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.

It has been suggested that having a physician present during interrogations makes it safer for the detainee. Like a referee in a boxing match, if things get too dangerous, the physician calls off the interrogator and everyone steps back to their corners.

Keller says the presence of a health professional can actually be a “catalyst” for torture. The interrogator may think that someone else is responsible for stopping anything that exceeds the limits of safe interrogation, and the physician may hesitate to step in because he or she is there to serve the CIA in addition to monitoring the health of the prisoner, a situation referred to as dual loyalty.

Professional organizations differ on where the lines are drawn for military medical professionals. The American Psychological Association has taken some heat for not going far enough to prevent ethical transgressions.

Psychologists in military prisons have taken information obtained during detainee evaluations and drawn on their clinical insights and knowledge of behavioral science to make interrogations more effective. Keller recounted an instance of a prisoner named Youssef, held at Guantanamo, who asked to speak with a psychologist about his distress and his concern for a brother with leukemia. When the interrogations resumed, the focus shifted to threats of permanent separation from his family and his brother’s health.

The prisoner had been subjected to physical stressors, but he said that such psychological anguish was what caused him to “come undone,” Keller said. Youssef believed that his psychologist had violated his confidentiality so that interrogators could exploit the information.

Certainly it is hard to find sympathy for terrorists who support killing Americans, but Keller argues that this kind of torture happens to innocent civilians who are swept up along with terrorists. The physical and psychological effects are not limited to the detainee. They ripple through the community, which ends up putting the United States in a more vulnerable position and threatens our moral authority when trying to stop abuses in other countries, said Keller.

In a previous post, Rob wrote about stress, memory and studies questioning the value of information obtained by using torture techniques. A scientific article published in August by Shane O’Mara in the journal Trends in Cognitive Sciences (summarized nicely by Newsweek’s Sharon Begley), “reviewed neurobiological literature on what stress does to areas of the brain associated with memory and concluded ‘coercive interrogations involving extreme stress are unlikely to facilitate the release of veridical information from long-term memory, given our current cognitive neurobiological knowledge.’ In other words: torture isn’t just morally questionable, it’s also ineffective.”

Taking psychologists out of the mix may solve one ethical dilemma, but does not address the larger issue of the United States’ involvement in torture, according to Keller. Enhanced interrogation techniques are torture, and America should be held accountable for it, he said.

“I think a shift will happen, where ultimately the next time something happens we’ll say, alright, we are not going to torture, but I believe….In order to prevent this from happening again, we need to understand the dynamics,” Keller said. “This wasn’t just the Department of Defense, or just the Department of Justice, or just the Executive, it was a perfect storm of all of the above.”

Yeah, that’s not a typo. Before the Fore people of Papua New Guinea were known for kuru, they were known for “mortuary feasts,” where villagers would mark the death of a family member by consuming him or her. And not just a nibble here or there - according to a 1979 book by anthropologist Shirley Lindenbaum, “meat, viscera, and brain were all eaten.” That’s a good way to spread a disease caused by prions - the mechanism for kuru eventually discovered by Daniel Carleton Gajdusek in research that won him the 1976 Nobel Prize in Physiology or Medicine. Now, kuru continues to fascinate the scientific community, as a new medical paper presents how the savage disease caused rapid natural selection in Papua New Guinea, selecting for a gene variant that may offer clues to how to treat prion diseases with no known cure.

Prions are also the culprit behind bovine spongiform encephalopathy, better known as Mad Cow Disease, which is thought to have broken out in Britain due to cannibalistic feeding practices in cattle. In short, prion diseases are caused by misshaped proteins that are a bad influence on native prion proteins present in all species, causing them to change shape, clump together, and eventually kill the cell. So when a prion disease enters a person’s nervous system - by, say, eating a person with a prion disease - it tends to wreak havoc in the brain, producing the odd symptoms of kuru or BSE.

At the height of kuru, 1 out of 50 people in some Fore villages succumbed to the untreatable, fatal disease. Women and children tended to die more often from kuru, likely because they usually were given the brains to eat while the men got the good, meaty parts. But what about those who participated in the mortuary feasts, but never contracted the disease? Was there something genetically different about them that made them resistant? Sounds like a case for…evolution!

