Chapter 10. Biological Rhythms and Sleep
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BY Bethany Brookshire We all need sleep, but attaining it can be delicate. Insomniacs can’t fall or stay asleep. Travelers suffer from jetlag. Anxiety keeps people up at night. Or maybe it’s just that jackhammer running across the street keeping your eyes open. Some people turn to earplugs, dark curtains or alcohol to soothe them to sleep. But others go to the supplement aisle and pick up melatonin. The hormone melatonin is secreted from our brains at night and helps regulate sleep. But this chemical is not restricted to humans, or even to mammals. The roots of melatonin’s role in our nightly slumbers go back much further in evolutionary history. A new paper focuses in on the role of melatonin in tiny marine creatures called zooplankton. It turns out that these animals use melatonin just as much as we do, suggesting that the origins of sleeplike behavior may lie under the sea. “For every system and feature that makes a human or other animal today, you can ask the question: Where did it start? How did it begin? What was its first role and function, and how did it become more complex?” says study coauthor Detlev Arendt, a zoologist at the University of Heidelberg in Germany. Arendt’s laboratory has been studying the answers to these questions in the marine ragworm Platynereis dumerilii. This unassuming, centipede-like, ocean-dwelling worm produces larvae that float through the open water as zooplankton. These small larvae propel themselves up and down in the water column with movements of their cilia, slender, hair-like appendages that protrude out from the organisms. © Society for Science & the Public 2000 - 2014.
By CLAIRE MALDARELLI Whether it’s lying wide awake in the middle of the night or falling asleep at an international business meeting, many of us have experienced the funk of jet lag. New research has uncovered some of the mysteries behind how our cells work together to maintain one constant daily rhythm, offering the promise of defense against this disorienting travel companion. Many organisms, including humans and fruit flies, have pacemaker neurons — specialized cells in the brain that have their own molecular clocks and oscillate in 24-hour cycles. But in order for an organism to regulate itself, all of these internal clocks must tick together to create one master clock. While scientists understood how individual neurons set their own clock, they didn’t know how that master clock was set. Working with young fruit flies, whose neuronal system is simpler than adults with fewer cells and easier to study, the researchers found that two types of neurons, which they called dawn cells and dusk cells, maintain a continuous cycle. As the sun rises, special “timeless” proteins, as they’re called, help the dawn cells to first signal to each other and then signal to the dusk cells. Then as the sun sets, proteins help the dusk cells signal to each other and then signal back to the dawn cells. Each signal tells the cells to synchronize with each other. Together, these two distinct signals drive the daily sleep and wake cycle. “This really shifts our view of these cells as super strong, independent oscillators to much more of a collective group working together to keep time,” said Justin Blau, a neurobiologist at New York University and co-author of the study. © 2014 The New York Times Company
Carl Zimmer As much as we may try to deny it, Earth’s cycle of day and night rules our lives. When the sun sets, the encroaching darkness sets off a chain of molecular events spreading from our eyes to our pineal gland, which oozes a hormone called melatonin into the brain. When the melatonin latches onto neurons, it alters their electrical rhythm, nudging the brain into the realm of sleep. At dawn, sunlight snuffs out the melatonin, forcing the brain back to its wakeful pattern again. We fight these cycles each time we stay up late reading our smartphones, suppressing our nightly dose of melatonin and waking up grumpy the next day. We fly across continents as if we could instantly reset our inner clocks. But our melatonin-driven sleep cycle lags behind, leaving us drowsy in the middle of the day. Scientists have long wondered how this powerful cycle got its start. A new study on melatonin hints that it evolved some 700 million years ago. The authors of the study propose that our nightly slumbers evolved from the rise and fall of our tiny oceangoing ancestors, as they swam up to the surface of the sea at twilight and then sank in a sleepy fall through the night. To explore the evolution of sleep, scientists at the European Molecular Biology Laboratory in Germany study the activity of genes involved in making melatonin and other sleep-related molecules. Over the past few years, they’ve compared the activity of these genes in vertebrates like us with their activity in a distantly related invertebrate — a marine worm called Platynereis dumerilii. The scientists studied the worms at an early stage, when they were ball-shaped 2-day-old larvae. The ocean swarms with juvenile animals like these. Many of them spend their nights near the ocean surface, feeding on algae and other bits of food. Then they spend the day at lower depths, where they can hide from predators and the sun’s ultraviolet rays. © 2014 The New York Times Company
