Archive for the ‘mental illness’ Category

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Psychedelic mushrooms can do more than make you see the world in kaleidoscope. Research suggests they may have permanent, positive effects on the human brain.

In fact, a mind-altering compound found in some 200 species of mushroom is already being explored as a potential treatment for depression and anxiety. People who consume these mushrooms, after “trips” that can be a bit scary and unpleasant, report feeling more optimistic, less self-centered, and even happier for months after the fact.

But why do these trips change the way people see the world? According to a study published today in Human Brain Mapping, the mushroom compounds could be unlocking brain states usually only experienced when we dream, changes in activity that could help unlock permanent shifts in perspective.

The study examined brain activity in those who’d received injections of psilocybin, which gives “shrooms” their psychedelic punch. Despite a long history of mushroom use in spiritual practice, scientists have only recently begun to examine the brain activity of those using the compound, and this is the first study to attempt to relate the behavioral effects to biological changes.

After injections, the 15 participants were found to have increased brain function in areas associated with emotion and memory. The effect was strikingly similar to a brain in dream sleep, according to Dr. Robin Carhart-Harris, a post-doctoral researcher in neuropsychopharmacology at Imperial College London and co-author of the study.

“You’re seeing these areas getting louder, and more active,” he said. “It’s like someone’s turned up the volume there, in these regions that are considered part of an emotional system in the brain. When you look at a brain during dream sleep, you see the same hyperactive emotion centers.”

In fact, administration of the drug just before or during sleep seemed to promote higher activity levels during Rapid Eye Movement sleep, when dreams occur. An intriguing finding, Carhart-Harris says, given that people tend to describe their experience on psychedelic drugs as being like “a waking dream.” It seems that the brain may literally be slipping into unconscious patterns while the user is awake.

Conversely, the subjects of the study had decreased activity in other parts of the brain—areas associated with high level cognition. “These are the most recent parts of our brain, in an evolutionary sense,” Carhart-Harris said. “And we see them getting quieter and less organized.”

This dampening of one area and amplification of another could explain the “mind-broadening” sensation of psychedelic drugs, he said. Unlike most recreational drugs, psychotropic mushrooms and LSD don’t provide a pleasant, hedonistic reward when they’re consumed. Instead, users take them very occasionally, chasing the strange neurological effects instead of any sort of high.

“Except for some naïve users who go looking for a good time…which, by the way, is not how it plays out,” Carhart-Harris said, “you see people taking them to experience some kind of mental exploration, and to try to understand themselves.”

Our firm sense of self—the habits and experiences that we find integral to our personality—is quieted by these trips. Carhart-Harris believes that the drugs may unlock emotion while “basically killing the ego,” allowing users to be less narrow-minded and let go of negative outlooks.

It’s still not clear why such effects can have more profound long-term effects on the brain than our nightly dreams. But Carhart-Harris hopes to see more of these compounds in modern medicine. “The way we treat psychological illnesses now is to dampen things,” he said. “We dampen anxiety, dampen ones emotional range in the hope of curing depression, taking the sting out of what one feels.”

But some patients seem to benefit from having their emotions “unlocked” instead. “It would really suit the style of psychotherapy where we engage in a patient’s history and hang-ups,” Carhart-Harris said. “Instead of putting a bandage over the exposed wound, we’d be essentially loosening their minds—promoting a permanent change in outlook.”

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

http://www.washingtonpost.com/news/to-your-health/wp/2014/07/03/psychedelic-drugs-put-your-brain-in-a-waking-dream-study-finds/

By Elizabeth Norton

A single dose of a century-old drug has eliminated autism symptoms in adult mice with an experimental form of the disorder. Originally developed to treat African sleeping sickness, the compound, called suramin, quells a heightened stress response in neurons that researchers believe may underlie some traits of autism. The finding raises the hope that some hallmarks of the disorder may not be permanent, but could be correctable even in adulthood.

That hope is bolstered by reports from parents who describe their autistic children as being caught behind a veil. “Sometimes the veil parts, and the children are able to speak and play more normally and use words that didn’t seem to be there before, if only for a short time during a fever or other stress” says Robert Naviaux, a geneticist at the University of California, San Diego, who specializes in metabolic disorders.

