Delay in Shifting Gaze Linked to Early Brain Development in Autism

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At 7 months of age, children who are later diagnosed with autism take a split second longer to shift their gaze during a task measuring eye movements and visual attention than do typically developing infants of the same age, according to researchers supported by the National Institutes of Health.

The difference between the groups’ test results was 25 to 50 milliseconds on average, the researchers found, too brief to be detected in social interactions with an infant. However, they showed that this measurable delay could be accounted for by differences in the structure and organization of actively developing neurological circuits of a child’s brain.

When they were infants, children who were later diagnosed with autism took longer to shift their gaze during a measure of eye movements than did infants who were not diagnosed with autism. The researchers believe that brain circuits involved with a brain structure known as the splenium of the corpus callosum (shown in this scan) may account for the differences in gaze shifting between the two groups. Image courtesy of Jason Wolff, Ph.D., University of North Carolina at Chapel Hill.

Efficiently shifting attention early in infancy is thought to be important for later social and cognitive development. Split-second delays, the researchers suggested, could be a precursor to such well known symptoms of autism as difficulty making eye contact or following a parent’s pointing finger, problems that generally emerge after a child turns 1. Typically, autism spectrum disorder (ASD) is not diagnosed until after 3 or 4 years of age.

–National Institutes for Health

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Twitter Chat on Wed. May 8th: NIMH Experts Discuss Childhood Rapid-onset OCD

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NIMH’s next Twitter Chat will focus on Pediatric Autoimmune Neuropsychiatric Disorders Associated with Strep Infections (PANDAS) and its related syndrome Pediatric Acute-onset Neuropsychiatric Syndrome (PANS). The chat is scheduled for Wednesday, May 8 at 11AM ET. You can find more information about PANDAS and the chat here:http://www.nimh.nih.gov/news/science-news/2013/twitter-chat-on-pandas-pans.shtml

Twitter: NIMH experts will discuss childhood rapid-onset #OCD called #PANDAS & #PANS in a Twitter chat May 8th @ 11am ET: http://1.usa.gov/YjGJd2

Facebook: NIMH will have a second Twitter chat in honor of National Children’s Mental Health Awareness Day on May 8th from 11 a.m. to noon ET on rapid-onset obsessive-compulsive disorder (OCD) in children, which is called Pediatric Autoimmune Neuropsychiatric Disorders Associated with Strep Infections (PANDAS) and its related syndrome Pediatric Acute-onset Neuropsychiatric Syndrome (PANS). For more on the chat and PANDAS/PANS, please visit: http://1.usa.gov/YjGJd2

Developing Male Brain Exposed to Less Stress-Protective Protein

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Why are rates of schizophrenia and autism higher in males? New evidence implicates an enzyme expressed in the placenta that helps protect the developing fetal brain from adverse effects of maternal stress early in pregnancy. Video: NIMH grantee Tracy Bale, Ph.D., of the University of Pennsylvania, discussed her line of research into how maternal stress might differentially affect the developing male brain during an interview at the 2011 Society for Neuroscience meeting.

Since then, Bale and colleagues discovered in mice that the gene that makes the enzyme, called OGT, is expressed less in placentas of male than in female offspring. Moreover, OGT was also expressed at relatively lower levels in placentas from stressed mothers. When they looked at evidence of its expression in human placentas, they saw a similar pattern of sex differences. Further experiments in mice confirmed that OGT plays a pivotal role in regulating the turning on-and-off of hundreds of brain genes and in protecting the developing brain from insults. The researchers suggest that OGT epigenetically places male fetuses at a disadvantage in adapting to environmental changes – a possible mechanism underlying males’ increased vulnerability to enduring effects of maternal stress on brain development.

–National Institute of Mental Health

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Adults Experiencing Mental Illness or a Substance Use Disorder Account for Nearly 40 Percent of all Cigarettes Smoked

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Adults aged 18 or older who experienced any mental illness or who have had a substance use disorder in the past year are more likely to smoke and to smoke more heavily than others according to a new report by the Substance Abuse and Mental Health Services Administration (SAMHSA).

