Researchers pinpoint brain region essential for social memory

Potential target for treating autism, schizophrenia, and other brain disorders NEW YORK, NY (February 23, 2014) — Columbia University Medical Center (CUMC) researchers have determined that a small region of the hippocampus known as CA2 is essential for social memory, the ability of an animal to recognize another of the same species. A better grasp of the function of CA2 could prove useful in understanding and treating disorders characterized by altered social behaviors, such as autism, schizophrenia, and bipolar disorder. The findings, made in mice, were published today in the online edition of Nature. Scientists have long understood that the hippocampus—a pair of seahorse-shaped structures in the brain's temporal lobes—plays a critical role in our ability to remember the who, what, where, and when of our daily lives. Recent studies have shown that different subregions of the hippocampus have different functions. For instance, the dentate gyrus is critical for distinguishing between similar environments, while CA3 enables us to recall a memory from partial cues (e.g., Proust's famous madeleine). The CA1 region is critical for all forms of memory. "However, the role of CA2, a relatively small region of the hippocampus sandwiched between CA3 and CA1, has remained largely unknown," said senior author Steven A. Siegelbaum, PhD, professor of neuroscience and pharmacology, chair of the Department of Neuroscience, a member of the Mortimer B. Zuckerman Mind Brain Behavior Institute and Kavli Institute for Brain Science, and a Howard Hughes Medical Institute Investigator. A few studies have suggested that CA2 might be involved in social memory, as this region has a high level of expression of a receptor for vasopressin, a hormone linked to sexual motivation, bonding, and other social behaviors. To learn more about this part of the hippocampus, the researchers created a transgenic mouse in which CA2 neurons could be selectively inhibited in adult animals. Once the neurons were inhibited, the mice were given a series of behavioral tests. "The mice looked quite normal until we looked at social memory," said first author Frederick L. Hitti, an MD-PhD student in Dr. Siegelbaum's laboratory, who developed the transgenic mouse. "Normally, mice are naturally curious about a mouse they've never met; they spend more time investigating an unfamiliar mouse than a familiar one. In our experiment, however, mice with an inactivated CA2 region showed no preference for a novel mouse versus a previously encountered mouse, indicating a lack of social memory." In two separate novel-object recognition tests, the CA2-deficient mice showed a normal preference for an object they had not previously encountered, showing that the mice did not have a global lack of interest in novelty. In another experiment, the researchers tested whether the animals' inability to form social memories might have to do with deficits in olfaction (sense of smell), which is crucial for normal social interaction. However, the mice showed no loss in ability to discriminate social or non-social odors. In humans, the importance of the hippocampus for social memory was famously illustrated by the case of Henry Molaison, who had much of his hippocampus removed by surgeons in 1953 in an attempt to cure severe epilepsy. Molaison (often referred to as HM in the scientific literature) was subsequently unable to form new memories of people. Scientists have observed that lesions limited to the hippocampus also impair social memory in both rodents and humans. "Because several neuropsychiatric disorders are associated with altered social behaviors, our findings raise the possibility that CA2 dysfunction may contribute to these behavioral changes," said Dr. Siegelbaum. This possibility is supported by findings of a decreased number of CA2 inhibitory neurons in individuals with schizophrenia and bipolar disorder and altered vasopressin signaling in autism. Thus, CA2 may provide a new target for therapeutic approaches to the treatment of social disorders. The paper is titled, "The hippocampal CA2 region is essential for social memory." ### The study was supported by a Ruth L. Kirschstein F30 National Research Service Award from the National Institute of Mental Health and the Howard Hughes Medical Institute. The authors declare no financial or other conflicts of interests. The Mortimer B. Zuckerman Mind Brain Behavior Institute Columbia University's Mortimer B. Zuckerman Mind Brain Behavior Institute is an interdisciplinary hub for scholars across the university, created on a scope and scale to explore the human brain and behavior at levels of inquiry from cells to society. The institute's leadership, which includes two Nobel Prize-winning neuroscientists, and many of its principal investigators will be based at the 450,000-square-foot Jerome L. Greene Science Center, now rising on the university's new Manhattanville campus. In combining Columbia's preeminence in neuroscience with its strengths in the biological and physical sciences, social sciences, arts, and humanities, the institute provides a common intellectual forum for research communities from Columbia University Medical Center, the Faculty of Arts and Sciences, the School of Engineering and Applied Science, and professional schools on both the Morningside Heights and Washington Heights campuses. Their collective mission is to further our understanding of the human condition and to find cures for disease. Columbia University Medical Center provides international leadership in basic, preclinical, and clinical research; medical and health sciences education; and patient care. The medical center trains future leaders and includes the dedicated work of many physicians, scientists, public health professionals, dentists, and nurses at the College of Physicians and Surgeons, the Mailman School of Public Health, the College of Dental Medicine, the School of Nursing, the biomedical departments of the Graduate School of Arts and Sciences, and allied research centers and institutions. Columbia University Medical Center is home to the largest medical research enterprise in New York City and State and one of the largest faculty medical practices in the Northeast. For more information, visit cumc.columbia.edu or columbiadoctors.org. For more information on related mental health, nursing and social work topics, visit Continuing Education for Social Workers

Gene found to be crucial for formation of certain brain circuitry

Identified using new technique that can speed identification of genes, drug candidates Using a powerful gene-hunting technique for the first time in mammalian brain cells, researchers at Johns Hopkins report they have identified a gene involved in building the circuitry that relays signals through the brain. The gene is a likely player in the aging process in the brain, the researchers say. Additionally, in demonstrating the usefulness of the new method, the discovery paves the way for faster progress toward identifying genes involved in complex mental illnesses such as autism and schizophrenia — as well as potential drugs for such conditions. A summary of the study appears in the Dec. 12 issue of Cell Reports. "We have been looking for a way to sift through large numbers of genes at the same time to see whether they affect processes we're interested in," says Richard Huganir, Ph.D., director of the Johns Hopkins University Solomon H. Snyder Department of Neuroscience and a Howard Hughes Medical Institute investigator, who led the study. "By adapting an automated process to neurons, we were able to go through 800 genes to find one needed for forming synapses — connections — among those cells." Although automated gene-sifting techniques have been used in other areas of biology, Huganir notes, many neuroscience studies instead build on existing knowledge to form a hypothesis about an individual gene's role in the brain. Traditionally, researchers then disable or "knock out" the gene in lab-grown cells or animals to test their hypothesis, a time-consuming and laborious process. In this study, Huganir's group worked to test many genes all at once using plastic plates with dozens of small wells. A robot was used to add precise allotments of cells and nutrients to each well, along with molecules designed to knock out one of the cells' genes — a different one for each well. "The big challenge was getting the neurons, which are very sensitive, to function under these automated conditions," says Kamal Sharma, Ph.D., a research associate in Huganir's group. The team used a trial-and-error approach, adjusting how often the nutrient solution was changed and adding a washing step, and eventually coaxed the cells to thrive in the wells. In addition, Sharma says, they fine-tuned an automated microscope used to take pictures of the circuitry that had formed in the wells and calculated the numbers of synapses formed among the cells. The team screened 800 genes in this way and found big differences in the well of cells with a gene called LRP6 knocked out. LRP6 had previously been identified as a player in a biochemical chain of events known as the Wnt pathway, which controls a range of processes in the brain. Interestingly, Sharma says, the team found that LRP6 was only found on a specific kind of synapse known as an excitatory synapse, suggesting that it enables the Wnt pathway to tailor its effects to just one synapse type. "Changes in excitatory synapses are associated with aging, and changes in the Wnt pathway in later life may accelerate aging in general. However, we do not know what changes take place in the synaptic landscape of the aging brain. Our findings raise intriguing questions: Is the Wnt pathway changing that landscape, and if so, how?" says Sharma. "We're interested in learning more about what other proteins LRP6 interacts with, as well as how it acts in different types of brain cells at different developmental stages of circuit development and refinement." Another likely outcome of the study is wider use of the gene-sifting technique, he says, to explore the genetics of complex mental illnesses. The automated method could also be used to easily test the effects on brain cells of a range of molecules and see which might be drug candidates Continuing Education for Social Workers ### Other authors on the paper are Se-Young Choi, now of Seoul National University School of Dentistry; Yong Zhang, Shunyou Long and Min Li of Johns Hopkins University School of Medicine; and Thomas J.F. Nieland, now of the Broad Institute of Harvard and MIT. This work was supported by grants from the Howard Hughes Medical Institute and the National Institute of Mental Health (grant numbers P50MH084020 and 5U54MH084691). Related stories: Gene Found to Foster Synapse Formation in the Brain http://www.hopkinsmedicine.org/news/media/releases/gene_found_to_foster_synapse_formation_in_the_brain Study Refutes Accepted Model of Memory Formation http://www.hopkinsmedicine.org/news/media/releases/study_refutes_accepted_model_of_memory_formation____ Newly Discovered "Switch" Plays Dual Role in Memory Formation http://m.hopkinsmedicine.org/news/media/releases/newly_discovered_switch_plays_dual_role_in_memory_formation

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

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.

