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By Anne Skomorowsky Because Germanwings pilot Andreas Lubitz killed himself when he purposefully drove a plane carrying 149 other people into a mountain in the Alps, there has been an assumption that he suffered from “depression”—an assumption strengthened by the discovery of antidepressants in his home and reports that he had been treated in psychiatry and neurology clinics. Many patients and other interested parties are rightly concerned that Lubitz’s murderous behavior will further stigmatize the mentally ill. It is certainly true that stigma may lead those in need to avoid treatment. When I was a psychiatrist at an HIV clinic, I was baffled by the shame associated with a visit to see me. Patients at the clinic had advanced AIDS, often contracted through IV drug use or sex work, and many had unprotected sex despite their high viral loads. Some were on parole. Many had lost custody of their children. Many lived in notorious single-room occupancy housing and used cocaine daily. But these issues, somehow, were less embarrassing than the suggestion that they be evaluated by a psychiatrist. Even doctors invoke “depression” to explain anything a reasonable adult wouldn’t do. For my clinic patients, it was shameful to be mentally ill. But to engage in antisocial behavior as a way of life? Not so bad. I think my patients were on to something. Bad behavior—even suicidal behavior—is not the same as depression. It is a truism in psychiatry that depression is underdiagnosed. But as a psychiatrist confronted daily with “problem” patients in the general hospital where I work, I find that depression is also overdiagnosed. Even doctors invoke “depression” to explain anything a reasonable adult wouldn’t do. © 2014 The Slate Group LLC.

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 20736 - Posted: 03.31.2015

By CELIA WATSON SEUPEL Every year, nearly 40,000 Americans kill themselves. The majority are men, and most of them use guns. In fact, more than half of all gun deaths in the United States are suicides. Experts and laymen have long assumed that people who died by suicide will ultimately do it even if temporarily deterred. “People think if you’re really intent on dying, you’ll find a way,” said Cathy Barber, the director of the Means Matters campaign at Harvard Injury Control Research Center. Prevention, it follows, depends largely on identifying those likely to harm themselves and getting them into treatment. But a growing body of evidence challenges this view. Suicide can be a very impulsive act, especially among the young, and therefore difficult to predict. Its deadliness depends more upon the means than the determination of the suicide victim. Now many experts are calling for a reconsideration of suicide-prevention strategies. While mental health and substance abuse treatment must always be important components in treating suicidality, researchers like Ms. Barber are stressing another avenue: “means restriction.” Instead of treating individual risk, means restriction entails modifying the environment by removing the means by which people usually die by suicide. The world cannot be made suicide-proof, of course. But, these researchers argue, if the walkway over a bridge is fenced off, a struggling college freshman cannot throw herself over the side. If parents leave guns in a locked safe, a teenage son cannot shoot himself if he suddenly decides life is hopeless. With the focus on who dies by suicide, these experts say, not enough attention has been paid to restricting the means to do it — particularly access to guns. © 2015 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 20674 - Posted: 03.10.2015

By Rachel Rabkin Peachman Many women with a history of depression who take antidepressants assume that once they get pregnant, they should try to wean themselves off their meds to avoid negative side effects for the baby. A new large study published in the journal Pediatrics challenges one reason behind that assumption. The research found that taking selective serotonin reuptake inhibitors (the antidepressants also known as S.S.R.I.s) while pregnant does not increase the risk of asthma in the resulting babies. What is associated with an increased risk of asthma? According to this study and other research, untreated prenatal depression. “The mechanisms underlying the association of prenatal depression and asthma are unknown,” said Dr. Xiaoqin Liu, the lead author of the Pediatrics study and an epidemiologist at Aarhus University in Denmark. An association between prenatal depression and asthma does not mean that prenatal depression causes asthma. There could be other reasons for the correlation, genetic or environmental, or both. For example, people who live in dense, polluted urban areas could be at an increased risk of both asthma and depression. The researchers used Denmark’s national registries to evaluate all singleton babies born from 1996 to 2007, and identify the mothers who had a diagnosis of depression or had used antidepressants, or both, during pregnancy or one year beforehand. Using a statistical model, the study authors found that prenatal depression — with or without the use of antidepressants — was associated with a 25 percent increased risk of asthma in children as compared with children whose mothers did not have a record of depression. © 2015 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 20671 - Posted: 03.10.2015

