If you called someone a rat, they probably wouldn’t take it as a compliment. But in a clever new study published today in Science, a team of University of Chicago neurobiologists show that rodents could serve as role models for how humans should behave. Rats were given a difficult choice between heart and stomach: either open a container of chocolate chips and enjoy the feast, or free a companion and share the chocolate chip bounty. The results argue that humans aren’t the only species to feel empathy for the distress of another and act upon it, suggesting a deep evolutionary basis for helping your fellow creature.

When Inbal Ben-Ami Bartal was a master’s student in Israel researching immunosuppression after surgery, she noticed a strange phenomenon in her laboratory rats. When rats were brought to the room where she regularly conducted surgical procedures, they grew extremely agitated.

“It was very obvious that rats could sense what was going on with other rats,” Bartal said. “They freaked out and were affected by the emotional state of the other rats once they were removed from the cages.”

Other researchers had previously noticed this phenomenon in both humans and animals and gave it the name “emotional contagion,” describing when the distress or pain of one individual spreads to others. In 2006, Jeffrey Mogil of McGill University found evidence of this effect in mice, observing that when one mouse is given a mildly painful stimulus, a second mouse viewing the first mouse’s pain will exhibit increased sensitivity to pain. When that paper was published, it was considered by some to be the first evidence for empathy in a rodent. But Bartal, having started as a graduate student advised by Jean Decety, Irving B. Harris Professor of Psychology and Psychiatry at the University of Chicago, wanted to find more definite proof of rat compassion.

Collaborating with the laboratory of Peggy Mason, professor of neurobiology, Bartal designed a test to see whether emotional contagion could actually drive a rat to take action. Two rats who live together in the same cage were placed in a special arena, with one held in a transparent, tube-shaped restrainer and one allowed to roam free. The restrainer’s door could be opened by a nudge from the outside, though the free rat - at least initially - didn’t know that. But after several sessions where the free rat was visibly agitated by his trapped companion’s distress, he figured out how to pop open the restrainer. As you can see in this video from Science, once the free rat learned this trick, he would take action almost immediately upon being placed in the arena during subsequent sessions.

“We are not training these rats in any way,” Bartal said. “These rats are learning because they are motivated by something internal. We’re not showing them how to open the door, they don’t get any previous exposure on opening the door, and it’s hard to open the door. But they keep trying and trying, and it eventually works.”

Proving that the free rat’s actions were motivated by empathy required more experimental conditions. When the restrainer was left empty, or when researchers put a stuffed toy rat in the tube, the free rat showed no interest in opening the restrainer door. He did, however, when the arena was rigged so that opening the restrainer released the trapped rat into a separate compartment from the free rat, showing that the free rat was not motivated by the “reward” of social interaction. The experiments left behavior motivated by empathy as the simplest explanation for the rats’ behavior.

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Loneliness has had a tough run of late, with a growing body of research blaming it for everything from high blood pressure to heart disease to depression and cognitive decline. The research group of John Cacioppo, director of the Center for Cognitive and Social Neuroscience at the University of Chicago, has been among the leaders in leveling these medical charges against loneliness. But one missing piece of the puzzle remains - what biological mechanism connects a person’s feelings of inadequate social contact with the negative health outcomes? A new collaboration with epidemiologists and geneticists at the Medical Center suggest that the missing link might be in the bedroom.

For decades, professor of human genetics Carole Ober has studied a unique society called the Hutterites [pdf]. A religious group that originated in the 16th century, the Hutterites have formed several communal farms in the United States where some 150 people live and work together. The stability and isolation of the Hutterites make them a perfect population for studying the interplay between genes, environment, and disease - the mission of Ober’s research. Those qualities also made them the perfect group of people for a team lead by Lianne Kurina, assistant professor of epidemiology in the University of Chicago Department of Health Studies, to test the link between loneliness and sleep quality.

The new study, which appears in the journal Sleep, is not the first to examine this connection. A 2002 study led by Cacioppo used the most accessible pool of subjects on a college campus - college students - and found that those who scored higher on a psychological loneliness test displayed reduced sleep “efficiency” with no change in sleep duration. In other words, the loneliest subjects slept just as long as their socially satisfied peers, but suffered more “microawakenings” and lower sleep quality.

Because college students reflect only a narrow band of society, it was important to replicate the result in an entirely different population. Enter the Hutterites, who were also tested using a loneliness scale and asked to wear wristband sleep monitors to track their activity during sleep. Because of their communal lifestyle, even the loneliest Hutterites were less lonely than the general population. But the same correlation was detected between loneliness and sleep quality - for each point increase on the loneliness scale used to test the subjects’ social feelings, the researchers observed an 8 percent increase in sleep fragmentation. Furthermore, the lonelier Hutterites did not themselves report poor sleep or daytime sleepiness, indicating that the effects are mostly subconscious.

“Loneliness has been associated with adverse effects on health,” Kurina said in a press release. “We wanted to explore one potential pathway for this, the theory that sleep - a key behavior to staying healthy - could be compromised by feelings of loneliness. What we found was that loneliness does not appear to change the total amount of sleep in individuals, but awakens them more times during the night.”

The evidence is still not strong enough to conclusively place sleep deficits as the intermediary between loneliness and poor health. As the paper admits, the opposite relationship could be true: sleep fragmentation could increase feelings of social disconnection. But a flood of recent evidence, much of it from the University of Chicago Sleep, Metabolism, and Health Center, suggests that the third of each day we spend sleeping can dramatically affect several different aspects of our health, including diabetes, obesity, dieting success, and testosterone levels. Certainly, the newly replicated connection between a lonely heart and restless nights offers an intriguing theory for future study.

