Links for Keyword: Depression

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Stacey Vanek Smith I'm in a booth with a computer program called Ellie. She's on a screen in front of me. Ellie was designed to diagnose post-traumatic stress disorder and depression, and when I get into the booth she starts asking me questions — about my family, my feelings, my biggest regrets. Emotions seem really messy and hard for a machine to understand. But Skip Rizzo, a psychologist who helped design Ellie, thought otherwise. When I answer Ellie's questions, she listens. But she doesn't process the words I'm saying. She analyzes my tone. A camera tracks every detail of my facial expressions. The doctor may see you now "Contrary to popular belief, depressed people smile as many times as non-depressed people," Rizzo says. "But their smiles are less robust and of less duration. It's almost like polite smiles rather than real, robust, coming from your inner-soul type of a smile." Ellie compares my smile to a database of soldiers who have returned from combat. Is my smile genuine? Is it forced? Ellie also listens for pauses. She watches to see whether I look off to the side or down. If I lean forward, she notices. All this analysis seems to work: In studies, Ellie could detect signs of PTSD and depression about as well as a large pool of psychologists. Jody Mitic served with the Canadian forces in Afghanistan. He lost both of his feet to a bomb. And Mitic remembers that Ellie's robot-ness helped him open up. "Ellie seemed to just be listening," Mitic says. "A lot of therapists, you can see it in their eyes, when you start talking about some of the grislier details of stuff that you might have seen or done, they are having a reaction." © 2015 NPR

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: 20961 - Posted: 05.21.2015

Dan Sung A 10-year study has revealed a startling link between high levels of anxiety and an increased risk of death from liver disease. The research, carried out by scientists at the University of Edinburgh, took account for obvious sociological and physiological factors such as alcohol consumption, obesity, diabetes and class, but still the data pointed to a clear relationship between the psychological conditions of stress and depression and the physical health of the hepatic system. There were over 165,000 participants surveyed for mental distress. They were each tracked for over a decade during which time the causes of death for those who passed on were recorded and categorised. What was found was that those who’d scored highly for signs of depression and stress were far more likely to suffer fatal liver disease. “This study provides further evidence for the important links between mind and body, and of the damaging effects psychological distress can have on physical wellbeing,” said Dr Tom Russ of the Centre for Clinical Brain Sciences. The work did not uncover any reasons for direct cause and effect but is the first to identify such a link between mental states and liver damage. Previous research has described how psychological conditions can lead to increased risk of cardiovascular disease which, in turn, may develop into obesity, raised blood pressure and then eventually to liver failure but, with this methodology controlling for such factors, it appears that the link is more direct than was previously thought.

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: 20960 - Posted: 05.20.2015

By Will Lippincott In January 2012, two weeks after my discharge from a psychiatric hospital in Connecticut, I made a plan to die. My week in an acute care unit that had me on a suicide watch had not diminished my pain. Back in New York, I stormed out of my therapist’s office and declared I wouldn’t return to the treatment I’d dutifully followed for three decades. Nothing was working, so what was the point? I fit the demographic profile of the American suicide — white, male and entering middle age with a history of depression. Suicide runs in families, research tells us, and it ran in mine. My father killed himself at age 49 in April 1990. A generation before, an aunt of his took her life; before her, there were others. Shame runs in families, too, and no one in mine talked much about mental illness. The first time I was hospitalized for wanting to kill myself, as a teenager, my dad visited me a few days in. I made an effort to greet him with a firm handshake; he shared a few jokes with me. Dad was visibly concerned and told me he loved me. Only after his suicide a few years later did I learn that he, too, had been hospitalized, for depression, when he was in his early 20s. Setting out to start my own life after college, I felt that suicide was a clear and present opportunity, one that glowed more brightly during my depressive episodes. But I had an ambitious plan to beat it. I’d be a performer: work hard, keep my goals in the line of sight at all times, and make as much money as I could. Professional success would be my first line of defense to keep hopelessness at bay. In parallel, I’d find excellent doctors and be a compliant patient, take my meds and show up for talk therapy. And for a long time, through my 20s and 30s, that plan worked. © 2015 The New York Times Company

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: 20949 - Posted: 05.19.2015

