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Mental Health News

Following are the latest news and information resources for the various mental health topics that we cover. We hope you will find the news educational and the links in the resources section useful in helping you to get even more in-depth data.

Brain Structure Could Predict Risky Behavior

Some people avoid risks at all costs, while others will put their wealth, health, and safety at risk without a thought. Researchers at Yale School of Medicine have found that the volume of the parietal cortex in the brain could predict where people fall on the risk-taking spectrum.

Led by Ifat Levy, assistant professor in comparative medicine and neurobiology at Yale School of Medicine, the team found that those with larger volume in a particular part of the parietal cortex were willing to take more risks than those with less volume in this part of the brain. The findings are published in the Sept. 10 issue of the Journal of Neuroscience.

Although several cognitive and personality traits are reflected in brain structure, there has been little research linking brain structure to economic preferences. Levy and her colleagues sought to examine this question in their study.

Study participants included young adult men and women from the northeastern United States. Participants made a series of choices between monetary lotteries that varied in their degree of risk, and the research team conducted standard anatomical MRI brain scans. The results were first obtained in a group of 28 participants, and then confirmed in a second, independent, group of 33 participants.

“Based on our findings, we could, in principle, use millions of existing medical brains scans to assess risk attitudes in populations,” said Levy. “It could also help us explain differences in risk attitudes based in part on structural brain differences.”

Levy cautions that the results do not speak to causality. “We don’t know if structural changes lead to behavioral changes or vice-versa,” she said.

Levy and her team had previously shown that risk aversion increases as people age, and we scientists also know that the cortex thins substantially with age. “It could be that this thinning explains the behavioral changes; we are now testing that possibility,” said Levy, who also notes that more studies in wider populations are needed.

The study was a collaboration of researchers from Yale, University College London, New York University, University of Pennsylvania, and the University of Sydney, Australia. In addition to Levy, authors include Sharon Gilaie-Dotan, Agnieszka Tymula, Nicole Cooper, Joseph W. Kable, and Paul W. Glimcher.

The study was funded by the National Institute of Aging (R01AG033406)

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Exercise Before School May Reduce ADHD Symptoms In Kids

Paying attention all day in school as a kid isn’t easy, especially for those who are at a higher risk of ADHD, or attention deficit hyperactivity disorder.

A new study from Michigan State University and University of Vermont researchers shows that offering daily before-school, aerobic activities to younger at-risk children could help in reducing the symptoms of ADHD in the classroom and at home. Signs can include inattentiveness, moodiness and difficulty getting along with others.

The study can be found in the Journal of Abnormal Child Psychology.

“Early studies suggest that physical activity can have a positive effect on children who suffer from ADHD,” said Alan Smith, chairperson of MSU’s Department of Kinesiology, who conducted the research along with lead author Betsy Hoza, a psychologist from the University of Vermont.

Previous MSU research has shown improved brain function and better math and reading skills in elementary students who were exposed to a bout of physical activity. Yet, it’s not as widely known how consistent exercise might improve the broad range of symptoms and impairments associated with the disorder.

Over a 12-week period, Smith and Hoza studied about 200 early elementary school students ranging from kindergarten to second grade that either exhibited signs of ADHD or didn’t. During the trial, students were randomly selected to participate in a group that completed moderate to vigorous physical activity each day before school, or a group that completed more sedentary classroom-type activities.

“Although our findings indicated that all participants showed improvements, children with ADHD risk receiving exercise benefited across a broader range of outcomes than those receiving the sedentary activities,” Smith said.

Smith indicated that further studies are needed to better understand the frequency and amount of physical activity that can provide benefits to children and added that the effects of exercise may be different based on a child’s age.

“Despite the number of remaining questions, physical activity appears to be a promising intervention method for ADHD with well-known benefits to health overall,” he said. “This gives schools one more good reason to incorporate physical activity into the school day.”

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Eating Is Addictive, Study Says

People can become addicted to eating for its own sake but not to consuming specific foods such as those high in sugar or fat, research suggests.

An international team of scientists has found no strong evidence for people being addicted to the chemical substances in certain foods.

