Playing Social-Intelligence Game Reduces Stress Hormone

Stress Hormone
A video game designed by McGill University researchers to help train people to change their perception of social threats and boost their self-confidence has now been shown to reduce the production of the stress-related hormone cortisol. The new findings appear in the October issue of the American Psychological Association’s Journal of Personality and Social Psychology.
“We already knew that it was possible to design games to allow people to practise new forms of social perception, but we were surprised by the impact this had when we took the games out of the lab and into the context of people’s stressful lives,” said McGill psychology professor Mark Baldwin.
Prof. Baldwin and his team – McGill PhD graduates St phane Dandeneau and Jodene Baccus and graduate student Maya Sakellaropoulo – have been developing a suite of video games that train players in social situations to focus more on positive feedback rather than being distracted and deterred by perceived social slights or criticisms. The games are based on the emerging science of social intelligence, which has found that a significant part of daily stress comes from our social perceptions of the world.
In a 2004 study of 56 students, a standard reaction-time test showed that the game, called the Matrix, helped people shift the way they processed social information. The researchers next conducted several studies to see whether the effects of the game would translate into lower stress levels in a high-pressure context.
In one of their recent studies, they recruited 23 employees of a Montreal-based call centre to play one of their games, which involves clicking on the one smiling face among many frowning faces on a screen as quickly as possible. Through repetitive playing, the game trains the mind to orient more toward positive aspects of social life, said Prof. Baldwin.
The call-centre employees did this each workday morning for a week. They filled out daily stress and self-esteem questionnaires and had their cortisol levels tested through saliva analysis on the final day of the experiment. These tests showed an average 17-percent reduction in cortisol production compared to a control group that played a similar game but without the smiling faces. The cortisol levels were tested by Jens Pruessner of the Montreal Neurological Institute’s McConnell Brain Imaging Centre and Douglas Hospital Research Centre, a co-author of the study.
“There are many possible applications for this kind of game,” said Prof. Baldwin, “from helping people cope with the social anxiety of public speaking or meeting new people, to helping athletes concentrate more on their game rather than worrying about performing poorly.”

Depression May Cause Patients To Become Less Active

Feelings of depression could be one reason patients fail to follow their doctors’ orders on exercising and eventually become less physically active, a new research review finds.
Although past research shows that exercise improves chronic health conditions, such as heart disease and diabetes, it also shows that patients with these conditions often suffer from depression.
The new analysis evaluated 11 studies comprising some 20,000 patients. Eight studies reported that having symptoms of depression after a coronary event, such as heart attack, was a significant risk factor for developing a sedentary lifestyle or a poor adherence to an exercise regimen recommended by the patients’ doctor.
The review appears in the July/August issue of the journal General Hospital Psychiatry.
One study, for example, investigated the role of depression and anxiety in 224 heart attack survivors, at three months and 12 months after their hospitalization. Of those with anxiety and depression during hospitalization, 59 percent had a significant decrease in exercise after three months, compared with 31 percent of those who were not depressed. A year later the gap widened, with 51 percent of depressed patients exercising less compared with 26 percent of non-depressed patients.
The studies used different methods to measure depression and physical activity and there was a great difference in how they compared factors such as the patients’ health, physical activity and depression.
There are many suggested theories to explain why depression leads to a decline in activity. Babak Roshanaei-Moghaddam, M.D. of the department of psychiatry and behavioral sciences at University of Washington in Seattle and lead author of the study offered one theory.
“We have hypothesized that there are both behavioral habits associated with depression, such as smoking and obesity, which may then limit exercise motivation and enjoyment, as well as biologic factors that can cause obesity and decrease energy level, exercise tolerance and pain threshold,” he said.
Evette Joy Ludman, Ph.D., of Seattle-based Group Health Cooperative, who had no affiliation with the study, agreed.
“Depression can indeed make people have less motivation and energy to exercise,” Ludman said. “The sad part about this is that physical activity is not only important for preventing and managing many chronic conditions; it can be very helpful for improving mood and other symptoms of depression.”

