May 29, 2012

Less couch time equals fewer cookies

Just 2 simple changes in health behavior spurs big and lasting results CHICAGO --- Simply ejecting your rear from the couch means your hand will spend less time digging into a bag of chocolate chip cookies. That is the simple but profound finding of a new Northwestern Medicine study, which reports simply changing one bad habit has a domino effect on others. Knock down your sedentary leisure time and you'll reduce junk food and saturated fats because you're no longer glued to the TV and noshing. It's a two-for-one benefit because the behaviors are closely related. The study also found the most effective way to rehab a delinquent lifestyle requires two key behavior changes: cutting time spent in front of a TV or computer screen and eating more fruits and vegetables. "Just making two lifestyle changes has a big overall effect and people don't get overwhelmed," said Bonnie Spring, a professor of preventive medicine at Northwestern University Feinberg School of Medicine, and lead author of the study published in Archives of Internal Medicine. "Americans have all these unhealthy behaviors that put them at high risk for heart disease and cancer, but it is hard for them and their doctors to know where to begin to change those unhealthy habits," Spring said. "This approach simplifies it." With this simplified strategy, people are capable of making big lifestyle changes in a short period of time and maintaining them, according to the study. Spring wanted to figure out the most effective way to spur people to change common bad health habits: eating too much saturated fat and not enough fruits and vegetables, spending too much sedentary leisure time and not getting enough physical activity. She and colleagues randomly assigned 204 adult patients, ages 21 to 60 years old, with all those unhealthy habits into one of four treatments. The treatments were: increase fruit/vegetable intake and physical activity, decrease fat and sedentary leisure, decrease fat and increase physical activity, and increase fruit/vegetable intake and decrease sedentary leisure. During the three weeks of treatment, patients entered their daily data into a personal digital assistant and uploaded it to a coach who communicated as needed by telephone or email. Participants could earn $175 for meeting goals during the three-week treatment phase. But when that phase was completed, patients no longer had to maintain the lifestyle changes in order to be paid. They were simply asked to send data three days a month for six months and received $30 to $80 per month. "We said we hope you'll continue to keep up these healthy changes, but you no longer have to keep them up to be compensated," Spring said. The results over the next six months amazed Spring. "We thought they'd do it while we were paying them, but the minute we stopped they'd go back to their bad habits," she said. "But they continued to maintain a large improvement in their health behaviors." From baseline to the end of treatment to the end of the six-month follow-up, the average servings of fruit/vegetables changed from 1.2 to 5.5 to 2.9; average minutes per day of sedentary leisure went from 219.2 to 89.3 to 125.7 and daily calories from saturated fat from 12 percent to 9.4 percent to 9.9 percent. About 86 percent of participants said once they made the change, they tried to maintain it. There was something about increasing fruits and vegetables that made them feel like they were capable of any of these changes," Spring said. "It really enhanced their confidence." "We found people can make very large changes in a very short amount of time and maintain them pretty darn well," Spring said. "It's a lot more feasible than we thought." ceus for social workers ### Other Northwestern authors included Donald Lloyd-Jones, M.D. Arlen Moller and Juned Siddique. The research is supported by the following National Institutes of Health grants: National Institute of Heart, Lung and Blood grant HL075451, for Multiple Behavior Change in Diet and Activity; the Robert H. Lurie Comprehensive Cancer Center of Northwestern University grant from the National Institute of Mental Health P30 CA060553; the National Institute of Mental Health grant F31 MH070107.

May 28, 2012

Most Children with ASD Diagnosed After Age 5, Use Multiple Services and Medications

Fewer than one out of five school-aged children with special health care needs were diagnosed with autism spectrum disorder (ASD) by age 2, according to new data from an NIMH-funded study. These diagnoses were made by a variety of health care providers, and most children in the study used multiple health care services (such as speech or language therapy) and multiple medications social worker continuing education Background Identifying ASD at an early age allows children to start treatment sooner, which can improve their later development and learning, and may also reduce a child’s need for specialized services or treatments later in life. To determine the experiences of school-aged children with special health care needs, Lisa Colpe, Ph.D., M.P.H., and Bev Pringle, Ph.D., of the NIMH Division of Services and Intervention Research, collaborated with colleagues who conducted more than 4,000 telephone interviews with parents or guardians of a child between the ages of 6-17 who had a confirmed diagnosis of ASD, intellectual disability, and/or developmental delay. These survey interviews were a part of the Pathways to Diagnosis and Services Study, sponsored by NIMH using funds available from the American Recovery and Reinvestment Act of 2009 (Recovery Act). Additional collaborators on this project include the National Center for Health Statistics at the Centers for Disease Control and Prevention (CDC) and the Maternal and Child Health Bureau at the Health Resources and Services Administration (HRSA). Results of the Study Key findings include: The median age when school aged children with special health care needs and ASD were first identified as having ASD was 5 years. Those identified as having ASD at younger than 5 years were diagnosed most often by generalists (such as pediatricians, family physicians, and nurse practitioners) and psychologists. Those identified later than 5 years were diagnosed primarily by psychologists and psychiatrists. Nine out of ten school-aged children with special health care needs and ASD used at least one health care service, such as behavioral intervention or modification services, sensory integration therapy, cognitive based therapy, occupational therapy, physical therapy, social skills training, or speech or language therapy. Social skills training and speech or language therapy were the most commonly used service, each used by almost 60 percent, or three out of five, of these children. More than half of school-aged children with special health care needs and ASD used at least one psychotropic medication. “Psychotropic medication” refers to any medication used to treat a mental disorder. Almost 33 percent of these children used stimulant medications 25 percent used anti-anxiety or mood-stabilizing medications 20 percent used antidepressants. Further findings are available in the NCHS Data Brief and Frequently Asked Questions. Significance The new data detail the experiences of young children with ASD, describing when they are first identified as having ASD, who is making those identifications, and the services and medications the children use to meet their developmental needs. What’s Next NIMH encourages researchers to access and analyze the new dataset to produce more studies on the early life experiences and the diagnostic, service, and treatment issues relevant to children with ASD and special health care needs. The Pathways to Diagnosis and Services Study dataset can be accessed at Reference Pringle BA, Colpe LJ, Blumberg SJ, Avila RM, Kogan MD. Diagnostic History and Treatment of School-Aged Children with Autism Spectrum Disorder and Special Health Care Needs. NCHS data brief, no 97. Hyattsville, MD: National Center for Health Statistics. 2012.