But why would feelings of social inadequacy disrupt a person’s time in bed?

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Loneliness can be deadly. In humans, there is a statistical relationship between social interaction and mortality - the more isolated you are, the lower your chances of living a long life. Rats kept in social isolation their entire life die at a younger age than littermates who lived in groups closer to their natural social structure. But how exactly does isolation kill a rat? Under normal conditions, an infectious disease such as pneumonia is typically the cause of earlier mortality in a lonely rat. But when rats are kept in the sterile conditions of a laboratory animal facility, the cause of death is something quite surprising: breast cancer.

Those experiments - conducted by the group of Martha McClintock, professor of psychology at the University of Chicago - sparked a fruitful collaboration between McClintock and Suzanne Conzen, professor of medicine and a cancer expert. Last week, McClintock and Conzen gave a tag-team talk at the Chicago Breast Cancer SPORE seminar to present an overview of their research into the connection between social isolation, stress, and breast cancer, a line of study that could flip the current thinking about the disease. Traditionally, the psychological and social effects of breast cancer are considered to be the consequence of its diagnosis and treatment, but the research of these two laboratories suggests that these factors could be a cause as well, just as much as genetics or other biological sources.

“What I brought to the classic traditional approach is trying to flip it on its head,” McClintock said, “where you recognize that there are truly social forces which then change the psychological states of individuals in those interactions, and in turn their hormone function, cell receptors for those hormones, and then ultimately changes in gene expression.”

The link between the two labs was made over a hormone known for its role in stress responses, cortisol. McClintock observed that solitary rats behaved more anxiously than their group-housed peers, and found that they exhibit a larger and prolonged cortisol increase after a stressful event. Conzen’s laboratory was already studying the role of a receptor for cortisol, the glucocorticoid receptor (GR), in breast cancer, because women with the harder-to-treat “triple negative” form of the disease often show increased GR levels. Researchers in Conzen’s laboratory discovered that activating GRs can stimulate proliferation of breast cells and block the effects of chemotherapy drugs.

Could this be the missing biological step between isolation stress and breast cancer? At the lecture, Conzen tagged back to McClintock to talk about experiments on the tumors from her socially isolated rats. Unlike more common animal models of breast cancer where the tumor is instigated by a toxin or a genetic mutation, the naturally-occurring tumors in isolated rats show a similar diversity to that seen in human tumors. Some rats grow benign tumors, some malignant, and different tumors have the different hormone receptor profiles that are used for classification and treatment choices in patients - including, in some cases, glucocorticoid receptors.

“This to me was very exciting because in the rat model we have a good model of the diversity of breast pathology that happens [in humans] and it is increased by isolation,” McClintock said. “I was happy to see it in the more natural, spontaneously-occurring cancer model rather than something that was induced.”

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Cancer used to be a black box, a disease that physicians could only monitor through surgical biopsies and indirect measures. But for the last thirty years, the use of computed tomography imaging, better known as CT scans, has allowed oncologists and cancer researchers to keep close watch on the growth or shrinkage of a tumor for many different types of cancer. A patient with a lung tumor, for example, can be scanned every few months in order to see whether their therapy is working - and if it’s not, doctors may choose to switch treatments. Clinical trials of new therapies for cancer also make use of CT scans, using the increase or decreased size of the tumor as a primary data point.

But for all the benefits of scans over surgeries to monitor tumor size, flaws remain for CT scans. A new study published this week in the Journal of Clinical Oncology shines a harsh light on one of the primary problems - the technology’s variability. Patients usually are given CT scans months apart, and trained radiologists measure the tumors to see whether they are growing or receding. But how much of those changes can be attributed to random error from the imperfect resolution of the scan or the breathing of the patient?

To test this baseline error, researchers from Memorial Sloan-Kettering Cancer Center got a little tricky. Instead of taking two scans from a patient months apart, they took two scans in quick succession, within 15 minutes. The scans were then handed off to experienced radiologists, who were told to measure the change in tumor size without knowing how much time had elapsed between the images. The results were sobering - despite the tumor being biologically identical between the two near-simultaneous scans, the radiologists found changes in size of 1mm or more in more than half of the samples and a 10 percent error range in either direction overall. Although the criteria for tumor progression is an increase in size of 20 percent or more, that 10 percent error could considerably distort the data when clinical and research decisions are made using normally-spaced scans.

The result doesn’t render CT scans obsolete, but offers new caution about the method’s shortcomings.

“It’s the sense of, ‘Really? Is this first happening now?’” Michael Maitland, assistant professor of medicine at the Medical Center, commented to Reuters Health about the study findings. “This is telling us scientifically how much noise is naturally there without any treatment or the cancer getting worse. It’s an important thing to do whenever you are going to use any kind of marker for a disease.”

In an accompanying editorial in the Journal of Clinical Oncology, Maitland went further, writing with his co-authors that it was time for oncologists to rely less upon CT scans alone and move toward integrating those images with other measures to create more precise monitoring technologies. As cancer edges toward more personalized treatment strategies, developing better diagnostic tools will become even more important, they argued.

“It is time to cast away familiar conventions and turn to better methods of evaluating malignant disease therapeutics,” they wrote. “It is time to replace these systems with more innovative, quantitative approaches that have the potential to define relationships between solid tumors, disease progression, and therapeutic outcomes in patients.”

