Chapter 10. Biological Rhythms and Sleep
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By Dina Fine Maron The game is a contemporary of the original Nintendo but it still appeals to today’s teens and lab monkeys alike—which is a boon for neuroscientists. It offers no lifelike graphics. Nor does it boast a screen. Primate players—whether human or not—are simply required to pull levers and replicate patterns of flashing lights. Monkeys get a banana-flavored treat as a reward for good performance whereas kids get nickels. But the game's creators are not really in it for fun. It was created by toxicologists at the U.S. Food and Drug Administration in the 1980s to study how chronic exposure to marijuana smoke affects the brain. Players with trouble responding quickly and correctly to the game’s commands may have problems with short-term memory, attention or other cognitive issues. The game has since been adapted to address a different question: whether anesthetics used to knock pediatric patients unconscious during surgery and diagnostic tests could affect a youngster's long-term neural development and cognition. Despite 20 years’ worth of experiments in young rodents and monkeys, there have been few definitive answers. To date, numerous studies suggest that being put under with anesthesia early in life seems somehow related to future cognitive problems. But whether this association is causal or merely coincidence is unclear. Researchers do know that the young human brain is exceptionally sensitive. When kids are exposed to certain harmful chemicals in their formative years, that experience can fundamentally alter the brain’s architecture by misdirecting the physical connections between neurons or causing cell deaths. But unraveling whether anesthetics may fuel such long-term damage in humans remains a challenge. © 2015 Scientific American
by Clare Wilson Do you dream of where you'd like to go tomorrow? It looks like rats do. When the animals are shown a food treat at the end of a path they cannot access and then take a nap, the neurons representing that route in their brains fire as they sleep – as if they are dreaming about running down the corridor to grab the grub. "It's like looking at a holiday brochure for Greece the day before you go – that night you might dream about the pictures," says Hugo Spiers of University College London. Like people, rats store mental maps of the world in their hippocampi, two curved structures on either side of the brain. Putting electrodes into rats' brains as they explore their environment has shown that different places are recorded and remembered by different combinations of hippocampal neurons firing together. These "place cells" fire not only when a rat is in a certain location, but also when it sleeps, as if it is dreaming about where it has been in the past. Spiers's team wondered whether this activity during sleep might also reflect where a rat wants to go in future. They placed four rats at the bottom of a T-shaped pathway, with entry to the top bar of the T blocked by a grille. Food was placed at the end of one arm, in a position visible to the animals. Next they encouraged the rats to sleep in a cosy nest and recorded their hippocampus activity with about 50 electrodes each as they rested. Finally they put the rats back into the maze, but now with the grille and the treat removed. © Copyright Reed Business Information Ltd.
Link ID: 21103 - Posted: 06.27.2015
by Colin Barras Bacteria aren't renowned for their punctuality – but perhaps one day they will be. A working circadian clock has been inserted in E. coli that allows the microbes to keep to a 24-hour schedule. The tiny timekeepers could eventually be used in biological computers or for combating the effects of jet lag. Many plants and animals use circadian clocks to regulate their daily activities – but bacterial circadian rhythms are much less well understood. The best studied belongs to photosynthetic cyanobacteria: other common microbes, like E. coli, don't carry clocks at all, says Pamela Silver of Harvard Medical School. The cyanobacterial clock is based around the kaiABC gene cluster and ATP – the molecular fuel that nearly all living cells rely on. During the day, while the cyanobacteria are active, the KaiA protein encourages the KaiC protein to bind to phosphate groups from ATP. At night, the KaiB protein kicks into action, disrupting the activity of KaiA and encouraging KaiC to hand back the phosphate. Silver, her former student Anna Chen and other colleagues have transplanted this kaiABC clock wholesale into E. coli – the first time such a sophisticated clock has been slotted into a new microbe. But would the bacteria use their new clocks to keep time? "That's the cleverest part – and it's down to Anna's genius," says Silver. Chen suggested hooking up the kaiABC clock to a green fluorescent protein so that the phosphorylated KaiC protein would make the E. coli glow. Sure enough, the E. coli became gradually more fluorescent and then returned to a non-fluorescent state over a 24-hour period, proving that the kaiABC clock kept ticking even after it was transplanted. © Copyright Reed Business Information Ltd.