May 21, 2012

Reducing off-label use of antipsychotic medications may save money

Reducing the non-FDA-approved use of antipsychotic drugs may be a way to save money while having little effect on patient care, according to a Penn State College of Medicine study. Researchers say that 57.6 percent of patients prescribed antipsychotic medications in data from 2003 did not have schizophrenia or bipolar disorder, the conditions for which the drugs were approved for use. Use of medication for treatments that is not FDA-approved is called off-label use. "Given healthcare reform and widespread crisis in state revenues, state Medicaid programs will be under pressure to serve larger patient populations, increasing their fiscal stress," said Douglass L. Leslie, Ph.D., professor of public health sciences. "Medicaid prescription drug programs covered 75 percent of all antipsychotic prescription medications in the United States in 2002. Reducing off-label antipsychotic use may generate savings with little impact on patient outcomes." Researchers looked at data for 42 states from 2003, the latest data available at the time of analysis, from the Centers for Medicare & Medicaid Services. They report their results in a recent issue of American Journal of Managed Care. Patients in a Medicaid fee-for-service plan for the entire year were chosen using de-identified patient information that could not be traced to the individuals. The researchers chose patients without a diagnosis of either schizophrenia or bipolar disorder during 2003 who received an antipsychotic medication. During 2003, 372,038 patients received an antipsychotic medication. Of these patients, 214,113, or 57.6 percent, did not have a diagnosis of schizophrenia or bipolar disorder. Diagnoses included other mental disorders: 35 percent, minor depression -- 25.4 percent, major depression -- 23.2 percent, no mental disorder -- 18.8 percent, conduct disorder -- 18.8 percent, and anxiety disorder -- 16.2 percent. "A high rate of off-label antipsychotic use would not necessarily be of concern if there were scientific evidence supporting the effectiveness of these medications for conditions other than schizophrenia and bipolar disorder," Leslie said. Off-label use is supported in the medical community, with the American Academy of Neurology endorsing the use of quinine for treatment-resistant leg cramps, for example. Since 2003, some of the antipsychotic medications have been approved by the FDA for the treatment of other conditions, including irritability in autism and treatment-resistant depression. However, at the time the data were collected they were considered off-label. The rate of off-label use of antipsychotics is high compared to other medications. Other studies have shown off-label medication use includes cardiovascular drugs: 46 percent, anticonvulsants -- 46 percent, and antiasthmatics -- 42 percent. "Antipsychotics were the highest selling medication class at $14.6 billion in 2009," Leslie said. "Medicaid bears a significant proportion of these costs. Hence, off-label use may be responsible for a considerable portion of state Medicaid budgets, with little or no documented clinical benefit and a substantial risk of adverse effects. Off-label use may be an area of potential savings with little impact on patient outcomes." The newest antipsychotic drugs can cost up to $10 per day at doses recommended for patients with schizophrenia. According to the researchers, more research is needed to determine if off-label use of antipsychotic medications yields substantial clinical benefit and to identify how doctors decide to prescribe these drugs for non-FDA approved conditions. Reasons why drugs may be prescribed off-label include a lack of research results showing the drug's effectiveness in certain patients or for other conditions, or that the drugs may be used as a last resort for those patients who have not responded to other treatments. Further research is needed on the decision-making process of doctors to prescribe off-label. "Where there is limited evidence of clinical benefit, greater caution should probably be used before prescribing these drugs off-label because they can have hazardous side effects," Leslie said. ### This study was funded in part by a grant from the National Institute of Mental Health and by the Department of Veterans Affairs Mental Illness Research, Education and Clinical Center. Researchers are continuing their analysis by incorporating newer data that was recently released. Also part of this study is Robert Rosenheck, M.D., Yale School of Medicine. Continuing Education for Social Workers

