Monya Baker Is psychology facing a ‘replication crisis’? Last year, a crowdsourced effort that was able to validate fewer than half of 98 published findings1 rang alarm bells about the reliability of psychology papers. Now a team of psychologists has reassessed the study and say that it provides no evidence for a crisis. “Our analysis completely invalidates the pessimistic conclusions that many have drawn from this landmark study,” says Daniel Gilbert, a psychologist at Harvard University in Cambridge, Massachusetts, and a co-author of the reanalysis, published on 2 March in Science2. But a response3 in the same issue of Science counters that the reanalysis itself depends on selective assumptions. And others say that psychology still urgently needs to improve its research practices. Statistical criticism In August 2015, a team of 270 researchers reported the largest ever single-study audit of the scientific literature. Led by Brian Nosek, executive director of the Center for Open Science in Charlottesville, Virginia, the Reproducibility Project attempted to replicate studies in 100 psychology papers. (It ended up with 100 replication attempts for 98 papers because of problems assigning teams to two papers.) According to one of several measures of reproducibility, just 36% could be confirmed; by another statistical measure, 47% could1. Either way, the results looked worryingly feeble. “Both optimistic and pessimistic conclusions about reproducibility are possible, and neither are yet warranted” Not so fast, says Gilbert. © 2016 Nature Publishing Group

Keyword: Attention
Link ID: 21953 - Posted: 03.05.2016

Heidi Ledford Obese mice — like obese humans — are at increased risk of colon cancer, and a study published today in Nature finally suggests why. Overweight mice fed a high-fat diet showed an increase in intestinal stem cells due to activation of a protein called PPAR-δ that regulates metabolism1. If the results hold true in humans, they could explain a phenomenon seen in epidemiological studies. “For quite some time there’s been an understanding that obesity leads to an increase in cancer in many tissues,” says Ömer Yilmaz, a cancer biologist at the Koch Institute for Integrative Cancer Research at the Massachusetts Institute of Technology (MIT) in Cambridge, and one of the leaders of the study. “We really wanted to understand the mechanism behind this.” Those molecular details could be important, says cell biologist P. Kay Lund who works at the University of North Carolina in Chapel Hill and the National Institutes of Health in Bethesda, Maryland. Tissue samples from people who have undergone colonoscopies could be tested to see if the same patterns hold true. Ultimately, the the increase in PPAR-δ activity could yield a useful indicator of cancer risk. “It could provide an opportunity to give those patients an earlier intervention,” says Lund, who was not involved in the obesity work. Yilmaz teamed up with David Sabatini, who studies metabolism at MIT and the Whitehead Institute, also in Cambridge, to learn more about the link between cancer and obesity. Their teams fed mice high-fat, high-calorie chow for about a year, and then tested the effects of the diet on the number and function of stem cells in their intestines. © 2016 Nature Publishing Group

Keyword: Obesity
Link ID: 21952 - Posted: 03.03.2016

Mo Costandi Most of us are well aware of the health risks associated with obesity. Being overweight or obese is associated with an increased risk of numerous other conditions, from high blood pressure, heart disease and stroke, to diabetes, gout and some forms of cancer. Self-control saps memory resources Read more Research published over the past few years shows that obesity also has neurological consequences – it is associated with altered function in, and shrinkage of, certain parts of the brain, particularly the frontal lobes, which are the seat of intelligence, and the hippocampus, which is critical for memory formation. A new study now shows that this in turn is associated with impaired memory function. Lucy Cheke of the University of Cambridge and her colleagues recruited 50 volunteers aged between 18 and 35, with Body Mass Indexes (BMIs) ranging from 18 (underweight) to 51 (extremely obese), and asked them to perform a computerised memory test called the “Treasure Hunt Task”. This involved moving food items around around complex scenes, such as a desert with palm trees, hiding them in various locations, and indicating afterwards where they had hidden them. The participants were then shown various locations from the computerised scenes, and some of the food items, and asked if they had hidden something in each of the locations, or where they had hidden each of the items. Finally, they were shown pairs of the food items they had seen, and asked to indicate which of each pair they had hidden first. © 2016 Guardian News and Media Limited

