Chapter 14. Biological Rhythms, Sleep, and Dreaming
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Ian Sample Science editor Too little sleep may bring on a form of the marijuana “munchies”, say scientists who found that sleep-deprived people craved crisps, sweets and biscuits far more than healthier foods. The US researchers believe that skimping on sleep alters brain chemicals in much the same way as the hunger-boosting ingredient in cannabis, which has long propped up snack sales at 24-hour convenience stores. After several nights of poor sleep, healthy volunteers who took part in the study reached for snacks containing more calories - and nearly twice as much fat - than ones they favoured after sleeping well for the same period, the scientists say. When sleepy, the participants had terrible trouble resisting the snacks, even when they were full, said Erin Hanlon, who led the study at the University of Chicago. Research has shown time and again that sleep loss raises the risk of obesity, but the reasons are complex and unclear. Insufficient sleep disrupts hormones that govern appetite and satiety. But those who sleep less have more time to eat, and may be too tired to exercise. To muddy the waters further, obesity can lead to breathing problems that themselves disrupt sleep patterns. In a small study published in the journal Sleep, Hanlon invited 14 men and women in their twenties to spend two four-day sessions at the university’s clinical research centre. The volunteers’ time in bed was controlled, so that on one visit they averaged 7.5 hours of sleep a night, but on the other only 4 hours 11 minutes a night. During their stays, the volunteers ate identical meals, dished out at 9am, 2pm and 7pm.
By Claire Asher A poor night's sleep is enough to put anyone in a bad mood, and although scientists have long suspected a link between mood and sleep, the molecular basis of this connection remained a mystery. Now, new research has found several rare genetic mutations on the same gene that definitively connect the two. Sleep goes hand-in-hand with mood. People suffering from depression and mania, for example, frequently have altered sleeping patterns, as do those with seasonal affective disorder (SAD). And although no one knows exactly how these changes come about, in SAD sufferers they are influenced by changes in light exposure, the brain’s time-keeping cue. But is mood affecting sleep, is sleep affecting mood, or is there a third factor influencing both? Although a number of tantalizing leads have linked the circadian clock to mood, there is “no definitive factor that proves causality or indicates the direction of the relationship,” says Michael McCarthy, a neurobiologist at the San Diego Veterans’ Affairs Medical Center and the University of California (UC), San Diego. To see whether they could establish a link between the circadian clock, sleep, and mood, scientists in the new study looked at the genetics of a family that suffers from abnormal sleep patterns and mood disorders, including SAD and something called advanced sleep phase, a condition in which people wake earlier and sleep earlier than normal. The scientists screened the family for mutations in key genes involved in the circadian clock, and identified two rare variants of the PERIOD3 (PER3) gene in members suffering from SAD and advanced sleep phase. “We found a genetic change in people who have both seasonal affective disorder and the morning lark trait” says lead researcher Ying-Hui Fu, a neuroscientist at UC San Francisco. When the team tested for these mutations in DNA samples from the general population, they found that they were extremely rare, appearing in less than 1% of samples. © 2016 American Association for the Advancement of Science.
