Antidepressant holds promise in treating Alzheimer's agitation

When non-medication options fail, it may prove to be an alternative treatment for this common, distressing symptom Feb. 19, 2014 (Toronto) - An antidepressant medication has shown potential in treating symptoms of agitation that occur with Alzheimer's disease and in alleviating caregivers' stress, according to a multi-site U.S.- Canada study. "Up to 90 per cent of people with dementia experience symptoms of agitation such as emotional distress, restlessness, aggression or irritability, which is upsetting for patients and places a huge burden on their caregivers," said Dr. Bruce G. Pollock, Vice President of Research at the Centre for Addiction and Mental Health (CAMH), who directed research at the CAMH site. "These symptoms are a major reason why people go into long-term care prematurely." The antidepressant citalopram, sold under the brand names Celexa and Cipramil, significantly relieved agitation in a group of Alzheimer's disease (AD) patients as reported in the February 19 issue of the Journal of the American Medical Association. "When agitation occurs, it's paramount to try non-medication approaches first, such as looking for underlying physical discomfort in a patient, reducing external triggers such as noise or overstimulation, and encouraging light exercise," said Dr. Pollock, Director of CAMH's Campbell Family Mental Health Research Institute. When these approaches don't work, antipsychotic medications are commonly used to treat agitation. "Antipsychotics are not an ideal therapy and significantly increase the risk of strokes, heart attacks and sudden death," he said. Based on promising early findings from Europe, Dr. Pollock began conducting studies on citalopram, which suggested it might be a viable treatment alternative to antipsychotics. To provide stronger evidence, the Citalopram for Agitation in Alzheimer's Disease Study (CitAD) was initiated with eight leading Alzheimer's research centres across the United States and Canada, including the Geriatric Program at CAMH. The study included 186 patients with Alzheimer's disease who showed symptoms of agitation. Their average age was in the late 70s. None had experienced symptom relief with non-medication therapies, and some had failed treatment with antipsychotic drugs. The study measured both patients' agitation levels as well as their caregivers' stress levels, a factor strongly linked to Alzheimer's patients' well-being. Patients were then randomly assigned to receive either citalopram for nine weeks, up to a dose of 30 milligrams per day, or an identical-looking placebo. At the end of the study period, the tests were repeated. Patients on the drug had significant relief from their agitation symptoms. In one measure of agitation, about 40 percent of patients who took citalopram had "considerable relief" compared to 26 percent of patients who took the placebo. In addition, caregivers for these patients had significantly lower levels of stress. ### Other CAMH collaborators were Dr. Tarek Rajji, Chief of Geriatric Psychiatry and Physician-in-Chief Dr. Benoit Mulsant. The other academic centres involved with the study were the University of Rochester, Johns Hopkins University, Columbia University, University of Calgary, Roper St. Francis Health Care, University of Southern California, University of Pennsylvania and Stanford University. This research was supported by a grant from the U.S. National Institute on Aging and National Institute of Mental Health. For further information, please contact Kate Richards, CAMH Media Relations at (416) 595-6015. The Centre for Addiction and Mental Health (CAMH) is Canada's largest mental health and addiction teaching hospital, and one of the world's leading research centres in the field. CAMH combines clinical care, research, education, policy development and health promotion to help transform the lives of people affected by mental health and addiction issues CEUs For Nurses CAMH is fully affiliated with the University of Toronto, and is a Pan American Health Organization/World Health Organization Collaborating Centre.

