The massive, long-term Diabetes Prevention Program study has now found (twice!) that altering one’s lifestyle in terms of diet and exercise is more effective than a common prescription drug in delaying the onset of the disease. To power this study and its recently published follow-up, dozens of medical centers conducted multiple examinations each year on thousands of patients - 3234 in the first 3-year study, and 2665 in the 10-year follow. It’s impressive - and more clinically useful - to look at the summary data accumulated from this very large population of patients. But what kind of impact does a huge study such as the DPP have on the individual participants?

With help from Margaret Matulik, the DPP program coordinator at the University of Chicago Medical Center, I connected with a couple of the study subjects to hear about the lives behind the data points. Both Katherine Seaberry, 80, and Robert Nolan, 61, are from Chicago, and enrolled in the study in the late 1990’s. Both were also motivated to join the DPP due to their respective families’ experience with diabetes - Nolan’s sister and mother suffered from the disease and died around the age of 60, and Seaberry said her “whole family” has been diagnosed with diabetes.

“It saved me,” Seaberry said of her involvement with the Diabetes Prevention Program. “It’s amazing that I’m the only one in my family that’s not diabetic. If I wasn’t in this study, I think I would be diabetic by now.”

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The classic slogan for Lay’s potato chips is “Betcha’ can’t eat just one!,” and anyone who’s ever sat down with a new bag of chips and systematically worked their way down to the bottom of the bag in an almost hypnotic state knows the truth of that message. Portion size has been shown in many studies to be a contributor to overeating, as scientists find that people tend to eat the food that’s placed in front of them rather than stopping when their hunger is satisfied. Some might say this behavior is culturally programmed by millions of mothers telling children to “clean their plates” - a good strategy for broccoli, but a rather unhealthy one when faced with a heaping mound of french fries.

But there may also be a biological reason driving people to eat whatever amount of food is placed in front of them, to the detriment of their own personal health. Today in the Journal of Neuroscience, University of Chicago neurobiologists Hayley Foo and Peggy Mason publish experiments that indicate rats get into a zone while eating or drinking something they like that actually reduces their sensitivity to pain. While eating a chocolate chip or having sugar water or regular water infused into their mouths, rats are slower to move their feet away from a hot light-bulb than when they are not eating or drinking. The implication is that rats are so focused on finishing the food in front of them, they are less susceptible to distractions…such as, for instance, a hot foot.

“It’s a strong, strong effect, but it’s not about hunger or appetite,” Mason said. “If you have all this food in front of you that’s easily available to reach out and get, you’re not going to stop eating, for basically almost any reason.”

In the wild, where food is scarce, a resistance to distraction while eating is a good skill to have. If a wild rat is eating a hard-earned nut, it would rather ignore that mild pain in its foot rather than flee the scene and risk losing the nut to another hungry animal. But for humans in modern society, where the next meal is only as far as the nearest supermarket or McDonald’s, an unshakable focus on finishing the food in front of you and drowning out distractions (like a little voice inside your head reminding you how many calories you’re consuming in that Big Mac), is decidedly unhealthy.

“We’ve gotten a lot more overweight in last 100 to 150 years,” Mason said. “We’re not more hungry; the fact of the matter is that we eat more because food is readily available and we are biologically destined to eat what’s readily available.”

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In all the hubbub over the Nobel Prizes this week, we don’t want to overlook the prestigious scientific prize that University of Chicago researchers recently received. To celebrate this momentous occasion, here’s a guest post from John Easton, Medical Center director of communications.Every year around this time a memo goes out defining the precise role for each member of the communications team if a University researcher should win a Nobel Prize. But this year, some unanticipated laureates caught the team with their pants down.

Well, not actually pants, and not quite Nobel. The University boasts ties to more than 80 winners of the big one. But on Oct. 1, 2009, three employees won an Ig Nobel Prize for multifunctional underwear.

Back in 2005, a few incidents, plus many rumors, triggered widespread fear in the United States that terrorists could set off a radioactive material-dispersal device–AKA a “dirty bomb.” Elena Bodnar and Raphael Lee from the university’s electrical trauma program were already working on a World Health Organization (WHO) project to study the Soviets’ public health response to similar challenges after the Chernobyl disaster. The 600,000 workers who cleaned up after that event had no more radiation-linked disease, according to WHO data, than unexposed controls.

