Posts tagged anxiety disorders
Articles and news from the latest research reports.
Research hints at why stress is more devastating for some
Some people take stress in stride; others are done in by it. New research at Rockefeller University has identified the molecular mechanisms of this so-called stress gap in mice with very similar genetic backgrounds — a finding that could lead researchers to better understand the development of psychiatric disorders such as anxiety and depression.
“Like people, each animal has unique experiences as it goes through its life. And we suspect that these life experiences can alter the expression of genes, and as a result, affect an animal’s susceptibility to stress,” says senior author Bruce McEwen, Alfred E. Mirsky Professor and head of the Harold and Margaret Milliken Hatch Laboratory of Neuroendocrinology. “We have taken an important step toward explaining the molecular origins of this stress gap by showing that inbred mice react differently to stress, with some developing behaviors that resemble anxiety and depression, and others remaining resilient.”
The results, published September 2 in Molecular Psychiatry, point toward potential new markers to aid the diagnosis of stress-related disorders, such as anxiety and depression, and a promising route to the development of new treatments for these devastating disorders.
In experiments, researchers stressed the mice by exposing them to daily, unpredictable bouts of cage tilting, altered dark-light cycles, confinement in tight spaces and other conditions mice dislike with the goal of reproducing the sort of stressful experiences thought to be a primary cause of depression in humans. Afterward, in tests to see if the mice displayed the rodent equivalent of anxiety and depression symptoms, they found about 40 percent showed high levels of behaviors that included a preference for a dark compartment over a brightly lit one, or a loss of interest in sugar water. The remaining 60 percent recovered well from the stress. This distinction between the susceptible mice and the resilient ones was so fundamental that it emerged even before the mice were subjected to stress; some unstressed mice showed an anxiety-like preference for a dark compartment over a lighted one.
The researchers found that the highly stress-susceptible mice had less of an important molecule known as mGlu2 in a stress-involved region of the brain known as the hippocampus. The mGlu2 decrease, they determined, resulted from an epigenetic change, which affects the expression of genes, in this case the gene that codes for mGlu2.
“If you think of the genetic code as words in a book, the book must be opened in order for you to read it. These epigenetic changes, which affect histone proteins associated with DNA, effectively close the book, so the code for mGlu2 cannot be read,” says first author Carla Nasca, a postdoc in the lab and a fellow of the American Foundation for Suicide Prevention. Previously, she and colleagues implicated mGlu2 in depression when they showed that a promising potential treatment known as acetyl carnitine rapidly alleviated depression-like symptoms in rats and mice by reversing these epigenetic changes to mGlu2 and causing its levels to increase.
“Currently, depression is diagnosed only by its symptoms,” Nasca says. “But these results put us on track to discover molecular signatures in humans that may have the potential to serve as markers for certain types of depression. Our work could also lead to a new generation of rapidly acting antidepressants, such as the candidate acetyl carnitine, which would be particularly important to reduce the risk of suicide.”
A reduction in mGlu2 matters because this molecule regulates the neurotransmitter glutamate. While glutamate plays a crucial role relaying messages between neurons as part of many important processes, too much can lead to harmful structural changes in the brain.
“The brain is constantly changing. When stressful experiences lead to anxiety and depressive disorders the brain becomes locked in a state it cannot spontaneously escape,” McEwen says. “Studies like this one are increasingly focusing on the regulation of glutamate as an underlying mechanism in depression and, we hope, opening promising new avenues for the diagnosis and treatment of this devastating disorder.”
Beneath the Surface: What Zebrafish Can Tell Us About Anxiety
The right tool for the job is important. A surgeon wouldn’t use a chainsaw when a scalpel offers more control. But sometimes the best treatments available aren’t precise. For example, anxiety medications available today are too blunt in how they target the brain, according to Ian Woods, assistant professor of biochemistry at Ithaca College.
“If you look at current treatments for anxiety disorders, the approach is a bit like taking a sledgehammer to a mosquito,” he said. “The treatments may work for anxiety, but they can have a lot of side effects.”
Woods researches how genetics influence responses to stimuli that can trigger anxiety, and he’s using zebrafish — a tropical member of the minnow family named for the black stripes on their bodies — to do so. He and his team of student researchers examine how fish with tweaked genes respond to different triggers compared to unmodified fish. The work could someday lead to better, more nuanced medications for anxiety disorders.