Link ID: 21926 - Posted: 02.23.2016
Tina Hesman Saey Sonia Vallabh knows what will probably kill her. In 2011, the Boston-area law school graduate learned she carries the same genetic mutation that caused her mother’s death from a rare brain-wasting prion disease. Prions are twisted forms of normal brain proteins that clump together and destroy nerves. About 10 to 15 percent of prion diseases are caused by a mutation in the PRNP gene, leading to such deadly diseases as Creutzfeldt-Jakob disease, Gerstmann-Sträussler-Scheinker syndrome and fatal familial insomnia, the disease that killed Vallabh’s mother. Grief, shared with family and friends, came first. Eventually, Vallabh realized, “We can’t get around this prognosis.… We’ve got to go through it.” So began her and husband Eric Minikel’s odyssey to learn about the disease that had turned their lives upside down. A scientist friend came by with a flash drive loaded with research papers about prion diseases. “We didn’t have the vocabulary” to understand the information, Vallabh says. So she took a sabbatical from her job to take biology and chemistry classes. Minikel kept writing transportation software, but attended night classes with his wife. Vallabh’s first foray into brain research was as a technician in a lab studying Huntington’s disease. During “science nights” at the couple’s home, scientist pals team-taught biology and biochemistry. The couple took the biggest step when Minikel left his consulting job and both enrolled in graduate school to study prion diseases. Prion proteins, some of which clump together or form fibrils, as in this E. coli bacteria, are often used to model how proteins misfold in some neurodegenerative disorders. © Society for Science & the Public 2000 - 2016
By Ariana Eunjung Cha The Centers for Disease Control and Prevention just published their first national survey of sleep for all 50 states and the District of Columbia. In many respects, it's consistent with our image of ourselves as bleary-eyed insomniacs downing triple espresso shots and melatonin pills as we stare at our iPhones like zombies. The CDC found that more than a third of American adults are not getting the recommended amount of seven-plus hours of sleep on a regular basis. Here's a look at what sleep looks like across the United States, as broken down by marital status, geography, race/ethnicity and employment. The results aren't always what you might expect. 1. First, here's a breakdown of how much sleep Americans are getting overall. This is based on a random telephone survey of 444,306 respondents. Overall, about 65 percent reported a "healthy sleep duration" (seven or more hours of sleep on a regular basis) and about 35 percent reported they were getting less than that. 2. Being unable to work or being unemployed appears to affect sleep in a negative way. That's consistent with previous research on sleep quality and mental health issues like depression that can be related to unemployment. 3. People with college degrees or higher were more likely to get enough sleep. Maybe it's because they are more likely to know how important good sleep is to your health or maybe because they have jobs or income that allow them to get more sleep?
By Jordana Cepelewicz Seasonal variations play a major role in the animal kingdom—in reproduction, food availability, hibernation, even fur color. Whether this seasonality has such a significant influence on humans, however, is an open question. Its best-known association is with mood—that is, feeling down during the colder months and up in the summer—and, in extreme cases, seasonal depression, a phenomenon known as seasonal affective disorder (SAD). A new study published in this week’s Proceedings of the National Academy of Sciences seeks to delve deeper into how human biology has adapted not only to day/night cycles (circadian rhythms) but to yearly seasonal patterns as well. Scientists have previously found seasonal variation in the levels and concentrations of certain compounds associated with mood (including dopamine and serotonin), conception and even mortality. Now for the first time, using functional MRI, “it’s [been] conclusively shown that cognition and the brain’s means of cognition are seasonal,” says neuroscientist Gilles Vandewalle of the University of Liège in Belgium, the study’s lead researcher. These findings come at a time when some scientists are disputing the links between seasonality and mental health. Originally aiming to investigate the impact of sleep and sleep deprivation on brain function, Vandewalle and his fellow researchers placed 28 participants on a controlled sleep/wake schedule for three weeks before bringing them into the laboratory, where they stayed for 4.5 days. During this time they underwent a cycle of sleep deprivation and recovery in the absence of seasonal cues such as natural light, time information and social interaction. Vandewalle’s team repeated the entire procedure with the same subjects several times throughout the course of nearly a year and a half. © 2016 Scientific American
By Michelle Roberts Health editor, Exposure to short flashes of light at night could help sleeping travellers adjust to new time zones and avoid jet lag, according to US scientists. The light beams travel through the eyelids and this tells the brain to re-set the body's inner biological clock, the Stanford researchers believe. They tested the method in 39 volunteers and found it shifted a person's body clock by about two hours. An hour of the flashlight therapy was enough to achieve this effect. People's bodies synchronise to the 24-hour pattern of daytime and night they are used to. And when they travel across time zones to a new light-dark schedule, they need to realign. While most people can easily manage a long-haul flight across one or two time zones, crossing several time zones messes with the body clock. Jet lag can leave travellers tired, irritable and disorientated for days. As a remedy, some people take melatonin tablets, which mimic a hormone released in the evening. Some try phototherapy - light boxes that simulate daylight. But Dr Jamie Zeitzer and colleagues at Stanford University School of Medicine believe sleeping in front of a strobe light could work better. They asked volunteers to go to bed and wake up at the same times every day for about two weeks. Next, they were asked to sleep in the lab, where some were exposed to continuous light and others a strobe light (two-millisecond flashes of light, similar to a camera flash, 10 seconds apart) for an hour. The flashing-light group reported a nearly two-hour delay in the onset of sleepiness the following night. In comparison, the delay in sleepiness was 36 minutes for the continuous-light group. Dr Zeitzer calls his therapy "biological hacking". Cells in the back of the eye that detect the light send messages to a part of the brain that sets the body clock. The light fools the brain into thinking the day is longer than it really is, which shifts the inner clock. © 2016 BBC.