According to the report, adults experiencing any mental illness or a substance use disorder in the past year represent 24.8 percent of the adult population, but that same group used 39.6 percent of all cigarettes smoked by adults.

In terms of rates of cigarette smoking, 38.3 percent of adults experiencing mental illness or substance use disorders were current smokers as opposed to 19.7 percent of those adults without these conditions. That means that the rate of current cigarette smoking among adults experiencing mental illness or substance use disorders is 94 percent higher than among adults without these disorders.

The report reveals that although people with substance use disorders and no mental disorder constitute only 4.9 percent of adults over age 18, they smoked 8.7 percent of all cigarettes. Similarly, although those who had experienced both mental illness and a substance use disorder represented only 3.8 percent of the population in the past year, they smoked 9.5 percent of all cigarettes.

The report defines any mental illness as any diagnosable mental, behavioral, or emotional disorder other than a substance use disorder. The report defines a substance use disorder as dependence on or abuse of alcohol or illicit drugs.

“It has long been a public health priority to develop effective smoking prevention and cessation programs,” said SAMHSA Administrator Pamela S. Hyde. “This report highlights a clear disparity. It shows that people dealing with mental illness or substance abuse issues smoke more and are less likely to quit. We need to continue to strengthen efforts to figure out what works to reduce and prevent smoking for people with mental health conditions,” said Administrator Hyde.

To address the high rates of tobacco use among people with mental or substance use disorders, SAMHSA, in partnership with the Smoking Cessation Leadership Center (SCLC), has developed a portfolio of activities designed to promote tobacco cessation efforts in behavioral health care. SAMHSA and the SCLC launched the 100 Pioneers for Smoking Cessation Campaign, which provides support for mental health and substance abuse treatment facilities and organizations to undertake tobacco cessation efforts. This program has been expanded in conjunction with state Leadership Academies for Wellness and Smoking Cessation, whose goal is to reduce tobacco use among those with behavioral health needs. Participating states bring together policymakers and stakeholders (including leaders in tobacco control, mental health, substance abuse, public health, and consumers) to develop a collaborative action plan.

–SAMHSA

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Five Major Mental Disorders Share Genetic Roots

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Five major mental disorders share some of the same genetic risk factors, the largest genome-wide study of its kind has found.  Evidence for such genetic overlap had previously been limited to pairs of disorders.

National Institutes of Health-funded researchers discovered that people with disorders traditionally thought to be distinct – autism, ADHD, bipolar disorder, major depression and schizophrenia – were more likely to have suspect genetic variation at the same four chromosomal sites. These included risk versions of two genes that regulate the flow of calcium into cells.

“These results will help us move toward diagnostic classification informed by disease cause,” said Jordan Smoller, M.D., of Massachusetts General Hospital, Boston, a coordinator of the study, which was supported by NIH’s National Institute of Mental Health. “Although statistically significant, each of these genetic associations individually can account for only a small amount of risk for mental illness, making them insufficient for predictive or diagnostic usefulness by themselves.”

Smoller, Kenneth Kendler, M.D.,, Virginia Commonwealth University, Richmond; Nicholas Craddock, PhD., Cardiff University, England; Stephan Ripke, M.D., Massachusetts General, Patrick Sullivan, M.D., University of North Carolina at Chapel Hill, and colleagues in the Cross-Disorder Group of the Psychiatric Genomics Consortium, report on their findings February 28, 2013 in The Lancet.

Prior to the study, researchers had turned up evidence of shared genetic risk factors for pairs of disorders, such as schizophenia and bipolar disorderautism and schizophrenia and depression and bipolar disorder. Such evidence of overlap at the genetic level has blurred the boundaries of traditional diagnostic categories and given rise to research domain criteria, or RDoC, an NIMH initiative to develop new ways of classifying psychopathology for research based on neuroscience and genetics as well as observed behavior.