by Sarah Zielinski Small, silver fish called Mexican tetra (Astyanax mexicanus) live in some Texas and Mexican rivers. Some members of the species — eyeless and blind — can be found in nearby freshwater caves. Sometimes the sighted fish wash into a cave, but they don’t do nearly as well as their blind brethren. Any surface dweller unlucky enough to end up in the dark would have some disadvantages: It would have to adapt to the loss of light and forage for unfamiliar foods, which may be not as abundant as those found in their home waters. But the fish’s biggest disadvantage may be its metabolism. Blind cavefish have lost their circadian rhythms and have developed more efficient metabolisms than the fish that live in the light, researchers report September 24 in PLOS ONE. To measure tetras’ metabolism, Damian Moran and colleagues at Lund University in Sweden placed fish in a contraption that let the fish swim in place while the researchers tracked their oxygen consumption, a measure of their metabolism. Surface and cave fish were placed in the tank under constant darkness or 12-hour light-and-dark cycles for 7 or 8 days. Then the researchers compared how the fish did under the different light regimes. All the fish took a few days to acclimate to the laboratory conditions. In the light-and-dark conditions, surface fish showed a clear circadian pattern to their oxygen consumption. These fish ramped up their metabolism by about 20 percent during the day. That increase in metabolism would let them have more energy for their hunts and feeding, which take place in the light. © Society for Science & the Public 2000 - 2014
Keyword: Biological Rhythms
Link ID: 20134 - Posted: 09.30.2014
Christie Nicholson reports. Shakespeare called sleep the chief nourisher in life’s feast. But today we know it’s so much more. Insufficient sleep contributes to the risk of cardiovascular disease, diabetes and obesity. And now a study finds that too little or too much sleep are both associated with a significant increase in sick days away from work. Almost 4,000 men and women between 30 and 64 years old (in Finland) participated in the study, which followed them for seven years. The research revealed that the absence from work due to illness increased dramatically for those who said they slept less than 6 hours or more than 9 hours per night. The sleep time that was associated with the lowest number of sick days was 7 hours 38 minutes for women and 7 hours 46 minutes for men. The study is in the journal Sleep. [Tea Lallukka, Sleep and Sickness Absence: A Nationally Representative Register-Based Follow-Up Study] Of course these findings are associative and not necessarily causal. Other factors may be responsible for the under- or oversleeping to begin with. But sleep patterns are still a warning sign for increased illness and health complications. Shakespeare put it best: Sleep…that knits up the ravell’d sleave of care. © 2014 Scientific American
Link ID: 20133 - Posted: 09.30.2014
By Tara Parker-Pope The most reliable workers are those who get seven to eight hours of sleep each night, a new study shows. Researchers from Finland analyzed the sleep habits and missed work days among 3,760 men and women over about seven years. The workers ranged in age from 30 to 64 at the start of the study. The researchers found that the use of sick days was associated with the worker’s sleep habits. Not surprisingly, they found that people who did not get enough sleep because of insomnia or other sleep problems were more likely to miss work. But notably, getting a lot of extra sleep was also associated with missed work. The workers who were most likely to take extra sick days were those who slept five hours or less or 10 hours or more. Short sleepers and long sleepers missed about five to nine more days of work than so-called optimal sleepers, workers who managed seven to eight hours of sleep each night. The workers who used the fewest number of sick days were women who slept an average of 7 hours 38 minutes a night and men who slept an average of 7:46. The study results were published in the September issue of the medical journal Sleep. © 2014 The New York Times Company
Link ID: 20074 - Posted: 09.15.2014
By Jennifer Balmer Each summer, leatherback sea turtles (Dermochelys coriacea) migrate thousands of kilometers from their tropical breeding grounds to feed in cooler waters. Yet how the animals know when to begin their long journey back south at the end of the season has mostly remained a mystery. New findings, to be published in an upcoming issue of the Journal of Experimental Marine Biology and Ecology, suggest that leatherback sea turtles may be able to sense seasonal changes in sunlight by means of an unpigmented spot on the crown of their head—known as the pink spot (pictured). Researchers conducted an examination of the anatomical structures beneath the pink spot and found that the layers of bone and cartilage were remarkably thinner than in other areas of the skull. This thin region of the skull allows the passage of light through to an area of the brain, called the pineal gland, that acts as biological clock, regulating night-day cycles and seasonal patterns of behavior. The authors suggest that the lack of pigment in the crowning pink spot and thin skull region underlying it act as a “skylight,” allowing the turtles to sense the subtle changes in sunlight that accompany changing seasons, signaling them to return south when autumn approaches. © 2014 American Association for the Advancement of Science