Research also shows that the veil can be parted. In 2007, scientists found that 83% of children with autism disorders showed temporary improvement during a high fever. The timing of a fever is crucial, however: A fever in the mother can confer a higher risk for the disorder in the unborn child.

As a specialist in the cell’s life-sustaining metabolic processes, Naviaux was intrigued. Autism is generally thought to result from scrambled signals at synapses, the points of contact between nerve cells. But given the specific effects of something as general as a fever, Naviaux wondered if the problem lay “higher up” in the cell’s metabolism.

To test the idea, he and colleagues focused on a process called the cell danger response, by which the cell protects itself from threats like infection, temperature changes, and toxins. As part of this strategy, Naviaux explains, “the cells behave like countries at war. They harden their borders. They don’t trust their neighbors.” If the cells in question are neurons, he says, disrupted communication could result—perhaps underlying the social difficulties; heightened sensitivity to sights, sounds, and sensations; and intolerance for anything new that often afflict patients with autism.

The key player may be ATP, the chief carrier of energy within a cell, which can also relay messages to other nearby cells. When too much ATP is released for too long, it can induce a hair-trigger cell danger response in neighboring neurons. In 2013, Naviaux spelled out his hypothesis that autism involves a prolonged, heightened cell danger response, disrupting pathways within and between neurons and contributing to the symptoms of the disorder.

The same year, he and his colleagues homed in on the drug suramin as a way to call off the response. The medication has been in use since the early 20th century to kill the organisms that cause African sleeping sickness. In 1988, it was found to block the so-called purinergic receptors, which bind to compounds called purines and pyrimidines—including ATP. These receptors are found on every cell in the body; on neurons, they help orchestrate many of the processes impaired in autism—such as brain development, the production of new synapses, inflammation, and motor coordination.

To determine if suramin could protect these receptors from overstimulation by ATP, Naviaux’s team worked with mice that developed an autism-like disorder after their mothers had been exposed to a simulated viral infection (and heightened cell danger responses) during pregnancy. Like children with autism, the mice born after these pregnancies were less social and did not seek novelty; they avoided unfamiliar mice and passed up the chance to explore new runs of a maze. In the 2013 paper, the researchers reported that these traits vanished after weekly injections of suramin begun when the mice were 6 weeks old (equivalent to 15-year-old humans). Many consequences of altered metabolism—including the structure of synapses, body temperature, the production of key receptors, and energy transport within neurons—were either corrected or improved.

In the new study, published online today in Translational Psychiatry, the researchers found equally compelling results after a single injection of suramin given to 6-month-old mice (equivalent to 30-year-old humans) with the same autism-like condition. Once again, previously reclusive animals approached unknown mice and investigated unfamiliar parts of a maze, suggesting that the animals had overcome the aversion to novelty that’s a hallmark of autism in children. After the single injection, the team lowered the levels of suramin by half each week. Within 5 weeks most, but not all, of the benefits of treatment had been lost. The drug also corrected 17 of 18 metabolic pathways that are disrupted in mice with autism-like symptoms.

Naviaux cautions that mice aren’t people, and therapies that are promising in rodents have a track record of not panning out in humans. He also says that prolonged treatment with suramin is not an option for children, because it can have side effects such as anemia with long-term use. He notes that there are 19 different kinds of purinergic receptors; if suramin does prove to be helpful in humans, newer drugs could be developed that would target only one or a few key receptors. The researchers are beginning a small clinical trial in humans of a single dose of suramin that they hope will be completed by the end of the year.

The study is exciting, says Bruce Cohen, a pediatric neurologist at Akron Children’s Hospital in Ohio. “The authors have come up with a novel idea, tested it thoroughly, and got a very positive response after one dose.” He notes, however, that the mice with a few characteristics of autism don’t necessarily reflect the entire condition in humans. “Autism isn’t a disease. It’s a set of behaviors contributing to hundreds of conditions and resulting from multiple genes and environmental effects. Great work starts with a single study like this one, but there’s more work to be done.”

http://news.sciencemag.org/biology/2014/06/century-old-drug-reverses-signs-autism-mice

Parkland Memorial Hospital said the patient-gagging incident in the psychiatric emergency room was discovered on April 8 during a routine review of security video from March 16. Parkland notified the Texas health department within a day, it said, in compliance with regulations.