In a paper published today in the New England Journal of Medicine (presumably the only article in the issue where “cannibalistic mortuary feasts” appears in the abstract) , a group of scientists from London, Papua New Guinea and Australia announce a newly-discovered gene variant that appears to have protected certain people from the ravages of kuru. Most excitingly, that variant shows up at an unusually high rate in the villages were kuru once ran rampant - an fascinating, if tragic, case of natural selection in action.

Researchers sequenced the DNA of more than 2500 people from areas hit hard by kuru and nearby areas that were unaffected, and compared their genes for the native prion protein. Sure enough, one population of older women that survived the kuru outbreak and young people of their families possess a polymorphism that reflects two small changes in their native prion protein gene. These subjects are heterozygous - meaning they have two different copies of the gene - while homozygous subjects with two identical genes for the native prion protein were sensitive to kuru. The most striking statistic is that 75% of young people who came down with kuru were homozygotes, while only about 20-25% of heterozygous older women (who lived during the outbreak) were afflicted with the disease - and even then, it started much later in life.

Those statistics reflect natural selection in action: people resistant to kuru (heterozygotes) stayed alive and reproduced, spreading their variant of the gene to the next generation, while those sensitive to kuru (homozygotes), well, died. Eventually, the heterozygous population wins out - the high number of heterozygotes in this region of Papua New Guinea violates the Hardy-Weinberg equilibrium, which states that gene frequencies should remain constant in a population unless some external force is disrupting the balance.

Furthermore, the identification of a genetic change that makes native prion proteins resistant to the bad influence of prion diseases could help develop treatment for what are currently untreatable diseases. But much more research must be done to figure out how it’s so effective - and why it became such an advantageous target for rapid selection. Raymond Roos, a neurologist at the University of Chicago who studies misfolded proteins and prion disease (and who worked in the past with Gajdusek), said via e-mail that looking at how the kuru-resistant polymorphism changes the shape of the native prion protein - and how it subsequently interacts with “invading” prions - could explain why it is protective. An antibody to that part of the protein that is different in kuru-resistant people could prevent prions from clumping together, creating a new treatment for kuru, BSE, and other prion diseases, Roos speculated.

“Even when diseases are essentially eliminated, they offer lessons,” Roos commented.

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.

The Argument for Fewer Mammograms

- Breast cancer is rare in young women: The task force noted that a 40-year-old woman only has a 0.19 percent chance of dying from a breast tumor. That’s slightly less than 2 out of every 1,000 women. Mortality rates for breast cancer don’t rise significantly until after age 50.

- False positives can cause harm: In the hands of experienced mammographers, false positives are rare, but more frequent screens will necessarily create more opportunities for a misreading, especially in young women, where the rate is higher. False positives can create anxiety in the patient, and lead to expensive tests or procedures that may not have been necessary.

- Younger women are harder to diagnose: Also noted by the task force is that it’s hard to predict what small tumors caught at very early stages will do - it’s possible that costs and treatments will be accrued to fight a tumor that will never become deadly in the woman’s lifetime.

The Argument for Routine Mammograms

- True benefits remain: Despite their recommendations, the task force still found that mammograms in 40-something women are beneficial. Women who received regular screening were 15 percent less likely to die of breast cancer. And the mortality from breast cancer overall has dropped 30 percent since 1990, as previous panels recommended routine screening for younger women.

- Less frequent screening may not reduce costs: The task force argues that doing fewer screens for women in the 40s and half the screens in women above age 50. But some are skeptical of that calculation, arguing that less frequent screening will create both more false positives and later detection of tumors, removing at least some of that cost decrease.

- Changing the recommendations may confuse patients: Some doctors also argued that creating a conflicting message will only create more questions in the minds of women already flooded with information about breast cancer risks and prevention. “It’s really going to roll back the small gains we’ve made over the past 30 years,” Schmidt said. “Negative recommendations for this significant public health issue, in the absence of any meaningful viable alternative for reducing breast cancer mortality, have consequences.”

