Posts tagged sleep deprivation
Articles and news from the latest research reports.
Russell Foster is a circadian neuroscientist: He studies the sleep cycles of the brain. And he asks: What do we know about sleep? Not a lot, it turns out, for something we do with one-third of our lives. In this talk, Foster shares three popular theories about why we sleep, busts some myths about how much sleep we need at different ages — and hints at some bold new uses of sleep as a predictor of mental health.
Russell Foster studies sleep and its role in our lives, examining how our perception of light influences our sleep-wake rhythms.
Sleep deprivation linked to junk food cravings
A sleepless night makes us more likely to reach for doughnuts or pizza than for whole grains and leafy green vegetables, suggests a new study from UC Berkeley that examines the brain regions that control food choices. The findings shed new light on the link between poor sleep and obesity.
Using functional magnetic resonance imaging (fMRI), UC Berkeley researchers scanned the brains of 23 healthy young adults, first after a normal night’s sleep and next, after a sleepless night. They found impaired activity in the sleep-deprived brain’s frontal lobe, which governs complex decision-making, but increased activity in deeper brain centers that respond to rewards. Moreover, the participants favored unhealthy snack and junk foods when they were sleep deprived.
“What we have discovered is that high-level brain regions required for complex judgments and decisions become blunted by a lack of sleep, while more primal brain structures that control motivation and desire are amplified,” said Matthew Walker, a UC Berkeley professor of psychology and neuroscience and senior author of the study published today (Tuesday, Aug. 6) in the journal Nature Communications.
Moreover, he added, “high-calorie foods also became significantly more desirable when participants were sleep-deprived. This combination of altered brain activity and decision-making may help explain why people who sleep less also tend to be overweight or obese.”
Previous studies have linked poor sleep to greater appetites, particularly for sweet and salty foods, but the latest findings provide a specific brain mechanism explaining why food choices change for the worse following a sleepless night, Walker said.
“These results shed light on how the brain becomes impaired by sleep deprivation, leading to the selection of more unhealthy foods and, ultimately, higher rates of obesity,” said Stephanie Greer, a doctoral student in Walker’s Sleep and Neuroimaging Laboratory and lead author of the paper. Another co-author of the study is Andrea Goldstein, also a doctoral student in Walker’s lab.
In this newest study, researchers measured brain activity as participants viewed a series of 80 food images that ranged from high-to low-calorie and healthy and unhealthy, and rated their desire for each of the items. As an incentive, they were given the food they most craved after the MRI scan.
Food choices presented in the experiment ranged from fruits and vegetables, such as strawberries, apples and carrots, to high-calorie burgers, pizza and doughnuts. The latter are examples of the more popular choices following a sleepless night.
On a positive note, Walker said, the findings indicate that “getting enough sleep is one factor that can help promote weight control by priming the brain mechanisms governing appropriate food choices.”
Tired and edgy? Sleep deprivation boosts anticipatory anxiety
UC Berkeley researchers have found that a lack of sleep, which is common in anxiety disorders, may play a key role in ramping up the brain regions that contribute to excessive worrying.
Neuroscientists have found that sleep deprivation amplifies anticipatory anxiety by firing up the brain’s amygdala and insular cortex, regions associated with emotional processing. The resulting pattern mimics the abnormal neural activity seen in anxiety disorders. Furthermore, their research suggests that innate worriers – those who are naturally more anxious and therefore more likely to develop a full-blown anxiety disorder – are acutely vulnerable to the impact of insufficient sleep.
“These findings help us realize that those people who are anxious by nature are the same people who will suffer the greatest harm from sleep deprivation,” said Matthew Walker, a professor of psychology and neuroscience at UC Berkeley and senior author of the paper, which was published in the Journal of Neuroscience.
The results suggest that people suffering from such maladies as generalized anxiety disorder, panic attacks and post-traumatic stress disorder, may benefit substantially from sleep therapy. At UC Berkeley, psychologists such as Allison Harvey, a co-author on the Journal of Neuroscience paper, have been garnering encouraging results in studies that use sleep therapy on patients with depression, bipolar disorder and other mental illnesses.