Elsewhere…

It might have come out a few days late for the 4th of July, but Travis Carter’s study of the effects of seeing the American flag on political beliefs is still timely. If the Booth Business School researcher is right, we’ll all be slightly more Republican for at least the next 8 months. Ed Yong at Not Exactly Rocket Science did a great writeup that was featured on the Colbert Report this week (and also wrote up our own Neil Shubin’s study on the origin of limb genetic programs this week as well).

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Popular Mechanics typically offers step-by-step guides for changing your oil or building a bookcase. But in a recent feature they seriously upped the instructional ante with an “Extreme How-To” - How to Perform Open Heart Surgery. The expert chosen to guide their readers through this don’t-try-this-at-home process was Medical Center cardiac and thoracic surgeons Jai Raman and Shahab Akhter who helped develop a new technique in heart surgery called the “wrap procedure.” The surgeons do a great job of explaining how the surgery has changed over the years, particularly in the materials used for repairing the heart and sternum after surgery to speed recovery and decrease scarring. “You’ve got to get comfortable putting stitches into a beating heart,” is just some of the sage advice that Raman offers in the piece.

The end of the academic year always brings a bounty of teaching honors, voted on by medical students, residents, and faculty peers. For the 2010-2011 year, more than two dozen awards were handed out by the Pritzker School of Medicine, the Biological Sciences Division, and departments of the Medical Center. For an awards roundup from both sides of campus, visit this article at the University of Chicago News Site.

The pediatric cancer patients at Comer were treated to a celebrity visit last weekend, though their parents and staff may have recognized her more by voice than by sight. Delilah, the easy listening disc jockey known for her “Love Someone” radio dedications, visited families at Comer before making 3-year-old leukemia patient Atia Lutarewych her “Brave Child of the Week.” You can listen to her segment on the visit here [mp3].

Another inspiring story of pediatric cancer was told in the Chicago Tribune this week, focusing on 6-year-old neuroblastoma patient Theofanis Yianas. After Theo’s hair fell out from chemotherapy treatment, 30 friends and family members shaved their heads in solidarity with the young boy. Theo’s doctor, professor of pediatrics Susan Cohn, comments on the importance of support in a patient’s recovery.

What did St. Vitus’ Dance - the 14th century outbreak of weeks and months-long uncontrolled dancing across Europe - have to do with mirror neurons in the brain? UChicago psychologist John Cacioppo weighs in on this fascinating phenomenon for ABC News.

An interesting plan to create “mystery shoppers” for assessing the primary care shortage in the United States was revealed in the New York Times on Sunday, then disappeared by Tuesday after doctors bristled about “snooping.” The survey, which would have been conducted by the University of Chicago National Opinion Research Center, shows how far the administration will go to collect data on the current health care system…and how stiff the medical field’s resistance can be to being measured.

Over the year-long discussion of health disparities in the MacLean Center for Clinical Medical Ethics seminar series, the health gaps presented between American whites and blacks have been predominantly a one-way street. On nearly every health measure - from infant mortality to diabetes to cardiovascular disease - higher rates are observed for African-Americans. But there’s one health gap where the racial positions are surprisingly flipped, said James Jackson of the University of Michigan in his visit to the series in early May. Over the course of a provocative talk, Jackson demonstrated how this strange reverse disparity in mental health could be hiding a model explaining the physical health gaps that continue to resist reduction efforts.

In a 2007 study, a survey project led by Jackson measured the lifetime prevalence of major depressive disorder in African-Americans, Caribbean blacks, and white Americans. An almost complete reversal from the normal health disparity was observed, with roughly 18% of whites diagnosed with major depression at some point in their lives, compared to only 10.4% of African-Americans. The data, though replicated several times, was initially greeted with skepticism by observers who were mostly familiar with biased data based on hospital admissions, Jackson said.

“When people noticed this, they really began to contort  the data,” said Jackson, a psychologist and director of the Institute for Social Research at the U. of M. “The argument was that there must be something wrong with the way it was assessed, because everybody knows that African-Americans have to have higher rates of psychiatric disorders than whites.”

But now that the reverse disparity has been verified in many different populations, Jackson has started to ask why these differences exist. His working theory hinges on two other observations: the delayed appearance of physical health disparities over the course of life, and cultural differences in the way people cope with stress. When well-known health disparities on measures such as diabetes or hypertension are broken down by age, there is not a consistent gap between blacks and whites, but a gap that emerges and rapidly grows in middle age (45-64 years old). Putting aside differences in infant mortality rates, some evidence actually suggests that black children are healthier than white children on many measures, Jackson said.

The growing gap in health measures over the life course is paralleled by another growing gap - in the frequency of poor health behaviors. In white populations, smoking rates peak in young adulthood and then decline, while the rate in black populations accelerates with age. The same pattern holds true for heavy alcohol use and drug use, Jackson said, while frequency of vigorous physical activity declines with age faster for black females than white females. Obesity is more complex - it is the only black-white difference observed early in life, at least for females - but this gap also widens over life course, regardless of socioeconomic status.

The core of Jackson’s theory was to cast those physically unhealthy behaviors not as mere vices, but as methods people use to self-medicate themselves against the stress of daily living.

“If you’re having a bad day…you know it. At the end of the day, your stomach is upset, you have a headache. There are palpable things that are present with regard to the stress reaction to the circumstances,” Jackson said. “But if you are growing a tumor for cancer, you don’t know it, until it reaches a certain stage.”

