Chapter 16. Psychopathology: Biological Basis of Behavior Disorders

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Story by Amy Ellis Nutt She relaxed in the recliner, her eyes closed, her hands resting lightly in her lap. The psychiatrist’s assistant made small talk while pushing the woman’s hair this way and that, dabbing her head with spots of paste before attaching the 19 electrodes to her scalp. In the struggle over the future of psychiatry, researchers are looking deep within the brain to understand mental illness and find new therapeutic tools. As the test started, her anxiety ticked up. And that’s when it began: the sensation of being locked in a vise. First, she couldn’t move. Then she was shrinking, collapsing in on herself like some human black hole. It was a classic panic attack — captured in vivid color on the computer screen that psychiatrist Hasan Asif was watching. “It’s going to be okay,” he said, his voice quiet and soothing. “Just stay with it.” The images playing out in front of him were entirely unexpected; this clearly wasn’t a resting state for his patient. With each surge of anxiety, a splotch of red bloomed on the computer screen. Excessive activity of high-energy brain waves near the top of her head indicated hyper-arousal and stress. Decreased activity in the front of her brain, where emotions are managed, showed she couldn’t summon the resources to keep calm.

Keyword: Depression; Brain imaging
Link ID: 21932 - Posted: 02.25.2016

Tina Hesman Saey Sonia Vallabh knows what will probably kill her. In 2011, the Boston-area law school graduate learned she carries the same genetic mutation that caused her mother’s death from a rare brain-wasting prion disease. Prions are twisted forms of normal brain proteins that clump together and destroy nerves. About 10 to 15 percent of prion diseases are caused by a mutation in the PRNP gene, leading to such deadly diseases as Creutzfeldt-Jakob disease, Gerstmann-Sträussler-Scheinker syndrome and fatal familial insomnia, the disease that killed Vallabh’s mother. Grief, shared with family and friends, came first. Eventually, Vallabh realized, “We can’t get around this prognosis.… We’ve got to go through it.” So began her and husband Eric Minikel’s odyssey to learn about the disease that had turned their lives upside down. A scientist friend came by with a flash drive loaded with research papers about prion diseases. “We didn’t have the vocabulary” to understand the information, Vallabh says. So she took a sabbatical from her job to take biology and chemistry classes. Minikel kept writing transportation software, but attended night classes with his wife. Vallabh’s first foray into brain research was as a technician in a lab studying Huntington’s disease. During “science nights” at the couple’s home, scientist pals team-taught biology and biochemistry. The couple took the biggest step when Minikel left his consulting job and both enrolled in graduate school to study prion diseases. Prion proteins, some of which clump together or form fibrils, as in this E. coli bacteria, are often used to model how proteins misfold in some neurodegenerative disorders. © Society for Science & the Public 2000 - 2016

Keyword: Prions; Sleep
Link ID: 21922 - Posted: 02.22.2016

By DONALD G. McNEIL Jr. A baby with a shrunken, misshapen head is surely a heartbreaking sight. But reproductive health experts are warning that microcephaly may be only the most obvious consequence of the spread of the Zika virus. Even infants who appear normal at birth may be at higher risk for mental illnesses later in life if their mothers were infected during pregnancy, many researchers fear. The Zika virus, they say, closely resembles some infectious agents that have been linked to the development of autism, bipolar disorder and schizophrenia. Schizophrenia and other debilitating mental illnesses have no single cause, experts emphasized in interviews. The conditions are thought to arise from a combination of factors, including genetic predisposition and traumas later in life, such as sexual or physical abuse, abandonment or heavy drug use. But illnesses in utero, including viral infections, are thought to be a trigger. “The consequences of this go way beyond microcephaly,” said Dr. W. Ian Lipkin, who directs The Center for Infection and Immunity at Columbia University. Here is a look at the most prominent rumors and theories about Zika virus, along with responses from scientists. Among children in Latin America and the Caribbean, “I wouldn’t be surprised if we saw a big upswing in A.D.H.D., autism, epilepsy and schizophrenia,” he added. “We’re looking at a large group of individuals who may not be able to function in the world.” © 2016 The New York Times Company