May 20, 2012

Zebrafish study isolates gene related to autism, schizophrenia and obesity

What can a fish tell us about human brain development? Researchers at Duke University Medical Center transplanted a set of human genes into a zebrafish and then used it to identify genes responsible for head size at birth. Researchers at Duke University Medical Center transplanted a set of human genes into a zebrafish and then used it to identify genes responsible for head size at birth. Head size in human babies is a feature that is related to autism, a condition that recent figures have shown to be more common than previously reported, 1 in 88 children in a March 2012 study. Head size is also a feature of other major neurological disorders, such as schizophrenia. "In medical research, we need to dissect events in biology so we can understand the precise mechanisms that give rise to neurodevelopmental traits," said senior author Nicholas Katsanis, Ph.D., Jean and George Brumley Jr., MD, Professor of Developmental Biology, and Professor of Pediatrics and Cell Biology. "We need expert scientists to work side by side with clinicians who see such anatomic and other problems in patients, if we are to effectively solve many of our medical problems." The study was published online in Nature journal on May 16. Katsanis knew that a region on chromosome 16 was one of the largest genetic contributors to autism and schizophrenia, but a conversation at a European medical meeting pointed him to information that changes within that same region of the genome also were related to changes in a newborn's head size. The problem was difficult to address because the region had large deletions and duplications in DNA, which are the most common mutational mechanisms in humans. "Interpretation is harrowingly hard," said Katsanis, who is also director of the Duke Center for Human Disease Modeling. The reason is that a duplication of DNA or missing DNA usually involves several genes. "It is very difficult to go from 'here is a region with many genes, sometimes over 50' to 'these are the genes that are driving this pathology,'" Katsanis said. "There was a light bulb moment," Katsanis said. "The area of the genome we were exploring gave rise to reciprocal (opposite) defects in terms of brain cell growth, so we realized that overexpressing a gene in question might give one phenotype – a smaller head, while shutting down the same gene might yield the other, a larger head." The researchers transplanted a common duplication area of human chromosome 16 known to contain 29 genes into zebrafish embryos and then systematically turned up the activity of each transplanted human gene to find which might cause a small head (microcephaly) in the fish. They then suppressed the same gene set and asked whether any of them caused the reciprocal defect: larger heads (macrocephaly). The researchers knew that deletion of the region that contained these 29 genes occurred in 1.7% of children with autism. It took the team a few months to dissect such a "copy number variant" – an alteration of the genome that results in an abnormal number of one or more sections of chromosomal DNA. "Now we can go from a genetic finding that is dosage-sensitive and start asking reasonable questions about this gene as it pertains to neurocognitive traits, which is a big leap," Katsanis said. Neurocognitive refers to the ability to think, concentrate, reason, remember, process information, learn, understand and speak. Many human conditions have anatomical features that are also related to genetics, he said. "There are major limitations in studying autistic or schizophrenic behavior in zebrafish, but we can measure head size, jaw size, or facial abnormalities." The single gene in question, KCTD13, is responsible for driving head size in zebrafish by regulating the creation and destruction of new neurons (brain cells). This discovery let the team focus on the analogous gene in humans. "This gene contributes to autism cases, and probably is associated with schizophrenia and also childhood obesity," Katsanis said. Once the gene has been uncovered, researchers can examine the protein it produces. "Once you have the protein, you can start asking valuable functional questions and learning what the gene does in the animal or human," Katsanis said. Copy number variants, such as the ones this team found on chromosome 16, are now thought to be one of the most common sources of genetic mutations. Hundreds, if not thousands, of such chromosomal deletions and duplications have been found in patients with a broad range of clinical problems, particularly neurodevelopmental disorders. "Now we may have an efficient tool for dissecting them, which gives us the ability to improve both diagnosis and understanding of disease mechanisms," Katsanis said. The current study suggests that KCTD13 is a major contributor to some cases of autism, but also points to the synergistic action of this gene with two other genes in the region, named MVP and MAPK3, Katsanis said. Other authors include lead author Christelle Golzio, Jason Willer and Edwin Oh of the Duke Center for Human Disease Modeling and Department of Cell Biology; Mike Talkowski, Mei Sun and Jim Guzella from the Molecular Neurogenetics Unit, Center for Human Genetic Research, Massachusetts General Hospital in Boston; Sebastien Jacquemont, Alexandre Reymond and Jacques Beckmann from the Service de Génétique Médicale, Centre Hospitalier Universitaire Vaudois, in Lausanne, Switzerland; and Yu Taniguchi, Akira Sawa and Atsushi Kamiya from the Department of Psychiatry, Johns Hopkins University School of Medicine in Baltimore. Funding is from a Silvio O. Conte Center grant from the National Institute of Mental Health (NIMH), National Institutes of Health grants, the Simons Foundation, the Autism Consortium of Boston, the Leenaards Foundation Prize, the Swiss National Science Foundation, a National Science Foundation Sinergia grant, an NIMH National Research Service Award, and an academic study award from the University of Lausanne. NIH-related grants: Silvio O. Conte center grant from the National Institute of Mental Health, NIH MH-084018 (AS, AK, and NK), grant MH-091230 (AK), grant HD06286 (JFG) and an NIMH National Research Service Award (F32MH087123) social worker continuing education

May 16, 2012

A walk in the park gives mental boost to people with depression

Study suggests nature walks improve cognitive abilities for people with clinical depression Toronto, CANADA – A walk in the park may have psychological benefits for people suffering from depression. In one of the first studies to examine the effect of nature walks on cognition and mood in people with major depression, researchers in Canada and the U.S. have found promising evidence that a walk in the park may provide some cognitive benefits. The study was led by Marc Berman, a post-doctoral fellow at Baycrest's Rotman Research Institute in Toronto, with partners from the University of Michigan and Stanford University. It is published online this week, ahead of print publication, in the Journal of Affective Disorders. "Our study showed that participants with clinical depression demonstrated improved memory performance after a walk in nature, compared to a walk in a busy urban environment," said Dr. Berman, who cautioned that such walks are not a replacement for existing and well-validated treatments for clinical depression, such as psychotherapy and drug treatment. "Walking in nature may act to supplement or enhance existing treatments for clinical depression, but more research is needed to understand just how effective nature walks can be to help improve psychological functioning," he said. Dr. Berman's research is part of a cognitive science field known as Attention Restoration Theory (ART) which proposes that people concentrate better after spending time in nature or looking at scenes of nature. The reason, according to ART, is that people interacting with peaceful nature settings aren't bombarded with external distractions that relentlessly tax their working memory and attention systems. In nature settings, the brain can relax and enter a state of contemplativeness that helps to restore or refresh those cognitive capacities. In a research paper he published in 2008 in Psychological Science, Dr. Berman showed that adults who were not diagnosed with any illness received a mental boost after an hour-long walk in a woodland park – improving their performance on memory and attention tests by 20 percent – compared to an hour-long stroll in a noisy urban environment. The findings were reported by The Wall Street Journal, The Boston Globe, The New York Times, and in the Pulitzer Prize finalist book by Nicholas Carr, The Shallows: What the internet is doing to our brains. In this latest study, Dr. Berman and his research team explored whether a nature walk would provide similar cognitive benefits, and also improve mood for people with clinical depression. Given that individuals with depression are characterized by high levels of rumination and negative thinking, the researchers were skeptical at the outset of the study that a solitary walk in the park would provide any benefit at all and may end up worsening memory and exacerbating depressed mood. For the study, 20 individuals were recruited from the University of Michigan and surrounding Ann Arbor area; all had a diagnosis of clinical depression. The 12 females and eight males (average age 26) participated in a two-part experiment that involved walking in a quiet nature setting and in a noisy urban setting. Prior to the walks, participants completed baseline testing to determine their cognitive and mood status. Before beginning a walk, the participants were asked to think about an unresolved, painful autobiographical experience. They were then randomly assigned to go for an hour-long walk in the Ann Arbor Arboretum (woodland park) or traffic heavy portions of downtown Ann Arbor. They followed a prescribed route and wore a GPS watch to ensure compliance. After completing their walk, they completed a series of mental tests to measure their attention and short-term/working memory and were re-asssessed for mood. A week later the participants repeated the entire procedure, walking in the location that was not visited in the first session. Participants exhibited a 16 percent increase in attention and working memory after the nature walk relative to the urban walk. Interestingly, interacting with nature did not alleviate depressive mood to any noticeable degree over urban walks, as negative mood decreased and positive mood increased after both walks to a significant and equal extent. Dr. Berman says this suggests that separate brain mechanisms may underlie the cognitive and mood changes of interacting with nature CADC I & II Continuing Education ### The study was supported by a grant from the National Institute of Mental Health and a private grant from the TKF Foundation. At Baycrest's Rotman Research Institute, Marc Berman's research explores the brain mechanisms involved in controlling thoughts, feeling and behaviors, and how to improve those abilities. Prior to joining Baycrest in 2011, Dr. Berman received his Ph.D. in Cognitive Neuroscience and Industrial and Operations Engineering at the University of Michigan.

