Posts tagged stress

Posts tagged stress
Early stress may sensitize girls’ brains for later anxiety
High levels of family stress in infancy are linked to differences in everyday brain function and anxiety in teenage girls, according to new results of a long-running population study by University of Wisconsin-Madison scientists.
The study highlights evidence for a developmental pathway through which early life stress may drive these changes. Here, babies who lived in homes with stressed mothers were more likely to grow into preschoolers with higher levels of cortisol, a stress hormone. In addition, these girls with higher cortisol also showed less communication between brain areas associated with emotion regulation 14 years later. Last, both high cortisol and differences in brain activity predicted higher levels of adolescent anxiety at age 18.
The young men in the study did not show any of these patterns.
"We wanted to understand how stress early in life impacts patterns of brain development which might lead to anxiety and depression,” says first author Dr. Cory Burghy of the Waisman Laboratory for Brain Imaging and Behavior. "Young girls who, as preschoolers, had heightened cortisol levels, go on to show lower brain connectivity in important neural pathways for emotion regulation — and that predicts symptoms of anxiety during adolescence."
To test this, scans designed by Dr. Rasmus Birn, assistant professor of psychiatry in the UW School of Medicine and Public Health, showed that teenage girls whose mothers reported high levels of family stress when the girls were babies show reduced connections between the amygdala or threat center of the brain and the ventromedial prefrontal cortex, a part of the brain responsible for emotional regulation. Birn used a method called resting-state functional connectivity (fcMRI), which looks at the brain connections while the brain is at a resting state.
The study was published in Nature Neuroscience.
PTSD linked to smaller brain area regulating fear response
Recent combat veterans who are diagnosed with post traumatic stress disorder have significantly smaller volume in an area of the brain critical for regulating fear and anxiety responses, according to research led by scientists at Duke University and the Durham VA Medical Center.
The finding, published Nov. 5, 2012, in the journal Archives of General Psychiatry, for the first time provides clear evidence that smaller amygdala volume is associated with PTSD, regardless of the severity of trauma. But it’s not clear whether the physiological difference was caused by a traumatic event, or whether PTSD develops more readily in people who naturally have smaller amygdalas.
“Researchers found 20 years ago that there were changes in volume of the hippocampus associated with PTSD, but the amygdala is more relevant to the disorder,” said Rajendra A. Morey, M.D., M.S., assistant professor at Duke and lead author of the study. Morey said studies in animals have established the amygdala’s role in regulating fear, anxiety and stress responses, but its effect on human behavior is less well known.
“It’s associated with how fear is processed, especially abnormal fear processing.” Morey said. “So it makes sense to look at the structure of the amygdala.”
(Photo: U.S. Army)
Studies report early childhood trauma takes visible toll on brain; changes found in regions controlling heart and behavior
Trauma in infancy and childhood shapes the brain, learning, and behavior, and fuels changes that can last a lifetime, according to new human and animal research released today. The studies delve into the effects of early physical abuse, socioeconomic status (SES), and maternal treatment. Documenting the impact of early trauma on brain circuitry and volume, the activation of genes, and working memory, researchers suggest it increases the risk of mental disorders, as well as heart disease and stress-related conditions in adulthood.
Today’s findings show:
• Physical abuse in early childhood may realign communication between key “body-control” brain areas, possibly predisposing adults to cardiovascular disease and mental health problems (Layla Banihashemi, PhD, abstract 691.12).
• Rodent studies provide insight into brain changes that allow tolerance of pain within mother-pup attachment (Regina Sullivan, PhD, abstract 399.19).
• Childhood poverty is associated with changes in working memory and attention years later in adults; yet training in childhood is associated with improved cognitive functions (Eric Pakulak, PhD, abstract 908.04).
• Chronic stress experienced by infant primates leads to fearful and aggressive behaviors; these are associated with changes in stress hormone production and in the development of the amygdala (Mar Sanchez, PhD, abstract 691.10).Another recent finding discussed shows that:
• Parent education and income is associated with children’s brain size, including structures important for memory and emotion (Suzanne Houston, MA).
Scientists reveal brain circuitry involved in post-traumatic stress and related disorders
Post-traumatic stress disorder (PTSD) is a severe anxiety disorder that can develop after experience of a traumatic or terrifying event, such as those experienced in combat or from sexual aggression. Such events can overwhelm the individual’s ability to cope and lead to a long-lasting disorder. Symptoms include re-experiencing the original trauma through flashbacks or nightmares, often triggered by seemingly innocuous events. PTSD can harm an individual’s relationships, ability to work, to sleep, and other aspects of life.
The lifetime prevalence of PTSD among adult Americans is 8 percent. Neither drug nor behavioral treatments currently available are consistently effective in treating PTSD. Therefore, scientists are studying brain changes associated with PTSD and related cognitive disorders, looking for clues to help in the development of new treatments.
Today’s findings show that:
- A fast-acting antidepressant, ketamine, appears to aid the formation of new nerve connections in the brain, helping to extinguish fearful memories. The mouse study could possibly lead to new PTSD treatments (Neil Fournier, PhD, abstract 399.09).