Zebrafish make ideal test subjects for several reasons. The embryos are transparent and develop outside the mother’s body, making it easy for Woods and his team to observe their growth under a microscope. They develop rapidly, are easy to care for and easy to breed in large quantities.
Specifically, Woods is looking at neuropeptides, which are the chemical messengers between brain cells. Different neuropeptides deliver different messages, which in turn produce different behaviors.
“Fish have the same neuropeptides as humans, and they mostly do the same things in the brain,” Woods said. “We can never faithfully model a complex human behavior like anxiety, but when we’re trying to figure out how the brain works, it’s useful to see inside a fish.”
Woods and his team isolate specific genes to disrupt, amplify, alter or replace, then analyze the movements of the modified fish with the aid of a computerized camera system. They examine responses to stimuli such as slight changes in water temperature, decreases in light intensity, or mild chemical irritants such as mustard oil.
“By observing the ensuing behavioral changes in the fish, we know how that replaced gene changed the message in the brain,” Woods explained. For example, fish exhibiting anxiety-like behaviors might hug the walls of the tank, while the rest will swim toward the middle. It’s not unlike social experiments in which the room temperature is raised gradually to see how human occupants will react.
“Genes typically don’t cause the anxiety,” Woods said. “But they can make organisms more susceptible to environmental triggers that might elicit what we’d call an anxious behavior.”
Anxiety disorders are the most common mental illness in the United States; over 40 million Americans suffer from some type in their lifetimes. But medications can be overprescribed and abused. For example, emergency room visits related to the use of Xanax and related drugs doubled from 2005 to 2011, according to the U.S. Substance Abuse and Mental Health Services Administration.
The anatomy of fear: Understanding the biological underpinnings of anxiety, phobias and PTSD
Fear in a mouse brain looks much the same as fear in a human brain.
When a frightening stimulus is encountered, the thalamus shoots a message to the amygdala — the primitive part of the brain — even before it informs the parts responsible for higher cognition. The amygdala then goes into its hard-wired fight-or-flight response, triggering a host of predictable symptoms, including racing heart, heavy breathing, startle response, and sweating.
The similarities of fear response in the brains of mice and men have allowed scientists to understand the neural circuitry and molecular processes of fear and fear behaviors perhaps better than any other response. That understanding has spurred breakthroughs in treatments for psychiatric disorders that are underpinned by fear.
Anxiety disorders are one of the most common mental illnesses in the country, with nearly one-third of Americans experiencing symptoms at least once during their lives. There are generalized anxiety disorders and fear-related disorders, which include panic disorders, phobias, and post-traumatic stress disorder (PTSD).
Emory psychiatrist and researcher Kerry Ressler is on the front lines of fear-disorder research. In his lab at Yerkes National Primate Research Center, he studies the molecular and cellular mechanisms of fear learning and extinction in mouse models. At Grady Memorial Hospital, he investigates the psychology, genetics, and biology of PTSD. And through the Grady Trauma Project, he works to draw attention to the problem of inner city intergenerational violence.
"If you look at Kerry’s work, it can seem like it’s all over the place — he’s got so many studies going on, and he collaborates with so many other scientists," says Barbara Rothbaum, associate vice chair of clinical research in psychiatry and director of the Trauma and Anxiety Recovery Program at Emory. "But they are all pieces to the same puzzle. All his work, from molecular to clinical to policy, fits together and starts telling a story." A Howard Hughes Medical Institute investigator, Ressler was recently elected to the Institute of Medicine — one of the highest honors in the fields of health and medicine. He was named a member of a new national PTSD consortium led by Draper Laboratory. And he recently appeared on the Charlie Rose show’s brain series.
Panic attacks seem to tie the fear-related disorders together, he explained on Charlie Rose. Everyone experiences fear, which evolved as a survival mechanism, but it only rises to a clinical level when people are unable to function normally in the face of it. For instance, PTSD includes not only intrusive thoughts, memories, nightmares, and startle responses, but also the concept of avoidance, which may extend to other areas of the individual’s life.
"There’s a patient I’ve seen who was attacked in a dark alley," Ressler shared on the show. "Initially it just felt dangerous to go out at night, but after a while she grew afraid of men and couldn’t go to that part of town. Then she couldn’t leave her house, and finally, her bedroom. The world got more and more dangerous."
