As another year comes to a close we’d like to look back at the fascinating research breakthroughs and inspiring patient stories from 2011. ScienceLife ran 168 posts this year, and while we wish we could highlight all of them, here are a handful of our favorites from each month.

January

Patrick Wilson found out that the H1N1 virus could end up helping us fight all types of flu. Stephen Pruett-Jones studied how some male birds mimic the sounds of predators to pick up the ladies (with an audio clip). We interviewed David Gozal about his study on the link between childhood obesity and lack of sleep, and took a look at NCAA regulations mandating sickle cell testing for athletes.

February

Harold Pollack gave a lecture on why violent crime in urban, minority communities should be considered a public health epidemic. Siri Atma Greeley studied the actual medical benefit of widespread genetic testing. Stacy Lindau wanted to know why so few women get help for sexual problems after surviving cancer. We talked to Bana Jabri about the causes of celiac disease, and Sliman Bensmaïa showed us how the brain processes the basic elements of touch very much like it handles visual information.

March

Sola Olopade educated women in Nigeria about using clean-burning stoves to prevent indoor pollution. Stefano Allesina and Jonathan Levine looked at how rock-paper-scissors helps explain evolution. Joshua Miller went to Yellowstone Park to see what stories the ghostly bones of animals can tell, and Scott Eggener questioned the wisdom of indiscriminate prostate cancer screening.

Photo by Gerald Waddell

Andrea King studied the wide range of responses to drinking alcohol, and why it can be fun for some people and a bummer for others. Cheryl Reed took a ride in a helicopter with our UCAN nurses. Kamal Sharma looked at the genes that control animals’ gait, and Ningqi Hou studied how urban environments can dictate how much exercise people get.

May

Daniel McGehee looked at the long-term effects of nicotine on the brain. Habibul Ahsan went to Bangladesh to study the health impacts of accidental exposure to arsenic in drinking water. The brain’s overlooked supporting cells got their due at a conference on neuroscience, and we remembered a landmark discovery about a once popular drug taken during pregnancy that we now know can cause cancer.

June

As we headed into summer, Diana Lauderdale used Google to track MRSA. We learned about an extraordinary transplant where a man received a new heart, liver AND kidney. Daniel Geynisman gave us the rundown on whether or not cell phones are killing us (they’re not, as long as you don’t use them in the car), and some UChicago undergrads studied what happens to gorillas on the birth control pill.

July

We spoke to Donald Jensen and Andrew Aronsohn about the new outlook for patients with hepatitis C. Igor Schneider made a time machine to find the genetic switch for limb development. Farr Curlin led a study about the benefits of addressing spiritual needs alongside medical care, and Adam Cifu looked at the phenomenon of scientific study reversals.

August

Stefano Allesina dug into the long, shady history of nepotism in academia in Italy. John Schneider talked about his work addressing sexual health and stigma in India. Michael Becker discovered a new treatment for the Royal Disease, and we had the rare chance to name check a Spiderman villain in a post.

September

Martha McClintock and Suzanne Conzen studied the connection between social isolation, stress and breast cancer. Gallego Romero traveled to India to search for the origins of lactose intolerance. Stephanie Dulawa developed a mouse model for OCD, and Paul Vezina looked at a different kind of obsession, compulsive gambling.

October

Arshiya Baig started a pilot project to help people learn about life with diabetes through pictures. Manyuan Long found that some of the youngest genes are in the brain. Jens Ludwig and Stacy Lindau published a landmark study about the connection between neighborhood poverty and health, and Issam Awad studied a rare brain disease that soon could be treated with a drug instead of surgery.

November

Cathy Pfister and Tim Wootton figured out how to use seashells to track climate change over the years. Lianne Kurina found a link between loneliness and sleep quality. Shantanu Nundy, Monica Peek and Marshall Chin developed a program to send text message reminders to people with diabetes, and Pan Chen looked at the links between childhood abuse and aggressive behavior in adults.

December

Inbal Ben-Ami Bartal, Jean Decety and Peggy Mason discovered that rats can show empathy for their fellow rats in distress. Maciej Lesniak performed a scary but amazing brain surgery on a patient who was awake. Cathryn Nagler searched for the source of food allergies within our bodies, while Stafano Guandalini uncovered the challenges in educating doctors about one of those allergies, celiac disease.

Whew. Hope you were able to click through at least a few of those. We look forward to another great year of research in 2012. We’re taking a break next week, but we’ll be back on January 5. Happy holidays!

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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Writing about science means looking up a lot of numbers. Trying to find a figure for the number of cells in the body or the protein-encoding genes in human DNA or patients diagnosed with ovarian cancer from 1980 through 1995 can eat up a lot of time and internet bandwidth. For some of these oft-cited numbers, there’s a mutually agreed upon estimate that science writers can drop into the articles, such as the 23,000 usually tossed around for the number of human genes. But it’s worth remembering that these figures are subject to change - after all, it was thought as recently as 10 years ago that there were 100,000 genes in human DNA.

A new counting kerfuffle broke out this week for yet another oft-cited scientific figure: the number of species on Earth. Last year, zoologist Robert May proposed in Science that the human race would be “embarrassed” should aliens show up tomorrow and ask how many different types of organisms live on our planet. Depending on the model used, one could argue for a number anywhere between 3 and 100 million eukaryotes, May wrote - and that doesn’t even count viruses and bacteria, which far outnumber the larger species.

