Richard A. Friedman: Why can’t doctors identify killers?

MASS killers like Elliot Rodger teach society all the wrong lessons about the connection between violence, mental illness and guns — and what we should do about it. One of the biggest misconceptions, pushed by our commentators and politicians, is that we can prevent these tragedies if we improve our mental health care system. It is a comforting notion, but nothing could be further from the truth.

And although the intense media attention might suggest otherwise, mass killings — when four or more people are killed at once — are very rare events. In 2012, they accounted for only about 0.15 percent of all homicides in the United States. Because of their horrific nature, however, they receive lurid media attention that distorts the public’s perception about the real risk posed by the mentally ill.

Anyone who watched Elliot Rodger’s chilling YouTube video, detailing his plan for murderous vengeance before he killed six people last week near Santa Barbara, Calif., would understandably conflate madness with violence. While it is true that most mass killers have a psychiatric illness, the vast majority of violent people are not mentally ill and most mentally ill people are not violent. Indeed, only about 4 percent of overall violence in the United States can be attributed to those with mental illness. Most homicides in the United States are committed by people without mental illness who use guns.

Mass killers are almost always young men who tend to be angry loners. They are often psychotic, seething with resentment and planning revenge for perceived slights and injuries. As a group, they tend to avoid contact with the mental health care system, so it’s tough to identify and help them. Even when they have received psychiatric evaluation and treatment, as in the case of Mr. Rodger and Adam Lanza, who killed 20 children and seven adults, including his mother, in Connecticut in 2012, we have to acknowledge that our current ability to predict who is likely to be violent is no better than chance.

Large epidemiologic studies show that psychiatric illness is a risk factor for violent behavior, but the risk is small and linked only to a few serious mental disorders. People with schizophrenia, major depression or bipolar disorder were two to three times as likely as those without these disorders to be violent. The actual lifetime prevalence of violence among people with serious mental illness is about 16 percent compared with 7 percent among people who are not mentally ill.

What most people don’t know is that drug and alcohol abuse are far more powerful risk factors for violence than other psychiatric illnesses. Individuals who abuse drugs or alcohol but have no other psychiatric disorder are almost seven times more likely than those without substance abuse to act violently.

As a psychiatrist, I welcome calls from our politicians to improve our mental health care system. But even the best mental health care is unlikely to prevent these tragedies.

If we can’t reliably identify people who are at risk of committing violent acts, then how can we possibly prevent guns from falling into the hands of those who are likely to kill? Mr. Rodger had no problem legally buying guns because he had neither been institutionalized nor involuntarily hospitalized, both of which are generally factors that would have prevented him from purchasing firearms.

Would lowering the threshold for involuntary psychiatric treatment, as some argue, be effective in preventing mass killings or homicide in general?

It’s doubtful.

The current guideline for psychiatric treatment over the objection of the patient is, in most states, imminent risk of harm to self or others. Short of issuing a direct threat of violence or appearing grossly disturbed, you will not receive involuntary treatment. When Mr. Rodger was interviewed by the police after his mother expressed alarm about videos he had posted, several weeks ago, he appeared calm and in control and was thus not apprehended. In other words, a normal-appearing killer who is quietly planning a massacre can easily evade detection.

In the wake of these horrific killings, it would be understandable if the public wanted to make it easier to force treatment on patients before a threat is issued. But that might simply discourage other mentally ill people from being candid and drive some of the sickest patients away from the mental health care system.

We have always had — and always will have — Adam Lanzas and Elliot Rodgers. The sobering fact is that there is little we can do to predict or change human behavior, particularly violence; it is a lot easier to control its expression, and to limit deadly means of self-expression. In every state, we should prevent individuals with a known history of serious psychiatric illness or substance abuse, both of which predict increased risk of violence, from owning or purchasing guns.

But until we make changes like that, the tragedy of mass killings will remain a part of American life.

Richard A. Friedman is a professor of clinical psychiatry and the director of the psychopharmacology clinic at the Weill Cornell Medical College.

Protecting new neurons reduces depression caused by stress, and may lead to a new class of molecules to treat depression.

Scientists probing the link between depression and a hormone that controls hunger have found that the hormone’s antidepressant activity is due to its ability to protect newborn neurons in a part of the brain that controls mood, memory, and complex eating behaviors. Moreover, the researchers also showed that a new class of neuroprotective molecules achieves the same effect by working in the same part of the brain, and may thus represent a powerful new approach for treating depression.

“Despite the availability of many antidepressant drugs and other therapeutic approaches, major depression remains very difficult to treat,” says Andrew Pieper, associate professor of psychiatry and neurology at the University of Iowa Carver College of Medicine and Department of Veterans Affairs, and co-senior author of the study.

