Posts tagged science

ScienceDaily (June 21, 2012) — Eating disorders are commonly seen as an issue faced by teenagers and young women, but a new study reveals that age is no barrier to disordered eating. In women aged 50 and over, 3.5% report binge eating, nearly 8% report purging, and more than 70% are trying to lose weight. The study published in the International Journal of Eating Disorders revealed that 62% of women claimed that their weight or shape negatively impacted on their life.

The researchers, led by Dr Cynthia Bulik, Director of the University of North Carolina Eating Disorders Program, reached 1,849 women from across the USA participating in the Gender and Body Image Study (GABI) with a survey titled, ‘Body Image in Women 50 and Over — Tell Us What You Think and Feel.’

"We know very little about how women aged 50 and above feel about their bodies," said Bulik. "An unfortunate assumption is that they ‘grow out of’ body dissatisfaction and eating disorders, but no one has really bothered to ask. Since most research focuses on younger women, our goal was to capture the concerns of women in this age range to inform future research and service planning."

The average age of the participants was 59, while 92% were white. More than a quarter, 27%, were obese, 29% were overweight, 42% were normal weight and 2% were underweight.

Results revealed that eating disorder symptoms were common. About 8% of women reported purging in the last five years and 3.5% reported binge eating in the last month. These behaviors were most prevalent in women in their early 50s, but also occurred in women over 75.

When it came to weight issues, 36% of the women reported spending at least half their time in the last five years dieting, 41% checked their body daily and 40% weighed themselves a couple of times a week or more.

62% of women claimed that their weight or shape negatively impacted their life, 79% said that it affected their self-perception and 64% said that they thought about it daily.

The women reported resorting to a variety of unhealthy methods to change their body, including diet pills (7.5%), excessive exercise (7%), diuretics (2.5%), laxatives (2%) and vomiting (1%).

Two-thirds, 66%, were unhappy with their overall appearance and this was highest when it came to their stomach, 84%, and shape, 73%.

"The bottom line is that eating disorders and weight and shape concerns don’t discriminate on the basis of age," concluded Bulik. "Healthcare providers should remain alert for eating disorder symptoms and weight and shape concerns that may adversely influence women’s physical and psychological wellbeing as they mature."

Source: Science Daily

ScienceDaily (June 21, 2012) — A pioneering report of genome-wide gene expression in autism spectrum disorders (ASDs) finds genetic changes that help explain why one person has an ASD and another does not. The study, published by Cell Press on June 21 in The American Journal of Human Genetics, pinpoints ASD risk factors by comparing changes in gene expression with DNA mutation data in the same individuals. This innovative approach is likely to pave the way for future personalized medicine, not just for ASD but also for any disease with a genetic component.

ASDs are a heterogeneous group of developmental conditions characterized by social deficits, difficulty communicating, and repetitive behaviors. ASDs are thought to be highly heritable, meaning that they run in families. However, the genetics of autism are complex.

Researchers have found rare changes in the number of copies of defined genetic regions that associate with ASD. Although there are some hot-spot regions containing these alterations, very few genetic changes are exactly alike. Similarly, no two autistic people share the exact same symptoms. To discover how these genetic changes might affect gene transcription and, thus, the presentation of the disorder, Rui Luo, a graduate student in the Geschwind lab at UCLA, studied 244 families in which one child (the proband) was affected with an ASD and one was not.

In addition to identifying several potential new regions where copy-number variants (CNVs) are associated with ASDs, Geschwind’s team found genes within these regions to be significantly misregulated in ASD children compared with their unaffected siblings. “Strikingly, we observed a higher incidence of haploinsufficient genes in the rare CNVs in probands than in those of siblings, strongly indicating a functional impact of these CNVs on expression,” says Geschwind. Haploinsuffiency occurs when only one copy of a gene is functional; the result is that the body cannot produce a normal amount of protein. The researchers also found a significant enrichment of misexpressed genes in neural-related pathways in ASD children. Previous research has found that these pathways include other genetic variants associated with autism, which Geschwind explains further legitimizes the present findings.

Source: Science Daily

June 21, 2012 By Janice Wood

Thanks to science, we know that love lives in the brain, not the heart.

Now a new international study has mapped out where love and sexual desire are in the brain.

“No one has ever put these two together to see the patterns of activation,” says Dr. Jim Pfaus, professor of psychology at Concordia University.

“We didn’t know what to expect –the two could have ended up being completely separate. It turns out that love and desire activate specific but related areas in the brain.”