- In a mouse model, when dopamine neurons in the brain’s reward system are turned on and off with a genetically engineered “light switch,” depressive symptoms also come and go. The research highlights the importance of this neural circuit as a potential target for new depression treatments (Dipesh Chaudhury, PhD, abstract 522.01).
- Brain images of adolescents taken before and after the 2011 Japanese earthquake reveal that pre-existing weakness in certain brain connections could be a risk factor for intensified anxiety and PTSD after a traumatic life experience (Atsushi Sekiguchi, MD, PhD, abstract 168.12).
- Rodent studies show that repeated violent, competitive encounters drive changes in brain activity that shapes the ongoing behavior of losers and winners in distinct ways, and can contribute to depression and/or anxiety (Tamara Franklin, PhD, abstract 399.10).
Other recent findings discussed show:
- How exposure to stress causes molecular changes that weaken the ability of the prefrontal cortex to regulate behavior, thought, and emotion, while strengthening more primitive brain circuits (Amy Arnsten, PhD, abstract 310).
Research identifies the mechanism that protects our brains from turning stress and trauma into post-traumatic stress disorder
Researchers from the University of Exeter Medical School have for the first time identified the mechanism that protects us from developing uncontrollable fear.
Our brains have the extraordinary capacity to adapt to changing environments – experts call this ‘plasticity’. Plasticity protects us from developing mental disorders as the result of stress and trauma.
Researchers found that stressful events re-programme certain receptors in the emotional centre of the brain (the amygdala), which the receptors then determine how the brain reacts to the next traumatic event.
These receptors (called protease-activated receptor 1 or PAR1) act in the same way as a command centre, telling neurons whether they should stop or accelerate their activity.
Before a traumatic event, PAR1s usually tell amygdala neurons to remain active and produce vivid emotions. However, after trauma they command these neurons to stop activating and stop producing emotions – so protecting us from developing uncontrollable fear.
This helps us to keep our fear under control, and not to develop exaggerated responses to mild or irrelevant fear triggers – for example, someone who may have witnessed a road traffic accident who develops a fear of cars or someone who may have had a dog jump up on them as a child and who now panics when they see another dog.
The research team used mice in which the PAR1 receptors were genetically de-activated and found that the animals developed a pathological fear in response to even mild, aversive stimuli.
The study was led by Professor Robert Pawlak of University of Exeter Medical School. He said: “The discovery that the same receptor can either awaken neurons or ‘switch them off’ depending on previous trauma and stress experience, adds an entirely new dimension to our knowledge of how the brain operates and emotions are formed.”
Professor Pawlak added: “We are now planning to extend our study to investigate if the above mechanisms, or genetic defects of the PAR1 receptor, are responsible for the development of anxiety disorders and depression in human patients. There is more work to be done, but the potential for the development of future therapies based on our findings is both exciting and intriguing.”
The article describing the above findings has recently been published in one of the most prestigious psychiatry journals, Molecular Psychiatry.
(Source: eurekalert.org)
Moderate exercise may help people cope with anxiety and stress for an extended period of time post-workout, according to a study by kinesiology researchers in the University of Maryland School of Public Health published in the journal Medicine and Science in Sports and Exercise.
"While it is well-known that exercise improves mood, among other benefits, not as much is known about the potency of exercise’s impact on emotional state and whether these positive effects endure when we’re faced with everyday stressors once we leave the gym," explains J. Carson Smith, assistant professor in the Department of Kinesiology. "We found that exercise helps to buffer the effects of emotional exposure. If you exercise, you’ll not only reduce your anxiety, but you’ll be better able to maintain that reduced anxiety when confronted with emotional events."
Smith, whose research explores how exercise and physical activity affect brain function, aging and mental health, compared how moderate intensity cycling versus a period of quiet rest (both for 30 minutes) affected anxiety levels in a group of healthy college students. He assessed their anxiety state before the period of activity (or rest), shortly afterward (15 minutes after) and finally after exposing them to a variety of highly arousing pleasant and unpleasant photographs, as well as neutral images. At each point, study participants answered 20 questions from the State-Trait Anxiety inventory, which is designed to assess different symptoms of anxiety. All participants were put through both the exercise and the rest states (on different days) and tested for anxiety levels pre-exercise, post-exercise, and post-picture viewing.
Smith found that exercise and quiet rest were equally effective at reducing anxiety levels initially. However, once they were emotionally stimulated (by being shown 90 photographs from the International Affective Picture System, a database of photographs used in emotion research) for ~20 minutes, the anxiety levels of those who had simply rested went back up to their initial levels, whereas those who had exercised maintained their reduced anxiety levels.
"The set of photographic stimuli we used from the IAPS database was designed to simulate the range of emotional events you might experience in daily life," Smith explains. "They represent pleasant emotional events, neutral events and unpleasant events or stimuli. These vary from pictures of babies, families, puppies and appetizing food items, to very neutral things like plates, cups, furniture and city landscapes, to very unpleasant images of violence, mutilations and other gruesome things."
The study findings suggest that exercise may play an important role in helping people to better endure life’s daily anxieties and stressors.