That’s been one of the questions studied in the Clinical Addictions Research Laboratory at the University of Chicago Medical Center, where director Andrea King has examined the phenomenon of alcohol-induced smoking. The studies put the spotlight on an interesting population of smokers - not the pack-a-day regulars, but those who smoke “socially,” a few cigarettes on nights out on the town with friends. That’s a demographic that hasn’t received as much study as addicted smokers, King said, in part due to psychiatric guidelines that classified people as either smokers or non-smokers with no space for people in the gray areas.

“Older studies wouldn’t even ask how frequently subjects smoked; if they smoke, they must be addicted, daily smokers,” said King, an associate professor of psychiatry and behavioral neuroscience. “But we see this percent that seems to be increasing in subsequent surveys…about 20-30 percent would be non-daily smokers. Some of these people may continue and become vulnerable to being a chronic habitual user, or this may be a new subclass of smokers.”

King was drawn to social, alcohol-induced smoking behavior when she was attempting to recruit heavy drinkers who were not smokers for a control group, a task she found exceptionally difficult. With rates of smoking among alcoholics as high as 75 percent, the non-smoking drinker was a rare breed, so King decided to flip it around to study what causes the two behaviors to frequently co-exist.

Behavioral studies in King’s lab confirmed that smoking increased people’s self-reported urge to smoke as well as the number of cigarettes actually smoked. But last week, the first jump from behavior to brain activation was published by King, with University of Chicago colleagues Patrick McNamara, Michael Angstadt and Luan Phan in the journal Neuropsychopharmacology. In the study, heavy drinkers (defined as consuming more than 10 drinks a week, including at least one “binge” session of at least 4 or 5 drinks) but light smokers (fewer than 50 cigarettes each week, with non-daily frequency) were given a Kool-Aid and ethanol mixture or a placebo drink, then placed in the fMRI machine and shown two types of pictures classified like an old restaurant’s seating plan: smoking and non-smoking.

The setup allowed researchers to test out two ideas about why drinking increases smoking behavior - the alcohol could make smoking cues more meaningful (the “Wow, that cigarette looks great” theory) or make people less inhibited (the “I wouldn’t normally smoke, but what the heck” theory). Or both, as the two theories are not mutually exclusive. Fortunately, both of those effects have been associated with particular brain areas - activation of an area called the ventral striatum is seen when people are craving drugs or other rewards such as food or sex, while decreased activity in an area at the front of the brain called the orbitofrontal cortex is associated with impulsive, less inhibited behavior.

Despite the intimidating setting of the fMRI chamber - a claustrophobic experience of being encased in a giant metal tube - subjects still reported an elevated urge to smoke for as long as 90 minutes after drinking alcohol vs. a placebo drink. That alone spoke volumes about how powerfully alcohol pushed people to smoke, King said.

“It’s so artificial [in the fMRI], but there’s still an increased desire to smoke as function of drinking or placebo,” King said. “It’s so robust, you don’t even have to be in a party or a bar.”

As the subjects sat in their tube craving a cigarette, their brains showed a ripple of activation that helped the researchers sort between theories of alcohol-induced smoking. Alcohol, by itself, increased activation in the ventral striatum, and when pictures of people holding, lighting or smoking cigarettes were shown, the striatum became even more excited. That offers support for the first theory - alcohol may make the sights and smells of smoking more appealing than they would be in otherwise sober conditions, leading casual smokers to bum a cigarette and light up.

Smoking bans may have pushed some of these cues away from social smokers as they sit inside the bar, but King said that their awareness of the crowd of smokers pushed outside to the sidewalk could be a subtle cue nonetheless.

“The ban is helping workers in the bar from being exposed to secondhand smoke, but it’s not necessarily changing behaviors,” King said. “After 4 or 5 drinks, activation in striatum will still make you want to go out outside and take your smoke. The cue two years ago might be a person right in front of you, but now you know they’re out there.”

Another recent paper from King’s lab suggested that men and women may be differentially sensitive to alcohol’s magnification of these social triggers - women given an alcohol drink reported an increased urge to smoke, but did not actually smoke more when given cigarettes in a laboratory setting. And the same study found that it may not be the nicotine that drinkers are craving, but something more abstract about the act of smoking - subjects who smoked while under the influence chose a regular cigarette and a denicotinized cigarette in equal measure. But characterizing what happens in the brains of people who smoke only on social occasions, rather than all-day, every-day, could help clinicians reach and treat a previously-unrecognized population of smokers that could still be risking serious health consequences.