Hannah Devlin, science correspondent Psychedelic drugs could prove to be highly effective treatments for depression and alcoholism, according to a study which has obtained the first brain scans of people under the influence of LSD. Early results from the trial, involving 20 people, are said to be “very promising” and add to existing evidence that psychoactive drugs could help reverse entrenched patterns of addictive or negative thinking. However, Prof David Nutt, who led the study, warned that patients are missing out on the potential benefits of such treatments due to prohibitive regulations on research into recreational drugs. Speaking at a briefing in London, the government’s former chief drugs adviser, said the restrictions amounted to “the worst censorship in the history of science”. After failing to secure conventional funding to complete the analysis of the latest study on LSD, Nutt and colleagues at Imperial College London, are now attempting to raise £25,000 through the crowd-funding site Walacea.com. “These drugs offer the greatest opportunity we have in mental health,” he said. “There’s little else on the horizon.” There has been a resurgence of medical interest in LSD and psilocybin, the active ingredient in magic mushrooms, after several recent trials produced encouraging results for conditions ranging from depression in cancer patients to post-traumatic stress disorder. © 2015 Guardian News and Media Limited

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 20656 - Posted: 03.05.2015

Anti-depressants are the most commonly-prescribed medication in the U.S., with one in 10 Americans currently taking pills like Zoloft and Lexapro to treat depression. But these pharmaceuticals are only fully effective roughly 30 percent of the time, and often come with troublesome side effects. In a controversial new paper published in the journal Neuroscience & Biobehavioral Reviews, psychologist Paul Andrews of McMaster University in Ontario argues that this failure of medication may be based in a misunderstanding of the underlying chemistry related to depression. Andrews surveyed 50 years' worth of research supporting the serotonin theory of depression, which suggests that the disease is caused by low levels of the "happiness" neurotransmitter, serotonin. But Andrews argues that depression may actually be caused by elevated levels of serotonin. And this fundamental misunderstanding may be responsible for inappropriate treatment: The most common form of antidepressants are selective serotonin re-uptake inhibitors (SSRIs), which operate by targeting serotonin receptors in the brain in an effort to amplify serotonin production. Currently, scientists are unable to measure precisely how the brain releases and uses serotonin, because it can't be safely observed in a human brain. But Andrews points to research on animals which suggests that serotonin might work just the opposite from what we've assumed. ©2015 TheHuffingtonPost.com, Inc.

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 20636 - Posted: 03.02.2015

Distinct changes in the immune systems of patients with ME or chronic fatigue syndrome have been found, say scientists. Increased levels of immune molecules called cytokines were found in people during the early stages of the disease, a Columbia University study reported. It said the findings could help improve diagnosis and treatments. UK experts said further refined research was now needed to confirm the results. People with ME (myalgic encephalopathy) or CFS (chronic fatigue syndrome) suffer from exhaustion that affects everyday life and does not go away with sleep or rest. They can also have muscle pain and difficulty concentrating. ME can also cause long-term illness and disability, although many people improve over time. It is estimated that around 250,000 people in the UK have the disease. Disease pattern The US research team, who published their findings in the journal Science Advances, tested blood samples from nearly 300 ME patients and around 350 healthy people. They found specific patterns of immune molecules in patients who had the disease for up to three years. These patients had higher levels of of cytokines, particularly one called interferon gamma, which has been linked to the fatigue that follows many viral infections. Healthy patients and those who had the disease for longer than three years did not show the same pattern. Lead author Dr Mady Hornig said this was down to the way viral infections could disrupt the immune system. "It appears that ME/CFS patients are flush with cytokines until around the three-year mark, at which point the immune system shows evidence of exhaustion and cytokine levels drop."

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 20631 - Posted: 02.28.2015

|By Gary Stix Implantation of electrodes deep within the brain is now commonly performed for treatment of the neurological disorders Parkinson’s disease and essential tremor. But the use of deep-brain stimulation, as it is known, is expanding. It is now being assessed in as many as 200 patients for major depression—and is being considered for other disorders such as anorexia. Helen Mayberg, a neurologist from Emory University, has pioneered the use of imaging techniques to understand the functioning of different brain circuits to determine how to tailor various treatments for depression, including deep-brain stimulation, to a patient’s needs. Learn about her work below in “Deep-Brain Stimulation: A Decade of Progress with Helen Mayberg,” a Webinar put on by the Brain & Behavior Research Foundation. © 2015 Scientific American