Keyword: Obesity; Learning & Memory
Link ID: 21951 - Posted: 03.03.2016

By Simon Makin Brain implants have been around for decades—stimulating motor areas to alleviate Parkinson's disease symptoms, for example—but until now they have all suffered from the same limitation: because brains move slightly during physical activity and as we breathe and our heart beats, rigid implants rub and damage tissue. This means that eventually, because of both movement and scar-tissue formation, they lose contact with the cells they were monitoring. Now a group of researchers, led by chemist Charles Lieber of Harvard University, has overcome these problems using a fine, flexible mesh. In 2012 the team showed that cells could be grown around such a mesh, but that left the problem of how to get one inside a living brain. The solution the scientists devised was to draw the mesh—measuring a few millimeters wide—into a syringe, so it would roll up like a scroll inside the 100-micron-wide needle, and inject it through a hole in the skull. In a study published in Nature Nanotechnology last year, the team injected meshes studded with 16 electrodes into two brain regions in mice. The mesh is composed of extremely thin, nanoscale polymer threads, sparsely distributed so that 95 percent of it is empty space. It has a level of flexibility similar to brain tissue. “You're starting to make this nonliving system look like the biological system you're trying to probe,” Lieber explains. “That's been the goal of my group's work, to blur the distinction between electronics as we know it and the computer inside our heads.” © 2016 Scientific American

Keyword: Brain imaging
Link ID: 21950 - Posted: 03.03.2016

By Gretchen Reynolds Learning in midlife to juggle, swim, ride a bicycle or, in my case, snowboard could change and strengthen the brain in ways that practicing other familiar pursuits such as crossword puzzles or marathon training will not, according to an accumulating body of research about the unique impacts of motor learning on the brain. When most of us consider learning and intelligence, we think of activities such as adding numbers, remembering names, writing poetry, learning a new language. Such complex thinking generally is classified as “higher-order” cognition and results in activity within certain portions of the brain and promotes plasticity, or physical changes, in those areas. There is strong evidence that learning a second language as an adult, for instance, results in increased white matter in the parts of the brain known to be involved in language processing. Regular exercise likewise changes the brain, as I frequently have written, with studies in animals showing that running and other types of physical activities increase the number of new brain cells created in parts of the brain that are integral to memory and thinking. But the impacts of learning on one of the most primal portions of the brain have been surprisingly underappreciated, both scientifically and outside the lab. Most of us pay little attention to our motor cortex, which controls how well we can move. “We have a tendency to admire motor skills,” said Dr. John Krakauer, a professor of neurology and director of the Center for the Study of Motor Learning and Brain Repair at Johns Hopkins University in Baltimore. We like watching athletes in action, he said. But most of us make little effort to hone our motor skills in adulthood, and very few of us try to expand them by, for instance, learning a new sport. We could be short-changing our brains. © 2016 The New York Times Company

Keyword: Learning & Memory; Glia
Link ID: 21949 - Posted: 03.03.2016

By Christian Jarrett Most of us like to think that we’re independent-minded — we tell ourselves we like Adele’s latest album because it suits our taste, not because millions of other people bought it, or that we vote Democrat because we’re so enlightened, not because all our friends vote that way. The reality, of course, is that humans are swayed in all sorts of different ways — some of them quite subtle — by other people’s beliefs and expectations. Our preferences don’t form in a vacuum, but rather in something of a social pressure-cooker. This has been demonstrated over and over, perhaps most famously in the classic Asch conformity studies from the ‘50s. In those experiments, many participants went along with a blatantly wrong majority judgment about the lengths of different lines — simply, it seems, to fit in. (Although the finding is frequently exaggerated, the basic point about the power of social influence holds true.) But that doesn’t mean all humans are susceptible to peer pressure in the same way. You only have to look at your own friends and family to know that some people always seem to roll with the crowd, while others are much more independent-minded. What accounts for these differences? A new study in Frontiers in Human Neuroscience led by Dr. Juan Dominguez of Monash University in Melbourne, Australia, offers the first hint that part of the answer may come down to certain neural mechanisms. In short, the study suggests that people have a network in their brains that is attuned to disagreement with other people. When this network is activated, it makes us feel uncomfortable (we experience “cognitive dissonance,” to use the psychological jargon) and it’s avoiding this state that motivates us to switch our views as much as possible. It appears the network is more sensitive in some people than in others, and that this might account for varying degrees of pushover-ness. © 2016, New York Media LLC.