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.

Phobia's effect on perception of feared object allows fear to persist

COLUMBUS, Ohio – The more afraid a person is of a spider, the bigger that individual perceives the spider to be, new research suggests. In the context of a fear of spiders, this warped perception doesn't necessarily interfere with daily living. But for individuals who are afraid of needles, for example, the conviction that needles are larger than they really are could lead people who fear injections to avoid getting the health care they need. A better understanding of how a phobia affects the perception of feared objects can help clinicians design more effective treatments for people who seek to overcome their fears, according to the researchers. In this study, participants who feared spiders were asked to undergo five encounters with live spiders – tarantulas, in fact – and then provide size estimates of the spiders after those encounters ended. The more afraid the participants said they were of the spiders, the larger they estimated the spiders had been. "If one is afraid of spiders, and by virtue of being afraid of spiders one tends to perceive spiders as bigger than they really are, that may feed the fear, foster that fear, and make it difficult to overcome," said Michael Vasey, professor of psychology at Ohio State University and lead author of the study. "When it comes to phobias, it's all about avoidance as a primary means of keeping oneself safe. As long as you avoid, you can't discover that you're wrong. And you're stuck. So to the extent that perceiving spiders as bigger than they really are fosters fear and avoidance, it then potentially is part of this cycle that feeds the phobia that leads to its persistence continuing education for social workers "We're trying to understand why phobias persist so we can better target treatments to change those reasons they persist." The study is published in a recent issue of the Journal of Anxiety Disorders. The researchers recruited 57 people who self-identified as having a spider phobia. Each participant then interacted at specific time points over a period of eight weeks with five different varieties of tarantulas varying in size from about 1 to 6 inches long. The spiders were contained in an uncovered glass tank. Participants began their encounters 12 feet from the tank and were asked to approach the spider. Once they were standing next to the tank, they were asked to guide the spider around the tank by touching it with an 8-inch probe, and later with a shorter probe. Throughout these encounters, researchers asked participants to report how afraid they were feeling on a scale of 0-100 according to an index of subjective units of distress. After the encounters, participants completed additional self-report measures of their specific fear of spiders, any panic symptoms they experienced during the encounters with the spiders, and thoughts about fear reduction and future spider encounters. Finally, the research participants estimated the size of the spiders – while no longer being able to see them – by drawing a single line on an index card indicating the length of the spider from the tips of its front legs to the tips of its back legs. An analysis of the results showed that higher average peak ratings of distress during the spider encounters were associated with estimates that the spiders were larger than they really were. Similar positive associations were seen between over-estimates of spider size and participants' higher average peak levels of anxiety, higher average numbers of panic symptoms and overall spider fear. These findings have been supported in later studies with broader samples of people with varying levels of fear of spiders. "It would appear from that result that fear is driving or altering the perception of the feared object, in this case a spider," said Vasey, also the director of research for the psychology department's Anxiety and Stress Disorders Clinic. "We already knew fear and anxiety alter thoughts about the feared thing. For example, the feared outcome is interpreted as being more likely than it really is. But this study shows that even perception is altered by fear. In this case, the feared spider is seen as being bigger. And that may serve as a maintaining factor for the fear." The approach tasks with the spiders are a classic example of exposure therapy, a common treatment for people with phobias. Though this therapy is known to be effective, scientists still do not fully understand why it works. And for some, the effects don't last – but it is difficult to predict who will have a relapse of fear, Vasey said. He and colleagues are studying these biased perceptions as well as attitudes with hopes that the new knowledge will enhance treatment for people with various phobias. The work suggests that fear not only alters one's perception of the feared thing, but also can influence a person's automatic attitude toward an object. Those who have developed an automatic negative attitude toward a feared object might have a harder time overcoming their fear. Though individuals with arachnophobia are unlikely to seek treatment, the use of spiders in this research was a convenient way to study the complex effects of fear on visual perception and how those effects might cause fear to persist, Vasey noted. "Ultimately, we are interested in identifying predictors of relapse so we can better measure when a person is done with treatment," he said. This work is supported by the National Institute of Mental Health. Co-authors include Michael Vilensky, Jacqueline Heath, Casaundra Harbaugh, Adam Buffington and Vasey's principal collaborator, Russell Fazio, all of Ohio State's Department of Psychology.

How stress influences disease: Carnegie Mellon study reveals inflammation as the culprit

PITTSBURGH—Stress wreaks havoc on the mind and body. For example, psychological stress is associated with greater risk for depression, heart disease and infectious diseases. But, until now, it has not been clear exactly how stress influences disease and health.

A research team led by Carnegie Mellon University's Sheldon Cohen has found that chronic psychological stress is associated with the body losing its ability to regulate the inflammatory response. Published in the Proceedings of the National Academy of Sciences, the research shows for the first time that the effects of psychological stress on the body's ability to regulate inflammation can promote the development and progression of disease continuing education for social workers

"Inflammation is partly regulated by the hormone cortisol and when cortisol is not allowed to serve this function, inflammation can get out of control," said Cohen, the Robert E. Doherty Professor of Psychology within CMU's Dietrich College of Humanities and Social Sciences.

Cohen argued that prolonged stress alters the effectiveness of cortisol to regulate the inflammatory response because it decreases tissue sensitivity to the hormone. Specifically, immune cells become insensitive to cortisol's regulatory effect. In turn, runaway inflammation is thought to promote the development and progression of many diseases.

Cohen, whose groundbreaking early work showed that people suffering from psychological stress are more susceptible to developing common colds, used the common cold as the model for testing his theory. With the common cold, symptoms are not caused by the virus — they are instead a "side effect" of the inflammatory response that is triggered as part of the body's effort to fight infection. The greater the body's inflammatory response to the virus, the greater is the likelihood of experiencing the symptoms of a cold.

In Cohen's first study, after completing an intensive stress interview, 276 healthy adults were exposed to a virus that causes the common cold and monitored in quarantine for five days for signs of infection and illness. Here, Cohen found that experiencing a prolonged stressful event was associated with the inability of immune cells to respond to hormonal signals that normally regulate inflammation. In turn, those with the inability to regulate the inflammatory response were more likely to develop colds when exposed to the virus.

In the second study, 79 healthy participants were assessed for their ability to regulate the inflammatory response and then exposed to a cold virus and monitored for the production of pro-inflammatory cytokines, the chemical messengers that trigger inflammation. He found that those who were less able to regulate the inflammatory response as assessed before being exposed to the virus produced more of these inflammation-inducing chemical messengers when they were infected.

"The immune system's ability to regulate inflammation predicts who will develop a cold, but more importantly it provides an explanation of how stress can promote disease," Cohen said. "When under stress, cells of the immune system are unable to respond to hormonal control, and consequently, produce levels of inflammation that promote disease. Because inflammation plays a role in many diseases such as cardiovascular, asthma and autoimmune disorders, this model suggests why stress impacts them as well."

He added, "Knowing this is important for identifying which diseases may be influenced by stress and for preventing disease in chronically stressed people."

###

In addition to Cohen, the research team included CMU's Denise Janicki-Deverts, research psychologist; Children's Hospital of Pittsburgh's William J. Doyle; University of British Columbia's Gregory E. Miller; University of Pittsburgh School of Medicine's Bruce S. Rabin and Ellen Frank; and the University of Virginia Health Sciences Center's Ronald B. Turner.

The National Center for Complementary and Alternative Medicine, National Institute of Mental Health, National Heart, Lung and Blood Institute and the MacArthur Foundation Research Network on Socioeconomic Status and Health funded this research.

Brain Chemical Linked to Joylessness Provides Insight Into Teen Depression

Depressed teens with anhedonia, or the inability to experience pleasure, have lower levels of the neurotransmitter GABA in a key mood-regulating region of the brain, according to an NIMH-funded study published online October 3, in the Archives of General Psychiatry. The researchers note that focusing on specific symptoms and using different types of measures may offer new clues to the pathways and processes underlying depression and other mental disorders continuing education for social workers

Background

Symptoms of depression in teens can be highly varied and tend to overlap with signs of other disorders. Because of this, adolescent depression can be hard to study using conventional research tools and methods.

Guided by findings in adults, Vilma Gabbay, M.D., of New York University School of Medicine, and colleagues decided to focus on the neurotransmitter GABA. GABA has many important roles throughout the body and is involved in regulating communication between brain cells. Abnormalities in GABA production or function in the brain have been linked to several mental disorders, including schizophrenia and postpartum depression, and possibly learning disorders. GABA has also been linked to anhedonia, a symptom present in up to 59 percent of depressed teens.

The researchers used a type of specialized MRI to measure GABA levels in the brain region known as the anterior cingulate cortex (ACC) in 20 teens with depression, half of whom also had anhedonia. They were compared to 21 matched controls who did not have depression or anhedonia. Levels of anhedonia were scored numerically according to clinician- and self-rated assessments.

Results of the Study

Compared to controls, teens with depression and anhedonia had significantly lower ACC GABA levels. Lower ACC GABA levels were associated with more severe anhedonia symptoms among all participants.

