Sugar makes you stupid
Posted on May 16, 2012 in Medical
Attention, college students cramming between midterms and finals: Binging on soda and sweets for as little as six weeks may make you stupid.
A new UCLA rat study is the first to show how a diet steadily high in fructose slows the brain, hampering memory and learning — and how omega-3 fatty acids can counteract the disruption. The peer-reviewed Journal of Physiology publishes the findings in its May 15 edition.
“Our findings illustrate that what you eat affects how you think,” said Fernando Gomez-Pinilla, a professor of neurosurgery at the David Geffen School of Medicine at UCLA and a professor of integrative biology and physiology in the UCLA College of Letters and Science. “Eating a high-fructose diet over the long term alters your brain’s ability to learn and remember information. But adding omega-3 fatty acids to your meals can help minimize the damage.”
While earlier research has revealed how fructose harms the body through its role in diabetes, obesity and fatty liver, this study is the first to uncover how the sweetener influences the brain.
The UCLA team zeroed in on high-fructose corn syrup, an inexpensive liquid six times sweeter than cane sugar, that is commonly added to processed foods, including soft drinks, condiments, applesauce and baby food. The average American consumes more than 40 pounds of high-fructose corn syrup per year, according to the U.S. Department of Agriculture.
“We’re not talking about naturally occurring fructose in fruits, which also contain important antioxidants,” explained Gomez-Pinilla, who is also a member of UCLA’s Brain Research Institute and Brain Injury Research Center. “We’re concerned about high-fructose corn syrup that is added to manufactured food products as a sweetener and preservative.”
Gomez-Pinilla and study co-author Rahul Agrawal, a UCLA visiting postdoctoral fellow from India, studied two groups of rats that each consumed a fructose solution as drinking water for six weeks. The second group also received omega-3 fatty acids in the form of flaxseed oil and docosahexaenoic acid (DHA), which protects against damage to the synapses — the chemical connections between brain cells that enable memory and learning.
“DHA is essential for synaptic function — brain cells’ ability to transmit signals to one another,” Gomez-Pinilla said. “This is the mechanism that makes learning and memory possible. Our bodies can’t produce enough DHA, so it must be supplemented through our diet.”
The animals were fed standard rat chow and trained on a maze twice daily for five days before starting the experimental diet. The UCLA team tested how well the rats were able to navigate the maze, which contained numerous holes but only one exit. The scientists placed visual landmarks in the maze to help the rats learn and remember the way.
Six weeks later, the researchers tested the rats’ ability to recall the route and escape the maze. What they saw surprised them.
“The second group of rats navigated the maze much faster than the rats that did not receive omega-3 fatty acids,” Gomez-Pinilla said. “The DHA-deprived animals were slower, and their brains showed a decline in synaptic activity. Their brain cells had trouble signaling each other, disrupting the rats’ ability to think clearly and recall the route they’d learned six weeks earlier.”
The DHA-deprived rats also developed signs of resistance to insulin, a hormone that controls blood sugar and regulates synaptic function in the brain. A closer look at the rats’ brain tissue suggested that insulin had lost much of its power to influence the brain cells.
“Because insulin can penetrate the blood–brain barrier, the hormone may signal neurons to trigger reactions that disrupt learning and cause memory loss,” Gomez-Pinilla said.
He suspects that fructose is the culprit behind the DHA-deficient rats’ brain dysfunction. Eating too much fructose could block insulin’s ability to regulate how cells use and store sugar for the energy required for processing thoughts and emotions.
“Insulin is important in the body for controlling blood sugar, but it may play a different role in the brain, where insulin appears to disturb memory and learning,” he said. “Our study shows that a high-fructose diet harms the brain as well as the body. This is something new.”
Gomez-Pinilla, a native of Chile and an exercise enthusiast who practices what he preaches, advises people to keep fructose intake to a minimum and swap sugary desserts for fresh berries and Greek yogurt, which he keeps within arm’s reach in a small refrigerator in his office. An occasional bar of dark chocolate that hasn’t been processed with a lot of extra sweetener is fine too, he said.