Keyword: Emotions; Attention
Link ID: 21948 - Posted: 03.03.2016

By Jonathan Webb Science reporter, BBC News Three British researchers have won a prize worth one million euros, awarded each year for an "outstanding contribution to European neuroscience". Tim Bliss, Graham Collingridge and Richard Morris revealed how strengthened connections between brain cells can store our memories. Our present understanding of memory is built on their work, which unpicked the mechanisms and molecules involved. This is the first time the Brain Prize has been won by an entirely UK team. It is awarded by a Danish charitable foundation and the 2016 winners were announced in London on Tuesday. Speaking to journalists at a media conference, Prof Morris explained it was the "chemistry of memory" that he and his colleagues had managed to illuminate. Fire together, wire together "Before this team got going, we had some idea about particular areas of the brain that might be involved in memory… but what we didn't have was any real understanding of how it worked," explained the professor, who works at the University of Edinburgh. The "team" of three winners never worked together in the same laboratory, but they have collaborated over the years. "Memories change the brain - the brain is plastic," said Prof Bliss, who worked for many years at the National Institute of Medical Research in London and is now affiliated with the Francis Crick Institute. Those changes occur at the junctions between nerve cells - synapses - and were described in a pioneering study by Bliss and a Norwegian colleague, Terje Lømo, in the 1970s. © 2016 BBC.

Keyword: Learning & Memory
Link ID: 21947 - Posted: 03.03.2016

Greg Miller The crime was brutal. On November 4, 1989, after a night of heavy drinking, David Scott Detrich and a male coworker picked up a woman walking along the side of the road in Tucson, Arizona. After scoring some cocaine, the trio went back to her place, where, according to court documents, Detrich slit the woman’s throat and stabbed her 40 times. Later, the two men dumped her body in the desert. A jury convicted Detrich of kidnapping and first-degree murder in 1995, and a judge sentenced him to death. Detrich is still on death row today as the appeals process drags on, but in 2010, his lawyers achieved a victory of sorts. They claimed that Detrich had received “ineffective assistance of counsel” at his trial, because his original legal team had failed to present evidence of neuropsychological abnormalities and brain damage that might have swayed the court to give him a lesser sentence. A federal appeals court agreed. The ruling said, in effect, that Detrich had been denied his Constitutional right to a fair trial because his lawyers hadn’t called an expert witness to talk about his brain. That judicial opinion is just one of nearly 1,600 examined in a recent study documenting the expanding use of brain science in the criminal-justice system. The study, by Nita Farahany at Duke University, found that the number of judicial opinions that mention neuroscientific evidence more than doubled between 2005 and 2012. “There are good reasons to believe that the increase in published opinions involving neurobiology are just the tip of the iceberg,” says Owen Jones, a law professor at Vanderbilt who directs the MacArthur Foundation Research Network on Law and Neuroscience.

Keyword: Aggression
Link ID: 21946 - Posted: 03.02.2016

Ewan Birney The Daily Mail recently ran an article about how alcohol abuse could harm future generations, via the (exciting-sounding) mechanism of trans-generational epigenetics. This is an emotive topic, combining a commonplace habit (drinking beer and wine) with a scary outcome (harming your children, grandchildren and future generations) and adding a twist of science for gravitas. It’s not surprising that this research has been handed a megaphone by the mainstream press – but does the science stack up? To start with, the research was carried out in rats, as multi-generational experiments on humans are both grossly unethical and logistically extremely hard. This crucial bit of information is missing from both the Daily Mail headline and the paper’s title. Secondly, the big effects of alcohol consumption were mainly seen on the rats’ children and grandchildren – the effects on their great grandchildren were smaller. That is really important, because if there’s no effect on great grandchildren, it’s probably not due to epigenetics. Drinking large amounts of alcohol (for a rat) whilst pregnant would be expected to have an effect on the children and even the grandchildren. This is because the eggs of female mammals are made early on in foetal development, whilst a daughter is developing in the womb. So if that cell (the egg) also gives rise to a daughter, she will have directly experienced exposures that occurred during her maternal grandmother’s pregnancy. © 2016 Guardian News and Media Limited or its affiliated companies.