But as the authors of the PLoS Biology article “How Many Species Are There on Earth and in the Ocean?” found out this week, picking a number within that range is hazardous territory. Using a mathematical model based on the roughly 1.2 million species we currently know about, the research team calculated a new estimate: approximately 8.7 million species from land and sea. Of those, only 14% of land species and 9% of sea species have so far been cataloged by humans, the authors concluded, and describing those remaining could take over 1,000 years and $364 billion. “Our results also suggest that this slow advance in the description of species will lead to species becoming extinct before we know they even existed,” they wrote.

Dramatic stuff, but what about the math? In Carl Zimmer’s article on the study for the New York Times, the first bubbles of discontent can be felt around the biology world, from fungi experts to entomologists who argue that the 8.7 million number is far too low. Scientists who study microbes were even less pleased with the mathematical model, which they said dramatically under-counted their favorite species. On his blog, Phylogenomics, microbiologist Jonathan Eisen pish-poshed the paper’s estimates of 10,000 prokaryote species: “I think without a doubt the number of bacterial and archaeal species on the planet is in the range of millions upon millions upon millions.  10,000 is clearly not even close.” Two other microbiologists wrote a letter to the Washington Post, pointing out that “a teaspoon of soil contains more than 10,000 species of bacteria.” For the time being, it looks like our alien visitors will have to be satisfied with the answer, “Lots.”

Elsewhere…

Speaking of the importance of bacteria and microbes, consider the discovery of antibiotic-resistance genes in 30,000-year-old bacteria from the Yukon Territory. Though these bacteria lived approximately 29,930 years before the discovery of penicillin, they possessed defenses against the naturally-occurring weapons scientists have seized upon to develop infection-fighting drugs. That long history means outsmarting drug-resistant bacteria may be even harder than scientists thought, and makes the case for even more selective use of antibiotics. “Bacteria share these genes like baseball cards with each other,” Stuart Levy at Tufts University told Nicholas Wade of the New York Times.

Has an important culprit in amyotrophic lateral sclerosis, aka Lou Gehrig’s disease, been discovered? The Medical Center’s Raymond Roos comments on a recent Northwestern University study.

On the blog, we’ve covered the link between sleep loss and testosterone, weight gain, and blood sugar. A new study from UCSD and Harvard now finds a connection between sleep quality and blood pressure. Our sleep research guru Eve Van Cauter commented on the research for TIME.

Just another reminder to check out the Medical Center’s new Facebook page, where this week you can find articles from the blog, information on the DNA Discovery Lab at the Field Museum, and President Sharon O’Keefe’s letter to the editor on hospital charity care. If you like it, please hit that “like” button!

To prepare for the grueling 2,200 miles of the Tour de France, cyclists train their muscles at both low and high altitudes. Riding at elevation does more than prepare them for the infamous mountain stages in the Alps, it has a biological effect, increasing the capacity of red blood cells to carry oxygen and improving how their muscles use energy. Though it may seem counter-intuitive, training in the low oxygen conditions found at high altitude is actually beneficial to an athlete’s muscular performance long-term. Could the same be said for another important muscle - the one located inside your skull?

That’s one implication of a new study from University of Chicago researchers on the relationship between the sleep disorder sleep apnea and strokes. Patients with sleep apnea suffer from repeated breathing “pauses” during the night, moments where their brain is briefly deprived of oxygen (known scientifically as “hypoxia”). One or two of these hypoxic episodes may not be dangerous by themselves, but cumulatively, they can be very harmful - sleep apnea has been associated with cognitive impairment, behavioral effects, and cardiovascular disease.

Indeed, sleep apnea increases the danger twice over for one especially serious vascular problem: stroke. Research indicates that patients with the disorder are more likely to suffer a stroke, and if a stroke occurs, it is more likely to cause severe brain damage than in people without sleep apnea. Both sides of this connection have been targeted by investigators from the Department of Pediatrics sleep research group at the University of Chicago Medical Center. In one recent study, led by David Gozal, chair and professor of pediatrics, and Richard Li, assistant professor of pediatrics, the researchers found a mechanism for why putting rats through “intermittent hypoxia” during sleep (an animal model of sleep apnea) can increase the risk of atherosclerosis, the hardening of the arteries involved in many cardiovascular conditions.

But another study, published last month in The Journal of Neuroscience, focused on stroke’s aftermath, testing whether the extra brain damage from a stroke in sleep apnea patients was due to the low-oxygen episodes or an associated risk factor such as obesity. A team led by Yang Wang, associate professor of pediatrics and director of basic research for the sleep medicine laboratory, again simulated sleep apnea in otherwise normal rats with intermittent hypoxia (IH), comparing them with rats that slept in normal oxygen conditions. When a controlled stroke was induced in each of these groups, the resulting damage was very different - the IH rats suffered more damage than controls, indicating a direct effect of hypoxic episodes upon recovery after stroke.

“It seems that something very bad is happening that affects the ability of the cells to survive or to recover after stroke,” Gozal said.

The researchers then focused on a possible mechanism for why intermittent hypoxia leads to more severe strokes, choosing energy metabolism as their primary suspect. When the brain is active - or trying to recover from damage - it needs a lot of fuel. As with the rest of the body, glucose is the first option for providing energy. But like muscles, a healthy brain can also use lactate as an alternative energy source in times of high demand. The gas pump for getting lactate into neurons is a protein called monocarboxylate transporter 2, or MCT2. Wang and colleagues looked at how intermittent hypoxia affected levels of MCT2 and how MCT2 levels affected the severity of stroke.