Keyword: Biological Rhythms
Link ID: 21881 - Posted: 02.10.2016
By John Bohannon Didn't get your 40 winks last night? Better not get yourself arrested, or you may admit to a crime you didn't commit. False confessions are surprisingly easy to extract from people simply by keeping them awake, according to a new study of sleep deprivation. It puts hard numbers to a problem that criminal law reformers have worried about for decades. The “crime” in question took place in a sleep lab run by Kimberly Fenn at Michigan State University in East Lansing. Together, she and Elizabeth Loftus, a psychologist at the University of California (UC), Irvine, and two of their former Ph.D. students recruited 88 Michigan State students to take part in an experiment. During two separate visits, the students worked at computers solving problems and filling out questionnaires. They were all given a stern warning: Do not press the escape key, because it will erase important study data. After their second session, the subjects were split into two groups. Half of them were forced to stay awake all night under the watch of the researchers. Scrabble, TV shows, and a card game called euchre seemed to do the trick. The rest were allowed to get a full night's sleep. But that also required policing. "We actually had a student leave the study because he wanted to stay awake all night to study for an exam the next day," Fenn says, adding that "I certainly do not advocate this!" The next morning, everyone received a typed statement describing their performance. The statement accused them of hitting the escape key on the first day, even though none of them actually did so—the computers recorded all keystrokes. © 2016 American Association for the Advancement of Science
Bruce Bower Winter doesn’t deserve its dour reputation as the season of depression, scientists say. Rates of major depression, a psychiatric condition marked by intense sadness, hopelessness, insomnia and a general loss of interest or pleasure, don’t markedly change from one season to another among U.S. adults, says a team led by psychologist Steven LoBello of Auburn University at Montgomery in Alabama. Neither do symptoms intensify or become more numerous during winter among those already suffering from depression, the researchers report online January 19 in Clinical Psychological Science. A small number of people with regular fall or winter depression may have gone undetected in the new study, which surveyed more than 30,000 U.S. adults. Still, it’s becoming harder to justify the current psychiatric diagnosis of major depression “with seasonal pattern,” LoBello and Auburn colleagues Megan Traffanstedt and Sheila Mehta conclude. Because it’s a recurring disorder, depression can strike in two consecutive winters by chance, the researchers say. Depression in three or more consecutive winters could be due to personal and social factors unrelated to shorter days, they add. “Being depressed during winter is not evidence that one is depressed because of winter,” LoBello says. © Society for Science & the Public 2000 - 2016
By Nicholas Bakalar Women with sleeping difficulties are at increased risk for Type 2 diabetes, researchers report. Scientists used data from 133,353 women who were generally healthy at the start of the study. During 10 years of follow-up, they found 6,407 cases of Type 2 diabetes. The researchers looked at four sleep problems: self-reported difficulty falling or staying asleep, frequent snoring, sleep duration of less than six hours, and either sleep apnea or rotating shift work. The study is in Diabetologia. Self-reported difficulty sleeping was associated with higher B.M.I., less physical activity, and more hypertension and depression. But even after adjusting for these and other health and behavioral characteristics, sleeping difficulty was still associated with a 22 percent increased risk for Type 2 diabetes. Compared to women with no sleep problems, those