“If sleep disruption is a key factor in anxiety disorders, as this study suggests, then it’s a potentially treatable target,” Walker said. “By restoring good quality sleep in people suffering from anxiety, we may be able to help ameliorate their excessive worry and disabling fearful expectations.”
While previous research has indicated that sleep disruption and psychiatric disorders often occur together, this latest study is the first to causally demonstrate that sleep loss triggers excessive anticipatory brain activity associated with anxiety, researchers said.
“It’s been hard to tease out whether sleep loss is simply a byproduct of anxiety, or whether sleep disruption causes anxiety,” said Andrea Goldstein, a UC Berkeley doctoral student in neuroscience and lead author of the study. “This study helps us understand that causal relationship more clearly.”
In their experiments, performed at UC Berkeley’s Sleep and Neuroimaging Laboratory, Walker and his research team scanned the brains of 18 healthy young adults as they viewed dozens of images, first after a good night’s rest, and again after a sleepless night. The images were either neutral, disturbing or alternated between both.
Participants in the experiments reported a wide range of baseline anxiety levels, but none fit the criteria for a clinical anxiety disorder. After getting a full night’s rest at the lab, which researchers monitored by measuring neural electrical activity, their brains were scanned via functional MRI as they waited to be shown, and then viewed 90 images during a 45-minute session.
To trigger anticipatory anxiety, researchers primed the participants using one of three visual cues prior to each series of images. A large red minus sign signaled to participants that they were about to see a highly unpleasant image, such as a death scene. A yellow circle portended a neutral image, such as a basket on a table. Perhaps most stressful was a white question mark, which indicated that either a grisly image or a bland, innocuous one was coming, and kept participants in a heightened state of suspense.
When sleep-deprived and waiting in suspenseful anticipation for a neutral or disturbing image to appear, activity in the emotional brain centers of all the participants soared, especially in the amygdala and the insular cortex. Notably, the amplifying impact of sleep deprivation was most dramatic for those people who were innately anxious to begin with.
“This discovery illustrates how important sleep is to our mental health,” said Walker. “It also emphasizes the intimate relationship between sleep and psychiatric disorders, both from a cause and a treatment perspective.”
(Source: newscenter.berkeley.edu)
Unusual comparison nets new sleep loss marker
For years, Paul Shaw, PhD, a researcher at Washington University School of Medicine in St. Louis, has used what he learns in fruit flies to look for markers of sleep loss in humans.
Shaw reverses the process in a new paper, taking what he finds in humans back to the flies and gaining new insight into humans as a result: identification of a human gene that is more active after sleep deprivation.
“I’m calling the approach cross-translational research,” says Shaw, associate professor of neurobiology. “Normally we go from model to human, but there’s no reason why we can’t take our studies from human to model and back again.”
Shaw and his colleagues plan to use the information they are gaining to create a panel of tests for sleep loss. The tests may one day help assess a person’s risk of falling asleep at the wheel of a car or in other dangerous contexts.
PLOS One published the results on April 24.
Scientists have known for years that sleep disorders and disruption raise blood serum levels of interleukin 6, an inflammatory immune compound. Shaw showed that this change is also detectable in saliva samples from sleep-deprived rats and humans.
Based on this link, Shaw tested the activity of other immune proteins in humans to see if any changed after sleep loss. The scientists took saliva samples from research participants after they had a normal night’s sleep and after they stayed awake for 30 hours. They found two immune genes whose activity levels rose during sleep deprivation.
“Normally we would do additional human experiments to verify these links,” Shaw says. “But those studies can be quite expensive, so we thought we’d test the connections in flies first.”
The researchers identified genes in the fruit fly that were equivalent to the human genes, but their activity didn’t increase when flies lost sleep. When they screened other, similar fruit fly genes, though, the scientists found one that did.
“We’ve seen this kind of switch happen before as we compared families of fly genes and families of human genes,” Shaw says. “Sometimes the gene performing a particular role will change, but the task will still be handled by a gene in the same family.”
