Chapter 10. Biological Rhythms and Sleep
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By Rachel Zelniker, A long dark winter can be mentally and physically exhausting, but a recent study published in the journal of Clinical Psychological Science challenges the idea that it's making people depressed. Seasonal affective disorder (SAD) is commonly believed to affect a significant portion of the population in the Northern Hemisphere during the darker winter months. As many as 35 per cent of Canadians complain of having the "winter blues," according to the Centre for Addiction and Mental Health. Another 10 to 15 per cent have a mild form of seasonal depression, while about two to five per cent of Canadians will have a severe, clinical form of SAD. The disorder is based on the theory that some depressions occur seasonally in response to reduced sunlight — but recent research says that theory may be unsubstantiated. "We conducted a study using data that looked at the relationship between depression in a fairly large sample of people distributed over several degrees latitude in the United States," said Steven G. LoBello, a psychology professor at Auburn University in Montgomery, Ala., and one of the study's authors. "We looked across the four seasons to see if there was an association with sunlight, and we simply didn't find a direct relationship with sunlight, the seasons, or latitude." LoBello's study does not look at populations north of the 49th parallel, but he is confident his findings hold. "We cite in our paper a paper by [Vidje Hansen] that looked at this problem in Norway, which is north of the Arctic Circle, and they experience the polar night." According to LeBello, that research "did not find any relationship between an increase in depression and the duration of the polar night." A "seasonal pattern" modifier for depression diagnoses was officially added to the Diagnostic and Statistical Manual of Mental Disorders (DSM) in 1987. ©2016 CBC/Radio-Canada.
By Jordana Cepelewicz Last week a senior National Football League official acknowledged for the first time the link between head injuries in professional football and a degenerative brain disease called chronic traumatic encephalopathy. The admission—which has been compared with Big Tobacco’s 1997 disclosure that smoking causes cancer—comes at a time when the dangers of less severe traumatic brain injuries (TBIs), including concussions, have also been making headlines. Scientists do not yet understand the biological mechanisms underlying the detrimental effects of TBI—and as a result, effective treatments remain elusive. In fact, how to deal with even a mild concussion is the subject of debate: Some doctors prescribe rest for several weeks whereas others claim this may have negative consequences and urge patients to stay active. Now it turns out that the type of rest patients get may be key. In a study on rats published this week in The Journal of Neuroscience a team of researchers at University Hospital Zurich (UHZ) found that enhancing the slow-wave cycle of sleep after a traumatic head injury preserves brain function and minimizes damage to axons, the long projections from neurons that send signals to other cells in the brain. Previous research has shown that TBIs cause axonal damage as well as the buildup of neurotoxic molecular waste products that result from injury. In the new study the researchers examined two different methods of inducing a slow-wave sleep state—the deepest sleep stage characterized by low-frequency, high-amplitude waves. During this stage, the brain clears out protein buildup, leading the researchers to question whether it could help treat rats that had suffered a brain injury. © 2016 Scientific American
Nicola Davis Suppressing bad memories from the past can block memory formation in the here and now, research suggests. The study could help to explain why those suffering from post-traumatic stress disorder (PTSD) and other psychological conditions often experience difficulty in remembering recent events, scientists say. Writing in Nature Communications, the authors describe how trying to forget past incidents by suppressing our recollections can create a “virtual lesion” in the brain that casts an “amnesiac shadow” over the formation of new memories. “If you are motivated to try to prevent yourself from reliving a flashback of that initial trauma, anything that you experience around the period of time of suppression tends to get sucked up into this black hole as well,” Dr Justin Hulbert, one of the study’s authors, told the Guardian. “I think it makes perfect sense because we know that people with a wide range of psychological problems have difficulties with their everyday memories for ordinary events,” said Professor Chris Brewin, an expert in PTSD from University College, London, who was not involved in the study. “Potentially this could account for the memory deficits we find in depression and other disorders too.” The phenomenon came to the attention of the scientists during a lecture when a student admitted to having suffered bouts of amnesia after witnessing the 1999 Columbine high school massacre. When the student returned to the school for classes after the incident she found she could not remember anything from the lessons she was in. “Here she was surrounded by all these reminders of these terrible things that she preferred not to think about,” said Hulbert. © 2016 Guardian News and Media Limited