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 20584 - Posted: 02.16.2015

By Rachel Ehrenberg SAN JOSE, Calif. — New moms suffering from postpartum depression change their activity on Facebook, suggesting that the social media site could help detect the onset of the baby blues. Many new parents share pictures and videos of their babies on Facebook and use the site to interact with friends they might be too busy to see in person. But compared with most typical new moms, those suffering from postpartum depression are less active on the social media site, Munmun De Choudhury of Georgia Tech reported February 14 at the annual meeting of the American Association for the Advancement of Science. She and her colleagues at Microsoft Research in Redmond, Wash., conducted an elaborate study that included a depression screening questionnaire, interviews and an analysis of Facebook activity and interactions of 165 mothers both before and after they had their babies. These women also tend to keep a stiff upper lip on the site, refraining from reporting on their emotional well-being and instead posting objective content geared toward getting feedback or advice on a specific matter, De Choudhury and her colleagues discovered. The scientists also found they could train a computer program to identify which moms had the blues. Such research might help with designing interventions, whereby moms could be warned that they might be sinking into depression and encouraged to reach out for social support or medical attention. M. De Choudhury. Online Social Dynamics and Emotional Wellbeing. American Association for the Advancement of Science Annual Meeting, San Jose, Calif., February 14, 2015. © Society for Science & the Public 2000 - 2015

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 8: Hormones and Sex
Link ID: 20583 - Posted: 02.16.2015

By David Tuller The Institute of Medicine on Tuesday proposed a new name and new diagnostic criteria for the condition that many still call chronic fatigue syndrome. Experts generally agree that the disease has a physical basis, but they have struggled for decades to characterize its symptoms. The new report may help improve diagnosis, but the recommendations are unlikely to end the long, contentious debate over who has the condition and what may be causing it. An institute panel recommended that the illness be renamed “systemic exertion intolerance disease,” a term that reflects what patients, clinicians and researchers all agree is a core symptom: a sustained depletion of energy after minimal activity, called postexertional malaise. The new name “really describes much more directly the key feature of the illness, which is the inability to tolerate both physical and cognitive exertion,” said Dr. Peter Rowe, a member of the panel and a pediatrician at Johns Hopkins who treats children with the condition. An alternate name for the illness, myalgic encephalomyelitis, meaning “brain and spinal cord inflammation with muscle pain,” was coined decades ago. Many experts now refer to the condition as M.E./C.F.S. About one million people in the United States are believed to have the syndrome. Many say they have been accused of imagining or exaggerating their symptoms, and many doctors have long viewed it as a psychological illness. The authors urged that doctors take patients’ physical complaints seriously. “This is not a figment of their imagination,” said Dr. Ellen Wright Clayton, the chairwoman of the Institute of Medicine panel and a professor of pediatrics and law at Vanderbilt University. Patients attribute much of their mistreatment to the name “chronic fatigue syndrome,” chosen by the Centers for Disease Control in 1988. © 2015 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 20573 - Posted: 02.13.2015

By ALAN SCHWARZ High numbers of students are beginning college having felt depressed and overwhelmed during the previous year, according to an annual survey released on Thursday, reinforcing some experts’ concern about the emotional health of college freshmen. The survey of more than 150,000 students nationwide, “The American Freshman: National Norms Fall 2014,” found that 9.5 percent of respondents had frequently “felt depressed” during the past year, a significant rise over the 6.1 percent reported five years ago. Those who “felt overwhelmed” by schoolwork and other commitments rose to 34.6 percent from 27.1 percent. Conducted by the Cooperative Institutional Research Program at the University of California, Los Angeles’s Higher Education Research Institute for almost 50 years, the survey assesses hundreds of matters ranging from political views to exercise habits. It is considered one of the most comprehensive snapshots of trends among recent high school seniors and is of particular interest to people involved in mental well-being. “It’s a public health issue,” said Dr. Anthony L. Rostain, a psychiatrist and co-chairman of a University of Pennsylvania task force on students’ emotional health. “We’re expecting more of students: There’s a sense of having to compete in a global economy, and they think they have to be on top of their game all the time. It’s no wonder they feel overwhelmed.” Other survey results indicated that students were spending more time on academics and socializing less — trends that would normally be lauded. But the lead author of the study, Kevin Eagan, cautioned that the shift could result in higher levels of stress. © 2015 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 20553 - Posted: 02.05.2015