Still planning to throw caution to the wind and indulge in a hot-fudge sundae? Then also eat foods rich in omega-3 fatty acids, like salmon, walnuts and flaxseeds, or take a daily DHA capsule. Gomez-Pinilla recommends one gram of DHA per day.
“Our findings suggest that consuming DHA regularly protects the brain against fructose’s harmful effects,” said Gomez-Pinilla. “It’s like saving money in the bank. You want to build a reserve for your brain to tap when it requires extra fuel to fight off future diseases.”
Source: UCLA
Mystery gene reveals new mechanism for anxiety disorders
Posted on May 16, 2012 in anxiety
A novel mechanism for anxiety behaviors, including a previously unrecognized inhibitory brain signal, may inspire new strategies for treating psychiatric disorders, University of Chicago researchers report.
By testing the controversial role of a gene called Glo1 in anxiety, scientists uncovered a new inhibitory factor in the brain: the metabolic by-product methylglyoxal. The system offers a tantalizing new target for drugs designed to treat conditions such as anxiety disorder, epilepsy, and sleep disorders.
The study, published in the Journal of Clinical Investigation, found that animals with multiple copies of the Glo1 gene were more likely to exhibit anxiety-like behavior in laboratory tests. Further experiments showed that Glo1 increased anxiety-like behavior by lowering levels of methylglyoxal (MG). Conversely, inhibiting Glo1 or raising MG levels reduced anxiety behaviors.
“Animals transgenic for Glo1 had different levels of anxiety-like behavior, and more copies made them more anxious,” said Abraham Palmer, PhD, assistant professor of human genetics at the University of Chicago Medicine and senior author of the study. “We showed that Glo1 was causally related to anxiety-like behavior, rather than merely correlated.”
In 2005, a comparison of different mouse strains found a link between anxiety-like behaviors and Glo1, the gene encoding the metabolic enzyme glyoxylase 1. However, subsequent studies questioned the link, and the lack of an obvious connection between glyoxylase 1 and brain function or behavior made some scientists skeptical.
“When people discover a gene, they’re always most comfortable when they discover something they already knew,” Palmer said. “The alarming thing here was there was a discovery of something that nobody knew, and therefore it seemed less likely to actually be correct.”
A 2009 study from Palmer’s laboratory suggested that differences in Glo1 expression between mouse strains were due to copy number variants, where the segment of the genome containing the gene is repeated multiple times. To test this hypothesis, lead author Margaret Distler inserted two, eight or ten copies of the Glo1 gene into mouse lines. She then ran experiments such as the open field test, in which researchers measure how much time a mouse spends in the center of an arena versus along the walls, to detect changes in anxiety behavior.
The results confirmed a causative role for Glo1 copy number variants, as mice with more copies of the Glo1 gene exhibited higher anxiety-like behavior in their experiments.
“It’s the first study to show that it’s the copy number variant that has the potential to change Glo1 expression and behavior,” said Distler, an MD/PhD student in the Pritzker School of Medicine’s Medical Scientist Training Program. “Our study was a physiological representation of what it means to increase Glo1 expression for anxiety.”
The researchers then set about answering the mystery of how Glo1 expression influences anxiety-like behaviors. The primary function of glyoxylase 1 is to metabolize and lower cellular levels of methylglyoxal, a waste product of glycolysis. Distler produced the opposite effect by injecting MG to artificially increase its levels in the brain, finding that raising MG levels quickly reduced anxiety symptoms in mice.
“Methylglyoxal changed behavior within 10 minutes of administration, which means it’s a rapid onset. It’s not changing gene expression, and it’s not having long-term downstream effects,” Distler said. “That was our first breakthrough.”
The short time course suggested that MG might have a direct effect on neuronal activity. MG also demonstrated sedative effects at high doses, a hallmark of drugs that activate inhibitory GABA receptors on neurons. In collaboration with Leigh Plant, now at Brandeis University, the researchers demonstrated that MG activated GABA-A receptors on neurons, a previously unknown inhibitory mechanism.