Why? Because they limited their exposures and wore masks to prevent inhaling radioactive particulates — standard practice. A well-designed mask that filters out aerosol particulates, in the right place at the right time, could save many lives.

Such a mask could have many applications. Nuclear accidents and dirty bombs are, fortunately, uncommon; lung damage from smoke inhalation in building or house fires is a major public health problem. But who plans for a house fire, much less a dirty bomb, or carries a mask at all times?

Enter a “garment device convertible to one or more facemasks wherein the garment device has a plurality of detachable cup sections,” patented by Bodnar, Lee, and Lee’s project assistant, Sandra Marijan. Patents have their own patois, but we’ll call number 7,255,627 the BraMask. “In one embodiment,” notes the patent, “the garment device is a bra or a brassiere garment… When both of the fasteners are released, the garment device converts into two facemasks, each facemask including a cup and the straps.”

The team partnered with Avocet Polymer Technologies, Inc., to prosecute the patent, refine the filtration material and design, and develop BraMask samples. The filters add only 25 cents to the cost. The device could potentially protect two people against smoke inhalation, a dirty bomb, and some forms of aerosolized biological or chemical warfare. Lee took patent, plan and prototype to an underwear maker.

As bras go, it was a tough sell. Maybe fire safety is hard to reconcile with lace. Maybe women would rather not cradle their glands in “a plurality of detachable cup sections” associated, however loosely, with bioterror. A mask that served as a shoulder insert for men’s suits and sport coats was similarly neglected. But the Ig Nobel committee immediately fastened on the BraMask’s brilliance, awarding it their top 2009 prize for public health.

In an acceptance speech, Bodnar proclaimed that “It only takes 25 seconds for any woman to use.” “Five seconds to convert and wear her own mask, and 20 seconds to wonder who the lucky man is to wear the second mask.”

For information about the grants that the University of Chicago received as part of the ARRA package, click here.

If the scientists you know have an extra spring in their step today, here’s why: over $5 billion in National Institutes of Health funding was announced this week, the scientific portion of the federal stimulus package passed in the spring. In his January inaugural address, President Barack Obama made researchers’ neck hair stand up when he promised to “restore science to its rightful place,” and this was the first installment of that pledge - a much-needed boost of cash after five years of flat NIH budgets put many laboratories in jeopardy.

“We’re announcing that we’ve awarded $5 billion — that’s with a b — in grants, through the Recovery Act, to conduct cutting-edge research all across America, to unlock treatments to diseases that have long plagued humanity, to save and enrich the lives of people all over the world,” Obama said Wednesday at an NIH event announcing the grants.

A $42 million slice of that $5 billion pie was awarded to the University of Chicago, and I’ve spent the day talking to some of the researchers who snagged the biggest awards. They are all, as you might guess, thrilled to have an infusion of money to help finally launch projects that have languished unfunded or undermanned. In all, more than 100 UChicago researchers shared in the $42 million pot, with grants ranging from $10,000 to $5.6 million. After the jump is some information on the day’s big winners and the projects their new grants will fund.

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Sam Volchenboum has his head shaved by Joshua Crosby, Sept. 24, 2009 (photos by David Christopher)

A researcher will do a lot for grant money, the fuel necessary to power a laboratory’s work. Sam Volchenboum, a pediatric oncologist at the University of Chicago Medical Center, took that adage to its follicular extreme last week, volunteering to go bald for funds from the St. Baldrick’s Foundation.

St. Baldrick’s, a California-based organization which raises funds for pediatric cancer research, asks their volunteers and award recipients to shave their heads in solidarity with cancer-stricken children who have lost their hair to chemotherapy. Thursday evening, Volchenboum went under the razor himself, shedding his dark brown hair with the help of Joshua Crosby, a 13-year-old cancer survivor. A small price to pay, Volchenboum said, for a $330,000 award that will help him design faster and more specific diagnostic tools for neuroblastoma.

“It can often take a while and be a little frustrating to get to the diagnosis,” Volchenboum said. “Despite all we know about this disease, even with aggressive treatment - chemo and radiation and surgery - over half of the kids will still die from their disease.”

Despite what its name implies, neuroblastoma is not brain cancer, but rather a cancer of the sympathetic nervous system that connects the spinal cord to organs of the body. Though it’s rare as far as diseases go - with only about 800 new cases a year in the US - it’s nevertheless the most common solid-tumor cancer seen in children and is responsible for about 15% of childhood cancer deaths. But not all neuroblastomas are fatal; in fact, some tumors in infants even regress spontaneously without treatment. That wide variation in prognosis presents a challenge to oncologists, Volchenboum said, who must decide the best course of treatment for a child with neuroblastoma, doing as much as possible to attack the tumor without over-treating with therapies that can be toxic and harmful in an adult, never mind a growing kid.

