Researchers Identify Risk-Factors for Addictive Video-Game Use among Adults

New research from the University of Missouri indicates escapism, social interaction and rewards fuel problematic video-game use among “very casual” to “hardcore” adult gamers. Understanding individual motives that contribute to unhealthy game play could help counselors identify and treat individuals addicted to video games.

“The biggest risk factor for pathological video game use seems to be playing games to escape from daily life,” said Joe Hilgard, a doctoral candidate in the Department of Psychological Sciences in the MU College of Arts and Science. “Individuals who play games to get away from their lives or to pretend to be other people seem to be those most at-risk for becoming part of a vicious cycle. These gamers avoid their problems by playing games, which in turn interferes with their lives because they’re so busy playing games.”

Problematic video game use is more than just excessive use of video games; it also includes a variety of unhealthy behaviors, such as lying to others about how much time is spent playing games and missing work or other obligations to play games.

“People who play games to socialize with other players seem to have more problems as well,” Hilgard said. “It could be that games are imposing a sort of social obligation on these individuals so that they have to set aside time to play with other players. For example, in games like World of Warcraft, most players join teams or guilds. If some teammates want to play for four hours on a Saturday night, the other players feel obligated to play or else they may be cut from the team. Those play obligations can mess with individuals’ real-life obligations.”

Problematic video game use isn’t all that different from other types of addictive behavior, such as alcohol or drug abuse, which can be spurred by poor coping strategies, Hilgard said.

“Gamers who are really into getting to the next level or collecting all of the in-game items seem to have unhealthier video-game use,” Hilgard said. “When people talk about games being ‘so addictive,’ usually they’re referring to games like Farmville or Diablo that give players rewards, such as better equipment or stronger characters, as they play. People who are especially motivated by these rewards can find it hard to stop playing.”

Understanding individuals’ motives for playing video games can inform researchers, game developers and consumers about why certain games attract certain individuals, Hilgard said.

“Researchers have suspected that Massively Multiplayer Online Role-Playing Games (MMORPGs) are the most addictive genre of video games,” Hilgard said. “Our study provides some evidence that supports that claim. The games provide opportunities for players to advance levels, to join teams and to play with others. In addition, the games provide enormous fantasy worlds that gamers can disappear into for hours at a time and forget about their problems. MMORPGs may be triple threats for encouraging pathological game use because they present all three risk factors to gamers.”

“Consistent with previous research, we did not find a perfect relationship between total time spent playing games and addictive video game behaviors,” said study co-author Christopher Engelhardt, a postdoctoral research fellow in the Department of Health Psychology in the MU School of Health Professions and the MU Thompson Center for Autism and Neurodevelopmental Disorders. “Additionally, other variables, such as the proportion of free time spent playing video games, seem to better predict game addiction above and beyond the total amount of time spent playing video games.”

The open-access journal, Frontiers in Psychology, published the article, “Individual differences in motives, preferences, and pathology in video games: the gaming attitudes, motives, and experiences scales (GAMES),” earlier in September.

Celebration of compassion

Unique multimedia eBook presents scientists’, practitioners’, and therapists’ experiences

Questions about the difference between empathy and compassion, or about whether compassion can be learned, are now answered by a newly published eBook. Edited by Tania Singer and Matthias Bolz from the Max Planck Institute for Human Cognitive and Brain Sciences, the book also explains how mental training transforms the human brain, and that compassion can reduce pain.

The eBook Compassion: Bridging Practice and Science has just been published and can be downloaded free of charge. It summarises fascinating results of the science of compassion, but also describes training programmes and practical experiences. The book thus provides not only a unique overview of current research into empathy and compassion, but also offers an exciting way of approaching the topic for interested readers—including useful advice for everyday life.

A major part of the eBook concerns the science of compassion. Tania Singer, director of the Department of Social Neuroscience, shows how empathy differs from compassion. In a recent study, she was able to show empirically that empathy—the ability to recognize emotions experienced by others—and compassion are supported by different biological systems and neuronal networks. In other chapters, researchers from Singer’s department explain how meditation-based compassion practices can reduce pain, and how compassion training can promote positive emotions and social closeness, which in turn can improve mental and physical health. In another chapter, the endocrinologist Charles Raison describes how compassion training can lead to a decrease in stress-related hormones such as cortisol. “With our research, and with this book, we hope to raise awareness of compassion in our society, and to support the development of a more caring and sustainable society which recognizes the importance of secular ethics and the interdependence of all beings”, Singer emphasises.