Keyword: Development of the Brain; Epigenetics
Link ID: 21945 - Posted: 03.02.2016

By Virginia Morell A fungal disease that has killed amphibians worldwide may be spreading by making the mating calls of infected males more attractive to females. The finding—one of the first—to show that the pathogen can alter a species’s reproductive behavior could explain why frogs and related animals continue to disappear across the globe. “If true—that the fungus is manipulating individuals’ behaviors to facilitate its spread—then this is extraordinary,” says Michael Ryan, a herpetologist at the University of Texas, Austin, who was not involved in the study. The pathogenic fungus, Batrachochytrium dendrobatidis (Bd), causes chytridiomycosis (also known as chytrid fungus disease, which kills amphibians by destroying their skin, disrupting their immune systems, and causing heart failure). Scientists first recognized its lethal effects in the 1990s when numerous species of frogs in Australia and Central and South America experienced massive die-offs; a related fungus attacks salamanders. Bd has been blamed for the extinction of hundreds of amphibian species, and poses a threat to up to one-third of the world’s frogs, salamanders, and other amphibians. There is no cure, but some frog species infected with the fungus are able to survive for years, indicating that they’ve adapted to the disease. Indeed, a recent study showed that Bd has been evolving with amphibians for some 40,000 years, although some species have only recently encountered it. But even amphibian populations adapted to Bd continue to suffer and decline from its effects, says Bruce Waldman, a behavioral ecologist at Seoul National University and one of the authors of the new paper. © 2016 American Association for the Advancement of Science

Keyword: Sexual Behavior; Neurotoxins
Link ID: 21944 - Posted: 03.02.2016

Ian Sample Science editor Too little sleep may bring on a form of the marijuana “munchies”, say scientists who found that sleep-deprived people craved crisps, sweets and biscuits far more than healthier foods. The US researchers believe that skimping on sleep alters brain chemicals in much the same way as the hunger-boosting ingredient in cannabis, which has long propped up snack sales at 24-hour convenience stores. After several nights of poor sleep, healthy volunteers who took part in the study reached for snacks containing more calories - and nearly twice as much fat - than ones they favoured after sleeping well for the same period, the scientists say. When sleepy, the participants had terrible trouble resisting the snacks, even when they were full, said Erin Hanlon, who led the study at the University of Chicago. Research has shown time and again that sleep loss raises the risk of obesity, but the reasons are complex and unclear. Insufficient sleep disrupts hormones that govern appetite and satiety. But those who sleep less have more time to eat, and may be too tired to exercise. To muddy the waters further, obesity can lead to breathing problems that themselves disrupt sleep patterns. In a small study published in the journal Sleep, Hanlon invited 14 men and women in their twenties to spend two four-day sessions at the university’s clinical research centre. The volunteers’ time in bed was controlled, so that on one visit they averaged 7.5 hours of sleep a night, but on the other only 4 hours 11 minutes a night. During their stays, the volunteers ate identical meals, dished out at 9am, 2pm and 7pm.

Keyword: Sleep; Obesity
Link ID: 21943 - Posted: 03.01.2016

By Nala Rogers Treatments that zap the brain with magnets or electricity are rising in popularity, and some evidence suggests they can help lift depression. But scientists are starting to wonder whether they could be hitting the wrong place in left-handed patients. Now, two small studies suggest this could very well be the case. “This is the kind of question that’s been desperately needed for many years,” says Jim Coan, a clinical psychologist at the University of Virginia in Charlottesville who was not involved in the project. “Most researchers in this area, including myself, have selected samples that are strongly right-handed, just in order to avoid mess in the data.” Past studies have suggested that the spots targeted by both kinds of stimulation—located in the left hemisphere—are likely to process “approach” emotions such as happiness, curiosity, and anger, which drive people to reach out and engage with the world. Some studies have also hinted that the brain’s right hemisphere is more involved in so-called “avoidance” emotions such as sorrow and fear. But the studies that support this separation of emotion into the two halves of the brain have relied almost exclusively on right-handed individuals. To figure out whether something else was happening with lefties, University of Chicago in Illinois neuroscientist Daniel Casasanto designed two studies: one to link personality to patterns of brain activity and another to measure the outcome of common brain stimulation treatments in right-handed and left-handed individuals. The brain stimulation treatments were originally designed to treat depression by boosting feelings of happiness and engagement, which motivate “approach” behaviors such as exploring the world and interacting with friends. © 2016 American Association for the Advancement of Science.