Significance

The findings support a role for GABA in anhedonia and depression among teens. Also, by correlating GABA levels with numeric measures of anhedonia severity, the researchers were able to assess participants’ symptoms along a continuum. Compared to traditional measures that categorize symptoms only as being either present or absent, such continuous or “dimensional” measurements may provide greater specificity to disease evaluations in research.

What’s Next

Additional studies in larger populations are needed to confirm these findings. Advances in imaging techniques and technology may help to identify differing roles for other neurotransmitters associated with depression.

Reference

Gabbay V, Mao X, Klein RG, Ely BA, Babb JS, Panzer AM, Alonso CM, Shungu DC. Anterior Cingulate Cortex {gamma}-Aminobutyric Acid in Depressed Adolescents: Relationship to Anhedonia. Arch Gen Psychiatry. 2011 Oct 3. [Epub ahead of print] PubMed PMID: 21969419.

Prescribed stimulant use for ADHD continues to rise steadily

NIH and AHRQ study finds pace of the rise has slowed in recent years


Source: NIMH

The prescribed use of stimulant medications to treat attention deficit hyperactivity disorder (ADHD) rose slowly but steadily from 1996 to 2008, according to a study conducted by the National Institutes of Health (NIH) and the Agency for Healthcare Research and Quality (AHRQ). The study was published online ahead of print September 28, 2011, in the American Journal of Psychiatry continuing education for Social Workers

ADHD is one of the most common childhood disorders, and can continue through adolescence and adulthood. Symptoms include difficulty staying focused and paying attention, difficulty controlling behavior, and hyperactivity (over-activity). The condition is frequently treated with stimulants such as methylphenidate (e.g., Ritalin), amphetamines (e.g., Adderall) or other types of medications. Behavioral therapies can also be effective.

During the 1990s, stimulant prescription use increased significantly, going from a prevalence rate among youth of 0.6 percent in 1987 to 2.7 percent in 1997, with the rate stabilizing around 2.9 percent in 2002. Recent reports, however, suggest that the prescribed use of these medications and the diagnosis of ADHD have continued to rise. Based on the Health Resources and Services Administration's National Survey of Children's Health, the percentage of children age 4-17 years diagnosed with ADHD increased from 7.8 percent in 2003 to 9.5 percent in 2007.

"Stimulant medications work well to control ADHD symptoms, but they are only one method of treatment for the condition. Experts estimate that about 60 percent of children with ADHD are treated with medication," said co-author Benedetto Vitiello, M.D., of NIH's National Institute of Mental Health (NIMH).

For this most recent survey, Dr. Vitiello and Samuel Zuvekas Ph.D., of AHRQ examined data from the AHRQ-sponsored Medical Expenditure Panel Survey, a nationally representative annual survey of U.S. households, to determine prescribed stimulant use among children under age 19 from 1996-2008. They found a slow but steady increase — from 2.4 percent in 1996 to 3.5 percent in 2008.The rate grew an average of 3.4 percent each year, which is substantially less than the growth rate between 1987 and 1996, which averaged about 17 percent per year.

Overall, prescription use among 6-12-year-olds was highest, going from 4.2 percent in 1996 to 5.1 percent in 2008. But the fastest growth of prescribed use occurred among 13-18-year-olds, going from 2.3 percent in 1996 to 4.9 percent in 2008. "This continuous increase among teens likely reflects a recent realization that ADHD often persists as children age. They do not always grow out of their symptoms," said Dr. Vitiello.

Prescription use among preschoolers remained very low at 0.1 percent from 2004 onward and decreased between 2002 and 2008, suggesting that stimulant use among very young children continues to be disfavored. Boys continued to be three times more likely to be prescribed a stimulant than girls, and use among white children continued to be higher than among black or Hispanic children (4.4 percent in 2008 among whites, compared to 2.9 percent in blacks and 2.1 percent in Hispanics). However, prescribed stimulant use is increasing among racial and ethnic minorities, likely suggesting more recognition of ADHD and acceptance of psychopharmacological treatment among these groups, according to the authors.

In addition, rates were substantially lower in Western states compared to other regions of the nation, with no increase in recent years, a finding consistent with other studies. In comparison, rates in the Northeast increased from 2.7 percent in 2002 to 4.6 percent in 2008.

"These persistent differences in prescribed stimulant use related to age, racial and ethnic background, and geographical location indicate substantial variability in how families and doctors approach ADHD treatment throughout the United States," said Dr. Zuvekas.

The researchers concluded that when comparing the rates of prescribed use with the estimated prevalence of ADHD diagnosis, it appears that many children with ADHD are not treated with stimulants. "The children with the most severe symptoms are more likely to be taking stimulants. Those with milder symptoms are more likely being treated with psychosocial treatments or other non-stimulant medications," they said.

Reference

Zuvekas S and Vitiello B. Stimulant medication use in children: a 12-year perspective. American Journal of Psychiatry. Online ahead of print September 28, 2011.

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The Agency for Healthcare Research and Quality (http://www.ahrq.gov) is part of the U.S. Department of Health and Human Services. AHRQ's mission is to improve the quality, safety, efficiency and effectiveness of health care for all Americans. AHRQ's research helps people make more informed decisions and improve the quality of health care services.

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.

Thinking Globally to Improve Mental Health

Source: NASA Jet Propulsion Laboratory (NASA-JPL)
Mental health experts are calling for a greater world focus on improving access to care and treatment for mental, neurological, and substance use (MNS) disorders, as well as increasing discoveries in research that will enable this goal to be met.

The Grand Challenges in Global Mental Health Initiative, led by the National Institutes of Health and the Global Alliance for Chronic Diseases, has identified the top 40 barriers to better mental health around the world. Similar to past grand challenges, which focused on infectious diseases and chronic, noncommunicable diseases, this initiative seeks to build a community of funders dedicated to supporting research that will significantly improve the lives of people living with MNS disorders within the next 10 years.

Twenty-five of the specific challenges and the process used to derive them are described in an article that will be published on July 7, 2011, in the journal Nature.

"Participating in global mental health research is an enormous opportunity, a means to accelerate advances in mental health care for the diverse U.S. population, as well as an extension of our vision of a world where mental illnesses are prevented and cured," said Thomas R. Insel, M.D., director of the National Institute of Mental Health (NIMH), the NIH institute heading this effort.

According to the paper's authors, the disorders targeted by the Grand Challenges in Global Mental Health—for example, schizophrenia, depression, epilepsy, dementia, and alcohol dependence—collectively account for more years of life lost to poor health, disability, or early death than either cardiovascular disease or cancer. Yet, compared to illnesses like cardiovascular disease and cancer, there are far fewer effective treatments or preventive methods. In addition, interventions are not widely available to those who need them most.

In recognizing the need to address this imbalance, Pamela Collins, M.D., M.P.H., of the NIMH Office for Research on Disparities and Global Mental Health, and colleagues assembled an international panel of experts to identify research priorities using the Delphi method, a widely accepted consensus-building tool. The panel consisted of 422 experts in fields such as neuroscience, basic behavioral science, mental health services, and epidemiology, and represented more than 60 countries social worker ceus

Over the course of two months, NIMH staff pared the panel's initial list of 1,565 challenges down to 154, with input from a scientific advisory board. From this list, the expert panel selected the top 40, of which the top five challenges identified after the third and final round of ranking are:

Integrate screening and core packages of services into routine primary health care
Reduce the cost and improve the supply of effective medications
Improve children's access to evidence-based care by trained health providers in low- and middle-income countries
Provide effective and affordable community-based care and rehabilitation
Strengthen the mental health component in the training of all health care personnel.
These top five challenges were ranked according to the ability to reduce the burden of disease, ability to reduce inequalities in health and health care, length of time until results can be observed, and the ability for the topic to be researched effectively.

"Addressing these challenges could have far-reaching effects, including increasing access to services and ultimately, reducing the treatment gap associated with these disorders," said Dr. Collins.

The Grand Challenges in Global Mental Health Initiative is led by NIMH and the Global Alliance for Chronic Diseases, in partnership with the Wellcome Trust, the McLaughlin-Rotman Centre for Global Health, and the London School of Hygiene and Tropical Medicine. Other NIH components participating in the Grand Challenges in Global Mental Health include the Fogarty International Center; the National Heart, Lung, and Blood Institute; and the National Institute of Neurological Disorders and Stroke.

Reference
Collins PY, Patel V, Joestl SS, March D, Insel TR, Daar A, on behalf of the Grand Challenges in Global Mental Health Scientific Advisory Board and Executive Committee. Grand Challenges in Global Mental Health. Nature. 2011 July 7. 474(7354):pp.

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.

Autism Blurs Distinctions Between Brain Regions

Erodes Molecular Identities in Cortex – NIH-funded Study
Autism blurs the molecular differences that normally distinguish different brain regions, a new study suggests. Among more than 500 genes that are normally expressed at significantly different levels in the front versus the lower middle part of the brain's outer mantle, or cortex, only 8 showed such differences in brains of people with autism, say researchers funded in part by the National Institutes of Health continuing education for social workers

"Such blurring of normally differentiated brain tissue suggests strikingly less specialization across these brain areas in people with autism," explained Daniel Geschwind, M.D., Ph.D., of the University of California, Los Angeles, a grantee of the NIH's National Institute of Mental Health. "It likely reflects a defect in the pattern of early brain development."