The pathway fell into place - exposing rats to IH decreased the expression of the MCT2 gene, while decreasing MCT2 activity through various methods increased brain damage after stroke. A transgenic mouse with elevated MCT2 was even created, and found to be protected against a stroke’s damaging effects. Thus, repeated hypoxia events during sleep could disrupt MCT2 and impair the brain’s ability to use lactate for energy - perhaps by “crying wolf” too many times. Gozal used the metaphor of a night watchman repeatedly running up the stairs for minor smoke alarms, only to be too tired to respond when the big fire starts.

“I think we have dissected in a very careful way, with a lot of work, the mechanisms that may explain why patients with sleep apnea are not only at increased risk of stroke, but also why when that stroke hits, they have a risk of not really recovering,” Gozal said.

The study also raised an intriguing idea about how to prevent this elevated sensitivity to stroke in sleep apnea patients.

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By Dianna Douglas

More research practically begging people to get a good night’s sleep has come out of the sleep labs at the University of Chicago. Eve Van Cauter and Rachel Leproult have discovered that a week of inadequate sleep means less testosterone in young men.

A lot less.

In the study, ten healthy young men gave blood samples after a week of sleeping just five hours a night. By the end of the week, they had 15 percent less testosterone than normal. “This is not an insignificant amount, since it is about the amount that occurs with normal aging by 10 to 15 years,” Van Cauter said. As a man ages, testosterone production decreases by 1 to 2 percent a year.

The lack of testosterone affected not only the reproductive function of these young men, but their happiness as well. Testosterone is a vital hormone for a man’s physical and mental health, and is released into the body during sleep.

“Low testosterone levels are associated with reduced well being and vigor,” Van Cauter said, explaining why the young men said they felt grumpy and lethargic, and their mood worsened as the study progressed.

Low testosterone is associated with low energy, reduced libido, and poor concentration. Consumer Reports Health found in a recent survey that feeling too tired is the reason men cite most often for a low sex drive.

This isn’t just a lab exercise - sleep loss is endemic in modern society. At least 15 percent of the adults in the US get less than 5 hours of sleep a night. Shift workers are especially at risk for lost sleep. The average American got nine hours of sleep in 1910 and got seven in 1975. The cumulative effects of short sleep are still being discovered, and they’re all bad. People who don’t get enough sleep are fatter, more likely to have diabetes, have all sorts of learning and cognitive problems, and die earlier. Van Cauter says that a nation that doesn’t sleep enough has an epidemic of obesity and diabetes.

“As research progresses, low sleep duration and poor sleep quality are increasingly recognized as endocrine disruptors,” Van Cauter said. Mess with the delivery of hormones throughout the body, and people become hungrier and sadder. Their blood pressure goes up and their insulin production goes haywire.

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[Cartoon from the University of Washington "Neuroscience for Kids" page.]

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In neuroscience, the neurons hog all the attention. Most research is focused on the 100 billion neurons of the brain, the elongated cells that fire electric action potentials and release chemical transmitters to communicate with each other. But the neurons are a minority in the brain, outnumbered 10 to 50 times over by their neglected stepbrothers, the glia. Traditionally, scientists think of glia as the mere support staff to the more fashionable neurons, playing the role of repairmen (microglia), wallpaper installers (oligodendrocytes), or janitors (astrocytes). When scientists go looking for the source of human behavior or disease in the brain, they tend to overlook the glia and go straight for the neurons.

But at the 2011 Chicago Symposium on Translational Neuroscience, held on campus last Friday, it was the glia who had their chance in the spotlight. Subtitled “Glia in Neuronal Health and Disease,” the day-long event steered away from the “glamour cells of the nervous system,” as the program described neurons. Instead, the focus was on mounting evidence concerning how glia play critical roles in sleep, depression, brain development, Lou Gehrig’s disease, and other notable neurological disorders. In a conference dedicated to transferring scientific discovery from the laboratory to the clinic, the talks described several possible new glial targets for treating some of the most common brain disorders.

Appropriately, the morning began with a talk about adenosine, a neurotransmitter known best by its very popular blocker, caffeine. As the audience sipped from cups of adenosine antagonist (coffee), Philip Hayden of the Tufts University School of Medicine described how this small nucleoside, made from ATP released by glial astrocytes, can have a big impact on an organism’s wakefulness and health. Most of Hayden’s discoveries were made using a special genetically-modified mouse, where the astrocyte release machinery was disrupted to reduce adenosine levels in the brain.

In normal mice (and humans), the amount of adenosine in the brain builds up over the course of the day, increasing drowsiness. When someone pulls an all-nighter, the elevated adenosine levels are responsible for the miserable feeling of the next day and the extra-long “catch-up” sleep most people need to recover. But in the mice with disrupted adenosine, there were no effects of sleep deprivation on their subsequent sleep, a sign of reduced “sleep pressure.”

“This is an awesome party pill,” Hayden joked. “You can stay up late at night, and wake up on time the next morning. You’re not getting the homeostatic response to sleep deprivation.”

As often discussed here, sleep disorders are linked with a wide range of diseases, from diabetes to depression to hypertension. Hayden added another sleep co-morbidity to the list: epilepsy. In epileptic mice, interfering with adenosine release also decreased the number of seizures and the damage caused by them, suggesting that astrocytes might be a good target for anti-epileptic drug design and other neuroprotective effects.