Working with colleagues in the United States and Switzerland, Pfaus analyzed the results of 20 separate studies that examined brain activity while subjects engaged in tasks such as viewing erotic pictures or looking at photographs of their significant others. Pooling this data enabled the scientists to form a map of love and desire in the brain.

They found that two brain structures, the insula and the striatum, are responsible for tracking the progression from sexual desire to love.

The insula is a portion of the cerebral cortex folded deep within an area between the temporal lobe and the frontal lobe, while the striatum is located nearby, inside the forebrain.

According to the researchers, love and sexual desire activate different areas of the striatum. The area activated by sexual desire is usually turned on by things that are inherently pleasurable, such as sex or food.

The area activated by love is involved in the process of conditioning in which things paired with reward or pleasure are given inherent value. That is, as feelings of sexual desire develop into love, they are processed in a different place in the striatum, the researchers explain.

This area of the striatum is also the part of the brain associated with drug addiction. Pfaus says there is good reason for this.

“Love is actually a habit that is formed from sexual desire as desire is rewarded,” he explains. “It works the same way in the brain as when people become addicted to drugs.”

However, the habit is not a bad one, he said, noting that love activates different pathways in the brain that are involved in monogamy and pair bonding. Some areas in the brain are actually less active when a person feels love than when they feel desire, he added.

“While sexual desire has a very specific goal, love is more abstract and complex, so it’s less dependent on the physical presence someone else,” says Pfaus.

Source: PsychCentral

June 20, 2012 By Robin Erb

Go ahead - do it: Grab a pencil. Right now. Write your name backward. And upside down. Awkward, right?

But if researchers and neurologists are correct, doing exercises like these just might buy you a bit more time with a healthy brain.

Some research suggests that certain types of mental exercises - whether they are memory games on your mobile device or jotting down letters backward - might help our gray matter maintain concentration, memory and visual and spatial skills over the years.

"There is some evidence of a use-it-or-lose-it phenomenon," says Dr. Michael Maddens, chief of medicine at Beaumont Hospital, Royal Oak, Mich.

Makers of computer brain games, in fact, are tapping into a market of consumers who have turned to home treadmills and gym memberships to maintain their bodies, and now worry that aging might take its toll on their mental muscle as well.

But tweaking every day routines can help.

Like brushing your teeth with your non-dominant hand. Or crossing your arms the opposite way you’re used to, says Cheryl Deep, who leads “Brain Neurobics” sessions on behalf of the Wayne State Institute of Gerontology.

At a recent session in Novi, Mich., Deep encouraged several dozen senior citizens to flip the pictures in their homes upside-down. It might baffle houseguests, but the exercise crowbars the brain out of familiar grooves cut deep by years of mindless habit.

"Every time you walk past and look, your brain has to rotate that image," Deep says. "Brain neurobics is about getting us out of those ruts, those pathways, and shaking things up."

Participants were asked to call out the color of ink that flashed on a screen in front them. The challenge: The colors spelled out names of other colors. Blue ink spelled o-r-a-n-g-e, for example.

Several in the crowd at Waltonwood Senior Living hesitated - a few scrunching up faces in concentration. The first instinct is to say “orange.”

In another exercise, participants had to try to name as many red foods as possible. Apple? Sure that’s an easy one. It took a while, but the crowd eventually made its way to pomegranate and pimento.

Elissa and Hal Leider chuckled with friends as they tested their recall.

Hal Leider, 82, a retired carpenter, was diagnosed with early-stage Alzheimer’s, and he tries to challenge himself mentally and physically - bowling and shooting pool and playing poker: “I think anything we can do might be helpful,” says Elissa Leider, 74.

The idea of mental workouts marks a dramatic shift in how we understand the brain these days.

"We want to stretch and flex and push" the brain, says Moriah Thomason, assistant professor in Wayne State University School of Medicine’s pediatrics department and in the Merrill Palmer Skillman Institute for Child and Family Development

Thomason also is a scientific adviser to http://www.Lumosity.com, one of the fastest-growing brain game websites.

"We used to think that what you’re born with is what you have through life. But now we understand that the brain is a lot more plastic and flexible than we ever appreciated," she says.

Still, like the rest of your body, aging takes its toll, she says.

The protective covering of the neural cells - white matter - begins to shrink first. Neural and glial cells, often called the gray matter, begin to shrink as well, but more slowly. Neurotransmitters, or chemical messengers, decrease.

But challenging the brain stimulates neural pathways - those tentacles that look like tree branches in a cluster of brain cells. It boosts the brain’s chemistry and connectivity, refueling the entire engine.

"Certain activities will lay more neural pathways that can be more readily re-engaged," Thomason says. "The hope is that there are ways to train and strengthen these pathways."