New evidence that chronic stress predisposes brain to mental illness

By Robert Sanders, Media Relations | February 11, 2014 BERKELEY — University of California, Berkeley, researchers have shown that chronic stress generates long-term changes in the brain that may explain why people suffering chronic stress are prone to mental problems such as anxiety and mood disorders later in life. myelin stained blue Myelin is stained blue in this cross section of a rat hippocampus. Myelin, which speeds electrical signals flowing through axons, is produced by oligodendrocytes, which increase in number as a result of chronic stress. New oligodendrocytes are shown in yellow. Image by Aaron Friedman and Daniela Kaufer. Their findings could lead to new therapies to reduce the risk of developing mental illness after stressful events. Doctors know that people with stress-related illnesses, such as post-traumatic stress disorder (PTSD), have abnormalities in the brain, including differences in the amount of gray matter versus white matter. Gray matter consists mostly of cells – neurons, which store and process information, and support cells called glia – while white matter is comprised of axons, which create a network of fibers that interconnect neurons. White matter gets its name from the white, fatty myelin sheath that surrounds the axons and speeds the flow of electrical signals from cell to cell. How chronic stress creates these long-lasting changes in brain structure is a mystery that researchers are only now beginning to unravel. In a series of experiments, Daniela Kaufer, UC Berkeley associate professor of integrative biology, and her colleagues, including graduate students Sundari Chetty and Aaron Freidman, discovered that chronic stress generates more myelin-producing cells and fewer neurons than normal. This results in an excess of myelin – and thus, white matter – in some areas of the brain, which disrupts the delicate balance and timing of communication within the brain. “We studied only one part of the brain, the hippocampus, but our findings could provide insight into how white matter is changing in conditions such as schizophrenia, autism, depression, suicide, ADHD and PTSD,” she said. The hippocampus regulates memory and emotions, and plays a role in various emotional disorders. Kaufer and her colleagues published their findings in the Feb. 11 issue of the journal Molecular Psychiatry. Does stress affect brain connectivity? Kaufer’s findings suggest a mechanism that may explain some changes in brain connectivity in people with PTSD, for example. One can imagine, she said, that PTSD patients could develop a stronger connectivity between the hippocampus and the amygdala – the seat of the brain’s fight or flight response – and lower than normal connectivity between the hippocampus and prefrontal cortex, which moderates our responses. “You can imagine that if your amygdala and hippocampus are better connected, that could mean that your fear responses are much quicker, which is something you see in stress survivors,” she said. “On the other hand, if your connections are not so good to the prefrontal cortex, your ability to shut down responses is impaired. So, when you are in a stressful situation, the inhibitory pathways from the prefrontal cortex telling you not to get stressed don’t work as well as the amygdala shouting to the hippocampus, ‘This is terrible!’ You have a much bigger response than you should.” white matter fibers in human brain White matter fiber architecture of the brain. Human Connectome Project. She is involved in a study to test this hypothesis in PTSD patients, and continues to study brain changes in rodents subjected to chronic stress or to adverse environments in early life. Stress tweaks stem cells Kaufer’s lab, which conducts research on the molecular and cellular effects of acute and chronic stress, focused in this study on neural stem cells in the hippocampus of the brains of adult rats. These stem cells were previously thought to mature only into neurons or a type of glial cell called an astrocyte. The researchers found, however, that chronic stress also made stem cells in the hippocampus mature into another type of glial cell called an oligodendrocyte, which produces the myelin that sheaths nerve cells. The finding, which they demonstrated in rats and cultured rat brain cells, suggests a key role for oligodendrocytes in long-term and perhaps permanent changes in the brain that could set the stage for later mental problems. Oligodendrocytes also help form synapses – sites where one cell talks to another – and help control the growth pathway of axons, which make those synapse connections. The fact that chronic stress also decreases the number of stem cells that mature into neurons could provide an explanation for how chronic stress also affects learning and memory, she said. Kaufer is now conducting experiments to determine how stress in infancy affects the brain’s white matter, and whether chronic early-life stress decreases resilience later in life. She also is looking at the effects of therapies, ranging from exercise to antidepressant drugs, that reduce the impact of stress and stress hormones. Kaufer’s coauthors include Chetty, formerly from UC Berkeley’s Helen Wills Neuroscience Institute and now at Harvard University; Friedman and K. Taravosh-Lahn at UC Berkeley’s Department of Integrative Biology; additional colleagues from UC Berkeley and others from Stanford University and UC Davis. The work was supported by a BRAINS (Biobehavioral Research Awards for Innovative New Scientists) award from the National Institute of Mental Health of the National Institutes of Health (R01 MH087495), a Berkeley Stem Cell Center Seed Grant, the Hellman Family Foundation and the National Alliance for Research on Schizophrenia and Depression. RELATED INFORMATION •Stress and glucocorticoids promote oligodendrogenesis in the adult hippocampus (2/11/14 Molecular Psychiatry) •Daniela Kaufer’s web site •Researchers find out why some stress is good for you (4/16/13 press release) For more information on this and other mental health topics, please visit Counselor CEUs

