Posts tagged psychology

FRIDAY, July 13 (HealthDay News) — Movies often stereotype people with schizophrenia as being violent and unpredictable, says a researcher who claims Hollywood dispenses misinformation about symptoms, causes and treatment of this mental illness.

Hollywood portrayals are often inaccurate, misleading, study shows.

For the study, published in the July issue of Psychiatric Services, Patricia Owen of the psychology department at St. Mary’s University in San Antonio, Texas, reviewed 41 English-language films released between 1990 and 2010 that featured at least one main character with schizophrenia.

Owen found that 83 percent of those characters were portrayed as dangerous or violent to others or themselves. Almost one-third engaged in homicidal behavior, and one-quarter committed suicide, the researcher said.

According to the U.S. National Institute of Mental Health, the risk of violence is small among people with schizophrenia. But suicide risk is higher than average. About 10 percent, mostly young men, do kill themselves, the agency notes.

Delusions, auditory and visual hallucinations, and disorganized speech or thought were displayed by most of the characters, the study author pointed out in a news release from the American Psychiatric Association.

But much more common symptoms of schizophrenia — such as flat affect, lack of speech and lack of motivation — were seen much less frequently.

Although schizophrenia incidence is nearly equal among women and men, almost 80 percent of the characters with schizophrenia were male, the study found.

The review noted, however, the movies did get some characterizations of schizophrenia right. Specifically, about half of the characters had low socioeconomic status, which is consistent with data on the illness. Moreover, about half of the movies depicted or alluded to the use of medication to treat the mental illness. Psychotherapy and group therapy were not portrayed often.

Owen suggested that more research is needed to understand how films influence public perceptions about schizophrenia, and to determine how to increase empathy and understanding.

Films featuring a character with schizophrenia include A Beautiful Mind and Donnie Darko.

Source: DoctorsLounge

ScienceDaily (July 13, 2012) — A new study by University of North Carolina School of Medicine researchers found that 31 percent of children identified as at risk for autism spectrum disorders (ASD) at 12 months received a confirmed diagnosis of ASD by age 3 years.

In addition, 85 percent of the children found to be at risk for ASD based on results from the First Year Inventory (FYI), a 63-item questionnaire filled out by their parents, had some other developmental disability or concern by age three, said Grace Baranek, PhD, senior author of the study and an autism researcher with the Program for Early Autism, Research, Leadership and Service (PEARLS) in the Department of Allied Health Sciences at the UNC School of Medicine.

"These results indicate that an overwhelming majority of children who screen positive on the FYI indeed experience some delay in development by age three that may warrant early intervention," she said.

Lead author of the study, Lauren Turner-Brown, PhD, also a researcher with PEARLS and the Carolina Institute for Developmental Disabilities said, “Identification of children at risk for ASD at 12 months could provide a substantial number of children and their families with access to intervention services months or years before they would otherwise receive a traditional diagnosis.”

The First Year Inventory was developed by Grace Baranek, PhD, Linda Watson, EdD, Elizabeth Crais, PhD and J. Steven Reznick, PhD, who are all researchers with PEARLS. All are also co-authors of the study with Turner-Brown, published online ahead of print on July 10, 2012 by Autism: The International Journal of Research & Practice.

In the study, parents of 699 children who had completed the FYI when their child was 12 months old completed additional screening questionnaires when their child reached age 3. In addition, children who were found to be at risk for ASD based on these measures were invited for in-person diagnostic evaluations.

"These findings are encouraging and suggest promise in the approach of using parent report of infant behaviors as a tool for identifying 12-month-olds who are at risk for an eventual diagnosis of ASD," Turner-Brown said.

Source: Science Daily

ScienceDaily (July 12, 2012) — Negative suggestion can induce symptoms of illness. Nocebo effects are the adverse events that occur during sham treatment and/or as a result of negative expectations. While the positive counterpart — the placebo effect — has been intensively studied in recent years, the scientific literature contains few studies on nocebo phenomena. In the latest issue of Deutsches Ärzteblatt International, Winfried Häuser of the Technical University of Munich and his co-authors present the underlying neurobiological mechanisms and highlight the relevance of the nocebo effect in everyday clinical practice.

Nocebo responses can, for instance, be brought about by unintended negative suggestion on the part of doctors or nurses, e.g., when informing the patient about the possible complications of a proposed treatment. It is also assumed that a certain proportion of the undesired effects of drugs can be attributed to nocebo effects. The mechanisms behind this phenomenon are — as with placebo effects — learning by Pavlovian conditioning and reaction to induced expectations.

What are the consequences for clinical practice? Doctors find themselves in an ethical dilemma between their obligation to tell the patient about the possible side effects of a treatment and their duty to minimize the risk of a medical intervention and thus to avoid triggering nocebo effects. As one possible strategy to solve this dilemma, Häuser et al. suggest emphasizing the tolerability of therapeutic measures. Another option, with the patient’s permission, would be to desist from discussing undesired effects during the patient briefing.