with two of the sleep conditions studied had double the risk, and those with all four had almost four times the risk of developing the illness. The senior author, Dr. Frank B. Hu, a professor of nutrition and epidemiology at Harvard, said that sleep problems are associated with excess secretion of two hormones: ghrelin, which increases appetite, and cortisol, which increases stress and insulin resistance. Both are linked to metabolic problems that increase the risk for diabetes. “And,” he added, “it’s not just quantity of sleep, but quality as well” that is associated with these health risks. © 2016 The New York Times Company
By JAN HOFFMAN One evening in the late fall, Lucien Majors, 84, sat at his kitchen table, his wife Jan by his side, as he described a recent dream. Mr. Majors had end-stage bladder cancer and was in renal failure. As he spoke with a doctor from Hospice Buffalo , he was alert but faltering. In the dream, he said, he was in his car with his great pal, Carmen. His three sons, teenagers, were in the back seat, joking around. “We’re driving down Clinton Street,” said Mr. Majors, his watery, pale blue eyes widening with delight at the thought of the road trip. “We were looking for the Grand Canyon.” And then they saw it. “We talked about how amazing, because there it was — all this time, the Grand Canyon was just at the end of Clinton Street!” Mr. Majors had not spoken with Carmen in more than 20 years. His sons are in their late 50s and early 60s. “Why do you think your boys were in the car?” asked Dr. Christopher W. Kerr, a Hospice Buffalo palliative care physician who researches the therapeutic role of patients’ end-of-life dreams and visions. “My sons are the greatest accomplishment of my life,” Mr. Majors said. He died three weeks later. For thousands of years, the dreams and visions of the dying have captivated cultures, which imbued them with sacred import. Anthropologists, theologians and sociologists have studied these so-called deathbed phenomena. They appear in medieval writings and Renaissance paintings, in Shakespearean works and set pieces from 19th-century American and British novels, particularly by Dickens. One of the most famous moments in film is the mysterious deathbed murmur in “Citizen Kane”: “Rosebud!” Even the law reveres a dying person’s final words, allowing them to be admitted as evidence in an unusual exception to hearsay rules. © 2016 The New York Times Company
Link ID: 21852 - Posted: 02.03.2016
Laura Sanders Signals in the brain can hint at whether a person undergoing anesthesia will slip under easily or fight the drug, a new study suggests. The results, published January 14 in PLOS Computational Biology, bring scientists closer to being able to tailor doses of the powerful drugs for specific patients. Drug doses are often given with a one-size-fits-all attitude, says bioengineer and neuroscientist Patrick Purdon of Massachusetts General Hospital and Harvard Medical School. But the new study finds clear differences in people’s brain responses to similar doses of an anesthetic drug, Purdon says. “To me, that’s the key and interesting point.” Cognitive neuroscientist Tristan Bekinschtein of the University of Cambridge and colleagues recruited 20 people to receive low doses of the general anesthetic propofol. The low dose wasn’t designed to knock people out, but to instead dial down their consciousness until they teetered on the edge of awareness — a point between being awake and alert and being drowsy and nonresponsive. While the drug was being delivered, participants repeatedly heard either a buzzing sound or a noise and were asked each time which they heard, an annoying question designed to gauge awareness. Of the 20 people, seven were sidelined by the propofol and they began to respond less. Thirteen other participants, however, kept right on responding, “fighting the drug,” Bekinschtein says. © Society for Science & the Public 2000 - 2016.