RI Hospital: Cognitive behavioral therapy benefits patients with body dysmorphic disorder

Patients reported considerable improvements in symptoms and disability PROVIDENCE, R.I. – In a recent study, researchers at Rhode Island Hospital found significant benefits of cognitive behavioral therapy as a treatment modality for patients with Body Dysmorphic Disorder (BDD). BDD is a common, often severe, and under-recognized body image disorder that affects an estimated 1.7 percent to 2.4 percent of the population. This study demonstrated significant improvement in patients' BDD symptoms and level of disability, as well as high levels of patient satisfaction with the treatment. The study is published online in advance of print in the journal Behavior Therapy. Researchers first developed the manualized treatment and then studied 36 adults with BDD who were randomly selected to either receive 22 cognitive behavioral therapy (CBT) sessions over 24 weeks, or placed on a 12-week wait list. Assessments were conducted pre-treatment, monthly, post-treatment and at three- and six-month follow-up appointments. Post-treatment, patients reported high satisfaction with the treatment, and BDD symptoms such as depression; insight regarding inaccurate beliefs about appearance; and disability in work, social life/leisure, and family life/home responsibilities significantly improved. "BDD is a common and often debilitating disorder, and there are very few proven effective treatments," said Katharine Phillips, M.D., director of the Body Dysmorphic Disorder program at Rhode Island Hospital, "This study suggests that using cognitive behavioral therapy that specifically targets BDD symptoms can result in significant improvements in symptoms and ability to function in daily life. We are currently conducting a study, funded by the National Institute of Mental Health, to more definitively test this treatment and compare it to the most commonly received type of therapy for BDD." CBT uses standard core elements relevant to all BDD patients, such as psychoeducation, cognitive interventions, exposure to avoided situations (which are usually social situations), and prevention of excessive repetitive behaviors (such as mirror checking or compulsive grooming). Treatment ends with relapse prevention strategies and booster sessions focused on helping patients maintain the gains they have made during treatment. Optional treatment modules focus on symptoms and behaviors that some, but not all, patients with this disorder engage in (such as compulsive skin picking or surgery seeking), which enables clinicians to tailor the treatment to individual patient needs. BDD typically starts during early adolescence. The disorder consists of intrusive, time-consuming preoccupations about perceived defects in one's physical appearance (for example, acne, hair loss, or nose size) whereas the perceived flaws are actually minimal or even nonexistent in the eyes of others. Individuals with BDD may engage in obsessive grooming, skin picking or plastic surgery (which appears to usually be ineffective). BDD also often leads to social impairments, missed work or school and difficulty forming and maintaining meaningful relationships. It is associated with high lifetime rates of psychiatric hospitalization and suicide. "Cognitive behavioral therapy is an often-helpful approach to treating BDD," Phillips said. "It can be tailored to meet the needs of a wide range of patients and includes unique strategies to address symptoms that distinguish BDD from other disorders." Phillips continued, "While more research is needed, we conclude from this study that CBT is an appropriate, feasible, and very promising alternative treatment for those suffering from this often misunderstood and severe mental illness." ### The study was funded in part by the National Institute of Mental Health (R34 MH070490). Phillips' principal affiliation is Rhode Island Hospital, a member hospital of the Lifespan health system in Rhode Island. She is also a member of the Department of Psychiatry and Human Behavior at The Warren Alpert Medical School of Brown University. Other researchers involved in the study were Elizabeth Didie of Rhode Island Hospital and the Alpert Medical School; and Sabine Wilhelm, Jeanne M. Fama, Jennifer L. Greenberg and Aparna Keshavia of Massachusetts General Hospital; Ulrike Buhlmann of the Institute of Psychology, Humboldt-Universität zu in Berlin, Germany; and Gail Steketee of Boston University. About Rhode Island Hospital Founded in 1863, Rhode Island Hospital in Providence, R.I., is a private, not-for-profit hospital and is the principal teaching hospital of The Warren Alpert Medical School of Brown University. A major trauma center for southeastern New England, the hospital is dedicated to being on the cutting edge of medicine and research. Last year, Rhode Island Hospital received more than $55 million in external research funding. It is also home to Hasbro Children's Hospital, the state's only facility dedicated to pediatric care. For more information on Rhode Island Hospital, visit http://www.rhodeislandhospital.org, follow us on Twitter @RIHospital or like us on Facebook http://www.facebook.com/rhodeislandhospitalpage. For more information on this and other mental health related topic, please visit MHC Continuing Education