Source: Science Daily

ScienceDaily (July 12, 2012) — University of Kansas researchers have found larger resting pupil size and lower levels of a salivary enzyme associated with the neurotransmitter norepinephrine in children with autism spectrum disorder.

However, even though the levels of the enzyme, salivary alpha-amylase (sAA), were lower than those of typically-developing children in samples taken in the afternoon in the lab, samples taken at home throughout the day showed that sAA levels were higher in general across the day and much less variable for children with ASD.

"What this says is that the autonomic system of children with ASD is always on the same level," Christa Anderson, assistant research professor, said. "They are in overdrive."

The sAA levels of typically-developing children gradually rise and fall over the day, said Anderson, who co-directed the study with John Colombo, professor of psychology.

Norepinephrine (NE) has been found in the blood plasma levels of individuals with ASD but some researchers have questioned whether these levels were just related to the stress from blood draws.

The KU study addressed this by collecting salivary measures by simply placing a highly absorbent sponge swab under the child’s tongue and confirmed that this method of collection did not stress the children by assessing their stress levels through cortisol, another hormone.

Collecting sAA levels has the potential for physicians to screen children for ASD much earlier, noninvasively and relatively inexpensively, said Anderson.

But Anderson and Colombo also see pupil size and sAA levels as biomarkers that could be the physiological signatures of a possible dysfunction in the autonomic nervous system.

"Many theories of autism propose that the disorder is due to deficits in higher-order brain areas," said Colombo. "Our findings, however, suggest that the core deficits may lie in areas of the brain typically associated with more fundamental, vital functions."

The study, published online in the May 29, 2012 Developmental Psychobiology compared children between the ages of 20 and 72 months of age diagnosed with ASD to a group of typically developing children and a third group of children with Down Syndrome.

Both findings address the Centers for Disease Control’s urgent public health priority goals for ASD: to find biological indicators that can both help screen children earlier and lead to better understanding of how the nervous system develops and functions in the disorder.

Source: Science Daily

ScienceDaily (July 12, 2012) — Researchers at Emory University School of Medicine have identified five rare mutations in a single gene that appear to increase the chances that a boy will develop an autism spectrum disorder (ASD).

Mutations in the AFF2 gene, and other genes like it on the X chromosome, may explain why autism spectrum disorders affect four times as many boys as girls.

The mutations in AFF2 appeared in 2.5 percent (5 out of 202) boys with an ASD. Mutations in X chromosome genes only affect boys, who have one X chromosome. Girls have a second copy of the gene that can compensate.

The results were published July 5 in the journal Human Molecular Genetics.

"Our data suggest that AFF2 could be one of the major X-linked risk factors for ASD’s," says senior author Michael Zwick, PhD, assistant professor of human genetics at Emory University School of Medicine.

The finding bolsters a growing consensus among geneticists that rare variants in many different genes contribute significantly to risk for autism spectrum disorders.

The mutations in the AFF2 gene probably do not cause ASDs all by themselves, Zwick says.

"We do not think that the variants we have identified are monogenic causes of autism," he says. "Our data does support the idea that this is an autism susceptibility gene."

In some situations, mutations in a single gene are enough by themselves to lead to a neurodevelopmental disorder with autistic features, such as fragile X syndrome or tuberous sclerosis complex. But these types of mutations are thought to account for a small number of ASD cases.

Recent large-scale genetic studies of autism spectrum disorders have identified several “rare variants” that sharply increase ASD risk. Scientists believe rare variants could explain up to 15 or 20 percent of ASD cases. However, until now no single variant has been found in more than one percent of ASD cases.

Working with Zwick, postdoctoral fellow Kajari Mondal and her colleagues read the sequence of the AFF2 gene in DNA from 202 boys diagnosed with autism spectrum disorders. The patient samples came from the Autism Genetic Resource Exchange and the Simons Simplex Collection.

Tests showed that in four cases, the affected boys had inherited the risk-conferring mutations from their mothers. One boy had a “de novo” (not coming from the parents) mutation. Compared with X-linked genes in unaffected people, mutations in AFF2 were five times more abundant in the boys with ASDs.

The AFF2 gene had already been identified as responsible for a rare inherited form of intellectual disability with autistic features. This effect is seen when the AFF2 gene is deleted or silenced completely.

AFF2 has some similarity to FMR1, the gene responsible for fragile X syndrome. Like FMR1, it can be silenced by a triplet repeat. In these cases, the presence of the triplet repeat (three genetic bases repeated dozens of times) triggers a change in chromosomal structure that prevents the gene from being turned on.

In contrast, the mutations Zwick’s team found are more subtle, slightly changing the sequence of the protein AFF2 encodes. Little is known about the precise function of the AFF2 protein. A related gene in fruit flies called lilliputian also appears to regulate the development of neurons.

Zwick says one of his laboratory’s projects is to learn more about the function of the AFF2 gene, and to probe how the mutations identified by his team affect the function. His team is also working on gauging the extent to which other genes on the X chromosome contribute to autism risk.