“We need to be able to sub-stratify the patients to predict outcome better,” Volchenboum said about the goals of his project. “There are probably some patients that will do poorly despite any conventional treatments, so let’s give this patient emerging therapy, let’s try something new. Likewise, there are some patients with apparent high-risk disease who get lots of therapy and are ultimately cured but may not have needed all that therapy.”

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Dr. Funmi Olopade and Dr. Mary Ann Malloy at the Harold Washington Public Library in Chicago, September 22, 2009 (photo by Rob Mitchum)

On Monday we previewed Dr. Funmi Olopade’s public lecture at the Harold Washington Public Library in Chicago titled “Nature, Nurture and Breast Cancer.” For that post, I talked about some recent work from Olopade’s research group that compared the types of breast tumors found in West African women with the tumors seen most often in black and white American women. That research indicated that there likely is a genetic difference between women of African origin and Caucasian, North American women that leads to fewer breast cancer cases but a  higher rate of aggressive, harder-to-treat tumors in black women here and abroad. But the patients from Senegal and Nigeria which Olopade’s group studied also showed different proportions of tumors when compared to African-American women, suggesting a strong role for environmental factors in causing breast cancer as well.

In her library appearance Tuesday evening with NBC reporter Dr. Mary Ann Malloy, Olopade expanded upon those mysterious “environmental factors” that likely contribute to the higher breast cancer numbers in North America. To a rapt audience, Olopade listed off the most well-known and common risk factors for breast cancer: age, family history and “the most important risk factor,” being a woman.

(Chicago Public Radio’s Chicago Amplified is supposed to post audio from Tuesday night’s event, but it’s not up yet. I’ll add a link when it’s available.)

But even to a crowd that, judging from their questions, was very well informed about breast cancer medicine and science, Olopade inspired gasps of surprise by rattling off some less-publicized environmental factors: breastfeeding, age at childbirth, even height. Many of these factors, in combination with more mundane things like lack of moderation in diet, exercise and alcohol intake, are behaviors more commonly seen in rich countries where women have achieved a more equal status in their work and private lives.

“I think what we’re still struggling with is, as we get more affluent and as people live the good life, then you see the rising incidence of breast cancer,” Olopade said. “We want people to have the good life, but what is it about the good life that is predisposing us to breast cancer?”

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A three-dimensional image of a "BK" cellular ion channel (Yale University/Futurity)

I apologize for the lack of a Linkage post last Friday - instead of blogging, your editors were learning about Chicago’s downtown architecture as we floated along the green if not Green Chicago River on one of summer’s final days. But like the reversed flow of that waterway, the science never stops, and last week saw the official launch of a new source for science news: Futurity.

Disclosure alert: the University of Chicago is one of the contributors to Futurity’s content, and our esteemed paleontologist Paul Sereno’s new “punk-size” T-Rex spent much of last week as the site’s featured story. But as both producers and consumers of science writing, we’re genuinely excited about the site, which will aggregate articles from an initial pool of 39 universities in an attempt to the gap left by shrinking science and medicine staffs at newspapers and television stations. With reduced space and time for science stories in the mainstream media, the news offices of these universities have taken it upon themselves to bring their science to the public directly, sometimes by employing refugees from those very same shrinking science staffs.

Yes, that largely means publishing press releases, though it must be said that many press releases are now themselves written and laid out like a news article, with an eye-catching lead, quotes from researchers and outside sources, historical perspective and photo or graphic art. Sites like ScienceDaily and Eurekalert are well-known depositories for these releases, but can be sensory overload for the casual reader with hundreds of new releases posted to the site each day. Futurity looks like it will filter out some of the noise and present the most exciting research in an aesthetically pleasing manner, with the hope that general audience readers, not just other science journalists and news office personnel, will find it entertaining and informative.

The site had a soft launch in the spring and went full-on live last Tuesday, so there’s already been a bit of attention paid to it by sites such as Inside Higher Ed, the San Jose Mercury News, and the Columbia Journalism Review. Skeptics note, appropriately, that there is a certain preaching-to-the-niche quality, where only people actively seeking out science news will be exposed to science news. But through deals with wider-audience news aggregators like Google and Yahoo!, the hope is that a casual reader will be distracted by interesting science news on their way to sports scores or celebrity gossip, just like they used to do in a newspaper.