By Veronique Greenwood Last year a new sleep drug called Belsomra came on the market, featuring a mechanism unlike any other pill: it mimics narcolepsy. That might sound odd, but the potential users are many. More than 8.5 million Americans take prescription sleep aids, and many others use snooze-inducing over-the-counter medications. All these pills, including Belsomra, do one of two things: they enhance the effects of the neurotransmitter GABA, known for quieting brain activity, or they arrest the actions of neurotransmitters that keep the brain aroused. Yet it's not quite as simple as flipping a switch; the drugs have a range of side effects, including daytime drowsiness, hallucinations and sleep-eating. Here's an overview of the sleeping pills currently available in the U.S.—plus a look at cognitive-behavior therapy for insomnia, which may be more successful than drugs alone. It requires a lot more work than popping a pill, but cognitive-behavior therapy for insomnia (CBT-I) has been shown to successfully alleviate sleep problems. Aimed at developing healthy habits, CBT-I comes with a lot of homework—between weekly or so visits with a specialist, a patient keeps track of hours spent in bed and hours sleeping and uses the bed only for sleep and sex. The patient must stay up until an established bedtime and get up on awakening, generating a sleep deficit that makes it easier to fall asleep at the right time. Avoiding caffeine and alcohol after 4 P.M. and timing exercise so that it doesn't interfere with drowsiness are also part of the system. © 2016 Scientific American
Link ID: 21770 - Posted: 01.11.2016
Jon Hamilton There's growing evidence that a lack of sleep can leave the brain vulnerable to Alzheimer's disease. "Changes in sleep habits may actually be setting the stage" for dementia, says Jeffrey Iliff, a brain scientist at Oregon Health & Science University in Portland. The brain appears to clear out toxins linked to Alzheimer's during sleep, Iliff explains. And, at least among research animals that don't get enough solid shut-eye, those toxins can build up and damage the brain. Iliff and other scientists at OHSU are about to launch a study of people that should clarify the link between sleep problems and Alzheimer's disease in humans. It has been clear for decades that there is some sort of link. Sleep disorders are very common among people with Alzheimer's disease. For a long time, researchers thought this was simply because the disease was "taking out the centers of the brain that are responsible for regulating sleep," Iliff says. But two recent discoveries have suggested the relationship may be more complicated. The first finding emerged in 2009, when researchers at Washington University in St. Louis showed that the sticky amyloid plaques associated with Alzheimer's develop more quickly in the brains of sleep-deprived mice. Then, in 2013, Iliff was a member of a team that discovered how a lack of sleep could be speeding the development of those Alzheimer's plaques: A remarkable cleansing process takes place in the brain during deep sleep, at least in animals. What happens, Iliff says, is "the fluid that's normally on the outside of the brain — cerebrospinal fluid, it's a clean, clear fluid — it actually begins to recirculate back into and through the brain along the outsides of blood vessels." This process, via what's known as the glymphatic system, allows the brain to clear out toxins, including the toxins that form Alzheimer's plaques, Iliff says. © 2016 npr
By Roni Caryn Rabin Melatonin has been shown to be effective in randomized clinical trials — the kind considered the gold standard in medicine — but it may work better for some sleep problems than others. “There is pretty strong evidence it’s effective for jet lag,” said D. Craig Hopp, a program director at the National Center for Complementary and Integrative Health, part of the National Institutes of Health. But “the evidence is more equivocal for chronic things like insomnia.” A 2002 Cochrane review that analyzed 10 randomized trials, most of them comparing oral melatonin to placebo, concluded that melatonin is “remarkably effective in preventing or reducing jet