May 15, 2012

Perceived racism may impact black Americans' mental health

For black American adults, perceived racism may cause mental health symptoms similar to trauma and could lead to some physical health disparities between blacks and other populations in the United States, according to a new study published by the American Psychological Association (APA). While previous studies have found links between racism and mental health, this is the first meta-analysis on the subject focusing exclusively on black American adults, according to the study published online in APA's Journal of Counseling Psychology. "We focused on black American adults because this is a population that has reported, on average, more incidents of racism than other racial minority groups and because of the potential links between racism and not only mental health, but physical health as well," said lead author Alex Pieterse, PhD, of the University at Albany, State University of New York. Researchers examined 66 studies comprising 18,140 black adults in the United States. To be included in the analysis, a study must have been published in a peer-reviewed journal or dissertation between 1996 and 2011; include a specific analysis of mental health indicators associated with racism; and focus specifically on black American adults in the United States. Black Americans' psychological responses to racism are very similar to common responses to trauma, such as somatization, which is psychological distress expressed as physical pain; interpersonal sensitivity; and anxiety, according to the study. Individuals who said they experienced more and very stressful racism were more likely to report mental distress, the authors said. While the researchers did not collect data on the impacts on physical health, they cite other studies to point out that perceived racism may also affect black Americans' physical health. "The relationship between perceived racism and self-reported depression and anxiety is quite robust, providing a reminder that experiences of racism may play an important role in the health disparities phenomenon," Pieterse said. "For example, African-Americans have higher rates of hypertension, a serious condition that has been associated with stress and depression." The authors recommended that therapists assess racism experiences as part of standard procedure when treating black Americans, and that future studies focus on how discrimination is perceived in specific settings, such as work, online or in school MFT Ceus

May 14, 2012

Healing Trauma’s Invisible Wounds

Mental Health Month Raises Awareness of Trauma and Impact on Children, Families, Communities; New Approaches to Treatment “Healing Trauma’s Invisible Wounds” ALEXANDRIA, Va. (April 23, 2012)—For May is Mental Health Month, Mental Health America is raising awareness of trauma, the devastating impact it has on physical, emotional, and mental well-being, and how therapeutic techniques based in neuroscience can mitigate these effects and create dramatic changes in people’s lives. “As a society, we are just beginning to deal with trauma—bringing it out of the shadows, finding new ways of healing its wounds, and casting off the shame that prevents trauma survivors from seeking help,” said David Shern, Ph.D., president and CEO of Mental Health America. “Most people think that “trauma” refers only to physical trauma that occurs as a result of a car accident or assault. But it’s much more than that.” Trauma includes: ■ Interpersonal violence – such as abuse, rape, domestic violence, and bullying; ■ Social violence — such as war, terrorism, and living under oppressive political regimes; ■ Natural disasters and accidents — such as hurricanes, floods, earthquakes, tornadoes, and auto crashes; ■ Serving in combat; ■ Chronic social stressors – such as racism, sexism, poverty, humiliation and cultural dislocation; ■ Childhood trauma—including physical, emotional and sexual abuse; emotional and physical neglect; a parent who’s an alcoholic or addicted to other drugs; a mother who’s been battered; a family member in prison or diagnosed with mental illness; and a loss of a parent through divorce or abandonment Dr. Shern said trauma has tremendous human and societal costs. Trauma is the leading cause of the death of children in this country. The effect of trauma on productive life years lost exceeds that of any other disease. The economic cost of 50 million injuries in the year 2000, alone, was $406 billion. This includes estimates of $80 billion in medical care costs, and $326 billion in productivity losses. And the predicted cost to the health care system from interpersonal violence and abuse ranges between $333 billion and $750 billion annually, or nearly 17 to 37.5 percent of total health care expenditures. When children or adults respond to traumas with fear, horror and/or helplessness, the extreme stress is toxic to their brains and bodies, and overwhelms their ability to cope, Dr. Shern said. “While many people who experience a traumatic event are able to move on with their lives without lasting negative effects, others may have more difficulty managing their responses to trauma.” Unresolved trauma can manifest in many ways, including anxiety disorders, panic attacks, intrusive memories (flashbacks), obsessive-compulsive behaviors, Post-Traumatic Stress Disorder, addictions, self-injury and a variety of physical symptoms. Trauma increases health-risk behaviors such as overeating, smoking, drinking and risky sex. Trauma survivors can become perpetrators themselves. Dr. Shern said unaddressed trauma can significantly increase the risk of mental and substance use disorders, suicide, chronic physical ailments, as well as premature death. The Adverse Childhood Experiences (ACE) Study, one of the largest investigations ever conducted to assess associations between childhood maltreatment and later-life health and well-being, demonstrated that trauma and other adverse experiences are associated with lifelong problems in behavioral health and general health. Until recently, trauma survivors were largely unrecognized by the formal treatment system. The costs of trauma and its aftermath to victims and society were not well documented. Inadvertently, treatment systems may have frequently re-traumatized individuals and failed to understand the impact of traumatic experiences on general and mental health. But that is changing. Researchers have learned how trauma changes the brain and alters behavior. A movement for trauma-informed care has emerged to ensure that trauma is recognized and treated and that survivors are not re-victimized when they seek care. Complementing these changes are programs to promote healthy development of children and healthy behaviors in families, schools and communities that reduce the likelihood of trauma. “It is critical that these efforts strengthened and we heal the invisible wounds of trauma,” Dr. Shern said. “They are crucial to promoting the healthy development of children and families.” For more than 50 years, Mental Health America and its affiliates around the country have led the observance of May is Mental Health Month by reaching millions of people through the media, local events and screenings. This unified effort includes educational messages about mental health and substance use conditions and the importance of mental health ceus for counselors Mental Health America ( is the nation’s largest and oldest community-based network dedicated to helping all Americans achieve wellness by living mentally healthier lives. With our more than 300 affiliates across the country, we touch the lives of millions—Advocating for changes in mental health and wellness policy; Educating the public & providing critical information; and delivering urgently needed mental health and wellness Programs and Services.