He and his colleagues published their study online May 26, 2011 in the journal Nature. The research was based on post mortem comparisons of brains of people with the disorder and healthy controls.

In fetal development, different mixes of genes turn on in different parts of the brain to create distinct tissues that perform specialized functions. The new study suggests that the pattern regulating this gene expression goes awry in the cortex in autism, impairing key brain functions.

"This study provides the first evidence of a common signature for the seemingly disparate molecular abnormalities seen in autism," said NIMH director Thomas R. Insel, M.D. "It also points to a pathway-based framework for understanding causes of other brain disorders stemming from similar molecular roots, such as schizophrenia and ADHD."

In an earlier study, the researchers showed that genes that turn on and off together at the same time hold clues to the brain's molecular instructions. These modules of co-expressed genes can reveal genetic co-conspirators in human illness, through what Geschwind and colleagues call "guilt by association." A gene is suspect if its expression waxes and wanes in sync with others in an illness-linked module.

Using this strategy, the researchers first looked for gene expression abnormalities in brain areas implicated in autism — genes expressed at levels different than in brains of healthy people. They found 444 such differently expressed genes in the cortexes of postmortem brains of people with autism.

Most of the same genes turned out to be abnormally expressed in the frontal cortex as in the temporal cortex (lower middle) of autistic brains. Of these, genes involved in synapses, the connections between neurons, tended to be under-expressed when compared with healthy brains. Genes involved in immune and inflammatory responses tended to be over-expressed. Significantly, the same pattern held in a separate sample of autistic and control brains examined as part of the study.

Autistic and healthy control brains were similarly organized –– modules of co-expressed genes correlated with specific cell types and biological functions.

Yet normal differences in gene expression levels between the frontal and temporal cortex were missing in the modules of autistic brains. This suggests that the normal molecular distinctions — the tissue differences — between these regions are nearly erased in autism, likely affecting how the brain works. Strikingly, among 174 genes expressed at different levels between the two regions in two healthy control brains, none were expressed at different levels in brains of people with autism.

An analysis of gene networks revealed two key modules of co-expressed genes highly correlated with autism.

One module was made up of genes in a brain pathway involved in neuron and synapse development, which were under-expressed in autism. Many of these genes were also implicated in autism in previous, genome-wide studies. So, several different lines of evidence now converge, pointing to genes in this M12 module (see picture below) as genetic causes of autism.

A second module of co-expressed genes, involved in development of other types of brain cells, was over-expressed in autism. These were determined not to be genetic causes of the illness, but likely gene expression changes related to secondary inflammatory, immune, or possible environmental factors involved in autism.

This newfound ability to see genes in the context of their positions in these modules, or pathways, provides hints about how they might work to produce illness, according to Geschwind and colleagues. For example, from its prominent position in the M12 module, the researchers traced a potential role in creating defective synapses to a gene previously implicated in autism.

Follow-up studies should explore whether the observed abnormalities in the patterning of gene expression might also extend to other parts of the brain in autism, say the researchers.

Cognitive Behavioral Therapy for Eating Disorders

Psychiatr Clin North Am. 2010 September; 33(3): 611–627.
doi: 10.1016/j.psc.2010.04.004. PMCID: PMC2928448