By Pam Belluck A large new study has documented unexpected links in the timing and severity of symptoms of maternal depression, which could help mothers and doctors better anticipate and treat the condition. The study of more than 8,200 women from 19 centers in seven countries, published last month in Lancet Psychiatry, found that in those with the severest symptoms — suicidal thoughts, panic, frequent crying — depression most often began during pregnancy, not after giving birth, as is often assumed. Moderately depressed women often developed their symptoms postpartum, and were more likely than severely depressed women to have experienced complications during pregnancy like pre-eclampsia, gestational diabetes or hypertension. Severely depressed women, however, more often reported complications during delivery. “This is the largest study to date on postpartum depressive symptoms,” said Leah Rubin, an assistant professor in the Women’s Mental Health Research Program at University of Illinois at Chicago, a co-author of a commentary about the study. “This is definitely a first step in the right direction, knowing that depression isn’t one-size-fits-all.” Ten to 20 percent of mothers experience depression, anxiety, bipolar disorder or other symptoms at some point from pregnancy to a year after giving birth. The study could aid efforts to find causes and treatments. The study participants were all mothers. Some had been found to have postpartum depression by clinicians, while others were assessed via a widely used questionnaire. (Some participants fell into both groups.) © 2015 The New York Times Company

Related chapters from BP7e: Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress
Link ID: 20546 - Posted: 02.03.2015

By Janice Neumann (Reuters Health) - Moderate-intensity exercise, or even just walking, can improve quality of life for depressed middle-aged women, a large Australian study suggests. Women who averaged 150 minutes of moderate exercise (golf, tennis, aerobics classes, swimming, or line-dancing) or 200 minutes of walking every week had more energy, socialized more, felt better emotionally, and weren't as limited by their depression when researchers followed up after three years. They also had less pain and did better physically, although the psychological benefit was greater. With depression so prevalent, "there is an urgent need" to identify treatments, including non-medical options that people can do themselves, said Kristiann Heesch, who led the study. Heesch, senior lecturer at Queensland University of Technology, and her colleagues point out in a January 13 online article in the American Journal of Preventive Medicine that depression is expected to be the second-leading cause of global disease by 2030 and the leading cause in high-income countries. One in 10 U.S. adults suffers from depression, according to the Centers for Disease Control and Prevention. Women are 70% more likely to be depressed at some point in their lives than men, according to the National Institute of Mental Health. In previous research, Heesch found that exercise and walking could boost physical and emotional health in women who are not depressed. © 2015 Scientific American

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 20536 - Posted: 01.31.2015

|By Tori Rodriguez Scientists have studied brain structure for decades, so most disease-related structural anomalies have been long known. New findings of this nature are rare—yet last summer one neuroscientist studying depression published just that. Over nine years of sorting through countless brain images, Jerome J. Maller of Monash University and Alfred Hospital in Melbourne noticed a particular type of brain abnormality that seemed to show up more often in depressed patients. Their occipital lobes were often wrapped around each other. Maller and his colleagues investigated further and found that depressed patients are indeed three times as likely to have wraparound lobes. Occipital bending occurred in 35.3 percent of the depressed patients and 12.5 percent of the control subjects, according to their paper, published in Brain. The effect was even more pronounced in women: 45.8 percent of female patients with major depressive disorder exhibited occipital bending versus only 5.9 percent of women without depression, possibly because women's brains fit more snugly in their skulls than men's do. Previous studies have also found that occipital bending is more common in patients with schizophrenia. Maller suggests the lobes may wrap around each other when space for brain growth becomes constricted, perhaps because the brain is not doing enough neural pruning—the process by which the brain gets rid of neurons that are no longer needed. Indeed, many other studies have found that depressed brains are hyperconnected. Maller does not know if the finding will have clinical implications beyond helping to diagnose depression, but experts hope that this avenue of research will eventually lead to a deeper understanding of the disorder. “It really suggests some significant biological basis for at least some forms of depression,” says William Hopkins, a professor of neuroscience at Georgia State University, who was not involved in the study. © 2015 Scientific American

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 20518 - Posted: 01.26.2015

|By Simon Makin People with depression process emotional information more negatively than healthy people. They show increased sensitivity to sad faces, for instance, or a weaker response to happy faces. What has been missing is a biological explanation for these biases. Now a study reveals a mechanism: an unusual balance of chemicals in a brain area crucial for the feeling of disappointment. A team led by Roberto Malinow of the University of California, San Diego, studied the lateral habenula, a evolutionarily ancient region deep in the brain [see diagram on bottom]. Neurons in this region are activated by unexpected negative events, such as a punishment out of the blue or the absence of an anticipated reward. For example, studies have shown that primates trained to expect a reward, such as juice, after a visual cue show heightened activity in the lateral habenula if the reward is withheld. Such findings have led to the idea that this area is a key part of a “disappointment circuit.” Past studies have also shown that hyperactivity in the lateral habenula is linked with depressionlike behavior in rodents. In people with depression, low levels of serotonin, the brain chemical targeted by antidepressants, are linked with a rise in lateral habenula activity. The region is unusual because it lacks the standard equipment the brain uses to reduce overactivity: opposing sets of neurons that either increase activity by secreting the chemical glutamate or decrease activity by secreting the chemical GABA. The lateral habenula has very few neurons that decrease activity, so Malinow and his colleagues set out to discover how the brain tamps down activity there. © 2015 Scientific American