May 10, 2012

Runaway Vigilance Hormone Linked to Panic Attacks

Translational Experiments in Rats, Humans Suggest New Medication Target A study has linked panic disorder to a wayward hormone in a brain circuit that regulates vigilance. While too little of the hormone, called orexin, is known to underlie narcolepsy, the new study suggests that too much of it may lead to panic attacks that afflict 6 million American adults. "Targeting the brain's orexin system may hold promise for a new generation of anti-anxiety treatments," said Thomas R. Insel, M.D., Director of the National Institute of Mental Health (NIMH), part of the National Institutes of Health. "This is a good example of how translational experiments in rats and humans can potentially yield clinical benefits." NIMH grantee Anantha Shekhar, M.B., Ph.D., and colleagues at Indiana University and Lund University, report on their findings online Dec. 27, 2009 in the journal Nature Medicine. They showed that blocking orexin gene expression or its receptor prevented panic attack-like responses in rats. The study also revealed that panic disorder patients have excess levels of the hormone Alcoholism and Drug Abuse Counselors Continuing Education Background Orexin, also called hypocretin, is secreted exclusively in a circuit emanating from the brain's hypothalamus, known to regulate arousal, wakefulness and reward. Panic attacks can be experimentally-induced by infusing susceptible humans with a normally innocuous salt called sodium lactate. The salt similarly triggers panic-like anxiety behaviors in susceptible rat strains, suggesting that something is altered in their arousal circuit. Since sodium lactate activated orexin-secreting neurons in panic-prone rats but not in control rats, the researchers hypothesized that something might be orexin. Results of This Study The investigators first discovered that increased gene expression in orexin-secreting neurons correlated with increases in anxiety-like behavior in panic-prone rats following sodium lactate infusions. Using a technique called RNA interference, they then protected the panic-prone rats from developing anxiety behaviors following the infusions by first injecting them with a genetically-engineered agent that prevented orexin genes from turning on. Blocking orexin receptors with a drug that specifically binds to it also blocked the anxiety like behavior following the infusions. This mirrored effects, seen in both rats and humans, of benzodiazepine medications used to treat panic disorder. The excess sleepiness of narcolepsy, traced a decade ago to loss of orexin-secreting neurons in the arousal circuit, might seem to be an opposite state of a panic attack. However, the researchers demonstrated in rats that such sedation could not account for orexin's effects on anxiety. Also in rats, they traced orexin neurons to their end target to pinpoint the specific brain site that accounts for the anxiety effects, disentangled from cardio-respiratory components of the panic response. Finally, by measuring orexin in cerebrospinal fluid of 53 patients, the researchers showed that those with just panic disorder had higher levels of orexin than those with both panic disorder and depression. Significance Taken together, these results and other evidence suggest a critical role for an overactive orexin system in producing panic attacks, say the researchers. What's Next? Medications that block the orexin receptor may provide a new therapeutic approach for the treatment of panic disorder, they add. The research was also supported, in part, by NIH's National Center for Research Resources. Reference A key role for orexin in panic anxiety. Johnson PL, Truitt W, Fitz SD, Kelley PE, Dietrich A, Sanghani S, Traskman-Bendz L, Goddard AW, Brundin, L, Shekhar A. Nature Medicine.