Here are a few of the Futurity stories that caught our eye in the website’s opening week:

• Scientists cure color blindness in monkeys with a human gene (University of Washington)
• Using Legos to model nanobiology (Johns Hopkins)
• Thin, overeating friends can inspire unhealthy eating behavior (Duke; with a slick YouTube video that makes us very envious)
• Using trees to generate electricity (University of Washington)
• An “open-source” camera with a brilliant name: Frankencamera (Stanford)

Dr. Funmi Olopade

A fact often lost in the charity walks and commercials that have dramatically raised awareness of breast cancer over the past two decades is that beneath the diagnostic umbrella of  “breast cancer” are numerous types of tumors. Other than the fact that all of these tumors are found in breast tissue, different forms of breast cancer grow at different rates, will express different types of hormone receptors or genes that can act as drug targets, and are more or less likely to become “invasive,” spreading throughout the body. To complicate matters further, not every population experiences these different types of breast cancer in equal proportions - black women in the United States have a poorer survival rate for breast cancer than white women, and women in Africa  have an equal breast cancer mortality rate to North American women despite four times as many diagnoses of the disease in the U.S., Canada and Mexico.

University of Chicago Medical Center researcher Olufunmilayo Olopade (Funmi, for short) has dedicated her career to the study of these discrepancies since moving to Chicago from her home country of Nigeria in the 1980’s. Olopade, a professor of medicine and human genetics, has received several accolades for her work, including the prestigious MacArthur fellowship (known sometimes as the “genius grant”) in 2005. On Tuesday evening, she’ll give a lecture at the Harold Washington Library Center in Chicago titled “Nature, Nurture and Breast Cancer” that will explain what we know about the genetic and environmental factors that cause the disease in more than 200,000 American women each year.

In a recent Journal of Clinical Oncology paper, Olopade and colleagues from Chicago, Senegal and Nigeria looked for physiological reasons to explain the differences in breast cancer rates and outcomes between American and African populations. Learning more about these differences could help direct women into the most effective treatments for their particular type of breast cancer, Olopade said, as well as offer clues as to how genes versus the environment cause breast tumors to arise.

“Breast cancer doesn’t affect all individuals the same way,” Olopade said this past weekend, as she prepared for Tuesday’s lecture. “What we found is that the types of cancer that people get in different populations differ, that’s why when we talk about personalized medicine at an individual level we also have to talk about it on a population level.”

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A relatively simple food web, believe it or not. (from Allesina & Pascual, 2009)

Ecologists drifted long ago from the simplistic model of the food chain to food webs, intricate, multi-tendril interactions between species that paint a more accurate picture of an ecosystem’s network. But, as with most sciences, as the models become more complex, so too does the analysis required to answer questions about the role each animal plays in an ecosystem. In a chain, if you remove one piece, the whole network falls apart. But how do you rank the importance of organisms in a system that looks like the tangle of wires behind an entertainment center?

Stefano Allesina, a brand new assistant professor in the University of Chicago Department of Ecology & Evolution (like, really brand new, as in moved into town last week) found the answer to this question in a brand name rapidly taking over our lives: Google. Specifically, he got a hunch that the algorithm Google uses to operate its search engine could be turned into a tool for detecting what species are most integral to an ecosystem’s health.

“One of the main problems in conservation is to forecast what’s going to happen if the species we are looking at is going down or going toward extinction,” Allesina said. “This single extinction can cascade in the loss of other species that are apparently unrelated, because all things are interdependent and it’s a very complex machinery. Or you could take away one piece and maybe the whole thing will reshape itself.”

So Allesina, and his collaborator Mercedes Pascual from the University of Michigan, constructed a computer model, published earlier this month in PLoS Computational Biology, to find vulnerabilities in an ecosystem. As Allesina describes it, they tried to help the cause of conservation by looking for the best way to destroy an ecosystem.

“How can we damage the network in the fastest possible way? How can we take away the most important species first so we can make the whole system collapse? It’s the best solution, but it’s actually not very good for the environment,” Allesina laughed.

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In each cell of the body is a busy factory, containing all of the elements needed for that cell to develop and perform its unique function. A neuron sprouts a long extension and develops the ability to conduct electrical impulses. A liver cell secretes bile and can absorb toxic substances to neutralize them. Muscle cells elongate, form multiple nuclei and build long fibers that contract powerfully when stimulated.