Create Your Happiness

The following article by by Ilchi Lee describes human emotions such as fear and happiness. What do you think? "Human emotion is a strong response coming out of our mental activities. Emotion itself is only a brain function; it is neither positive nor negative. Fear makes you avoid danger, resentment makes you fight, and loving makes you care for others. People cannot remove their emotions from the brain functions. That’s why it is not a good idea to suppress emotions or ignore them; they will eventually damage the body and relationships with others. There are two things people can do with their emotions. One is admitting emotions, the other is regulating them. Admitting and regulating emotions are possible when people don’t drown in their emotions. Emotion is not an ocean; it is a wave. It is not the whole; it is a response on the surface. Just like waves rise always on the surface of the ocean, people feel emotion rising all the time. Being emotional is a very natural phenomenon in the body, but what’s important is how to process it. People’s emotions are changed by their hormones, and people’s happiness and unhappiness are influenced by their hormones. Men and women, when they love each other, have pounding hearts and are happy. In the end, that’s about information. When certain information is input into our brains, we become happy or unhappy as a result. That’s why we say that our bodies are chemical factories that secrete hormones. The human brain secretes hormones as a result of certain information. For example, good hormones are always produced in the brains of those who continually receive praise. Consequently, they live with confidence. Those who are continually nagged frequently lose confidence, are fearful of people, and cringe even at the sight of people. Bad hormones are secreted when they just think about being nagged. When this happens, certain functions of the brain can even be destroyed. So I thought, “I can cause the secretion of hormones through information! Wouldn’t it be great if we could just produce the hormones we want?” And I always say that I am the owner of my brain and emotions. I can watch my emotions rising and process them as an owner. If we don’t realize that we are the owners of our brains, our fickle emotion will take over and become the owner of our brains. We should use our brains proactively as an owner. We usually think emotion comes from outside of our body and we respond to it. Of course, emotion comes from outside stimulation, but how we respond to it depends on how we use our brains. If we use our brains well, we can develop a natural ability to not be swept away by our emotions. Because happiness is hormonal, we don’t need to wait for happiness in life, we can make our body produce good hormones. Everybody can create happiness knowing this theory. When neurotransmitters secrete well, information transfers well in the brain. Serotonin is a neurotransmitter that contributes to the feeling of happiness. I want to call it happy hormone or peace messenger. Serotonin increases when we are creative and it decreases when we are stressed. When serotonin secretes less than normal levels, people can have trouble managing stress and get easily angry or depressed. If you feel comfortable, peaceful and joyful, it secretes well. Meditation can help to make us feel comfortable, peaceful and joyful. Or, if we say it the other way around, any activity that increases serotonin can be a good meditation. Meditation is not a difficult thing to do. Meditation is not only sitting in a lotus posture and breathing, but also laughing, praising and loving. You don’t need to stick to a certain posture or form of meditation. If meditation helps activate your brain function and you can feel healthy, happy and peaceful from the meditation, then that is the best meditation for you. Meditation is giving positive stimulation to the brain besides the habitual and daily stimulation. If you build a sense of meditating, you can meditate in your daily activities. Sit down on the chair or the floor with your back straight. Shake your head side to side. Start with tapping your lower abdomen with your two fists and continue for three to five minutes. You will feel warmth in your lower abdomen and your head refreshed. And you will produce saliva in your mouth. This is the condition of happiness which serotonin produces in your body. This simple way is called Brain Wave Vibration meditation. Please make your brain overflow with serotonin from this simple method and create your happiness in any time and situation. And here’s a video on how to do Brain Wave Vibration! - See more at: http://brainworldmagazine.com/create-your-happiness/#sthash.hcIoU4Kd.dpuf" For more information on the human brain and emotions, please visit our course listing at Aspira Continuing Education Online Courses

