Chapter 10. Biological Rhythms and Sleep
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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
By Karen Weintraub Is sleep induced by a benzodiazepine counted as restorative sleep? Researchers hate to admit it, but they don’t know enough about sleep to answer this question. Their best guess, several experts said, is that sleep is sleep. Dr. John Weyl Winkelman, a sleep disorders expert at Massachusetts General Hospital and Harvard Medical School, said if a patient asked him whether medicated sleep was restorative, “I’d say: ‘You tell me.’” There is quite a bit of evidence about the negative health consequences of insomnia, but researchers don’t know precisely what it is in the brain and body that is "restored" by sleep to aid optimal function. And it is unlikely that any specific stage of sleep is uniquely restorative, said Dr. Daniel J. Buysse, a sleep medicine expert and professor of psychiatry at the University of Pittsburgh. More sleep, less interrupted sleep, and sleep at the right time of night are all likely to be important, he said. There are two types of sleep: REM, when people dream, and non-REM, which has light, medium and deep portions. Sleeping pills mainly increase the amount of medium-depth non-REM sleep, Dr. Buysse said. Medications can help people fall asleep faster and reduce nighttime wakefulness, he said, and those changes are usually considered to contribute to restorative sleep. But different people respond differently. “Do you feel more rested, more alert, more able to concentrate, less irritable on medication versus off?" Dr. Buysse said. "If all those things are true then I would say it’s more restorative. If a hypnotic drug leaves you feeling hung over or more anxious, if it causes you to order five hickory smoked turkeys on the Internet without remembering, then it’s probably not good.” © 2015 The New York Times Company
Link ID: 21691 - Posted: 12.12.2015
By Lindzi Wessel Nighttime restlessness is common among people with Alzheimer’s, and many stay awake agitated and pacing long after their family members have gone to sleep. Now, scientists may have figured out why: The disease appears to degrade a special type of eye cell that tells the brain when it’s day or night. If the discovery holds up, it might offer clinicians a new way to monitor the progression of Alzheimer’s and could lead to treatments that restore a good night’s sleep. The cells in question are known as melanopsin retinal ganglion cells. They send signals to the brain center responsible for circadian rhythms, our body’s daily clock. The cells make up 1% to 2% of the eye’s light-responsive sensors, but they play no role in vision, says lead author Chiara La Morgia, a neuroscientist at the University of Bologna in Italy. Rather, they sense light levels around us, telling us when to get sleepy and when to be alert. La Morgia and her colleagues, aware of the profound sleep problems often seen in Alzheimer’s, wondered whether the cells may stop doing their job as the disease progresses. “If you lose them, you should see dysfunction of the circadian rhythms and see disrupted sleep,” says Alfredo Sadun, neuro-opthamologist at the University of California, Los Angeles, and co-author of the study. “That is the exact symptomology we see in Alzheimer’s disease.” To learn more, the researchers used dyes to mark melanopsin cells in the eyes of 30 recently deceased organ donors. They found approximately 24% fewer melanopsin cells in the eyes of people with Alzheimer’s than in the eyes of donors without the disease. © 2015 American Association for the Advancement of Science.
Aimee Cunningham For a child with attention deficit hyperactivity disorder, meeting the daily expectations of home and school life can be a struggle that extends to bedtime. The stimulant medications commonly used to treat ADHD can cause difficulty falling and staying asleep, a study finds. And that can make the next day that much harder. As parents are well aware, sleep affects a child's emotional and physical well-being, and it is no different for those with ADHD. "Poor sleep makes ADHD symptoms worse," says Katherine M. Kidwell, a doctoral student in clinical psychology at the University of Nebraska, Lincoln, who led the study. "When children with ADHD don't sleep well, they have problems paying attention the next day, and they are more impulsive and emotionally reactive." Stimulant medications boost alertness, and some studies have found a detrimental effect on children's sleep. However, other studies have concluded that the stimulants' ameliorating effects improve sleep. The drugs include amphetamines such as Adderall and methylphenidate such as Ritalin. To reconcile the mixed results on stimulants and children's sleep, Kidwell and her colleagues undertook a meta-analysis, a type of study that summarizes the results of existing research. The team found nine studies that met their criteria. These studies compared children who were taking stimulant medication with those who weren't. The studies also randomly assigned children to the experimental group or the control group and used objective measures of sleep quality and quantity, such as assessing sleep in a lab setting or with a wristwatch-like monitor at home rather than a parent's report. © 2015 npr
By Nicholas Bakalar Bright light therapy has been used effectively for seasonal affective disorder, the kind of depression that comes on at a specific time every year, often the dark days of late fall and winter, and then lifts. Now a new study has found that it may work to treat nonseasonal depression as well. Researchers randomly assigned 122 patients, 19 to 60 years old, with major depression to receive one of four treatments: 30 minutes of daily exposure to fluorescent light; 20 milligrams of Prozac daily; both light and Prozac; and a control group that received a dummy pill and exposure to an electric air purifier. The study, in JAMA Psychiatry, lasted eight weeks. Using well-validated scales that quantify depression severity, the researchers found improvements in all four groups. The difference between Prozac alone and the placebo was not statistically significant, but light therapy alone was significantly better than placebo, and light therapy with medication was the most effective treatment of all. “This is the first study to show that light treatment is an option for people with nonseasonal depression, which is much more common than seasonal depression,” said the lead author, Dr. Raymond W. Lam, a professor of psychiatry at the University of British Columbia. “Light treatment can be combined with medicine and psychotherapy, and it’s a safe treatment without a lot of side effects.” © 2015 The New York Times Company