“The way we think of the brain is NASCAR racing,” Hayden said. “Though the car and driver are important - they’re the neurons - in the difference between a car winning and coming second, how well the pit crew is changing the engine can really make a difference. We feel the astrocyte is tuning the system and helping to optimize performance.”

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Kristen Knutson, PhD, recently added to the growing body of research from the University of Chicago on the long-term consequences of skimping on sleep. She found that diabetics who sleep poorly have a harder time controlling their insulin and glucose levels than diabetics who sleep well. The research was published in the journal Diabetes Care. We conducted an extended interview with Kristen Knutson about her research, and below are some of the highlights.

Q: Why study diabetes and chronic sleep problems?

A: Many of our laboratory studies, led by Dr. Eve Van Cauter, have shown that restriction of sleep is associated with alterations in glucose metabolism. Usually, these lab studies are a week. But we wonder about the long-term effects of being a chronic short sleeper.

We think that chronic poor sleep could put people at risk of many health problems, including diabetes.

Q: How did you design your study?

A: We used data from an epidemiologic study called CARDIA (coronary artery risk development in young adults). It started in 1985, and has been going on for more than 20 years.

We gave the participants wrist activity monitors—it’s like a wristwatch that measures the subject’s sleep duration. The participants wore the activity monitors for three nights in a row. A year later, they wore the monitors three more nights. So we had a total of six days of data.

We also asked them about their sleep. Did they wake up frequently during the night, three or more times per week? Did they have trouble falling asleep?

To get the measurements of their fasting blood glucose and fasting blood insulin, we used the data from the CARDIA study, in which the participants gave fasting blood samples. Their fasting blood glucose and insulin give us an estimate of insulin resistance.

Q: Explain your most striking findings, especially with the diabetics who slept poorly.

A: We saw more significant associations between measures of sleep and glucose metabolism markers in the patients with diabetes. In particular, we saw that poor sleep quality was associated with higher fasting glucose and greater estimated insulin resistance. So poor sleep quality meant worse control of their blood glucose levels.

Also, we separated people with and without insomnia. Among the people with type 2 diabetes, those who also had insomnia had worse glucose levels and greater estimated insulin resistance. That suggests that it’s not just sleep duration that’s important, which laboratory studies have shown. But sleep quality is important as well.

The data show that people with diabetes who are poor sleepers will have a more difficult time controlling their glucose levels.

Q: Does this mean that sleeping poorly makes diabetes worse?

A: It could go the other way. It could be that people who are having trouble controlling their glucose will have more complications, more pain, more need to get up in the middle of the night to urinate, and therefore they’re not sleeping as well. What we need to do now is find people with diabetes who aren’t sleeping well, and see if improving their sleep also improves their glucose metabolism.

This study is observational, but suggests that there is a relationship between poor sleep and controlling glucose. We don’t know which factor leads to which outcome. read more

We are pleased to announce a new way to keep up with research news from the University of Chicago Medical Center, in the form of a regular audio podcast. Because we are all about evolution at ScienceLife, we will start by posting the pilot episode - Episode #0, if you will - and asking for help in shaping the podcast’s development. For starters, the podcast needs a name; if you have any suggestions, leave them in the comments or e-mail us at robert.mitchum@uchospitals.edu and/or dianna.douglas@uchospitals.edu. We would also love to hear what you want in a University of Chicago Medical Center podcast: more research news, patient stories, Q&As with doctors and scientists, or other segment ideas. Whether you’re in your car, in your office, or on the treadmill, enjoy listening to our debut effort!

In the pilot episode of the podcast to be named later, hear from Dianna Douglas and Rob Mitchum about the inaugural symposium of the new Sleep, Metabolism, and Health Center (SMAHC), a study of sexuality in female cancer survivors, and the identification of new targets in celiac disease.

University of Chicago Research Podcast Episode #0 by robmitchum

“If sleep does not serve an absolutely vital function, then it is the biggest mistake the evolutionary process ever made.” - Allan Rechtschaffen.

We spend approximately one-third of our lives asleep, and yet there is still much to learn about why. Modern sleep research only began less than a century ago, when Nathaniel Kleitman founded the world’s first sleep laboratory at the University of Chicago in 1925. Since then, many of the mysteries of sleep have been uncovered by UChicago researchers, including the discovery of REM sleep by Kleitman and Eugene Aserinsky in 1953, and the characterization of the first sleep disorder, narcolepsy, by Rechtschaffen and Gerry Vogel in the early 1960’s.

But in the last two decades, the study of sleep has shifted from how it works and doesn’t work to the serious consequences when sleep is lacking. Locally, the hub of this new wave of sleep research is Eve Van Cauter, who has linked insufficient or irregular sleep to a long list of chronic diseases including diabetes, obesity, and heart disease. Earlier this week, Van Cauter was doubly honored in receiving the Frederick H. Rawson Professorship and headlining the christening of the new University of Chicago Sleep, Metabolism, and Health Center (SMAHC, pronounced “Smack”). Sleep scientists from UChicago, Northwestern University, and Harvard University gathered to discuss the latest evidence on just how important sufficient sleep is for good health. The consensus message was frightening: From infancy to the golden years, the failure to get a good night’s sleep can cause a wide variety of problems - and may be a major contributor to today’s most worrisome health trends.