May 09, 2012

Effects on Personality May Be Mechanism of Antidepressant Effectiveness

Results of a study of antidepressant treatment for major depression suggest that changes in personality traits seen in patients taking the drug paroxetine (Paxil) may not be the result of the medication’s lifting of mood but may instead be a direct effect of this class of drugs and part of the mechanism by which they relieve depression ceus for social workers Background People with a high level of the personality trait neuroticism—characterized by a tendency to experience negative emotions and moodiness—are more likely than others to develop depression. Neuroticism is one of five personality traits that psychologists use as an organizing scheme for understanding personality: the other four traits are extraversion, openness, conscientiousness, and agreeableness. People who take anti-depressants report lower levels of neuroticism and increased extroversion, in addition to a lifting of depression. The assumption has been that these changes in personality measures were the result, not the cause, of a lifting of depression. Studies in twins suggest that to a large degree the same genetic factors underlie both neuroticism and depression risk. Research also suggests that the neurotransmitter serotonin plays a role in the expression of both neuroticism and extraversion. The class of anti-depressant drugs to which paroxetine belongs—the selective serotonin reuptake inhibitors (SSRIs)—increase the neurotransmitter’s availability in the brain. This Study To test the relationship between SSRIs and personality, investigator Tony Tang and colleagues at Northwestern University, Evanston, IL, the University of Pennsylvania in Philadelphia, and Vanderbilt University in Nashville, TN, randomly assigned patients with major depressive disorder (MDD) to receive paroxetine (120 patients), placebo (60 patients), or cognitive therapy (60 patients). After 8 weeks, medication and cognitive therapy (CT) each proved more effective than placebo in reducing depression. In addition, measures of neuroticism (based on standard surveys) in the groups receiving medication or cognitive therapy dropped, while extraversion scores rose. The changes were striking; while patients receiving placebo also reported small changes in both traits, the changes in patients on paroxetine were four to eight times as large. Patients receiving paroxetine had much greater changes in personality traits than patients receiving placebo even when the degree of improvement in depression was the same. This suggested that the effects on personality traits were not the result of the drug’s lifting of depression. After accounting for decreases in depression in patients receiving CT, the improvement in extraversion, but not neuroticism, remained significant. In further comparison of paroxetine with placebo, patients who had initially taken placebo were given the option after 8 weeks to take paroxetine. During the placebo phase, there were small changes in neuroticism and extraversion; much greater changes occurred after 8 weeks on paroxetine. Finally, those patients on paroxetine with the greatest degree of change in neuroticism (but not extraversion) were least likely to relapse to depression; the degree of changes in personality in those receiving CT did not affect the chances of relapse. Significance While the neurochemical effects of SSRIs are known, how those changes act to reduce depression is not clear. These results contradict the prevailing assumption that changes seen in personality traits in patients taking SSRIs are a result of the drugs’ effects on depression. SSRIs may alter personality directly—and thus lift depression—or may act on a third factor that underlies both. CT may alter personality by a different path. Continued research on how these treatments work can provide a clearer understanding of the mechanism of action of SSRIs and how treatment can be best used to reduce depression and minimize relapse. Reference Tang, T.Z., DeRubeis, R.J., Hollon, S.D., Amsterdam, J., Shelton, R., and Schalet, B. Personality change during depression treatment. Archives of General Psychiatry 2009 Dec;66(12):1322-30.

May 08, 2012

Teens Who Recover from Hard-to-treat Depression Still at Risk for Relapse

Teens with hard-to-treat depression who reach remission after 24 weeks of treatment are still at a significant risk for relapse, according to long-term, follow-up data from an NIMH-funded study published online ahead of print November 16, 2010, in the Journal of Clinical Psychiatry. The long-term data reiterate the need for aggressive treatment decisions for teens with stubborn depression continuing education for social workers Background In the Treatment of Resistant Depression in Adolescents (TORDIA) study, teens whose depression had not improved after an initial course of selective serotonin reuptake inhibitor (SSRI) antidepressant treatment were randomly assigned to one of four interventions for 12 weeks: Switch to another SSRI-paroxetine (Paxil), citalopram (Celexa) or fluoxetine (Prozac) Switch to a different SSRI plus cognitive behavioral therapy (CBT), a type of psychotherapy that emphasizes problem-solving and behavior change Switch to venlafaxine (Effexor), a different type of antidepressant called a serotonin and norepinephrine reuptake inhibitor (SNRI) Switch to venlafaxine plus CBT As reported in May 2010, nearly 40 percent of those who completed 24 weeks of treatment achieved remission, regardless of the treatment to which they had initially been assigned. However, those who achieved remission were more likely to have responded to treatment early—during the first 12 weeks. After 24 weeks of treatment, the participants were discharged from the study and urged to continue care within their community. They were then asked to return for an assessment at 72 weeks. Results of the Study Of the 334 original TORDIA participants, about 61 percent had reached remission by week 72. Symptoms of depression steadily decreased after the initial 24 weeks of treatment. But at 72 weeks, many participants still reported having residual symptoms of depression, such as irritability, fatigue and low self-esteem. Those with more severe depression at baseline were less likely to reach remission. Those who responded early to treatment—within the first six weeks of treatment—were more likely to reach remission. Initial treatment assignment during the study did not appear to influence the remission rate or time to remission. However, of the 130 participants who had remitted by week 24, 25 percent had relapsed by week 72. Ethnic minorities tended to have a higher risk for relapse than whites. Significance Because more than one-third of the teens did not recover and the relapse rate was high, the authors conclude that more effective interventions early in the treatment process are needed. In addition, the higher risk of relapse for ethnic minorities suggests that cultural factors may influence the long-term course of depression and recovery, but it is unclear what those factors may be. What's Next The findings indicate that new methods are needed to accurately identify those who may not respond early in treatment so that patients unlikely to reach remission using a particular treatment may be offered alternative treatments earlier in the process. More data is needed, however, to be able to predict who might be more likely to remit and who may not. Reference Vitiello B, Emslie G, Clarke G, Wagner K, Asarnow JR, Keller M, Birmaher B, Ryan N, Kennard B, Mayes T, DeBar L, Lynch F, Dickerson J, Strober M, Suddath R, McCraken JT, Spirito A, Onorato M, Zelazny J, Porta G, Iyengar S, Brent D. Long-term outcome of adolescent depression initially resistant to SSRI treatment. Journal of Clinical Psychiatry.