Nick Davis Mood disorders such as depression are devastating to sufferers, and hugely costly to treat. The most severe form of depression, often called clinical depression or major depressive disorder (MDD), increases the person’s likelihood of suicide and contributes significantly to a person’s disability-adjusted life years (DALYs), a measure of quality of life taking into account periods of incapacity. The healthcare burden of MDD is large in most countries, especially when the person requires a stay in hospital. Putting these factors together, it’s clear we need to develop effective treatments to combat depression. The mechanisms of depressive disorders are not well understood, and it seems likely that there is no single cause. Most modern therapies use drugs that target neurotransmitters – the chemicals that carry signals between neurons. For example, the class of drugs known as SSRIs, or selective serotonin reuptake inhibitors, prevent the neurotransmitter serotonin from being reabsorbed by a neuron; this means that more serotonin is available to wash around between the nerve cells, and is more likely to activate cells in the brain networks that area affected in MDD. But SSRIs and other drugs are not a pharmacological ‘free lunch’. Drug treatments for depression are ineffective for many people, cause side-effects, and may lose their therapeutic effect over time. For these reasons, many researchers are searching for alternative treatments for MDD that overcome these problems, and are more effective or less unpleasant. One potential treatment involves the use of pulses of magnetic energy over the head to target the brain’s mood circuits. This technique, called transcranial magnetic stimulation (TMS), may potentially address some of the problems of pharmaceutical treatments, but we still don’t know exactly how it works, or how effective it will be in treating MDD. © 2015 Guardian News and Media Limited

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 20946 - Posted: 05.18.2015

John Crace After over a year working in Westminster as this paper’s parliamentary sketchwriter, I thought I had learned a thing or two about bearpits. That was before I agreed to second Prof Allan Young in speaking against the motion that “This House believes that the long-term use of psychiatric medications is causing more harm than good”. It turned out that politicians are almost models of decency compared to psychiatrists fighting their own corner. I had wondered why I had been invited. I have no scientific knowledge of the subject under discussion; all I had to offer was my own personal experience of living with episodes of depression and acute anxiety for more than 20 years. For me, a combination of medication and therapy has proved effective; not so effective as to prevent recurrences of these mental health problems all together, but effective enough for me to have managed them without having to return as an in-patient at the psychiatric hospital I wound up in 20 years earlier. I could perhaps have done more to look after myself, I suppose. I could have given up my Spurs season ticket. But apart from that … Having raised concerns about my credentials, I was assured that it was important to have a patient’s voice heard. I thought so, too. So I agreed. But on the way home from the debate last night, I did wonder if the reason I had been asked was because everyone else had turned them down. Things didn’t get off to a great start, when there was a pre-debate vote in the packed theatre at King’s College’s Institute of Psychiatry, Psychology and Neuroscience, which had apparently sold out within hours of the tickets being made available in March. 126 people – a mixture of mental health practitioners, students and members of the public – believed the motion to be correct; 28 abstained, and only 64 were on my side. © 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: 20936 - Posted: 05.16.2015

Haroon Siddique Long-term depression in people over 50 could more than double their risk of suffering a stroke, with the risk remaining significantly higher even after the depression allays, research suggests. The US study of more than 16,000 people, which documented 1,192 strokes, found that onset of recent depression was not associated with higher stroke risk, suggesting the damage is done by depressive symptoms accumulating over time. The study’s lead author, Paola Gilsanz, from Harvard University’s TH Chan School of Public Health, said: “Our findings suggest that depression may increase stroke risk over the long term. Looking at how changes in depressive symptoms over time may be associated with strokes allowed us to see if the risk of stroke increases after elevated depressive symptoms start or if risk goes away when depressive symptoms do. We were surprised that changes in depressive symptoms seem to take more than two years to protect against or elevate stroke risk.” The research, published on Wednesday in the Journal of the American Heart Association, used data from between 1998 and 2010 from the Health and Retirement Study, which interviews a panel of representative Americans aged over 50 every two years, on their depressive symptoms, history of stroke, and stroke risk factors. Gilsanz, with colleagues from universities in Washington, California and Minnesota, and Bronx Partners for Healthy Communities, found that people with high depressive symptoms at two consecutive interviews had a 114% higher risk of suffering a first stroke, compared with people without depression at either interview. Those who had depressive symptoms at one interview but not at the next had a 66% higher risk. © 2015 Guardian News and Media Limited

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 19: Language and Hemispheric Asymmetry
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 15: Language and Our Divided Brain
Link ID: 20928 - Posted: 05.14.2015