By MILES MOFFEIT AND BROOKS EGERTON

The psychiatric patient spat at Parkland Memorial Hospital staff as they strapped her into a chair. Then a nurse shoved a toilet paper roll into her mouth, while a co-worker put a sheet over her head.

“Blood stains can be seen on the toilet tissue” after its removal, says a police report that describes security camera footage. A follow-up report says a third employee warned the caregivers that their actions were “illegal.”

Texas health authorities are investigating the March incident — the first abuse in Parkland’s psychiatric emergency room to become public since the hospital hired a new chief executive. One nurse involved in the gagging was also involved in the 2011 restraint of a psych ER patient whose death triggered a federal investigation and virtual takeover of Parkland.

State health regulations prohibit restraint that obstructs a psychiatric patient’s airway or ability to communicate. A prior state enforcement action against Parkland requires hospital managers to report patient abuse within two days of becoming aware of it.

Parkland reported the gagging incident more than three weeks after it occurred. The hospital said managers didn’t know about it initially but acted promptly once they did.

“Employees on site did not elevate this incident appropriately,” Parkland spokeswoman April Foran said. The hospital fired two of five employees who were present during the restraint, she said. Two others resigned, and a fifth “received corrective action.”

Parkland, which collects hundreds of millions of dollars a year from Dallas County taxpayers, would not name the employees. But The Dallas Morning News confirmed the identities of two: Charles Enyinna-Okeigbo, the nurse who forced the toilet paper roll into the patient’s mouth, and Sherwin De Guzman, a supervising nurse.

Authorities have previously investigated both nurses: Enyinna-Okeigbo for domestic violence, and De Guzman in connection with the 2011 death of psych ER patient George Cornell. State and federal regulators found that Cornell was illegally restrained shortly before dying. They cited De Guzman for failing to supervise the technicians who subdued Cornell.

Parkland’s in-house police department investigated the March incident and asked the Dallas County district attorney’s office whether assault charges should be filed. A prosecutor said that the use of force was “unfortunate” but not criminal.

Both nurses declined to comment to The News. Enyinna-Okeigbo told police that he was merely trying to stop the spitting and was not angry with the patient, according to Parkland records.

UT Southwestern Medical Center, whose physicians supervise care at the public hospital, identified the psychiatrist in charge as Dr. Uros Zrnic. He “was not informed or aware of the incident until the videotape was reviewed” in April, UTSW said.

Terrified patient

Experts criticized Parkland after reading police reports on the latest incident at The News’ request.

“When a patient spits, it’s the last resort of a terrified human being, and being restrained like this is terrifying,” said Dr. Peter Breggin, a New York psychiatrist and former consultant for the National Institute of Mental Health.

“Trained mental health workers in this day and age know that spitting is a cause for staff to back off,” he said, adding that forcing objects into patients’ mouths can escalate violence. “There’s no excuse for this abuse.”

Dennis Borel, executive director of the Coalition of Texans with Disabilities, said some Parkland psych workers “still don’t get it.”

“This is pretty outrageous when it was just a few years ago that these kinds of actions were supposed to trigger training and other safe approaches at Parkland,” Borel said. “Everything in the patient’s behavior indicates she was desperately trying to protect herself, and they were making it worse. They failed the patient miserably.”

The state health department hit Parkland in 2012 with a $1 million fine because of Cornell’s death and several other “egregious deficiencies.” It was by far the largest hospital fine in Texas history.

Under a settlement, the hospital paid $750,000. It can avoid paying the rest if, by later this summer, it demonstrates compliance with safety requirements.

Because of the gagging incident, regulators are investigating whether there have been more “significant, egregious deficiencies and a failure to correct them or an attempt to hide them,” said health department spokeswoman Carrie Williams. “It’s an open investigation, and there have been no findings in this case so far.”