Keyword: Laterality; Depression
Link ID: 21942 - Posted: 03.01.2016

It’s the most ancient nervous system we’ve ever seen, preserved inside 520 million-year-old fossils. What’s more, the nervous systems of these creatures’ modern-day descendants are less intricate, proving that evolution isn’t a one-way street to complexity. Found in South China, the five Cambrian fossils belonged to a group of organisms that gave rise to the arthropods, including insects, spiders and crustaceans. The fossils are of Chengjiangocaris kunmingensis, a creature around 10 centimetres long, with a segmented body, multiple pairs of legs and a heart-shaped head. But most interesting of all is its nerve cord and associated neurons. Together, the fossils show the entire nervous system of the organism, apart from its brain – making this the oldest preserved nervous system that has ever been found. “The detail of this fossil is exquisite,” says Rob DeSalle of the American Museum of Natural History in New York, who was not involved in the work. “The information from this specimen unravels transitions in how the nervous systems of arthropods evolved.” The animal had a nerve cord that ran the length of its body, with bulbous nodes of neurons called ganglia located between each pair of legs. “It’s almost like a mini-brain for each pair of legs,” says Javier Ortega-Hernández of the University of Cambridge, whose team analysed and described the fossil. Surprisingly, the team found dozens of fine, subsidiary nerves fanning out across the entire length of the nerve cord, making this nervous system more complex than those seen in today’s descendants. © Copyright Reed Business Information Ltd.

Keyword: Evolution
Link ID: 21941 - Posted: 03.01.2016

Interview by Tim Adams Professor John Cacioppo has been studying the effects and causes of loneliness for 21 years. He is the director of the University of Chicago’s Center for Cognitive and Social Neuroscience. His book Loneliness: Human Nature and the Need for Social Connection examines the pathology and public health implications of the subject. You have been studying social connection and loneliness for more than two decades. How did you come to it as a subject? It was not biographical, I don’t think. Back in the early 90s I had outlined the new field called social neuroscience, the study of the neural mechanisms within a defined social species. Social species are those that create stable bonds, which have societies and cultures. And neuroscience hadn’t really studied those things. Was it something that neuroscientists, with their emphasis on individual brains and cells, resisted? When I proposed it in 1992, I anticipated some kickback from colleagues, so in the original papers I proposed that “social neuroscience isn’t an oxymoron”, and I explained why. That was all well and good, but I quickly realised that theoretical arguments were not going to be enough on their own. I needed to have a convincing demonstration of social neuroscience. And you chose loneliness for that? Well, I was originally interested in social connections. I argued we are defined by social connections, so what happens in the brain when you absent those? I took one other step. I said that the brain is the organ for creating, monitoring, nurturing and retaining these social connections, so it didn’t matter whether you actually had these connections, what was important was whether you felt that you had them. © 2016 Guardian News and Media Limited

Keyword: Emotions; Stress
Link ID: 21940 - Posted: 03.01.2016

Laura Sanders For some adults, Zika virus is a rashy, flulike nuisance. But in a handful of people, the virus may trigger a severe neurological disease. About one in 4,000 people infected by Zika in French Polynesia in 2013 and 2014 got a rare autoimmune disease called Guillain-Barré syndrome, researchers estimate in a study published online February 29 in the Lancet. Of 42 people diagnosed with Guillain-Barré in that outbreak, all had antibodies that signaled a Zika infection. Most also had recent symptoms of the infection. In a control group of hospital patients who did not have Guillain-Barré, researchers saw signs of Zika less frequently: Just 54 out of 98 patients tested showed signs of the virus. The message from this earlier Zika outbreak is that countries in the throes of Zika today “need to be prepared to have adequate intensive care beds capacity to manage patients with Guillain-Barré syndrome,” writes study coauthor Arnaud Fontanet of the Pasteur Institute in Paris and colleagues, some of whom are from French Polynesia. The study, says public health researcher Ernesto Marques of the University of Pittsburgh, “tells us what I think a lot of people already thought: that Zika can cause Guillain-Barré syndrome.” As with Zika and the birth defect microcephaly (SN: 2/20/16, p. 16), though, more work needs to be done to definitively prove the link. Several countries currently hard-hit by Zika have reported upticks in Guillain-Barré syndrome. Colombia, for instance, usually sees about 220 cases of the syndrome a year. But in just five weeks between mid-December 2015 to late January 2016, doctors diagnosed 86 cases, the World Health Organization reports. Other Zika-affected countries, including Brazil, El Salvador and Venezuela, have also reported unusually high numbers of cases. © Society for Science & the Public 2000 - 2016. All rights reserved.