“While someone who is a light smoker, or non-daily smoker, might believe they are reducing their risk for lung cancer, heart disease, and all the other aspects of smoking that prematurely kill people, this may not be the case. They may compensate on a subconscious level by inhaling more deeply or closing off the ventilation holes in a cigarette and exposure themselves to similar amounts of nicotine and cancer-causing chemicals as in regular daily smokers, ” King said. “There’s no such thing as a safe level of smoking.”

The “Speech Gene” Gains a Function

One of the more intriguing genes discovered since the flood of genetic sequences began to arrive at the beginning of this decade is FOXP2. Encoding for a humble transcription factor (sort of a DNA light switch), FOXP2 nevertheless gained lofty status when it was found in the late 1990’s to be associated with human language - one of the most complex behaviors of all. Previously associated with speech and language disorders in humans, FOXP2 gained steam when a team of scientists (including University of Chicago professor of human genetics Molly Przeworski) compared our FOXP2 with our close primate relatives and found only two amino acids different between the human and chimpanzee versions of the gene. With only 715 amino acids total in the FOXP2 protein, that small difference suggests a recent evolution event, which that research group estimated at roughly 100,000 years ago - right around the time that “modern humans” appeared on the scene. This has led some to conclude that this fortuitous small change in the FOXP2 gene is one of the key moments in our evolutionary history that separated man from beast.

But what exactly does FOXP2 do, and how could such a minute change mean the difference between chimpanzee grunts and Shakespeare? One way to answer that question is to put the human version of the FOXP2 gene into another animal, an experiment that was published earlier this year by a very large team of German researchers. That mouse didn’t suddenly start reciting soliloquies, but it did show differences in “ultrasonic vocalizations,” as well as cellular changes in a part of the brain associated with movement - which makes sense given that FOXP2 is thought to mediate motions related to speaking. Still, changing just one gene to the “human version” in an animal and leaving all the other mouse genes intact would presumably limit the impact of the human FOXP2 gene in changing the mouse brain. (Jerry Coyne wrote about the media reaction to this paper here)

Thursday, another group got down to the dirty details of the human FOXP2 gene, examining how the protein it encodes is functionally different from the chimpanzee version. Despite the small changes (again, the two genes are only 0.2% different), the number of genes that respond in different ways to human vs. chimp FOXP2 is over 100, a dramatic change in function. Interestingly, the human FOXP2 gene actually changes the expression of fewer gene targets than the chimp version - another blow to the idea that complex behavior must result from greater numbers of genes (fruit flies have twice as many genes as humans, for instance). Many of the genes that FOXP2 turns on or off have to do, unsurprisingly, with the development of the brain. But as for how that combination of FOXP2-related genes work together to help humans talk where other animals cannot remains unanswered. Hence the conclusion of an accompanying commentary in Nature by Martin Dominguez and Pasko Rakic that the paper “does what important discoveries usually do: it answers many questions, but raises even more.”

When Sleestaks Roamed the Earth

Lizard creatures are a fixture of science fiction from Land of the Lost to the recently-revived V miniseries to David Icke conspiracies. But until reading this post at Darren Naish’s Tetrapod Zoology blog, I had no idea that upright lizards have actually been floated as a scientific theory of what dinosaurs might have evolved into had they not been wiped out 65 million years ago or evolved into birds. Okay, it’s not really an accepted theory or anything - Naish, who studies the theropod dinosaurs that Canadian paleontologist Dale Russell based his intelligent “dinosauroid” thought experiment on in 1982, is clearly irritated by the premise. But the reason slightly disturbing upright humanoid dinosaurs are back in the blog conversation is because they were name-dropped by none other than Richard Dawkins in a recent Scientific American article about whether aliens would resemble humans.