Parkland also remains under a 2013 corporate integrity agreement with the U.S. Department of Health & Human Services. It requires periodic reports on patient safety, among other steps.

Compliance with that agreement is a top stated priority of Dr. Fred Cerise, Parkland’s new chief executive. He started work about a week after the March gagging incident.

Cerise and other hospital officials declined to be interviewed for this report. In written responses to questions, Parkland said “the event was discovered” on April 8 during a routine review of security video from March 16. Parkland notified the Texas health department within a day, they said, in compliance with state regulations.

Parkland also said that in addition to taking personnel actions, it now requires video reviews of restraints within 24 hours. But it would not say whether it previously had a schedule for reviewing the security videos, or why it took more than three weeks to detect the gagging incident.

Quick investigation

The criminal investigation lasted less than 48 hours before the case was closed as “unfounded,” police reports show. A News investigation last year found that Parkland police have a history of quickly closing cases in which hospital employees are accused of abuse.

The hospital released nine pages of reports on the investigation, blacking out the names of employees and the patient. It released no information about why the patient was in the psych ER or whether she was injured in the restraint incident. There is no indication in the records that police tried to interview the woman.

When asked, the hospital spokeswoman told The News that “Parkland made multiple attempts to locate the patient” but failed.

The reports contain conflicting versions of what led to strapping the patient to the chair.

Enyinna-Okeigbo told police the woman became “extremely agitated” while in a common area of the psych ER. He said he gave her medication to calm down, but it didn’t work. When staff then directed her toward seclusion rooms, she began to “spit, swing, and kick at the staff,” police wrote, summarizing Enyinna-Okeigbo’s account.

A fellow caregiver who was interviewed “does not recall seeing the patient strike or attempt to strike any staff members,” a police report says. This caregiver also said he didn’t recall seeing the toilet paper roll put into the patient’s mouth or any bleeding. He denied covering the patient’s face with the sheet. The police report noted that “video of the incident contradicts this.”

The reports quote another staffer as saying he saw the bleeding and thought the patient had been “struck by a nurse.” He described the scene as “very chaotic” and said employees lacked training for such situations.

The police description of video footage begins as the patient resists efforts to strap her into a restraint chair: “She appeared to be acting aggressively toward to the medical staff, including spitting on multiple occasions in the direction of the staff.”

Five staffers approached the woman, including one who “immediately placed the roll of toilet tissue over the patient’s mouth,” a report says. “The patient began to resist,” leading Enyinna-Okeigbo to “shove the end of the roll into the patient’s mouth, at one point even appearing to force the patient’s jaw open to completely insert the roll.”

Then another employee secured the sheet around the patient’s head, and the bloody toilet paper was removed from her mouth. Next, a surgical mask was put on the patient. It, too, later showed blood stains.

A Parkland officer met with Assistant District Attorney Craig McNeil on April 10 to discuss potential criminal charges against Enyinna-Okeigbo. “McNeil stated that he felt the culpable mental state exhibited was negligence, and the mental state that has to be met for assault is reckless,” a police report says. “Therefore, McNeil stated that he did not feel that [Enyinna-Okeigbo] met the culpable state to be charged with a crime.”

McNeil told The News he did not know why the hospital didn’t consider charges against the staff member who put the sheet around the patient’s head. Foran, the Parkland spokeswoman, said hospital police gave the DA’s office “complete details” of the incident and noted that prosecutors have “full discretion” about how to proceed.

No assault

The News became aware of the incident on May 28 and asked Parkland for all related police reports. That same day, a Parkland detective asked McNeil for a written explanation of his reasoning, which the hospital gave The News.

“The use of force against a patient in an altered mental state is always unfortunate and should be avoided,” McNeil wrote. But it “does not appear to have been done with the intent to harm the patient.”

In an interview with The News, McNeil identified Enyinna-Okeigbo as the nurse who stuffed the toilet paper roll into the patient’s mouth.

The prosecutor said that spitting could be considered assault because of the potential for disease transmission. In using that term, he said, he did not mean to suggest that the patient should be charged with assault but added: “You have the right to defend yourself.”