May 07, 2012

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May 06, 2012

Rats recall past to make daily decisions

UCSF study offers path for studying learning, decision-making, PTSD UCSF scientists have identified patterns of brain activity in the rat brain that play a role in the formation and recall of memories and decision-making. The discovery, which builds on the team's previous findings, offers a path for studying learning, decision-making and post-traumatic stress syndrome. The researchers previously identified patterns of brain activity in the rat hippocampus, a brain region critical for memory storage. The patterns sometimes represented where an animal was in space, and, at other times, represented fast-motion replays of places the animal had been, but no one knew whether these patterns indicated the process of memory formation and recollection. In the journal Science this week (online May 3, 2012), the UCSF researchers demonstrated that the brain activity is critical for memory formation and recall. Moreover, they showed that the brain patterns through which the rats see rapid replays of past experiences are fundamental to their ability to make decisions. Disturbing those particular brain patterns impaired the animals' ability to learn rules based on memories of things that had happened in the past lsw ceus "We think these memory-replay events are central to understanding how the brain retrieves past experiences and uses them to make decisions," said neuroscientist Loren Frank, PhD, a associate professor of physiology and a member of the Keck Center for Integrative Neuroscience at UCSF, who led the research with Shantanu Jadhav, PhD, a post-doctoral fellow. "They offer insight into how a past experience can have such a profound effect on how we think and feel." The finding gives scientists a new way to investigate fundamental processes like learning and decision-making in animals and in people. It also may help shed light on memory disorders like post-traumatic stress disorder (PTSD), which is characterized by strong, disturbing and uncontrolled memories. WITHOUT LINKS TO THE PAST, RATS FACE INDECISION Seeking to understand how the recall of specific memories in the brain guides our thinking, Frank and his colleagues built a system for detecting the underlying patterns of neuronal activity in rats. They fitted the animals with electrodes and built a system that enabled them to detect a specific pattern, called a sharp-wave ripple, in the hippocampus. Whenever they detected a ripple, they would send a small amount of electricity into another set of electrodes that would immediately interrupt the ripple event, in effect turning off all memory replay activity without otherwise affecting the brain. The UCSF researchers knew that these sharp-wave ripples would be activated when the animals had to make choices about which direction to turn as they wended their way toward their reward: a few drops of sweetened condensed milk. These signals seem to be flashes of memory recall, said Frank, a rat's past knowledge flooding back to inform it on what had happened in the past and where it might go in the future. Squashing the sharp-wave ripples, the UCSF team found, disrupted the recall and subverted the rat's ability to correctly navigate the maze. This shows, said Frank, that the sharp-wave ripples are critical for this type of memory recall. Through these brain waves, the rat reprocesses and replays old experiences in a fleeting instant—lessons from the past essential for shaping their perception of the present. "We think these memory replay events are a fundamental constituent of memory retrieval and play a key role in human perspective and decision-making as well," he said. "These same events have been seen in memory tasks in humans, and now we know they are critical for memory in rats. We think that these fast-forward replays make up the individual elements of our own memories, which jump rapidly from event to event." Next, the team wants to tease out information about how the rats actually use these memory replay events to make decisions and how amplifying or blocking specific replay events will change the way an animal learns and remembers. They also think that these events could be important for understanding memory problems, as when stressful memories intrude into daily life. The article, "Awake Hippocampal Sharp-Wave Ripples Support Spatial Memory" by Shantanu P. Jadhav, Caleb Kemere, P. Walter German and Loren M. Frank is published by Science on May 4, 2012. After that date, the article can be accessed at: This work was funded by grants from the Helen Hay Whitney Foundation and the National Institute of Mental Health, a component of the National Institutes of Health. Additional support was provided through a Wheeler Center Fellowship. UCSF is a leading university dedicated to promoting health worldwide through advanced biomedical research, graduate-level education in the life sciences and health professions, and excellence in patient care.

May 05, 2012

Awake Mental Replay of Past Experiences Critical for Learning

Blocking It Stumps Memory-Guided Decision-Making in Rats – NIH-Funded Study Awake mental replay of past experiences is essential for making informed choices, suggests a study in rats. Without it, the animals’ memory-based decision-making faltered, say scientists funded by the National Institutes of Health. The researchers blocked learning from, and acting on, past experience by selectively suppressing replay – encoded as split-second bursts of neuronal activity in the memory hubs of rats performing a maze task. “It appears to be these ripple-like bursts in electrical activity in the hippocampus that enable us to think about future possibilities based on past experiences and decide what to do,” explained Loren Frank, Ph.D., of the University of California, San Francisco, a grantee of the NIH’s National Institute of Mental Health (NIMH). “Similar patterns of hippocampus activity have been detected in humans during similar situations.” continuing education for social workers Frank, Shantanu Jadhav, Ph.D., and colleagues, report on their discovery online in the journal Science, Thursday, May 3, 2012. “These results add to evidence that the brain encodes information not only in the amount of neuronal activity, but that its rhythm and synchronicity also play a crucial role,” said Bettina Osborn, Ph.D., of the NIMH Division of Neuroscience and Basic Behavioral Science, which funded the research. Frank and colleagues had discovered in previous studies that the rhythmic ripple-like activity in the hippocampus coincided with awake mental replay of past experiences, which occurs during lulls in the rats’ activity. The same signal during sleep is known to help consolidate memories. So the researchers hypothesized that these awake ripple states are required for memory-guided decision-making. To test this in the current study, they selectively suppressed the ripple activity without disturbing other functions, while monitoring any effects on the animals’ performance in a maze task. Individual neurons in certain areas of the hippocampus become associated with a particular place. These place cells fire when the animal is in that place or – it turns out – is just mentally replaying the experience of being in that place. In the experimental situation, the rat needs to learn a rule to get a reward. It must remember which of two outer arms of a W-shaped maze it had visited previously and alternate between them – visiting the opposite arm after first visiting the center arm. The ripple activity occurs when rats are inactive during breaks between trials. Place cells associated with the maze fire in rapid succession and in synchrony with other neurons in the neighborhood. The same place cells fire in the same sequence as they did when the rat first walked through the maze – suggesting that the rat is mentally replaying the earlier experience, but on a much faster timescale. In the current study, an automatic feedback system shut down place cell firing, via mild electrical stimulation, whenever it detected ripple activity, thereby also preventing the replay of the maze memory. Without benefit of mental replay, rats’ performance on the maze task deteriorated. The impairment was in the animals’ spatial working memory – their ability to link immediate and earlier past experience to the reward. This ability was required to correctly decide which outside arm to visit after exiting the center arm during outbound trials. The researchers propose that awake replay in the hippocampus provides such information about past locations and future options to the brain’s executive hub, the prefrontal cortex, which learns the alternation rule and applies it to guide behavior. Even though the replay events in rats last just a fraction of a second, Frank notes that they are not unlike our own experience of memories, which tend to compress often lengthy events into snippets of just the highlights of what happened to us. “We think the brain is using these same ripple-like bursts for many things,” he explained. “It’s using them for retrieving memories, exploring possibilities – day-dreaming – and for strengthening memories.”
During breaks in trials when the rat was awake but inactive, areas in the brain’s memory hub emitted split-second bursts of ripple-like electrical activity (SWRs). This indicated that the rat was mentally replaying an earlier experience in the maze. Individual neurons in the areas become associated with a particular place. These place cells spike when the animal is in that place or – it turns out – is just mentally replaying the experience of being in that place. Embedded in the ripple-like signal above are place cells spiking in the same sequence as they did when the rat first walked through the maze. (Color-coded hatch marks match the path in the maze.) Rats’ performance in the maze task faltered when these awake mental replay events were blocked, revealing that they are important for memory-guided decision-making. Source: Shantanu Jadhav, Ph.D., University of California San Francisco In this YouTube clip, NIMH grantee Loren Frank, Ph.D., explains how rats mentally replay recent experiences in a maze. Reference Jadhav SP, Kemere C, German PW, Frank LM. Awake Hippocampal Sharp-Wave Ripples Support Spatial Memory. 2012, May 3, Science Express. The mission of the NIMH is to transform the understanding and treatment of mental illnesses through basic and clinical research, paving the way for prevention, recovery and cure. For more information, visit the NIMH website. About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit the NIH website.