By Victoria Sayo Turner Seasonal affective disorder was categorized under major depression to signify depression with a yearly recurrence, a condition far more debilitating than your average “winter blues.” Credit: ©iStock Around March, some of us take a kick at the snow mounded on the curb and wonder if spring is finally going to drop by. The sun sets before we go home, and the cold coops us up except for runs to the grocery store. All of this amounts to something known informally as the winter blues, because those wintry days and dead trees can put us in a glum mood. But in the 1980s, research at the National Institutes of Mental Health led to recognition of a form of depression known as seasonal affective disorder (shortened, of course, to SAD). Seasonal affective disorder was categorized under major depression to signify depression with a yearly recurrence, a condition far more debilitating than your average “winter blues.” Mention of SAD in research and books peaked in the 1990s, and today SAD is considered a diagnosable (and insurable) disorder. Treatment ranges from psychotherapy to antidepressants to light therapy — large boxes filled with lightbulbs that look like tanning beds for your face. However, a recent study questions the existence of seasonal depression entirely. Each year, the Centers for Disease Control conducts a large cross-sectional study of the US population. A group of researchers realized they could use the CDC results independently to investigate how much depression changes by season. The 2006 version of the CDC study included a set of questions typically used to screen for depression. By analyzing the answers gathered from 34,000 adults over the course of the year, the researchers might detect flareups of seasonal affective disorder. They might see wintertime surges in depression. “To be honest, we initially did not question the [SAD] diagnosis,” writes investigator Dr. Steven LoBello, the goal being “to determine the actual extent to which depression changes with the seasons.” © 2016 Scientific American
By HEATHER MURPHY Good morning. Or confusing morning, really. Come Daylight Saving Time each year, people often complain about how thrown off they feel by the shift of an hour. I thought they were just whiny. That is, until my dinosaur got jet lag and refused to glow. Since that’s not an everyday occurrence, let me explain the dinosaur first, and then I’ll get to how my dinosaur’s problems may be connected to your own struggles to function over the next few days. (Hint: It’s not only the loss of sleep that causes problems.) Created by a company called BioPop, my Dino Pet contains lots of itty bitty dinoflagellates. Dinoflagellates, if you are having trouble summoning a sixth-grade biology lesson, are usually ocean-dwelling, single-celled organisms also known as marine plankton. People typically encounter them when they clean the inside of their aquarium (this form is often referred “brown slime algae”) or if they happen to be kayaking through a bay filled with lots of bioluminescent ones. The ones that live in my plastic dinosaur (a Christmas gift) are the latter kind. Shake them just a bit and the transparent creatures become a glow-in-the-dark snow globe. Except that a week after I set my dinosaur up, it still refused to put on its shimmer show. I tried everything. I moved it from darker to lighter spots. I played it music and whispered encouraging words. But when I turned off the lights, my little dino remained depressingly dark. © 2016 The New York Times Company
Keyword: Biological Rhythms
Link ID: 21981 - Posted: 03.14.2016
By Jerome Siegel To say whether an animal sleeps requires that we define sleep. A generally accepted definition is that sleep is a state of greatly reduced responsiveness and movement that is homeostatically regulated, meaning that when it is prevented for a period of time, the lost time is made up—an effect known as sleep rebound. Unfortunately, the application of this definition is sometimes difficult. Can an animal sleep while it is moving and responsive? How unresponsive does an animal have to be? How much of the lost sleep has to be made up for it to be considered homeostatically regulated? Is the brain activity that characterizes sleep in humans necessary and sufficient to define sleep in other animals? Apart from mammals, birds are the only other animals known to engage in both slow-wave and rapid eye movement (REM) sleep. Slow-wave sleep, also called non-REM sleep, is characterized by slow, high-amplitude waves of electrical activity in the cortex and by slow, regular respiration and heart rate. During REM sleep, animals exhibit a waking-like pattern of cortical activity, as well as physiological changes including jerky eye twitches and increased variability of heart rate and respiration. (See “The A, B, Zzzzs.”) But many more animals, including some insects and fish, engage in behaviors that might be called sleep, such as resting with slow but regular respiration and heart rates and a desensitization to environmental stimuli. In addition to diversity in the neural and physiological correlates of sleep, species vary tremendously in the intensity, frequency, and duration of sleep. Some animals tend to nap intermittently throughout the day, while others, including humans, tend to consolidate their sleep into a single, long slumber. The big brown bat is the current sleep champion, registering 20 hours per day; giraffes and elephants doze less than four hours daily. © 1986-2016 The Scientist
By Kerry Grens On a closed-circuit television I watch Marie settle into her room, unpacking her toiletries in the bathroom and arranging her clothes for the next day. Her digs at the University of Chicago sleep lab look like an ordinary hotel room, with a bed, TV, desk, nightstand. Ordinary, except for the camera keeping watch from across the bed and the small metal door in the wall next to the headboard. The door, about one foot square, is used when researchers want to sample the study participants’ blood during the night without disturbing them; an IV line passes from the person’s arm through the door and into the master control room where I’m watching Marie on the screen. She’s come to the lab on a weekday evening to be screened for possible inclusion in a study on insomnia. Marie says her sleep problems started almost 20 years ago, on the first day of her job as a flight attendant. “The phone rang in the middle of the night,” she recalls. It was work, scheduling her for a flight. “Something was triggered in my mind. It was the first time in my life I experienced a night with no sleep. Something clicked. Then the second night I couldn’t sleep. It just went on. I lost my ability to sleep.” After a few years, Marie (not her real name—she asked to remain anonymous for privacy) stopped working. Most nights she’ll sleep for a short stretch—maybe a few hours—then wake up and lie awake for hours as pain in her neck consumes her and makes her uneasy and restless. “I’ve seen psychologists, physical therapists, doctors. I’ve been prescribed medications for depression. But it didn’t work,” she says. “Every single day it’s a struggle . . . I feel like when Job was attacked by the devil. Someone is trying to take my vitality away.” © 1986-2016 The Scientist
Link ID: 21959 - Posted: 03.07.2016
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