Moreover, scientifically validated compassion training programmes are introduced for the first time, and expert users describe their experiences with some of these in schools, therapy, or end-of-life care situations. These reports provide interesting, enlightening, but also touching insights into the everyday-life effects of compassion training. One chapter, for example, shows how compassion training gains increasing significance for clinical staff—not only for their interactions with terminally ill or dying patients, but also for their processing of daily events, thus helping to prevent burnout-related illnesses among physicians and caretakers.

The book also provides theories and concepts of compassion from different perspectives. Paul Gilbert presents an evolutionary model of compassion, which argues that compassion is deeply rooted in our caring system. From a cognitive neuroscientific point of view, compassion is based on attentional, cognitive, and socio-affective processes, each of which draws on specific neuronal networks. The book also offers a Buddhist perspective on compassion, which insists compassion must begin with the move from self- to other-centredness.

The eBook has evolved from a successful workshop, How to Train Compassion, which was organised by Singer’s department in artist Olafur Eliasson’s studio in Berlin back in 2011. After the event, participants all agreed that the topics shared and discussed at the workshop should be made accessible to a wider range of people. Thus, with the support of the Max Planck Society, the eBook was produced—offering its readers many videos from the workshop, sound art collages by Nathalie Singer, as well as impressive pieces of visual art by Olafur Eliasson.

The documentary Raising Compassion, produced by Tania Singer und Olafur Eliasson, shows a unique exchange between the very different participants of the workshop.

Perception of Marijuana as a “Safe Drug” Is Scientifically Inaccurate

The nature of the teenage brain makes users of cannabis amongst this population particularly at risk of developing addictive behaviors and suffering other long-term negative effects, according to researchers at the University of Montreal and New York’s Icahn School of Medicine at Mount Sinai.

“Of the illicit drugs, cannabis is most used by teenagers since it is perceived by many to be of little harm. This perception has led to a growing number of states approving its legalization and increased accessibility. Most of the debates and ensuing policies regarding cannabis were done without consideration of its impact on one of the most vulnerable population, namely teens, or without consideration of scientific data,” wrote Professor Didier Jutras-Aswad of the University of Montreal and Yasmin Hurd, MD, PhD, of Mount Sinai. “While it is clear that more systematic scientific studies are needed to understand the long-term impact of adolescent cannabis exposure on brain and behavior, the current evidence suggests that it has a far-reaching influence on adult addictive behaviors particularly for certain subsets of vulnerable individuals.”

The researchers reviewed over 120 studies that looked at different aspects of the relationship between cannabis and the adolescent brain, including the biology of the brain, chemical reaction that occurs in the brain when the drug is used, the influence of genetics and environmental factors, in addition to studies into the “gateway drug” phenomenon. “Data from epidemiological studies have repeatedly shown an association between cannabis use and subsequent addiction to heavy drugs and psychosis (i.e. schizophrenia). Interestingly, the risk to develop such disorders after cannabis exposure is not the same for all individuals and is correlated with genetic factors, the intensity of cannabis use and the age at which it occurs. When the first exposure occurs in younger versus older adolescents, the impact of cannabis seems to be worse in regard to many outcomes such as mental health, education attainment, delinquency and ability to conform to adult role,” Dr Jutras-Aswad said.

Although it is difficult to confirm in all certainty a causal link between drug consumption and the resulting behavior, the researchers note that rat models enable scientists to explore and directly observe the same chemical reactions that happen in human brains. Cannabis interacts with our brain through chemical receptors (namely cannabinoid receptors such as CB1 and CB2.) These receptors are situated in the areas of our brain that govern our learning and management of rewards, motivated behavior, decision-making, habit formation and motor function. As the structure of the brain changes rapidly during adolescence (before settling in adulthood), scientists believe that the cannabis consumption at this time greatly influences the way these parts of the user’s personality develop. In adolescent rat models, scientists have been able to observe differences in the chemical pathways that govern addiction and vulnerability – a receptor in the brain known as the dopamine D2 receptor is well known to be less present in cases of substance abuse.