by Simon Makin Talking in your sleep might be annoying, but listening may yet prove useful. Researchers have shown that sleeping brains not only recognise words, but can also categorise them and respond in a previously defined way. This could one day help us learn more efficiently. Sleep appears to render most of us dead to the world, our senses temporarily suspended, but sleep researchers know this is a misleading impression. For instance, a study published in 2012 showed that sleeping people can learn to associate specific sounds and smells. Other work has demonstrated that presenting sounds or smells during sleep boosts performance on memory tasks – providing the sensory cues were also present during the initial learning. Now it seems the capabilities of sleeping brains stretch even further. A team led by Sid Kouider from the Ecole Normale Supérieur in Paris trained 18 volunteers to classify spoken words as either animal or object by pressing buttons with their right or left hand. Brain activity was recorded using EEG, allowing the researchers to measure the telltale spikes in activity that indicate the volunteers were preparing to move one of their hands. Since each hand is controlled by the motor cortex on the opposite side of the brain, these brainwaves can be matched to the intended hand just by looking at which side of the motor cortex is active. © Copyright Reed Business Information Ltd.
By Helen Briggs Health editor, BBC News website Long-term use of pills for anxiety and sleep problems may be linked to Alzheimer's, research suggests. A study of older Canadian adults found that past benzodiazepine use for three months or more was linked to an increased risk (up to 51%) of dementia. NHS guidelines say the drugs should be used for eight to 12 weeks at most. The French-Canadian team says while the link is not definitive, it is another warning that treatments should not exceed three months. "Benzodiazepine use is associated with an increased risk of Alzheimer's disease," lead researcher, Sophie Billioti de Gage of the University of Bordeaux, France, and colleagues wrote in the BMJ. "Unwarranted long-term use of these drugs should be considered as a public health concern." The study involved about 2,000 cases of Alzheimer's disease in adults aged over 66 living in Quebec. All had been prescribed benzodiazepines. They were compared with about 7,000 healthy people of the same age living in the same community. While an increased risk was found in those on benzodiazepines, the nature of the link was unclear. Dr Eric Karran, director of research at Alzheimer's Research UK, said: "This study shows an apparent link between the use of benzodiazepines and Alzheimer's disease although it's hard to know the underlying reason behind the link. BBC © 2014
By Smitha Mundasad Health reporter, BBC News More than 300 people a year in the UK and Ireland report they have been conscious during surgery - despite being given general anaesthesia. In the largest study of its kind, scientists suggests this happens in one in every 19,000 operations. They found episodes were more likely when women were given general anaesthesia for Caesarean sections or patients were given certain drugs. Experts say though rare, much more needs to be done to prevent such cases. Led by the Royal College of Anaesthetists and Association of Anaesthetists of Great Britain and Ireland, researchers studied three million operations over a period of one year. More than 300 people reported they had experienced some level of awareness during surgery. Most episodes were short-lived and occurred before surgery started or after operations were completed. But some 41% of cases resulted in long-term psychological harm. Patients described a variety of experiences - from panic and pain to choking - though not all episodes caused concern. The most alarming were feelings of paralysis and being unable to communicate, the researchers say. One patient, who wishes to remain anonymous, described her experiences of routine orthodontic surgery at the age of 12. She said: "I could hear voices around me and I realised with horror that I had woken up in the middle of the operation but couldn't move a muscle. BBC © 2014
Greta Kaul, Stanford researchers say poor sleep may be an independent risk factor for suicide in adults over 65. Researchers used data from a previous epidemiological study to compare the sleep quality of 20 older adults who committed suicide and 400 who didn't, over 10 years. Researchers found that those who didn't sleep well were 1.4 times more likely to commit suicide within a decade. Older adults have disproportionately high suicide rates in the first place, especially older men. The Stanford researchers believe that on its own, sleeping poorly could be a risk factor for suicide later in life. It may even be a more powerful predictor of suicide risk than symptoms of depression. They found that the strongest predictor of suicide was the combination of bad sleep and depression. Unlike many biological, psychological and social risk factors for suicide, sleep disorders tend to be treatable, said Rebecca Bernert, the lead author of the study. Sleep disorders are also less stigmatized than other suicide risk factors. Bernert is now studying whether treating insomnia is effective in preventing depression and suicide. The study was published in JAMA Psychiatry in August. © 2014 Hearst Communications, Inc.