Keyword: Development of the Brain; Schizophrenia
Link ID: 21918 - Posted: 02.20.2016

By Nancy Szokan It’s well known that physical activity is a mood elevator. But writing in “The Athlete’s Way” blog on Psychology Today’s website, endurance athlete Christopher Bergland discusses a study indicating that combining movement with the attention-focusing benefits of meditation can be an extra-effective tool in fighting depression. The small study, conducted at Rutgers University in New Jersey, was based on a set of assumptions: Healthy brains are constantly producing neurons. Brains of people under stress or suffering depression produce fewer neurons. Physical activity increases neuron production, as do antidepressant medications. (Meanwhile, a certain number of newborn neurons die off.) Mental exercise — “effortful learning,” which requires focus — reduces those deaths. People with depression often have problems with focus. The researchers tested a novel intervention — it’s called MAP because it involves mental and physical training — aimed at both increasing neuron production and keeping those neurons alive. Fifty-two people completed the study — 22 with major depressive disorder, or MDD, and 30 who were not depressed. Twice a week, they performed 30 minutes of meditation during which they were directed to constantly focus on their breathing; they began each session seated, but for the last 10 minutes they meditated while walking slowly. Then they performed 30 minutes of moderate physical activity on a treadmill or stationary cycle. After eight weeks, the researchers found that the MDD patients’ depressive symptoms had been reduced by 40 percent. (The non-depressed participants also said they felt happier.)

Keyword: Depression
Link ID: 21899 - Posted: 02.16.2016

By Dominic Howell BBC News A new therapy which involves a patient embodying themselves in a virtual reality avatar of a crying child could help with depression, research has suggested. Patients wear a headset that projects a life-sized image, firstly of an adult and then of a child. The new research tested the technology for the first time on patients with a mental health problem. The project is part of a continuing study at University College London. The university, which is working in collaboration with ICREA-University of Barcelona, has suspected for several years that virtual therapy could help with mental health conditions. This latest research - which has been published in the British Journal of Psychiatry Open and was funded by the Medical Research Council - lays the basis for a large-scale clinical trial to be carried out in the future. The study took 15 people who were all being treated by the NHS for depression and put them through the avatar experience. Firstly, the patients - 10 of whom were female and the rest male - put on a headset which projected an adult version of themselves into a virtual reality mirror. The patient was asked to mentally identify with the adult avatar, which exactly replicated the patient's body movements, in a process known as "embodiment". They then noticed a separate avatar of a small crying child, who was also in the mirror. They were told to say compassionate phrases to the child to try and comfort and console it. Patients asked the child to think of a time when it was happy, and to think of someone who loved them. At this stage of the experiment the roles were then reversed. © 2016 BBC

Keyword: Depression
Link ID: 21897 - Posted: 02.15.2016

By Ann Gibbons Depressed? Your inner Neandertal may be to blame. Modern humans met and mated with these archaic people in Europe or Asia about 50,000 years ago, and researchers have long suspected that genes picked up in these trysts might be shaping health and well-being today. Now, a study in the current issue of Science details their impact. It uses a powerful new method for scanning the electronic health records of 28,000 Americans to show that some Neandertal gene variants today can raise the risk of depression, skin lesions, blood clots, and other disorders. Neandertal genes aren’t all bad. “These variants sometimes protect against a disease, sometimes make people more susceptible to disease,” says paleogeneticist Svante Pääbo of the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany. Two other new studies identified three archaic genes that boost immune response. And most archaic genes that persist in humans were likely beneficial in prehistoric times. But some now cause disease because modern lifestyles and environments are so different. Living people carry only trace amounts of Neandertal DNA, which makes its impact on health more striking. “The Neandertal genetic contribution to present-day people seems to have larger physiological effects than I would have naïvely thought,” says Pääbo, who helped launch this avenue of research by sequencing the first ancient genomes but was not involved in these studies. On average, Europeans and Asians have inherited about 1.5% of their genomes from Neandertals. Island Melanesians carry an additional 2% to 3% of DNA inherited from another extinct group, the Denisovans. Most Africans lack this archaic DNA because the interbreeding happened after modern humans left Africa. © 2016 American Association for the Advancement of Science