“It’s a completely different system that is tying neuronal inhibitory tone into metabolic activity,” Palmer said. “That’s potentially really exciting in terms of re-evaluating what we thought we knew about inhibitory tone in the CNS. It turns out now that methylglyoxal, which has been around ever since glycolysis evolved, was also acting at these receptors, and nobody knew that.”
Conventionally, anxiety has been treated with drugs that activate the GABA-A receptor, such as benzodiazepines and barbiturates, which are prone to abuse and dangerous side effects. The researchers theorized that targeting the Glo1/MG interaction could provide a more selective strategy for reducing anxiety symptoms by subtly influencing inhibitory tone.
“The GABA-A receptor agents already out there have a lot of side effects, such as sedation and hypothermia, as well as a high abuse liability,” Distler said. “It’s possible that taking a Glo1 inhibitor will increase only MG levels to a certain maximum. You could have the potential for more specificity, given that you’re activating a system that’s already in place, not just dumping methylglyoxal or some other GABA-A receptor agent throughout the brain.”
Preliminary experiments with a small molecule inhibitor of Glo1 supported the theory. Injections of the inhibitor, developed by John Termini at the Beckman Research Institute of the City of Hope, reduced anxiety-like symptoms in mice.
“It’s a different way of hitting these GABA-A receptors,” Palmer said. “We have yet to determine if that’s a better way of doing it, but it’s certainly different, and it gives us a unique angle of attack on this system and potential advantages that we have yet to evaluate.”
Such a drug may also be useful in treating epilepsy and sleep disorders, where GABA-A drugs have shown success. While the therapeutic potential of manipulating this system is yet to be determined, the research clears the fog around the role of Glo1 in anxiety by adding behavioral and cellular evidence.
“What’s neat is that we started with exploratory, open-ended genetic studies in mice, and we’ve now gotten into some fundamental new physiology that nobody had appreciated or put together before,” Palmer said. “Now we’re starting to reap some of the fruit from those types of genetic studies to enrich our understanding of more classical aspects of biology.”
Source: Eurekalert
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A walk in the park gives mental boost to people with depression
Posted on May 14, 2012 in Co-Occuring Disorders
Woodland Walk Wassand Park When open to the public Wassand Hall has a "half mile walk" taking you around the park. (Photo credit: Wikipedia)
A walk in the park may have psychological benefits for people suffering from depression.
In one of the first studies to examine the effect of nature walks on cognition and mood in people with major depression, researchers in Canada and the U.S. have found promising evidence that a walk in the park may provide some cognitive benefits.
The study was led by Marc Berman, a post-doctoral fellow at Baycrest’s Rotman Research Institute in Toronto, with partners from the University of Michigan and Stanford University. It is published online this week, ahead of print publication, in the Journal of Affective Disorders.
“Our study showed that participants with clinical depression demonstrated improved memory performance after a walk in nature, compared to a walk in a busy urban environment,” said Dr. Berman, who cautioned that such walks are not a replacement for existing and well-validated treatments for clinical depression, such as psychotherapy and drug treatment.
“Walking in nature may act to supplement or enhance existing treatments for clinical depression, but more research is needed to understand just how effective nature walks can be to help improve psychological functioning,” he said.
Dr. Berman’s research is part of a cognitive science field known as Attention Restoration Theory (ART) which proposes that people concentrate better after spending time in nature or looking at scenes of nature. The reason, according to ART, is that people interacting with peaceful nature settings aren’t bombarded with external distractions that relentlessly tax their working memory and attention systems. In nature settings, the brain can relax and enter a state of contemplativeness that helps to restore or refresh those cognitive capacities.
In a research paper he published in 2008 in Psychological Science, Dr. Berman showed that adults who were not diagnosed with any illness received a mental boost after an hour-long walk in a woodland park – improving their performance on memory and attention tests by 20 percent – compared to an hour-long stroll in a noisy urban environment. The findings were reported by The Wall Street Journal, The Boston Globe, The New York Times, and in the Pulitzer Prize finalist book by Nicholas Carr, The Shallows: What the internet is doing to our brains.
