bones; some time after puberty, those growth plates disappear. With Ben Nwosu and Ola Nilsson, we studied whether the telomeres in those growth plates grow shorter with age - I mostly helped by doing dissections on our chosen animal model, the rabbit, as we bantered about World Cup results. Somewhat unfortunately, we found that the telomere length does not change as a rabbit grows older, suggesting that telomeres are not responsible for the closing of the growth plate after puberty. But disproving a hypothesis is just as important sometimes as proving one, and we were able to publish the results in the journal Hormone Research.

So on behalf of telomere researchers the world over, I’d like to thank the Nobel Committee for their award. But I’ll happily defer the prize money to Blackburn, Grieder and Szostak.

Convincing people to stop smoking is no easy task, as family members or friends of smokers know all too well. But consider a situation where roughly three-quarters of active smokers find themselves ready to quit, willing to make that all-important first step of deciding to go smoke-free. When is this short window of vulnerability and motivation open? The time is when a smoker is in the hospital, said Dr. Lisa Shah, instructor in the section of hospital medicine at the University of Chicago Medical Center, a time when the patient is also surrounded by the infrastructure needed to nurture a desire to stop smoking into a successful change of behavior.

But Shah, a researcher focused on studying inpatient tobacco cessation, said in her Medicine Grand Rounds presentation Tuesday afternoon that many doctors miss this opportunity to help their patients kick a dangerous habit. In fact, it was right there on a slide titled The Missed Opportunity, which laid out why inpatients find themselves ready to quit: the no-smoking policies in place at hospitals*, the shock of being hospitalized for an illness that may be a direct result of smoking, and the isolation from environmental cues at home or work that may trigger the urge to smoke.

“For the smokers we see here, often one big barrier to quitting smoking is that they have family members and friends who also smoke cigarettes, Shah said. “Social smoking is a huge impetus to smoke, and makes it hard to quit. So hospitalization helps them succeed in quitting smoking without the temptation.”

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(photo courtesy hivresearch.org)

Rare Encouraging News in HIV and Parkinson’s Disease

HIV/AIDS and Parkinson’s Disease are two areas of medical research where good news is hard to come by, as researchers encounter countless setbacks in trying to translate promising laboratory findings into clinical practice. Both diseases have seen progress in the past decade in ex post facto treatments - preventing the maturity of HIV into AIDS with antiretroviral treatment or reducing the motor symptoms associated with Parkinson’s. But drugs that seemed to offer a cure for either disease, or in the case of Parkinson’s a mere brake to the progression of symptoms, have consistently disappointed in human trials.

That changed - slightly - this week, as two highly-publicized studies were published offering faint glimmers of hope on both disease fronts. Grabbing the most headlines was the first-ever demonstration of a successful HIV vaccine in a study conducted in Thailand but funded by the U.S. Army and the National Institutes of Health. The caveats are flying hot and heavy - the researchers saw only a 31% decrease in the number of HIV cases after treatment with a vaccine and a booster drug, one of the HIV strains protected against is specific to southeast Asia, and mystery lingers over why this particular combination of drugs was protective where so many others have failed. The two drugs used in the Thai trial - one a “primer” and one a “booster” - had themselves failed in previous large clinical trials. But the first small success in protecting against the deadly virus nevertheless encouraged many HIV/AIDS researchers; Dan Barouch, an immunologist at the Beth Israel Deaconess Medical Center in Boston, Massachusetts, told Nature “It’s the largest step forward that’s ever occurred in the HIV-vaccine field, but there’s a tremendous amount of more work that will need to be done.”

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The question was a welcome one, given the heated, exhausting health care debate that has raged through the summer: On the day after health care reform (whatever form it takes), what are the potential stumbling blocks and opportunities?

That’s how moderator Michele Norris (of NPR’s All Things Considered) thoughtfully began the panel at the University of Chicago-curated “Chicago Contributes” health care forum, held Thursday in Washington, DC less than a day after President Barack Obama’s speech to Congress. Reform supporters might consider that question to be a jinx as Obama and the Democrats struggle to find a consensus plan, but it allowed the forum’s panelists to clear the political fog and put the focus back where it should be - on the challenging questions of access and cost reduction that face modern American medicine.