Keyword: Depression; Genes & Behavior
Link ID: 21894 - Posted: 02.13.2016

Bruce Bower Winter doesn’t deserve its dour reputation as the season of depression, scientists say. Rates of major depression, a psychiatric condition marked by intense sadness, hopelessness, insomnia and a general loss of interest or pleasure, don’t markedly change from one season to another among U.S. adults, says a team led by psychologist Steven LoBello of Auburn University at Montgomery in Alabama. Neither do symptoms intensify or become more numerous during winter among those already suffering from depression, the researchers report online January 19 in Clinical Psychological Science. A small number of people with regular fall or winter depression may have gone undetected in the new study, which surveyed more than 30,000 U.S. adults. Still, it’s becoming harder to justify the current psychiatric diagnosis of major depression “with seasonal pattern,” LoBello and Auburn colleagues Megan Traffanstedt and Sheila Mehta conclude. Because it’s a recurring disorder, depression can strike in two consecutive winters by chance, the researchers say. Depression in three or more consecutive winters could be due to personal and social factors unrelated to shorter days, they add. “Being depressed during winter is not evidence that one is depressed because of winter,” LoBello says. © Society for Science & the Public 2000 - 2016

Keyword: Depression; Biological Rhythms
Link ID: 21876 - Posted: 02.09.2016

By Jordana Cepelewicz As the Panthers and Broncos faced off in the third quarter of last night’s Super Bowl, wide receiver Philly Brown suffered a possible concussion—and to the disappointment of Panthers fans, he never returned to the game. But for good reason: concussions are now known to be much more serious injuries than once thought. And the danger may not be limited to the immediate repercussions. Researchers have already linked more severe traumatic brain injury to later suicide—particularly in military veterans and professional athletes—and have more recently explored the connection between concussion and depression. Now, new research published in the Canadian Medical Association Journal shows that even mild concussions sustained in ordinary community settings might be more detrimental than anyone anticipated; the long-term risk of suicide increases threefold in adults if they have experienced even one concussion. That risk increases by a third if the concussion is sustained on a weekend instead of a weekday—suggesting recreational concussions are riskier long-term than those sustained on the job. “The typical patient I see is a middle-aged adult, not an elite athlete,” says Donald Redelmeier, a senior scientist at the University of Toronto and one of the study’s lead authors. “And the usual circumstances for acquiring a concussion are not while playing football; it is when driving in traffic and getting into a crash, when missing a step and falling down a staircase, when getting overly ambitious about home repairs—the everyday activities of life.” Redelmeier and his team wanted to examine the risks of the concussions acquired under those circumstances. © 2016 Scientific American

Keyword: Brain Injury/Concussion; Depression
Link ID: 21875 - Posted: 02.09.2016

By Steven Petrow I have slogged through a number of difficult situations in recent months, among them the ongoing crises of my elderly parents’ illnesses and the suicide of a friend. I never lost my appetite nor burst into tears, and I didn’t suffer from any of the other typical symptoms of depression. Maybe I was more irritable than usual, a bit more prone to snap. And yes, I buried myself in my work. But I didn’t think I’d tripped down into the rabbit hole of depression. You would think I would have been more self-aware, both personally and professionally. As a health journalist, I have often used my own stories to write about difficult-to-discuss medical conditions, including learning I had testicular cancer at age 26 and my misdiagnosis with H.I.V./AIDS — back when it was a death sentence. But I had never written about suffering from depression, even though it’s plagued me since I first put pen to paper, at age 11, when I started keeping a diary. Still, I’m far from alone. At least six million men in the United States suffer from depression, according to the National Institute of Mental Health. The true number is likely to be even higher, said Dr. Matthew Rudorfer, the institute’s associate director for treatment research, since men are less likely than women to report classic symptoms like low mood, sadness or crying, so they often go undiagnosed. Men, he told me, more often demonstrate “externalizing” symptoms like irritability, anger and aggressiveness, substance and alcohol abuse, risk-taking behaviors and “workaholism.” Oh, that macho thing: Men don’t get depressed; they just work, drink and compete harder. Andrew Solomon, author of the pathbreaking memoir about depression, “Noonday Demon,” told me that ridiculous attitude is part of the mind-set that guys should “cover up our moods with militarism or athleticism.” © 2016 The New York Times Company