When the scientists looked for the human version of the newly identified fly marker for sleep deprivation, they found ITGA5 and realized it hadn’t been among the human immune genes they screened at the start of the study. Testing ITGA5 activity in the saliva samples revealed that its activity levels increased during sleep deprivation.
“We will need more time to figure out how useful this particular marker will be for detecting sleep deprivation in humans,” Shaw says. “In the meantime, we’re going to continue jumping between our flies and humans to maximize our insights.”
Red Light Increases Alertness During “Post-Lunch Dip”
Acute or chronic sleep deprivation resulting in increased feelings of fatigue is one of the leading causes of workplace incidents and related injuries. More incidents and performance failures, such as automobile accidents, occur in the mid-afternoon hours known as the “post-lunch dip.” The post-lunch dip typically occurs from 2-4 p.m., or about 16-18 hours after an individual’s bedtime from the previous night.
A new study from the Lighting Research Center (LRC) at Rensselaer Polytechnic Institute shows that exposure to certain wavelengths and levels of light has the potential to increase alertness during the post-lunch dip. The research was a collaboration between Mariana Figueiro, LRC Light and Health Program director and associate professor at Rensselaer, and LRC doctoral student Levent Sahin. Results of the study titled “Alerting effects of short-wavelength (blue) and long-wavelength (red) lights in the afternoon,” were recently published in Physiology & Behavior journal.
The collaboration between Figueiro and Sahin lays the groundwork for the possible use of tailored light exposures as a non-pharmacological intervention to increase alertness during the daytime. Figueiro has previously conducted studies that show that light has the potential to increase alertness at night. Exposure to more than 2500 lux of white light at night increases performance, elevates core body temperature, and increases heart rate.
In most studies to date, the alerting effects of light have been linked to its ability to suppress melatonin. However, results from another study led by Figueiro demonstrate that acute melatonin suppression is not needed for light to affect alertness during the nighttime. They showed that both short-wavelength (blue) and long-wavelength (red) lights increased measures of alertness but only short-wavelength light suppressed melatonin. Melatonin levels are typically lower during the daytime, and higher at night.
Figueiro and Sahin hypothesized that if light can impact alertness via pathways other than melatonin suppression, then certain wavelengths and levels of light might also increase alertness during the middle of the afternoon, close to the post-lunch dip hours.
During the study conducted at the LRC, participants experienced two experimental lighting conditions in addition to darkness. Long-wavelength “red” light (λmax = 630 nanometers) and short-wavelength “blue” light (λmax = 470 nanometers) were delivered to the corneas of each participant by arrays of light emitting diodes (LEDs) placed in 60 × 60 × 60 cm light boxes. Participant alertness was measured by electroencephalogram (EEG) and subjective sleepiness (KSS scale).
The team found that, compared to remaining in darkness, exposure to red light in the middle of the afternoon significantly reduces power in the alpha, alpha theta, and theta ranges. Because high power in these frequency ranges has been associated with sleepiness, these results suggest that red light positively affects measures of alertness not only at night, but also during the day. Red light also seemed to be a more potent stimulus for modulating brain activities associated with daytime alertness than blue light, although they did not find any significant differences in measures of alertness after exposure to red and blue lights. This suggests that blue light, especially higher levels of blue light, could still increase alertness in the afternoon. It appears that melatonin suppression is not needed for light to have an impact on objective measures of alertness.
“Our study suggests that photoreceptors other than the intrinsically photosensitive retinal ganglion cells respond to light for the arousal system,” said Figueiro. “Future research should look into the spectral sensitivity of alertness and how it changes over the course of 24 hours.”
Sahin, who has more than 10 years of experience in railway engineering, was interested in this study from a transportation safety perspective, and what the results could mean to the transportation industry. “Safety is a prerequisite and one of the most important quality indicators in the transportation industry,” said Sahin. “Our recent findings provided the scientifically valid underpinnings in approaching fatigue related safety problems in 24 hour transportation operations.”