Keyword: Biological Rhythms
Link ID: 21055 - Posted: 06.16.2015
Hannah Devlin Science correspondent When Lucy Tonge started drifting off in front of the television as a 13-year-old, her parents put it down to typical teenage lethargy. And when she developed a strange habit of slumping forward when she laughed, her mum told her: “Stop doing that stupid thing when you laugh. It makes you look silly.” But she couldn’t. It was only when she started collapsing with no warning that her family sought medical advice that led to a diagnosis of narcolepsy. Soon afterwards, Tonge discovered that her sleeping disorder was very likely to have been triggered by the swine flu vaccine, which she had received in 2009 a couple of months before her symptoms first emerged. Swine flu vaccine can trigger narcolepsy, UK government concedes The government has acknowledged the rare side-effect of the Pandemrix jab, which was given to 6 million people in Britain during the 2009 and 2010 swine flu pandemic, but the Department for Work and Pensions (DWP)has rejected the compensation claims of about 80 people including Tonge on the grounds that their disabilities were not “severe”. This week, the group was given fresh hope that the challenges they face will be acknowledged after a tribunal ordered the government to pay £120,000 in damages to a 12-year-old boy whose narcolepsy was also linked to Pandemrix. © 2015 Guardian News and Media Limited
Link ID: 21052 - Posted: 06.15.2015
By David Noonan Every night, before he goes to sleep, Al Pierce, whose thunderous snoring used to drive his wife out of their bedroom, uses a small remote control to turn on an electronic sensor implanted in his chest. The sensor detects small changes in his breathing pattern—early signs that Pierce's airway is beginning to collapse on itself. When the device senses these changes, it triggers a mild jolt of electricity that travels through a wire going up his neck. The wire ends at a tiny electrode wrapped around a nerve that controls muscles in his tongue. The nerve, stimulated by the charge, activates muscles that thrust Pierce's tongue forward in his mouth, which pulls his airway open. Throughout the night the 65-year-old plumber in Florence, S.C., gets hundreds of little jolts, yet he sleeps quietly. In the morning, rested and refreshed, Pierce uses the remote to turn off the device. This new technology, called upper-airway electronic stimulation and approved by the U.S. Food and Drug Administration last summer, offers much more than relief from an annoying noise. Pierce's loud snoring was the most obvious symptom of obstructive sleep apnea, a drastically underdiagnosed disorder shared by an estimated 25 million Americans. It can lead to high blood pressure, heart disease, diabetes, depression and an impaired ability to think clearly. Overall, people with severe sleep apnea have triple the risk of death from all causes as compared with those without the disorder. © 2015 Scientific American
Link ID: 21035 - Posted: 06.10.2015
Austin Frakt One weekend afternoon a couple of years ago, while turning a page of the book I was reading to my daughters, I fell asleep. That’s when I knew it was time to do something about my insomnia. Data, not pills, was my path to relief. Insomnia is common. About 30 percent of adults report some symptoms of it, though less than half that figure have all symptoms. Not all insomniacs are severely debilitated zombies. Consistent sleeplessness that causes some daytime problems is all it takes to be considered an insomniac. Most function quite well, and the vast majority go untreated. I was one of the high-functioning insomniacs. In fact, part of my problem was that I relished the extra time awake to work. My résumé is full of accomplishments I owe, in part, to my insomnia. But it took a toll on my mood, as well as my ability to make it through a children’s book. Insomnia is worth curing. Though causality is hard to assess, chronic insomnia is associated with greater risk of anxiety, depression, hypertension, diabetes, accidents and pain. Not surprisingly, and my own experience notwithstanding, it is also associated with lower productivity at work. Patients who are successfully treated experience improved mood, and they feel healthier, function better and have fewer symptoms of depression. Which remedy would be best for me? Lunesta, Ambien, Restoril and other drugs are promised by a barrage of ads to deliver sleep to minds that resist it. Before I reached for the pills, I looked at the data. © 2015 The New York Times Company
Link ID: 21031 - Posted: 06.09.2015
David Shariatmadari Maybe we should ask the duck-billed platypus. Back in the 1950s, scientists working on humans identified a state marked by increased brain activation, accelerated breathing and heart rate, and muscular paralysis. But perhaps the most remarkable feature was a flickering of the eyes beneath closed eyelids – because all these physiological changes took place while the subjects were fast asleep. What the researchers had discovered became known as the “rapid eye movement” (REM) phase. Under normal circumstances, it recurs every 90 minutes or so, and takes up around 25% of our total time spent sleeping. It quickly became clear that people woken during REM had much better recall of their dreams; in fact, they would often say they’d just that moment been dreaming. As a result, the scientific community began to think of REM as the outward manifestation of the dream state. For the first time in human history, the most extraordinary and fantastical part of our lives had been subject to experimental observation. Not only that, but animals were found to experience REM as well – some of them more often and for longer than humans. We now know that the REM-iest mammal of them all is, bizarrely enough, Ornithorhynchus anatinus, known to you and me as the duck-billed platypus. Perhaps we shouldn’t be surprised, since, as Nature notes, “an account from as long ago as 1860, before REM sleep was discovered, reported that young platypus showed ‘swimming’ movements of their forepaws while asleep”. © 2015 Guardian News and Media Limited