Cognitive Behavioral Therapy for Eating Disorders
Rebecca Murphy, Suzanne Straebler, Zafra Cooper, and Christopher G. Fairburn
Department of Psychiatry, Warneford Hospital, Warneford Lane, Oxford University, Oxford OX3 7JX, UK
redistributed and reused, subject to certain conditions.
This document was posted here by permission of the publisher. At the time of the deposit, it included all changes made during peer review, copy editing, and publishing. The U. S. National Library of Medicine is responsible for all links within the document and for incorporating any publisher-supplied amendments or retractions issued subsequently. The published journal article, guaranteed to be such by Elsevier, is available for free, on ScienceDirect, at: http://dx.crossref.org/10.1016/j.psc.2010.04.004AbstractCognitive behavioral therapy (CBT) is the leading evidence-based treatment for bulimia nervosa. A new “enhanced” version of the treatment appears to be more potent and has the added advantage of being suitable for all eating disorders, including anorexia nervosa and eating disorder not otherwise specified. This article reviews the evidence supporting CBT in the treatment of eating disorders and provides an account of the “transdiagnostic” theory that underpins the enhanced form of the treatment. It ends with an outline of the treatment's main strategies and procedures.Keywords: Cognitive behavioral therapy, Eating disorders, Anorexia nervosa, Bulimia nervosa Other Sections▼
AbstractEating disorders and their clinical featuresThe empirical status of cognitive behavioral therapy for eating disordersThe cognitive behavioral account of eating disordersEnhanced cognitive behavioral therapyAn overview of the core aspects of treatmentPreparation for treatment and changeStage oneStage twoStage threeStage fourUnderweight patientsFinal commentsReferences The eating disorders provide one of the strongest indications for cognitive behavioral therapy (CBT). Two considerations support this claim. First, the core psychopathology of eating disorders, the overevaluation of shape and weight, is cognitive in nature. Second, it is widely accepted that CBT is the treatment of choice for bulimia nervosa1 and there is evidence that it is as effective with cases of “eating disorder not otherwise specified” (eating disorder NOS),2 the most common eating disorder diagnosis. This article starts with a description of the clinical features of eating disorders and then reviews the evidence supporting cognitive behavioral treatment. Next, the cognitive behavioral account of eating disorders is presented and, last, the new “transdiagnostic” form of CBT is described. Other Sections▼
AbstractEating disorders and their clinical featuresThe empirical status of cognitive behavioral therapy for eating disordersThe cognitive behavioral account of eating disordersEnhanced cognitive behavioral therapyAn overview of the core aspects of treatmentPreparation for treatment and changeStage oneStage twoStage threeStage fourUnderweight patientsFinal commentsReferencesEating disorders and their clinical featuresClassification and Diagnosis
Eating disorders are characterized by a severe and persistent disturbance in eating behavior that causes psychosocial and, sometimes, physical impairment. The DSM-IV classification scheme for eating disorders recognizes 2 specific diagnoses, anorexia nervosa (AN) and bulimia nervosa (BN), and a residual category termed eating disorder NOS.3The diagnosis of anorexia nervosa is made in the presence of the following features:
1. The overevaluation of shape and weight; that is, judging self-worth largely, or even exclusively, in terms of shape and weight. This has been described in various ways and is often expressed as strong desire to be thin combined with an intense fear of weight gain and fatness.
2. The active maintenance of an unduly low body weight. This is commonly defined as maintaining a body weight less than 85% of that expected or a body mass index (BMI; weight kg/height m2 or weight lb/[height in]2 × 703) of 17.5 or less.
3. Amenorrhea, in postpubertal females not taking an oral contraceptive.
The unduly low weight is pursued in a variety of ways with strict dieting and excessive exercise being particularly prominent. A subgroup also engages in episodes of binge eating and/or “purging” through self-induced vomiting or laxative misuse.For a diagnosis of bulimia nervosa 3 features need to be present:
1. Overevaluation of shape and weight, as in anorexia nervosa.
2. Recurrent binge eating. A “binge” is an episode of eating during which an objectively large amount of food is eaten for the circumstances and there is an accompanying sense of loss of control.
3. Extreme weight-control behavior, such as recurrent self-induced vomiting, regular laxative misuse, or marked dietary restriction.
In addition, the diagnostic criteria for anorexia nervosa should not be met. This “trumping rule” ensures that patients do not receive both diagnoses at one time.There are no positive criteria for the diagnosis of eating disorder NOS. Instead, this diagnosis is reserved for eating disorders of clinical severity that do not meet the diagnostic criteria of AN or BN. Eating disorder NOS is the most common eating disorder encountered in clinical settings constituting about half of adult outpatient eating-disordered samples, with patients with bulimia nervosa constituting about a third, and the rest being cases of anorexia nervosa.4 In inpatient settings the great majority of cases are either underweight forms of eating disorder NOS or anorexia nervosa.5In addition, DSM-IV recognizes “binge eating disorder” (BED) as a provisional diagnosis in need of further study. The criteria for BED are recurrent episodes of binge eating in the absence of extreme weight-control behavior. It is proposed that BED be recognized as a specific eating disorder in DSM-V.6Clinical Features
Anorexia nervosa, bulimia nervosa, and most cases of eating disorder NOS share a core psychopathology: the overevaluation of the importance of shape and weight and their control. Whereas most people judge themselves on the basis of their perceived performance in a variety of domains of life (such as the quality of their relationships, their work performance, their sporting prowess), for people with eating disorders self-worth is dependent largely, or even exclusively, on their shape and weight and their ability to control them. This psychopathology is peculiar to the eating disorders (and to body dysmorphic disorder).In anorexia nervosa, patients become underweight largely as a result of persistent and severe restriction of both the amount and the type of food that they eat. In addition to strict dietary rules, some patients engage in a driven form of exercising, which further contributes to their low body weight. Patients with anorexia nervosa typically value the sense of control that they derive from undereating. Some practice self-induced vomiting, laxative and/or diuretic misuse, especially (but not exclusively) those who experience episodes of loss of control over eating. The amount of food eaten during these “binges” is often not objectively large; hence, they are described as “subjective binges.” Many other psychopathological features tend to be present, some as a result of the semistarvation. These include depressed and labile mood, anxiety features, irritability, impaired concentration, loss of libido, heightened obsessionality and sometimes frank obsessional features, and social withdrawal. There are also a multitude of physical features, most of which are secondary to being underweight. These include poor sleep, sensitivity to the cold, heightened fullness, and decreased energy.Patients with bulimia nervosa resemble those with anorexia nervosa both in terms of their eating habits and methods of weight control. The main feature distinguishing these 2 groups is that in patients with bulimia nervosa attempts to restrict food intake are regularly disrupted by episodes of (objective) binge eating. These episodes are often followed by compensatory self-induced vomiting or laxative misuse, although there is also a subgroup of patients who do not purge (nonpurging bulimia nervosa). As a result of the combination of undereating and overeating the weight of most patients with bulimia nervosa tends to be unremarkable and is within the healthy range, BMI = 20–25. Features of depression and anxiety are prominent in these patients. Certain of these patients engage in self-harm and/or substance and alcohol misuse and may attract the diagnosis of borderline personality disorder. Most have few physical complaints, although electrolyte disturbance may occur in those who vomit or take laxatives or diuretics frequently.The clinical features of patients with eating disorder NOS closely resemble those seen in anorexia nervosa and bulimia nervosa and are of comparable duration and severity.7 Within this diagnostic grouping 3 subgroups may be distinguished, although there are no sharp boundaries among them. The first group consists of cases that closely resemble anorexia nervosa or bulimia nervosa but just fail to meet the threshold set by the diagnostic criteria (eg, binge eating may not be frequent enough to meet criteria for BN or weight may be just above the threshold in AN); the second and largest subgroup comprises cases in which the features of AN and BN occur in different combinations from that seen in the prototypic disorders—these states may be best viewed as “mixed” in character—and the third subgroup comprises those with binge-eating disorder. Most patients with binge-eating disorder are overweight (BMI = 25–30) or meet criteria for obesity (BMI ≥ 30). Other Sections▼
AbstractEating disorders and their clinical featuresThe empirical status of cognitive behavioral therapy for eating disordersThe cognitive behavioral account of eating disordersEnhanced cognitive behavioral therapyAn overview of the core aspects of treatmentPreparation for treatment and changeStage oneStage twoStage threeStage fourUnderweight patientsFinal commentsReferencesThe empirical status of cognitive behavioral therapy for eating disordersConsistent with the current way of classifying eating disorders, the research on their treatment has focused on the particular disorders in isolation. Wilson and colleagues8 have provided a narrative review of the studies of the treatment of the 2 specific eating disorders as well as eating disorder NOS, and an authoritative meta-analysis has been conducted by the UK National Institute for Health and Clinical Excellence (NICE).1 This systematic review is particularly rigorous and, as with all NICE reviews, it forms the basis for evidence-based guidelines for clinical management.The conclusion from the NICE review, and 2 other recent systematic reviews,9,10 is that cognitive behavioral therapy (CBT-BN) is the clear leading treatment for bulimia nervosa in adults. However, this is not to imply that CBT-BN is a panacea, as the original version of the treatment resulted in only fewer than half of the patients who completed treatment making a full and lasting recovery.8 The new “enhanced” version of the treatment (CBT-E) appears to be more effective.2Interpersonal psychotherapy (IPT) is a potential evidence-based alternative to CBT-BN in patients with bulimia nervosa and it involves a similar amount of therapeutic contact, but there have been fewer studies of it.11,12 IPT takes 8 to 12 months longer than CBT-BN to achieve a comparable effect. Antidepressant medication (eg, fluoxetine at a dose of 60 mg daily) has also been found to have a beneficial effect on binge eating in bulimia nervosa but not as great as that obtained with CBT-BN and the long-term effects remain largely untested.13 Combining CBT-BN with antidepressant medication does not appear to offer any clear advantage over CBT-BN alone.13 The treatment of adolescents with bulimia nervosa has received relatively little research attention to date.There has been much less research on the treatment of anorexia nervosa. Most of the studies suffer from small sample sizes and some from high rates of attrition. As a result, there is little evidence to support any psychological treatment, at least in adults. In adolescents the research has focused mainly on family therapy, with the result that the status of CBT in younger patients is unclear.Preliminary findings have been reported from a 3-site study of the use of the enhanced form of CBT (CBT-E) to treat outpatients with anorexia nervosa.14 This is the largest study of the treatment of anorexia nervosa to date. In brief, it appears that the treatment can be used to treat about 60% of outpatients with the disorder (BMI 15.0 to 17.5) and that in these patients about 60% have a good outcome. Interestingly and importantly the relapse rate appears low.There is a growing body of research on the treatment of binge-eating disorder. This research has been the subject of a recent narrative review15 and several systematic reviews.1,16,17 The strongest support is for a form of CBT similar to that used to treat BN (CBT-BED). This treatment has been found to have a sustained and marked effect on binge eating, but it has little effect on body weight, which is typically raised in these patients. Arguably the leading first-line treatment is a form of guided cognitive behavioral self-help as it is relatively simple to administer and reasonably effective.18Until recently, there had been almost no research on the treatment of forms of eating disorder NOS other than binge-eating disorder despite their severity and prevalence.7 However, recently the first randomized controlled trial of the enhanced form of CBT found that CBT-E was as effective for patients with eating disorder NOS (who were not significantly underweight; BMI >17.5) as it was for patients with bulimia nervosa with two-thirds of those who completed treatment having a good outcome.2In summary, CBT is the treatment of choice for bulimia nervosa and for binge-eating disorder with the best results being obtained with the new “enhanced” form of the treatment. Recent research provides support for the use of this treatment with patients with eating disorder NOS and those with anorexia nervosa.The remainder of this article provides a description of this transdiagnostic form of CBT. Other Sections▼
AbstractEating disorders and their clinical featuresThe empirical status of cognitive behavioral therapy for eating disordersThe cognitive behavioral account of eating disordersEnhanced cognitive behavioral therapyAn overview of the core aspects of treatmentPreparation for treatment and changeStage oneStage twoStage threeStage fourUnderweight patientsFinal commentsReferencesThe cognitive behavioral account of eating disordersAlthough the DSM-IV classification of eating disorders encourages the view that they are distinct conditions, each requiring their own form of treatment, there are reasons to question this view. Indeed, it has recently been pointed out that what is most striking about the eating disorders is not what distinguishes them but how much they have in common.19 As noted earlier, they share many clinical features, including the characteristic core psychopathology of eating disorders: the overevaluation of the importance of shape and weight. In addition, longitudinal studies indicate that most patients migrate among diagnoses over time.20 This temporal movement among diagnostic categories, together with the shared psychopathology, has led to the proposal that there may be limited utility in distinguishing among the disorders19 and furthermore that common “transdiagnostic” mechanisms may be involved in their maintenance.The transdiagnostic cognitive behavioral account of the eating disorders19 extends the original theory of bulimia nervosa21 to all eating disorders. According to this theory, the overevaluation of shape and weight and their control is central to the maintenance of all eating disorders. Most of the other clinical features can be understood as resulting directly from this psychopathology. It results in dietary restraint and restriction; preoccupation with thoughts about food and eating, weight and shape; the repeated checking of body shape and weight or its avoidance; and the engaging in extreme methods of weight control. The one feature that is not a direct expression of the core psychopathology is binge eating. This occurs in all cases of bulimia nervosa, many cases of eating disorder NOS, and some cases of anorexia nervosa. The cognitive behavioral account proposes that such episodes are largely the result of attempts to adhere to multiple extreme, and highly specific, dietary rules. The repeated breaking of these rules is almost inevitable and patients tend to react negatively to such dietary slips, generally viewing them as evidence of their poor self-control. They typically respond by temporarily abandoning their efforts to restrict their eating with binge eating being the result. This in turn maintains the core psychopathology by intensifying patients' concerns about their ability to control their eating, shape, and weight. It also encourages more dietary restraint, thereby increasing the risk of further binge eating.Three further processes may also maintain binge eating. First, difficulties in the patient's life and associated mood changes make it difficult to maintain dietary restraint. Second, as binge eating temporarily alleviates negative mood states and distracts patients from their difficulties, it can become a way of coping with such problems. Third, in patients who engage in compensatory purging, the mistaken belief in the effectiveness of vomiting and laxative misuse as a means of weight control results in a major deterrent against binge eating being removed.In patients who are underweight, the physiological and psychological consequences may also contribute to the maintenance of the eating disorder. For example, delayed gastric emptying leads to feelings of fullness even after patients have eaten only modest amounts of food. In addition, the social withdrawal and loss of previous interests prevent patients from being exposed to experiences that might diminish the importance they place on shape and weight.The composite “transdiagnostic” formulation is shown in Fig. 1. This illustrates the core processes that are hypothesized to maintain the full range of eating disorders. When applied to individual patients, its precise form will depend on the psychopathology present. In some patients, most of the processes are in operation (for example, in cases of anorexia nervosa binge-purge subtype) but in others only a few are active (for example, in binge-eating disorder). Thus, for each patient the formulation is driven by their individual psychopathology rather than their DSM diagnosis. As such, the formulation provides a guide to those processes that need to be addressed in treatment. Fig. 1
The composite “transdiagnostic” cognitive behavioral formulation.