But as different as the end product may be, the machines that make up the inner workings of these cells are largely the same, built from the identical set of genetic instructions that all cells share. Indeed, all of the body’s hundreds of cell types originate from one ambitious type of cell with the potential to become almost anything – the pluripotent stem cell to which so much scientific attention has been recently paid. What destiny that neutral cell follows is largely determined by how it organizes its factory, placing its machines in various orders that can have dramatically different outcomes.

Charting those interactions in specialized cells is a frequent goal of scientific research, as understanding a cell’s inner workings will help doctors make repairs when something goes wrong. The laboratory of Dr. Marcus Clark, chief of the Section of Rheumatology at the University of Chicago Medical Center, has devoted itself to the machinery of the B cell, the immune system cells responsible for producing antibodies that fight off disease. In a paper published this week in the journal Nature Immunology, Clark’s group fills in much of the story of what signals are involved in a crucial step of early B cell development, and shows that one of those signals, called Ras and typically associated with cancer in other cells, is surprisingly a key component in the healthy formation of a B cell.

“Ras is one of the best described oncogenes out there, it contributes to cancer in a variety of different formats.” Clark said. “It’s always seen as this pro-proliferative thing: if you put Ras in, the cells start dividing autonomously, and that’s cancer. In our hands, Ras turned off proliferation, it was very unexpected.”

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The development of the human brain is a massive biological construction project that scientists are still only beginning to understand. From the first few cells of the human embryo, billions of neurons and glia cells must be formed and positioned in exactly the right place with all of the proper connections. Hundreds of genes, chemical signals and growth factors have been found to be foremen and tradesmen on this neurological construction site, and if any one of those workers doesn’t show up for work or does their job incorrectly, the consequences can range from severe mental retardation to prenatal death.

That incredible feat of engineering is the backdrop for a new paper published online Sunday in Nature Genetics by a team of scientists and clinicians led by Kathleen Millen, assistant professor human genetics at the University of Chicago, and William Dobyns, a professor of human genetics, neurology and pediatrics at the University of Chicago Medical Center. For the last 8 years, Millen and Dobyns have been looking at a case where the brain’s construction goes awry: a common birth defect of the brain called Dandy-Walker malformation (DWM). In 2004, they found the first two genes that contribute to some children born with DWM, which can lead to motor delays, mental retardation, hydrocephalus and autism. In their new paper, a third gene is implicated in the development of DWM – and it was not one that the authors expected to find.

The researchers found that people with a missing or defective version of a gene called FOXC1 exhibited the characteristic deformity of Dandy-Walker: an improperly formed cerebellum, the region at the back of the brain that controls coordination, balance and other motor processes. But FOXC1 is not a likely culprit for a brain disorder, as it’s never actually expressed in the brain. Instead, it shows up in embryonic tissue called mesenchyme, which later develops into the skull and membranes that wrap around the brain.

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Decades of research advances have made depression less mysterious and less stigmatized in most circles, accepted as a neurobiological disorder rather than a more abstract (and untreatable) entity. But some news about depression remains surprising, at least to people outside the realm of psychiatry. Tuesday’s newspaper had one such example: a new study out of Washington University in St. Louis following a group of clinically depressed and young – very young – children, between the ages of 3 and 6.

Diagnosing a preschool child with major depressive disorder was a new concept to me. But it turns out that it’s relatively old news to psychiatrists, who have been studying the diagnosis and treatment of early childhood depression cases since at least the mid-1980’s. Prior to that, even practitioners  had trouble grappling with the idea of toddlers and kindergartners suffering from a traditionally “adult” disorder like depression, said Sharon Hirsch, section chief for child and adolescent psychiatry in the Department of Psychiatry and Behavioral Neuroscience at the University of Chicago Medical Center.

“People used to have a different concept about kids,” Hirsch said. “They figured, from a developmental point of view, that if you didn’t understand abstract concepts – if you only knew right and wrong, black and white – you didn’t have to worry about the larger concepts in life. Therefore, you weren’t really capable of becoming depressed, because you were only focused on food and basic necessities, which are all provided for you, so what is there to get depressed about?”

But as theories of depression focused less on psychoanalysis and more on neurochemical causes, researchers began asking whether the brains of very young children might be vulnerable to mood disorders such as depression. They found that depression does strike kids, but it takes distinct physical and emotional forms.