From the present results, it is not possible to determine the underlying mechanisms contributing to light-induced changes in alertness because the optical radiation incident on the retina has multiple effects on brain activity through parallel neural pathways. According to Figueiro, that is an area that she would like to explore in future research.
Sleep Deprivation May Disrupt Your Genes
Far more than just leaving you yawning, a small amount of sleep deprivation disrupts the activity of genes, potentially affecting metabolism and other functions in the human body, a new study suggests.
It’s not clear how your health may be affected by the genetic disruption if you don’t get enough sleep. Still, the research raises the possibility that the effects of too little sleep could have long-lasting effects on your body.
"If people regularly restrict their sleep, it is possible that the disruption that we see … could have an impact over time that ultimately determines their health outcomes as they age in later life," said study co-author Simon Archer, who studies sleep at the University of Surrey, in England.
The study was published online Feb. 25 in the Proceedings of the National Academy of Sciences.
At issue is how a lack of enough sleep affects the human body. While it’s obvious that people get tired when they don’t sleep, scientists have only recently started to understand how sleep deprivation affects more than the brain, said Dr. Charles Czeisler, chief of the division of sleep medicine at Brigham and Women’s Hospital, in Boston. Research has suggested that sleep is important all the way down to the level of cells, said Czeisler, who was not involved in the new study.
For the study, researchers recruited 26 volunteers who spent a week getting a normal amount of sleep (8.5 hours) and a week getting less than normal (5.7 hours). The participants were still able to enter periods of deep sleep.
The researchers then studied the genes of the participants in blood samples and found that numerous genes, including some related to metabolism, became less active.
So what does that mean for the body? “We have no idea,” Archer said, “but these effects are not minor.” They appear to be similar to those that separate normal from abnormal types of tissue in the body, he said.
Archer said the next step will be to investigate how a lack of sleep affects the body in the long term and to figure out whether some kinds of people are more vulnerable to sleep deprivation’s negative effects on health.
For his part, Czeisler praised the study and said it raises the prospect of a blood test that will tell doctors if a patient’s body is being affected because he or she isn’t getting enough sleep. That’s important because substances such as caffeine can hide the effects of lack of sleep so patients don’t realize there’s a problem, he said.
What about the possibility of a pill that mimics the effects of sleep so people don’t have to bother getting some shut-eye in the first place? There’s no evidence to support the idea of such a pill, Czeisler said, although there’s ongoing research into how to improve the quality of sleep that people do manage to get.
(Image: iStock)
Astrocytes Identified as Target for New Depression Therapy
Neuroscience researchers from Tufts University have found that our star-shaped brain cells, called astrocytes, may be responsible for the rapid improvement in mood in depressed patients after acute sleep deprivation. This in vivo study, published in the current issue of Translational Psychiatry, identified how astrocytes regulate a neurotransmitter involved in sleep. The researchers report that the findings may help lead to the development of effective and fast-acting drugs to treat depression, particularly in psychiatric emergencies.
Drugs are widely used to treat depression, but often take weeks to work effectively. Sleep deprivation, however, has been shown to be effective immediately in approximately 60% of patients with major depressive disorders. Although widely-recognized as helpful, it is not always ideal because it can be uncomfortable for patients, and the effects are not long-lasting.
During the 1970s, research verified the effectiveness of acute sleep deprivation for treating depression, particularly deprivation of rapid eye movement sleep, but the underlying brain mechanisms were not known.
Most of what we understand of the brain has come from research on neurons, but another type of largely-ignored cell, called glia, are their partners. Although historically thought of as a support cell for neurons, the Phil Haydon group at Tufts University School of Medicine has shown in animal models that a type of glia, called astrocytes, affect behavior.
Haydon’s team had established previously that astrocytes regulate responses to sleep deprivation by releasing neurotransmitters that regulate neurons. This regulation of neuronal activity affects the sleep-wake cycle. Specifically, astrocytes act on adenosine receptors on neurons. Adenosine is a chemical known to have sleep-inducing effects.