“If you know you’re having these stress-related kinds of problems, this awareness motivates you to action - you are motivated to do something about the physiological and psychological consequences of stressors in your life. And what do you want to do? People eat comfort food to reduce stress, the activity in the chronic stress response network,” Jackson said. “If I’m stressed, a Twinkie makes me feel better.”

Self-regulating stress can also go beyond junk food, Jackson said, to severe drug and alcohol use. All of these coping strategies may help dampen the stress response and protect mental health, but only at the cost of exacerbating physical health problems.

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TED Comes to Campus

This weekend, the students of the University of Chicago are putting together a local edition of the renowned TED conference called TEDxUChicago. The theme, “Reinventing the Life of the Mind,” nicely blends the goals of TED and the University, the idea-sharing mission of the conference sutured to the intellectual spirit of our campus. Among the talks taking place at the Reynolds Club this Sunday are a few UChicago scientists: paleontologist and educator Paul Sereno (speaking on the topic of “Art In Science”), psychologist and child language expert Susan Goldin-Meadow (”What Our Hands Can Tell Us About Our Minds”), and student speaking contest winner Bruno Cabral (“The Life of the Mind Lived Through Noise”), an undergraduate working in the laboratory of psychologist Howard Nusbaum. Other speakers include Mark Inglis, the first double amputee to climb Mount Everest, Jonathan Greenblatt, the former CEO of GOOD magazine, and cybernetics expert Kevin Warwick giving probably the talk with the coolest title: “The Last Remaining Hurdles to Cyborg Technology.” Tickets are still for sale on the TEDxUChicago website, but if you can’t make it down to Hyde Park, the talks will be webcast live at the UChicago Facebook page.

The Rules of Language

Last week, the Joseph P. Kennedy Intellectual and Developmental Diabetes Research Center held a symposium called “Variations in Language Learning,” a series of talks about how languages are acquired by children, adults, and cultures. Elissa Newport, a professor of brain & cognitive sciences and linguistics at the University of Rochester, presented fascinating data on the concept of “statistical learning,” the theory that the brain uses mathematical tricks to learn the arcane rules of a new language. To test this idea, Newport and her colleagues played a made-up language of nonsense syllables for 20 minutes (!) to volunteers, showing that combinations of syllables that show up more frequently (such as “dutaba” or “babupu”) are eventually perceived as “words” by the listener. The researchers also went on to show that children are better at this “statistical learning” than adults when confronted with a new language, offering an explanation for why languages are easier to pick up when learned at a younger age.

The idea of a universal foundation for learning and developing language echoes the “universal grammar” theories of Noam Chomsky and others, if peripherally so - Newport’s experiments showing that the same statistical learning can be used for tones and visual sequences implies that it’s a universal learning mechanism, not specific to language. But a new phylogenetic analysis of the world’s languages appearing in Nature this week argues against innate rules for language, demonstrating deep grammatical differences between “families” of languages go against the idea of a universal human grammar. Most linguists seem skeptical or underwhelmed about the result, and the debate smacks of a false dichotomy, with the truth about language development less a battle between cognition and culture than a combination of the two forces. Discover, the LA Times’ Amina Khan, and Ars Technica’s John Timmer all weigh in on the study.

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In the 11 years since the blueprint of human life was decoded by the Human Genome Project, much of the focus has been on when those instructions fail. Scientists have used our newfound genetic knowledge to look for the roots of common and rare diseases, the gene or genes that can increase the risk of everything from heart disease to cancer to asthma. But setting the stage for future illness is not the purpose of genes, of course. By coding for the proteins that make up the body and brain, genes lay the foundation for everything we do, feel, and probably even think.

Like the study of disease, genetic studies of human behavior have mostly focused on the abnormal - the targets of psychiatry. Mental illnesses such as schizophrenia, depression, and drug addiction have been the subjects of genetic hunts, known as genome wide association studies, where the ill are compared to controls to reveal genes that might be involved in the a particular disorder. As with diseases in the rest of the body, psychiatric disorders have mostly resisted easy genetic explanations - only a small percentage of schizophrenia, for instance, has been traced to genetic causes.

A more useful, but also vastly more complicated, approach might be to study not the binary comparison of healthy vs. sick, but the whole spectrum of human behavior. For example, rather than just looking at those with extreme enough depression symptoms for a clinical diagnosis and those who don’t, scientists could look at genes in subjects who are rarely, mildly, or frequently affected by depression, as well as those on the extremes. Such analyses may get closer to the genes and brain structures that control human behavior, both in everyday life and when it breaks down.

These types of experiments have caught the imagination of Abraham Palmer, assistant professor of human genetics at the Medical Center. In collaboration with the laboratory of Harriet de Wit, professor of psychiatry, Palmer has started to look at the behavioral trait of impulsivity, which has been associated with attention deficit disorder and predisposition to drug abuse.

“We’re coming at it from a tradition that’s very psychology, drug abuse-based, but we’re really interested in asking questions that get at the broadest range possible of behaviors,” Palmer said. “These are continuous traits that everybody in the population will have some value for. We’re not talking about it exclusively from a disease perspective. These are healthy people coming in.”

Palmer used Donald Rumsfeld’s infamous quote about known knowns, known unknowns, and unknown unknowns, to illustrate how studies of genes and behavior have classically been limited by the tunnel vision of previous knowledge. If a particular gene is already known to play a role in a behavior, scientists can study how individual variants in that gene correspond to behavior. In one such project, Palmer was part of a team that looked at the D2 dopamine receptor - a neurotransmitter receptor linked with the response to drugs of abuse - and impulsive decision-making.