By Meeri Kim The pervasive glow of electronic devices may be an impediment to a good night’s sleep. That’s particularly noticeable now, when families are adjusting to early wake-up times for school. Teenagers can find it especially hard to get started in the morning. For nocturnal animals, it spurs activity. For daytime species such as humans, melatonin signals that it’s time to sleep. As lamps switch off in teens’ bedrooms across America, the lights from their computer screens, smartphones and tablets often stay on throughout the night. These devices emit light of all colors, but it’s the blues in particular that pose a danger to sleep. Blue light is especially good at preventing the release of melatonin, a hormone associated with nighttime. Ordinarily, the pineal gland, a pea-size organ in the brain, begins to release melatonin a couple of hours before your regular bedtime. The hormone is no sleeping pill, but it does reduce alertness and make sleep more inviting. However, light — particularly of the blue variety — can keep the pineal gland from releasing melatonin, thus warding off sleepiness. You don’t have to be staring directly at a television or computer screen: If enough blue light hits the eye, the gland can stop releasing melatonin. So easing into bed with a tablet or a laptop makes it harder to take a long snooze, especially for sleep-deprived teenagers who are more vulnerable to the effects of light than adults. During adolescence, the circadian rhythm shifts, and teens feel more awake later at night. Switching on a TV show or video game just before bedtime will push off sleepiness even later even if they have to be up by 6 a.m. to get to school on time.
|By Mark Fischetti Parents, students and teachers often argue, with little evidence, about whether U.S. high schools begin too early in the morning. In the past three years, however, scientific studies have piled up, and they all lead to the same conclusion: a later start time improves learning. And the later the start, the better. Biological research shows that circadian rhythms shift during the teen years, pushing boys and girls to stay up later at night and sleep later into the morning. The phase shift, driven by a change in melatonin in the brain, begins around age 13, gets stronger by ages 15 and 16, and peaks at ages 17, 18 or 19. Does that affect learning? It does, according to Kyla Wahlstrom, director of the Center for Applied Research and Educational Improvement at the University of Minnesota. She published a large study in February that tracked more than 9,000 students in eight public high schools in Minnesota, Colorado and Wyoming. After one semester, when school began at 8:35 a.m. or later, grades earned in math, English, science and social studies typically rose a quarter step—for example, up halfway from B to B+. Two journal articles that Wahlstrom has reviewed but have not yet been published reach similar conclusions. So did a controlled experiment completed by the U.S. Air Force Academy, which required different sets of cadets to begin at different times during their freshman year. A 2012 study of North Carolina school districts that varied school times because of transportation problems showed that later start times correlated with higher scores in math and reading. Still other studies indicate that delaying start times raises attendance, lowers depression rates and reduces car crashes among teens, all because they are getting more of the extra sleep they need. © 2014 Scientific American
Ever wonder why it’s hard to focus after a bad night’s sleep? Using mice and flashes of light, scientists show that just a few nerve cells in the brain may control the switch between internal thoughts and external distractions. The study, partly funded by the National Institutes of Health, may be a breakthrough in understanding how a critical part of the brain, called the thalamic reticular nucleus (TRN), influences consciousness. “Now we may have a handle on how this tiny part of the brain exerts tremendous control over our thoughts and perceptions,” said Michael Halassa, M.D., Ph.D., assistant professor at New York University’s Langone Medical Center and a lead investigator of the study. “These results may be a gateway into understanding the circuitry that underlies neuropsychiatric disorders.” The TRN is a thin layer of nerve cells on the surface of the thalamus, a center located deep inside the brain that relays information from the body to the cerebral cortex. The cortex is the outer, multi-folded layer of the brain that controls numerous functions, including one’s thoughts, movements, language, emotions, memories, and visual perceptions. TRN cells are thought to act as switchboard operators that control the flow of information relayed from the thalamus to the cortex. To understand how the switches may work, Dr. Halassa and his colleagues studied the firing patterns of TRN cells in mice during sleep and arousal, two states with very different information processing needs. The results published in Cell, suggest that the TRN has many switchboard operators, each dedicated to controlling specific lines of communication. Using this information, the researchers could alter the attention span of mice.