In this latest study, Dr. Berman and his research team explored whether a nature walk would provide similar cognitive benefits, and also improve mood for people with clinical depression. Given that individuals with depression are characterized by high levels of rumination and negative thinking, the researchers were skeptical at the outset of the study that a solitary walk in the park would provide any benefit at all and may end up worsening memory and exacerbating depressed mood.
For the study, 20 individuals were recruited from the University of Michigan and surrounding Ann Arbor area; all had a diagnosis of clinical depression. The 12 females and eight males (average age 26) participated in a two-part experiment that involved walking in a quiet nature setting and in a noisy urban setting.
Prior to the walks, participants completed baseline testing to determine their cognitive and mood status. Before beginning a walk, the participants were asked to think about an unresolved, painful autobiographical experience. They were then randomly assigned to go for an hour-long walk in the Ann Arbor Arboretum (woodland park) or traffic heavy portions of downtown Ann Arbor. They followed a prescribed route and wore a GPS watch to ensure compliance.
After completing their walk, they completed a series of mental tests to measure their attention and short-term/working memory and were re-asssessed for mood. A week later the participants repeated the entire procedure, walking in the location that was not visited in the first session.
Participants exhibited a 16 percent increase in attention and working memory after the nature walk relative to the urban walk. Interestingly, interacting with nature did not alleviate depressive mood to any noticeable degree over urban walks, as negative mood decreased and positive mood increased after both walks to a significant and equal extent. Dr. Berman says this suggests that separate brain mechanisms may underlie the cognitive and mood changes of interacting with nature.
Source: Eurekalert
College men find steroids for better game less ethical than stimulants for better grades, study says
Posted on May 10, 2012 in Addiction
Adderall (Photo credit: Wikipedia)
In the eyes of young college men, it’s more unethical to use steroids to get an edge in sports than it is to use prescription stimulants to enhance one’s grades, according to new research published by the American Psychological Association.
And students who had themselves used stimulants without a prescription were more inclined to see such drug use as acceptable, according to the findings, which were published online in the APA journal Psychology of Addictive Behaviors. This is one of the first studies to compare perceptions of off-label prescription drug use with perceptions of steroids performance enhancers.
“This is consistent with the idea that using performance enhancers is viewed as less ethical in the sporting world than in the academic world,” said the study’s lead author, Tonya Dodge, PhD, of George Washington University. “Interestingly, the students in our study considered off-label prescription drug use as more effective for success than using steroids.”
Approximately 1,200 college freshmen (73 percent white) at Pennsylvania State University answered a questionnaire that presented two scenarios. One described “Bill,” a sprinter for his college track team who does not have a lot of time to train before the championship meet and is worried he won’t be able to improve. He gets steroids from a friend and ends up performing better than expected and wins the championship race.
The second scenario presents “Jeff,” a college student facing midterm exams who is worried that his grades in class may be low. He doesn’t have much time to study so he gets some Adderall, a prescription stimulant, from a friend who tells him it will help him focus at exam time. Jeff takes the pills and ends up getting better midterm grades than he expected.
After reading both scenarios, the students were asked how strongly they agreed or disagreed with four statements: “Bill/Jeff is a cheater for using steroids/Adderall,” and, “Taking steroids/Adderall was necessary for Bill/Jeff to do well.”
The students were also asked if they had ever misused prescription stimulant drugs, such as Adderall, Ritalin or Dexedrine, or if they had ever used steroids. Less than 1 percent of the sample reported having ever used steroids while about 8 percent said they had misused prescription stimulants in the last 12 months. This compares to 8 percent to 34 percent of college students who have reported misusing prescription stimulants and 1.5 percent of adolescents and young adults who have misused anabolic steroids.
The researchers also asked the men if they had played a sport in high school to determine if that would affect their judgments.
Participants significantly rated Bill, the steroid user, as more of a cheater than Jeff, the prescription drug user. This difference got bigger if the students reported having misused prescription stimulants themselves in the past or if they had played a sport.