by Penny Sarchet The common pet budgerigar (or parakeet) is loved for its ability to mimic its owners. But it has another special trick – it can catch yawns from other budgies, suggesting it has some kind of empathy. "Practically all vertebrates yawn," says Ramiro Joly-Mascheroni of City University, London. In 2008, he showed that dogs can catch yawns from humans. The only other species shown to yawn contagiously are humans, chimpanzees and a type of rodent called the high-yawning Sprague-Dawley rat. But Andrew Gallup of the State University of New York and his colleagues have now shown for the first time that the same happens for a species of non-mammals. To see whether budgies, a sociable parrot species, can make each other yawn, his team designed two experiments. In the first, budgies were placed in adjacent cages, either with a barrier between them, or with nothing obstructing their view of each other. They found that, when budgies could see each other, they were around three times as likely to yawn within five minutes of a yawn from their neighbour. In their second experiment, budgies were shown a video – either one that showed clips of budgies yawning, or one that had no yawning at all. Every bird that watched the yawning video also yawned, while fewer than half of the birds shown the other video yawned. "Thus far, yawning has been demonstrated to be contagious in a few highly social species," said Gallup. "To date, this is the first experimental evidence of contagious yawning in a non-mammalian species." © Copyright Reed Business Information Ltd
Link ID: 20997 - Posted: 05.30.2015
By Tara Haelle Thousands of infants each year die in their cribs from sudden infant death syndrome (SIDS) for reasons that have remained largely a mystery. A study published May 25 provides strong evidence that oxygen deprivation plays a big role. One reason the cause of SIDS has been so difficult to study is the sheer number of variables researchers have had to account for: whether the infant sleeps face down, breathes secondhand smoke or has an illness as well as whether the child has an unidentified underlying susceptibility. To isolate the effects of oxygen concentration, researchers from the University of Colorado compared the rate of SIDS in infants living at high altitudes, where the air is thin, to those living closer to sea level. Infants at high altitudes, they found, were more than twice as likely to die from SIDS. It was “very clever of the authors,” says Michael Goodstein, a pediatrician and member of the 2010–2011 Task Force on Sudden Infant Death Syndrome who was not involved in the study. “The authors did a good job controlling for other variables,” he adds. Beyond the risk of living at high altitudes, the study suggests a common link among different risk factors about the causes of SIDS. For example, the authors note that sleeping on the stomach and exposure to tobacco smoke can also contribute to hypoxia—insufficient oxygen reaching the tissues. Similarly, past research has suggested that sleeping on soft surfaces may shift the chin down, partly obstructing the airway, which might cause an infant to breathe in less oxygen. It’s unclear how hypoxia might contribute to SIDS but it could have to do with a buildup of carbon dioxide in the tissues when a child does not wake up. © 2015 Scientific American
Rob Stein The seasons appear to influence when certain genes are active, with those associated with inflammation being more active in the winter, according to new research released Tuesday. A study involving more than 16,000 people found that the activity of about 4,000 of those genes appears to be affected by the season, researchers reported in the journal Nature Communications. The findings could help explain why certain diseases are more likely than others to strike for the first time during certain seasons, the researchers say. "Certain chronic diseases are very seasonal — like seasonal affective disorder or cardiovascular disease or Type 1 diabetes or multiple sclerosis or rheumatoid arthritis," says John Todd, a geneticist at the University of Cambridge who led the research. "But people have been wondering for decades what the explanation for that is." Todd and his colleagues decided to try to find out. They analyzed the genes in cells from more than 16,000 people in five countries, including the United States and European countries in the Northern Hemisphere, and Australia in the Southern Hemisphere. And they spotted the same trend — in both hemispheres, and among men as well as women. "It's one of those observations where ... the first time you see it, you go, 'Wow, somebody must have seen this before,' " Todd says. Not all young girls avoid dirt. Hannah Rose Akerley, 7, plays in a gigantic lake of mud at the annual Mud Day event in Westland, Mich., last July. © 2015 NPR