Fig. 1The composite “transdiagnostic” cognitive behavioral formulation. Other Sections▼
AbstractEating disorders and their clinical featuresThe empirical status of cognitive behavioral therapy for eating disordersThe cognitive behavioral account of eating disordersEnhanced cognitive behavioral therapyAn overview of the core aspects of treatmentPreparation for treatment and changeStage oneStage twoStage threeStage fourUnderweight patientsFinal commentsReferencesEnhanced cognitive behavioral therapy“Enhanced” cognitive behavioral therapy (CBT-E) is based on the transdiagnostic theory outlined earlier and was derived from CBT-BN. It is designed to treat eating disorder psychopathology rather than an eating disorder diagnosis, with its exact form in any particular case depending on an individualized formulation of the processes maintaining the disorder. CBT-E is designed to be delivered on an individual basis to adult patients with any eating disorder of clinical severity who are appropriate to treat on an outpatient basis. It is described as “enhanced” because it uses a variety of new strategies and procedures to improve outcome and because it includes modules to address certain obstacles to change that are “external” to the core eating disorder, namely clinical perfectionism, low self-esteem, and interpersonal difficulties.There are 2 forms of CBT-E. The first is the “focused” form (CBT-Ef) that exclusively addresses eating disorder psychopathology. Current evidence suggests that this form should be viewed as the “default” version, as it is optimal for most patients with eating disorders.2 The second, a broad form of the treatment (CBT-Eb), addresses external obstacles to change, in addition to the core eating disorder psychopathology. Preliminary evidence suggests that this more complex form of CBT-E should be reserved for patients in whom clinical perfectionism, core low self-esteem, or interpersonal difficulties are pronounced and maintaining the eating disorder.2There are also 2 intensities of CBT-E. With patients who are not significantly underweight (BMI above 17.5), it consists of 20 sessions over 20 weeks. This version is suitable for the great majority of adult outpatients. For patients who have a BMI below 17.5, a commonly used threshold for anorexia nervosa, treatment involves 40 sessions over 40 weeks. The additional sessions and treatment duration are designed to allow sufficient time for 3 additional clinical features to be addressed, namely, limited motivation to change, undereating, and being underweight.In addition CBT-E has been adapted for younger patients22 and for inpatient and day patient settings treatment.23,24 Limitations on space preclude a description of these other forms of CBT-E. Further details of these adaptations of CBT-E, together with a comprehensive account of the treatment and its implementation, can be found in the main treatment guide.25 Other Sections▼
AbstractEating disorders and their clinical featuresThe empirical status of cognitive behavioral therapy for eating disordersThe cognitive behavioral account of eating disordersEnhanced cognitive behavioral therapyAn overview of the core aspects of treatmentPreparation for treatment and changeStage oneStage twoStage threeStage fourUnderweight patientsFinal commentsReferencesAn overview of the core aspects of treatmentCBT-E is a form of cognitive behavioral therapy and in common with other empirically supported forms of CBT it focuses primarily on the maintaining processes, in this case those maintaining the eating disorder psychopathology. It uses specified strategies and a flexible series of sequenced therapeutic procedures to achieve both cognitive and behavioral changes. The style of treatment is similar to other forms of CBT, that of collaborative empiricism. Although CBT-E uses a variety of generic cognitive and behavioral interventions (such as addressing cognitive biases), unlike some forms of CBT, it favors the use of strategic changes in behavior to modify thinking rather than direct cognitive restructuring. The eating disorder psychopathology may be likened to a house of cards with the strategy being to identify and remove the key cards that are supporting the eating disorder, thereby bringing down the entire house. Following, we summarize the core features of the focused and broad versions of CBT-E, including adaptations that need to be made for patients who are underweight. The treatment has 4 defined stages. Other Sections▼
AbstractEating disorders and their clinical featuresThe empirical status of cognitive behavioral therapy for eating disordersThe cognitive behavioral account of eating disordersEnhanced cognitive behavioral therapyAn overview of the core aspects of treatmentPreparation for treatment and changeStage oneStage twoStage threeStage fourUnderweight patientsFinal commentsReferencesPreparation for treatment and changeAn evaluation interview assessing the nature and extent of the patient's psychiatric problems is conducted before starting treatment.26 This interview usually takes place over 2 or more appointments. The assessment process is collaborative and designed to put the patient at ease and begin to engage the patient in treatment and in change. Information from the assessment informs how best to proceed and, in particular, whether CBT-E is appropriate. If CBT-E is deemed to be appropriate, the main aspects of the therapy are described and patients are encouraged to make the most of the opportunity to overcome their eating disorder.It is important that from the outset of CBT-E the patient is in a position to make optimum use of treatment. For this reason any potential barriers to benefiting from CBT-E should be explored. Important contraindications to beginning treatment immediately are physical features of concern, the presence of severe clinical depression, significant substance abuse, major distracting life events or crises, and competing commitments. Such factors should be addressed first before embarking on treatment. Other Sections▼
AbstractEating disorders and their clinical featuresThe empirical status of cognitive behavioral therapy for eating disordersThe cognitive behavioral account of eating disordersEnhanced cognitive behavioral therapyAn overview of the core aspects of treatmentPreparation for treatment and changeStage oneStage twoStage threeStage fourUnderweight patientsFinal commentsReferencesStage oneIt is crucial that treatment starts well. This is consistent with evidence that the magnitude of change achieved early in treatment is a good predictor of treatment outcome.27,28 This initial intensive stage, designed to achieve initial therapeutic momentum, involves approximately 8 sessions held twice weekly over 4 weeks. The aims of this first stage are to engage the patient in treatment and change, to derive a personalized formulation (case conceptualization) with the patient, to provide education about treatment and the disorder, and to introduce and implement 2 important procedures: collaborative “weekly weighing” and “regular eating.” The changes made in this first stage of treatment form the foundation on which other changes are built.Engaging the Patient in Treatment and Change
Many patients with eating disorders are ambivalent about treatment and change. Getting patients “on board” with treatment is a necessary first step. Engagement can be enhanced by conducting the assessment of the eating disorder in a way that helps the patient to become involved in, and hopeful about, the possibility of change and encourages the patient to take “ownership” of treatment.Jointly Creating the Formulation
This is usually done in the first treatment session and is a personalized visual representation of the processes that appear to be maintaining the eating problem. The therapist draws out the relevant sections of Fig. 1 in collaboration with the patient, incorporating the patient's own experiences and words. It is usually best to start with something the patient wishes to change (eg, binge eating). The formulation helps patients to realize both that their behavior is comprehensible and that it is maintained by a series of interacting self-perpetuating mechanisms that are open to change. It is explained that “the diagram” provides a guide to what needs to be targeted in treatment if patients are to achieve a full and lasting recovery. At this early stage in treatment the therapist should explain that it is provisional and may need to be modified as treatment progresses and understanding of the patient's eating problem increases.Establishing Real-time Self-monitoring
This is the ongoing “in-the-moment” recording of eating and other relevant behavior, thoughts, feelings, and events (Fig. 2 is an example of a monitoring record). Self-monitoring is introduced in the initial session and continues to occupy an essential and central role throughout most of treatment. Therapists should clearly explain the reasons for self-monitoring. First, that it enables further understanding of the eating problem and it identifies progress. Second, and more importantly, it helps patients to be more aware of what is happening in the moment so that they can begin to make changes to behavior that may have seemed automatic or beyond their control. Fundamental to establishing accurate recording is jointly reviewing the patient's records each session and discussing the process of recording and any difficulties with this. The records also help inform the agenda for the session: it is best to save any problems identified in the records for the main part of the session. Fig. 2
An example monitoring record.