Overall, the students were more likely to consider Jeff’s Adderall use more necessary to succeed than Bill’s steroid use regardless of whether they had misused prescription stimulants in the past or had played a sport. “One reason students may have felt Adderall was more necessary than steroids for success is because people may believe intelligence is less malleable than athletic ability. This view of intelligence might have led the students in this study to believe that taking Adderall would increase intellectual capacity,” said Dodge. “This research can help mold future prevention efforts around off-label prescription stimulant use in the academic world.”
Source: Eurekalert
Chronic cocaine use may speed up aging of brain
Posted on May 8, 2012 in Addiction
Deutsch: Struktur von Kokain English: Structure of cocaine (Photo credit: Wikipedia)
New research by scientists at the University of Cambridge suggests that chronic cocaine abuse accelerates the process of brain ageing. The study, published today 25 April in Molecular Psychiatry, found that age-related loss of grey matter in the brain is greater in people who are dependent on cocaine than in the healthy population.
For the study, the researchers scanned the brains of 120 people with similar age, gender and verbal IQ. Half of the individuals had a dependence on cocaine while the other 60 had no history of substance abuse disorders.
The researchers found that the rate of age-related grey matter volume loss in cocaine-dependent individuals was significantly greater than in healthy volunteers. The cocaine users lost about 3.08 ml brain volume per year, which is almost twice the rate of healthy volunteers (who only lost about 1.69 ml per year). The accelerated age-related decline in brain volume was most prominent in the prefrontal and temporal cortex, important regions of the brain which are associated with attention, decision-making, and self-regulation as well as memory.
Previous studies have shown that psychological and physiological changes typically associated with old age such as cognitive decline, brain atrophy and immunodeficiency are also seen in middle-aged cocaine-dependent individuals. However, this is the first time that premature ageing of the brain has been associated with chronic cocaine abuse.
Dr Karen Ersche, of the Behavioural and Clinical Neuroscience Institute (BCNI) at the University of Cambridge, said: “As we age, we all lose grey matter. However, what we have seen is that chronic cocaine users lose grey matter at a significantly faster rate ,which could be a sign of premature ageing. Our findings therefore provide new insight into why the cognitive deficits typically seen in old age have frequently been observed in middle aged chronic users of cocaine.”
The scientists also highlight concerns that premature ageing in chronic cocaine users is an emerging public health concern. The United Nations Office on Drugs and Crime estimates that cocaine is used by up to 21 million individuals worldwide, with approximately 1 per cent of these individuals becoming dependent.
Dr Ersche said: “Our findings clearly highlight the need for preventative strategies to address the risk of premature ageing associated with cocaine abuse. Young people taking cocaine today need to be educated about the long-term risk of ageing prematurely.”
The concern of accelerated ageing is not limited to young people but also affects older adults who have been abusing drugs such as cocaine since early adulthood.
Dr Ersche added: “Our findings shed light on the largely neglected problem of the growing number of older drug users, whose needs are not so well catered for in drug treatment services. It is timely for heath care providers to understand and recognise the needs of older drug users in order to design and administer age-appropriate treatments.”
Huge Study Finds Brain Networks Connected to Teen Drug Abuse
Posted on May 7, 2012 in Addiction
Ritalin (Photo credit: Wikipedia)
Why do some teenagers start smoking or experimenting with drugs — while others don’t? In the largest imaging study of the human brain ever conducted — involving 1,896 14-year-olds — scientists have discovered a number of previously unknown networks that go a long way toward an answer.
Robert Whelan and Hugh Garavan of the University of Vermont, along with a large group of international colleagues, report that differences in these networks provide strong evidence that some teenagers are at higher risk for drug and alcohol experimentation — simply because their brains work differently, making them more impulsive.
Their findings are presented in the journal Nature Neuroscience, published online April 29, 2012.
This discovery helps answer a long-standing chicken-or-egg question about whether certain brain patterns come before drug use — or are caused by it.