May 02, 2012

Prenatal exposure to insecticide chlorpyrifos linked to alterations in brain structure and cognition

While chlorpyrifos is no longer registered for household use in the US, it continues to be widely used around the world, as well as on many food and agricultural products throughout the US Even low to moderate levels of exposure to the insecticide chlorpyrifos during pregnancy may lead to long-term, potentially irreversible changes in the brain structure of the child, according to a new brain imaging study by researchers from the Columbia Center for Children's Environmental Health at the Mailman School of Public Health, Duke University Medical Center, Emory University, and the New York State Psychiatric Institute. The changes in brain structure are consistent with cognitive deficits found in children exposed to this chemical. Results of the study appear online in the April 30 PNAS. The new study is the first to use MRI to identify the structural evidence for these cognitive deficits in humans, confirming earlier findings in animals. Changes were visible across the surface of the brain, with abnormal enlargement of some areas and thinning in others. The disturbances in brain structure are consistent with the IQ deficits previously reported in the children with high exposure levels of chlorpyrifos, or CPF, suggesting a link between prenatal exposure to CPF and deficits in IQ and working memory at age 7 ceus for social workers The study also reports evidence that CPF may eliminate or reverse the male-female differences that are ordinarily present in the brain. Further study is needed to determine the consequences of these changes before and after puberty, the researchers say. Notably, the brain abnormalities appeared to occur at exposure levels below the current EPA threshold for toxicity, which is based on exposures high enough to inhibit the action of the key neurological enzyme cholinesterase. The present findings suggest that the mechanism underlying structural changes in the brain may involve other pathways. According to the lead author, Virginia Rauh, ScD, Professor at the Mailman School of Public Health and Deputy Director of the Columbia Center for Children's Environmental Health, "By measuring a biomarker of CPF exposure during pregnancy, and following the children prospectively from birth into middle childhood, the present study provides evidence that the prenatal period is a vulnerable time for the developing child, and that toxic exposure during this critical period can have far-reaching effects on brain development and behavioral functioning." "By combining brain imaging and community-based research, we now have much stronger evidence linking exposure to chlorpyrifos with neurodevelopmental problems," adds senior author Bradley S. Peterson, MD, Chief of Child & Adolescent Psychiatry, New York State Psychiatric Institute, and Director of MRI Research in the Department of Psychiatry, Columbia University Medical Center. In the current study, the researchers used MRI to evaluate the brains of 40 New York City children, ages 5 to 11, whose mothers were enrolled prenatally in a larger cohort study. Researchers compared 20 children with high exposures to CPF with 20 children with lower exposures; all exposures occurred prior to the EPA ban on household use of the chemical in 2001. They found brain anomalies were associated with the higher exposure. Since the 2001 ban, a drop in residential exposure levels of CPF has been documented by Robin Whyatt, DrPH, a co-author on the present study and Professor of Clinical Environmental Health Sciences and Co-Deputy Director of the Columbia Center for Children's Environmental Health at the Mailman School. However, the chemical continues to be present in the environment through its widespread use in agriculture (food and feed crops), wood treatments, and public spaces such as golf courses, some parks, and highway medians. People near these sources can be exposed by inhaling the chemical, which drifts on the wind. Low-level exposure can also occur by eating fruits and vegetables that have been sprayed. Although the chemical is degraded rapidly by water and sunlight outdoors, it has been detected by the Columbia researchers in many urban residences years after the ban went into effect. The study was supported by the National Institute of Environmental Health Sciences Grants 5P01ES09600, P50ES015905, and 5R01ES08977, as well as pilot funding through ES009089; EPA STAR Grants RD834509, RD832141, and R827027; National Institute of Mental Health Grants MH068318 and K02-74677; and the John and Wendy Neu Family Foundation. Additional co-authors included Frederica P. Perera and Megan K. Horton, Mailman School; Ravi Bansal, Xuejun Hao, and Jun Liu, Columbia University Medical Center; Dana Boyd Barr, Emory University; and Theodore A. Slotkin, Duke University.