In the new study, Pieper and colleagues from University of Texas Southwestern Medical Center led by Jeffrey Zigman, associate professor of internal medicine and psychiatry at UT Southwestern, focused on understanding the relationship between depression, the gut hormone ghrelin, and the survival of newborn neurons in the hippocampus, the brain region involved in mood, memory, and eating behaviors.

“Not only did we demonstrate that the P7C3 compounds were able to block the exaggerated stress-induced depression experienced by mice lacking ghrelin receptors, but we also showed that a more active P7C3 analog was able to complement the antidepressant effect of ghrelin in normal mice, increasing the protection against depression caused by chronic stress in these animals,” Zigman explains.

“The P7C3 compounds showed potent antidepressant activity that was based on their neurogenesis-promoting properties,” Pieper adds. “Another exciting finding was that our experiments showed that the highly active P7C3 analog acted more rapidly and was more effective [at enhancing neurogenesis] than a wide range of currently available antidepressant drugs.”

The findings suggest that P7C3-based compounds may represent a new approach for treating depression. Drugs based on P7C3 might be particularly helpful for treating depression associated with chronic stress and depression associated with a reduced response to ghrelin activity, which may occur in conditions such as obesity and anorexia nervosa.

Future studies, including clinical trials, will be needed to investigate whether the findings are applicable to other forms of depression, and determine whether the P7C3 class will have antidepressant effects in people with major depression.

The hippocampus is one of the few regions in the adult brain where new neurons are continually produced – a process known as neurogenesis. Certain neurological diseases, including depression, interfere with neurogenesis by causing death of these new neurons, leading to a net decrease in the number of new neurons produced in the hippocampus.

Ghrelin, which is produced mainly by the stomach and is best known for its ability to stimulate appetite, also acts as a natural antidepressant. During chronic stress, ghrelin levels rise and limit the severity of depression caused by long-term stress. When mice that are unable to respond to ghrelin experience chronic stress they have more severe depression than normal mice.

In the new study, Pieper and Zigman’s team showed that disrupted neurogenesis is a contributing cause of depression induced by chronic stress, and that ghrelin’s antidepressant effect works through the hormone’s ability to enhance neurogenesis in the hippocampus. Specifically, ghrelin helps block the death of these newborn neurons that otherwise occurs with depression-inducing stress. Importantly, the study also shows that the new “P7C3-class” of neuroprotective compounds, which bolster neurogenesis in the hippocampus, are powerful, fast-acting antidepressants in an animal model of stress-induced depression. The results were published online April 22 in the journal Molecular Psychiatry.

Potential for new antidepressant drugs

The neuroprotective compounds tested in the study were discovered about eight years ago by Pieper, then at UT Southwestern Medical Center, and colleagues there, including Steven McKnight and Joseph Ready. The root compound, known as P7C3, and its analogs protect newborn neurons from cell death, leading to an overall increase in neurogenesis. These compounds have already shown promising neuroprotective effects in models of neurodegenerative disease, including Parkinson’s disease, amyotrophic lateral sclerosis (ALS), and traumatic brain injury. In the new study, the team investigated whether the neuroprotective P7C3 compounds would reduce depression in mice exposed to chronic stress, by enhancing neurogenesis in the hippocampus.

http://now.uiowa.edu/2014/04/protecting-new-neurons-reduces-depression-caused-stress

When doctors prescribe books to heal the mind

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By Leah Price

More than 350 million people worldwide suffer from depression. Fewer than half receive any treatment; even fewer have access to psychotherapy. Around the turn of the millennium, antidepressants became the most prescribed kind of drug in the United States. In the United Kingdom, 1 in 6 adults has taken one.

But what if a scientist were to discover a treatment that required minimal time and training to administer, and didn’t have the side effects of drugs? In 2003, a psychiatrist in Wales became convinced that he had. Dr. Neil Frude noticed that some patients, frustrated by year-long waits for treatment, were reading up on depression in the meantime. And of the more than 100,000 self-help books in print, a handful often seemed to work.

This June, a program was launched that’s allowing National Health Service doctors across England to act upon Frude’s insight. The twist is that the books are not just being recommended, they’re being “prescribed.” If your primary care physician diagnoses you with “mild to moderate” depression, one of her options is now to scribble a title on a prescription pad. You take the torn-off sheet not to the pharmacy but to your local library, where it can be exchanged for a copy of “Overcoming Depression,” “Mind Over Mood,” or “The Feeling Good Handbook.” And depression is only one of over a dozen conditions treated. Other titles endorsed by the program include “Break Free from OCD,” “Feel the Fear and Do it Anyway,” “Getting Better Bit(e) by Bit(e),” and “How to Stop Worrying.”