Keyword: Depression
Link ID: 21874 - Posted: 02.09.2016

It’s well known that some people report that their mood is influenced by the seasons. But can the time of year affect other cognitive functions? To find out, Gilles Vandewalle and colleagues at the University of Liege in Belgium scanned the brains of 28 volunteers while they performed attention and working memory tests at different times of the year. To ensure the results were influenced by the seasons rather than the environmental conditions on the test day, the participants were confined to a lab for 4.5 days prior to the test, exposed to a constant light level and temperature. Although their test scores didn’t change with the seasons, activity in some brain areas showed a consistent seasonal pattern among the volunteers: brain activity peaked in the summer on the attention task and in the autumn on the memory task. Many seasonally changing factors could regulate such a pattern, including day length (known as photoperiod), temperature, humidity, social interaction and physical activity. Since these weren’t all controlled for in the study, it’s impossible to say what is responsible for the seasonal changes seen. “In our data it seems that photoperiod, or the rate of change of photoperiod, was more likely to explain what we were seeing. But we can’t exclude all the others,” says Vandewalle. The results suggest that over the course of a year, the brain might work in different ways to compensate for seasonal factors that could affect its function, enabling it to maintain a stable performance. Vandewalle speculates that these mechanisms might not work as well in some people, for example, those vulnerable to the winter blues. © Copyright Reed Business Information Ltd.

Keyword: Depression; Learning & Memory
Link ID: 21872 - Posted: 02.09.2016

By Jonathan Leo Last week, according to many media accounts, scientists from Harvard Medical School, Boston Children’s Hospital, and the Broad Institute discovered the genetic basis of schizophrenia. The researchers reported in Nature that people with schizophrenia were more likely to have the overactive forms of a gene called complement component 4, or C4, which is involved in pruning synapses during adolescence. However, suggesting a biologic mechanism for a small subset of those diagnosed with schizophrenia is not the same as confirming the genetic theory of schizophrenia. Benedict Carey, science reporter for the New York Times, delved into the details and reported the all-important fact that having the C4 variant would increase a person’s risk by about 25 percent over the 1-percent base rate of schizophrenia—that is, to 1.25 percent. Genes for schizophrenia and depression have been discovered before, and in those cases, the subsequent enthusiastic headlines were shortly followed by retractions and more sober thinking. There are so many open questions (for instance, why do many people with the problematic variant not develop schizophrenia, and why do many people who don’t have the variant develop schizophrenia?) that the same may occur with the C4 discovery. The idea that mental illness is the result of a genetic predisposition is the foundation for modern-day psychiatry and has been the driving force for how research money is allocated, how patients are treated, and how society views people diagnosed with conditions identified in the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition. Schizophrenia holds a unique spot in the annals of mental health research because of its perceived anatomical underpinnings and is often cited as evidence in favor of a genetic predisposition to other conditions.

Keyword: Schizophrenia; Genes & Behavior
Link ID: 21863 - Posted: 02.06.2016

By Diana Kwon Antidepressants are some of the most commonly prescribed medications out there. More than one out of 10 Americans over age 12—roughly 11 percent—take these drugs, according to a 2011 report by the National Center for Health Statistics. And yet, recent reports have revealed that important data about the safety of these drugs—especially their risks for children and adolescents—has been withheld from the medical community and the public. In the latest and most comprehensive analysis, published last week in BMJ (the British Medical Journal),a group of researchers at the Nordic Cochrane Center in Copenhagen showed that pharmaceutical companies were not presenting the full extent of serious harm in clinical study reports, which are detailed documents sent to regulatory authorities such as the U.S. Food and Drug Administration and the European Medicines Agency (EMA) when applying for approval of a new drug. The researchers examined documents from 70 double-blind, placebo-controlled trials of two common types of antidepressants—selective serotonin reuptake inhibitors (SSRI) and serotonin and norepinephrine reuptake inhibitors (SNRI)—and found that the occurrence of suicidal thoughts and aggressive behavior doubled in children and adolescents who used these medications. This paper comes on the heels of disturbing charges about conflicts of interest in reports on antidepressant trials. Last September a study published in the Journal of Clinical Epidemiology revealed that a third of meta-analyses of antidepressant studies were written by pharma employees and that these were 22 times less likely than other meta-studies to include negative statements about the drug. © 2016 Scientific American