By Rachel Feltman At every waking moment, your brain is juggling two very different sets of information. Input from the world around you, like sights and smells, has to be processed. But so does internal information — your memories and thoughts. Right now, for example, I’m looking at a peach: It’s yellow and pink, and has a lot of fuzz. But I also know that it smells nice (a personal assessment) and I’m imagining how good it will taste, based on my previous experience with fragrant pink fruits. The brain’s ability to handle these different signals is key to cognitive function. In some disorders, particularly autism and schizophrenia, this ability is disrupted. The brain has difficulty keeping internal and external input straight. In a new study published Thursday in Cell, researchers observe the switching method in action for the first time. While the research used mice, not humans, principal investigator and NYU Langone Medical Center assistant professor Michael Halassa sees this as a huge step toward understanding and manipulating the same functions in humans. “This is one of the few moments in my life where I’d actually say yes, absolutely this is going to translate to humans,” Halassa said. “This isn’t something based on genes or molecules that are specific to one organism. The underlying principles of how the brain circuitry works are likely to be very similar in humans and mice.” That circuitry has been hypothesized for decades. Neurologists know that the cortex of the brain is responsible for higher cognitive functions, like music and language. And the thalamus, which is an egg-like structure in the center of the brain, works to direct the flow of internal and external information before it gets to the cortex.
The news of Robin Williams’s suicide has brought mental health into the spotlight this week. According to data from the Massachusetts Violent Death Reporting System at the department of public health, the number of deaths per year as a result of suicide in the state has increased 4 percent per year since 2003. The rate increased from 424 suicides in 2003 to a peak of 600 in 2010, before dropping back down to 588. That’s 8.9 suicides per 100,000, a total of 4,500 deaths for this preventable public health problem. There are many biological, sociological, and psychological risk factors that can increase an individual’s risk for committing suicide. But did you know that poor sleep could be a major factor pushing people over the edge, even if they aren’t depressed? We all know the feeling that when we’re under slept, we aren’t quite ourselves, but according to the Substance Abuse and Mental Health Services Administration, sleep complaints are actually one of the top 10 warning signs for suicide. A study published today in JAMA Psychiatry is the first research of its kind to draw a correlation between poor sleep habits and an increased risk for death by suicide by controlling for signs of depression. Stanford University School of Medicine researchers have found that over a 10 year observation period, people with poor sleep quality and no other depressive symptoms demonstrated a 1.2 times greater risk for death by suicide.
|By Piercarlo Valdesolo In the summer of 2009 I tried to cure homemade sausages in my kitchen. One of the hazards of such a practice is preventing the growth of undesirable molds and diseases such as botulism. My wife was not on board with this plan, skeptical of my ability to safely execute the procedure. And so began many weeks of being peppered with warnings, relevant articles and concerned looks. When the time came for my first bite, nerves were high. My throat itched. My heart raced. My vision blurred. I had been botulized! Halfway through our walk to the hospital I regained my composure. Of course I had not been instantaneously struck by an incredibly rare disease that, by the way, takes at least 12 hours after consumption to manifest and does not share many symptoms with your garden variety anxiety attack. My experience had been shaped by my mindset. A decade of learning about the psychological power of expectations could not inoculate me from its effect. Psychologists know that beliefs about how experiences should affect us can bring about the expected outcomes. Though these “placebo effects” have primarily been studied in the context of pharmaceutical interventions (e.g. patients reporting pain relief after receiving saline they believed to be an analgesic), recent research has shown their strength in a variety of domains. Tell people that their job has exercise benefits and they will lose more weight than their coworkers who had no such belief. Convince people of a correlation between athleticism and visual acuity and they will show better vision after working out . Trick people into believing they are consuming caffeine and their vigilance and cognitive functioning increases. Some evidence shows that such interventions can even mitigate the negative effects of other experiences. For example, consuming placebo caffeine alleviates the cognitive consequences of sleep deprivation. © 2014 Scientific American