Smith plans to explore if exercise could have the same persistent beneficial effect in patients who regularly experience anxiety and depression symptoms. In collaboration with the new Maryland Neuroimaging Center, he is also exploring the addition of functional magnetic resonance imaging, or fMRI, to measure brain activity during the period of exposure to emotionally stimulating images to see how exercise may alter the brain’s emotion-related neural networks.
Smith also investigates the role of exercise in preventing cognitive decline in older adults. His research has shown that physical activity promotes changes in the brain that may protect those at high risk for Alzheimer’s disease.
(Source: newsdesk.umd.edu)
Stress has long been pegged as the enemy of attention, disrupting focus and doing substantial damage to working memory — the short-term juggling of information that allows us to do all the little things that make us productive.
By watching individual neurons at work, a group of psychologists at the University of Wisconsin-Madison has revealed just how stress can addle the mind, as well as how neurons in the brain’s prefrontal cortex help “remember” information in the first place.
Working memory is short-term and flexible, allowing the brain to hold a large amount of information close at hand to perform complex tasks. Without it, you would have forgotten the first half of this sentence while reading the second half. The prefrontal cortex is vital to working memory.

"In many respects, you’d look pretty normal without a prefrontal cortex," said Craig Berridge, UW-Madison psychology professor. "You don’t need that part of the brain to hear or talk, to keep long-term memories, or to remember what you did as a child or what you read in the newspaper three days ago."
But without your prefrontal cortex you’d be unable to stay on task or modulate your emotions well.
"People without a prefrontal cortex are very distractible," Berridge said. "They’re very impulsive. They can be very argumentative."
The neurons of the prefrontal cortex help store information for short periods. Like a chalkboard, these neurons can be written with information, erased when that information is no longer needed, and rewritten with something new.
It’s how the neurons maintain access to that short-term information that leaves them vulnerable to stress. David Devilbiss, a scientist working with Berridge and lead author on a study published today in the journal PLOS Computational Biology, applied a new statistical modeling approach to show that rat prefrontal neurons were firing and re-firing to keep recently stored information fresh.

"Even though these neurons communicate on a scale of every thousandth of a second, they know what they did one second to one-and-a-half seconds ago," Devilbiss said. "But if the neuron doesn’t stimulate itself again within a little more than a second, it’s lost that information."
Apply some stress — in the researchers’ case, a loud blast of white noise in the presence of rats working on a maze designed to test working memory — and many neurons are distracted from reminding themselves of … what was it we were doing again?
"We’re simultaneously watching dozens of individual neurons firing in the rats’ brains, and under stress those neurons get even more active," said Devilbiss, whose work was supported by the National Science Foundation and National Institutes of Health. "But what they’re doing is not retaining information important to completing the maze. They’re reacting to other things, less useful things."
Without the roar of white noise, which has been shown to impair rats in the same way it does monkeys and humans, the maze-runners were reaching their goal about 90 percent of the time. Under stress, the animals completed the test at a 65 percent clip, with many struggling enough to fall to blind chance.
Recordings of the electrical activity of prefrontal cortex neurons in the maze-running rats showed these neurons were unable to hold information key to finding the next chocolate chip reward. Instead, the neurons were frenetic, reacting to distractions such as noises and smells in the room.
The effects of stress-related distraction are well-known and dangerous.
"The literature tells us that stress plays a role in more than half of all workplace accidents, and a lot of people have to work under what we would consider a great deal of stress," Devilbiss said. "Air traffic controllers need to concentrate and focus with a lot riding on their actions. People in the military have to carry out these thought processes in conditions that would be very distracting, and now we know that this distraction is happening at the level of individual cells in the brain."
The researchers’ work may suggest new directions for treatment of prefrontal cortex dysfunction.
"Based on drug studies, it had been believed stress simply suppressed prefrontal cortex activity," Berridge said. "These studies demonstrate that rather than suppressing activity, stress modifies the nature of that activity. Treatments that keep neurons on their self-stimulating task while shutting out distractions may help protect working memory."
(Source: news.wisc.edu)
Results of a study led by researchers at Boston University School of Medicine (BUSM) and the Veterans Affairs (VA) Boston Healthcare System indicate that the proposed changes to the diagnosis of post-traumatic stress disorder (PTSD) will not substantially affect the number of people who meet criteria for the disorder.
The Diagnostic and Statistical Manual of Mental Disorders (DSM), the handbook that defines psychiatric disorders, has been undergoing revisions for the past decade in advance of the publication of its fifth edition (DSM-5). Included in the proposed revisions are the first major changes to the PTSD diagnosis since its initial appearance in DSM-III back in 1980. These include the addition of new symptoms, revision of existing ones and a new set of diagnostic criteria.
According to DSM-IV, the criteria for a diagnosis of PTSD include exposure to a traumatic event, persistent re-experiencing of the traumatic event, avoidance and emotional numbing, and persistent hyperarousal and hypervigilance. The proposed revisions for DSM-5 involve clarification regarding what constitutes a traumatic event, the addition symptoms such as self-destructive behavior and distorted blaming of oneself or others for the traumatic event and a reorganization of the diagnostic decision rules for establishing a diagnosis of PTSD.