Posts tagged anxiety
Articles and news from the latest research reports.
Worms May Shed Light on Human Ability to Handle Chronic Stress
New research at Rutgers University may help shed light on how and why nervous system changes occur and what causes some people to suffer from life-threatening anxiety disorders while others are better able to cope.
Maureen Barr, a professor in the Department of Genetics, and a team of researchers, found that the architectural structure of the six sensory brain cells in the roundworm, responsible for receiving information, undergo major changes and become much more elaborate when the worm is put into a high stress environment.
Scientists have known for some time that changes in the tree-like dendrite structures that connect neurons in the human brain and enable our thought processes to work properly can occur under extreme stress, alter brain cell development and result in anxiety disorders like depression and Post Traumatic Stress Disorder affecting millions of Americans each year.
What scientists don’t understand for sure, Barr says, is the cause behind these molecular changes in the brain.
“This type of research provides us necessary clues that ultimately could lead to the development of drugs to help those suffering with severe anxiety disorders,” Barr says.
In the study published today in Current Biology, scientists at Rutgers have identified six sensory nerve cells in the tiny, transparent roundworm, known as the C. elegans and an enzyme called KPC-1/furin which triggers a chemical reaction in humans that is needed for essential life functions like blood-clotting.
While the enzyme also appears to play a role in the growth of tumors and the activation of several types of virus and diseases in humans, in the roundworm the enzyme enables its simple neurons to morph into new elaborately branched shapes when placed under adverse conditions.
Normally, this one-millimeter long worm develops from an embryo through four larval stages before molting into a reproductive adult. Put it under stressful conditions of overcrowding, starvation and high temperature and the worm transforms into an alternative larval stage known as the dauer that becomes so stress-resistant it can survive almost anything – including the Space Shuttle Columbia disaster in 2003 of which they were the only living things to survive.
“These worms that normally have a short life cycle turn into super worms when they go into the dauer stage and can live for months, although they are no longer able to reproduce,” Barr says.
What is so interesting to Barr is that when a perceived threat is over, these tiny creatures and their IL2 neurons transform back to a normal lifespan and reproductive state like nothing had ever happened. Under a microscope, the complicated looking tree-like connectors that receive information are pruned back and the worm appears as it did before the trauma occurred.
This type of neural reaction differs in humans who can suffer from extreme anxiety months or even years after the traumatic event even though they are no longer in a threatening situation.
The ultimate goal, Barr says, is to determine how and why the nervous system responds to stress. By identifying molecular pathways that regulate neuronal remodeling, scientists may apply this knowledge to develop future therapeutics.
(Source: news.rutgers.edu)
Robots Strike Fear in the Hearts of Fish
Anxious Zebrafish Help NYU-Poly Researchers Understand How Alcohol Affects Fear
The latest in a series of experiments testing the ability of robots to influence live animals shows that bio-inspired robots can not only elicit fear in zebrafish, but that this reaction can be modulated by alcohol. These findings may pave the way for new methodologies for understanding anxiety and other emotions, as well as substances that alter them.
Maurizio Porfiri, associate professor of mechanical and aerospace engineering at the Polytechnic Institute of New York University (NYU-Poly) and Simone Macrì, a collaborator at the Istituto Superiore di Sanità in Rome, Italy, published their findings in PLOS ONE, an international, peer-reviewed, open-access, online publication.
This latest study expands Porfiri and Macrì’s efforts to determine how bio-inspired robots can be employed as reliable stimuli to elicit reactions from live zebrafish. Previous studies have established that zebrafish show a strong affinity for robotic members designed to swim and appear as one of their own and that this preference can be abolished by exposing the fish to ethanol.
Porfiri and Macri, along with students Valentina Cianca and Tiziana Bartolini, hypothesized that robots could be used to induce fear as well as affinity and designed a robot mimicking the morphology and locomotion pattern of the Indian leaf fish, a natural predator of the zebrafish. In the lab, they simulated a harmless predatory scenario, placing the zebrafish and the robotic Indian leaf fish in separate compartments of a three-section tank. The other compartment was left empty. The control group uniformly avoided the robotic predator, showing a preference for the empty section.