To learn more, the consortium researchers analyzed the five key disorders as if they were the same illness. They screened for evidence of illness-associated genetic variation across the genomes of 33,332 patients with all five disorders and 27,888 controls, drawing on samples from previous consortium mega-analyses.

For the first time, specific variations significantly associated with all five disorders were among several suspect genomic sites that turned up. These included variation in two genes that code for the cellular machinery for regulating the flow of calcium into neurons. Variation in one of these, called CACNA1C, which had previously been implicated in susceptibility to bipolar disorder, schizophrenia and major depression, is known to impact brain circuitry involved in emotion, thinking, attention and memory – functions disrupted in mental illnesses. Variation in another calcium channel gene, called CACNB2, was also linked to the disorders.

Alterations in calcium-channel signaling could represent a fundamental mechanism contributing to a broad vulnerability to psychopathology, suggest the researchers.

They also discovered illness-linked variation for all five disorders in certain regions of chromosomes 3 and 10. Each of these sites spans several genes, and the specific causal factors within them remain elusive. However, one region, called 3p21, which produced the strongest signal of illness association, harbors suspect variations identified in previous genome-wide studies of bipolar disorder and schizophrenia.

–National Institute of Mental Health

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Autism Risk Unrelated to Total Vaccine Exposure in Early Childhood

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A child’s risk for developing an autism spectrum disorder (ASD) is not increased by receiving “too many vaccines too soon,” according to a new study published in The Journal of Pediatrics.

Although previous scientific evidence has shown that vaccines do not cause autism, more than 1 in 10 parents refuse or delay vaccinations for their young children. A main safety concern of these parents is the number of vaccines administered, both on a single day and over the course of a child’s first 2 years of life.

In the first study of its kind, researchers from the CDC and Abt Associates, Inc. compared vaccine records for over 1000 children born from 1994–1999, some of whom were later diagnosed with ASD. The researchers calculated the total number of vaccine antigens each child received between birth and age 2, as well as the maximum number of antigens each child received on a single day.

The study found that the total number of vaccine antigens received was the same between children with ASD and those without ASD. Additionally, antigen number was also found to be unrelated to the development of two sub-categories of ASD—autistic disorder and ASD with regression.

The researchers concluded, “The possibility that immunological stimulation from vaccines during the first 1 or 2 years of life could be related to the development of ASD is not well-supported by what is known about the neurobiology of ASDs.”

–National Institute of Mental Health

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Study Shows That People With Serious Mental Illness Can Lose Weight

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People with serious mental illnesses such as schizophrenia, bipolar disorder, and major depression can lose weight and keep it off through a modified lifestyle intervention program, a National Institute of Mental Health (NIMH)-funded study reported online in The New England Journal of Medicine.

Over 80 percent of people with serious mental illnesses are overweight or obese, which contributes to them dying at three times the rate of the overall population. They succumb mostly to the same things the rest of the population experiences—cardiovascular disease, diabetes and cancer. Although antipsychotic medications increase appetite and cause weight gain in these patients, it is not the only culprit. Like the general population, sedentary lifestyle and poor diet also play a part. Lifestyle modifications such as diet and exercise should work for these patients, yet they are often left out of weight loss studies.

“People with serious mental illnesses are commonly excluded from studies to help them help themselves about their weight,” said Gail L. Daumit, M.D., of Johns Hopkins University, Baltimore, and the study’s lead author. “We’re showing that serious mentally ill patients can make successful, sustained changes with proper interventions.”

This study could usher in new forms of weight loss treatment for people with serious mental illness.

“Until now, obesity among those with serious mental illnesses has not received adequate attention,” said NIMH Director Thomas R. Insel, M.D. “People with serious mental illnesses need more attention to their physical health. This study provides convincing evidence these individuals can make substantial lifestyle changes and therefore should suffer fewer medical complications as they age.”