During our waking hours, adenosine accumulates and increases the urge to sleep, known as sleep pressure. Chemicals, such as caffeine, are adenosine receptor antagonists and promote wakefulness. In contrast, an adenosine receptor agonist creates sleepiness.
“In this study, we administered three doses of an adenosine receptor agonist to mice over the course of a night that caused the equivalent of sleep deprivation. The mice slept as normal, but the sleep did not reduce adenosine levels sufficiently, mimicking the effects of sleep deprivation. After only 12 hours, we observed that mice had decreased depressive-like symptoms and increased levels of adenosine in the brain, and these results were sustained for 48 hours,” said first author Dustin Hines, Ph.D., a post-doctoral fellow in the department of neuroscience at Tufts University School of Medicine (TUSM).
“By manipulating astrocytes we were able to mimic the effects of sleep deprivation on depressive-like symptoms, causing a rapid and sustained improvement in behavior,” continued Hines.
“Further understanding of astrocytic signaling and the role of adenosine is important for research and development of anti-depressant drugs. Potentially, new drugs that target this mechanism may provide rapid relief for psychiatric emergencies, as well as long-term alleviation of chronic depressive symptoms,” said Naomi Rosenberg, Ph.D., dean of the Sackler School of Graduate Biomedical Sciences and vice dean for research at Tufts University School of Medicine. “The team’s next step is to further understand the other receptors in this system and see if they, too, can be affected.”
(Image: Paul De Koninck)
The image of mental fatigue
Functional magnetic resonance imaging offers insights into mental fatigue
We all perhaps know the feeling of mental exhaustion, but what does it mean physiologically to have mental fatigue? A new study carried out using brain scans could help scientists uncover the neurobiological mechanisms underlying mental fatigue.
According to Bui Ha Duc and Xiaoping Li of the National University of Singapore writing in a forthcoming issue of the International Journal Computer Applications in Technology, mental fatigue has become commonplace as many people face increasing mental demands from stressful jobs, longer working hours with less time to relax and increasingly suffer sleep problems. Mental fatigue has received attention from those involved generally in health and well being as well as from the military and transport industry. After all, mental fatigue not only affects the health of individuals but can also have implications for road safety and international security.
The researchers used functional magnetic resonance imaging (fMRI) to monitor activity in the brains of ten student volunteers (male and female aged 19 to 25 years) deprived of sleep for 25 hours and given a simple task repeatedly through that period. They carried out scans at 9am, 2pm, 3am, 9am the following day. All volunteers had to have avoided alcohol and caffeine for the 24 hours prior to the experiment, were all physically and mentally fit prior to participation and none had any sleep problems.
The activation of the left thalamus increases with sleep deprivation, going in an exactly opposite trend to the inferior parietal that (following the circadian rhythm) decreases in activation from 9 am to 3 am next day and then increases in activation. This finding fits with logic as the inferior parietal cortex integrates information from different sensory modalities. As all the information has to go through the thalamus and then is sent by the thalamus to the inferior parietal, when the inferior parietal decreases in activation, the thalamus must increase its activation to get the information sent through.
The team explains that a gradual increase in mental fatigue led to decreased activity in the volunteers’ brains in specific regions: the anterior cingulate gyrus, right inferior frontal, left middle frontal and right superior temporal cortex. The anterior cingulate cortex has been described as an interface between motivation, cognition and action, and has been implicated in using reinforcement information to control behavior. The fMRI scans suggest that decreased activity in this part of the brain is therefore linked to those familiar feelings of mental fatigue including lethargy and slowness of thinking.
"The research provides a neurophysiologic basis for measuring the level of mental fatigue by EEG, as well as for the intervention by non-invasive neural stimulation to maintain wakefulness," the team says. "We have developed devices for both, which will be commercialized by our spinoff company, Newrocare Pte Ltd."