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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?

The Chicago Tribune’s new medical reporter Trine Tsouderos (my successor at the paper) has a must-read article in today’s Trib about misguided efforts to use the “chemical castration” drug Lupron as a treatment for young kids with autism. It’s part one in a two-part series, with contributions from an all-star cast including veteran national reporter Tim Jones and investigative reporters Patricia Callahan and Steve Mills.

I can’t say enough good things about the piece. It draws on an impressive array of endocrinologists and pediatricians who attest that the children being treated are not suitable for the testosterone-lowering drug. Bonus: They quote the brother of the actor who plays “Borat,” noted Cambridge University autism researcher Simon Baron-Cohen.

The father-and-son physician team who developed the suspect protocol claim that many experts back their approach, including Baron-Cohen - but Baron-Cohen delivers a stinging rebuke of their reliance on Lupron: “The idea of using it with vulnerable children with autism, who do not have a life-threatening disease and pose no danger to anyone, without a careful trial to determine the unwanted side effects or indeed any benefits, fills me with horror,” Baron-Cohen said. So much for that endorsement.

One of the best things about the piece that it gives both sides room to make their case without falling into a “he said/she said” routine, which would not reflect the consensus against using this therapy. Autism is a terrifying condition, but that doesn’t justify trying powerful treatments without evidence that they will work safely. These physicians claim to have seen some effect in patients, but that’s not surprising - any potent drug with psychiatric effects could influence a child’s behavior in the short term. The article indicates that the daily dose the doctors use for autism patients is 10 times the normal amount typically given for children with early puberty. With that kind of dosage I’d be surprised if there weren’t some psychiatric effect. But that doesn’t mean it’s the right effect, or that the drug is safe for children. Only a trial can determine that.

So kudos to Trine, and to the Tribune for giving these careful reporters the time and space to explain a difficult issue and a treatment that could put kids at risk. It’s a heartening sign during a gut-wrenching time for newspapers. I can’t wait for part two.

News outlets reported this week on a new JAMA study showing that having a heart defibrillator implanted by an electrophysiologist produces fewer complications for patients than if a doctor outside that specialty does the procedure.

I asked Martin C. Burke, DO, to comment on the article and the background that makes this important for patients and physicians, and he graciously agreed. Here is Dr. Burke’s post:

The new JAMA article regarding physician certification for implantable cardioverter defibrillator (ICD) implantation and patient outcome is interesting to me as a practicing electrophysiologist, or electrician of the heart, as well as a trainer of the next generation of electrophysiologists.

In 2004, the medical society that represents the heart electricians called the Heart Rhythm Society or HRS published criteria for certification that allowed non-electrophysiologists to implant ICDs without going through the rigors of a fellowship in clinical cardiac electrophysiology.  The electrophysiology fellowship training pathway provides a one- or two-year intense exposure to the management of heart rhythm disorders as well as training in the complex interventional procedures such as the ICD implantations and more complex cardiac resynchronization ICD implantations mentioned in the JAMA article.  The HRS certification criteria for non electrophysiologists has been used by hospitals and third-party payors to allow non-electrophysiology board eligible or certified physicians to get credentialed by hospitals to implant and get paid for such implants.

At the time of the publication of the 2004 paper, the membership of  the heart rhythm society was mystified as to why our own society would sanction such a document and essentially ‘throw under the bus’ our training pathway in heart rhythm disorders that we take quite seriously.  We as the heart rhythm society and I as a trainer of electrophysiologists have spent the last 20 plus years advancing the science and application of such devices in a methodical and expert way.  So, the logical deduction is that this policy has been the agenda of the device manufacturing companies who felt that there weren’t enough cardiac electrophysiologists to meet the needs of the public indicated for such devices.  

This is an incendiary topic as the financial implications at stake are large for all parties. Consequently there has been great controversy within the HRS membership, and it has recently bubbled into a call for our medical societies to sever all relationship with industry, a typically American over-reaction. Industry working with clinician scientists is of huge value to society at large as long as it is disclosed and managed ethically.  Of more concern to me are cases where study authors do not disclose potential conflicts of interest - a practice that remains distressingly common.

Still, patients should be assured that in science, the true path eventually becomes evident and now patients can move forward with expert device implantation and management with the best-trained physicians in the world to do so: the clinical cardiac electrophysiologists.