Source: Science Daily

July 12, 2012

(HealthDay) — A supplement mixture (Souvenaid) containing dietary precursors and specific nutrients can improve memory in drug-naive patients with mild Alzheimer’s disease (AD), according to a study published in the July issue of the Journal of Alzheimer’s Disease.

Philip Scheltens, M.D., from the VU University Medical Center in Amsterdam, and colleagues conducted a 24-week, randomized, controlled trial in which drug-naive patients with mild AD were randomized in a 1:1 ratio to receive Souvenaid or an iso-caloric control product once daily. Memory function was assessed using the domain z-score of the Neuropsychological Test Battery (NTB).

The researchers found that, over the intervention period, the NTB memory domain z-score was significantly increased in patients taking Souvenaid versus the control group (P = 0.023), with a trend toward improvement in the NTB total composite z- score (P = 0.053). Functional connectivity in the delta band, as measured by an electroencephalography, was significantly different between the study groups in favor of the active group. There was very high adherence to the intervention (96.6 percent for the control and 97.1 percent for the active group). Both products were well tolerated and there was no between-group difference in the occurrence of serious adverse events.

"In conclusion, this study confirms that Souvenaid is well tolerated and improves memory performance,” the authors write. “Our results warrant further investigation of the clinical potential of Souvenaid in preclinical or clinical conditions characterized by synaptic loss, in particular AD.”

Several authors disclosed financial ties to Danone Research BV and Nutricia Advanced Medical Nutrition, which sponsored the study and manufacture Souvenaid.

Source: medicalxpress.com

ScienceDaily (July 12, 2012) — Obesity is not to blame for poor educational performance, according to early findings from research funded by the Economic and Social Research Council (ESRC). In a study that combines statistical methods with genetic information, researchers dispel the false idea that being overweight has damaging educational consequences.

Previous studies have shown that children who are heavier are less likely to do well at school. However, Dr Stephanie von Hinke Kessler Scholder from University of York argues it’s vital to understand what drives this association. “We sought to test whether obesity ‘directly’ hinders performance due to bullying or health problems, or whether kids who are obese do less well because of other factors that are associated with both obesity and lower exam results, such as coming from a disadvantaged family,” Dr Scholder explains.

Researchers examined data on almost 4,000 members of the Children of the 90s Birth Cohort Study. These data include the children’s DNA. It is well known that genes are randomly allocated within a population, irrespective of factors such as socio-economic position. The researchers combined the latest developments from genetic epidemiology with statistical methodologies in economic and econometric research. Using two carefully chosen ‘genetic markers’, the research team was able to identify children with a slightly higher genetic pre-disposition to obesity.

“Based on a simple correlation between children’s obesity as measured by their fat mass and their exam results, we found that heavier children did do slightly worse in school,” Dr Scholder points out. “But, when we used children’s genetic markers to account for potentially other factors, we found no evidence that obesity causally affects exam results. So, we conclude that obesity is not a major factor affecting children’s educational outcomes.”

These findings suggest that the previously found negative relationship between weight and educational performance is driven by factors that affect both weight and educational attainment. Future research should focus on other determinants of poor educational outcomes, such as social class or a family’s socio-economic circumstances, Dr Scholder points out.

The finding that obesity is not a cause of poorer educational performance is, the researchers suggest, a positive thing. “Clearly there are reasons why there are differences in educational outcomes, but our research shows that obesity is not one of them,” Dr Scholder argues.

Source: Science Daily

July 12, 2012

Biologists at UC San Diego have discovered a chemical that offers a completely new and promising direction for the development of drugs to treat metabolic disorders such as type 2 diabetes—a major public health concern in the United States due to the current obesity epidemic.

Their discovery, detailed in a paper published July 13 in an advance online issue of the journal Science, initially came as a surprise because the chemical they isolated does not directly control glucose production in the liver, but instead affects the activity of a key protein that regulates the internal mechanisms of our daily night and day activities, which scientists call our circadian rhythm or biological clock.

Scientists had long suspected that diabetes and obesity could be linked to problems in the biological clock. Laboratory mice with altered biological clocks, for example, often become obese and develop diabetes. Two years ago, a team headed by Steve Kay, dean of the Division of Biological Sciences at UC San Diego, discovered the first biochemical link between the biological clock and diabetes. It found that a key protein, cryptochrome, that regulates the biological clocks of plants, insects and mammals also regulates glucose production in the liver and that altering the levels of this protein could improve the health of diabetic mice.

Now Kay and his team have discovered a small molecule—one that can be easily developed into a drug—that controls the intricate molecular cogs or timekeeping mechanisms of cryptochrome in such a manner that it can repress the production of glucose by the liver. Like mice and other animals, humans have evolved biochemical mechanisms to keep a steady supply of glucose flowing to the brain at night, when we’re not eating or otherwise active.

"At the end of the night, our hormones signal that we’re in a fasting state," said Kay. "And during the day, when we’re active, our biological clock shuts down those fasting signals that tell our liver to make more glucose because that’s when we’re eating."

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