The brain does not respond to nutrients in the same way as it does to addictive drugs such as heroin or cocaine, the researchers say.

Instead, people can develop a psychological compulsion to eat, driven by the positive feelings that the brain associates with eating.

New approach

This is a behavioral disorder and could be categorized alongside conditions such as gambling addiction, say scientists at Edinburgh.

They add that the focus on tackling the problem of obesity should be moved from food itself towards the individual’s relationship with eating.

The study, which examined the scientific evidence for food addiction as a substance-based addiction, is published in Neuroscience & Biobehavioral Reviews.

The researchers also say that the current classification of mental disorders, which does not permit a formal diagnosis of eating addiction, could be redrawn.

However, more research would be needed to define a diagnosis, the scientists add.

They add that the focus on tackling the problem of obesity should be moved from food itself towards the individual’s relationship with eating.

International collaboration

The study, which examined the scientific evidence for food addiction as a substance-based addiction, is published in Neuroscience & Biobehavioral Reviews.

The researchers also say that the current classification of mental disorders, which does not permit a formal diagnosis of eating addiction, could be redrawn. However, more research would be needed to define a diagnosis, the scientists add.

The work was carried at the Universities of Edinburgh, Aberdeen, Gothenburg, Essen, Utrecht and Santiago de Compostela.

The researchers are involved in the NeuroFAST consortium, which is an EU-funded project studying the neurobiology of eating behavior, addiction and stress.

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When Antidepressant Drugs Cause Depression

A new study published in the current issue of Psychotherapy and Psychosomatics provides alarming data on the likelihood that antidepressant drugs may produce untoward effects.

Mixed depression is narrowly defined in the DSM-IV and somewhat broader in the DSM-5, although both exclude psychomotor agitation as a diagnostic criterion. This article proposes a clinical description for defining mixed depression, which emphasizes psychomotor excitation.

Two hundred and nineteen consecutive outpatients were diagnosed with an mixed depression episode using criteria proposed by Koukopoulos et al. Results showed that the most frequent mixed depression symptoms were psychic agitation or inner tension (97%), absence of retardation (82%), dramatic description of suffering or weeping spells (53%), talkativeness (49%), and racing or crowded thoughts (48%). Mixed depression was associated with antidepressants in 50.7% of patients, with similar frequency for tricyclic antidepressants (45%) versus selective serotonin reuptake inhibitors (38.5%).

Positive predictors of antidepressant-associated mixed depression were bipolar disorder type II diagnosis, higher index depression severity, and higher age at index episode. Antipsychotic or no treatment was protective against antidepressant-associated mixed depression.

Mixed depression, defined as depression with excitatory symptoms, can be clinically identified, is common, occurs in both unipolar depression and bipolar disorder, and is frequently associated with antidepressant use. If replicated, this view of mixed depression could be considered a valid alternative to the DSM-5 criteria for depression with mixed features.

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The Neural Circuits Activated By Cognitive Behavioral Therapy (CBT)

A new study published in the current issue of Psychotherapy and Psychosomatics provides new insights on how psychotherapy works. Cognitive behavioral therapy (CBT) is an effective treatment for panic disorder with agoraphobia (PD/AG). It is unknown, how variants of CBT differentially modulate brain networks involved in PD/AG.                   

This study evaluated the effects of therapist-guided (T+) versus self-guided (T-) exposure on the neural correlates of fear conditioning in PD/AG.

In a randomized, controlled multicenter clinical trial in medication-free patients with PD/AG who were treated with 12 sessions of manualized CBT, functional magnetic resonance imaging (fMRI) was used during fear conditioning before (t1) and after CBT (t2). Quality-controlled fMRI data from 42 patients and 42 healthy subjects (HS) were obtained.

Patients were randomized to two variants of CBT (T+, n = 22, and T-, n = 20). Results: The interaction of diagnosis (PD/AG, HS), treatment group (T+, T-), time point (t1, t2) and stimulus type (conditioned stimulus: yes, no) revealed activation in the left hippocampus and the occipitotemporal cortex. The T+ group demonstrated increased activation of the hippocampus at t2 (t2 > t1), which was positively correlated with treatment outcome, and a decreased connectivity between the left inferior frontal gyrus and the left hippocampus across time (t1 > t2).