The NHS’s Books on Prescription program is only the highest-profile example of a broader boom in “bibliotherapy.” The word is everywhere in Britain this year, although—or because—it means different things to different people. In London, a painter, a poet, and a former bookstore manager have teamed up to offer over-the-counter “bibliotherapy consultations”: after being quizzed about their literary tastes and personal problems, the worried well-heeled pay 80 pounds for a customized reading list. At the Reading Agency, a charity that developed and administers Books on Prescription, a second program called Mood-Boosting Books recommends fiction and poetry. The NHS’s public health and mental health budgets also fund nonprofits such as The Reader Organization, which gathers people who are unemployed, imprisoned, old, or just lonely to read poems and fiction aloud to one another.

At best, Books on Prescription looks like a win-win for both patients and book lovers. It boosts mental health while also bringing new library users in the door. Libraries loaned out NHS-approved self-help books 100,000 times in the first three months of the program; no doubt some of their borrowers must have picked up a novel or a memoir en route to the circulation desk. At worst, it’s hard to see what harm the program can do. Unlike drugs, books carry no risk of side effects like weight gain, dampened libido, or nausea (unless you read in the car).

For book lovers, an organization with as much clout as the NHS would seem to be a welcome ally. Yet its initiatives raise troubling questions about why exactly a society should value reading. What’s lost when a bookshelf is repurposed as a medicine cabinet—and when a therapist’s job gets outsourced to the page?

In 1916, the clergyman Samuel Crothers coined the term “bibliotherapy,” positing tongue-in-cheek that “a book may be a stimulant or a sedative or an irritant or a soporific.” In the intervening century, doctors, nurses, librarians, and social workers have more seriously championed “bibliopathy,” “bibliocounseling,” “biblioguidance,” and “literatherapy”—all variations on the notion that reading can heal.

Only recently, however, have the mental health effects of one genre—self-help books—been rigorously studied. As early as 1997, a randomized trial found bibliotherapy supervised by therapists no less effective in treating unipolar depression than individual or group therapy. More surprisingly, a 2007 literature review by the same researcher found that books treated anxiety just as effectively without a therapist’s guidance as with it. A 2004 meta-analysis comparing bibliotherapy for anxiety and depression to short-term talk therapy found books “as effective as professional treatment of relatively short duration.”

None of this means a book can outperform a therapist, even if it can underbid him. A 2012 meta-analysis of anxiety disorders concluding that “comparing self-help with waiting list gave a significant effect size of 0.84 in favour of self-help” nevertheless cautioned that “comparison of self-help with therapist-administered treatments revealed a significant difference in favour of the latter.” Translation: A book does worse than a therapist, but it’s better than nothing. And in the short term, at least, nothing is what many patients get.

Books on Prescription can be understood as an extension of larger changes in psychiatry over the past few decades. For most of the 20th century, psychodynamic therapy placed more emphasis on the therapist-patient relationship than on the content of the therapist’s words. More recently, insurers’ interest in cutting costs and researchers’ interest in protocols that can be measured and replicated have combined to nudge treatment toward short-term, standardized methods such as cognitive-behavioral therapy. Books take this trajectory to its logical conclusion. If your aim is less to help patients explore the underlying causes of their condition than to offer step-by-step instructions for managing it, then who cares whether the exercises emanate from a mouth, a manual, or even a smartphone app?

But even therapies like cognitive-behavioral therapy require the patient to feel recognized and understood by another human being. Asked how a printed page can mimic that face-to-face encounter, Frude comes up with an unexpected word: “magic.” The best books give the illusion of listening and caring, he explains, because authors who are also clinicians can draw on years of experience interacting with patients to leave each reader saying “that book was about me.” He does acknowledge that not every case fits books “off the peg” (or off the rack, as we say in the United States). But it’s a striking metaphor to choose—one that makes psychodynamic therapy sound like a luxury good as unattainable as Savile Row tailoring.

Where Frude sees magic, a cynic might smell pragmatism. Even short-term cognitive-behavioral therapy costs more than a $24.95 hardcover. But in any case, many patients read whether or not they have the NHS’s blessing. If recommended titles crowd out the misinformation that patients might otherwise stumble upon, whether in print or online, Books on Prescription will already have helped.

It’s hard not to notice that Books on Prescription was developed in the same years when American universities began to offer MOOCs, or massive open online courses. Even if an online course lacks the give-and-take of a seminar, it’s better than nothing. Like Books on Prescription, MOOCs scale up an activity whose face-to-face version was traditionally out of reach of the masses. Also like Books on Prescription, MOOCs create a cost-effective alternative that may eventually squeeze out personal contact even at the high end of the market.

That concern aside, it’s no surprise that self-help books can help the self. That literature might help, however, is a more controversial proposition. The other half of the Reading Agency’s two-pronged Reading Well initiative, Mood-Boosting Books, promotes fiction, poetry, and memoirs. Its annual list of “good reads for people who are anxious or depressed” mixes titles that represent characters experiencing anxiety or depression (Mark Haddon’s “A Spot of Bother”) with others calculated to combat those conditions. Some go for laughs (Sue Townsend’s “The Secret Diary of Adrian Mole Aged 13¾”); others, such as “A Street Cat Named Bob” and “The Bad Dog’s Diary,” read like printouts of PetTube.com. Others are darker and more demanding: Reading Well anointed Alice Munro’s short stories as a selection before the Nobel Prize Committee did.