According to the National Institute of Mental Health, over 18 percent of American adults suffer from anxiety disorders, characterized as excessive worry or tension that often leads to other physical symptoms. Previous studies of anxiety in the brain have focused on the amygdala, an area known to play a role in fear. But a team of researchers led by biologists at the California Institute of Technology (Caltech) had a hunch that understanding a different brain area, the lateral septum (LS), could provide more clues into how the brain processes anxiety. Their instincts paid off—using mouse models, the team has found a neural circuit that connects the LS with other brain structures in a manner that directly influences anxiety.
"Our study has identified a new neural circuit that plays a causal role in promoting anxiety states," says David Anderson, the Seymour Benzer Professor of Biology at Caltech, and corresponding author of the study. "Part of the reason we lack more effective and specific drugs for anxiety is that we don’t know enough about how the brain processes anxiety. This study opens up a new line of investigation into the brain circuitry that controls anxiety."
The team’s findings are described in the January 30 version of the journal Cell.
Led by Todd Anthony, a senior research fellow at Caltech, the researchers decided to investigate the so-called septohippocampal axis because previous studies had implicated this circuit in anxiety, and had also shown that neurons in a structure located within this axis—the LS—lit up, or were activated, when anxious behavior was induced by stress in mouse models. But does the fact that the LS is active in response to stressors mean that this structure promotes anxiety, or does it mean that this structure acts to limit anxiety responses following stress? The prevailing view in the field was that the nerve pathways that connect the LS with different brain regions function as a brake on anxiety, to dampen a response to stressors. But the team’s experiments showed that the exact opposite was true in their system.
In the new study, the team used optogenetics—a technique that uses light to control neural activity—to artificially activate a set of specific, genetically identified neurons in the LS of mice. During this activation, the mice became more anxious. Moreover, the researchers found that even a brief, transient activation of those neurons could produce a state of anxiety lasting for at least half an hour. This indicates that not only are these cells involved in the initial activation of an anxious state, but also that an anxious state persists even after the neurons are no longer being activated.
"The counterintuitive feature of these neurons is that even though activating them causes more anxiety, the neurons are actually inhibitory neurons, meaning that we would expect them to shut off other neurons in the brain," says Anderson, who is also an investigator with the Howard Hughes Medical Institute (HHMI).
So, if these neurons are shutting off other neurons in the brain, then how can they increase anxiety? The team hypothesized that the process might involve a double-inhibitory mechanism: two negatives make a positive. When they took a closer look at exactly where the LS neurons were making connections in the brain, they saw that they were inhibiting other neurons in a nearby area called the hypothalamus. Importantly, most of those hypothalamic neurons were, themselves, inhibitory neurons. Moreover, those hypothalamic inhibitory neurons, in turn, connected with a third brain structure called the paraventricular nucleus, or PVN. The PVN is well known to control the release of hormones like cortisol in response to stress and has been implicated in anxiety.
This anatomical circuit seemed to provide a potential double-inhibitory pathway through which activation of the inhibitory LS neurons could lead to an increase in stress and anxiety. The team reasoned that if this hypothesis were true, then artificial activation of LS neurons would be expected to cause an increase in stress hormone levels, as if the animal were stressed. Indeed, optogenetic activation of the LS neurons increased the level of circulating stress hormones, consistent with the idea that the PVN was being activated. Moreover, inhibition of LS projections to the hypothalamus actually reduced the rise in cortisol when the animals were exposed to stress. Together these results strongly supported the double-negative hypothesis.
"The most surprising part of these findings is that the outputs from the LS, which were believed primarily to act as a brake on anxiety, actually increase anxiety," says Anderson.
Knowing the sign—positive or negative—of the effect of these cells on anxiety, he says, is a critical first step to understanding what kind of drug one might want to develop to manipulate these cells or their molecular constituents. If the cells had been found to inhibit anxiety, as originally thought, then one would want to find drugs that activate these LS neurons, to reduce anxiety. However, since the group found that these neurons instead promote anxiety, then to reduce anxiety a drug would have to inhibit these neurons.
"We are still probably a decade away from translating this very basic research into any kind of therapy for humans, but we hope that the information that this type of study yields about the brain will put the field and medicine in a much better position to develop new, rational therapies for psychiatric disorders," says Anderson. "There have been very few new psychiatric drugs developed in the last 40 to 50 years, and that’s because we know so little about the brain circuitry that controls the emotions that go wrong in a psychiatric disorder like depression or anxiety."