The importance of sleep starts with birth, said David Gozal in his talk, and maybe even before due to epigenetic imprinting during the mother’s pregnancy. Gozal reviewed his paper from last month on the elevated risk of obesity in children with shorter and less consistent sleep patterns, but also presented even newer findings, including altered expression of metabolic genes in children who snore and mouse studies that found frequently-disrupted sleep can cause animals to ingest more food and retain more fat tissue. Meanwhile, more and more studies are finding that young children are not getting nearly as much sleep as recommended.

“Sleep curtailment is not only a problem of our adult society, but clearly has pervasively infiltrated to infants and young toddlers,” Gozal said.

The effect of poor sleep upon children may go beyond metabolic issues such as obesity and diabetes, proposed neurobiologist Daniel Margoliash. In both humans and birds, Margoliash’s laboratory has found evidence that sleep helps the brain consolidate information learned during the day into memory. As young birds sleep after a day of practicing their distinctive song, the brain recreates its activity patterns from those earlier performances, presumably part of the process of making that newly learned skill permanent. For schoolchildren, the lesson is clear: lose out on sleep, and you could be losing what you were taught during the preceding day.

Later in life, the problems associated with insufficient sleep only appear to grow worse. In older adults, chronic insomnia has been linked to cognitive decline, perturbations in hormones associated with hunger, and insulin sensitivity, said Northwestern’s Phyllis Zee. Women with polycystic ovary syndrome, a condition marked by infertility, hormonal dysregulation, obesity, and diabetes, are more than 8 times more likely to suffer from obstructive sleep apnea, said David Ehrmann. And the medical effects of poor sleep can literally appear overnight - Vineet Arora’s study of poor sleep in noisy hospital wards found an average blood pressure increase of 6.2 mmHg for every hour of sleep lost. read more

photo by Cheryl Reed

A quick round-up of science around the web to end a busy, snowy week:

The “facepalm” has become a popular piece of the internet lexicon, alongside peers such as “epic fail” and “OMG.” But, as Ed Yong writes at Not Exactly Rocket Science, humans aren’t the only ones who make the universal expression of disgust and embarrassment. A group of Mandrill monkeys in an English zoo have started to make the expression. However, he writes, they may be signaling something different than facepalming humans: “Why are they doing it? It’s unlikely that they’ve found something stupid on the Internet.”

Jerry Coyne posts another example of purportedly human behavior observed in animals with the green heron - a bird that not only has a crazy expandable neck, but also has been filmed “fishing” by using a piece of bread as bait (yes, there is video). A webpage he links to at Tufts University contains a few other examples of bird tool use.

Earlier this week, in discussing his study on sleep and child obesity, David Gozal theorized that the modern family structure of two working parents has disturbed sleep routines for adults and children alike. Another study, released this week, appears to support that hypothesis, as a team including Ariel Kalil of the Harris School for Public Policy found an association between working mothers and their children’s body-mass index. Lead author Taryn Morrissey of American University stressed to Time magazine that the study is not meant to bash working moms, but rather to remind busy families about the importance of maintaining sleep schedules.”If all moms were to leave the workforce tomorrow, it wouldn’t solve childhood obesity,” she says.

With the Super Bowl coming up this weekend, allow us to point you back to a post written last year at the start of the World Cup about heart attacks in sports fans while watching important games. Some new research has come out in time for this year’s Big Game, including a study of LA fans during the 1980 and 1984 Super Bowls profiled by Ferris Jabr at New Scientist.

When you’re a hospital, you can’t call a snow day. If you’re curious as to how the Medical Center handled this week’s third-snowiest Chicago blizzard ever, here’s your answer: a lot of cots, and free lunch.

University of Chicago chemistry post-doc Niels Holton-Andersen views evolution as a “beautiful, amazingly huge experiment” that has produced elegant solutions to biological problems. His latest discovery is a self-healing, powerful adhesive produced by mussels, published last week in the Proceedings of the National Academy of Sciences. Mussels secrete the substance to stick to rocks in rivers and lakes, and researchers found that tweaking the pH of the adhesive can turn it into a self-healing gel, “kind of like Silly Putty,” Holton-Anderson said. The potential of the discovery was covered by “Green movement” blog Tainted Green.

Photo by woodleywonderworks/Wikimedia Commons

It’s a fight all parents are familiar with: the nightly battle to get their children to bed. Kids will try almost any tactic to avoid being tucked in for the night, and even then have long found ways to delay sleep with under-the-cover flashlights. But the deficit of sleep for today’s children and the degree to which that could be harming their short-term and long-term health was underscored last week by a new paper from University of Chicago and University of Louisville researchers. Led by David Gozal, professor and chair of pediatrics, and Karen Spruyt, assistant professor of pediatrics, the study used wristwatch-like activity monitors to objectively measure the sleep of more than 300 children between the ages of 4 and 10 for a week. Their results found that children are sleeping nowhere near the recommended amount of time, and that reduced or irregular sleep increases the risk of childhood obesity.

Like other studies dealing with sleep and weight gain, the research received a flood of media coverage, from sources such as CNN, the New York Times, and Time Magazine. ScienceLife conducted an extended interview with Dr. Gozal to dig deeper into the issues raised by the study, including how sleep deprivation is like an overdrawn bank account, how poor childhood sleep can predispose a child to a lifetime of health problems, and what parents can do to make sure their child is getting adequate rest at night. Here is an edited transcript of that conversation.