Volunteers came to the laboratory and performed a “stop task,” a common psychology test. The subject is trained to look for a “go signal” and start hitting a certain keyboard key as quickly as possible until the “stop signal” sounds. The delay between the go and stop signals is steadily decreased with each round, and the ability of the subject to stop on time is measured. Researchers then compared their D2 genotype to their behavioral score, and found a link between different D2 variants and more “impulsive” results on the stop task.

These results help researchers study possible genetic predisposition for drug abuse or addition. But Palmer said he wants to expand the search beyond genes that are already implicated in behaviors and beyond psychiatric conditions.

“We’ve mostly looked at candidate genes, genes where we had reason to think it might modulate a behavior,” Palmer said. “But the more interesting question, if you had a sufficiently large sample and enough power, is to say let’s go at this with a blank state, let’s look at all the polymorphisms in a genome and pull out novel things maybe in genes we had never thought to be related to these processes.”

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For some diseases, taking a census is easy. Most people who have cancer are diagnosed with the disease before they die and seek treatment, allowing for the collection of detailed national cancer statistics. But other diseases tend to hide in the shadows, undetected and under-counted due to infrequent diagnosis or an unwillingness of patients to seek treatment. Into this latter group falls the eating disorders: anorexia nervosa, bulimia nervosa, and other conditions. Because many of these patients try to avoid treatment, psychiatrists have long suspected the numbers are skewed because only a subset of people suffering from eating disorders find their way to their clinical practice.

“We only see the tip of the iceberg,” said Daniel Le Grange, professor of psychiatry and director of the University of Chicago Eating Disorders Program. “As clinicians and researchers, we’ve known that in the community there are thousands of people out there with eating disorder behaviors that we never see in our clinics.”

Hard data on the frequency of eating disorders in the broader community has been hard to come by. But a new survey study of over 10,000 adolescents, released last week in the Archives of General Psychiatry, confirmed that the iceberg of eating disorder prevalence among American teens is as broad below the surface as psychiatrists suspected. Almost 6 percent of those surveyed in the study met the criteria for one of the five eating disorders tested at some point in their lifetime, a number extrapolated by some media outlets to 500,000 teens in the United States.

But the total numbers were just one of the eyebrow-raising results of the research. Le Grange, a co-author on the study, sat down with ScienceLife and detailed the most significant findings of this long-awaited census, and discussed its implications for the nature of these diseases and the patients who are slipping through the field’s fingers.

1. The Myth of Rarity

Health care dollars are not infinite, and cynical as it may sound, diseases must compete for research funding and insurance reimbursements. So when conditions such as eating disorders are perceived as rare occurrences, the people who treat and study those conditions face an uphill struggle for attention and support. Thus, the under-reporting of eating disorder prevalence has held the field back from being considered as a priority concern in adolescents. The new numbers - lifetime prevalences of 0.3% for anorexia nervosa, 0.9% for bulimia nervosa, 1.6% for binge-eating disorder, and 3.3% for sub-threshold disorders - lift eating disorders into a higher tier of concern for teenage and adult health.

“The myth has been that eating disorders and especially anorexia nervosa are relatively rare disorders, and we constantly have to argue that they’re not, because that’s what it feels like when we sit in clinical practice and we are inundated by patients,” Le Grange said. “This is robust data to demonstrate that eating disorders are not rare.”

2. A Gender-Blind Illness

In the clinic, psychiatrists see far more girls with eating disorders than boys - a ratio of 9-to-1. But surprisingly, the community survey revealed roughly equal prevalence for anorexia nervosa in males and females, suggesting that boys are not less likely to suffer from the condition, but are much less likely to be diagnosed and treated. Le Grange said he suspects that physician bias may lead them to more quickly consider an eating disorder  when the patient is a she rather than a he.

“We are so convinced that anorexia nervosa is predominantly a female disorder that pediatricians and mental health professionals, when presented with a boy who’s lost weight, do not consider anorexia to be a legitimate  diagnosis,” he said. “When we do see boys in our clinic, they usually have had an extensive preliminary workup, as the clinicians don’t consider an eating disorder…until everything comes back negative.”

3. Effects Beyond Mealtime

Psychiatrists observe that eating disorders don’t typically occur in isolation, as patients often carry “co-morbid” psychiatric issues such as depression or anxiety. The community survey puts a number on this observation, finding that the majority of those that met the criteria of an eating disorder also met the criteria of at least one other psychiatric disorder. Perhaps most alarming was the very high occurrence of suicidal thoughts and attempts in adolescents with eating disorders - more than half of those with bulimia nervosa reported thinking about suicide, and more than a third reported attempts.

Also striking was that these associations were just as common for kids who exhibited “sub-threshold” eating disorders, those did not meet the full criteria for anorexia nervosa or bulimia nervosa. In the DSM-IV, the diagnostic bible of psychiatry, such patients would be lumped into the category of Eating Disorders Not Otherwise Specified (EDNOS). The health risks associated with these patients suggest that EDNOS should not be seen as any less severe an illness, Le Grange said.

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One of the most important functions of the brain is to make decisions. Even the simplest animals need to make choices based on sensory information: is that thing over there food or a predator, and should I eat it, or run from it? Making the right decision is literally a matter of life or death. In humans, our decision-making can grow far more complex, encompassing matters from choosing where to eat dinner to whether a defendant is guilty or innocent.