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 20508 - Posted: 01.22.2015

By Richard A. Friedman, M.D. You’re feeling down, and your doctor or therapist has confirmed it: You have depression. Now what? Until recently, many experts thought that your clinician could literally pick any antidepressant or type of psychotherapy at random because, with a few clinical exceptions, there was little evidence to favor one treatment over another for a given patient. In fact, I used to delight in tormenting the drug company representatives when they asked me how I picked an antidepressant. I would take a quarter out of my pocket, flip the coin and say I’d let chance decide because their drug was no better or worse than their competitors’. Although the holy grail of personalized therapy — be it with psychotropic drugs or psychotherapy — has proved elusive, we’ve learned a lot recently about individual factors that might predict a better response to one type of treatment over another. Dr. Helen Mayberg, a professor of psychiatry at Emory University, recently published a study in JAMA Psychiatry that identified a potential biomarker in the brain that could predict whether a depressed patient would respond better to psychotherapy or antidepressant medication. Using PET scans, she randomized a group of depressed patients to either 12 weeks of treatment with the S.S.R.I. antidepressant Lexapro or to cognitive behavior therapy, which teaches patients to correct their negative and distorted thinking. Over all, about 40 percent of the depressed subjects responded to either treatment. But Dr. Mayberg found striking brain differences between patients who did well with Lexapro compared with cognitive behavior therapy, and vice versa. Patients who had low activity in a brain region called the anterior insula measured before treatment responded quite well to C.B.T. but poorly to Lexapro; conversely, those with high activity in this region had an excellent response to Lexapro, but did poorly with C.B.T. © 2015 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 20468 - Posted: 01.10.2015

Sara Reardon Ketamine, a psychoactive ‘party drug’ better known as Special K, has pharma­ceutical companies riding high. Used clinically as an anaesthetic in animals and humans, it has proved an extremely effective treatment for depression, bipolar disorder and suicidal behaviour. It also works incredibly fast. Unlike conventional antidepressants, which generally take weeks to start working, ketamine lifts depression in as little as two hours. “It blew the doors off what we thought we knew about depression treatment,” says psychiatrist James Murrough at Mount Sinai Hospital in New York City. Companies are racing to develop patentable forms of the drug, and researchers are battling to understand how it affects the brain. An increasing number of clinicians are prescribing ketamine off-label for their patients, even as some of their colleagues worry that too little is known about its long-term effects. The excitement over ketamine shows how badly new depression drugs are needed, says Thomas Insel, director of the US National Institute of Mental Health (NIMH) in Bethesda, Maryland. Many drug companies have closed their mental-health divisions in the past five years, and there have been no significant advances in medication for depression in decades. Today’s most common antidepressants target the brain’s serotonin or noradrenaline pathways (some target both). Ketamine blocks the signalling molecule NMDA, a component of the glutamate pathway, which is involved in memory and cognition. Before ketamine was studied, no one even knew that the pathway was involved in depression, Murrough says. © 2015 Nature Publishing Group

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 20461 - Posted: 01.08.2015

Haroon Siddique Research that aims to map the activity of serotonin in the brain could revolutionise the use of antidepressants and behavioural therapy for people with mental illnesses. The neurotransmitter serotonin has long been associated with mood, with drugs that boost the chemical in the brain helping to alleviate the symptoms of common illnesses such as depression and anxiety, but scientists lack a deep understanding of how it mediates different mood disorders. By understanding the biology of serotonin, the hope is that drugs can be created that only target cells relevant to a particular disorder and behavioural therapies can be made more effective, reducing the need for antidepressants. Dr Jeremiah Cohen, an assistant professor at the Johns Hopkins Brain Science Institute in Baltimore, said: “The ultimate aim is to understand the biology of mood and how groups of cells in the brain connect to produce our emotional behaviour. Most antidepressants operate broadly in the entire serotonin system. What we hope to do with this map is use drugs that are available or design new drugs that will target only the components of that system relevant to a particular disorder.” The use of antidepressants in England has soared since the late 1990s, raising concerns in some quarters about over-prescription. Researchers from the Nuffield Trust and the Health Foundation found that 40m prescriptions for antidepressants were made in 2012, compared to 15m in 1998. Doctors write prescriptions for more than one in 10 adults in developed countries, with Iceland, Australia, Canada and European Nordic countries leading the way, according to 2013 data from the Organisation for Economic Co-operation and Development. More than 10% of American adults have used antidepressants.