McNeil said he could not tell from the video why the patient had blood in her mouth. He said he saw no footage of the patient being struck.

McNeil handled a 2011 case in which security video showed Parkland psychiatric technician Johnny Roberts choking a patient into unconsciousness. The hospital fired Roberts, but grand jurors declined to indict him.

“I was not happy about that,” McNeil said. “I still don’t know why they did that.”

Troubled pasts

The News’ reporting of George Cornell’s death ultimately led to a regulatory crackdown and two years of round-the-clock federal monitoring of Parkland.

The hospital installed security cameras — the same ones that captured the recent gagging incident. It also promised to fire problem employees and retrain others, especially on patient restraints.

Parkland would not say whether Enyinna-Okeigbo or De Guzman received this training.

De Guzman left his job at Parkland at some point after Cornell’s death in February 2011. He returned to work later the same year, according to hospital employment data. Parkland would not explain his departure or return.

Cornell’s death also led to a federal civil rights lawsuit that’s still pending against the hospital, UTSW, De Guzman and other caregivers. In court records, Cornell’s family has noted ways that regulators found fault with De Guzman.

Enyinna-Okeigbo, who was hired at Parkland in 2005, was charged with misdemeanor assault of his wife in 2008.

Dallas County prosecutors initially proposed a deal under which he could plead guilty and serve probation, court records show. Instead, for reasons the records don’t explain, they dismissed the charge in exchange for his completion of an anger management class. He never entered a plea and has no conviction record.

Parkland would not say whether it was aware of the allegations against Enyinna-Okeigbo. The hospital said that before 2011 it conducted criminal background checks only on prospective employees. It said it now checks existing employees, too.

In 2013, Parkland hired privately owned Green Oaks Hospital to manage its psychiatric services. Green Oaks, which receives $1.1 million a year under the deal, declined to comment for this report. Parkland would not discuss the company’s performance.

http://www.dallasnews.com/investigations/20140614-parkland-psych-er-is-again-scene-of-patient-abuse.ece

A high-tech helmet has reduced symptoms of depression in two-thirds of people who’ve worn it, BBC reports. Now undergoing clinical trials, the hood works by sending electromagnetic impulses to the brain to activate the formation of new blood vessels. Patients who wear the device daily for half an hour to an hour show mood improvement in as little as week, according to the results, published in Acta Neuropsychiatrica.

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

http://news.sciencemag.org/sifter/2014/05/watch-electromagnetic-helmet-treats-depression

In the inner city, a health problem is making it harder for young people to learn. inner-city kids suffer from post-traumatic stress disorder (PTSD).

“Youth living in inner cities show a higher prevalence of post-traumatic stress disorder than soldiers,” according to Howard Spivak M.D., director of the U.S. Centers for Disease Control and Prevention’s Division of Violence Prevention.

Spivak presented research at a congressional briefing in April 2012 showing that children are essentially living in combat zones. Unlike soldiers, children in the inner city never leave the combat zone and often experience trauma repeatedly.

One local expert says national data suggests one in three urban youth have mild to severe PTSD. “You could take anyone who is experiencing the symptoms of PTSD, and the things we are currently emphasizing in school will fall off their radar. Because frankly it does not matter in our biology if we don’t survive the walk home,” said Jeff Duncan-Andrade, Ph.D. of San Francisco State University.

In 2013, there were 47 recorded lockdowns in Oakland public schools – again, almost all in East and West Oakland.

Students at Fremont High showed where one classmate was shot.

“If someone got shot that they knew or that they cared about… they’re going to be numb,” one student said. “If someone else in their family got shot and killed they will be sad, they will be isolated because I have been through that.”

Gun violence is only one of the traumas or stressors in concentrated areas of deep poverty.

“Its kids are unsafe, they’re not well fed,” Duncan-Andrade said. “And when you start stacking those kids of stressors on top of each other, that’s when you get these kinds of negative health outcomes that seriously disrupt school performance.”