Only a minority (approximately one in four) of teenage users of cannabis will develop an abusive or dependant relationship with the drug. This suggests to the researchers that specific genetic and behavioral factors influence the likelihood that the drug use will continue. Studies have also shown that cannabis dependence can be inherited through the genes that produce the cannabinoid receptors and an enzyme involved in the processing of THC. Other psychological factors are also likely involved. “Individuals who will develop cannabis dependence generally report a temperament characterized by negative affect, aggressivity and impulsivity, from an early age. Some of these traits are often exacerbated with years of cannabis use, which suggests that users become trapped in a vicious cycle of self-medication, which in turn becomes a dependence” Jutras-Aswad said.

The researchers stress that while a lot remains unknown about the mechanics of cannabis abuse, the body of existing research has clear implications for society. “It is now clear from the scientific data that cannabis is not harmless to the adolescent brain, specifically those who are most vulnerable from a genetic or psychological standpoint. Identifying these vulnerable adolescents, including through genetic or psychological screening, may be critical for prevention and early intervention of addiction and psychiatric disorders related to cannabis use. The objective is not to fuel the debate about whether cannabis is good or bad, but instead to identify those individuals who might most suffer from its deleterious effects and provide adequate measures to prevent this risk” Jutras-Aswad said. “Continuing research should be performed to inform public policy in this area. Without such systematic, evidenced-based research to understand the long-term effects of cannabis on the developing brain, not only the legal status of cannabis will be determined on uncertain ground, but we will not be able to innovate effective treatments such as the medicinal use of cannabis plant components that might be beneficial for treating specific disorders,” Dr Hurd said.

(Image: AP)

Brain circuit can tune anxiety

New findings may help neuroscientists pinpoint better targets for antianxiety treatments.

Anxiety disorders, which include posttraumatic stress disorder, social phobias and obsessive-compulsive disorder, affect 40 million American adults in a given year. Currently available treatments, such as antianxiety drugs, are not always effective and have unwanted side effects.

To develop better treatments, a more specific understanding of the brain circuits that produce anxiety is necessary, says Kay Tye, an assistant professor of brain and cognitive sciences and member of MIT’s Picower Institute for Learning and Memory.

“The targets that current antianxiety drugs are acting on are very nonspecific. We don’t actually know what the targets are for modulating anxiety-related behavior,” Tye says.

In a step toward uncovering better targets, Tye and her colleagues have discovered a communication pathway between two brain structures — the amygdala and the ventral hippocampus — that appears to control anxiety levels. By turning the volume of this communication up and down in mice, the researchers were able to boost and reduce anxiety levels.

Lead authors of the paper, which appears in the Aug. 21 issue of Neuron, are technical assistant Ada Felix-Ortiz and postdoc Anna Beyeler. Other authors are former research assistant Changwoo Seo, summer student Christopher Leppla and research scientist Craig Wildes.

Measuring anxiety

Both the hippocampus, which is necessary for memory formation, and the amygdala, which is involved in memory and emotion processing, have previously been implicated in anxiety. However, it was unknown how the two interact.

To study those interactions, the researchers turned to optogenetics, which allows them to engineer neurons to turn their electrical activity on or off in response to light. For this study, the researchers modified a set of neurons in the basolateral amygdala (BLA); these neurons send long projections to cells of the ventral hippocampus.

The researchers tested the mice’s anxiety levels by measuring how much time they were willing to spend in a situation that normally makes them anxious. Mice are naturally anxious in open spaces where they are easy targets for predators, so when placed in such an area, they tend to stay near the edges.

When the researchers activated the connection between cells in the amygdala and the hippocampus, the mice spent more time at the edges of an enclosure, suggesting they felt anxious. When the researchers shut off this pathway, the mice became more adventurous and willing to explore open spaces. However, when these mice had this pathway turned back on, they scampered back to the security of the edges.

Complex interactions

In a study published in 2011, Tye found that activating a different subset of neurons in the amygdala had the opposite effect on anxiety as the neurons studied in the new paper, suggesting that anxiety can be modulated by many different converging inputs.

“Neurons that look virtually indistinguishable from each other in a single region can project to different regions and these different projections can have totally opposite effects on anxiety,” Tye says. “Anxiety is such an important trait for survival, so it makes sense that you want some redundancy in the system. You want a couple of different avenues to modulate anxiety.”