The Reading Agency’s endorsement of imaginative reading stops short of recommending specific titles. Its website bristles with disclaimers that the works of literature are nominated by reading groups rather than tested by scientists. Yet the charity has given Mood-Boosting Books prestige—and the NHS has put hard cash behind them as well, providing some libraries with grants to purchase the recommended works of literature along with the “prescribed” self-help titles.

I ask Judith Shipman, who runs the Mood-Boosting Books program, whether recommending books “for people who are anxious or depressed” implies that poems or novels can treat those conditions. “I don’t think we could claim that they are therapy or a substitute for therapy,” she hazards after a long pause. “But for those who don’t quite need therapy, Mood-Boosting Books could be a nice little lift.”

Today it might seem commonplace to suggest that books are good for you. In the longer view, though, the hope that both literature and practical nonfiction can cure reverses an older belief by doctors that reading could cause physical and mental illness. In 1867, one expert cautioned that taking a book to bed could “injure your eyes, your brain, your nervous system.” Some social reformers proposed regulating books as if they were drugs. In 1883, the New York State Legislature debated whether to fine “any person who shall sell, loan, or give to any minor under sixteen years of age any dime novel or book of fiction, without first obtaining the written consent of the parent or guardian of such a minor.” As late as 1889, one politician called fiction “moral poison.”

As radio, TV, gaming, and eventually the Internet began to compete with books, though, fiction-reading came to look wholesome by comparison. Today, with only half of Americans reading any book for pleasure in a given year, reading is finding new champions from an unlikely quarter: science. This year, Science published a study concluding that reading about fictional characters increases empathy; in his 2011 book “The Better Angels of Our Nature,” the psychologist Steven Pinker correlated the rise of imaginative literature with a centuries-long decline in violence. And while correlation doesn’t imply causation, randomized trials have also attempted to link fiction-reading to physical health. In a 2008 study of 81 preteens, girls assigned fiction in which characters eat balanced breakfasts ended up with a lower body mass index than the control group. The Reading Well website itself cites a 2009 study that compared heart rates and muscle tension before and after various activities and found that reading is “68% better at reducing stress levels than listening to music; 100% more effective than drinking a cup of tea.” The numbers may be less telling than the fact that someone would think to compare books to tea in the first place.

It’s too early to predict the long-term effects of bibliotherapy programs. There’s little precedent for a government to make neuroscientists and psychiatrists the arbiters of what books should be read and why. And literary critics like me recoil from reducing the value of reading to a set of health metrics. But as library budgets shrink and any text longer than 140 characters gets crowded out by audio and video, white-coated experts may be the only ones prospective readers can hear. Racing to find out what happens next, seeing the world through a character’s eyes, wallowing in the play of language—all are becoming means to medical ends. Today, for an increasing number of people, the pleasures of reading require a doctor’s note.

http://www.bostonglobe.com/ideas/2013/12/22/when-doctors-prescribe-books-heal-mind/H2mbhLnTJ3Gy96BS8TUgiL/story.html

‘Jumping Genes’ Linked to Schizophrenia

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Roaming bits of DNA that can relocate and proliferate throughout the genome, called “jumping genes,” may contribute to schizophrenia, a new study suggests. These rogue genetic elements pepper the brain tissue of deceased people with the disorder and multiply in response to stressful events, such as infection during pregnancy, which increase the risk of the disease. The study could help explain how genes and environment work together to produce the complex disorder and may even point to ways of lowering the risk of the disease, researchers say.

Schizophrenia causes hallucinations, delusions, and a host of other cognitive problems, and afflicts roughly 1% of all people. It runs in families—a person whose twin sibling has the disorder, for example, has a roughly 50-50 chance of developing it. Scientists have struggled to define which genes are most important to developing the disease, however; each individual gene associated with the disorder confers only modest risk. Environmental factors such as viral infections before birth have also been shown to increase risk of developing schizophrenia, but how and whether these exposures work together with genes to skew brain development and produce the disease is still unclear, says Tadafumi Kato, a neuroscientist at the RIKEN Brain Science Institute in Wako City, Japan and co-author of the new study.

Over the past several years, a new mechanism for genetic mutation has attracted considerable interest from researchers studying neurological disorders, Kato says. Informally called jumping genes, these bits of DNA can replicate and insert themselves into other regions of the genome, where they either lie silent, doing nothing; start churning out their own genetic products; or alter the activity of their neighboring genes. If that sounds potentially dangerous, it is: Such genes are often the culprits behind tumor-causing mutations and have been implicated in several neurological diseases. However, jumping genes also make up nearly half the current human genome, suggesting that humans owe much of our identity to their audacious leaps.