How those decisions are made has fascinated philosophers as far back as Plato, and been the subject of science books as recently as Jonah Lehrer’s How We Decide. Plato’s metaphorical tug of war between the rational mind and the emotional mind has been updated with brain imaging and psychological experiments to a balance between emotional centers of the brain (the amygdala, the insula) and the “rational” calculations of the prefrontal cortex. But as Lehrer nicely illustrates via airplane pilots, poker players, and Tom Brady, the prefrontal cortex doesn’t always make the best decisions, and human choices are often the product of an argument between a Congress of different brain regions.

One brain area that doesn’t appear in Lehrer’s book is the parietal lobe, a region located roughly in the upper middle of the human brain. An old-fashioned name for the parietal lobe is the “association cortex,” named for the region’s role in integrating sensory and motor information primarily mediated by other parts of the brain. As a hub between incoming sensory inputs (such as the sight of an attacking tiger) to behavioral motor outputs (such as RUN!!!), the parietal lobe would seem an obvious place for decision-making. But it was a different phenomenon that first led David Freedman, assistant professor of neuroscience at the University of Chicago, to the decision-making role of the parietal lobe.

As a graduate student and postdoctoral researcher, Freedman was interested in visual categorization, how the brain classifies the many objects around us into useful groups. Freedman trained subjects to form categories about shapes they were shown, such as the difference between dogs and cats. By recording from different areas of the brain, including the prefrontal cortex that is often implicated in decision-making, Freedman found that learned categories could be encoded in the activity of individual neurons - some began responding preferentially to cats, others responded to dogs.

“We’re not born knowing about things like furniture and vehicles, you have to learn about that through experience,” Freedman said. “So the experiments we did suggested that learned information about these kinds of visual categories can be encoded in the activity of individual neurons at the highest stages of the visual system and the frontal lobe.”

While at Harvard working with John Assad, Freedman found another area of the brain that seemed to play a role in categorization: a region of the parietal lobe called lateral intraparietal area, or LIP. The region had already attracted the attention of scientists studying decision-making at the University of Washington, Stanford, and NYU, who found activity there when monkeys performed a simple visual choice task.

In those experiments, subjects were shown an array of dots moving in one direction, and were rewarded when they darted their eyes (a motion called a saccade) in the same direction as the dots. When the researchers looked in the LIP - previously known to play a role in saccades - they saw an increase in activity as the subjects processed the dot stimulus, peaking with the decision to move their eyes in the correct direction. The dynamics suggested that such decisions might be encoded in an intentional framework, in which making a decision is inseparable from the motion to execute it. In other words, both deciding on a Diet Coke and moving your arm to press the right button on the pop machine originate from the same brain region and activity.

But Freedman wondered if the real job of LIP was obscured by the simplicity of the eye movement task. Because of its quickfire look-and-respond nature, the experiment could give a false impression about the tightness of the link between decision-making and action. So Freedman designed a more complex experiment, where subjects first learned to group the movement of dots into two directional categories, and then were shown two different arrays of moving dots one second apart. If the movement of the two arrays belonged to the same category, the subjects released a lever; if they were from different categories, they maintained their hold.

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As Chicago digs out from under two feet of snow and summer feels a million years away, it’s time for the usual jokes doubting the existence of global warming to come from certain quarters of society. It’s apparently a human reflex to start questioning the gradual climb of Earth’s temperatures while shivering knee-deep in snow at the bus stop - even if the intense snowstorms of the current winter may, in fact, be related to climate change. But something about our brains seems designed to prioritize immediate impressions over long-term data and hunches over evidence, a problem that has consistently plagued scientists and policymakers arguing for urgency in the fight against climate change.

But if a run of cold, snowy days predisposes people to doubt global warming, could the opposite influence also be true? The hypothesis that “warmth” could tip people toward believing reports of climate change was recently put to the test by the Booth Business School’s Jane Risen and Clayton Critcher of UC-Berkeley. In a series of experiments, published in the Journal of Personality and Social Psychology (pdf), they tested whether people were more likely to agree with statements about global warming when they themselves were in a warm environment, either outside or in an artificially-heated indoor setting.

The concept of humans being easily influenced by their surroundings is not new to psychologists. As much as we like to think we have solid, evidence-based reasons for our beliefs, the literature contains countless examples of people being easily swayed by seemingly minor stimuli. Risen and Critcher cite studies where subjects were more likely to believe a statement based on what color it was printed in, judge people as more hostile after being primed with words related to hostility, and believe a disease is more likely if they are able to imagine its symptoms. To explain this phenomenon, the authors propose a theory of “visceral fit,” where a person is more prone to agree with a proposed state of the world that aligns with their own current personal state.

So, Risen and Critcher had undergraduate volunteers fill out a survey assessing their views in various environments: outside on a hot day vs. a cold day, in a heated cubicle vs. an unheated cubicle, or before and after eating a bowl full of salty pretzels. Subjects were consistently more likely to rate the statement “global warming is a proven fact” over “global warming is a theory that has not yet been proven” as closer to their own views when in a warmer setting - outside, inside, and even when researchers directly pointed out the room’s warmth to subjects. In several experiments, warmth was more strongly correlated with responses than even the self-reported political views of the subjects (and warmth had no effect on perception of other political issues such as gun control and the death penalty). As for the pretzel experiment, think the Seinfeld line “these pretzels are making me thirsty” - subjects were more likely to believe concerns about drought after consuming the salty snacks.

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The late December quiet has given way to a post-holiday flurry of exciting research news, most of which I can’t tell you about until next week. But in the meantime, here’s our first weekly roundup for 2011 of the most interesting science and medical news around the web.