By David Shultz We no longer live in a world governed by the sun. Artificial light lets millions of people stay up late, or work in the predawn hours. But the price many of us pay for this extra illumination is a disrupted internal clock—and, growing evidence suggests, obesity. Now, a study of mice suggests that excessive light exposure causes the rodents to burn less fat, a finding that if confirmed could lead to new paths to weight loss in humans. Many mammals have two types of tissues that store fat: brown fat and white fat. Both store energy, but white fat releases its energy stores to power other cells, while brown fat produces heat from metabolizing its contents. For years, scientists have been trying to coax brown fat into action as a way to stimulate weight loss. They’ve identified a protein called β3 adrenergic receptor that, when activated, encourages brown fat cells to burn off more fat and produce more heat. To test the relationship between light exposure and brown fat activity, researchers exposed groups of mice to artificial light for 12, 16, or 24 hours per day and monitored their levels of β3 adrenergic receptor activity. The team also monitored the rate at which energy molecules such as glucose and fatty acids were absorbed from the bloodstream by brown fat tissue to test whether the tissue was using less energy to begin with. Both metrics showed the same trend: Brown fat in mice exposed to prolonged periods of light, 16 or 24 hours compared with a normal 12, absorbed less nutrients from the blood and burned less fat as a result of reduced β3 adrenergic receptor activity. In essence, their furnaces were using less fuel and burning less intensely. To compound the problem, the fatty molecules left in the blood stream were absorbed elsewhere—often in white adipose tissue that makes up the classical body fat that causes obesity, says team leader Patrick Rensen, a biochemist at Leiden University Medical Center in the Netherlands. © 2015 American Association for the Advancement of Science.
By Lena H. Sun Most babies in the United States are born on a weekday, with the highest percentages delivered between 8 a.m. to 9 a.m., and from noon to 1 p.m., according to a report published Friday by the National Center for Health Statistics. That won't come as too much of a surprise to many pregnant women who had cesarean deliveries. Most births in the United States take place in hospitals. And as C-sections and induced labor have increased during the past few decades, more deliveries take place during the day, to maximize coordination and care with doctors and hospital staff. But what happens if the baby isn't born in the hospital, but in the home, where most out-of-hospital births occur? (Less than 2 percent of all U.S. births take place outside the hospital.) Those births were most likely to take place in the wee morning hours between 1 a.m. and 4:59 a.m., the report found. The reason: mother nature. "Where nature is taking its course, infants are more likely to be born when it's completely dark out," said T.J. Mathews, a demographer with the National Center for Health Statistics, part of the U.S. Centers for Disease Control and Prevention. Researchers think evolution may have something to do with making the middle of the night an optimal time for delivery. Say you were pregnant and part of a nomadic tribe. Having your baby in the middle of the day could mean the rest of the tribe leaves you behind as they move from place to place. "You probably bled to death," said Aaron Caughey, chairman of the Department of Obstetrics and Gynecology at Oregon Health & Science University's School of Medicine.
Keyword: Biological Rhythms
Link ID: 20904 - Posted: 05.09.2015
Douwe Draaisma When we sleep, wrote English psychiatrist Havelock Ellis over a hundred years ago, we enter a ‘dim and ancient house of shadow’. We wander through its rooms, climb staircases, linger on a landing. Towards morning we leave the house again. In the doorway we look over our shoulders briefly and with the morning light flooding in we can still catch a glimpse of the rooms where we spent the night. Then the door closes behind us and a few hours later even those fragmentary memories we had when we woke have been wiped away. That is how it feels. You wake up and still have access to bits of the dream. But as you try to bring the dream more clearly to mind, you notice that even those few fragments are already starting to fade. Sometimes there is even less. On waking you are unable to shake off the impression that you have been dreaming; the mood of the dream is still there, but you no longer know what it was about. Sometimes you are unable to remember anything at all in the morning, not a dream, not a feeling, but later in the day you experience something that causes a fragment of the apparently forgotten dream to pop into your mind. No matter what we may see as we look back through the doorway, most of our dreams slip away and the obvious question is: why? Why is it so hard to hold on to dreams? Why do we have such a poor memory for them? In 1893, American psychologist Mary Calkins published her ‘Statistics of Dreams’, a numerical analysis of what she and her husband dreamed about over a period of roughly six weeks. They both kept candles, matches, pencil and paper in readiness on the bedside table. But dreams are so fleeting, Calkins wrote, that even reaching out for matches was enough to make them disappear. Still with an arm outstretched, she was forced to conclude that the dream had gone. © 2015 Salon Media Group, Inc