Fig. 2An example monitoring record.Establishing Collaborative “Weekly Weighing”
The patient and therapist check the patient's weight once a week and plot it on an individualized weight graph. Patients are strongly encouraged not to weigh themselves at other times. Weekly in-session weighing has several purposes. First, it provides an opportunity for the therapist to educate patients about body weight and help patients to interpret the numbers on the scale, which otherwise they are prone to misinterpret. Second, it provides patients with accurate data about their weight at a time when their eating habits are changing. Third, and most importantly, it addresses the maintaining processes of excessive body weight checking or its avoidance.Providing Education
From session 1 onward, an important element of treatment is education about weight and eating, as many patients have misconceptions that maintain their eating disorder. Some of the main topics to cover are as follows:
• The characteristic features of eating disorders including their associated physical and psychosocial effects
• Body weight and its regulation: the body mass index and its interpretation; natural weight fluctuations; and the effects of treatment on weight
• Ineffectiveness of vomiting, laxatives, and diuretics as a means of weight control
• Adverse effects of dieting: the types of dieting that promote binge eating; dietary rules versus dietary guidelines.
To provide reliable information on these topics, patients are asked to read relevant sections from one of the authoritative books on eating disorders29,30 and their reading is discussed in subsequent treatment sessions.Establishing “Regular Eating”
Establishing a pattern of regular eating is fundamental to successful treatment whatever the form of the eating disorder. It addresses an important type of dieting (“delayed eating”); it displaces most episodes of binge eating; it structures people's days and, for underweight patients, it introduces meals and snacks that can be subsequently increased in size. Early in treatment (usually by the third session) patients are asked to eat 3 planned meals each day plus 2 or 3 planned snacks so that there is rarely more than a 4-hour interval between them. Patients are also asked to confine their eating to these meals and snacks. They should choose what they eat with the only condition being that the meals and snacks are not followed by any compensatory behavior (eg, self-induced vomiting or laxative misuse). The new eating pattern should take precedence over other activities but should not be so inflexible as to preclude the possibility of adjusting timings to suit the patients' commitments each day.Patients should be helped to adhere to their regular eating plan and to resist eating between the planned meals and snacks. Two rather different strategies may be used to achieve the latter goals. The first involves helping patients to identify activities that are incompatible with eating and likely to distract them from the urge to binge eat (eg, taking a brisk walk) and strategies that make binge eating less likely (eg, leaving the kitchen). The second is to help patients to recognize that the urge to binge eat is a temporary phenomenon that can be “surfed.” Some “residual binges” are likely to persist, however, and these are addressed later.Involving Significant Others
The treatment is primarily an individual treatment for adults. Despite this, “significant others” are seen if this is likely to facilitate treatment and the patient is willing for this to happen. There are 2 reasons for seeing others: if they could help the patient in making changes or if others are making it difficult for the patient to change, for example, by commenting adversely on eating or appearance. Other Sections▼
AbstractEating disorders and their clinical featuresThe empirical status of cognitive behavioral therapy for eating disordersThe cognitive behavioral account of eating disordersEnhanced cognitive behavioral therapyAn overview of the core aspects of treatmentPreparation for treatment and changeStage oneStage twoStage threeStage fourUnderweight patientsFinal commentsReferencesStage twoStage two is a brief, but essential, transitional stage that generally comprises 2 appointments, a week apart. While continuing with the procedures introduced in Stage one, the therapist and patient take stock and conduct a joint review of progress, the goal being to identify problems still to be addressed and any emerging barriers to change, to revise the formulation if necessary, and to design Stage three. The review serves several purposes. If patients are making good progress they should be praised for their efforts and helpful changes reinforced. If patients are not doing well, the explanation needs to be understood and addressed. If clinical perfectionism, core low self-esteem or relationship difficulties appear to be responsible, this would be an indication for implementing the broad version of the treatment. Other Sections▼
AbstractEating disorders and their clinical featuresThe empirical status of cognitive behavioral therapy for eating disordersThe cognitive behavioral account of eating disordersEnhanced cognitive behavioral therapyAn overview of the core aspects of treatmentPreparation for treatment and changeStage oneStage twoStage threeStage fourUnderweight patientsFinal commentsReferencesStage threeThis is the main body of treatment. Its aim is to address the key processes that are maintaining the patient's eating disorder. The mechanisms addressed, and the order in which these are tackled, depend upon their role and relative importance in maintaining the patient's psychopathology. There are generally 8 weekly appointments.Addressing the Overevaluation of Shape and Weight
Identifying the overevaluation and its consequences
The first step involves explaining the concept of self-evaluation and helping patients identify how they evaluate themselves. The relative importance of the various domains that are relevant may be represented as a pie chart (Fig. 3 is an example of a pie chart with extended formulation), which for most patients is dominated by a large slice representing shape and weight and controlling eating. Fig. 3
The overevaluation of shape and weight and their control: an extended formulation.