Russell’s basic idea (and again, this is all in the territory of what-if speculation), is that a dinosaur called a Troodon, with a brain six times larger than the average dinosaur, might have eventually developed a human-size brain if not for that whole extinction thing. Russell decided to estimate what a dinosaur with a human-size brain would look like, and came up with something that looked very similar to the denizen of many a sci-fi movie (pictured above). Since then, paleontologists have dismissed Russell’s hypothetical “dinosauroid” as being much too human in shape, arguing that there’s no reason “intelligence” would necessitate human-like features of standing upright and the lack of a tail or long, toothy snout. 

On his blog, Naish points out that signs of intelligence have been observed in dinosaur descendants - we just know them as boring old birds. Birds such as parrots and crows can use tools, count and according to one recent paper, hold “funerals” for deceased relatives. Naish argues there’s no reason why standing upright on two legs should be considered the “best shape” for an intelligent organism with a big brain, it’s just the shape evolution happened to deal us. He also argues that Dawkins “should have known better” than to rely upon the poor, freakish dinosauroid even in the context of what is, for all intents and purposes, another scientific thought experiment. But I think it’s a pretty interesting cautionary tale about the difficulty of trying to predict what path evolution might take and a reminder that similar circumstances won’t necessarily produce similar creatures. Sorry, Sleestaks.

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.

Organismal biology can use the shared ancestry of species to answer questions about humans by conducting experiments in animals. Obviously, this is not a groundbreaking concept - research on lab animals such as rats and mice have been part of science and medicine for centuries. But while it’s generally accepted to study cancer in a rat, studying the syntax of language in a bird and extending those results to humans is a reach for linguists who believe human language to be unique or recently evolved.

“Dan and I have been amazed that even those people who readily acknowledge the importance of evolution in understanding language will restrict the evolution of language to the last few million years,” said Nusbaum, professor and chair of psychology at the University of Chicago. “In essence, by moving the developmental language past apes and saying there are no extant species besides humans who have that capability, that limits the comparative study of language to one species - which makes comparison impossible.”

But the more scientists look at animals that use vocal communication, the fewer items remain on the “human language is unique” list. One example from Margoliash and Nusbaum’s paper is “creolization,” the ability of children to create a new hybrid language from two different languages that still retains normal structure. This phenomenon is used as evidence for Chomsky’s universal grammar, the idea that humans (and only humans) share an innate template for language that is filled in by whatever language they grow up hearing.

But earlier this year, Olga Feher at the City University of New York found that zebra finches raised in isolation - who develop their own unique birdsong - are nonetheless able to tutor younger finches toward a “normal” birdsong. That’s evidence for an innate language template in birds, perhaps similar to the one that helps human children construct a language with normal structure out of erroneous input. Such similarities throw open the doors to further experiments that test the “universal grammar” of humans in a model species where more dramatic manipulations are possible.

“I wouldn’t say that birds have universal grammar,” Nusbaum said. “But we now have a model system to do very fundamental neurophysiological experiments.”

Jumping between species can push the science forward in many different ways, Margoliash and Nusbaum point out from personal experience. In 2000, Margoliash’s lab found that sleep helps zebra finches consolidate song learning from the previous day. That discovery led to a collaboration with Nusbaum’s lab, and the pair published a paper in 2003 with Kimberly Fenn that found sleep helped college students retain perceptual learning of computer generated speech, much like learning to understand a foreign accent.

“It gives us an enormous amount of power be able to look in a different kind of system and understand how sleep plays a neurophsysiological role compared to humans,” Nusbaum said. “Biology seems to find similar solutions to similar problems even when they occur in different species, and that’s information we can use in scientifically understanding  something like language.”

That is, until today, when University of Chicago researchers Jeanette Chung and David Meltzer published a letter in the Journal of the American Medical Association that measures the health care sector’s carbon footprint. By running the economic data about how health care spends its resources through a model, created at Carnegie-Mellon University’s Green Design Institute, that estimates the emissions of various greenhouse gases. Chung said she was surprised that nobody had run these numbers on health care effect, but thought it might have to do with the other priorities of the industry of late.

“In this country, the primary focus is on issues surrounding patient safety, health care quality, and cost containment at this current point in time. The health care sector, in general, may be a bit slower than other sectors to put this on their radar screen,” said Chung, a Research Associate in the Section of Hospital Medicine. “But given the focus on health care policy and environmental policy, it might be interesting - if not wise - to start accounting for environmental externalities in health care.”