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 20455 - Posted: 01.06.2015

By Dr. Mitesh Popat It’s common knowledge that eating better, exercising more, limiting alcohol intake and not smoking can lead to a healthier, longer life. For many, sustaining healthy behaviors is not easy. For diabetics, maintaining healthy behaviors is even more challenging, although it is critical. If well managed, the disease can be held in check; if not, it can be devastating, leading to kidney failure, blindness, stroke and even death. It may be a surprise that there is strong association between depression, anxiety and diabetes. Not only can depression and anxiety seriously affect the ability to manage the disease, but there also is evidence that, for some, depression plays a role in actually causing diabetes. Research indicates that depression is unrecognized and untreated in approximately two-thirds of patients with diabetes. Whether cause or effect, the medical profession needs to do more to address the psychological issues associated with the disease. As a family medicine physician, I see the association on daily basis. Some patients are so overwhelmed by the necessary daily self-care that comes with diabetes that they become highly anxious and depressed. Others who are suffering from complications or are having trouble managing their blood sugar levels may feel a loss of control and get anxious or depressed. These symptoms are often compounded in people who live in poverty, including the low-income Latinos, African Americans and seniors whom we care for at Marin Community Clinics. Diabetes has become an epidemic in these groups. Working three jobs and constantly worrying about making ends meet can trigger depression and anxiety in anyone. Add to that the need to adopt a disciplined healthy lifestyle, and it can be a real struggle.

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 20410 - Posted: 12.13.2014

By ANDREW POLLACK It is either the most exciting new treatment for depression in years or it is a hallucinogenic club drug that is wrongly being dispensed to desperate patients in a growing number of clinics around the country. It is called ketamine — or Special K, in street parlance. While it has been used as an anesthetic for decades, small studies at prestigious medical centers like Yale, Mount Sinai and the National Institute of Mental Health suggest it can relieve depression in many people who are not helped by widely used conventional antidepressants like Prozac or Lexapro. And the depression seems to melt away within hours, rather than the weeks typically required for a conventional antidepressant. But some psychiatrists say the drug has not been studied enough to be ready for use outside of clinical trials, and they are alarmed that clinics are springing up to offer ketamine treatments, charging hundreds of dollars for sessions that must be repeated many times. “We don’t know what the long-term side effects of this are,” said Dr. Anthony J. Rothschild, a professor of psychiatry at the University of Massachusetts Medical School. Some psychiatrists say the drug has not been studied enough to be ready for use outside of clinical trials. Credit Sandy Huffaker for The New York Times Pharmaceutical companies hope to solve the problem by developing drugs that work like ketamine but without the side effects, which are often described as out-of-body experiences. © 2014 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 20407 - Posted: 12.10.2014

By Tina Rosenberg When Ebola ends, the people who have suffered, who have lost loved ones, will need many things. They will need ways to rebuild their livelihoods. They will need a functioning health system, which can ensure that future outbreaks do not become catastrophes. And they will need mental health care. Depression is the most important thief of productive life for women around the world, and the second-most important for men. We sometimes imagine it is a first-world problem, but depression is just as widespread, if not more so, in poor countries, where there is a good deal more to be depressed about. And it is more debilitating, as a vast majority of sufferers have no safety net. Health care for all must include mental health care. It’s hard to believe but both Liberia and Sierra Leone have only a single psychiatrist. The Ebola crisis has exposed these countries’ malignant neglect of their health systems. People can’t get care for diarrhea and malaria. How will these countries take care of an epidemic of depression? This isn’t really a medical question. We know how to treat depression. What we don’t know yet is how to make effective treatment cheap, culturally appropriate, convenient and non-stigmatizing — all needed to get treatment out to millions and millions of people. But some researchers are finding out. They are doing so despite the fact that growing attention to this issue hasn’t been accompanied by money. The U.S. National Institute of Mental Health last year provided just $24.5 million for global mental health efforts, and the Canadian government’s Grand Challenges Canada, which is said to have the largest portfolio of mental health innovation in developing countries, has spent only $28 million on them since it began in 2010. © 2014 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 20404 - Posted: 12.08.2014