Keyword: Movement Disorders; Neuroimmunology
Link ID: 21939 - Posted: 03.01.2016

By SABRINA TAVERNISE WASHINGTON — Half of one satisfying sexual encounter a month. That is the average benefit a woman gets when she takes the new female libido drug, sometimes called the “female Viagra,” researchers reported Monday. Last year the Food and Drug Administration approved the drug, flibanserin, making it the first drug available to treat low sexual desire in women. It was promoted by a group of women’s rights activists who argued it was unfair that men had numerous drugs to boost sexual function while women had nothing. But public health groups and some other women’s groups contended that the science did not justify its approval. The drug’s effects were modest, they said, and not worth side effects such as sleepiness, dizziness, fatigue and nausea. And the risk of some side effects increased with alcohol consumption. In the new study, published in JAMA Internal Medicine, researchers found benefits that were slightly more modest than those submitted to the F.D.A. during the approval process. The researchers analyzed eight studies of about 5,900 women, using a method that involved pooling the data. They concluded that treatment with flibanserin, now marketed as Addyi, resulted in “one-half of an additional sexually satisfying encounter per month.” (The study did not define what “one-half” of a sexually satisfying encounter was.) That result was not very different from original findings of three clinical trials submitted to the F.D.A. as support for the drug’s approval. Those trials found that once women started taking the drug, they had an average of about one additional satisfying sexual encounter a month, on top of the two to three they were having already. That result lifted the benefits above the bar of being scientifically meaningful, but barely. Still, it was enough for the agency’s approval. © 2016 The New York Times Company

Keyword: Sexual Behavior
Link ID: 21938 - Posted: 03.01.2016

Cathleen O'Grady When we speak, listen, read, or write, almost all of the language processing that happens in our brains goes on below the level of conscious awareness. We might be aware of grasping for a particular forgotten word, but we don’t actively think about linguistic concepts like morphemes (the building blocks of words, like the past tense morpheme “-ed”). Psycholinguists try to delve under the surface to figure out what’s actually going on in the brain, and how well this matches up with our theoretical ideas of how languages fit together. For instance, linguists talk about morphemes like “-ed”, but do our brains actually work with morphemes when we’re producing or interpreting language? That is, do theoretical linguistic concepts have any psychological reality? An upcoming paper in the journal Cognition suggests an unusual way to investigate this: by testing synaesthetes. Synaesthesia comes in many forms. Some synaesthetes associate musical tones or notes with particular colours; others attach personalities to letters or numbers. A huge number of synaesthetes have associations that are in some way linguistic, and one of the most common forms of all is grapheme-colour (GC) synaesthesia, which is the association of colours with particular letters or numbers. For instance, a GC synaesthete might have a consistent perception of the letter “A” being red. This association often extends to a whole word, so “ant” might be red, too. © 2016 Guardian News and Media Limited