Maddens explains it this way: Consider the neurons of your brain like electrical wires and the white matter like the insulation. When the insulation breaks down over time, things can misfire.

In labs, those who engaged in mentally challenging games do, in fact, show improvement in cognitive functioning. They get faster at speed games and stronger in memory games, for example.

What’s less clear is whether this improvement transfers to everyday tasks, like remembering where you parked the car or the name of your child’s teacher, both Thomason and Maddens say.

But when it comes to the link between physical exercise and the brain, researchers and clinicians agree: physical exercise is good for the brain; it has also been linked to lower rates of chronic disease. Good nutrition is essential too.

Oxygen, itself, is essential, Deep said: “Your brain is an oxygen hog.”

Diet, exercise and mental maneuvers all may boost brain health in ways science still doesn’t understand. In the best cases, the right mix might stave off the effects of Alzheimer’s and other age-related disease too, Maddens says.

All this is good news for an aging, stressed out, and too-busy society, he says.

Reading a book, engaging with friends or going out for a walk and paying attention to what’s around you - that’s not really about goofing off. Rather, it’s critical time that stimulates neural pathways and boosts the odds of long-time brain health.

"It’s talking to friends. It’s getting out socially. It’s engaging in life. The question is ‘How do I force myself to learn?’" Thomason says.

The same might be true when it comes to mentally changing computer games.

Says Maddens: “Would I have patients playing computer games eight hours a day in hopes that they can delay Alzheimer’s by two months? No. But you can enjoy (playing such games) and possibly get a benefit from it, too.”

Read more …

ScienceDaily (June 20, 2012) — Most of us assume that confidence and certainty are preferred over uncertainty and bewilderment when it comes to learning complex information. But a new study led by Sidney D’Mello of the University of Notre Dame shows that confusion when learning can be beneficial if it is properly induced, effectively regulated and ultimately resolved.

Most of us assume that confidence and certainty are preferred over uncertainty and bewilderment when it comes to learning complex information. But a new study shows that confusion when learning can be beneficial if it is properly induced, effectively regulated and ultimately resolved. (Credit: © Ana Blazic Pavlovic / Fotolia)

The study will be published in a forthcoming issue of the journal Learning and Instruction.

Notre Dame psychologist and computer scientist D’Mello, whose research areas include artificial intelligence, human-computer interaction and the learning sciences, together with Art Graesser of the University of Memphis, collaborated on the study, which was funded by the National Science Foundation.

They found that by strategically inducing confusion in a learning session on difficult conceptual topics, people actually learned more effectively and were able to apply their knowledge to new problems.

In a series of experiments, subjects learned scientific reasoning concepts through interactions with computer-animated agents playing the roles of a tutor and a peer learner. The animated agents and the subject engaged in interactive conversations where they collaboratively discussed the merits of sample research studies that were flawed in one critical aspect. For example, one hypothetical case study touted the merits of a diet pill, but was flawed because it did not include an appropriate control group. Confusion was induced by manipulating the information the subjects received so that the animated agents sometimes disagreed with each other and expressed contradictory or incorrect information. The agents then asked subjects to decide which opinion had more scientific merit, thereby putting the subject in the hot spot of having to make a decision with incomplete and sometimes contradictory information.

In addition to the confusion and uncertainty triggered by the contradictions, subjects who were confused scored higher on a difficult post-test and could more successfully identify flaws in new case studies.

"We have been investigating links between emotions and learning for almost a decade, and find that confusion can be beneficial to learning if appropriately regulated because it can cause learners to process the material more deeply in order to resolve their confusion," D’Mello says.

According to D’Mello, it is not advisable to intentionally confuse students who are struggling or induce confusion during high-stakes learning activities. Confusion interventions are best for higher-level learners who want to be challenged with difficult tasks, are willing to risk failure, and who manage negative emotions when they occur.

"It is also important that the students are productively instead of hopelessly confused. By productive confusion, we mean that the source of the confusion is closely linked to the content of the learning session, the student attempts to resolve their confusion, and the learning environment provides help when the student struggles. Furthermore, any misleading information in the form of confusion-induction techniques should be corrected over the course of the learning session, as was done in the present experiments."

According to D’Mello, the next step in this body of research is to apply these methods to some of the more traditional domains such as physics, where misconceptions are common.

Source: Science Daily

ScienceDaily (June 20, 2012) — Most of us have experienced it. You are introduced to someone, only to forget his or her name within seconds. You rack your brain trying to remember, but can’t seem to even come up with the first letter. Then you get frustrated and think, “Why is it so hard for me to remember names?”