SHY hypothesis explains that sleep is the price we pay for learning

MADISON — Why do animals ranging from fruit flies to humans all need to sleep? After all, sleep disconnects them from their environment, puts them at risk and keeps them from seeking food or mates for large parts of the day. Two leading sleep scientists from the University of Wisconsin School of Medicine and Public Health say that their synaptic homeostasis hypothesis of sleep or "SHY" challenges the theory that sleep strengthens brain connections. The SHY hypothesis, which takes into account years of evidence from human and animal studies, says that sleep is important because it weakens the connections among brain cells to save energy, avoid cellular stress, and maintain the ability of neurons to respond selectively to stimuli. "Sleep is the price the brain must pay for learning and memory," says Dr. Giulio Tononi, of the UW Center for Sleep and Consciousness. "During wake, learning strengthens the synaptic connections throughout the brain, increasing the need for energy and saturating the brain with new information. Sleep allows the brain to reset, helping integrate, newly learned material with consolidated memories, so the brain can begin anew the next day. " Tononi and his co-author Dr. Chiara Cirelli, both professors of psychiatry, explain their hypothesis in a review article in today's issue of the journal Neuron. Their laboratory studies sleep and consciousness in animals ranging from fruit flies to humans; SHY takes into account evidence from molecular, electrophysiological and behavioral studies, as well as from computer simulations. "Synaptic homeostasis" refers to the brain's ability to maintain a balance in the strength of connections within its nerve cells. Why would the brain need to reset? Suppose someone spent the waking hours learning a new skill, such as riding a bike. The circuits involved in learning would be greatly strengthened, but the next day the brain will need to pay attention to learning a new task. Thus, those bike-riding circuits would need to be damped down so they don't interfere with the new day's learning. "Sleep helps the brain renormalize synaptic strength based on a comprehensive sampling of its overall knowledge of the environment," Tononi says, "rather than being biased by the particular inputs of a particular waking day." The reason we don't also forget how to ride a bike after a night's sleep is because those active circuits are damped down less than those that weren't actively involved in learning. Indeed, there is evidence that sleep enhances important features of memory, including acquisition, consolidation, gist extraction, integration and "smart forgetting," which allows the brain to rid itself of the inevitable accumulation of unimportant details. However, one common belief is that sleep helps memory by further strengthening the neural circuits during learning while awake. But Tononi and Cirelli believe that consolidation and integration of memories, as well as the restoration of the ability to learn, all come from the ability of sleep to decrease synaptic strength and enhance signal-to-noise ratios. While the review finds testable evidence for the SHY hypothesis, it also points to open issues. One question is whether the brain could achieve synaptic homeostasis during wake, by having only some circuits engaged, and the rest off-line and thus resetting themselves. Other areas for future research include the specific function of REM sleep (when most dreaming occurs) and the possibly crucial role of sleep during development, a time of intense learning and massive remodeling of brain Counselor CEUs