Keyword: Language
Link ID: 21937 - Posted: 02.27.2016

By James Gallagher Health editor, BBC News website People who are obese have a worse memory than their thinner friends, a small study shows. Tests on 50 people showed being overweight was linked to worse "episodic memory" or the ability to remember past experiences. The study in the Quarterly Journal of Experimental Psychology argues that a less vivid memory of recent meals may lead to overeating. However, other aspects of memory - such as general knowledge - were unaffected. Tests on rats have previously shown that with burgeoning waistlines come poorer performances in memory tests, but the evidence in humans has been mixed. The latest experiments looked at episodic memory - the video tape in your mind - that remembers the smell of a cup of coffee or the feel of holding someone's hand. Fifty people with a Body Mass Index (BMI) ranging from 18 (healthy) to 51 (very obese) took part in a memory test - a bit like doing a treasure hunt on your own. They had to "hide" objects at different times and on different scenes displayed on a computer screen. They were later asked to recall what they had hidden, when and where. The results showed obese people's scores were 15% lower than thinner people. Dr Lucy Cheke, from the University of Cambridge, told the BBC News website: "The suggestion we're making is that a higher BMI is having some reduction on the vividness of memory, but they're not drawing blanks and having amnesia. "But if they have a less strong memory of a recent meal, with a less strong impact in the mind, then they may have less ability to regulate how much they eat later on." Hunger hormones play a huge role in how much we eat, but it is already recognised that our minds have a key role too. © 2016 BBC

Keyword: Obesity; Learning & Memory
Link ID: 21936 - Posted: 02.27.2016

With the opioid epidemic reaching into every corner of the U.S., more people are talking about addiction as a chronic disease rather than a moral failing. For researcher A. Thomas McLellan, who has spent his entire career studying substance abuse, the shift is a welcome one, though it has come frustratingly late. McLellan is co-founder of the Treatment Research Institute in Philadelphia and former deputy director of the White House Office of National Drug Control Policy. His work has focused on understanding addiction as a disease and improving the ways it is treated, a mission that took a personal turn midway through his career when he lost a son to overdose. NPR's Audie Cornish spoke with McLellan about how addiction is viewed and how that view has shaped the treatment system we have today. He also has suggestions on how to make it better. On why addiction has traditionally been seen as a criminal justice issue, not a health issue Think about it. If you didn't have brain science, which has just really emerged in the last two or three decades, all you had to look at was the behavior of addicted people. They are not pleasant people when they are in full addiction. They steal, they lie, they swear they're going to do something and they don't. It's quite easy to think of this as it has been thought of for literally hundreds of years: as a character disorder, as poor upbringing as a problem of parenting. And that's how we approached it. It's not coincidence that the Justice Department has played such a pivotal role. The emerging science shows this is a brain disease. It's got the same genetic transmutability as a lot of chronic illnesses. And the organ that it affects is the brain, and within the brain it is motivation, inhibition, cognition, all those things that produce the aberrant, unpleasant behaviors that are associated with addiction. © 2016 npr

Keyword: Drug Abuse
Link ID: 21935 - Posted: 02.27.2016

By Roni Caryn Rabin Fatal prescription-drug overdoses in the United States have increased sharply in recent years. But while most of the deaths have involved opioid painkillers like oxycodone, a new study suggests that anti-anxiety medications now are playing an outsize role in overdose deaths. The number of Americans filling prescriptions for anti-anxiety drugs — benzodiazepines like Valium and Xanax that are used to treat anxiety, panic disorders and insomnia — increased 67 percent between 1996 and 2013, the study found. But the rate of overdose deaths involving these drugs increased more than fourfold. The analysis, published online last week in The American Journal of Public Health, found that 5.6 percent of American adults filled a benzodiazepine prescription in 2013, up from 4.1 percent in 1996. (The actual number of Americans filling a benzodiazepine prescription rose to 13.5 million in 2013, up from 8.1 million in 1996.) Meanwhile, the rate of overdose deaths involving anti-anxiety drugs reached 3.07 per 100,000 adults in 2013, up from 0.58 per 100,000 adults in 1996. With public attention focused primarily on opioid painkillers, the role of anti-anxiety drugs “fell under the radar,” said Dr. Marcus Bachhuber, the study’s author and an assistant professor of medicine at Montefiore Medical Center/Albert Einstein College of Medicine in the Bronx. Yet when benzodiazepines are abused or combined with other drugs or alcohol, they contribute to depressing the respiratory system, which can be deadly, he said. “If we’re going to address the prescription drug crisis, we can’t just focus on opioids,” he said. “We need to think more broadly about other drugs, like benzodiazepines.” © 2016 The New York Times Company

Keyword: Drug Abuse
Link ID: 21934 - Posted: 02.27.2016