To determine whether alcohol would affect fear responses, the researchers exposed separate groups of fish to different doses of ethanol in water. Ethanol has been shown to influence anxiety-related responses in humans, rodents and some species of fish. The zebrafish exposed to the highest concentrations of ethanol showed remarkable changes in behavior, failing to avoid the predatory robot. Acute administration of ethanol causes no harm and has no lasting effect on zebrafish.
“These results are further evidence that robots may represent an exciting new approach in evaluating and understanding emotional responses and behavior,” said Porfiri. “Robots are ideal replacements as independent variables in tests involving social stimuli—they are fully controllable, stimuli can be reproduced precisely each time, and robots can never be influenced by the behavior of the test subjects.”
To validate their findings and ensure that the zebrafish behavior being modulated was, in fact, a fear-based response, Porfiri and his collaborators conducted two traditional anxiety tests and evaluated whether the results obtained therein were sensitive to ethanol administration.
They placed test subjects in a two-chamber tank with one well-lit side and one darkened side, to establish which conditions were preferable. In a separate tank, they simulated a heron attack from the water’s surface—herons also prey on zebrafish—and measured how quickly and how many fish took shelter from the attack. As expected, the fish strongly avoided the dark compartment, and most sought shelter very quickly from the heron attack. Ethanol exposure significantly modulated these fear responses as well, abolishing the preference for the light compartment and significantly slowing the fishes’ retreat to shelter during the simulated attack.
“We hoped to see a correlation between the robotic Indian leaf fish test results and the results of the other anxiety tests, and the data support that,” Porfiri explained. “The majority of control group fish avoided the robotic predator, preferred the light compartment and sought shelter quickly after the heron attack. Among ethanol-exposed fish, there were many more who were unaffected by the robotic predator, preferred the dark compartment and were slow to swim to shelter when attacked.”
Porfiri and his colleagues believe zebrafish may be a suitable replacement for higher-order animals in tests to evaluate emotional responses. This novel robotic approach would also reduce the number of live test subjects needed for experiments and may inform other areas of inquiry, from collective behavior to animal protection.
The Love Hormone is Two-Faced
Finding shows oxytocin strengthens bad memories and can increase fear and anxiety
It turns out the love hormone oxytocin is two-faced. Oxytocin has long been known as the warm, fuzzy hormone that promotes feelings of love, social bonding and well-being. It’s even being tested as an anti-anxiety drug. But new Northwestern Medicine® research shows oxytocin also can cause emotional pain, an entirely new, darker identity for the hormone.
Oxytocin appears to be the reason stressful social situations, perhaps being bullied at school or tormented by a boss, reverberate long past the event and can trigger fear and anxiety in the future.
That’s because the hormone actually strengthens social memory in one specific region of the brain, Northwestern scientists discovered.
If a social experience is negative or stressful, the hormone activates a part of the brain that intensifies the memory. Oxytocin also increases the susceptibility to feeling fearful and anxious during stressful events going forward.
(Presumably, oxytocin also intensifies positive social memories and, thereby, increases feelings of well being, but that research is ongoing.)
The findings are important because chronic social stress is one of the leading causes of anxiety and depression, while positive social interactions enhance emotional health. The research, which was done in mice, is particularly relevant because oxytocin currently is being tested as an anti-anxiety drug in several clinical trials.
“By understanding the oxytocin system’s dual role in triggering or reducing anxiety, depending on the social context, we can optimize oxytocin treatments that improve well-being instead of triggering negative reactions,” said Jelena Radulovic, the senior author of the study and the Dunbar Professsor of Bipolar Disease at Northwestern University Feinberg School of Medicine. The paper was published July 21 in Nature Neuroscience.