After a keynote address by Kathleen Sebelius, Obama’s Secretary of Health and Human Services, echoed many of the points the President made himself the night before, the stage was turned over to a national group of university experts that were grappling with these issues long before health care became the season’s political hot potato. The importance of access to health care, not just insurance, was summarized nicely (and immediately) by Gerard Clancy, Dean of the University of Oklahoma-Tulsa College of Medicine: “If we have 40-50 million people now with health care coverage, who’s going to take care of them?”

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First of all: OUCH.

The rather painful X-ray to the left was taken from a 48-year-old patient who, it should be said immediately, survived his unfortunate encounter with a nail-gun and its 6-inch long projectile. But it’s what happened after the nail’s removal that merited the publication of this photograph in the medical journal The Lancet last month by University of Chicago doctors Babak Mokhlesi and Mohsin Khan.

Some time after the patient’s recovery from this very severe brain injury, he presented to the University of Chicago Sleep Disorders Center with hypersomnolence - sleeping, on average, 20 hours each day. The man’s sleep patterns were also unusual; he fell from the awake state into sleep faster, achieved REM sleep more rapidly than normal and woke up frequently during a 7-hour polysomnogram, or sleep test. Doctors were able to treat the man’s narcolepsy with methylphenidate (commonly known as Ritalin) and modafinil, two stimulants commonly prescribed to treat the disorder.

According to the article, the man’s hypersomnolence improved under medication. There was also a secondary side-effect of the gruesome injury - the man’s obsessive compulsive disorder “completely resolved.” read more

The committee members who make up the shortlist for the  Nobel Prize in Physiology or Medicine each year might want to start listing an unlikely trio of medical researchers: The Brothers Gibb, otherwise known as The Bee Gees.

Last fall, David Matlock, a medical resident with the University of Illinois School of Medicine presented a study at the American College of Emergency Physicians meeting that found listening to the Bee Gees’ “Stayin’ Alive” during a CPR refresher course helped doctors and medical students perform the lifesaving method accurately. Retesting the same subjects five weeks later, with the subjects instructed to replay the song in their heads, the doctors and students continued to show excellent CPR technique. Though Matlock’s proof appeared to be the first scientific study of Bee Gee-related emergency medicine, inside medical sources (i.e. my wife), say that the song has been an instructional CPR tool for some time. [Conveniently, the song is also a health threat in its own right. - ed.]

Since it’s already stuck in your head by now…

The song’s medical benefits had little to do with the soothing sound of falsetto harmonies or fond memories of John Travolta, but rather with the pace: “Stayin’ Alive” struts along at 103 beats per minute, very near the 100 compressions per minute recommended for CPR. As such, any 100bpm song would do, but the uplifting message of the Bee Gees chorus makes for an irresistible and memorable lesson.

That tempo was harnessed for the powers of health again recently, this time as a guide for  aerobic activity. Earlier this week, the website of the Department of Health and Human Services spotlighted a May paper in the American Journal of Preventive Medicine that found “Stayin’ Alive” sets the internal metronome for a healthy walking pace. Researcher Simon Marshall of San Diego State University determined that 100 steps per minute was the ideal rate for “moderate intensity walking,” which public health guidelines recommend adults do for at least 150 minutes each week. Therefore, humming the tune and making like Travolta is a low-budget solution for those unwilling to purchase a pedometer to track their feet.

“The tempo of it is such that – as with most disco music from the ‘70s – the beat is fairly consistent throughout the whole song, and most people find it hard to sit still to,” the pro-disco Marshall told HHS.

Of course, an anti-disco attitude can also help you burn off some calories, but may result in legal charges. If you’re planning on performing CPR or walking at a moderate intensity pace and can’t stand the Bee Gees (or just prefer “Night Fever”), here’s a list of songs that are exactly 100 beats per minute, so you’ll be even more accurate. Perhaps Ricky Martin’s “Shake Your Bon-Bon” suits you better? I won’t judge.

The Heliscope Single Molecule Sequencer

An idea that may be close to jumping from the world of science fiction to your local hospital is the concept of full, individualized genome scans - a personal genetic profile that could, at least in theory, help a doctor assess your risk for certain diseases and prescribe more effective treatment. That’s the prize a number of biotechnology engineers are currently chasing, producing a scientific race to invent quick, cheap and accurate sequencing machines that could open up a new world of genetic research and medicine. An important step was announced in that race this week, as a group based out of Stanford University detailed the sequencing of the 8th full human genome using a new machine with the delightfully sci-fi name of the Heliscope Single Molecule Sequencer.