“The differences in these networks seem to precede drug use,” says Garavan, Whelan’s colleague in UVM’s psychiatry department, who also served as the principal investigator of the Irish component of a large European research project, called IMAGEN, that gathered the data about the teens in the new study.
In a key finding, diminished activity in a network involving the “orbitofrontal cortex” is associated with experimentation with alcohol, cigarettes and illegal drugs in early adolescence.
“These networks are not working as well for some kids as for others,” says Whelan, making them more impulsive.
Faced with a choice about smoking or drinking, the 14-year-old with a less functional impulse-regulating network will be more likely to say, “yeah, gimme, gimme, gimme!” says Garavan, “and this other kid is saying, ‘no, I’m not going to do that.’”
Testing for lower function in this and other brain networks could, perhaps, be used by researchers someday as “a risk factor or biomarker for potential drug use,” Garavan says.
The researchers were also able to show that other newly discovered networks are connected with the symptoms of attention-deficit hyperactivity disorder. These ADHD networks are distinct from those associated with early drug use.
In recent years, there has been controversy and extensive media attention about the possible connection between ADHD and drug abuse. Both ADHD and early drug use are associated with poor inhibitory control — they’re problems that plague impulsive people.
But the new research shows that these seemingly related problems are regulated by different networks in the brain — even though both groups of teens can score poorly on tests of their “stop-signal reaction time,” a standard measure of overall inhibitory control used in this study and other similar ones. This strengthens the idea that risk of ADHD is not necessarily a full-blown risk for drug use as some recent studies suggest.
The impulsivity networks — connected areas of activity in the brain revealed by increased blood flow — begin to paint a more nuanced portrait of the neurobiology underlying the patchwork of attributes and behaviors that psychologists call impulsivity — as well as the capacity to put brakes on these impulses, a set of skills sometimes called inhibitory control.
Edythe London, Professor of Addiction Studies and Director of the UCLA Laboratory of Molecular Pharmacology, who was not part of the new study, described it as “outstanding,” noting that the work by Whelan and others “substantially advances our understanding of the neural circuitry that governs inhibitory control in the adolescent brain.”
Using a complex mathematical approach called factor analysis, Whelan and colleagues were able to fish out seven networks involved when impulses were successfully inhibited and six networks involved when inhibition failed — from the vast and chaotic actions of a teenage brain at work. These networks “light up,” Whelan says, in a functional MRI scanner during trials when the teenagers were asked to perform a repetitive task that involved pushing a button on a keyboard, but then were able to successfully stop — or inhibit — the act of pushing the button in mid-action. Those teens with better inhibitory control were able to succeed at this task faster.
But the underlying networks behind these tasks could not have been detectable in a “typical fMRI study of about 16 or 20 people,” says Whelan. “This study was orders of magnitude bigger, which lets us overcome much of the randomness and noise — and find the brain regions that actually vary together.”
“The take-home message is that impulsivity can be decomposed, broken down into different brain regions,” says Garavan, “and the functioning of one region is related to ADHD symptoms, while the functioning of other regions is related to drug use.
The new study draws on the multi-year work of the IMAGEN Consortium, funded by the European Union, and headed by Prof. Gunter Schumann at the Institute of Psychiatry, King’s College London. IMAGEN, lead by a team of scientists across Europe, carried out neuroimaging, genetic and behavioral analyses in 2000 teenage volunteers in Ireland, England, France, and Germany and will be following them for several years, investigating the roots of risk-taking behavior and mental health in teenagers.
That teenagers push against boundaries — and sometimes take risks — is as predictable as the sunrise. It happens in all cultures and even across all mammal species: adolescence is a time to test limits and develop independence.
But death among teenagers in the industrialized world is largely caused by preventable or self-inflicted accidents that are often launched by impulsive risky behaviors, often associated with alcohol and drug use. Additionally, “addiction in the western world is our number one health problem,” says Garavan. “Think about alcohol, cigarettes or harder drugs and all the consequences that has in society for people’s health.” Understanding brain networks that put some teenagers at higher risk for starting to use them could have large implications for public health.
Source: Sciencedaily