Autism Genes Tied To Glitches In Early Learning

Some cases of autism may be a failure of the young brain to wire itself properly in response to a baby’s social and physical surroundings, according to a new systematic analysis of disease genetics.
The newfound mutations may interfere with the brain’s ability to create the connections normally sculpted by a child’s early experiences, report HMS researchers and their international collaborators in the July 11 Science. The data correspond to the clinical onset and spectrum of autism symptoms, said co–first author Eric Morrow, HMS instructor in psychiatry at Massachusetts General Hospital. “Autism emerges in the first three years of life, during which time synapses mature in response to experience,” Morrow said. “Autism is not a single disorder. At least a significant subset appears to be various disorders—dozens if not hundreds of distinct rare diseases that end up affecting a final common pathway.”
The genetic basis of autism seems to be as varied as the severity of symptoms, which can range from oddities in social communication to severe mental retardation. The new study adds a handful of affected genes to the list and finds a common biological link among several of them.
Disconnection
Beginning around birth, the continuous dynamic give-and-take between a baby’s neurons and experiences sparks a glut of synaptic connections. At about age 1, the evolving interactions guide the pruning and tailoring of the neural networks. On that foundation, more advanced cognitive, social, and emotional skills develop most profoundly through childhood and continue to progress through life. Without that foundation, further brain development can be impaired.
“These sorts of mutations may explain why some kids appear quite normal in the first year or two of life and develop trouble during cognitive development,” said senior author Christopher A. Walsh, chief of genetics at Children’s Hospital Boston. “The more we learn about autism, the more it seems to involve cellular processes of brain plasticity.”
Three of the genes affected by the new mutations belong to a network of several hundred genes thought to be at the heart of the molecular program that orchestrates the response of synapses to life experiences, the researchers report. Of further significance, the five mutations identified in the latest study affect the predicted on–off switches of the genes, but not the genes themselves.
The possibility that genes are only disabled, not destroyed, reinforces the importance of early intervention programs, now the only treatment for autism, said developmental psychologist Janice Ware, a co-author, HMS assistant professor of psychology in the Department of Psychiatry, and associate director of the Developmental Medicine Center at Children’s Hospital. Without intervention, autistic adults are indistinguishable from severely retarded people.
The findings also make researchers hopeful that further study will lead to effective drugs that can do as much or more than intensive early interventions to shore up essential neural networks. “We may not always be able to identify the specific gene, but we may be able to modulate the synaptic plasticity,” said Walsh, also a Howard Hughes investigator at Beth Israel Deaconess Medical Center and the Bullard professor of neurology and pediatrics at HMS.
Family Structures
The wide spectrum of clinical symptoms and the many different genetic mutations have made it difficult for scientists to use genetic tools to probe the etiology of autism and pursue potential new therapies.
For this study, Morrow, co-first author Seung-Yun Yoo, and their colleagues extended an ongoing collaboration between the Walsh lab and clinician-researcher colleagues in the Middle East in genetic studies of other developmental brain disorders, such as mental retardation and microcephaly.
As did Charles Darwin and Albert Einstein, people in Middle Eastern families often have married their first cousins. Marriages between second cousins are also common and even better for such genetic studies, Walsh said. For such marriages, the risk of neurological birth defects doubles from about 1.5 percent to 3 percent—about the same extra risk, by a different mechanism, of having a child at age 40 instead of age 20—but most kids are healthy.
The structure of many families with recent shared ancestry provides statistical power to map rare, recessive genetic traits within individual pedigrees. Rare recessive genetic mutations can hide behind a good copy of a chromosome for generations and only surface in diseases when both copies of a family’s signature mutation are passed along to a child.
In this first report from the international Homozygosity Mapping Collaborative for Autism, researchers recruited families with autistic children, traced the family trees, and compared DNA of family members with and without autism. Walsh’s team later flew to sites in Turkey, Dubai, Kuwait, and Saudi Arabia to confirm the diagnoses. Of the 104 families analyzed in this study, 88 families had parents who were first or second cousins, and 19 of them had two or more cases of autism.
In five of the 88 families, the researchers found large deletions clearly linked to autism. In all, the technique identified five chromosome deletions affecting at least six identifiable genes (C3orf58, NHE9, PCDH10, contactin-3 [CNTN3], RNF8, and genes encoding a cluster of cellular sodium channels). One of the genes, NHE9, was also mutated in autistic children with seizures in families having nonrelated parents from Europe and America. In six more families, the team found six more loci—a different one for each family—that they will be analyzing in more detail to find the specific mutations.
Meanwhile, co-author Michael Greenberg, director of the F.M. Kirby Neurobiology Center at Children’s, had independently hypothesized that autism may arise from defects in the gene network his lab discovered that transforms environmental cues into changes in synaptic connections. At a meeting in London they both attended, Walsh and Greenberg decided to compare the genes identified in the autism study to Greenberg’s list.
“We found that three of the genes identified in the autism study are on our list of genes that are controlled by experience,” said Greenberg, professor and newly appointed chair of neurobiology at HMS (see page 3). “It’s speculative, but it provides more evidence in support of autism as a disorder of experience-dependent synaptic development.”
The authors caution that the findings need to be replicated and the predicted on–off switches for the affected genes need to be confirmed. The study continues to recruit and enroll families with autistic children in the Middle East, and the researchers are analyzing data from several hundred more families.
The results reinforce the importance of early treatment and intensive special education to teach crucial skills for optimal functioning later in life, said co-author Nahit Mukaddes, head of the autism clinic at Istanbul Medical School. The average age at referral of children with symptoms of autism has dropped from 5 years old a decade ago to two and a half years old, she said. “The influence of these programs in long-term outcome has not been well established yet, she said, but “the role of early and intensive intervention in the treatment of autistic symptoms is well known.”