Fig. 3The overevaluation of shape and weight and their control: an extended formulation.
The patient and therapist then identify the problems inherent in this scheme for self-evaluation. Briefly there are 3 related problems: first, self-evaluation is overly dependent on performance in one area of life with the result that domains other than shape and weight are marginalized; second, the area of controlling shape and weight is one in which success is elusive, thus undermining self-esteem; and third, the overevaluation is responsible for the behavior that characterizes the eating disorder (dieting, binge eating, and so forth).31The final step in the consideration of self-evaluation is the creation of an “extended formulation” depicting the main expressions of the overevaluation of shape and weight: dieting, body checking and body avoidance, feeling fat, and marginalization of other areas of life. The therapist uses this extended formulation to explain how these behaviors and experiences serve to maintain and magnify the patient's concerns about shape and weight and thus they need to be addressed in treatment.Enhancing the importance of other domains for self-evaluation
An indirect, yet powerful, means of diminishing the overevaluation of shape and weight is helping patients increase the number and significance of other domains for self-evaluation. Engaging in other aspects of their life that may have been pushed aside by the eating disorder results in these other areas becoming more important in the patient's self-evaluation. Briefly, this involves identifying activities or areas of life that the patient would like to engage in and helping them do so.A second, direct, strategy is to target the behavioral expressions of the overevaluation of shape and weight. This is done at the same time as enhancing the other domains for self-evaluation and it involves tackling body checking, body avoidance, and feeling fat.Addressing body checking and avoidance
Patients are often not aware that they are engaging in body checking and that it is maintaining their body dissatisfaction. The first step is therefore to obtain detailed information about their checking behavior by asking patients to monitor it. Patients are then educated about the adverse effects of repeated body checking as the way in which they check tends to provide biased information that leads them to feel dissatisfied. For example, scrutinizing parts of one's body magnifies apparent defects, and only comparing oneself to thin and attractive people leads one to draw the conclusion that one is unattractive. Most patients need substantial and detailed help to curb their repeated body checking and invariably attention needs to be devoted to their mirror use.Patients who avoid seeing their bodies also need considerable help. They should be encouraged to progressively get used to the sight and feel of their body. This may take many successive sessions.Addressing “feeling fat”
“Feeling fat” is an experience reported by many women but the intensity and frequency of this feeling appears to be far greater among people with eating disorders. Feeling fat is a target for treatment because it tends to be equated with being fat (irrespective of the patient's actual shape and weight) and hence maintains body dissatisfaction. Although this topic has received little research attention, clinical observation suggests that feeling fat is a result of mislabeling certain emotions and bodily experiences. Consequently, patients are helped to identify the triggers of their feeling fat experiences and the accompanying feelings. These typically are negative mood states (eg, feeling bored or depressed) or physical sensations that heighten body awareness (eg, feeling full, bloated, or sweaty). Patients are then helped to view “feeling fat” as a cue to ask themselves what else they are feeling at the time and once recognized to address it directly.Exploring the origins of overevaluation
Toward the end of Stage three it is often helpful to explore the origins of the patient's sensitivity to shape, weight, and eating. A historical review can help to make sense of how the problem developed and evolved, highlight how it might have served a useful function in its early stages, and the fact that it may no longer do so. If a specific event appears to have played a critical role in the development of the eating problem, the patient should be helped to reappraise this from the vantage point of the present. This review helps patients distance themselves further from the eating disorder frame of mind or “mindset.”Addressing Dietary Rules
Patients are helped to recognize that their multiple extreme and rigid dietary rules impair their quality of life and are a central feature of the eating disorder. A major goal of treatment is therefore to reduce, if not eliminate altogether, dieting. The first step in doing so is to identify the patient's various dietary rules together with the beliefs that underlie them. The patient is then helped to break these rules to test the beliefs in question and to learn that the feared consequences that maintain the dietary rule (typically weight gain or binge eating) are not an inevitable result. With patients who binge eat, it is important to pay particular attention to “food avoidance” (the avoidance of specific foods) as this is a major contributory factor. These patients need to systematically re-introduce the avoided food into their diet.Addressing Event-related Changes in Eating
Among many patients with eating disorders, eating habits change in response to outside events and changes in their mood. The change may involve eating less, stopping eating altogether, overeating, or binge eating. If these changes are prominent, patients need help to deal directly with the triggers. Generally this may be achieved by training them in “proactive” problem solving coupled with the use of functional means of modulating mood.Addressing Clinical Perfectionism, Low Self-esteem, and Interpersonal Problems
As noted earlier, there are 2 main forms of CBT-E. The components of the focused version are described previously. The “broad” version also includes these strategies and procedures but, in addition, addresses one or more “external” (to the core eating disorder) processes that may be maintaining the eating disorder. It is designed for patients in whom clinical perfectionism, core low self-esteem, or marked interpersonal problems are pronounced and appear to be contributing to the eating disorder. If the therapist decides, in the review of progress (Stage two), to use one or more of these modules, they should become a major component of all subsequent sessions. In the original version of the broad form of CBT-E a fourth module, “mood intolerance,” was included but this has since been integrated in to the standard, focused, form of the treatment as part of addressing events and moods. A description of the main elements of the 3 modules follows. A more detailed account is available in the main treatment guide.32Addressing clinical perfectionism
The psychopathology of clinical perfectionism is similar to that of an eating disorder.33 Its core is the overevaluation of striving to achieve and achievement itself. People with clinical perfectionism judge themselves largely, or exclusively, in terms of working hard toward, and meeting, personally demanding standards in areas of life that they value. If they have a coexisting eating disorder such extreme standards are applied to their eating, weight, and shape. This intensifies key aspects of the eating disorder including dietary restraint, exercise, and shape checking. It is usually evident from the patient's behavior and it can interfere with important aspects of treatment, leading to, for example, overly detailed recording and a strong resistance to relaxing dietary restraint.The strategy for addressing clinical perfectionism mirrors that used to address the overevaluation of shape and weight and the two can be addressed more or less at the same time. The first step is to add perfectionism to the patient's formulation and to consider the consequences of this for the patient and his or her life, including the self-evaluation pie-chart. Patients are then encouraged to take steps to enhance the importance of other, nonperformance related, domains for self-evaluation.It is helpful to consider collaboratively patients' goals in areas of life that they value, which are usually multiple, rigid, and extreme, and whether these goals are in fact counterproductive and impairing their actual performance. Performance checking is addressed similarly to shape checking, beginning by first asking patients to record times when they are checking their performance. Then the therapist helps them appreciate that the data they obtain is likely to be skewed as a result of using biased assessment processes, such as selective attention to failure. Avoidance and procrastination also need to be addressed, as they interfere with patients being able to assess their true ability with the result that their fears of failure are maintained.Addressing core low self-esteem
People with core low self-esteem (CLSE) have a longstanding and pervasive negative view of themselves. It is largely independent of the person's actual performance in life (ie, it is unconditional) and is not secondary to the presence of the eating disorder. The presence of CLSE results in the individual striving especially hard to control eating, weight, and shape to retain some sense of self-worth. It is generally a barrier to engaging in treatment as patients do not feel they deserve treatment nor do they believe that they can benefit from it.If it is to be directly addressed in treatment, it is added to the patient's formulation in Stage two and tackled alongside, although slightly later than, the steps addressing the overevaluation of shape and weight. This involves educating patients about the role of CLSE in maintaining the eating disorder and contributing to other difficulties in their life. Patients are helped to identify and modify the main cognitive maintaining processes, including discounting positive qualities and the overgeneralization of apparent failures. Previous views of the self are reappraised, using both cognitive restructuring and behavioral experiments, to help patients to reach a more balanced view of their self-worth.Addressing interpersonal problems
Interpersonal problems are common among patients with eating disorders, although they generally improve as the eating disorder resolves. Such problems may include conflict with others and difficulties developing close relationships. If these problems, and the resulting effects on mood, directly influence the patient's eating, they may be addressed through the use of proactive problem solving and functional mood modulation and acceptance (as described earlier). However, in some cases interpersonal problems powerfully maintain the eating disorder through a variety of direct and indirect processes or they interfere with treatment itself. Under these circumstances, they need to become a focus of treatment in their own right.The strategy used in CBT-E is to use a different psychological treatment to achieve interpersonal change, namely Interpersonal Psychotherapy (IPT). This is an evidence-based treatment that helps patients identify and address current interpersonal problems. In style and content IPT is very different from CBT-E. For this reason it is not “integrated” with CBT-E as such: rather, each session has a CBT-E component and an IPT one. More detailed information about IPT and its use with patients with eating disorders is available in a recent book chapter.34 Other Sections▼
AbstractEating disorders and their clinical featuresThe empirical status of cognitive behavioral therapy for eating disordersThe cognitive behavioral account of eating disordersEnhanced cognitive behavioral therapyAn overview of the core aspects of treatmentPreparation for treatment and changeStage oneStage twoStage threeStage fourUnderweight patientsFinal commentsReferencesStage fourStage four, the final stage in treatment, is concerned with ending treatment well. The focus is on maintaining the progress that has already been made and reducing the risk of relapse. Typically there are 3 appointments about 2 weeks apart. During this stage, as part of their preparation for the ending of treatment, patients discontinue self-monitoring and begin weekly weighing at home.To maximize the chances that progress is maintained, the therapist and patient jointly devise a personalized plan for the following few months until a posttreatment review appointment (usually about 20 weeks later). Typically this includes further work on body checking, food avoidance, and perhaps further practice at problem solving. In addition, patients are encouraged to continue their efforts to develop new interests and activities.There are 2 elements to minimizing the risk of relapse. First, patients need to have realistic expectations regarding the future. Expecting never to experience any eating difficulties again makes patients vulnerable to relapse because it encourages a negative reaction to even minor setbacks. Instead, patients should view their eating problem as an Achilles heel. The goal is that patients identify setbacks as early as possible, view them as a “lapse” rather than a “relapse,” and actively address them using strategies that they learned during treatment. Other Sections▼
AbstractEating disorders and their clinical featuresThe empirical status of cognitive behavioral therapy for eating disordersThe cognitive behavioral account of eating disordersEnhanced cognitive behavioral therapyAn overview of the core aspects of treatmentPreparation for treatment and changeStage oneStage twoStage threeStage fourUnderweight patientsFinal commentsReferencesUnderweight patientsThe strategies and procedures described so far are also relevant to patients who are underweight (mostly cases of anorexia nervosa but some cases of eating disorder NOS). However, CBT-E has to be modified to address certain characteristics of these patients.The first priority is to address motivation, as often these patients do not view undereating or being underweight as a problem. This may be done in several ways and relies on a good therapeutic alliance. The patient is provided with a personalized education about the psychological and physical effects of being underweight. This helps them to understand that some of the things that they find difficult (eg, being obsessive and indecisive, being unable to be spontaneous, being socially avoidant, lacking sexual appetite) are a direct consequence of being a low weight rather than being a reflection of their true personality. The patient is helped to think through the advantages and disadvantages of change, including a consideration of how things are likely to be in the future if they choose not to change and how this would fit with their aspirations. The therapist shows intense interest in the patient as a person, beyond the eating disorder, and helps them to reflect on the state of all aspects of their life, including their relationships, their physical and psychological well-being, their work, and their personal values. The patient is encouraged to experiment with making changes to learn more about the pros and cons of their current behavior. The goal is for patients themselves to decide to regain weight rather than this decision being imposed by the therapist. If this is successful, it greatly assists subsequent weight regain.Second, the undereating and the consequent state of starvation must be addressed. It is important to help patients to realize that undereating, and being underweight maintain the eating disorder and this is illustrated in a personalized formulation. Once the patient has agreed to regain weight it is explained that weight regain should be gradual and steady and that they should aim to maintain an average energy surplus of 500 calories each day to regain an average of 0.5 kg (1.1 lb) per week. The therapist helps the patient to devise and implement a daily plan of eating (which may be supplemented by energy-rich drinks) that meets this target.Treatment needs to be extended from the typical 20 weeks to about 40 weeks to allow sufficient time for patients to decide to change, to reach a healthy weight, and then practice maintaining it. It can be helpful to involve others in the weight-gain process to facilitate the patient's own efforts. This is especially so with young patients who are living at home with their parents. Other Sections▼
AbstractEating disorders and their clinical featuresThe empirical status of cognitive behavioral therapy for eating disordersThe cognitive behavioral account of eating disordersEnhanced cognitive behavioral therapyAn overview of the core aspects of treatmentPreparation for treatment and changeStage oneStage twoStage threeStage fourUnderweight patientsFinal commentsReferencesFinal commentsHopefully it will be clear from this brief account of CBT for eating disorders that major advances have been made and are continuing to be made. Perhaps most prominent among these is the adoption of a transdiagnostic approach to treatment whereby treatment is no longer for a specific eating disorder (eg, bulimia nervosa) but is directed at eating disorder psychopathology and the processes that maintains it. As a result, an empirically supported treatment approach has evolved that is suitable for all forms of eating disorder and one that is highly individualized.Many challenges remain. First and foremost, treatment outcome needs to be further improved, especially in the case of patients who are substantially underweight. Second, understanding more about the way in which treatment works, and the active ingredients of treatment, could inform the design of a more potent version. Doubtless some elements could be discarded whereas others may need to be enhanced.35 We need treatments that are effective and efficient. Last, we need to facilitate the dissemination of evidence-based practice. Many patients receive suboptimal treatment. There are several possible reasons for this but prominent among them is the fact that few therapists have received the necessary training.FootnotesC.G.F. is supported by a Principal Research Fellowship from the Wellcome Trust (046386). R.M., S.S., and Z.C. are supported by a program grant from the Wellcome Trust (046386). Other Sections▼
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