Q: What differentiates this study from previous studies of childhood sleep and obesity?

Gozal: Other investigators have conducted studies assessing sleep objectively using an actigraph, but the usual duration of those studies was either one day or three days. There was a study out of China where they actually identified for the first time that kids who slept more during the weekend were somewhat protected from the risk of obesity. Our study set out to look at a US population, to look objectively at both the week and the weekend, and to look at blood correlates of risk. This has never been done, to really look at what impact relatively short sleep or irregular sleep would have on the risk of disease later in life.

Q: What links did the study find between this lack of sleep and obesity?

We found that kids that slept the normally recommended number of hours were actually at the least risk. The kids that slept the least and had irregular sleep schedules were not only at very high risk, over fourfold, of obesity, but also showed a similar increase in metabolic and cardiovascular risk factors. When they tried to compensate during the weekends, the risk was less, but not eliminated. These kids were still at almost a threefold increased risk in obesity, but it’s better than a fourfold increased risk.

Q: The study revealed that he kids (aged 4-10) slept on average about 8 hours a night. Was this a surprise? Is it a concern?

It was a suspected surprise, because in the process of verifying the validity of actigraph recordings in children, we already became fully appraised of the misclassification that parents will assign to the duration of their own children’s sleep. On average, parents tend to overestimate the duration of sleep that their kids get by between 60 and 90 minutes. The moment parents close the door on their children, when they’re a certain age and above, they really don’t know what’s happening. They assume that 15-30 minutes later their kids will be asleep, when in fact it’s not true at all. I remember as a kid myself telling good night to my mom and then taking a little flashlight and book and reading for a long time. Now I’m sure what kids do is pull out their gadgets: phones, computers, mini-TVs, and video games.

The other thing that actually is rather remarkable is that over 80 percent of our kids in our country don’t wake up by themselves, they actually need to be awoken by their parents, which indicates that they still need more sleep, but aren’t getting it. There’s a paper from 1913 which measured and observed that kids of this age would sleep, on average, 10 hours. So the recommendations of all the organizations that are involved in sleep coincide on the need in this age group being 9-1/2 to 10 hours.

I’ve always said you need to look at this as if you were running a bank account. Call it a sleep account. If kids on average have an overdraft every night of two hours of sleep, by the end of the week, after five days of school, they will owe themselves and owe the account about 10 hours. If they continue doing the same during the weekend because they have friends, they want to do all these activities, and sleep is not perceived by the family as important, then they will further owe themselves an additional 4 hours, which gives an overdraft of 14 hours.

Q: So is “catch-up” sleep on the weekend an advisable way to recover from a sleep deficit?

Even if kids are catching up on sleep during the weekend, and let’s say they over-sleep two hours, then they would only reduce the debt of 10 hours accumulated during the week to about 6 hours. In both cases, they’re on overdraft, and long-term their credit history is gone. Also, you must remember, like a real bank account you’re going to pay a penalty every time you are going into overdraft.

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ScienceLife ran 219 posts in 2010, and choosing the best of them is as hard as picking a favorite gene.  So here’s a month-by-month scan of a busy year at the University of Chicago Medical Center, full of exciting discoveries in the laboratory and the clinic. The impact of some of this research is already being felt by patients receiving improved, evidence-based medical care. For other studies, the clinical benefit may be years in the future, and may take unpredictable forms. As a closing message for 2010, we’ll re-quote the recently departed Eugene Goldwasser, whose laboratory research isolating and purifying the hormone erythropoietin has helped millions of people worldwide.

“It is a particularly impressive example of how basic research can pay a dividend that could not be anticipated at the start,” Goldwasser wrote about his life’s work, “and it is a pity that the lesson still has not been learned by those who control public funding of science.”

January: Tong Chuan-He looked at how cancer may result from cells who don’t want to grow up. Scientists studied how sleep affects the language learning skills of starlings (with painstakingly acquired video of the experiment!). Richard Jones combined two laboratory staples - Western blots and DNA micro-arrays - to develop a new method for studying protein networks. While physicians such as Tammy Utset treat patients with lupus, UChicago scientists are looking for the genetic origins of the autoimmune disorder.

February: Many Medical Center employees returned from volunteering with relief efforts in Haiti, and we filmed video interviews with Rex Haydon, Tiffany Cupp, Richard Cook, and Dima Awad on their experiences. Most of the human genome is “junk” between protein-encoding regions, but Marcelo Nobrega developed a way to find important regulatory elements in that genetic sea. Like birds, human learning can be affected by sleep, and Leila Kheirandish-Gozal reported on the impact of obstructive sleep apnea upon learning in children. Can a single protein in the brain create behaviors associated with drug addiction in rats?

March: Everyone knows air travel is stressful, but did you know that eastbound flights cause stronger cortisol changes than westbound trips? The laboratory of Milan Mrksich found a way to direct stem cells to form fat or bone by shaping them into stars or flowers, a brilliant example of bioengineering. Computational neuroscientists discovered how touch is like vision in the brain, knowledge that could be used to someday re-engineer Luke Skywalker’s robot hand. Dartmouth president and Partners in Health co-founder Jim Yong Kim visited to talk about a new, needed area of research: health care delivery.

April: Researchers at the Field Museum and the University of Chicago teamed up for the Emerging Pathogens Project, an effort to find new viruses in animals before they jump to humans. Cardiologist Martin Burke tested out a new type of internal defibrillator device that can go under the skin, instead of into the heart (the clinical trial, reported in May, was a success). In a lecture to the MacLean Center of Clinical Medical Ethics, transplant surgeon J. Michael Millis described his efforts to bring American organ transplant practices to China.