By Kenneth Miller At first, no one noticed that Joe Borelli was losing his mind — no one, that is, but Borelli himself. The trim, dark-haired radiologist was 43 years old. He ran two practices, was an assistant professor at the Medical University of South Carolina and played a ferocious game of tennis. Yet he began to have trouble recalling friends’ names, forgot to run important errands and got lost driving in his own neighborhood. He’d doze off over paperwork and awaken with drool dampening his lab coat. Borelli feared he had a neurodegenerative disease, perhaps early onset Alzheimer’s. But as a physician, he knew that memory loss coupled with fatigue could also indicate obstructive sleep apnea (OSA), a disorder in which sagging tissue periodically blocks the upper airway during slumber. The sufferer stops breathing for seconds or minutes, until the brain’s alarm centers rouse him enough to tighten throat muscles. Although the cycle may repeat hundreds of times a night, the patient is usually unaware of any disturbance. Borelli checked in to a sleep clinic for tests, which came out negative. He went to a neurologist, who found nothing wrong. At another sleep clinic, Borelli was diagnosed with borderline OSA; the doctor prescribed a CPAP (continuous positive airway pressure) machine, designed to keep his airway open by gently inflating it. But he still awoke feeling exhausted, and he quit using the device after a couple of months. Borelli’s fingers soon grew so clumsy that he couldn’t button his shirt cuffs.
Link ID: 20869 - Posted: 05.02.2015
by Jessica Hamzelou You open your front door to find your boss – who is also a cat. The bizarre can seem completely normal when you're dreamingMovie Camera, perhaps because parts of your brain give up trying to figure out what's going on. Armando D'Agostino of the University of Milan in Italy thinks that the strangeness of dreams resembles psychosis, because individuals are disconnected from reality and have disrupted thought processes that lead to wrong conclusions. Hoping to learn more about psychotic thoughts, D'Agostino and his colleagues investigated how our brains respond to the bizarre elements of dreams. Because it is all but impossible to work out what a person is dreaming about while they're asleep, D'Agostino's team asked 12 people to keep diaries in which they were to write detailed accounts of seven dreams. When volunteers could remember one, they were also told to record what they had done that day and come up with an unrelated fantasy story to accompany an image they had been given. Using a "bizarreness" scoring system, the researchers found that dreams were significantly weirder than the waking fantasies the volunteers composed. "It seems counterintuitive, but there was almost no bizarreness in fantasies," says D'Agostino. "There are logical constraints on waking fantasies and they are never as bizarre as a dream." © Copyright Reed Business Information Ltd
Link ID: 20865 - Posted: 04.30.2015
By Chris Cesare The beautiful color of a sunset might be more than just a pretty picture. It could be a signal to our bodies that it’s time to reset our internal clock, the biological ticktock that governs everything from sleep patterns to digestion. That’s the implication of a new study in mice that shows these small rodents use light’s changing color to set their own clocks, a finding that researchers expect will hold for humans, too. “I think this work opens up how we're just starting to scratch the surface and look at the environmental adaptations of clocks,” says Carrie Partch, a biochemist at the University of California, Santa Cruz, who was not involved in the new study. Scientists have long known about the role light plays in governing circadian rhythms, which synchronize life’s ebb and flow with the 24-hour day. But they weren’t sure how different properties of light, such as color and brightness, contributed to winding up that clock. “As a sort of common sense notion people have assumed that the clock somehow measures the amount of light in the outside world,” says Tim Brown, a neuroscientist at the University of Manchester in the United Kingdom and an author of the new study. “Our idea was that it might be doing something more sophisticated than that.” To find out, Brown and his colleagues targeted an area in the brain called the suprachiasmatic nucleus, or SCN, a region common to all vertebrates. It’s where the body keeps time using chemical and electrical rhythms that last, on average, 24 hours. The team wanted to know if color signals sent from the eyes reached the SCN and whether that information affected the timing of the clock. © 2015 American Association for the Advancement of Science
By Lenny Bernstein The dangers associated with night-time breathing disturbances, such as obstructive sleep apnea, are well known: increased risk of high blood pressure, heart attack, stroke and diabetes, not to mention sometimes dangerous daytime drowsiness, according to the National Heart, Lung and Blood Institute. Now a study suggests that such sleep conditions can hasten the onset of both Alzheimer's disease and "moderate cognitive impairment," such as memory loss, by quite a few years. But in a bit of good news, it concludes that using a continuous positive airway pressure (CPAP) machine, the treatment of choice for sleep apnea, can prevent or delay cognitive problems. A team of researchers led by Ricardo Osorio, an assistant professor of psychiatry at NYU Langone Medical Center determined that the sleep disturbances brought on mild cognitive impairment at least 11 years earlier in groups of people enrolled in a long-term Alzheimer's disease study, even when they controlled for other factors. In the largest group, that meant self-reported or family-reported cognitive problems, such as memory loss, at about 72 instead of 83. The same was true for Alzheimer's disease itself, which started in one group at a little older than 83, instead of about 88, when other factors were ruled out. The study was published online in the journal Neurology. It could be that the intermittent cutoff of oxygen to the brain is responsible for the problems, or the sleep disruption itself may be affecting cognition, Osorio said. Studies are underway to determine the cause.