The team will continue to map out this area of the brain in greater detail to understand more about its role in controlling stress-induced anxiety.
"There is no shortage of new questions that have been raised by these findings," Anderson says. "It may seem like all that we’ve done here is dissect a tiny little piece of brain circuitry, but it’s a foothold onto a very big mountain. You have to start climbing someplace."
Drugs that weaken traumatic memories hold promise for PTSD treatment
Memories of traumatic events often last a lifetime because they are so difficult to treat through behavioral approaches. A preclinical study in mice published by Cell Press January 16th in the journal Cell reveals that drugs known as histone deacetylase inhibitors (HDACis) can enhance the brain’s ability to permanently replace old traumatic memories with new memories, opening promising avenues for the treatment of posttraumatic stress disorder (PTSD) and other anxiety disorders.
Caption: Metabolic activity (green and red colors) in the hippocampus (white dotted line) of animals that underwent extinction training in combination with HDACis (right) is significantly higher than in animals that underwent extinction training alone (left). Metabolic activity serves to estimate the learning capacity of an animal. Credit: Cell, Gräff et al.
"Psychotherapy is often used for treating PTSD, but it doesn’t always work, especially when the traumatic events occurred many years earlier," says senior study author Li-Huei Tsai of the Massachusetts Institute of Technology. "This study provides a mechanism explaining why old memories are difficult to extinguish and shows that HDACis can facilitate psychotherapy to treat anxiety disorders such as PTSD."
One common treatment for anxiety disorders is exposure-based therapy, which involves exposing patients to fear-evoking thoughts or events in a safe environment. This process reactivates the traumatic memory, opening a short time window during which the original memory can be disrupted and replaced with new memories. Exposure-based therapy is effective when the traumatic events occurred recently, but until now, it was not clear whether it would also be effective for older traumatic memories.
To address this question, Tsai and her team used a protocol for studying fear responses associated with traumatic memories. In the first phase, the researchers exposed mice to a tone followed by an electrical footshock. Once the mice learned to associate these two events, they began to freeze in fear upon hearing the tone by itself, even when they did not receive a shock. Using an extinction protocol, which is similar to exposure-based therapy, the researchers repeatedly presented the tone without the shock to test whether the mice could unlearn the association between these two events and would stop freezing in response to the tone. The extinction protocol was successful for mice that were exposed to the tone-shock pairing just one day earlier, but it was not effective for mice that originally formed the traumatic memory one month earlier. The researchers hypothesized that epigenetic modification of genes involved in learning and memory might be responsible for the diminished response of treatment for older memories.
The researchers tested whether HDACis, which promote long-lasting activation of genes involved in learning and memory, could help replace old traumatic memories with new memories. Mice previously exposed to the tone-shock pairing received HDACis and then underwent the extinction protocol. These mice learned to stop freezing in response to the tone, even when they originally formed the traumatic memory one month earlier. “Collectively, our findings suggest that exposure-based therapy alone does not effectively weaken traumatic memories that were formed a long time ago, but that HDACis can be combined with exposure-based therapy to substantially improve treatment for the most enduring traumatic memories,” Tsai says.
(Source: eurekalert.org)
Sniffing Out Danger: Rutgers Scientists Say Fearful Memories Can Trigger Heightened Sense of Smell
Most people – including scientists – assumed we can’t just sniff out danger.
It was thought that we become afraid of an odor – such as leaking gas – only after information about a scary scent is processed by our brain.
But neuroscientists at Rutgers University studying the olfactory – sense of smell – system in mice have discovered that this fear reaction can occur at the sensory level, even before the brain has the opportunity to interpret that the odor could mean trouble.
In a new study published today in Science, John McGann, associate professor of behavioral and systems neuroscience in the Department of Psychology, and his colleagues, report that neurons in the noses of laboratory animals reacted more strongly to threatening odors before the odor message was sent to the brain.
“What is surprising is that we tend to think of learning as something that only happens deep in the brain after conscious awareness,” says McGann whose laboratory studies the sense of smell. “But now we see how the nervous system can become especially sensitive to threatening stimuli and that fear-learning can affect the signals passing from sensory organs to the brain.”
McGann and students Marley Kass and Michelle Rosenthal made this discovery by using light to observe activity in the brains of genetically engineered mice through a window in the mouse’s skull. They found that those mice that received an electric shock simultaneously with a specific odor showed an enhanced response to the smell in the cells in the nose, before the message was delivered to the neurons in the brain.