In Chung and Meltzer’s analysis, health care accounted for 8% of the country’s total emission of carbon dioxide, methane, nitrous oxide and chlorofluorocarbons. That sounds pretty good - health care’s slice of the carbon pie only half the size of its slice of the economic pie - but Chung and Meltzer emphasize that such a huge contribution makes health care a ripe target for environmental improvement.

“If one sector is very large, even if it’s somewhat less carbon-intensive than others, simply the fact that it’s large means it’s a big target, and that’s the case with health care,” said Meltzer, Chief of the Section of Hospital Medicine, Associate Professor in the Department of Medicine, the Harris School of Public Policy and the Department of Economics.

“Obviously, health care and health is very highly valued; you’re not going to shut down a hospital because of its environmental impact or not produce a drug that you think is going to save lives because of carbon output,” Meltzer said. “But this reminds people in health care that we’re not a trivial part of the issue.”

Fortunately, the University of Chicago Medical Center has already been walking the walk on minding our effects on the Earth. Under the umbrella of the University’s Sustainability program, the Medical Center has put a number of programs in place to try and conserve waste and resources. Some of these efforts are as high-tech as the scientific research it supports - the diagram on top of this post isn’t from an immunology paper, it’s a diagram of the new microfiber mops the Medical Center uses to soak up pollen, viruses and bacteria.

Mark Lestina, the Sustainability Manager at the Medical Center, said that hospitals are a challenging place for conservation efforts do their unusual demands and schedules.

“Hospitals are very unique in the way they operate,” Lestina said. “We’re a 24/7 operation, so we need to keep our lights on all the time, our spaces cooled and heated all the time. We operate somewhat like a hotel in a way: people stay here, and we continuously use resources to make them comfortable.”

But Lestina, who first advised the Medical Center as a consultant in 2005 before being hired full-time in 2007, still found places to cut waste…and costs. When he first arrived, the Medical Center only recycled about 5% of its waste - it now recycles 26% percent. In the operating room alone, where sterile procedure tends to generate a ton of trash, Lestina helped institute a plastic recycling program that diverts more than 500 pounds of waste from landfills each day. And helpfully, all of this saves money - the monthly waste bill has dropped from $55,000 to $35,000 at the Medical Center, Lestina said.

“Sustainability does not necessarily just equal garbage and minimization,” Lestina said. “You’re incorporating energy efficiencies, saving water, using less, re-using more and so on, and it almost always leads to lower costs.”

It doesn’t take a PhD in neurobiology to conclude that slot machines are designed to lure people into a money-draining repetition, just as it doesn’t take expertise in the casino business to realize slots are absurdly profitable - there’s a reason why they outnumber table games 100-to-1. But I wanted to go back to the scientific literature to confirm a faint glimmer of information I retained from graduate school, specifically that slot machines are masterful manipulators of our brain’s natural reward system. Every feature - the incessant noise, the flashing lights, the position of the rolls and the sound of the coins hitting the dish - is designed to hijack the parts of our brain designed for the pursuit of food and sex and turn it into a river of quarters. Or so I remember.

Fortunately, there is a robust amount of research into why slot machines are so addictive, despite paying out only about 75% of what people put in. They are, some scientists have concluded, the most addictive of all the ways humans have designed to gamble, because pathological gambling appears faster in slots players and more money is spent on the machines than other forms of gambling. In Spain, where gambling is legal and slot machines can be found in most bars, more than 20.3 billion dollars was spent on slots in 2008 - 44% of the total money spent by Spaniards on gambling last year.

That data was published earlier this month by a psychologist from the Universidad de Valencia named Mariano Choliz in the Journal of Gambling Studies. Yes, such a publication exists! In the background of the paper, Choliz outlines the tricks that slot machines use to keep people feeding them:

• Operating on a random payout schedule, but appearing to be a variable payout; i.e. fooling the player into thinking that the more money they play, the more likely they are to win.
• “The illusion of control” in pressing buttons or pulling a lever to produce the outcome.
• The “near-miss” factor (more on this below)
• Increased arousal (where the sounds and flashing lights come in)
• Able to be played with very little money; the allure of “penny” slots.
• And perhaps most importantly, immediate gratification.