Alcohol, tobacco, drug use far higher in severely mentally ill

In the largest ever assessment of substance use among people with severe psychiatric illness, researchers at Washington University School of Medicine in St. Louis and the University of Southern California have found that rates of smoking, drinking and drug use are significantly higher among those who have psychotic disorders than among those in the general population. The study is published online in the journal JAMA Psychiatry. The finding is of particular concern because individuals with severe mental illness are more likely to die younger than people without severe psychiatric disorders. "These patients tend to pass away much younger, with estimates ranging from 12 to 25 years earlier than individuals in the general population," said first author Sarah M. Hartz, MD, PhD, assistant professor of psychiatry at Washington University. "They don't die from drug overdoses or commit suicide — the kinds of things you might suspect in severe psychiatric illness. They die from heart disease and cancer, problems caused by chronic alcohol and tobacco use." The study analyzed smoking, drinking and drug use in nearly 20,000 people. That included 9,142 psychiatric patients diagnosed with schizophrenia, bipolar disorder or schizoaffective disorder — an illness characterized by psychotic symptoms such as hallucinations and delusions, and mood disorders such as depression. The investigators also assessed nicotine use, heavy drinking, heavy marijuana use and recreational drug use in more than 10,000 healthy people without mental illness. The researchers found that 30 percent of those with severe psychiatric illness engaged in binge drinking, defined as drinking four servings of alcohol at one time. In comparison, the rate of binge drinking in the general population is 8 percent. Among those with mental illness, more than 75 percent were regular smokers. This compares with 33 percent of those in the control group who smoked regularly. There were similar findings with heavy marijuana use: 50 percent of people with psychotic disorders used marijuana regularly, versus 18 percent in the general population. Half of those with mental illness also used other illicit drugs, while the rate of recreational drug use in the general population is 12 percent. "I take care of a lot of patients with severe mental illness, many of whom are sick enough that they are on disability," said Hartz. "And it's always surprising when I encounter a patient who doesn't smoke or hasn't used drugs or had alcohol problems." Hartz said another striking finding from the study is that once a person develops a psychotic illness, protective factors such as race and gender don't have their typical influence. Previous research indicates that Hispanics and Asians tend to have lower rates of substance abuse than European Americans. The same is true for women, who tend to smoke, drink and use illicit drugs less often than men. "We see protective effects in these subpopulations," Hartz explained. "But once a person has a severe mental illness, that seems to trump everything." That's particularly true, she said, with smoking. During the last few decades, smoking rates have declined in the general population. People over age 50 are much more likely than younger people to have been regular smokers at some point in their lives. For example, about 40 percent of those over 50 used to smoke regularly. Among those under 30, fewer than 20 percent have been regular smokers. But among the mentally ill, the smoking rate is more than 75 percent, regardless of the patient's age. "With public health efforts, we've effectively cut smoking rates in half in healthy people, but in the severely mentally ill, we haven't made a dent at all," she said. Until recently, smoking was permitted in most psychiatric hospitals and mental wards. Hartz believes that many psychiatrists decided that their sickest patients had enough problems without having to worry about quitting smoking, too. There also were concerns about potential dangers from using nicotine-replacement therapy, while continuing to smoke since smoking is so prevalent among the mentally ill. Recent studies, however, have found those concerns were overblown. The question, she said, is whether being more aggressive in trying to curb nicotine, alcohol and substance use in patients with severe psychiatric illness can lengthen their lives. Hartz believes health professionals who treat the mentally ill need to do a better job of trying to get them to stop smoking, drinking and using drugs. "Some studies have shown that although we psychiatrists know that smoking, drinking and substance use are major problems among the mentally ill, we often don't ask our patients about those things," she said. "We can do better, but we also need to develop new strategies because many interventions to reduce smoking, drinking and drug use that have worked in other patient populations don't seem to be very effective in these psychiatric patients." CADC I & II Continuing Education ### Funding for this research comes from the National Institute on Drug Abuse (NIDA), the National Institute on Alcohol Abuse and Alcoholism (NIAAA), the National Institute of Mental Health (NIMH) and the National Cancer Institute (NCI) of the National Institutes of Health (NIH), and the American Cancer Society. NIH grant numbers R01 DA032843, R01 DA025888, U10 AA008401, UL1 RR024992, P01 CA089392, R01 MH085548, R01 MH085542, K08 DA032680-1, Kl2 RR024994, K01 DA025733. Hartz SM, Pato CN, Medeiros H, Cavazos-Rehg P, Sobell JL, Knowles JA, Bierut LJ, Pato MT and the Genomic Psychiatry Cohort Consortium. JAMA Psychiatry Published online Jan. 1, 2014. doi:10.1001/jamapsychiatry.2013.3276 Washington University School of Medicine's 2,100 employed and volunteer faculty physicians also are the medical staff of Barnes-Jewish and St. Louis Children's hospitals. The School of Medicine is one of the leading medical research, teaching and patient care institutions in the nation, currently ranked sixth in the nation by U.S. News & World Report. Through its affiliations with Barnes-Jewish and St. Louis Children's hospitals, the School of Medicine is linked to BJC HealthCare.