Other factors that preclude people with serious mental illnesses from losing weight include memory impairments or residual psychiatric symptoms that impede learning and adopting new behaviors such as counting calories. Socioeconomics are also a factor as many can’t afford or can’t get to physical activity programs like fitness gyms. Some patients additionally suffer from social phobia or have poor social interactions, and are simply afraid to work out in a public area.

Daumit’s group attempted to solve these issues by bringing the gyms and nutritionists to places most of these patients frequent—psychiatric rehabilitation outpatient programs. Under the trial name ACHIEVE, the researchers randomized 291 participants in 10 rehab centers around Maryland to receive the usual care, consisting of nutrition and physical activity information, or six months of intensive intervention consisting of exercise classes three times a week along with individual or group weight loss classes once a week. Both groups were followed for an additional year, during which the weight loss classes of the intervention arm tapered down but the exercise classes remained constant. The intervention arm included goals such as reducing caloric intake by avoiding sugar-sweetened beverages and junk food; eating five servings of fruits and vegetables daily; choosing smaller portions and healthy snacks; and moderate intensity aerobic exercise.

Participants in the specially tailored weight loss program lost seven pounds more than the controls—and continued to lose weight and did not regain, despite the reduced frequency of classes and counseling sessions. In contrast, the general population tends to experience peak weight loss in the first six months and then rebound and gain part or all of their weight back.

On average, each participant was on three psychotropic medications, with half on lithium or mood stabilizers, all known to cause weight gain. But no matter what they were on, they lost the weight.

“We’re showing behavioral interventions work regardless of what they’re taking,” Daumit said. Her group is now looking for ways to spread the program.

–National Institute of Mental Health

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Association Between Parental Hospital-Treated Infection and the Risk of Schizophrenia in Adolescence and Early Adulthood

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It has been suggested that infection during perinatal life may lie at the etiological root of schizophrenia. It has thus been hypothesized that the origin of schizophrenia may lie either in direct fetal infection and/or in a generally increased familial susceptibility to infections, some of which may occur during pregnancy. We explored these 2 hypotheses by assessing maternal infection during pregnancy and maternal as well as paternal infection in general as predictors of schizophrenia in their offspring. We found a slightly increased risk to be associated with prenatal infection exposure. However, the effect of prenatal infection exposure was not statistically significantly different from the effect of infection exposure in general. Parental infection appeared to be associated with development of schizophrenia in adolescence and early adulthood. Our study does not exclude a specific effect of infection during fetal life; yet, it does suggest that schizophrenia is associated with an increased familial liability to develop severe infection.

In a landmark study, Mednick et al[1] presented data that suggested that prenatal exposure to influenza infection during the second trimester was associated with schizophrenia illness later in life. Many studies have since tried to verify and expand this finding, though with mixed results. A recent meta-analysis by Selten et al[2] concludes that evidence to support the maternal influenza hypothesis remains insufficient. Studies on the association between infection and schizophrenia may be grouped into ecological studies and studies of birth cohorts. A majority have used an ecological design and therefore lack information on individual exposure status as stated in a review by Brown et al.[3] Some birth cohort studies have investigated the possible association between maternal infection during pregnancy and schizophrenia. A study following offspring of women examined serologically for rubella has related rubella to schizophrenia and related disorders in the offspring.[4] Studies using stored sera from pregnant women have linked the presence of maternal antibodies to influenza A virus,[5] herpes simplex virus type 2 (HSV-2),[6] and the protozoan Toxoplasma Gondii [7] to the subsequent development of schizophrenia spectrum disorders. Mortensen et al[8] using neonatal blood spots found an association with maternal IgG against T. Gondii and HSV-2.[9] Although these studies measured maternal IgG antibodies against specific infections, they could not determine if the mother became infected during pregnancy. Despite numerous well performed studies linking congenital or neonatal viral infections to schizophrenia, the viral hypothesis remains compelling but is as yet unproven. New data continue to emerge linking viral infections to the etiopathogenesis of schizophrenia and the use of biomarkers of prenatal infections in rigorous epidemiological

by Philip R. Nielsen, Thomas M. Laursen, Preben B. Mortensen

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