Link ID: 20810 - Posted: 04.18.2015
By Nicholas Bakalar Breathing problems during sleep may be linked to early mental decline and Alzheimer’s disease, a new study suggests. But treating apnea with a continuous positive airway pressure machine can significantly delay the onset of cognitive problems. In a group of 2,470 people, average age 73, researchers gathered information on the incidence of sleep apnea, a breathing disorder marked by interrupted breathing and snoring, and the incidence of mild cognitive impairment and Alzheimer’s disease. After adjusting for a range of variables, they found that people with disordered breathing during sleep became cognitively impaired an average of about 10 years sooner than those without the disorder. But compared with those whose sleep disorder was untreated, those using C.P.A.P. machines delayed the appearance of cognitive impairment by an average of 10 years — making their age of onset almost identical to those who had no sleep disorder at all. The lead author, Dr. Ricardo S. Osorio, a research professor of psychiatry at New York University, said the analysis, published online in Neurology, is an observational study that does not prove cause and effect. “But,” he added, “we need to increase the awareness that sleep disorders can increase the risk for cognitive impairment and possibly for Alzheimer’s. Whether treating sleep disorders truly slows the decline is still not known, but there is some evidence that it might.” © 2015 The New York Times Company
Jon Hamilton There's new evidence that the brain's activity during sleep isn't random. And the findings could help explain why the brain consumes so much energy even when it appears to be resting. "There is something that's going on in a very structured manner during rest and during sleep," says Stanford neurologist Dr. Josef Parvizi, "and that will, of course, require energy consumption." For a long time, scientists dismissed the brain's electrical activity during rest and sleep as meaningless "noise." But then studies using fMRI began to reveal patterns suggesting coordinated activity. To take a closer look, Parvizi and a team of researchers studied three people awaiting surgery for epilepsy. These people spent several days with electrodes in their brains to help locate the source of their seizures. And that meant Parvizi's team was able to monitor the activity of small groups of brain cells in real time. "We wanted to know exactly what's going on during rest," Parvizi says, "and whether or not it reflects what went on during the daytime when the subject was not resting." In the study published online earlier this month in Neuron, the team first studied the volunteers while they were awake and answering simple questions like: Did you drive to work last week? "In order to answer yes or no, you retrieve a lot of facts; you retrieve a lot of visualized memories," Parvizi says. © 2015 NPR
By Nicholas Bakalar A new study suggests that early to bed and early to rise makes a man healthy — although not necessarily wealthy or wise. Korean researchers recruited 1,620 men and women, ages 47 to 59, and administered a questionnaire to establish whether they were morning people or night owls. They found 480 morning types, 95 night owls, and 1,045 who fit into neither group. The scientists measured all for glucose tolerance, body composition and waist size, and gathered information on other health and behavioral characteristics. The study is online in The Journal of Clinical Endocrinology & Metabolism. After controlling for an array of variables, they found that compared with morning people, men who were night owls were significantly more likely to have diabetes, and women night owls were more than twice as likely to have metabolic syndrome — high blood sugar levels, excess body fat around the waist, and abnormal lipid readings. The reasons for the effect are unclear, but the scientists suggest that consuming more calories after 8 p.m. and exposure to artificial light at night can both affect metabolic regulation. Can a night owl become a morning person? “Yes,” said the lead author, Dr. Nan Hee Kim, an endocrinologist at the Korea University College of Medicine. “It can be modified by external cues such as light, activity and eating behavior. But it isn’t known if this would improve the metabolic outcomes.” © 2015 The New York Times Company
Link ID: 20781 - Posted: 04.10.2015