The ultimate goal, laid out by the Genomics X Prize , is to invent a method that can sequence 100 human genomes in 10 days, at an average cost of no more than $10,000 per genome. The HSMS scan of Stephen R. Quake, one if the machine’s inventors, published in Nature Biotechnology this week, is said to have taken about two weeks and cost roughly $50,000 - still far from the X Prize standard. But by contrast, the sequencing of James Watson’s DNA in 2007 took 2 months and cost $2 million.

Kevin White, a professor of human genetics at the University of Chicago, said by e-mail that the HSMS demonstration was a “ a powerful demonstration of what can be done with the current technologies,” but points out that the Helicos sequencer is one of several machines, each with their own innovation that speeds up sequencing, to have hit the market recently. It’s also not a new effort: first proposed in a 2003 paper, the refrigerator-sized machine (which costs about $1 million) was used to sequence a viral genome last year.

However, White notes that even these new technologies are limited by the enzymes they use to indirectly deduce the ingredients of the DNA molecule. For the technology to truly achieve the speed and affordability necessary to be a clinical game-changer, White said, they must be capable of directly “reading” the base-pair language of DNA. 

“This ‘ultimate’ machine is what many of us are looking forward to, but in the meantime the current batch of next generation sequencers is enabling a vast array of new research to be performed by individuals or small teams of researchers who otherwise would not have access to genome sequencing,” White wrote. “Because of this, more focused and often more interesting questions are being asked than the days when genome sequencing was dominated by just a few centers. ”

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Gina Kolata has an interesting story in the New York Times today about the lack of volunteers for cancer research trials, but she left out a facet that has puzzled me: Even though few adults enter cancer studies, the vast majority of kids with cancer do get enrolled in trials. Why?

Kolata offers many possible reasons for the shortage of adult volunteers, including anxiety and a reluctance to make the extra office visits that a trial often requires. But those are factors in pediatric cancer too. And yet at least 75 percent of kids with cancer get enrolled in trials, compared with just 3 percent for adult patients. We did a piece recently for the University of Chicago Medical Center magazine describing how clinical trials have transformed pediatric cancer care for the better. Among other things, the studies probably raise adherence to treatment regimens because each center must document that participants follow the required course of therapy.

One likely reason for the adult-pediatric gap, as Kolata mentions, is that many adult patients are satisfied with existing treatments, especially for types of cancer with a good prognosis. If a regimen of surgery plus chemotherapy is likely to work, and patients can get the chemo at a local cancer treatment center, they’re less motivated to make the trip to a major research center conducting a trial.

But once again, the same factors could affect pediatric trials. Many pediatric treatments are highly successful, and parents would seem to have less incentive to enter their children in trials. Yet they do enter those trials, time after time.

Could one answer be that we adults are sometimes more hyper-vigilant about our children’s health than our own? Are we just more willing to suffer inconveniences for the sake of our kids? Perhaps entering a study that could result in extending the lives of other adult patients by a few months or years seems like insufficient payoff. But give those same months or years to a pediatric patient, and the calculus starts to look better, the time gained somehow more precious.

Maybe recruiters for cancer trials should try an experiment with prospective patients: Imagine you were making this decision not for yourself, but for your child. Would you be satisfied with the standard of care, or would you want to try something that might improve your child’s outcome, if only by a little? And if you would do it for your child (and most people do), why not do it for yourself?

One of the interesting riddles of evolution is how single-celled organisms became integrated into larger communities of cells, finally resulting in cumbersome creatures like us. But sometimes even we get glimpses of what life before the multi-cellular era might have looked like.

When cancer develops, the affected cells abandon the body’s well-regulated union and revert to form as freelancers. They become single cells with ravenous needs. Genetic mutations make those cells ditch polite conventions, like having the courtesy to self-destruct when they collect too many harmful changes. Immortal and more prolific than the surrounding cells, they gain an advantage and start undermining the body’s essential functions.

Here’s Dr. Ezra Cohen, a specialist in head and neck cancer here, explaining how Darwinian principles aid the study of cancer.