This new research – which indicates that fearful memories can influence the senses – could help to better understand conditions like Post Traumatic Stress Disorder, in which feelings of anxiety and fear exist even though an individual is no longer in danger.
“We know that anxiety disorders like PTSD can sometimes be triggered by smell, like the smell of diesel exhaust for a soldier,” says McGann who received funding from the National Institute of Mental Health and the National Institute on Deafness and Other Communication Disorders for this research. “What this study does is gives us a new way of thinking about how this might happen.”
In their study, the scientists also discovered a heightened sensitivity to odors in the mice traumatized by shock. When these mice smelled the odor associated with the electrical shocks, the amount of neurotransmitter – chemicals that carry communications between nerve cells – released from the olfactory nerve into the brain was as big as if the odor were four times stronger than it actually was.
This created mice whose brains were hypersensitive to the fear-associated odors. Before now, scientists did not think that reward or punishment could influence how the sensory organs process information.
The next step in the continuing research, McGann says, is to determine whether the hypersensitivity to threatening odors can be reversed by using exposure therapy to teach the mice that the electrical shock is no longer associated with a specific odor. This could help develop a better understanding of fear learning that might someday lead to new therapeutic treatments for anxiety disorders in humans, he says.
(Source: news.rutgers.edu)
Missing “brake in the brain” can trigger anxiety states
Fear, at the right level, can increase alertness and protect against dangers. Disproportionate fear, on the other hand, can disrupt the sensory perception, be disabling, reduce happiness and therefore become a danger in itself. Anxiety disorders are therefore a psychiatric condition that should not be underestimated. In these disorders, the fear is so strong that there is tremendous psychological strain and living a normal life appears to be impossible. Researchers at the MedUni Vienna have now found a possible explanation as to how social phobias and fear can be triggered in the brain: a missing inhibitory connection or missing “brake” in the brain.
Inside the brain, the amygdala and the orbitofrontal cortex in the frontal lobe form an important control circuit for regulating the emotions. This control circuit is termed the brain’s emotional control centre. Whereas in healthy subjects, this circuit has “negative feedback” and “calmness” was identified, scientists used functional magnetic resonance imaging (MRI) on people with social phobias and found the opposite to be true: an important inhibitory connection is different in these patients, which may explain why they are unable to control their fears.
In collaboration with the Centre for Medical Physics and Biomedical Technology and the University Department of Psychiatry and Psychotherapy at the MedUni Vienna, the research team lead by Christian Windischberger was also able to discover through its recent study at the MedUni Vienna’s High Field MR Centre of Excellence how the areas of the brain that are involved with processing emotions are able to influence each other.
The study participants were shown a series of “emotional faces” while undergoing functional magnetic resonance imaging. fMRI is a non-invasive method which uses radio waves and magnetic fields to measure changes in the levels of oxygen in the blood and therefore neuronal activity in individual regions of the brain. An analysis method developed at University College London was used to provide new perspectives on the data obtained.
Breaking the circle of fear
When emotional facial expressions were shown - from laughing to crying, from happiness to anger - neuronal activity was triggered in the brain. The result: on a purely external basis, the test subjects looked no different, but the healthy subjects were kept calm thanks to their automatic “brake”, despite the emotional nature of the images. For the social phobics, on the other hand, the photographs put their brains into “overdrive”, triggering very strong neuronal activity. This was demonstrated very clearly using the new analysis method: “We have the opportunity not only to localise brain activity and compare it between groups, but we can now also make statements regarding functional connections within the brain. In psychiatric conditions especially, we can assume that there are not complete failures of these connections going on, but rather imbalances in complex regulatory processes,” says Ronald Sladky, the study’s primary author.
This better understanding of the neuronal mechanisms involved will now be used to develop new approaches to treatment. The aim is to understand what effect medications and psycho-therapeutic support have on the networks involved in order to help patients break out of their circles of fear.
(Source: meduniwien.ac.at)
Studies pinpoint specific brain areas and mechanisms associated with depression and anxiety
Research released today reveals new mechanisms and areas of the brain associated with anxiety and depression, presenting possible targets to understand and treat these debilitating mental illnesses. The findings were presented at Neuroscience 2013, the annual meeting of the Society for Neuroscience and the world’s largest source of emerging news about brain science and health.