This is the first study to link oxytocin to social stress and its ability to increase anxiety and fear in response to future stress. Northwestern scientists also discovered the brain region responsible for these effects — the lateral septum – and the pathway or route oxytocin uses in this area to amplify fear and anxiety.
The scientists discovered that oxytocin strengthens negative social memory and future anxiety by triggering an important signaling molecule — ERK (extracellular signal regulated kinases) — that becomes activated for six hours after a negative social experience. ERK causes enhanced fear, Radulovic believes, by stimulating the brain’s fear pathways, many of which pass through the lateral septum. The region is involved in emotional and stress responses.
The findings surprised the researchers, who were expecting oxytocin to modulate positive emotions in memory, based on its long association with love and social bonding.
“Oxytocin is usually considered a stress-reducing agent based on decades of research,” said Yomayra Guzman, a doctoral student in Radulovic’s lab and the study’s lead author. “With this novel animal model, we showed how it enhances fear rather than reducing it and where the molecular changes are occurring in our central nervous system.’
The new research follows three recent human studies with oxytocin, all of which are beginning to offer a more complicated view of the hormone’s role in emotions.
All the new experiments were done in the lateral septum. This region has the highest oxytocin levels in the brain and has high levels of oxytocin receptors across all species from mice to humans.
“This is important because the variability of oxytocin receptors in different species is huge,” Radulovic said. “We wanted the research to be relevant for humans, too.”
Experiments with mice in the study established that 1) oxytocin is essential for strengthening the memory of negative social interactions and 2) oxytocin increases fear and anxiety in future stressful situations.
Experiment 1: Oxytocin Strengthens Bad Memories
Three groups of mice were individually placed in cages with aggressive mice and experienced social defeat, a stressful experience for them. One group was missing its oxytocin receptors, essentially the plug by which the hormone accesses brain cells. The lack of receptors means oxytocin couldn’t enter the mice’s brain cells. The second group had an increased number of receptors so their brain cells were flooded with the hormone. The third control group had a normal number of receptors.
Six hours later, the mice were returned to cages with the aggressive mice. The mice that were missing their oxytocin receptors didn’t appear to remember the aggressive mice and show any fear. Conversely, when mice with increased numbers of oxytocin receptors were reintroduced to the aggressive mice, they showed an intense fear reaction and avoided the aggressive mice.
Experiment 2: Oxytocin Increases Fear and Anxiety in Future Stress
Again, the three groups of mice were exposed to the stressful experience of social defeat in the cages of other more aggressive mice. This time, six hours after the social stress, the mice were put in a box in which they received a brief electric shock, which startles them but is not painful. Then 24 hours later, the mice were returned to the same box but did not receive a shock.
The mice missing their oxytocin receptors did not show any enhanced fear when they re-entered the box in which they received the shock. The second group, which had extra oxytocin receptors showed much greater fear in the box. The third control group exhibited an average fear response.
“This experiment shows that after a negative social experience the oxytocin triggers anxiety and fear in a new stressful situation,” Radulovic said.
(Source: northwestern.edu)
Exercise reorganizes the brain to be more resilient to stress
Physical activity reorganizes the brain so that its response to stress is reduced and anxiety is less likely to interfere with normal brain function, according to a research team based at Princeton University.
The researchers report in the Journal of Neuroscience that when mice allowed to exercise regularly experienced a stressor — exposure to cold water — their brains exhibited a spike in the activity of neurons that shut off excitement in the ventral hippocampus, a brain region shown to regulate anxiety.
These findings potentially resolve a discrepancy in research related to the effect of exercise on the brain — namely that exercise reduces anxiety while also promoting the growth of new neurons in the ventral hippocampus. Because these young neurons are typically more excitable than their more mature counterparts, exercise should result in more anxiety, not less. The Princeton-led researchers, however, found that exercise also strengthens the mechanisms that prevent these brain cells from firing.