(Source: eurekalert.org)
Forget All-Night Studying, a Good Night’s Sleep Is Key to Doing Well on Exams
As fall semesters wind down at the country’s colleges and universities, students will be pulling all-night study sessions to prepare for final exams. Ironically, the loss of sleep during these all-nighters could actually work against them performing well, says a Harris Health System sleep specialist.
Dr. Philip Alapat, medical director, Harris Health Sleep Disorders Center, and assistant professor, Baylor College of Medicine, recommends students instead study throughout the semester, set up study sessions in the evening (the optimal time of alertness and concentration) and get at least 8 hours of sleep the night before exams.
“Memory recall and ability to maintain concentration are much improved when an individual is rested,” he says. “By preparing early and being able to better recall what you have studied, your ability to perform well on exams is increased.”
Alapat’s recommendations:
• Get 8-9 hours of sleep nightly (especially before final exams)• Try to study during periods of optimal brain function (usually around 6-8 p.m.)
• Avoid studying in early afternoons, usually the time of least alertness
• Don’t overuse caffeinated drinks (caffeine remains in one’s system for 6-8 hours)
• Recognize that chronic sleep deprivation may contribute to development of long-term diseases like diabetes, high blood pressure and heart disease
If suffering from bouts of chronic sleep deprivation or nightly insomnia that lasts for more than a few weeks, Alapat suggests consulting a sleep specialist.
Sleep-deprived bees have difficulty relearning
Everyone feels refreshed after a good night’s sleep, but sleep does more than just rejuvenate, it can also consolidate memories. ‘The rapid eye movement form of sleep and slow wave sleep are involved in cognitive forms of memory such as learning motor skills and consciously accessible memory’, explains Randolf Mezel from the Freie Universtät Berlin, Germany. According to Menzel, the concept that something during sleep reactivates a memory for consolidation is a basic theory in sleep research. However, the human brain is far too complex to begin dissecting the intricate neurocircuits that underpin our memories, which is why Menzel has spent the last four decades working with honey bees: they are easy to train, well motivated and it is possible to identify the miniaturised circuits that control specific behaviours in their tiny brains. Intrigued by the role of sleep in memory consolidation and knowing that a bee is sleeping well when its antennae are relaxed and collapsed down, Menzel decided to focus on the role of sleep in one key memory characteristic: relearning (p. 3981). The challenge that Menzel set the bees was to learn a new route home after being displaced from a familiar path.
Menzel and his colleague Lisa Beyaert provided a hive with a well-stocked feeder and trained the bees to visit the feeder and return home fully laden. Then, when the duo were convinced that the bees had memorized the routine, they cunningly intercepted the bees at the feeder and transported them to a new location before releasing the insects to find their way home. According to Menzel, foragers learn the general lay of the land as novices before specialising in a few well-travelled routes later in their careers. He explains that the displaced bees had to rely on their earlier experiences to learn their new way home. How would loss of sleep affect the bee’s ability to learn the new route? To determine this, Menzel and Beyeart first had to check that the bees could learn the new route and that sleep deprivation hadn’t made them too tired or altered their motivation to forage.
Teaming up with electrical engineer Uwe Greggers, Menzel kitted the bees out with tiny RADAR transponders; the RADAR technology was particularly demanding to operate. Tracking the insects’ progress as they tried to learn the alternative route home, Menzel and his colleagues saw that by the second run home, the displaced bees had learned the new route. And when the trio disturbed the insects’ sleep during the night before the initial displacement by shaking them awake every 5 min, they found that the bees were unfazed. In fact they didn’t seem to need sleep to maintain their foraging energy levels and the foragers that were deprived of sleep before the first displacement run had no problems learning the new route home.
However, when the team disrupted the bees’ sleep after they had allowed the bees a single run along the new displaced route, the lack of sleep played havoc with their memories on the following day. Fewer than half of the sleep-deprived foragers made it home successfully, and those that did took more than twice as long as bees that had enjoyed an uninterrupted night’s sleep.
Sleep deprivation had dramatically affected the bees’ ability to alter a well-established memory and the team is now keen to see whether they can identify characteristic activity patterns in the slumbering insects’ brains that could represent memory formation.