After T+ exposure, contingency-encoding processes related to the posterior hippocampus are augmented and more decoupled from processes of the left inferior frontal gyrus, previously shown to be dysfunctionally activated in PD/AG. Linking single procedural variants to neural substrates offers the potential to inform about the optimization of targeted psychotherapeutic interventions.

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13 Things You Probably Don’t Know About Laughing

1. Contrary to popular belief, the number one catalyst for laughter isn’t a joke: It’s interacting with another person.

2. That’s because the modern-day ha-ha! probably evolved as a form of communication. Our primate ancestors used a similar sound—a sort of pant-pant—to reassure one another that their rough-and-tumble play was all in good fun and not an attack, says Robert R. Provine, a professor of psychology at the University of Maryland, Baltimore County, the author of Curious Behavior, and one of the foremost experts on laughter.

3. One of Provine’s earliest experiments proved that just listening to recorded laughing could evoke fits of giggles in subjects (which is why television studios use laugh tracks on sitcoms). In fact, according to his research, you’re 30 times more likely to laugh when someone else is around than when you’re by yourself.

4. The ideal number of words in a joke? 103.

5. “There is no magic formula or key for what’s funny,” says Scott Weems, Ph.D., a research scientist at the University of Maryland, College Park, and the author of Ha! The Science of When We Laugh and Why. But, in general, he says, what often makes us laugh is when our brain is expecting one thing and then, in the space of a few words, that expectation is turned on its head. Take the classic Groucho Marx joke: “One morning I shot an elephant in my pajamas. How he got in my pajamas, I don’t know.”

6. Ten to 15 minutes of daily laughing burns 10 to 40 calories.

7. Our appreciation for the unexpected starts as early as infancy, although on a very basic level. “Parents will notice that they can elicit a giggle from their baby by making a funny face, talking in a funny voice, or playing peekaboo,” says Merideth Gattis, Ph.D., a psychologist at Cardiff University, in Wales.

8. British psychologist Richard Wiseman, Ph.D., the author of Quirkology, has revealed clear regional preferences for what we find funny. Americans often like jokes that include a sense of superiority. (Texan: “Where are you from?” Harvard grad: “I come from a place where we do not end our sentences with prepositions.” Texan: “OK, where are you from, jackass?”) Europeans tend to laugh at jokes that make light of anxiety-provoking topics, like marriage and illness. (A patient says, “Doctor, last night I made a Freudian slip. I was having dinner with my mother-in-law and wanted to say, ‘Could you please pass the butter?’ But instead I said, ‘You silly cow. You have completely ruined my life.'”) And Brits? Wiseman finds that they are tickled most by wordplay. (Patient: “Doctor, I’ve got a strawberry stuck up my bum.” Doctor: “I’ve got some cream for that.”)

9. An adult laughs an estimates 15 to 20 times a day.

10. “The same pleasure sensors in the brain that are activated when we eat chocolate become active when we find something funny,” says Weems. “It’s a natural high.” In fact, a 2003 brain-scan study published in the journal Neuron found that the dopamine reward centers and pathways in the brains of subjects lit up when they were treated to a funny cartoon, but not when they were shown an unfunny version.

11. Research has linked laughter with boosts in immune function, pain tolerance, cardiovascular health and maybe even memory retention.

12. A typical 10-minute conversation has an average of 5.8 bouts of laughter.

13. Even those with zero sense of humor can reap the benefits of laughter. How? Fake it. A 2002 study in Psychological Reports reveals that forcing yourself to laugh (or even just to smile) can improve your mood. The human brain is not able to distinguish spontaneous laughter from self-induced; therefore the corresponding health-related benefits are alleged to be alike, according to a 2010 report in Alternative Therapies in Health and Medicine by Ramon Mora-Ripoll, M.D., Ph.D., an advisory board member of the Laughter Online University, a supplier of online laughter education.