You may think it’s just how you were born, but that’s not the case, according to Kansas State University’s Richard Harris, professor of psychology. He says it’s not necessarily your brain’s ability that determines how well you can remember names, but rather your level of interest.

"Some people, perhaps those who are more socially aware, are just more interested in people, more interested in relationships," Harris said. "They would be more motivated to remember somebody’s name."

This goes for people in professions like politics or teaching where knowing names is beneficial. But just because someone can’t remember names doesn’t mean they have a bad memory.

"Almost everybody has a very good memory for something," Harris said.

The key to a good memory is your level of interest, he said. The more interest you show in a topic, the more likely it will imprint itself on your brain. If it is a topic you enjoy, then it will not seem like you are using your memory.

For example, Harris said a few years ago some students were playing a geography game in his office. He started to join in naming countries and their capitals. Soon, the students were amazed by his knowledge, although Harris didn’t understand why. Then it dawned on him that his vast knowledge of capitals didn’t come from memorizing them from a map, but rather from his love of stamps and learning their whereabouts.

"I learned a lot of geographical knowledge without really studying," he said.

Harris said this also explains why some things seem so hard to remember — they may be hard to understand or not of interest to some people, such as remembering names.

Harris said there are strategies for training your memory, including using a mnemonic device.

"If somebody’s last name is Hefty and you notice they’re left-handed, you could remember lefty Hefty," he said.

Another strategy is to use the person’s name while you talk to them — although the best strategy is simply to show more interest in the people you meet, he said.

Source: Science Daily

June 20, 2012

A “brain pacemaker” called deep brain stimulation (DBS) remains an effective treatment for Parkinson’s disease for at least three years, according to a study in the June 2012 online issue of Neurology, the medical journal of the American Academy of Neurology.

But while improvements in motor function remained stable, there were gradual declines in health-related quality of life and cognitive abilities.

First author of the study is Frances M. Weaver, PhD, who has joint appointments at Edward Hines Jr. VA Hospital and Loyola University Chicago Stritch School of Medicine.

Weaver was one of the lead investigators of a 2010 paper in the New England Journal of Medicine that found that motor functions remained stable for two years in DBS patients. The new additional analysis extended the follow-up period to 36 months.

DBS is a treatment for Parkinson’s patients who no longer benefit from medication, or who experience unacceptable side effects. DBS is not a cure, and it does not stop the disease from progressing. But in the right patients, DBS can significantly improve symptoms, especially tremors. DBS also can relieve muscle rigidity that causes decreased range of motion.

In the DBS procedure, a neurosurgeon drills a dime-size hole in the skull and inserts an electrode about 4 inches into the brain. A connecting wire from the electrode runs under the skin to a battery implanted near the collarbone. The electrode delivers mild electrical signals that effectively reorganize the brain’s electrical impulses. The procedure can be done on one or both sides of the brain.

Researchers evaluated 89 patients who were stimulated in a part of the brain called the globus pallidus interna and 70 patients who were stimulated in a different part of the brain called the subthalamic nucleus. (Patients received DBS surgery at seven VA and six affiliated university medical centers.) Patients were assessed at baseline (before DBS surgery) and at 3, 6, 12, 18, 24 and 36 months. Patients were rated on a Parkinson’s disease scale that includes motor functions such as speech, facial expression, tremors, rigidity, finger taps, hand movements, posture, gait, bradykinesia (slow movement) etc. The lower the rating, the better the function.

Improvements in motor function were similar in both groups of patients, and stable over time. Among patients stimulated in the globus pallidus interna, the score improved from 41.1 at baseline to 27.1 at 36 months. Among patients stimulated in the subthalamic nucleus, the score improved from 42.5 at baseline to 29.7 at 36 months.

By contrast, some early gains in quality of life and the abilities to do the activities of daily living were gradually lost, and there was a decline in neurocognitive function. This likely reflects the progression of the disease, and the emergence of symptoms that are resistant to DBS and medications.

Researchers concluded that both the globus pallidus interna and the subthalamic nucleus areas of the brain “are viable DBS targets for treatment of motor symptoms, but highlight the importance of nonmotor symptoms as determinants of quality of life in people with Parkinson’s disease.”

Source: medicalxpress.com

June 20, 2012

With a single drug treatment, researchers at the Ludwig Institute for Cancer Research at the University of California, San Diego School of Medicine can silence the mutated gene responsible for Huntington’s disease, slowing and partially reversing progression of the fatal neurodegenerative disorder in animal models.