Recent research by neuroscientist Fred Gage and colleagues at the University of California (UC), San Diego, has shown that one of the most common types of jumping gene in people, called L1, is particularly abundant in human stem cells in the brain that ultimately differentiate into neurons and plays an important role in regulating neuronal development and proliferation. Although Gage and colleagues have found that increased L1 is associated with mental disorders such as Rett syndrome, a form of autism, and a neurological motor disease called Louis-Bar syndrome, “no one had looked very carefully” to see if the gene might also contribute to schizophrenia, he says.

To investigate that question, principal investigator Kazuya Iwamoto, a neuroscientist; Kato; and their team at RIKEN extracted brain tissue of deceased people who had been diagnosed with schizophrenia as well as several other mental disorders, extracted DNA from their neurons, and compared it with that of healthy people. Compared with controls, there was a 1.1-fold increase in L1 in the tissue of people with schizophrenia, as well as slightly less elevated levels in people with other mental disorders such as major depression, the team reports today in Neuron.

Next, the scientists tested whether environmental factors associated with schizophrenia could trigger a comparable increase in L1. They injected pregnant mice with a chemical that simulates viral infection and found that their offspring did, indeed, show higher levels of the gene in their brain tissue. An additional study in infant macaques, which mimicked exposure to a hormone also associated with increased schizophrenia risk, produced similar results. Finally, the group examined human neural stem cells extracted from people with schizophrenia and found that these, too, showed higher levels of L1.

The fact that it is possible to increase the number of copies of L1 in the mouse and macaque brains using established environmental triggers for schizophrenia shows that such genetic mutations in the brain may be preventable if such exposures can be avoided, Kato says. He says he hopes that the “new view” that environmental factors can trigger or deter genetic changes involved in the disease will help remove some of the disorder’s stigma.

Combined with previous studies on other disorders, the new study suggests that L1 genes are indeed more active in the brain of patients with neuropsychiatric diseases, Gage says. He cautions, however, that no one yet knows whether they are actually causing the disease. “Now that we have multiple confirmations of this occurring in humans with different diseases, the next step is to determine if possible what role, if any, they play.”

One tantalizing possibility is that as these restless bits of DNA drift throughout the genomes of human brain cells, they help create the vibrant cognitive diversity that helps humans as a species respond to changing environmental conditions, and produces extraordinary “outliers,” including innovators and geniuses such as Picasso, says UC San Diego neuroscientist Alysson Muotri. The price of such rich diversity may be that mutations contributing to mental disorders such as schizophrenia sometimes emerge. Figuring out what these jumping genes truly do in the human brain is the “next frontier” for understanding complex mental disorders, he says. “This is only the tip of the iceberg.”

Thanks to Dr. Rajadhyaksha for bringing this to the attention of the It’s Interesting community.

http://news.sciencemag.org/biology/2014/01/jumping-genes-linked-schizophrenia

New research shows that sleep functions to allow the brain to eliminate toxins that accumulate while we are awake

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While the brain sleeps, it clears out harmful toxins, a process that may reduce the risk of Alzheimer’s, researchers say.

During sleep, the flow of cerebrospinal fluid in the brain increases dramatically, washing away harmful waste proteins that build up between brain cells during waking hours, a study of mice found.

“It’s like a dishwasher,” says Dr. Maiken Nedergaard, a professor of neurosurgery at the University of Rochester and an author of the study in Science.

The results appear to offer the best explanation yet of why animals and people need sleep. If this proves to be true in humans as well, it could help explain a mysterious association between sleep disorders and brain diseases, including Alzheimer’s.

Nedergaard and a team of scientists discovered the cleaning process while studying the brains of sleeping mice. The scientists noticed that during sleep, the system that circulates cerebrospinal fluid through the brain and nervous system was “pumping fluid into the brain and removing fluid from the brain in a very rapid pace,” Nedergaard says.

The team discovered that this increased flow was possible in part because when mice went to sleep, their brain cells actually shrank, making it easier for fluid to circulate. When an animal woke up, the brain cells enlarged again and the flow between cells slowed to a trickle. “It’s almost like opening and closing a faucet,” Nedergaard says. “It’s that dramatic.”

Nedergaard’s team, which is funded by the National Institute of Neurological Disorders and Stroke, had previously shown that this fluid was carrying away waste products that build up in the spaces between brain cells.

The process is important because what’s getting washed away during sleep are waste proteins that are toxic to brain cells, Nedergaard says. This could explain why we don’t think clearly after a sleepless night and why a prolonged lack of sleep can actually kill an animal or a person, she says.

So why doesn’t the brain do this sort of housekeeping all the time? Nedergaard thinks it’s because cleaning takes a lot of energy. “It’s probably not possible for the brain to both clean itself and at the same time [be] aware of the surroundings and talk and move and so on,” she says.