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Fighting Addiction Requires Dedicated Approach On A Variety Of Fronts

Whenever celebrities like Philip Seymour Hoffman or Robin Williams die, the media shines a light for a brief period on the terrible cost of addiction. The moment soon passes, though, and the subject returns to the shadows where countless individuals struggle with addiction outside of the limelight.

People may think that they have learned something about addiction — whether through media coverage or from personal experience — but for most, addiction remains a mystery. What is addiction? How do people become addicted? And why do addicts continue to use drugs and alcohol even in the face of serious negative consequences?

The short answer is that addiction is a chronic brain disease, and it shares a great deal with other diseases. Addiction causes persistent changes in the structure and function of the brain, and it leads to compulsive behavior and an inability to stop using the very drugs or alcohol that lead to the development of the disease. Like other chronic diseases, it is preventable and responds to treatment, but if it is left untreated, it will last for a person’s entire life.

Furthermore, addiction, like other diseases, is a result of the combination of genetic predisposition, environmental factors, and an individual’s behavior. Relapse rates for addiction (40 percent to 60 percent) are comparable to relapse from other chronic diseases, like type 1 diabetes (30 percent-50 percent), hypertension (50%-70 percent) and asthma (50 percent-70 percent).

Addiction often begins in adolescence. A little more than two-thirds of those who meet criteria for substance dependence — the term used by substance-abuse professionals to refer to addiction — first do so between the ages of 12 and 17. Another quarter of addicted people meet dependence criteria between the ages of 18 and 25, which means that more than 90 percent of addicts become addicted before the age of 25.

Addiction is also more prevalent among certain groups; individuals who come from lower socioeconomic class backgrounds, who witness violence or are victims of abuse at an early age, who are exposed to drugs and alcohol as children, who suffer from a lack of family or other social supports or who have mental health disorders are at an increased risk of becoming addicted.

The good news is that, with treatment, the disease can be brought under control. Individuals can learn to avoid the people, places and things associated with drug and alcohol use and can be taught coping strategies to help them deal with stress and the cravings brought on by exposure to environmental cues for substance use. They also can begin to deal with any mental health issues that either may have led to substance use or resulted from it, and to build a support network of family and sober friends to help them once they have completed treatment.

Without these tools, individuals struggling with addiction increase the chances that they will relapse. Since relapse can be a part of any chronic disease, addicts may need to return to treatment more than once before they can achieve a sustained abstinence. For many, addiction is a lifetime struggle, but recovery is always possible.

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Sibling Bullying Increases Depression Risk

Being bullied regularly by a sibling could put children at risk of depression when they are older, a study led by the University of Oxford suggests.

Around 7,000 children aged 12 were asked if they had experienced a sibling saying hurtful things, hitting, ignoring or lying about them.

The children were followed up at 18 and asked about their mental health.

A charity said parents should deal with sibling rivalry before it escalates.

Previous research has suggested that victims of peer bullying can be more susceptible to depression, anxiety and self-harm.

This study claims to be the first to examine bullying by brothers or sisters during childhood for the same psychiatric problems in early adulthood.

Researchers from the Universities of Oxford, Warwick and Bristol and University College London sent questionnaires to thousands of families with 12-year-old children in 2003-04 and went back to them six years later to assess their mental health.

If they had siblings they were asked about bullying by brothers and sisters. The questionnaire said: "This means when a brother or sister tries to upset you by saying nasty and hurtful things, or completely ignores you from their group of friends, hits, kicks, pushes or shoves you around, tells lies or makes up false rumors about you."

'Twice as likely'

Most children said they had not experienced bullying. Of these, at 18, 6.4% had depression scores in the clinically significant range, 9.3% experienced anxiety and 7.6% had self-harmed in the previous year.

The 786 children who said they had been bullied by a sibling several times a week were found to be twice as likely to have depression, self-harm and anxiety as the other children.

In this group, depression was reported by 12.3%, self-harm by 14%, and 16% of them reported anxiety.

Girls were slightly more likely to be victims of sibling bullying than boys, particularly in families where there were three or more children.

Older brothers were often found to be responsible.

On average, victims said that sibling bullying had started at the age of eight, the study said.