This image shows stained mouse neurons. Credit: Image courtesy of Taylor Bayouth

The findings are published in the June 21, 2012 online issue of the journal Neuron.

Researchers suggest the drug therapy, tested in mouse and non-human primate models, could produce sustained motor and neurological benefits in human adults with moderate and severe forms of the disorder. Currently, there is no effective treatment.

Huntington’s disease afflicts approximately 30,000 Americans, whose symptoms include uncontrolled movements and progressive cognitive and psychiatric problems. The disease is caused by the mutation of a single gene, which results in the production and accumulation of toxic proteins throughout the brain.

Don W. Cleveland, PhD, professor and chair of the UC San Diego Department of Cellular and Molecular Medicine and head of the Laboratory of Cell Biology at the Ludwig Institute for Cancer Research, and colleagues infused mouse and primate models of Huntington’s disease with one-time injections of an identified DNA drug based on antisense oligonucleotides (ASOs). These ASOs selectively bind to and destroy the mutant gene’s molecular instructions for making the toxic huntingtin protein.

The singular treatment produced rapid results. Treated animals began moving better within one month and achieved normal motor function within two. More remarkably, the benefits persisted, lasting nine months, well after the drug had disappeared and production of the toxic proteins had resumed.

"For diseases like Huntington’s, where a mutant protein product is tolerated for decades prior to disease onset, these findings open up the provocative possibility that transient treatment can lead to a prolonged benefit to patients,” said Cleveland. “This finding raises the prospect of a ‘huntingtin holiday,’ which may allow for clearance of disease-causing species that might take weeks or months to re-form. If so, then a single application of a drug to reduce expression of a target gene could ‘reset the disease clock,’ providing a benefit long after huntingtin suppression has ended.”

Beyond improving motor and cognitive function, researchers said the ASO treatment also blocked brain atrophy and increased lifespan in mouse models with a severe form of the disease. The therapy was equally effective whether one or both huntingtin genes were mutated, a positive indicator for human therapy.

Cleveland noted that the approach was particularly promising because antisense therapies have already been proven safe in clinical trials and are the focus of much drug development. Moreover, the findings may have broader implications, he said, for other “age-dependent neurodegenerative diseases that develop from exposure to a mutant protein product” and perhaps for nervous system cancers, such as glioblastomas.

Provided by University of California - San Diego

Source: medicalxpress.com

June 20, 2012

Researchers from Boston University School of Medicine (BUSM) have demonstrated in experimental models that blocking the Sigma-1 receptor, a cellular protein, reduced binge eating and caused binge eaters to eat more slowly. The research, which is published online in Neuropsychopharmacology, was led by Pietro Cottone, PhD, and Valentina Sabino, PhD, both assistant professors in the pharmacology and psychiatry departments at BUSM.

Binge eating disorder, which affects approximately 15 million Americans, is believed to be the eating disorder that most closely resembles substance dependence. In binge eating subjects, normal regulatory mechanisms that control hunger do not function properly. Binge eaters typically gorge on “junk” foods excessively and compulsively despite knowing the adverse consequences, which are physical, emotional and social in nature. In addition, binge eaters typically experience distress and withdrawal when they abstain from junk food.

The researchers developed an experimental model of compulsive binge eating by providing a sugary, chocolate diet only for one hour a day while the control group was given a standard laboratory diet. Within two weeks, the group exposed to the sugary diet exhibited binge eating behavior and ate four times as much as the controls. In addition, the experimental binge eaters exhibited compulsive behavior by putting themselves in a potentially risky situation in order to get to the sugary food while the control group avoided the risk.

The researchers then tested whether a drug that blocks the Sigma-1 receptor could reduce binge eating of the sugary diet. The experimental data showed the drug successfully reduced binge eating by 40 percent, caused the binge eaters to eat more slowly and blocked the risky behavior.

The abnormal, risky behavior exhibited by the binge eating experimental group suggested to the researchers that there could be something wrong with how decisions were made. Because evaluation of risks and decision making are functions executed in the prefronto-cortical regions of the brain, the researchers tested whether the abundance of Sigma-1 receptors in those regions was abnormal in the binge eaters. They found that Sigma-1 receptor expression was unusually high in those areas, which could explain why blocking its function could decrease both compulsive binge eating and risky behavior.

"These findings suggest that the Sigma-1 receptor may contribute to the neurobiological adaptations that cause compulsive-like eating, opening up a new potential therapeutic treatment target for binge eating disorder,” said Cottone, who also co-directs the Laboratory of Addictive Disorders at BUSM with Sabino.

Provided by Boston University Medical Center

Source: medicalxpress.com