Tears for Fears

Scientists have discovered a multitude of ways by which animals communicate through chemical signals, such as those in the urine that dogs use to mark their territory and the path left by ants to guide their compatriots to food sources. But whether such pheromone signals exist in humans has been much more controversial. Martha McClintock, professor of psychology at the University of Chicago, has published many papers showing evidence for communicative signals in human sweat that can influence menstrual cycling, mood, and brain function in other people. But the behavioral effects of human chemical signals have so far been small, producing nowhere near the sensational effects that marketers of “pheromone” perfumes claim on less than reputable websites.

But another mediator of chemical communication in humans may have been traced this week, in a paper published by Science on the ability of women’s tears to affect sexual interest in males. The Israeli study used a hilarious method of collecting their experimental substance, sitting women down in front of sad movies and catching their tears in test tubes (”We obtained negative-emotion tears from 2 donor women who watched sad movies in isolation,” the authors right in scientist-ese). The fluid was then placed under the nose of male subjects, who viewed pictures of women’s faces and rated their attractiveness. As described by Ed Yong at Not Exactly Rocket Science, the males’ sexual interest decreased when exposed to the tears, as compared to being exposed to a control of saline. Differences in brain activity and testosterone levels were also detected while men sniffed the tears of sadness.

Consulted by the New York Times, McClintock said the study “really broadens the possibilities of where signals are coming from,” but expressed skepticism that the tears’ effect would be restricted to sexual behavior. “I have no doubt that it affected sexuality as they report, but I would be very surprised if it doesn’t turn out to affect other emotions in other contexts. Maybe it’s affecting some deeper, more fundamental psychological process that drives the effect that they’re reporting,” she told the newspaper. Other critics have asked whether the chemical signal lies in the tears themselves, or are collected by the tear from the skin as they roll down a subject’s cheeks. The nature of the chemical still remains to be found, but the evidence suggests another entry in the previously hidden chemical vocabulary of humans.

Fraudulent Science, Human Cost

Last year, the infamous 1998 Lancet paper purporting to show a link between the measles, mumps, rubella vaccine and childhood autism was finally retracted after years of criticism for biased selection of subjects and unethical behavior. But the research, led by Andrew Wakefield, went beyond scientific mistakes to fraudulent falsification of data, a new report from the British Medical Journal released this week discovered. Investigative reporter Brian Deer found that Wakefield, who was being receiving payments from a lawyer seeking to file a lawsuit against vaccine manufacturers before he started the study, changed the timeline of autistic symptoms appearing in patients to make it look more like vaccines were the cause. The article is a rigorous and thorough deconstruction of a scientific fraud that has had concrete consequences for children around the world - in the  12 years since the article was published, measles cases have spiked in England and America as vaccination rates have dropped, and other vaccination-sensitive diseases such as whooping cough have also made a resurgence.

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Imagine There’s No Hunger

This post is going up around lunchtime, and you might be just now picturing what you’re going to eat. There are those healthy whole-wheat pasta leftovers in the fridge, but just down the street is a deli where you can purchase a giant Italian sub with hot peppers and cheese and a bag of chips on the side. Just the thought of that delicious sandwich is making your mouth salivate and your stomach grumble in anticipation. Wait, were we talking about you, or me?

The ability of people to make themselves hungry just by imagining food has always baffled psychologists, who would predict just the opposite response. Using imagination for habituation, the gradual diminishing of a stimuli’s power to provoke a response with repetition, is a classic tool of psychological treatment. For example, people with phobias are often instructed to repeatedly imagine the cause of their fear (spiders, heights, airplanes) until their emotional response subsides. By that theory, repeatedly imagining a delicious pizza should eventually make you less hungry for a slice, rather than increase craving.

But maybe people are just imagining the wrong thing, thought researchers from the business school at Carnegie-Mellon in this week’s Science. Instead of imagining the food before it is eaten, perhaps people could imagine actually eating that food to habituate themselves against its wily charms. Using a particularly seductive denizen of the office vending machine, M&M’s, the authors instructed their subjects to imagine eating 30 pieces of the candy in succession, like picturing the process of inserting 30 quarters into a vending machine. This tedious fantasy actually worked when the subjects were subsequently given a nice big bowl of M&Ms - subjects who imagined eating 30 pieces of candy ate less than subjects who only imagined a 3-piece snack, or no snack at all. The trick was found to be stimulus-specific, in that a session of imaginary M&M eating had no effect on subsequent eating of another snack; in this case, cheese cubes.

Aside from it’s dietary implications, the study is a pretty amazing demonstration of the power of imagination - “The difference between actual experience and mental representations of experience may be smaller than previously assumed,” the authors write. But it’s unlikely that anyone will incorporate this imagination trick into a get-thin quick diet plan, as you can’t sell a customer the ability to imagine eating unhealthy food, and therefore can’t hire Kirstie Alley to endorse it. But it is something we can all try for free, at home or at our office desk. So while I write the rest of this post, I’ll devote part of my mind to imagining the laborious consumption of that delicious Italian sub sandwich, rather than the sandwich in all it’s pre-eaten glory.

[H/T to the Wall Street Journal Health Blog for the article.]