More than teasing

Lead author Dr Lucy Bowes, from the department of social policy and intervention at the University of Oxford, said although they couldn't say sibling bullying caused depression, the result were significant.

"We need to change the conversation we have about this. If it occurred in a school setting there would be repercussions.

"It may be causing long-term harm. We need to do more research, but we also need parents to listen to their children.

She added: "We are not talking about the sort of teasing that often goes on within families, but incidents that occur several times a week, in which victims are ignored by their brothers or sisters, or are subjected to verbal or physical violence."

Emma Jane Cross, from the bullying prevention charity, BeatBullying, said: "Being bullied as a child can have a devastating effect which lasts a lifetime. Parents who are concerned about this issue should speak to their children as early as possible before the problem escalates.

"It's important to tackle the underlying issues behind more frequent bullying behavior rather than dismissing it as normal sibling rivalry."

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Shining Light On Brain Circuits To Study Learning, Memory

Univ. of California, Berkeley neuroscientists plan to use light to tweak the transmission of signals in the brain to learn more about how the mouse brain and presumably the human brain process information.

Last month, the research project was awarded one of 36 new $300,000, two-year grants from the National Science Foundation in support of President Obama’s BRAIN Initiative, a multi-agency research effort that seeks to accelerate the development of new neuro-technologies that promise to help researchers answer fundamental questions about how the brain works.

NSF’s Early Concept Grants for Exploratory Research (EAGER) are designed to “enable new technologies to better understand how complex behaviors emerge from the activity of brain circuits,” according to an Aug. 18 announcement by the agency.

The new technology involves optogenetics, “an incredibly powerful approach to do circuit breaking to understand how the brain works,” said lead researcher Ehud Isacoff, UC Berkeley professor of molecular and cell biology and director of the Helen Wills Neuroscience Institute. “This is a way of exploring the basic principles of brain processing, and how these govern learning and memory.”

“And because these circuits play roles in anxiety, depression and schizophrenia, we can help define what goes wrong with brain circuits in disease,” he added.

Innovative optogenetic technology

Isacoff said that there is the critical need for new technologies that can record the activity of thousands of neurons at once, rather than the few now possible with standard electrophysiological recording. Optogenetics complements cell recording with the ability to control the activity of nerve cells. UC Berkeley’s optogenetic technique “goes a step further by controlling the way the cells communicate in the network.”

About a decade ago, Isacoff and UC Berkeley scientists Richard Kramer and Dirk Trauner—now at the University of Munich—developed ways to chemically synthesize a light-sensitive switch and attach it to signaling proteins on cell membranes so that a flash of light could turn the cells on and off. This allowed researchers to explore the function of the brain’s ion channels and the connectivity of neural circuits, offering the possibility of restoring sight to those with blinding retinal diseases such as retinitis pigmentosa.

Recently, Isacoff, Trauner and colleagues extended this optogenetic technique to the largest family of membrane receptors, which are involved in complex signaling not only in the brain but throughout the body. The ability to switch these G-protein coupled receptors (GPCRs) on and off with light now allows neuroscientists to manipulate fundamental modulatory functions of the synapse, the critical junction between nerve cells where signals are transmitted.

“Now we can directly probe the synapse, turning on and off the very receptors that mediate information filtering and adjust the strength of synapses,” he said. “The NSF-EAGER grant and a linked grant from the U.S.-Israel Binational Science Foundation to collaborator Eitan Reuveny at the Weizmann Institute enable us to take the next step: to generate a new family of light-controlled GPCRs that will make it possible to probe one of the central mechanisms of learning and memory in motor control.”

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Dozens Of Schizophrenia Risk Loci Identified

A few years back, there was but a handful of genetic markers that could confidently be linked with schizophrenia risk. But on July 21, Nature published findings from the National Institutes of Mental Health (NIMH)-supported Psychiatric Genomic Consortium (PGC). In an unprecedented effort of collaboration and data sharing, the PGC had pinpointed 108 genetic loci associated with schizophrenia, 83 of which had not been previously identified.