More than 350 million people worldwide suffer from clinical depression and between 5 and 25 percent of adults suffer from generalized anxiety, according to the World Health Organization. The resulting emotional and financial costs to people, families, and society are significant. Further, antidepressants are not always effective and often cause severe side effects.
Today’s new findings show that:
- A molecule in the immune system may contribute to depression, suggesting a potential biomarker for the disease (Georgia Hodes, PhD, abstract 542.1, see attached summary).
- Decreasing a chemical signal in the amygdala, a brain area associated with emotional processing, produces antidepressant-like effects in mice (Yann Mineur, PhD, abstract 504, see attached summary).
- MicroRNAs, tiny molecules that alter gene expression, correlate with how mice respond to socially stressful situations that cause depressive-like behavior. The findings may help determine why some people are more likely to suffer from depression than others (Karen Scott, PhD, abstract 731.2, see attached summary).
Other recent findings discussed show that:
- A pathway between two brain regions, the amygdala and the hippocampus, plays a significant role in anxiety. Shutting down this connection can decrease anxiety-like behavior in mice (Ada Felix-Ortiz, MS, presentation 393.01, see attached speaker summary).
- Aversive experiences can change how humans, particularly those with anxiety disorders, perceive stimuli. After a severe negative incident, patients with anxiety disorders over-generalize the experience and have increased emotional responses to subsequent similar situations (Rony Paz, PhD, presentation 295.05, see attached speaker summary).
“Today’s findings represent our rapidly growing understanding of the individual molecules and brain circuits that may contribute to depression and anxiety,” said press conference moderator Lisa Monteggia, PhD, of the University of Texas Southwestern Medical Center, an expert on mechanisms of antidepressant action. “These exciting discoveries represent the potential for significant changes in how we diagnose and treat these illnesses that touch millions.”
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)
To suppress or to explore? Emotional strategy may influence anxiety
When trouble approaches, what do you do? Run for the hills? Hide? Pretend it isn’t there? Or do you focus on the promise of rain in those looming dark clouds?
New research suggests that the way you regulate your emotions, in bad times and in good, can influence whether – or how much – you suffer from anxiety.
The study appears in the journal Emotion.
In a series of questionnaires, researchers asked 179 healthy men and women how they managed their emotions and how anxious they felt in various situations. The team analyzed the results to see if different emotional strategies were associated with more or less anxiety.
The study revealed that those who engage in an emotional regulation strategy called reappraisal tended to also have less social anxiety and less anxiety in general than those who avoid expressing their feelings. Reappraisal involves looking at a problem in a new way, said University of Illinois graduate student Nicole Llewellyn, who led the research with psychology professor Florin Dolcos, an affiliate of the Beckman Institute at Illinois.
"When something happens, you think about it in a more positive light, a glass half full instead of half empty," Llewellyn said. "You sort of reframe and reappraise what’s happened and think what are the positives about this? What are the ways I can look at this and think of it as a stimulating challenge rather than a problem?"
Study participants who regularly used this approach reported less severe anxiety than those who tended to suppress their emotions.
Anxiety disorders are a major public health problem in the U.S. According to the National Institute of Mental Health, roughly 18 percent of the U.S. adult population is afflicted with general or social anxiety that is so intense that it warrants a diagnosis.
"The World Health Organization predicts that by 2020, anxiety and depression –which tend to co-occur – will be among the most prevalent causes of disability worldwide, secondary only to cardiovascular disease," Dolcos said. "So it’s associated with big costs."
Not all anxiety is bad, however, he said. Low-level anxiety may help you maintain the kind of focus that gets things done. Suppressing or putting a lid on your emotions also can be a good strategy in a short-term situation, such as when your boss yells at you, Dolcos said. Similarly, an always-positive attitude can be dangerous, causing a person to ignore health problems, for example, or to engage in risky behavior.
Previous studies had found that people who were temperamentally inclined to focus on making good things happen were less likely to suffer from anxiety than those who focused on preventing bad things from happening, Llewellyn said. But she could find no earlier research that explained how this difference in focus translated to behaviors that people could change. The new study appears to explain the strategies that contribute to a person having more or less anxiety, she said.
"This is something you can change," she said. "You can’t do much to affect the genetic or environmental factors that contribute to anxiety. But you can change your emotion regulation strategies."