Emily Underwood Since swine flu swept the globe in 2009, scientists have scrambled to determine why a small percentage of children in Europe who received the flu vaccine Pandemrix developed narcolepsy, an incurable brain disorder that causes irresistible sleepiness. This week, a promising explanation was dealt a setback when prominent sleep scientist Emmanuel Mignot of Stanford University in Palo Alto, California, and colleagues retracted their influential study reporting a potential link between the H1N1 virus used to make the vaccine and narcolepsy. Some researchers were taken aback. “This was one of the most important pieces of work on narcolepsy that has come out,” says neuroimmunologist Lawrence Steinman, a close friend and colleague of Mignot’s, who is also at Stanford. The retraction, announced in Science Translational Medicine (STM), “really caught me by surprise,” he says. Others say that journal editors should have detected problems with the study’s methodology. The work provided the first substantiation of an autoimmune mechanism for narcolepsy, which could explain the Pandemrix side effect, researchers say. The vaccine, used only in Europe, seems to have triggered the disease in roughly one out of 15,000 children who received it. The affected children carried a gene variant for a particular human leukocyte antigen (HLA) type—a molecule that presents foreign proteins to immune cells—considered necessary for developing narcolepsy. In the 18 December 2013 issue of STM, Mignot and colleagues reported that T cells from people with narcolepsy, but not from healthy controls, are primed to attack by hypocretin, a hormone that regulates wakefulness. They also showed molecular similarities between fragments of the H1N1 virus and the hypocretin molecule and suggested that these fragments might fool the immune system into attacking hypocretin-producing cells. © 2014 American Association for the Advancement of Science
By PAULA SPAN Call me nuts, but I want to talk more about sleeping pill use. Hold your fire for a few paragraphs, please. Just a week after I posted here about medical efforts to help wean older patients off sleeping pills — causing a flurry of comments, many taking exception to the whole idea as condescending or dismissive of the miseries of insomnia — researchers at the Centers for Disease Control and Prevention and Johns Hopkins published findings that reinforce concerns about these drugs. I say “reinforce” because geriatricians and other physicians have fretted for years about the use of sedative-hypnotic medications, including benzodiazepines (like Ativan, Klonopin, Xanax and Valium) and the related “Z-drugs” (like Ambien) for treating insomnia. “I’m not comfortable writing a prescription for these medications,” said Dr. Cara Tannenbaum, the geriatrician at the University of Montreal who led the weaning study. “I haven’t prescribed a sedative-hypnotic in 15 years.” In 2013, the American Geriatrics Society put sedative-hypnotics on its first Choosing Wisely campaign list of “Five Things Physicians and Patients Should Question,” citing heightened fall and fracture risks and automobile accidents in older patients who took them. Now the C.D.C. has reported that a high number of emergency room visits are associated with psychiatric medications in general, and zolpidem — Ambien — in particular. They’re implicated in 90,000 adult E.R. visits annually because of adverse reactions, the study found; more than 19 percent of those visits result in hospital admissions. Among those taking sedatives and anxiety-reducing drugs, “a lot of visits were because people were too sleepy or hard to arouse, or confused,” said the lead author, Dr. Lee Hampton, a medical officer at the C.D.C. “And there were also a lot of falls.” © 2014 The New York Times Company
|By Jillian Rose Lim and LiveScience People who don't get enough sleep could be increasing their risk of developing false memories, a new study finds. In the study, when researchers compared the memory of people who'd had a good night's sleep with the memory of those who hadn't slept at all, they found that, under certain conditions, sleep-deprived individuals mix fact with imagination, embellish events and even "remember" things that never actually happened. False memories occur when people's brains distort how they remember a past event — whether it's what they did after work, how a painful relationship ended or what they witnessed at a crime scene. Memory is not an exact recording of past events, said Steven Frenda, a psychology Ph.D. student at the University of California, Irvine, who was involved in the study. Rather, fresh memories are constructed each time people mentally revisit a past event. During this process, people draw from multiple sources — like what they've been told by others, what they've seen in photographs or what they know as stereotypes or expectations, Frenda said. The new findings "have implications for people's everyday lives —recalling information for an exam, or in work contexts, but also for the reliability of eyewitnesses who may have experienced periods of restricted or deprived sleep," said Frenda, who noted that chronic sleep deprivation is on the rise. In a previous study, Frenda and his colleagues observed that people with restricted sleep (less than 5 hours a night) were more likely to incorporate misinformation into their memories of certain photos, and report they had seen video footage of a news event that didn't happen. In the current study, they wanted to see how a complete lack of sleep for 24 hours could influence a person's memory. © 2014 Scientific American