Sarah Boseley Health editor Psychiatric drugs do more harm than good and the use of most antidepressants and dementia drugs could be virtually stopped without causing harm, an expert on clinical trials argues in a leading medical journal. The views expressed in a British Medical Journal debate by Peter Gøtzsche, professor and director of the Nordic Cochrane Centre in Denmark, are strongly opposed by many experts in mental health. However, others say the debate around the use of psychiatric drugs is important and acknowledge that there has been overuse of antipsychotics to quieten aggressive patients with dementia. Gøtzsche says more than half a million people over the age of 65 die as a result of the use of psychiatric drugs every year in the western world. “Their benefits would need to be colossal to justify this, but they are minimal,” he writes. He claims that trials carried out with funding from drug companies into the efficacy of psychiatric drugs have almost all been biased, because the patients involved have usually been on other medication first. They stop their drugs and often experience a withdrawal phase prior to starting the trial drug, which then appears to have a big benefit. He also claims that deaths from suicide in clinical trials are under-reported. In trials of the modern antidepressants fluoxetine and venlafaxine, says Gøtzsche, it takes only a few extra days for depression in the placebo group – given dummy pills – to lift as much as in the group given the drugs. He argues that there is spontaneous remission of the disease over time. © 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: 20919 - Posted: 05.13.2015

By Tina Hesman Saey People with depression have more mitochondrial DNA and shorter telomeres than nondepressed people do, an international team of researchers reports online April 23 in Current Biology. Mitochondria are organelles that produce energy for cells. Mitochondria seem to become inefficient under stress, the team found, so more mitochondria may be needed to produce enough energy. Telomeres are the DNA endcaps on chromosomes that prevent the genetic material from unraveling. Short telomeres are associated with shorter life spans. The altered DNA may reflect metabolic changes associated with depression, the researchers say. Experiments with mice showed that these DNA changes are brought on by stress or by stress hormones. Four weeks after scientists stopped stressing the mice, their mitochondrial and telomere DNA had returned to normal. Those results indicate that the molecular changes are reversible. Researchers also studied DNA from more than 11,000 people to learn whether past stress was responsible for the molecular changes seen in people with depression. Depression was associated with the DNA changes, but having a stressful life was not. For instance, people who had experienced childhood sexual abuse but were not depressed did not have statistically meaningful changes to their DNA compared with people who had no history of abuse. The findings suggest that stress can change DNA but many people can bounce back. Depressed people may have a harder time recovering from the molecular damage. © Society for Science & the Public 2000 - 2015.

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: 20850 - Posted: 04.28.2015

By Smitha Mundasad Health reporter, BBC News A mindfulness-based therapy could offer a "new choice for millions of people" with recurrent depression, a Lancet report suggests. Scientists tested it against anti-depressant pills for people at risk of relapse and found it worked just as well. The therapy trains people to focus their minds and understand that negative thoughts may come and go. In England and Wales doctors are already encouraged to offer it. Patients who have had recurrent clinical depression are often prescribed long-term anti-depressant drugs to help prevent further episodes. And experts stress that drug therapy is still essential for many. In this study, UK scientists enrolled 212 people who were at risk of further depression on a course of mindfulness-based cognitive therapy (MBCT) while carefully reducing their medication. Patients took part in group sessions where they learned guided meditation and mindfulness skills. The therapy aimed to help people focus on the present, recognise any early warning signs of depression and respond to them in ways that did not trigger further reoccurrences. Researchers compared these results to 212 people who continued to take a full course of medication over two years. By the end of the study, a similar proportion of people had relapsed in both groups. And many in the MBCT group had been tapered off their medication. Scientists say these findings suggest MBCT could provide a much-needed alternative for people who cannot or do not wish to take long-term drugs. In their report, they conclude it "may be a new choice for millions of people with recurrent depression on repeat prescriptions." © 2015 BBC

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: 20826 - Posted: 04.21.2015

Arran Frood A psychedelic drink used for centuries in healing ceremonies is now attracting the attention of biomedical scientists as a possible treatment for depression. Researchers from Brazil last month published results from the first clinical test of a potential therapeutic benefit for ayahuasca, a South American plant-based brew1. Although the study included just six volunteers and no placebo group, the scientists say that the drink began to reduce depression in patients within hours, and the effect was still present after three weeks. They are now conducting larger studies that they hope will shore up their findings. The work forms part of a renaissance in studying the potential therapeutic benefits of psychedelic or recreational drugs — research that was largely banned or restricted worldwide half a century ago. Ketamine, which is used medically as an anaesthetic, has shown promise as a fast-acting antidepressant; psilocybin, a hallucinogen found in ‘magic mushrooms’, can help to alleviate anxiety in patients with advanced-stage cancer2; MDMA (ecstasy) can alleviate post-traumatic stress disorder; and patients who experience debilitating cluster headaches have reported that LSD eases their symptoms. Ayahuasca, a sacramental drink traditionally brewed from the bark of a jungle vine (Banisteriopsis caapi) and the leaves of a shrub (Psychotria viridis), contains ingredients that are illegal in most countries. But a booming ayahuasca industry has developed in South America, where its religious use is allowed, and where thousands of people each year head to rainforest retreats to sample its intense psychedelic insights. © 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: 20765 - Posted: 04.07.2015

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