By Nicholas Bakalar Several studies have shown that there is an association between shift work and an increased risk for heart disease and diabetes. Now a new study, in the Journal of Clinical Endocrinology & Metabolism, has found a similar association in people whose sleeping schedules change on the weekend. For seven days, 447 men and women ages 30 to 54 wore devices that measured movement and tracked when they fell asleep and woke. Almost 85 percent of the group went to sleep and woke later on their days off than during the workweek. The researchers found that the greater the mismatch in sleep timing between weekdays and weekends, the higher the metabolic risk. Sleeping late on days off was linked to lower HDL (good) cholesterol, higher triglycerides, higher insulin resistance and higher body mass index. The associations persisted after controlling for physical activity, caloric intake, alcohol use and other factors. “It’s not clear yet that this is a long-term effect,” said the lead author, Patricia M. Wong, a graduate student at the University of Pittsburgh. “But we think of this as people having to sleep and work out of sync with their internal clock, and that having to be out of sync may be having these health effects.” © 2015 The New York Times Company
Link ID: 21651 - Posted: 11.21.2015
By Elahe Izadi The days growing shorter and colder can be more than just a nuisance; the seasonal change can also trigger clinical depression. Those who suffer from seasonal affective disorder, or SAD, may turn to a light box to help make them feel better. But a new study suggests another form of therapy could be more powerful and enduring: talking. The benefits of cognitive behavioral therapy — a form of talk therapy — outlasted light therapy sessions for people suffering from SAD, according to a study published Thursday in the American Journal of Psychiatry. "Light therapy is a treatment that suppresses symptoms as long as you're using it," said lead author Kelly Rohan, a psychology professor at the University of Vermont. "So if you're not using it, there's no reason to expect the continued benefit for a treatment that works that way, whereas cognitive behavioral therapy teaches skills." And the people who learn those skills can use them long after their therapy sessions. For the study, researchers tracked 177 people who suffer from major depression that follows a recurring seasonal pattern. About half of the subjects received six weeks of daily light therapy; the others received 12 sessions of cognitive behavioral therapy over the same period of time.
By Rachel E. Gross For decades, Michael Jackson had struggled to fall asleep at night. But in 2009 the pop singer was preparing for his worldwide comeback tour, and he couldn’t afford to be at anything less than 100 percent. Desperate for sleep, he convinced an unscrupulous physician to give it to him synthetically in the form of an anesthetic so strong that it sent him almost immediately into a “druglike coma.” At first, Jackson would wake up feeling refreshed. But the nightly injections conferred only the shadow of true sleep, with none of the deep, dream-filled REM cycles that his body needed. Soon he was fading fast, his mind and mood slipping away. Within two months Jackson was dead of an overdose. If that hadn’t killed him, doctors later testified during his wrongful death trial, he would have died of sleep deprivation. Jackson’s is a particularly dramatic case. But his struggle for oblivion rings true to anyone who has dealt with insomnia. “I’m for anything that gets you through the night,” Frank Sinatra once said, “be it prayer, tranquilizers, or a bottle of Jack Daniel’s.” If you have insomnia, you’ll understand this sentiment, and you’re not alone: Regular sleep eludes up to 15 percent of the population, making insomnia the most commonly diagnosed sleep problem in America. Fortunately, the nighttime affliction is becoming steadily less mysterious—at least from the perspective of neuroscience. While insomniacs toss and turn, researchers are finally starting to understand this elusive disease. As it turns out, chronic insomnia may be more hard-wired into our brains than we had thought, and indicative of larger differences that separate the brains of the sleepless from those who so effortlessly enter the land of dreams. © 2015 The Slate Group LLC
Link ID: 21614 - Posted: 11.07.2015
By Jan Hoffman As the first semester of the school year reaches the halfway mark, countless college freshmen are becoming aware that their clothes are feeling rather snug. While the so-called freshman 15 may be hyperbole, studies confirm that many students do put on five to 10 pounds during that first year away from home. Now new research suggests that an underlying cause for the weight gain may be the students’ widely vacillating patterns of sleep. A study in the journal Behavioral Sleep Medicine looked at the sleep habits of first-semester freshmen. Researchers followed 132 first-year students at Brown University who kept daily sleep diaries. After nine weeks, more than half of them had gained nearly six pounds. There are many poor sleep habits that might have exacerbated their weight gains, a growing body of research indicates. Was it abbreviated sleep? Optimally, experts say, teenagers need about nine hours and 15 minutes a night. These freshmen averaged about seven hours and 15 minutes. In a study earlier this year, in the journal PLOS One, researchers found that when teenagers are sleep-deprived, they more readily reach for candy and desserts. Or were the Brown students’ late bedtimes the scale-tipping factor? On average, they went to bed around 1:30 a.m. A study this month in the journal Sleep that followed teenagers into adulthood found that each hour later bedtime was pushed during the school or workweek was associated with about a two-point increase in body mass index. While both the amount of sleep and the lateness of bedtime may have played a role, the researchers in the Brown study identified a new sleep factor for predicting weight gain: variability, or the extent to which a student’s bedtime and waking time changed daily. © 2015 The New York Times Company