May: A trial testing the erectile dysfunction drug Viagra for a rare, untreatable lung disease failed, but pulmonologist Imre Noth found a silver lining. Lauren Sallan and Michael Coates uncovered evidence of a previously unappreciated mass extinction event 360 million years ago that changed the path of life on Earth. Researchers from the University of Chicago and around the world presented science at the frontier of biotechnology at the annual BIO conference.

June: In a study that is literally the size of an entire country, epidemiologist Habibul Ahsan measured the toll of a tragic, accidental exposure of millions to arsenic in Bangladesh. Putting a gene from fireflies into the pancreas of mice isn’t mad science, it’s an imaging tool that will help study cures for diabetes. Epigenetics, the modifications that turn genes on and off, took off in 2010, and cardiologists Stephen Archer and Jalees Rehman linked one epigenetic factor to pulmonary artery hypertension.

July: Scientists don’t often get to see the fruits of their research in the flesh, but the Celebrating the Miracles gathering of diabetic children weaned off injected insulin thanks to genetic research was a moving exception (video of the event can also be viewed). Another hot topic in science and medicine this year was the use of computational analysis to sift through rapidly accumulating data, topics explored by Gary An and Andrey Rzhetsky. Or you can build a computer model of a brain network to study the dynamics of epilepsy, like neurologist Wim van Drongelen.

August: Air pollution is a problem indoors as well as outdoors in developing countries where dung and firewood are used to cook food - a problem being tackled in a project led by Sola Olopade. A study of the hormonal changes induced by a stressful test revealed a surprising protective effect of marriage and long relationships. Microbiologist Olaf Schneewind’s laboratory developed two new strategies against MRSA, the most-wanted cause of hospital-acquired infections.

September: To study multiple sclerosis, neurologist Brian Popko’ s laboratory developed a new mouse model that can replicate the disease, then spontaneously recover. Meanwhile, a new drug to treat MS, originally isolated from fungus found in wasps, was approved by the FDA and is being studied for broader uses at the Medical Center. The micro-organisms that live in humans were analyzed as part of a “microbiome” study looking at the protective effects of breast-feeding against a intestinal disease.

October: Common wisdom on quitting smoking says to stay away from cigarette-associated cues, but research from psychiatrist Harriet de Wit’s laboratory revealed that abstinence could make craving even worse. A study of how getting a good night’s rest affects dieting results suggested that “sleeping off the pounds” isn’t merely a fantasy. Graduate student Daniel Matute solved a 100-year-old riddle about how quickly new species become reproductively incompatible with each other.

November: In perhaps our favorite study of the year, geneticist George Perry found a way to acquire the genomic information of endangered species from…poop. The evolutionary biologist Leigh Van Valen passed away, but his Lewis Caroll-inspired Red Queen Hypothesis lives on. Sometimes statistics don’t tell the whole truth, as in the curious case of the aspirin paradox - why the cardio-protective drug may actually predict worse outcomes after heart attack.

December: Evolution textbooks may need a rewrite after geneticist Manyuan Long’s laboratory discovered that new genes can be just as essential as old genes. A study by neurobiologist Nicholas Hatsopoulos proved that the only thing better than a thought-controlled device is a thought-controlled device equipped with a robot arm. Ripped from the headlines: microbiologist Jack Miller weighed in on the hype over arsenic-based bacteria, and ethicist/physician/friar Daniel Sulmasy discussed the Presidential Bioethics Commission’s report on synthetic biology.

All told, it was a great year of science and medicine. Let’s do it again in 2011! Regular posting will resume Jan. 3rd. Happy Holidays.

Losing weight can be described at its simplest as a matter of counting calories during the daytime. Consume fewer calories and burn more through activity and exercise, and you’re likely to lose weight. Eat more high-calorie foods and sit on the couch all day watching football, and you get the opposite effect. But according to a new study from University of Chicago Medical Center researchers, another number should be taken into account by dieters: hours of sleep.

Given people generally do not eat or exercise while asleep (aside from some Ambien users), the link between weight and sleep may seem unlikely. But previous research at the University of Chicago found that sleep loss can wreak havoc with a person’s endocrine system, the hormones that control appetite and metabolism. In a 2004 study, men limited to only four hours of sleep a night reported increased appetite and showed hormonal changes consistent with increased hunger - increased ghrelin, which signals hunger, and decreased leptin, which signals satiety. But the long-term influence of those sleep pattern changes on weight gain or loss remained to be studied.

Monday, an experiment testing that connection was published by Plamen Penev, assistant professor of medicine, and colleagues in the Annals of Internal Medicine. And this was no easy experiment: 10 subjects had to spend two 14-day periods essentially living in a laboratory, so that scientists could control their diet, their daily activity, and the amount of sleep. But the small study reached a compelling, unexpected conclusion.

On the surface, the results may look disappointing. Subjects were allowed 8-1/2 hours in bed during one two-week period, and limited to 5-1/2 hours in bed the other two weeks. Diet and exercise were kept the same between the two periods, so that the effect of sleep alone could be isolated. But when the researchers looked at weight loss during the two periods, it was almost identical. Subjects lost about 3 kilograms, or 6 pounds, over the two weeks, whether they were getting a long night’s sleep or the reduced amount.