lag.” It not only helped people fall asleep faster and sleep more soundly, but also led to less daytime fatigue and improved general well-being. Eight of the 10 trials found that taking melatonin for several days after arriving at a destination reduced jet lag from flights crossing at least five time zones. In many of the trials, people also took melatonin on the day of the flight or for several days before the trip, usually in the late afternoon or early evening. Once at the destination, melatonin should be taken close to bedtime, aiming for the local hours between 10 p.m. and midnight. Doses of 0.5 milligrams and 5 milligrams were both effective, though people fell asleep faster and slept better with the larger dose. For others with insomnia, melatonin has more modest benefits. A 2013 analysis that looked at 19 randomized controlled trials involving 1,683 subjects determined that on average, melatonin reduced the amount of time it took to fall asleep by seven minutes when compared with placebo and increased total sleep time by eight minutes. © 2015 The New York Times Company
Carl Zimmer Throughout the day, a clock ticks inside our bodies. It rouses us in the morning and makes us sleepy at night. It raises and lowers our body temperature and at the right times, and regulates the production of insulin and other hormones. From Our Advertisers The body’s circadian clock even influences our thoughts and feelings. Psychologists have measured some of its effects on the brain by having people take cognitive tests at different times of day. As it turns out, late morning turns out to be the best time to try doing tasks such as mental arithmetic that demand that we hold several pieces of information in mind at once. Later in the afternoon is the time to attempt simpler tasks, like searching for a particular letter in a page of gibberish. Another clue about the clock in our brains comes from people with conditions such as depression and bipolar disorder. People with these disorders often have trouble sleeping at night, or feel groggy during the day. Some people with dementia experience “sundowning,” becoming confused or aggressive at the end of the day. “Sleep and activity cycles are a very big part of psychiatric illnesses,” said Huda Akil, a neuroscientist at the University of Michigan. Yet neuroscientists have struggled to understand exactly how the circadian clock affects our minds. After all, researchers can’t simply pop open a subject’s skull and monitor his brain cells over the course of each day. A few years ago, Dr. Akil and her colleagues came up with an idea for the next best thing. © 2015 The New York Times Company
Need to remember something important? Take a break. A proper one – no TV or flicking through your phone messages. It seems that resting in a quiet room for 10 minutes without stimulation can boost our ability to remember new information. The effect is particularly strong in people with amnesia, suggesting that they may not have lost the ability to form new memories after all. “A lot of people think the brain is a muscle that needs to be continually stimulated, but perhaps that’s not the best way,” says Michaela Dewar at Heriot-Watt University in Edinburgh, UK. New memories are fragile. They need to be consolidated before being committed to long-term storage, a process thought to happen while we sleep. But at least some consolidation may occur while we’re awake, says Dewar – all you need is a timeout. In 2012, Dewar’s team showed that having a rest helps a person to remember what they were told a few minutes earlier. And the effect seems to last. People who had a 10-minute rest after hearing a story remembered 10 per cent more of it a week later than those who played a spot-the-difference game immediately afterwards. “We dim the lights and ask them to sit in an empty, quiet room, with no mobile phones,” says Dewar. When asked what they had been thinking about afterwards, most volunteers said they had let their minds wander. Now Dewar, along with Michael Craig at the University of Edinburgh and their colleagues, have found that spatial memories can also be consolidated when we rest. © Copyright Reed Business Information Ltd.