The Neuron study contributes significantly to scientists’ understanding of the roles of the amygdala and hippocampus in anxiety and offers directions for seeking new drug targets, says Joshua Gordon, an associate professor of psychiatry at Columbia University.

“The study specifies a particular connection in the brain as being important for anxiety. One could imagine, then, identifying components of the machinery of that connection — synaptic proteins or ion channels, for example — that are particularly important for amygdala-hippocampal connectivity. If such specific components could be identified, they would be potential targets for novel antianxiety drugs,” says Gordon, who was not part of the research team.

In future studies, the MIT team plans to investigate the effects of the amygdala on other targets in the hippocampus and the prefrontal cortex, which has also been implicated in anxiety. Deciphering these circuits could be an important step toward finding better drugs to help treat anxiety.

Study finds night owls more likely to be psychopaths

People who stay up late at night are more likely to display anti-social personality traits such as narcissism, Machiavellianism, and psychopathic tendencies, according to a study published by a University of Western Sydney researcher.

Dr Peter Jonason, from the UWS School of Social Sciences and Psychology, assessed over 250 people’s tendency to be a morning- or evening-type person to discover whether this was linked to the ‘Dark Triad’ of personality traits.

The results, published in Personality and Individual Differences, found students who were awake in the twilight hours displayed greater anti-social tendencies than those who went to bed earlier.

“Those who scored highly on the Dark Triad traits are, like many other predators such as lions and scorpions, creatures of the night,” he says.

"For people pursuing a fast life strategy like that embodied by the Dark Triad traits, it’s better to occupy and exploit a lowlight environment where others are sleeping and have diminished cognitive functioning."

Dr Jonason says there may be an evolutionary basis for the link between anti-social behaviour and a preference to being awake late at night.

“There is likely to be a co-evolutionary arms race between cheaters and those who wish to detect and punish them, and the Dark Triad traits may represent specialized adaptations to avoid detection,” he says.

“The features of the night - a low-light environment where others are sleeping - may facilitate the casual sex, mate-poaching, and risk-taking the Dark Triad traits are linked to.”

“Indeed, most crimes and most sexual activity peak at night, suggesting just such a link.”

Dr Jonason adds that far more work is needed, but these results represent an important advance in behavioural ecological and evolutionary psychological models of the Dark Triad, as well as ‘darker’ aspects of human nature and personality.

Nicotinic receptor essential for cognition and mental health

The ability to maintain mental representations of ourselves and the world — the fundamental building block of human cognition — arises from the firing of highly evolved neuronal circuits, a process that is weakened in schizophrenia. In a new study, researchers at Yale University School of Medicine pinpoint key molecular actions of proteins that allow the creation of mental representations necessary for higher cognition that are genetically altered in schizophrenia. The study was released July 1 in the Proceedings of the National Academy of Sciences.

Working memory, the mind’s mental sketch pad, depends upon the proper functioning of a network of pyramid-shaped brain cells in the prefrontal cortex, the seat of higher order thinking in humans. To keep information in the conscious mind, these pyramidal cells must stimulate each other through a special group of receptors. The Yale team discovered this stimulation requires the neurotransmitter acetylcholine to activate a specific protein in the nicotinic family of receptors — the alpha7 nicotinic receptor.

Acetycholine is released when we are awake — but not in deep sleep. These receptors allow prefrontal circuits to come “online” when we awaken, allowing us to perform complex mental tasks. This process is enhanced by caffeine in coffee, which increases acetylcholine release. As their name suggests, nicotinic alpha-7 receptors are also activated by nicotine, which may may help to explain why smoking can focus attention and calm behavior, functions of the prefrontal cortex.

The results also intrigued researchers because alpha7 nicotinic receptors are genetically altered in schizophrenia, a disease marked by disorganized thinking. “Prefrontal networks allow us to form and hold coherent thoughts, a process that is impaired in schizophrenia,” said Amy Arnsten, professor of neurobiology, investigator for Kavli Institute, and one of the senior authors of the paper. “A great majority of schizophrenics smoke, which makes sense because stimulation of the nicotinic alpha7 receptors would strengthen mental representations and lessen thought disorder.”

Arnsten said that new medications that stimulate alpha-7 nicotinic receptors may hold promise for treating cognitive disorders.