But not all weight loss is created equal. When the researchers looked more closely at what kind of weight was lost over the two-week periods, an important difference was revealed. With adequate sleep time, more than half of what was lost was fat. But when sleep was limited to less than 5-1/2 hours, only a quarter of the lost weight was due to reduced fat, suggesting that important protein and muscle were being shed instead of unsightly flab.

“If your goal is to lose fat, skipping sleep is like poking sticks in your bicycle wheels,” Penev said. “Cutting back on sleep, a behavior that is ubiquitous in modern society, appears to compromise efforts to lose fat through dieting. In our study it reduced fat loss by 55 percent.”

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Imagine a child who gets good grades in school, listens well to his teacher, and is commended for his good behavior in the classroom. Then slowly, his grades start to decline, he grows moodier, and his teacher reports that his attention often drifts in class. The parents are stumped - they can’t think of anything that has changed, except for the appearance of a snoring habit as the child sleeps at night. The parents wonder if their child may be showing signs of ADHD, but could the seemingly innocuous snoring be to blame?

That’s a story often heard in pediatric sleep clinics, said Leila K. Gozal, associate professor of Pediatrics and director of clinical research for the section of pediatric sleep medicine at the University of Chicago Medical Center. Over the past decade, many studies have shown that several behavioral symptoms commonly associated with ADHD - hyperactivity, mood swings, difficulty in school - have been linked in some children to obstructive sleep apnea, the disorder where sleep is frequently interrupted by episodes of blocked breathing.

Pediatric obstructive sleep apnea, or OSA, can have long-term, detrimental effects on a child’s cardiovascular and respiratory health. But it can also create neurocognitive effects, such as a reduced ability to learn and retain information, Gozal said. Previous research conducted by David Gozal, professor and chairman of pediatrics at the Medical Center, found that OSA can reduce a child’s IQ by as many as 10 points, while treatment in children with OSA can improve grades.

But many of these measurements of the neurocognitive effects of OSA on child require extensive testing and expert examiners, Leila Gozal said. So she wanted to develop a simpler test, one that could be used in any sleep clinic to directly test the effect of a sleep disorder upon a child’s memory.

“I wanted to come up with something fairly simple that can be easily done in any sleep center with almost no training or background in neuropsychology,” Gozal said. “The theory is if we come up with a simple test of pictorial memory - what you see and memorize - can we actually see any difference between kids who have OSA and kids who don’t have it?”

Using a $3.95 children’s picture book and a simple testing protocol, Gozal and her colleagues found a strong effect of OSA upon learning and memory. Published online earlier this year by the European Respiratory Journal, the study found that children with OSA were slower to learn the task, and retained less of the information the following morning when compared to normal children.

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When an adult snores, it’s annoying. When a kid snores, it’s mostly cute. But as David Gozal, chairman of pediatrics at Comer Children’s Hospital explains, those nighttime noises aren’t always innocuous.

“Snoring is not benign in kids,” Gozal said. “Snoring is clearly something that we need to not just make fun of but actually think that it has consequences on learning, behavior, the cardiovascular system, and diabetes. It can also exacerbate many existing conditions associated with learning, intelligence and behavior.”

“Those effects are silent for the most part in children, but nevertheless, if let go for a long time, they can cause damage that could be irreversible and lead to onset of disease in adults earlier and more severe than otherwise would be appropriate.”

Yet while awareness and diagnosis of sleep disorders in adults has improved over recent years, the pediatric end of the field has lagged somewhat behind. Conducting an overnight sleep study - which involves a night in the hospital or sleep center bed attached to a multitude of wires - is unpleasant enough for adults; just try performing one on a sleep-deprived 8-year-old. The number of sleep technicians and doctors trained to record and analyze the unique characteristics of sleep in children is also a fraction of those available for adult studies, Gozal said. That means very few sleep centers are able to conduct sleep studies in children, which produces waiting lists as long as one year in some areas.

And yet, better screening technology is needed to sort out relatively harmless “primary snoring,” seen in around 1 out of every 10 kids, from the more harmful obstructive sleep apnea (OSA). Often associated with adult, overweight males, OSA reflects the occurrence of frequent breathing “pauses” during sleep, which may lead to as many as hundreds of  short episodes without oxygen and abrupt awakenings during a single night of sleep. Gozal’s research found that about 3 percent of children suffer from OSA, but the condition is often undiagnosed, and sometimes even treated (through surgical removal of the tonsils and adenoids) based upon mere reports of chronic snoring.

“This is not a trivial proposition,” Gozal said. “And yet because there’s so little choice, parents and physicians decide to pursue surgery because there’s not enough access to the diagnostic tool. If it were easy, and not as expensive and inconvenient, it would allow everybody to get tested and know whether you have sleep apnea or you don’t before going to surgery.”

That’s the kind of clinical problem that inspires creative science, and Gozal’s research group at his old home, the University of Louisville, and his new, the University of Chicago, have been working toward a simpler way of testing children for obstructive sleep apnea. Recognizing that OSA causes changes in kidney function in mice and humans, Gozal hypothesized that kids with sleep apnea could be identified due to differences in what comes out of their kidney: urine. By measuring the proteins from kids diagnosed with OSA and comparing their “urinary proteome” to kids without the sleep disorder, Gozal’s team hoped to identify candidate proteins that could be used in, simply put, a pee test for sleep apnea.

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