This rapid growth is reminiscent of Dubai, which also transformed from a modest city to a skyscraper-filled metropolis almost overnight. But just as a shiny office tower is only useful if it’s productive, so too these schizophrenia loci need to lead to tangible scientific and clinical benefits down the road.

The immediate thought is whether these loci can be used to predict schizophrenia before it manifests or determine the optimal treatment if it does develop.

“In terms of individual-level prediction, whether a person will or won’t get the disease, we are not there yet,” said Philip Wang, M.D., deputy director of NIMH. “Though we uncovered a large number of genetic variants, they only account for a small percentage of someone’s schizophrenia risk.

“But we are getting to the point where we can begin to act on our genetic findings,” Wang added, noting the PGC study did develop risk profile scores by adding up the various genetic signals and demonstrated that people in the highest category had a 20-fold increased schizophrenia risk.

Having a robust genetic profile will help identify certain subgroups that might be more prone to the disease or to specific schizophrenia phenotype manifestations, but even if hundreds more genetic variants for schizophrenia are uncovered, the complexity and rarity of the disease would make true individual prediction unfeasible, given the near certainty of false positive results.

More potential lies in digging deeper into these associations to uncover potential drug targets. About three-quarters of the loci identified in the PGC study were on or adjacent to a protein-encoding gene, including some well-established players. “Finding a strong association for the D2 dopamine receptor, which is the target of antipsychotics, was particularly reassuring, as it shows that we are dealing with biologically important variants.” said Wang. Additional variants identified in regions relevant to schizophrenia included genes involved in the transport of glutamate—the brain’s major neurotransmitter—and in calcium channels, which regulate how well the connections between neurons strengthen or weaken over time.

Perhaps the most intriguing variations identified were in several genes involved in the immune system, such as for B-cells involved in acquiring pathogen-specific defense mechanisms. “The connection between immunity and mental health has been postulated for decades, but it’s been a puzzle,” said William Eaton, Ph.D., a professor in the Department of Mental Health at the Johns Hopkins Bloomberg School of Public Health. “These genetic findings add more pieces to that puzzle, notably in supporting the importance of adaptive immunity. But, next to the brain, the human immune system is probably the most complex thing on the planet, so we still have many connections to establish.”

Wang agrees with this assessment. “This study has pointed us in several good directions, but it’s just the first installment,” he said. “This coming together of individuals and institutions is happening across the research landscape of mental health, so we will be seeing more variants for schizophrenia and other psychiatric conditions on the horizon. And as we progress, I think we will find more risk factors in the noncoding areas of the genome that regulate gene expression, which will open up even more mechanisms underlying this disease.”

The challenge now is shifting from a research area that has too much information, as opposed to too little. While many of the variants were found in biologically plausible regions, only a handful will end up being integral to disease. Like an old-time prospector, research will have to sift through a great deal of peripheral association to find their nuggets of causation.

Even then the underlying gene, or the protein it makes, may not be a clinical gold mine. “An important thing to remember about this study is that the consortium identified common variants, which by nature have only minor influence on risk,” said William Carpenter, M.D., a professor of psychiatry at the University of Maryland School of Medicine and former director of the Maryland Psychiatric Research Center. “It’s possible, but unlikely, that you will find a specific protein that will make a good drug target.”

Instead, researchers should map out known common—and rare—variants to identify pathways and networks where variants cluster. Then, scan those pathways and find proteins that could be the most “druggable,” as opposed to having the strongest risk, he said.

The necessities of drug development will mean that any approved products are still years away, but Carpenter noted that genetic findings might offer more immediate hope for some patients. “There’s a lot of focus on using genetics to find new drugs, but we could also test psychological therapies, which do not require all the regulatory hurdles,” he said. “If we identify defects in a cognition pathway in a patient, for example, we could try cognitive remediation or other behavioral approaches to see if they benefit.”

Even psychological strategies are still likely a ways off, but clinicians, patients, and others affected by schizophrenia should still consider this genetic bonanza a positive step forward. Mental health has been lagging behind other fields when it comes to genetic discoveries, but now it appears ready to join the party. 

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Did You Know?

Vitamin D Supplementation Does Not Relieve Depressive Symptoms.


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