Anxiety linked to higher long-term risk of stroke

American Heart Association Rapid Access Journal Report The greater your anxiety level, the higher your risk of having a stroke, according to new research published in the American Heart Association journal Stroke. The study is the first in which researchers linked anxiety and stroke independent of other factors such as depression. Anxiety disorders are one of the most prevalent mental health problems. Symptoms include feeling unusually worried, stressed, nervous or tense. Over a 22 year period, researchers studied a nationally representative group of 6,019 people 25-74 years old in the first National Health and Nutrition Examination Survey (NHANES I). Participants underwent an interview and took blood tests, medical examinations and completed psychological questionnaires to gauge anxiety and depression levels. Researchers tracked strokes through hospital or nursing home reports and death certificates. After accounting for other factors, they found that even modest increases in anxiety were associated with greater stroke risk. People in the highest third of anxiety symptoms had a 33 percent higher stroke risk than those with the lowest levels. "Everyone has some anxiety now and then. But when it's elevated and/or chronic, it may have an effect on your vasculature years down the road," said Maya Lambiase, Ph.D., study author and cardiovascular behavioral medicine researcher in the Department of Psychiatry at the University of Pittsburgh School of Medicine, in Pittsburgh, Penn. People with high anxiety levels are more likely to smoke and be physically inactive, possibly explaining part of the anxiety-stroke link. Higher stress hormone levels, heart rate or blood pressure could also be factors, Lambiase said. In earlier work, researchers found that depression was linked to greater risk of stroke. In contrast to anxiety, depression is a persistent feeling of hopelessness, dejection, and lack of energy, among other symptoms. Stroke is the No. 4 killer and a leading cause of disability in the United States Continuing Education for MFTs ### Co-authors are Laura Kubzansky, Ph.D. and Rebecca Thurston, Ph.D. Author disclosures are on the manuscript. The National Heart, Lung, and Blood Institute and the National Institute of Mental Health funded the study. For the latest heart and stroke news, follow us on Twitter: @HeartNews. For stroke science, follow the Stroke journal at @StrokeAHA_ASA. Statements and conclusions of study authors published in American Heart Association scientific journals are solely those of the study authors and do not necessarily reflect the association's policy or position. The association makes no representation or guarantee as to their accuracy or reliability. The association receives funding primarily from individuals; foundations and corporations (including pharmaceutical, device manufacturers and other companies) also make donations and fund specific association programs and events. The association has strict policies to prevent these relationships from influencing the science content. Revenues from pharmaceutical and device corporations are available at http://www.heart.org/corporatefunding.