The brain-cleaning process has been observed in rats and baboons, but not yet in humans, Nedergaard says. Even so, it could offer a new way of understanding human brain diseases including Alzheimer’s. That’s because one of the waste products removed from the brain during sleep is beta amyloid, the substance that forms sticky plaques associated with the disease.

That’s probably not a coincidence, Nedergaard says. “Isn’t it interesting that Alzheimer’s and all other diseases associated with dementia, they are linked to sleep disorders,” she says.

Researchers who study Alzheimer’s say Nedergaard’s research could help explain a number of recent findings related to sleep. One of these involves how sleep affects levels of beta amyloid, says Randall Bateman, a professor of neurology Washington University in St. Louis who wasn’t involved in the study.

“Beta amyloid concentrations continue to increase while a person is awake,” Bateman says. “And then after people go to sleep that concentration of beta amyloid decreases. This report provides a beautiful mechanism by which this may be happening.”

The report also offers a tantalizing hint of a new approach to Alzheimer’s prevention, Bateman says. “It does raise the possibility that one might be able to actually control sleep in a way to improve the clearance of beta amyloid and help prevent amyloidosis that we think can lead to Alzheimer’s disease.”

http://www.npr.org/blogs/health/2013/10/17/236211811/brains-sweep-themselves-clean-of-toxins-during-sleep

http://m.sciencemag.org/content/342/6156/373.abstract

Thanks to Kebmodee for bringing this to the It’s Interesting community.

The Virtual Therapist

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Ellie is a creation of ICT, and could serve as an important diagnostic and therapeutic tool for veterans with Post-Traumatic Stress Disorder.

By Alastair Leithead
BBC News, Los Angeles

The University of Southern California’s Institute for Creative Technologies is leading the way in creating virtual humans. The result may produce real help for those in need.

The virtual therapist sits in a big armchair, shuffling slightly and blinking naturally, apparently waiting for me to get comfortable in front of the screen.

“Hi, I’m Ellie,” she says. “Thanks for coming in today.”

She laughs when I say I find her a little bit creepy, and then goes straight into questions about where I’m from and where I studied.

“I’m not a therapist, but I’m here to learn about people and would love to learn about you,” she asks. “Is that OK?”

Ellie’s voice is soft and calming, and as her questions grow more and more personal I quickly slip into answering as if there were a real person in the room rather than a computer-generated image.

“How are you at controlling your temper?” she probes. “When did you last get into an argument?”

With every answer I’m being watched and studied in minute detail by a simple gaming sensor and a webcam.

How I smile, which direction I look, the tone of my voice, and my body language are all being precisely recorded and analysed by the computer system, which then tells Ellie how best to interact with me.

“Wizard of Oz mode” is how researcher Louis-Philippe Morency describes this experiment at the University of Southern California’s Institute for Creative Technologies (ICT).

In the next room his team of two are controlling what Ellie says, changing her voice and body language to get the most out of me.

Real people come in to answer Ellie’s questions every day as part of the research, and the computer is gradually learning how to react in every situation.

It is being taught how to be human, and to respond as a doctor would to the patients’ cues.

Soon Ellie will be able to go it alone. That opens up a huge opportunity for remote therapy sessions online using the knowledge of some of the world’s top psychologists.

But Dr Morency doesn’t like the expression “virtual shrink”, and doesn’t think this method will replace flesh-and-blood practitioners.

“We see it more as being an assistant for the clinician in the same way you take a blood sample which is analysed in a lab and the results sent back to the doctor,” he said.

The system is designed to assess signs of depression or post-traumatic stress, particularly useful among soldiers and veterans.

“We’re looking for an emotional response, or perhaps even any lack of emotional response,” he says.

“Now we have an objective way to measure people’s behaviour, so hopefully this can be used for a more precise diagnosis.”

The software allows a doctor to follow a patient’s progress over time. It objectively and scientifically compares sessions.

“The problem we have, particularly with the current crisis in mental health in the military, is that we don’t have enough well trained providers to handle the problem,” says Skip Rizzo, the associate director for medical virtual reality at the ICT.

“This is not a replacement for a live provider, but it might be a stop-gap that helps to direct a person towards the kind of care they might need.”

The centre does a lot of work with the US military, which after long wars in Iraq and Afghanistan has to deal with hundreds of thousands of troops and veterans suffering from various levels of post-traumatic stress disorder.

“We have an issue in the military with stigma and a lot of times people feel hesitant talking about their problems,” he says. A virtual counselling tool can alleviate some of this reluctance.

“We see this as a way for service members or veterans to talk openly and explore their issues.”

The whole lab is running experiments with virtual humans. To do so, it blends a range of technologies and disciplines such as movement sensing and facial recognition.

Dr Morency has won awards for his work into the relationship between psychology and minute physical movements in the face.

