Most Recent Links

Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.


Links 1 - 20 of 22806

By Mo Costandi This map of London shows how many other streets are connected to each street, with blue representing simple streets with few connecting streets and red representing complex streets with many connecting streets. Credit: Joao Pinelo Silva The brain contains a built-in GPS that relies on memories of past navigation experiences to simulate future ones. But how does it represent new environments in order to determine how to navigate them successfully? And what happens in the brain when we enter a new space, or use satellite navigation (SatNav) technology to help us find our way around? Research published Tuesday in Nature Communications reveals two distinct brain regions that cooperate to simulate the topology of one’s environment and plan future paths through it when one is actively navigating. In addition, the research suggests both regions become inactive when people follow SatNav instructions instead of using their spatial memories. In a previous study researchers at University College London took participants on a guided tour through the streets of London’s Soho district and then used functional magnetic resonance imaging (fMRI) to scan their brains as they watched 10 different simulations of navigating those streets. Some of the movies required them to decide at intersections which way would be the shortest path to a predetermined destination; others came with instructions about which way to go at each junction. © 2017 Scientific American,

Keyword: Learning & Memory
Link ID: 23391 - Posted: 03.22.2017

Hannah Devlin Scientists have developed a new genetic test for Alzheimer’s risk that can be used to predict the age at which a person will develop the disease. A high score on the test, which is based on 31 genetic markers, can translate to being diagnosed many years earlier than those with a low-risk genetic profile, the study found. Those ranked in the top 10% in terms of risk were more than three times as likely to develop Alzheimer’s during the course of the study, and did so more than a decade before those who ranked in the lowest 10%. Strobe lighting provides a flicker of hope in the fight against Alzheimer’s Read more Rahul Desikan, of the University of California – who led the international effort, said the test could be used to calculate any individual’s risk of developing Alzheimer’s that year. “That is, if you don’t already have dementia, what is your yearly risk for AD onset, based on your age and genetic information,” he said. The so-called polygenic hazard score test was developed using genetic data from more than 70,000 individuals, including patients with Alzheimer’s disease and healthy elderly people. It is already known that genetics plays a powerful role in Alzheimer’s. Around a quarter of patients have a strong family history of the disease, and scientists have shown this is partly explained by a gene called ApoE, which comes in three versions, and is known to have a powerful influence on the risk of getting the most common late-onset type of Alzheimer’s. One version of ApoE appears to reduce risk by up to 40%, while those with two copies (one from each parent) of the high-risk version can increase risk by 12 times.

Keyword: Alzheimers
Link ID: 23390 - Posted: 03.22.2017

By KIM SEVERSON SONOMA, Calif. — The first thing Paula Wolfert wants to make a guest is coffee blended with butter from grass-fed cows and something called brain octane oil. She waves a greasy plastic bottle of the oil around her jumble of a kitchen like a preacher who has taken up a serpent. Never mind that this is the woman who introduced tagines, Aleppo pepper and cassoulet to American kitchens, wrote nine cookbooks and once possessed a palate the food writer Ruth Reichl declared the best she’d ever encountered. Ms. Wolfert, 78, has dementia. She can’t cook much, even if she wanted to. Which, by the way, she doesn’t. She learned she probably had Alzheimer’s disease in 2013, but she suspected something wasn’t right long before. Words on a page sometimes made no sense. Complex questions started to baffle her. Since she has always been an audacious and kinetic conversationalist with a touch of hypochondria, friends didn’t notice anything was wrong. Doctors spoke of “senior moments.” But she knew. One day, Ms. Wolfert went to make an omelet for her husband, the crime novelist William Bayer. She had to ask him how. The woman who once marched up to the French chef Jean-Louis Palladin and told him a dish didn’t have enough salt can no longer taste the difference between a walnut and a pecan, or smell whether the mushrooms are burning. The list of eight languages she once understood has been reduced to English. Maybe 40 percent of the words she knew have evaporated. “What am I going to do, cry about it?” Ms. Wolfert said in an interview at her home this month, the slap of her Brooklyn accent still sharp. After all, she points out, her first husband left her in Morocco with two small children and $2,000: “I cried for 20 minutes and I thought, ‘This isn’t going to do any good.’” © 2017 The New York Times Company