Keyword: Depression
Link ID: 21860 - Posted: 02.04.2016

Heidi Ledford Difficulty with concentration, memory and other cognitive tasks is often associated with depression. In the past quarter of a century, a wave of drugs has transformed the treatment of depression. But the advances have struggled to come to grips with symptoms that often linger long after people start to feel better: cognitive problems such as memory loss and trouble concentrating. On 3 February, the US Food and Drug Administration (FDA) will convene a meeting of its scientific advisers to discuss whether such cognitive impairments are components of the disorder that drugs might be able to target — or just a result of depressed mood. The discussion will help the agency to decide whether two companies that sell the antidepressant vortioxetine should be allowed to label it as a treatment for the cognitive effects. A ‘yes’ could spur drug developers to invest in ways to test cognitive function during their antidepressant trials. Psychiatrists have long noted that some people with depression also struggle to concentrate and to make decisions. The question has been whether such difficulties are merely an offshoot of altered mood and would thus clear up without specific treatment, says Diego Pizzagalli, a neuroscientist at McLean Hospital, an affiliate of Harvard Medical School in Belmont, Massachusetts. But some patients who report improved mood after treatment still struggle with cognitive deficits — so psychiatrists sometimes prescribe concentration-enhancing drugs that are approved to treat attention deficit hyperactivity disorder to people with depression. © 2016 Nature Publishing Group

Keyword: Depression; Attention
Link ID: 21855 - Posted: 02.03.2016

By Sara Solovitch It was November 2012 when Dennis Hartman, a Seattle business executive, managed to pull himself out of bed, force himself to shower for the first time in days and board a plane that would carry him across the country to a clinical trial at the National Institute of Mental Health (NIMH) in Bethesda. After a lifetime of profound depression, 25 years of therapy and cycling through 18 antidepressants and mood stabilizers, Hartman, then 46, had settled on a date and a plan to end it all. This clinical trial would be his last stab at salvation. For 40 minutes, he sat in a hospital room as an IV drip delivered ketamine through his system. Several more hours passed before it occurred to him that all his thoughts of suicide had evaporated. “My life will always be divided into the time before that first infusion and the time after,” Hartman says today. “That sense of suffering and pain draining away. I was bewildered by the absence of pain.” Ketamine, popularly known as the psychedelic club drug Special K, has been around since the early 1960s. It is a staple anesthetic in emergency rooms, regularly used for children when they come in with broken bones and dislocated shoulders. It’s an important tool in burn centers and veterinary medicine, as well as a notorious date-rape drug, known for its power to quickly numb and render someone immobile.

Keyword: Depression; Drug Abuse
Link ID: 21846 - Posted: 02.02.2016

By BENEDICT CAREY A new approach to treating early schizophrenia, which includes family counseling, results in improvements in quality of life that make it worth the added expense, researchers reported on Monday. The study, published by the journal Schizophrenia Bulletin, is the first rigorous cost analysis of a federally backed treatment program that more than a dozen states have begun trying. In contrast to traditional outpatient care, which generally provides only services covered by insurance, like drugs and some psychotherapy, the new program offers other forms of support, such as help with jobs and school, as well as family counseling. The program also tries to include the patients — people struggling with a first psychotic “break” from reality, most of them in their late teens and 20s — as equals in decisions about care, including drug dosage. In a widely anticipated study last fall, called the Raise trial, researchers reported that after two years, people who got this more comprehensive care did better on a variety of measures than those who received the standard care. But the study found no evidence of related cost savings or differences in hospitalization rates, a prime driver of expense. As lawmakers in Washington are considering broad changes in mental health care, cost issues loom especially large. Outside experts said this analysis — which was based on the Raise trial data — was an important test of the new care program’s value. “This is the way cost analysis should be done,” Sherry Glied, a professor of public service and the dean of New York University’s graduate school of public service, said. “One way to think about it is to ask, if this program were a drug, would we pay for it? And the answer is yes.” © 2016 The New York Times Company