The impact of physical activity on the ventral hippocampus specifically has not been deeply explored, said senior author Elizabeth Gould, Princeton’s Dorman T. Warren Professor of Psychology. By doing so, members of Gould’s laboratory pinpointed brain cells and regions important to anxiety regulation that may help scientists better understand and treat human anxiety disorders, she said.
From an evolutionary standpoint, the research also shows that the brain can be extremely adaptive and tailor its own processes to an organism’s lifestyle or surroundings, Gould said. A higher likelihood of anxious behavior may have an adaptive advantage for less physically fit creatures. Anxiety often manifests itself in avoidant behavior and avoiding potentially dangerous situations would increase the likelihood of survival, particularly for those less capable of responding with a “fight or flight” reaction, she said.
"Understanding how the brain regulates anxious behavior gives us potential clues about helping people with anxiety disorders. It also tells us something about how the brain modifies itself to respond optimally to its own environment," said Gould, who also is a professor in the Princeton Neuroscience Institute.
The research was part of the graduate dissertation for first author Timothy Schoenfeld, now a postdoctoral fellow at the National Institute of Mental Health, as well as part of the senior thesis project of co-author Brian Hsueh, now an MD/Ph.D. student at Stanford University. The project also included co-authors Pedro Rada and Pedro Pieruzzini, both from the University of Los Andes in Venezuela.
For the experiments, one group of mice was given unlimited access to a running wheel and a second group had no running wheel. Natural runners, mice will dash up to 4 kilometers (about 2.5 miles) a night when given access to a running wheel, Gould said. After six weeks, the mice were exposed to cold water for a brief period of time.
The brains of active and sedentary mice behaved differently almost as soon as the stressor occurred, an analysis showed. In the neurons of sedentary mice only, the cold water spurred an increase in “immediate early genes,” or short-lived genes that are rapidly turned on when a neuron fires. The lack of these genes in the neurons of active mice suggested that their brain cells did not immediately leap into an excited state in response to the stressor.
Instead, the brain in a runner mouse showed every sign of controlling its reaction to an extent not observed in the brain of a sedentary mouse. There was a boost of activity in inhibitory neurons that are known to keep excitable neurons in check. At the same time, neurons in these mice released more of the neurotransmitter gamma-aminobutyric acid, or GABA, which tamps down neural excitement. The protein that packages GABA into little travel pods known as vesicles for release into the synapse also was present in higher amounts in runners.
The anxiety-reducing effect of exercise was canceled out when the researchers blocked the GABA receptor that calms neuron activity in the ventral hippocampus. The researchers used the chemical bicuculine, which is used in medical research to block GABA receptors and simulate the cellular activity underlying epilepsy. In this case, when applied to the ventral hippocampus, the chemical blocked the mollifying effects of GABA in active mice.
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)
1 in 4 Stroke Patients Suffer PTSD
One in four people who survive a stroke or transient ischemic attack (TIA) suffer from symptoms of post-traumatic stress disorder (PTSD) within the first year post-event, and one in nine experience chronic PTSD more than a year later. The data suggest that each year nearly 300,000 stroke/TIA survivors will develop PTSD symptoms as a result of their health scare. The study, led by Columbia University Medical Center researchers, was published today in the online edition of PLOS ONE.
“This work builds on recent findings of ours that PTSD is common among heart attack survivors and that it contributes to a doubled risk of a future cardiac event or of dying within one to three years. Our current results show that PTSD in stroke and TIA survivors may increase their risk for recurrent stroke and other cardiovascular events,” said first author Donald Edmondson, PhD, MPH, assistant professor of behavioral medicine (Center for Behavioral Cardiovascular Health) at CUMC. “Given that each event is life-threatening and that strokes/TIAs add hundreds of millions of dollars to annual health expenditures, these findings are important to both the long-term survival and health costs of these patient populations.”
“PTSD is not just a disorder of combat veterans and sexual assault survivors, but strongly affects survivors of stroke and other potentially traumatic acute cardiovascular events as well,” said Ian M. Kronish, MD, MPH, assistant professor of medicine (Center for Behavioral Cardiovascular Health) and the study’s senior author. “Surviving a life-threatening health scare can have a debilitating psychological impact, and health care providers should make it a priority to screen for symptoms of depression, anxiety, and PTSD among these patient populations.”