This last point is the subject of Choliz’s experiment, which puts a group of ten pathological gamblers in front of two different slot machines. One machine produces a result (win or lose) 2 seconds after the coin was virtually dropped (it was computer program), the other delayed the result until 10 seconds after the gambler hit play. In support of the immediate gratification theory, gamblers played almost twice as long on the 2-second machines than they did on the 10-second machines…even though the 10-second machines paid out more money on average!

Choliz concluded that the immediacy of the reward was part of what kept people at slot machines, making them so addictive. The quick turnaround between action and reward also allows people to get into a repetitious, uninterrupted behavior, which Choliz compares to the “Skinner boxes” of operant conditioning - the specialized cages where rats hit a lever for food or some other reward. It seems like a cruel comparison, but after my three days walking through the casinos, not an inaccurate one.

Another trick up the slot machine’s sleeve was profiled earlier this year by a group of scientists from the University of Cambridge. In the journal Neuron, Luke Clark and colleagues examined the “near-miss” effect, the observation that barely missing a big payout (i.e. two cherries on the payline while the third cherry is just off) is a powerful stimulator of gambling behavior.

The Cambridge researchers put their subjects in an fMRI machine to take images of their brains while they played a two-roll slot machine game. When the players hit a match and won money, the reward systems of the brain predictably got excited - the activation of areas classically associated to respond to food or sex I mentioned earlier. When players got a “near-miss,” they reported it as a negative experience, but also reported an increased desire to play! That feeling matched up with activation of two brain areas commonly associated with drug addiction: the ventral striatum and the insula (smokers who suffer insular damage suddenly lose the desire to smoke).

Clark and co. conclude that near-misses produce an “illusion of control” in gamblers, exploiting the credo of “practice makes perfect.” If you were learning a normal task such as hitting a baseball, a “near-miss” foul ball would suggest that you’re getting closer - it’s better than a complete whiff, after all. But for a slot machine, where pulling the lever has no impact on the rolls other than to start them moving and start the internal computer calculating, a “near-miss” is as meaningless as any miss.

Nevertheless, it’s this type of “cognitive distortion,” as Clark and colleagues name it, that makes slot machines such effective manipulators of our brains. Those massive, gaudy casino-hotels that I wore out a pair of shoes strolling through last week weren’t just built on a crafty use of probability, they were built on a exploitation of brain functions we are only just beginning to understand.

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.”

Seaberry, who first heard about the study on the news, was placed in the “lifestyle intervention” group, where subjects were given instruction and assistance from health professionals in improving their diet and exercise with the goal of reducing total weight by 7 percent. Looking back, Seaberry said she recalls how valuable that education and encouragement was to her health - she proudly says now that the only pill she takes is her daily vitamin, her morning eggs and bacon has been replaced by a bowl of oatmeal, and she walks five miles almost every day.

“I didn’t even didn’t know what a fat gram was, I would just eat,” Seaberry said. “It’s a beautiful life once you learn. So many people now are diabetic because of their lifestyle, what they’re eating and drinking. They say ‘you’re so silly to get up and walk,’ but I enjoy it. I’ll walk as long as I’m on the Earth, even though I’m 80 years old. I’m old, but I don’t feel that way.”

Nolan enrolled in the study with his brother, and was placed in the group receiving the anti-diabetes drug metformin. Though he was ultimately diagnosed with diabetes (under new, reduced guidelines for the diagnosis) two years ago, he has remained off of insulin and feels that the study delayed and dampened his disease. Not all of the lifestyle interventions have stuck - “the habits you get into are tougher to change,” Nolan said - but when he compares his health to his sister and mother’s issues before their early deaths, he said he felt like “something’s happened right.”

Nolan also wondered if the experience of him and others in the study could ultimately factor into the current national debate about the cost of health care.

“I think people are concerned about diabetes and one of the things that has to be looked at is what are we doing about it,” Nolan said. “My sister and mother both had extensive medical treatment at the end of their lives because of diabetes. Maybe one way to keep health care costs down is to educate people with these kinds of studies.”