Keyword: Schizophrenia
Link ID: 21842 - Posted: 02.01.2016

By CHARLES SIEBERT Nearly 30 years ago, Lilly Love lost her way. She had just completed her five-year tour of duty as an Alaska-based Coast Guard helicopter rescue swimmer, one of an elite team of specialists who are lowered into rough, frigid seas to save foundering fishermen working in dangerous conditions. The day after she left active service, the helicopter she had flown in for the previous three years crashed in severe weather into the side of a mountain, killing six of her former crewmates. Devastated by the loss and overcome with guilt, Love chose as her penance to become one of the very fishermen she spent much of her time in the Coast Guard rescuing. In less than a year on the job, she nearly drowned twice after being dragged overboard in high seas by the hooks of heavy fishing lines. Love would not formally receive a diagnosis of severe post-traumatic stress disorder for another 15 years. In that time, she was married and divorced three times, came out as transgender and retreated periodically to Yelapa, Mexico, where she lived in an isolated cabin accessible only by water. She eventually ended up living on a boat in a Los Angeles marina, drinking heavily and taking an array of psychotropic drugs that doctors at the West Los Angeles Veterans Administration Medical Center began to prescribe with increasing frequency as Love proved resistant to traditional treatments like counseling and group therapy. One night, after her fifth stay in the center’s psych ward, she crashed her boat into a sea wall. Finally, in 2006, she was in the veterans’ garden and happened to catch sight of the parrots being housed in an unusual facility that opened a year earlier on the grounds of the center. ‘‘This place is why I’m still here,’’ Love, now 54, told me one day last summer as I watched her undergo one of her daily therapy sessions at the facility, known as Serenity Park, a name that would seem an utter anomaly to anyone who has ever been within 200 yards of the place. © 2016 The New York Times Company

Keyword: Stress
Link ID: 21839 - Posted: 01.30.2016

By BENEDICT CAREY Scientists reported on Wednesday that they had taken a significant step toward understanding the cause of schizophrenia, in a landmark study that provides the first rigorously tested insight into the biology behind any common psychiatric disorder. More than two million Americans have a diagnosis of schizophrenia, which is characterized by delusional thinking and hallucinations. The drugs available to treat it blunt some of its symptoms but do not touch the underlying cause. The finding, published in the journal Nature, will not lead to new treatments soon, experts said, nor to widely available testing for individual risk. But the results provide researchers with their first biological handle on an ancient disorder whose cause has confounded modern science for generations. The finding also helps explain some other mysteries, including why the disorder often begins in adolescence or young adulthood. “They did a phenomenal job,” said David B. Goldstein, a professor of genetics at Columbia University who has been critical of previous large-scale projects focused on the genetics of psychiatric disorders. “This paper gives us a foothold, something we can work on, and that’s what we’ve been looking for now, for a long, long time.” The researchers pieced together the steps by which genes can increase a person’s risk of developing schizophrenia. That risk, they found, is tied to a natural process called synaptic pruning, in which the brain sheds weak or redundant connections between neurons as it matures. During adolescence and early adulthood, this activity takes place primarily in the section of the brain where thinking and planning skills are centered, known as the prefrontal cortex. People who carry genes that accelerate or intensify that pruning are at higher risk of developing schizophrenia than those who do not, the new study suggests. Some researchers had suspected that the pruning must somehow go awry in people with schizophrenia, because previous studies showed that their prefrontal areas tended to have a diminished number of neural connections, compared with those of unaffected people. © 2016 The New York Times Company