Keyword: Alzheimers
Link ID: 23389 - Posted: 03.22.2017

By NICHOLAS BAKALAR Some research has suggested that vitamin E and selenium supplements might lower the risk for Alzheimer’s disease, but a new long-term trial has found no evidence that they will. The study began as a randomized clinical trial in 2002 testing the supplements for the prevention of prostate cancer. When that study was stopped in 2009 because no effect was found, 3,786 of the original 7,540 men participated in a continuing study to test the antioxidants as a preventive for Alzheimer’s. The study, in JAMA Neurology, randomly assigned the men, whose average age was 67 at the start, to take either vitamin E, selenium, both supplements, or a placebo. By 2015, 4.4 percent of the men had dementia, but there was no difference between the groups. Neither selenium, vitamin E, nor both in combination were any more effective than a placebo. The study controlled for age, family history of Alzheimer’s disease, education, race, diabetes and other factors. The lead author, Richard J. Kryscio, a professor of statistics at the University of Kentucky, said that it is possible that different dosages or different types of selenium or vitamin E might show an effect. “We could have picked the wrong version or the wrong dose,” he said. “But there’s really no evidence that these supplements will make a difference down the road in preventing dementia.” © 2017 The New York Times Company

Keyword: Alzheimers
Link ID: 23388 - Posted: 03.22.2017

By Jill Serjeant NEW YORK (Reuters) - Long-running children's television show "Sesame Street" is welcoming a new kid to the block - a Muppet with autism called Julia. A redhead who loves to sing and remembers the words to lots of songs, Julia will debut on the show for preschoolers on April 10 after a five-year outreach effort to families and experts on autism, Sesame Workshop said on Monday. "For years, families of children with autism have asked us to address the issue," Dr. Jeanette Betancourt, senior vice president of U.S. social impact at the nonprofit Sesame Workshop, said in a statement. One in 68 American children is currently diagnosed with autism, according to the Centers for Disease Control and Prevention, an increase of some 119 percent since 2000. Autism is a developmental disorder present from early childhood, characterized by difficulty in communicating and forming relationships with other people and in using language and abstract concepts Stacey Gordon, the puppeteer who will perform the role of Julia, and Christine Ferraro who wrote her part, both have family members who are on the autism spectrum. "It's important for kids without autism to see what autism can look like," Gordon told the CBS show "60 Minutes" in a preview on Sunday. "Had my son's friends been exposed to his behaviors through something that they had seen on TV before they experienced them in the classroom, they might not have been frightened. They might not have been worried when he cried. They would have known that he plays in a different way and that that's okay," she added. © 2017 Scientific American

Keyword: Autism
Link ID: 23387 - Posted: 03.22.2017

by Helen Thompson Aside from being adorable, sea otters and Indo-Pacific bottlenose dolphins share an ecological feat: Both species use tools. Otters crack open snails with rocks, and dolphins carry cone-shaped sponges to protect their snouts while scavenging for rock dwelling fish. Researchers have linked tool use in dolphins to a set of differences in mitochondrial DNA — which passes from mother to offspring — suggesting that tool-use behavior may be inherited. Biologist Katherine Ralls of the Smithsonian Institution in Washington, D.C., and her colleagues looked for a similar pattern in otters off the California coast. The team tracked diet (primarily abalone, crab, mussels, clams, urchins or snails) and tool use in the wild and analyzed DNA from 197 individual otters. Otters that ate lots of hard-shelled snails — and used tools most frequently — rarely shared a common pattern in mitochondrial DNA, nor were they more closely related to other tool-users than any other otter in the population. Unlike dolphins, sea otters may all be predisposed to using tools because their ancestors probably lived off mollusks, which required cracking open. However, modern otters only take up tools when their diet requires them, the researchers report March 21 in Biology Letters. |© Society for Science & the Public 2000 - 2017.