Publication of the PNAS paper comes on the eve of the 10^th anniversary of the death of  Yale neurobiologist Patricia Goldman-Rakic, who was hit by a car in Hamden Ct. on July 31, 2003. Goldman-Rakic first identified the central role of prefrontal cortical circuits in working memory.

“Patricia’s work has provided the neural foundation for current studies of molecular influences on cognition and their disruption in cognitive disorders,” said Arnsten. “Our ability to apply a scientific approach to perplexing disorders such as schizophrenia is due to her groundbreaking research.”

Genes Involved in Birth Defects May Also Lead to Mental Illness

Gene mutations that lead to major birth defects may also cause subtle disruptions in the brain that contribute to psychiatric disorders such as schizophrenia, autism, and bipolar disorder, according to new research by UC San Francisco scientists.

Over the past several years, researchers in the laboratory of psychiatrist Benjamin Cheyette, MD, PhD, have shown that mutations in a gene called Dact1 cause cell signaling networks to go awry during embryonic development. Researchers observed that mice with Dact1 mutations were born with a range of severe malformations, including some reminiscent of spina bifida in humans.

This new study was designed to explore whether Dact1 mutations exert more nuanced effects in the brain that may lead to mental illness. In doing so, Cheyette, John Rubenstein, MD, PhD, and colleagues in UCSF’s Nina Ireland Laboratory of Developmental Neurobiology used a genetic technique in adult mice to selectively delete the Dact1 protein only in interneurons, a group of brain cells that regulates activity in the cerebral cortex, including cognitive and sensory processes. Poor function of interneurons has been implicated in a range of psychiatric conditions.

As reported in the June 24 online issue of PLOS ONE, researchers found that the genetically altered interneurons appeared relatively normal and had managed to find their proper position in the brain’s circuitry during development. But the cells had significantly fewer synapses, the sites where communication with neighboring neurons takes place. In additional observations not included in the new paper, the team also noted that the cells’ dendrites – fine extensions that normally form bushy arbors studded with synapses – were poorly developed and sparsely branched.

“When you delete this gene function after initial, early development – just eliminating it in neurons after they’ve formed – they migrate to the right place and their numbers are correct, but their morphology is a little off,” Cheyette said. “And that’s very much in line with the kinds of pathology that people have been able to identify in psychiatric illness.

"Neurological illnesses tend to be focal, with lesions that you can identify or pathology you can see on an imaging study," Cheyette explained. "Psychiatric illnesses? Not so much. The differences are really subtle and hard to see.”

Key Gene’s Role in Development of Human Nervous System

The Dact1 protein is part of a fundamental biological system known as the Wnt (pronounced “wint”) signaling pathway. Interactions among proteins in the Wnt pathway orchestrate many processes essential to life in animals as diverse as fruit flies, mice and humans, including the proper development of the immensely complex human nervous system from a single fertilized egg cell.

One way the Wnt pathway manages this task is by maintaining the “polarity” of cells during development, said Cheyette, “a process of sequestering, increasing the concentration of one set of proteins on one side of the cell and a different set of proteins on the other side of the cell.” Polarity is particularly important as precursor cells transform into nerve cells, Cheyette said, because neurons are “the most polarized cells in the body,” with specialized input and output zones that must wind up in the proper spots if the cells are to function normally.

Cheyette said his group is now conducting behavioral experiments with the mice analyzed in the new PLOS ONE paper and with genetically related mouse lines to test whether these mice have behavioral abnormalities in sociability, sensory perception, anxiety or motivation that resemble symptoms in major psychiatric disorders.

He also hopes to collaborate with UCSF colleagues on follow-up experiments to determine whether the activity of neurons lacking Dact1 is impaired in addition to the structural flaws identified in the new study and prior published work from his lab.

Meanwhile, as-yet-unpublished findings from human genetics research conducted by Cheyette’s group suggest that individuals with autism are significantly more likely than healthy comparison subjects to carry mutations in a Wnt pathway gene called WNT1.

“Just because a gene plays an important role in the embryo doesn’t mean it isn’t also important in the brain later, and might be involved in psychiatric pathology,” said Cheyette. “When these genes are mutated, someone may look fine, develop fine and have no obvious medical problems at birth, but they may also develop autism in childhood or have a psychotic break in adulthood and develop schizophrenia.”