“People who are anxious fidget with their hands more, and people who are distressed often have a shorter smile with less intensity. People who are depressed are looking away a lot more,” he says.

Making computer-generated images appear human isn’t easy, but if believable they can be powerful tools for teaching and learning. To that end, the lab is involved in several different projects to test the limits and potential of virtual interactions.

In the lab’s demonstration space a virtual soldier sits behind a desk and responds to a disciplinary scenario as part of officer training.

The team have even built a Wild West style saloon, complete with swinging doors and bar.

Full-size characters appear on three projection screens and interact with a real person walking in, automatically responding to questions and asking their own to play out a fictional scenario.

Downstairs, experiments are creating 3D holograms of a human face.

Throughout the building, the work done is starting to blur the lines between the real world and the virtual world.

And the result just may be real help for humans who need it.

http://www.bbc.co.uk/news/magazine-22630812

Many thanks to Jody, for bringing this to the attention of the It’s Interesting community.

US suicide rate has risen sharply among middle-aged white men and women

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The suicide rate among middle-aged Americans climbed a startling 28 percent in a decade, a period that included the recession and the mortgage crisis, the government reported Thursday. The trend was most pronounced among white men and women in that age group. Their suicide rate jumped 40 percent between 1999 and 2010. But the rates in younger and older people held steady. And there was little change among middle-aged blacks, Hispanics and most other racial and ethnic groups, the report from the Centers for Disease Control and Prevention found.

Why did so many middle-aged whites — that is, those who are 35 to 64 years old — take their own lives?

One theory suggests the recession caused more emotional trauma in whites, who tend not to have the same kind of church support and extended families that blacks and Hispanics do.

The economy was in recession from the end of 2007 until mid-2009. Even well afterward, polls showed most Americans remained worried about weak hiring, a depressed housing market and other problems.

Pat Smith, violence-prevention program coordinator for the Michigan Department of Community Health, said the recession — which hit manufacturing-heavy states particularly hard — may have pushed already-troubled people over the brink. Being unable to find a job or settling for one with lower pay or prestige could add “that final weight to a whole chain of events,” she said.

Another theory notes that white baby boomers have always had higher rates of depression and suicide, and that has held true as they’ve hit middle age. During the 11-year period studied, suicide went from the eighth leading cause of death among middle-aged Americans to the fourth, behind cancer, heart disease and accidents.

“Some of us think we’re facing an upsurge as this generation moves into later life,” said Dr. Eric Caine, a suicide researcher at the University of Rochester.

One more possible contributor is the growing sale and abuse of prescription painkillers over the past decade. Some people commit suicide by overdose. In other cases, abuse of the drugs helps put people in a frame of mind to attempt suicide by other means, said Thomas Simon, one of the authors of the CDC report, which was based on death certificates.

People ages 35 to 64 account for about 57 percent of suicides in the U.S.

The report contained surprising information about how middle-aged people kill themselves: During the period studied, hangings overtook drug overdoses in that age group, becoming the No. 2 manner of suicide. But guns remained far in the lead and were the instrument of death in nearly half of all suicides among the middle-aged in 2010.

The CDC does not collect gun ownership statistics and did not look at the relationship between suicide rates and the prevalence of firearms.

For the entire U.S. population, there were 38,350 suicides in 2010, making it the nation’s 10th leading cause of death, the CDC said. The overall national suicide rate climbed from 12 suicides per 100,000 people in 1999 to 14 per 100,000 in 2010. That was a 15 percent increase.

For the middle-aged, the rate jumped from about 14 per 100,000 to nearly 18 — a 28 percent increase. Among whites in that age group, it spiked from about 16 to 22.

Suicide prevention efforts have tended to concentrate on teenagers and the elderly, but research over the past several years has begun to focus on the middle-aged. The new CDC report is being called the first to show how the trend is playing out nationally and to look in depth at the racial and geographic breakdown.

Thirty-nine out of 50 states registered a statistically significant increase in suicide rates among the middle-aged. The West and the South had the highest rates. It’s not clear why, but one factor may be cultural differences in willingness to seek help during tough times, Simon said.

Also, it may be more difficult to find counseling and mental health services in certain places, he added.

Suicides among middle-aged Native Americans and Alaska Natives climbed 65 percent, to 18.5 per 100,000. However, the overall numbers remain very small — 171 such deaths in 2010. And changes in small numbers can look unusually dramatic.

The CDC did not break out suicides of current and former military service members, a tragedy that has been getting increased attention. But a recent Department of Veterans Affairs report concluded that suicides among veterans have been relatively stable in the past decade and that veterans have been a shrinking percentage of suicides nationally.