Stroke is the fourth-leading cause of death and the top cause of disability in the United States. According to data from the American Stroke Association, nearly 795,000 Americans each year suffer a new or recurrent stroke, and up to an additional 500,000 suffer a TIA.
PTSD is an anxiety disorder initiated by exposure to a traumatic event. Common symptoms include nightmares, avoidance of reminders of the event, and elevated heart rate and blood pressure. Chronic PTSD is a duration of these symptoms for three months or longer (as defined by the DSM-IV).
Since only a few studies have assessed PTSD due to stroke, Drs. Edmondson and Kronish and their colleagues performed the first meta-analysis of clinical studies of stroke- or TIA-induced PTSD. The nine studies in the meta-analysis included a total of 1,138 stroke or TIA survivors.
The study found that 23 percent, or roughly one in four, of the patients developed PTSD symptoms within the first year after their stroke or TIA, with 11 percent, or roughly one in nine, experiencing chronic PTSD more than a year later.
“PTSD and other psychological disorders in stroke and TIA patients appear to be an under-recognized and undertreated problem,” said Dr. Kronish.
“Fortunately, there are good treatments for PTSD,” said Dr. Edmondson. “But first, physicians and patients have to be aware that this is a problem. Family members can also help. We know that social support is a good protective factor against PTSD due to any type of traumatic event.”
“The next step is further research to assess whether mental health treatment can reduce stroke- and TIA-induced PTSD symptoms and help these patients regain a feeling of normalcy and calm as soon as possible after their health scare,” said Dr. Edmondson.
(Source: newsroom.cumc.columbia.edu)
PD-Like Sleep and Motor Problems Observed in α-Synuclein Mutant Mice
The presence of Lewy bodies in nerve cells, formed by intracellular deposits of the protein α-synuclein, is a characteristic pathologic feature of Parkinson’s Disease (PD). In the quest for an animal model of PD that mimics motor and non-motor symptoms of human PD, scientists have developed strains of mice that overexpress α-synuclein. By studying a strain of mice bred to overexpress α-synuclein via the Thy-1 promoter, scientists have found these mice develop many of the age-related progressive motor symptoms of PD and demonstrate changes in sleep and anxiety. Their results are published in the latest issue of Journal of Parkinson’s Disease.
PD is the second most common neurodegenerative disorder in the United States, affecting approximately one million Americans and five million people worldwide. Its prevalence is projected to double by 2030. The most obvious symptoms are movement-related, such as involuntary shaking and muscle stiffness; non-motor symptoms, such as increases in anxiety and sleep disturbances, can appear prior to the onset of motor symptoms. Although the drug levodopa can relieve some symptoms, there is no cure – intensifying the pressure to find an animal model that can help clarify the pathological processes underlying human PD and find new medications to treat the pathology and/or relieve symptoms.
Investigators at the National Institute on Aging compared wild type mice with specially bred mice that were transgenic for the A53T mutation of the human α-synuclein (SNCA) gene under the control of a human thymus cell antigen 1, theta (THY-1) promoter. As the mice aged, their motor performance on a rotarod test (which measures how long the mouse can remain on a rotating rod) became impaired and the length of their strides were significantly shorter than the wild type control mice.
The study also found that SNCA mice displayed fragmented nighttime activity patterns compared to wild type controls and appeared to have a reduced overall sleep time. “Despite the prevalence of abnormal sleep patterns in PD, very few studies to date have outlined sleep disturbances in animal models of PD,” says Sarah M. Rothman, PhD, a researcher with the National Institute on Aging, in Baltimore, MD.