Keyword: Schizophrenia; Genes & Behavior
Link ID: 21835 - Posted: 01.28.2016

Angus Chen When she was 22, Rachel Star Withers uploaded a video to YouTube called "Normal: Living With Schizophrenia." It starts with her striding across her family's property in Fort Mill, S.C. She looks across the rolling grounds, unsmiling. Her eyes are narrow and grim. She sits down in front of a deserted white cottage and starts sharing. "I see monsters. I see myself chopped up and bloody a lot. Sometimes I'll be walking, and the whole room will just tilt. Like this," she grasps the camera and jerks the frame crooked. She surfaces a fleeting grin. "Try and imagine walking." She becomes serious again. "I'm making this because I don't want you to feel alone whether you're struggling with any kind of mental illness or just struggling." At the time, 2008, there were very few people who had done anything like this online. "As I got diagnosed [with schizophrenia], I started researching everything. The only stuff I could find was like every horror movie," she says. "I felt so alone for years." She decided that schizophrenia was really not that scary. "I want people to find me and see a real person." Over the past eight years, she has made 53 videos documenting her journey with schizophrenia and depression and her therapy. And she is not the only one. There are hundreds of videos online of people publicly sharing their experiences with mental illness. © 2016 npr

Keyword: Schizophrenia
Link ID: 21834 - Posted: 01.28.2016

Heidi Ledford Addie plays hard for an 11-year-old greater Swiss mountain dog — she will occasionally ignore her advanced years to hurl her 37-kilogram body at an unwitting house guest in greeting. But she carries a mysterious burden: when she was 18 months old, she started licking her front legs aggressively enough to wear off patches of fur and draw blood. Addie has canine compulsive disorder — a condition that is thought to be similar to human obsessive–compulsive disorder (OCD). Canine compulsive disorder can cause dogs to chase their tails for hours on end, or to suck on a toy or body part so compulsively that it interferes with their eating or sleeping. Addie may soon help researchers to determine why some dogs are more prone to the disorder than others. Her owner, Marjie Alonso of Somerville, Massachusetts, has enrolled her in a project called Darwin’s Dogs, which aims to compare information about the behaviour of thousands of dogs against the animals’ DNA profiles. The hope is that genetic links will emerge to conditions such as canine compulsive disorder and canine cognitive dysfunction — a dog analogue of dementia and possibly Alzheimer’s disease. The project organizers have enrolled 3,000 dogs so far, but hope to gather data from at least 5,000, and they expect to begin analysing DNA samples in March. “It’s very exciting, and in many ways it’s way overdue,” says Clive Wynne, who studies canine behaviour at Arizona State University in Tempe. © 2016 Nature Publishing Group,

Keyword: OCD - Obsessive Compulsive Disorder; Genes & Behavior
Link ID: 21833 - Posted: 01.28.2016

By Ellen Hendriksen This topic comes by request on the Savvy Psychologist Facebook page from listener Anita M. of Detroit. Anita works with foster kids and, too often, sees disadvantaged kids who have been on a cocktail of psychiatric medications from as early as age 6. She asks, does such early use alter a child’s brain or body? And have the effects of lifelong psychiatric medication been studied? Childhood mental illness (and resulting medication) is equally overblown and under-recognized. Approximately 21% of American kids - that’s 1 in 5 - will battle a diagnosable mental illness before they reach the age of 17, whether or not they actually get treatment. The problem is anything but simple. Some childhood illnesses - ADHD and autism, for example - often get misused as “grab-bag” diagnoses when something’s wrong but no one knows what. This leads to overdiagnosis and sometimes, overmedicating. Other illnesses, like substance abuse, get overlooked or written off as rebellion or experimentation, leading to underdiagnosis and kids slipping through the cracks. But the most common problem is inconsistent diagnosis. For example, a 2008 study found that fewer than half of individuals diagnosed with bipolar disorder actually had the illness, while 5% of those diagnosed with something completely different actually had bipolar disorder. But let’s get back to Anita’s questions: Does early psychotropic medication alter a child’s brain? The short answer is yes, but the long answer might be different than you think. © 2016 Scientific American

Keyword: ADHD; Schizophrenia
Link ID: 21831 - Posted: 01.28.2016