In fact, one (impossible to implement) form of treatment that might lead people to healthier lifestyles and diabetes prevention would be to enroll everyone at risk into studies. Matulik said roughly a third of the original participants based at UChicago continue to keep their weight at the target level as much as 13 years after enrollment, while another third fluctuate between the target and higher weights. That’s an impressive figure, likely down to the quarterly health classes, check-ups and weigh-ins each subject undergoes - not to mention the firm encouragement of coordinators such as Matulik, who says she is known by the intimidating moniker of the “Margerator.”

Matulik said that Seaberry was a perfect example of the positive effect of simple lifestyle changes once they are assimilated into a person’s life.

“Everyone says know what supposed to do, they just don’t do it,” Matulik said. “For those that do it, who lost the 7 percent and kept it off, they are so routine now we don’t really have to do a whole lot with them - they walk no matter what, in the rain, snow, or cold.”

This train of thought stems from a study published last week by medical journal The Lancet, in which one of the largest diabetes studies showed (again) that changes in lifestyle are more effective than a leading medication in preventing the disease. Originally published in 2001, the Diabetes Prevention Program (DPP) followed more than 3000 people at risk for diabetes at hospitals across the United States as they underwent either a lifestyle intervention, treatment with anti-diabetic drug metformin, or a placebo treatment. After nearly 3 years of study, the authors reported that lifestyle changes (meaning diet and exercise to reduce weight) reduced diabetes incidence by almost 60%. Metformin also reduced the disease, but only by about 31% - results so strong that the authors stopped the study and began offering both treatments to everyone in their study.

But the study didn’t end, and the medical centers involved continued to monitor as many patients as were willing to stay in contact. All told, 2766 of the original 3234 participants continued to be monitored, allowing the publication last week of a followup study examining how many of these at-risk patients had developed diabetes 10 years after the original study began. What they found was somewhat status quo - after 10 years, the lifestyle group still showed twice the decrease of new diabetes cases than the drug group, 34% vs 18% lower compared to placebo. But that also means there was no difference in the number of new diabetes cases between lifestyle and drug groups in the 7 years between the original study’s end and the followup study’s end, which authors attributed to the mixture of treatments - the group receiving lifestyle interventions was now allowed access to metformin, and vice versa.

The University of Chicago Medical Center was one of the hospitals involved in planning and conducting this massive study, and I spoke over e-mail with David Ehrmann, professor of medicine and one of the Diabetes Prevention Program Research Group’s principal investigators.

Q: What is the importance of revisiting these patients ~7 years after the initial interventions?

Ehrmann: The idea is to look for durability of the effects of interventions, lifestyle vs. pharmacologic. The intitial study was short term. This study reports the long term results.

Q: What would you say the bottom line of the new study is for patients and doctors?

Ehrmann: I think that the persistent effects of interventions speak for the fact that lifestyle modification is the ideal manner by which to reduce the risk for development of diabetes among high risk persons. Alternate therapy would be metformin which is also effective, albeit to a lesser degree.

Q:  Did the results of the original DPP study impact clinical treatment of people at risk for diabetes? Is metformin commonly used for this purpose?

Ehrmann: Yes, the original study had a major impact on the way in which impaired glucose tolerance (also referred to as “prediabetes”) is perceived and treated. Until the results of the initial study were published, it could only be assumed that intervention would delay or prevent conversion to diabetes. The results nailed that concept and raised awareness both in the medical and lay communities about the importance of early diagnosis and aggressive intervention.

Q:  Do you expect the 10-year follow-up results to modify that clinical treatment in any way?

Ehrmann: They reinforce the initial findings and provide further evidence that intervention at an early stage of glucose intolerance is effective at reducing conversion to diabetes and further, that the intervention is durable.

Q:  Is there any other conclusions that patients or physicians should take away from this study?

Ehrmann: Patients and physicians should be overwhelmingly convinced that those at risk for diabetes should be tested early and, if found to have impaired glucose tolerance (also referred to as prediabetes), should accept the need for intervention with lifestyle and/or metformin treatment.