Many PD patients typically show an increase in anxiety and depression, and in this respect the SNCA mouse model did not replicate the human condition. SNCA mice displayed an early and significant decrease in anxiety-like behavior that persisted throughout their lifespan, as shown by both open field and elevated plus maze tests (in which mice have the choice of spending time in open or closed arms of a maze). Other rodent models that utilize changes in expression of α-synuclein have also reported lower anxiety levels. The authors suggest that higher levels of serotonin found in the hypothalamus of the SNCA mice may be associated with the reduced anxiety observed.
The authors say it is important to remember that the SNCA “model utilizes the presence of a mutation that only occurs very rarely in PD. While all PD patients display α-synuclein pathology, they do not all express the mutated form of the protein,” says Dr. Rothman.
(Source: alphagalileo.org)
Anxious? Activate Your Anterior Cingulate Cortex With a Little Meditation
Scientists, like Buddhist monks and Zen masters, have known for years that meditation can reduce anxiety, but not how. Scientists at Wake Forest Baptist Medical Center, however, have succeeded in identifying the brain functions involved.
“Although we’ve known that meditation can reduce anxiety, we hadn’t identified the specific brain mechanisms involved in relieving anxiety in healthy individuals,” said Fadel Zeidan, Ph.D., postdoctoral research fellow in neurobiology and anatomy at Wake Forest Baptist and lead author of the study. “In this study, we were able to see which areas of the brain were activated and which were deactivated during meditation-related anxiety relief.”
The study is published in the current edition of the journal Social Cognitive and Affective Neuroscience.
For the study, 15 healthy volunteers with normal levels of everyday anxiety were recruited for the study. These individuals had no previous meditation experience or anxiety disorders. All subjects participated in four 20-minute classes to learn a technique known as mindfulness meditation. In this form of meditation, people are taught to focus on breath and body sensations and to non-judgmentally evaluate distracting thoughts and emotions.
Both before and after meditation training, the study participants’ brain activity was examined using a special type of imaging – arterial spin labeling magnetic resonance imaging – that is very effective at imaging brain processes, such as meditation. In addition, anxiety reports were measured before and after brain scanning.
The majority of study participants reported decreases in anxiety. Researchers found that meditation reduced anxiety ratings by as much as 39 percent.
“This showed that just a few minutes of mindfulness meditation can help reduce normal everyday anxiety,” Zeidan said.
The study revealed that meditation-related anxiety relief is associated with activation of the anterior cingulate cortex and ventromedial prefrontal cortex, areas of the brain involved with executive-level function. During meditation, there was more activity in the ventromedial prefrontal cortex, the area of the brain that controls worrying. In addition, when activity increased in the anterior cingulate cortex – the area that governs thinking and emotion – anxiety decreased.
“Mindfulness is premised on sustaining attention in the present moment and controlling the way we react to daily thoughts and feelings,” Zeidan said. “Interestingly, the present findings reveal that the brain regions associated with meditation-related anxiety relief are remarkably consistent with the principles of being mindful.”
Research at other institutions has shown that meditation can significantly reduce anxiety in patients with generalized anxiety and depression disorders. The results of this neuroimaging experiment complement that body of knowledge by showing the brain mechanisms associated with meditation-related anxiety relief in healthy people, he said.
Hormone levels may provide key to understanding psychological disorders in women
Women at a particular stage in their monthly menstrual cycle may be more vulnerable to some of the psychological side-effects associated with stressful experiences, according to a study from UCL.
The results suggest a monthly window of opportunity that could potentially be targeted in efforts to prevent common mental health problems developing in women. The research is the first to show a potential link between psychological vulnerability and the timing of a biological cycle, in this case ovulation.
A common symptom of mood and anxiety problems is the tendency to experience repetitive and unwanted thoughts. These ‘intrusive thoughts’ often occur in the days and weeks after a stressful experience.
In this study, the researchers examined whether the effects of a stressful event are linked to different stages of the menstrual cycle. The participants were 41 women aged between 18 and 35 who had regular menstrual cycles and were not using the pill as a form of contraception. Each woman watched a 14-minute stressful film containing death or injury and provided a saliva sample so that hormone levels could be assessed. They were then asked to record instances of unwanted thoughts about the video over the following days.