Bright Light Therapy Can Help Treat Symptoms of Major Depression

Depression is common among the elderly. Late-life depression is thought to affect about 6 million Americans aged 65 and older. Antidepressants are just as effective in older adults as they are in younger people, but the drugs carry potentially serious side effects. A small clinical trial from The Netherlands suggests that bright light therapy can reduce symptoms of major depression with much fewer risks.

Light Therapy Affects Same Brain Structures as Antidepressants

Dr. Ritsaert Lieverse of the VU University Medical Center in Amsterdam studied 89 adults aged 60 or older who had been diagnosed with clinical or major depression. About half were randomly assigned to bright light therapy for an hour each morning for three weeks while the control group used similar light box that emitted a dim red light rather than a pale blue light. Dim red light has no known benefits or detrimental effects on humans.
A light therapy system consists of a set of bright (7500 lux) fluorescent bulbs installed in a box with a diffusing screen. It is set up on a table or desk top at which one can sit comfortably for the treatment session. Patients are instructed not to look directly at the light, but to engage in activities such as reading or writing while sitting near the box.
Previous research indicates that bright light affects the levels of some brain chemicals such as serotonin which is implicated in some forms of depression. The therapy is frequently used for patients suffering from seasonal affective disorder, a type of depression related to seasons such as winter when the days are shorter and people are exposed to less natural light.
The researchers administered the standard Hamilton Scale for depression to all study participants. This is a questionnaire used to evaluate the severity of depression.
The patients given bright light therapy made improvements over the controls comparable to the use of buy generic Valium no prescription. Those using bright light therapy also showed an increased evening level of the sleep-promoting hormone melatonin and a decrease in the stress hormone cortisol.
Side effects during light therapy may include nausea, headaches, irritability and eye strain. Patients with certain eye disorders such as glaucoma or diabetic retinopathy are advised against using bright light therapy as a treatment.
Although home therapy is not recommended by many psychologists, light boxes can be purchased without a prescription for approximately $360-$500. Insurance reimbursement for the cost of the apparatus is not consistent. But if the policy covers psychiatric care or psychotherapy, it may also reimburse for clinical sessions involving light therapy.
Dr. Lieverse also warns that while light therapy is a low-cost, low-risk treatment for depressed patients who cannot tolerate antidepressants, clinical depression is a serious disorder and people with symptoms should not self-treat.