Duncan-Andrade said doctors at Harvard’s School of Public Health have come up with a new diagnosis of complex PTSD, describing people who are repeatedly re-exposed to trauma, which Duncan-Andrade said, would include many inner-city youth.

In Oakland, about two-thirds of the murders last year were actually clustered in East Oakland, where 59 people were killed.

Teachers and administrators who graduated from Fremont High School in East Oakland and have gone back to work there spoke with KPIX 5.

“These cards that (students) are suddenly wearing around their neck that say ‘Rest in peace.’ You have some kids that are walking around with six of them. Laminated cards that are tributes to their slain friends,” said teacher Jasmene Miranda.

Jaliza Collins, also a teacher at Fremont, said, “It’s depression, it’s stress, it’s withdrawal, it’s denial. It’s so many things that is encompassed and embodied in them. And when somebody pushes that one button where it can be like, ‘please go have a seat,’ and that can be the one thing that just sets them off.”

Even the slang nickname for the condition, “Hood Disease,” itself causes pain, and ignites debate among community leaders, as they say the term pejoratively refers to impoverished areas, and distances the research and medical community from the issue.

“People from afar call it ‘Hood Disease,’ – it’s what academics call it,” said Olis Simmons, CEO of Youth UpRising working in what she describes as the epicenter of the issue: East Oakland.

She said the term minimizes the pain that her community faces, and fails to capture the impact this has on the larger community.

“In the real world where this affects real lives, people are suffering from a chronic level of trauma that doesn’t have a chance to heal because they’re effectively living in a war zone within your town,” said Simmons.

“Terms like ‘hood disease’ mean it’s someone else’s problem, but it’s not. That’s a lie. It’s a collective problem, and the question is what are we prepared to do about it?”

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

http://sanfrancisco.cbslocal.com/2014/05/16/hood-disease-inner-city-oakland-youth-suffering-from-post-traumatic-stress-disorder-ptsd-crime-violence-shooting-homicide-murder/

by Joe Palca

There are smartphone apps for monitoring your diet, your drugs, even your heart. And now a Michigan psychiatrist is developing an app he hopes doctors will someday use to predict when a manic episode is imminent in patients with bipolar disorder.

People with the disorder alternate between crushing depression and wild manic episodes that come with the dangerous mix of uncontrollable energy and impaired judgment.

There are drugs that can prevent these episodes and allow people with bipolar disorder to live normal lives, according to Dr. Melvin McInnis, a psychiatrist at the University of Michigan Medical Center. But relapses are common.

“We want to be able to detect that well in advance,” McInnis says. “The importance of detecting that well in advance is that they reach a point where their insight is compromised, so they don’t feel themselves that anything is wrong.”

Early detection would give doctors a chance to adjust a patient’s medications and stave off full-blown manic episodes.

McInnis says researchers have known for some time that when people are experiencing a manic or depressive episode, their speech patterns change. Depressed patients tend to speak slowly, with long pauses, whereas people with a full-blown manic attack tend to speak extremely rapidly, jumping from topic to topic.

“It occurred to me a number of years ago that monitoring speech patterns would be a really powerful way to devise some kind of an approach to have the ability to predict when an episode is imminent,” says McInnis.

So he and some computer science colleagues invented a smartphone app. The idea is that doctors would give patients the app. The app would record whenever they spoke on the phone. Once a day, the phone would send the recorded speech to a computer in the doctor’s office that would analyze it for such qualities as speed, energy and inflection.

Right now the app is being tested with 12 or 15 volunteers who are participating in a longitudinal study of bipolar disorder.

McInnis and his colleagues presented preliminary results at this year’s International Conference on Acoustics, Speech and Signal Processing, and so far, things are looking encouraging. McInnis says the software is reasonably good at detecting signs of an impending manic attack. It’s not quite as good catching an oncoming depression.

For now, this app is only intended for patients with bipolar disorder, but McInnis thinks that routinely listening for changes in speech could be an important tool for early detection of a variety of diseases.

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.

http://www.nytimes.com/2014/05/28/opinion/why-cant-doctors-identify-killers.html?_r=0

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

bibliotherapy_WEB

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

sn-schizophrenia

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