Rae Ellen Bichell Ever notice the catnaps that older relatives take in the middle of the day? Or how grandparents tend to be early risers? You're not alone. Colleen McClung did, too. A neuroscientist at the University of Pittsburgh Medical Center, McClung wanted to know what was going on in the brain that changes people's daily rhythms as they age. We all have a set of so-called clock genes that keep us on a 24-hour cycle. In the morning they wind us up, and at night they help us wind down. A study out Monday in Proceedings of the National Academy of Sciences found that those genes might beat to a different rhythm in older folks. "When you think about the early bird dinner specials, it sort of fits in with their natural shift in circadian rhythms," says McClung. "There is a core set of genes that has been described in every animal — every plant all the way down from fungus to humans — and they're pretty much the same set of genes." The genes are the master controllers of a bunch of other genes that control processes ranging from metabolism to sleep. When you woke up this morning, the timekeeping genes told a gland in your brain to give a jolt of the stress hormone cortisol to wake up. Tonight, they'll tell a gland to spit out melatonin, a hormone that makes you sleepy. "You can think of them as sort of the conductor of an orchestra," says McClung. They make sure all the other genes keep time. © 2015 npr
Carl Zimmer Over the past few million years, the ancestors of modern humans became dramatically different from other primates. Our forebears began walking upright, and they lost much of their body hair; they gained precision-grip fingers and developed gigantic brains. But early humans also may have evolved a less obvious but equally important advantage: a peculiar sleep pattern. “It’s really weird, compared to other primates,” said Dr. David R. Samson, a senior research scientist at Duke University. In the journal Evolutionary Anthropology, Dr. Samson and Dr. Charles L. Nunn, an evolutionary biologist at Duke, reported that human sleep is exceptionally short and deep, a pattern that may have helped give rise to our powerful minds. Until recently, scientists knew very little about how primates sleep. To document orangutan slumber, for example, Dr. Samson once rigged up infrared cameras at the Indianapolis Zoo and stayed up each night to watch the apes nod off. By observing their movements, he tracked when the orangutans fell in and out of REM sleep, in which humans experience dreams. “I became nocturnal for about seven months,” Dr. Samson said. “It takes someone who wants to get their Ph.D. to be motivated enough to do that.” In the new study. Dr. Samson and Dr. Nunn combined that information with studies of 19 other primate species. The researchers found wide variations in how long the animals slept. Mouse lemurs doze for seventeen hours a day, for example, while humans sleep just seven hours or so a day — “the least of any primate on the planet,” said Dr. Samson. © 2015 The New York Times Company
Scientists hunting for a drug that speeds stroke recovery might find one in the bedside cabinets of millions of Americans. Mice treated with small doses of the sleeping pill Ambien recovered more quickly from strokes than those given a placebo. Ambien is the best-known incarnation of the drug zolpidem, which was prescribed 40 million times in the US in 2011. The researchers say that the finding should be replicated by other labs before proceeding with clinical trials, but it’s an intriguing result for a problem in desperate need of solutions. Strokes cut off the blood supply to part of the brain, leading to the death of oxygen-starved tissue. Some tissue repair can take place in the months afterwards, but most people never fully recover. Although physical therapy can help, there are no drugs that increase the amount of brain tissue repaired. “There are various natural mechanisms that promote a degree of normal recovery in animals and people, but it’s limited”, says Gary Steinberg of Stanford University School of Medicine, who was lead author of the study. One such mechanism may be an increase in signalling by the GABA neurotransmitter in parts of the brain that are able to rewire themselves. Because Ambien acts on GABA receptors, Steinberg and his team wondered whether they could use it to hack this mechanism to improve recovery. © Copyright Reed Business Information Ltd.
Tina Hesman Saey SAN DIEGO — New research may help explain why chronic stress, sleep deprivation and other disruptions in the body’s daily rhythms are linked to obesity. Chronic exposure to stress hormones stimulates growth of fat cells, Mary Teruel of Stanford University reported December 16 at the annual meeting of the American Society for Cell Biology. Normally, stress hormones, such as cortisol, are released during waking hours in regular bursts that follow daily, or circadian, rhythms. Those regular pulses don’t cause fat growth, Teruel and colleagues discovered. But extended periods of exposure to the hormones, caused by such things as too little sleep, break up that rhythm and lead to more fat cells. Even though only about 10 percent of fat cells are replaced each year, the body maintains a pool of prefat cells that are poised to turn into fat. “If they all differentiated at once, you’d be drowning in fat,” Teruel said. Previous studies have shown that a protein called PPAR-gamma controls the development of fat cells and that stress hormones turn on production of PPAR-gamma. Teruel’s team discovered that prefat cells with levels of PPAR-gamma below a certain threshold don’t transform into fat in laboratory tests. Steady hormone exposure eventually allowed the precursor cells to build up enough PPAR-gamma to cross the threshold into fat making. But in cells given the same total amount of stress hormone in short pulses, PPAR-gamma levels rose and fell. © Society for Science & the Public 2000 - 2015