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The common wisdom about kicking an addiction is to “isolate and conquer.” People trying to give up smoking, or coffee, or something more serious, are usually advised to stay away from reminders of their drug, such as other people smoking, the smell of coffee, or other cues that might remind them of their habit. Taken to its extreme, this isolation policy is the backbone of inpatient drug treatment programs, which remove an addict from their environment and away from addiction “triggers” for 30 days or more. At the hospital, addicts can safely pass through withdrawal symptoms, receive psychiatric care, and return to society equipped to resist the siren call of their vice.

However, research in animals throws a wrench into that theory of addiction treatment. In animals taught to hit a lever to receive addictive substances such as cocaine, heroin, or sucrose, an extended period of abstinence away from drug-related cues produces an unintended effect. Rather than decreasing the animals’ response to the cues (which in the world of a rat’s cage is usually a light or a sound rather than an ashtray or a syringe), longer periods of abstinence inspire a more robust and energetic “relapse” of lever-pressing.

This “incubation effect” suggests that the longer addicts stay away from their drug, the more likely they are to succumb to a relapse when they see or smell a drug-related trigger. But that idea had not been translated from rats to humans until an experiment performed by Gillinder Bedi and colleagues in the laboratory of Harriet de Wit, professor of psychiatry at the University of Chicago Medical Center. Published last month in the journal Biological Psychiatry, the experiment shows the first evidence that incubation of drug cues also occurs in humans. Further, their results suggest that current treatments for addiction may miss, or even run counter to, an important cause of relapse.

“Many factors contribute to relapse,” de Wit said. “One is the presence of withdrawal symptoms, the other is just the immediate difficulty of removing a habit that you had. But there might be this other factor, incubation, that grows over time without dissipating, at least for weeks or perhaps months.”

In Bedi’s experiment, cigarette smokers were paid $30 a day to abstain from smoking for as long as 35 days. As testament to the allure of nicotine, only half of the subjects recruited for the study reached their smoke-free target despite the financial rewards, de Wit said. The participants who did successfully abstain until their goal (7, 14, or 35 days) returned to the lab where they were exposed to either smoking-related cues (pictures of people smoking, lit cigarettes, ashtrays, etc.) or neutral cues or a matched show of neutral, non-smoking cues. To enhance the sensory experience, subjects held a lit cigarette while viewing the smoking cues or a pencil during the neutral session. Before and after the cues, subjects completed surveys to report how strongly they craved cigarettes.

Before the slide show sessions, participants reported expected, positive results of quitting: withdrawal symptoms and craving decreased with the more days since their last cigarette. But after viewing the parade of cigarette-related images, the opposite effect was observed. Subjects assigned to the group that abstained from smoking for a longer period of time (35 days) reported more cue-driven craving compared to those who only abstained for 7 or 14 days.

That looks a lot like the incubation effect seen in rats, and according to de Wit, may actually be an even more impressive effect than what was seen in animal studies. Whereas rats can be kept totally isolated from drug cues for as long as necessary, the subjects in Bedi’s study were presumably exposed to some smoking-related cues - friends smoking, cigarettes in movies, etc. - during a typical day of their paid abstinence. Yet in the laboratory, the cues still held the power to spark craving, and this craving increased with the number of days of abstinence. In a further surprise, most subjects returned to their smoking habits after their part in the research was finished, regardless of how long they had abstained from smoking for the study.

“I think one of the really interesting things is that almost everybody goes back to smoking, even after a month of not smoking,” de Wit said. “You would think if they could go drug-free for a month it would be pretty easy to stay quit after that, and yet they went back.”

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Yesterday we talked about how Kathleen Cagney’s research appeared to reveal an effect of the 9/11 terrorist attacks on the body mass index of people more than a thousand miles away in Dallas. By coincidence, Discover magazine published a book excerpt (from “Origins: How the Nine Months Before Birth Shape the Rest of Our Lives” by Annie Murphy Paul) yesterday that touches on how the fall of the World Trade Center might have caused post-traumatic stress disorder not just in people near the towers that morning, but also the fetuses being carried by pregnant women near the towers. Can PTSD be transmitted from mother to unborn child? And did 9/11 leave a wide swath of medical impact across the country? Fascinating research.

Oh cruel search for alien habitable worlds: new data released at an astronomy symposium this week appears to refute the existence of Gliese 581g, the “Goldilocks” planet that had everyone daydreaming of intergalactic travel two weeks ago. Though the debate over the planet’s existence is far from settled, it’s a quick, nasty reminder that leaping from a handful of data points to bold claims of Earth-like planets and alien life is a dangerous gamble. (Also, Google News hits for original Gliese 581g story = 1407 articles. For the “Gliese 581g may not exist” story = 91.)

As part of the “It Gets Better” campaign reacting to the recent run of tragic suicides by homosexual teenagers, Scientific American’s psychology blogger Jesse Bering begins a long, detailed look at the evolutionary history of suicide. Why would an organism evolve the capacity to kill itself? Bering dials down to insects that are cannibalized after copulation and explains a mathematical equation for suicidal motivation in the first part of his series.

If University of Chicago evolutionary biologist Jerry Coyne is too prolific for you on his blog, Why Evolution is True, you can get a primer on his views regarding the incompatibility of science and religion from his USA Today editorial this week. There were, of course, letters,  and a blog response from Albert Mohler of the Southern Baptist Theological Seminary.

An in-depth Reuters article about the increasing use of cardiac assist devices and the end-of-life ethics questions they raise talks to our chief of cardiac and thoracic surgery Valluvan Jeevanandam, among other experts. For more on the topic, see our post on ethicist Daniel Sulmasy, who has written about when it is ethical for physicians to turn off a person’s cardiac device, knowing that it may hasten death.