“We found that women in the ‘early luteal’ phase, which falls roughly 16 to 20 days after the start of their period, had more than three times as many intrusive thoughts as those who watched the video in other phases of their menstrual cycle,” explains author Dr Sunjeev Kamboj, Lecturer in UCL’s Department of Clinical, Educational and Health Psychology.
“This indicates that there is actually a fairly narrow window within the menstrual cycle when women may be particularly vulnerable to experiencing distressing symptoms after a stressful event.”
The findings could have important implications for mental health problems and their treatment in women who have suffered trauma.
“Asking women who have experienced a traumatic event about the time since their last period might help identify those at greatest risk of developing recurring symptoms similar to those seen in psychological disorders such as depression and post-traumatic stress disorder (PTSD),” said Dr Kamboj.
“This work might have identified a useful line of enquiry for doctors, helping them to identify potentially vulnerable women who could be offered preventative therapies,” continued Dr Kamboj.
“However, this is only a first step. Although we found large effects in healthy women after they experienced a relatively mild stressful event, we now need to see if the same pattern is found in women who have experienced a real traumatic event. We also need further research to investigate how using the contraceptive pill affects this whole process.”
(Source: ucl.ac.uk)
Chronic trauma can inflict lasting damage to brain regions associated with fear and anxiety. Previous imaging studies of people with post-traumatic stress disorder, or PTSD, have shown that these brain regions can over-or under-react in response to stressful tasks, such as recalling a traumatic event or reacting to a photo of a threatening face. Now, researchers at NYU School of Medicine have explored for the first time what happens in the brains of combat veterans with PTSD in the absence of external triggers.
Their results, published in Neuroscience Letters, and presented today at the annual meeting of the American Psychiatry Association in San Francisco, show that the effects of trauma persist in certain brain regions even when combat veterans are not engaged in cognitive or emotional tasks, and face no immediate external threats. The findings shed light on which areas of the brain provoke traumatic symptoms and represent a critical step toward better diagnostics and treatments for PTSD.
A chronic condition that develops after trauma, PTSD can plague victims with disturbing memories, flashbacks, nightmares and emotional instability. Among the 1.7 million men and women who have served in the wars in Iraq and Afghanistan, an estimated 20% have PTSD. Research shows that suicide risk is higher in veterans with PTSD. Tragically, more soldiers committed suicide in 2012 than the number of soldiers who were killed in combat in Afghanistan that year.
"It is critical to have an objective test to confirm PTSD diagnosis as self reports can be unreliable," says co-author Charles Marmar, MD, the Lucius N. Littauer Professor of Psychiatry and chair of NYU Langone’s Department of Psychiatry. Dr. Marmar, a nationally recognized expert on trauma and stress among veterans, heads The Steven and Alexandra Cohen Veterans Center for the Study of Post-Traumatic Stress and Traumatic Brain Injury at NYU Langone Medical Center.
The study, led by Xiaodan Yan, a research fellow at NYU School of Medicine, examined “spontaneous” or “resting” brain activity in 104 veterans of combat from the Iraq and Afghanistan wars using functional MRI, which measures blood-oxygen levels in the brain. The researchers found that spontaneous brain activity in the amygdala, a key structure in the brain’s “fear circuitry” that processes fearful and anxious emotions, was significantly higher in the 52 combat veterans with PTSD than in the 52 combat veterans without PTSD. The PTSD group also showed elevated brain activity in the anterior insula, a brain region that regulates sensitivity to pain and negative emotions.
Moreover, the PTSD group had lower activity in the precuneus, a structure tucked between the brain’s two hemispheres that helps integrate information from the past and future, especially when the mind is wandering or disengaged from active thought. Decreased activity in the precuneus correlates with more severe “re-experiencing” symptoms—that is, when victims re-experience trauma over and over again through flashbacks, nightmares and frightening thoughts.