Thanks to Kebmodee for bringing this to the attention of the It’s Interesting community.

http://bigstory.ap.org/article/us-suicide-rate-rose-sharply-among-middle-aged

Our failed approach to treating schizophrenia

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By PAUL STEINBERG
Published: December 25, 2012
New York Times

TOO many pendulums have swung in the wrong directions in the United States. I am not referring only to the bizarre all-or-nothing rhetoric around gun control, but to the swing in mental health care over the past 50 years: too little institutionalizing of teenagers and young adults (particularly men, generally more prone to violence) who have had a recent onset of schizophrenia; too little education about the public health impact of untreated mental illness; too few psychiatrists to talk about and treat severe mental disorders — even though the medications available in the past 15 to 20 years can be remarkably effective.

Instead we have too much concern about privacy, labeling and stereotyping, about the civil liberties of people who have horrifically distorted thinking. In our concern for the rights of people with mental illness, we have come to neglect the rights of ordinary Americans to be safe from the fear of being shot — at home and at schools, in movie theaters, houses of worship and shopping malls.
“Psychosis” — a loss of touch with reality — is an umbrella term, not unlike “fever.” As with fevers, there are many causes, from drugs and alcohol to head injuries and dementias. The most common source of severe psychosis in young adults is schizophrenia, a badly named disorder that, in the original Greek, means “split mind.” In fact, schizophrenia has nothing to do with multiple personality, a disorder that is usually caused by major repeated traumas in childhood. Schizophrenia is a physiological disorder caused by changes in the prefrontal cortex, an area of the brain that is essential for language, abstract thinking and appropriate social behavior. This highly evolved brain area is weakened by stress, as often occurs in adolescence.

Psychiatrists and neurobiologists have observed biochemical changes and alterations in brain connections in patients with schizophrenia. For example, miscommunications between the prefrontal cortex and the language area in the temporal cortex may result in auditory hallucinations, as well as disorganized thoughts. When the voices become commands, all bets are off. The commands might insist, for example, that a person jump out of a window, even if he has no intention of dying, or grab a set of guns and kill people, without any sense that he is wreaking havoc. Additional symptoms include other distorted thinking, like the notion that something — even a spaceship, or a comic book character — is controlling one’s thoughts and actions.

Schizophrenia generally rears its head between the ages of 15 and 24, with a slightly later age for females. Early signs may include being a quirky loner — often mistaken for Asperger’s syndrome — but acute signs and symptoms do not appear until adolescence or young adulthood.

People with schizophrenia are unaware of how strange their thinking is and do not seek out treatment. At Virginia Tech, where Seung-Hui Cho killed 32 people in a rampage shooting in 2007, professors knew something was terribly wrong, but he was not hospitalized for long enough to get well. The parents and community-college classmates of Jared L. Loughner, who killed 6 people and shot and injured 13 others (including a member of Congress) in 2011, did not know where to turn. We may never know with certainty what demons tormented Adam Lanza, who slaughtered 26 people at an elementary school in Newtown, Conn., on Dec. 14, though his acts strongly suggest undiagnosed schizophrenia.

I write this despite the so-called Goldwater Rule, an ethical standard the American Psychiatric Association adopted in the 1970s that directs psychiatrists not to comment on someone’s mental state if they have not examined him and gotten permission to discuss his case. It has had a chilling effect. After mass murders, our airwaves are filled with unfounded speculations about video games, our culture of hedonism and our loss of religious faith, while psychiatrists, the ones who know the most about severe mental illness, are largely marginalized.

Severely ill people like Mr. Lanza fall through the cracks, in part because school counselors are more familiar with anxiety and depression than with psychosis. Hospitalizations for acute onset of schizophrenia have been shortened to the point of absurdity. Insurance companies and families try to get patients out of hospitals as quickly as possible because of the prohibitively high cost of care.

As documented by writers like the law professor Elyn R. Saks, author of the memoir “The Center Cannot Hold: My Journey Through Madness,” medication and treatment work. The vast majority of people with schizophrenia, treated or untreated, are not violent, though they are more likely than others to commit violent crimes. When treated with medication after a rampage, many perpetrators who have shown signs of schizophrenia — including John Lennon’s killer and Ronald Reagan’s would-be assassin — have recognized the heinousness of their actions and expressed deep remorse.

It takes a village to stop a rampage. We need reasonable controls on semiautomatic weapons; criminal penalties for those who sell weapons to people with clear signs of psychosis; greater insurance coverage and capacity at private and public hospitals for lengthier care for patients with schizophrenia; intense public education about how to deal with schizophrenia; greater willingness to seek involuntary commitment of those who pose a threat to themselves or others; and greater incentives for psychiatrists (and other mental health professionals) to treat the disorder, rather than less dangerous conditions.

Too many people with acute schizophrenia have gone untreated. There have been too many Glocks, too many kids and adults cut down in their prime. Enough already.

Paul Steinberg is a psychiatrist in private practice.

Thanks to David Frey for bringing this to the attention of the It’s Interesting community.