Keyword: Evolution
Link ID: 23386 - Posted: 03.22.2017

Laura Sanders Not too long ago, the internet was stationary. Most often, we’d browse the Web from a desktop computer in our living room or office. If we were feeling really adventurous, maybe we’d cart our laptop to a coffee shop. Looking back, those days seem quaint. Today, the internet moves through our lives with us. We hunt Pokémon as we shuffle down the sidewalk. We text at red lights. We tweet from the bathroom. We sleep with a smartphone within arm’s reach, using the device as both lullaby and alarm clock. Sometimes we put our phones down while we eat, but usually faceup, just in case something important happens. Our iPhones, Androids and other smartphones have led us to effortlessly adjust our behavior. Portable technology has overhauled our driving habits, our dating styles and even our posture. Despite the occasional headlines claiming that digital technology is rotting our brains, not to mention what it’s doing to our children, we’ve welcomed this alluring life partner with open arms and swiping thumbs. Scientists suspect that these near-constant interactions with digital technology influence our brains. Small studies are turning up hints that our devices may change how we remember, how we navigate and how we create happiness — or not. Somewhat limited, occasionally contradictory findings illustrate how science has struggled to pin down this slippery, fast-moving phenomenon. Laboratory studies hint that technology, and its constant interruptions, may change our thinking strategies. Like our husbands and wives, our devices have become “memory partners,” allowing us to dump information there and forget about it — an off-loading that comes with benefits and drawbacks. Navigational strategies may be shifting in the GPS era, a change that might be reflected in how the brain maps its place in the world. Constant interactions with technology may even raise anxiety in certain settings. |© Society for Science & the Public 2000 - 2017

Keyword: Attention; Learning & Memory
Link ID: 23385 - Posted: 03.21.2017

Ian Sample Science editor Doctors have stumbled on an unlikely source for a drug to ward off brain damage caused by strokes: the venom of one of the deadliest spiders in the world. A bite from an Australian funnel web spider can kill a human in 15 minutes, but a harmless ingredient found in the venom can protect brain cells from being destroyed by a stroke, even when given hours after the event, scientists say. If the compound fares well in human trials, it could become the first drug that doctors have to protect against the devastating loss of neurons that strokes can cause. Researchers discovered the protective molecule by chance as they sequenced the DNA of toxins in the venom of the Darling Downs funnel web spider (Hadronyche infensa) that lives in Queensland and New South Wales. Venom from three spiders was gathered for the study after scientists trapped and “milked exhaustively” three spiders on Orchid beach, about 400km north of Brisbane. The molecule, called Hi1a, stood out because it looked like two copies of another brain cell-protecting chemical stitched together. It was so intriguing that scientists decided to synthesise the compound and test its powers. “It proved to be even more potent,” said Glenn King at the University of Queensland’s centre for pain research. Strokes occur when blood flow to the brain is interrupted and the brain is starved of oxygen. About 85% of strokes are caused by blockages in blood vessels in the brain, with the rest due to bleeds when vessels rupture. Approximately six million people a year die from stroke, making it the second largest cause of death worldwide after heart attacks. © 2017 Guardian News and Media Limited

Keyword: Stroke; Neurotoxins
Link ID: 23384 - Posted: 03.21.2017

As the father of two sons with schizophrenia, author Ron Powers is familiar with the pain and frustration of dealing with a chronic, incurable disease of the brain. Powers' younger son, Kevin, was a talented musician whose struggles with schizophrenia began at age 17. Just before his 21st birthday, in 2005, Kevin took his own life. A few years later, Powers' older son, Dean, started experiencing symptoms of schizophrenia and had a psychotic break. "There is no greater ... feeling of helplessness than to watch two beloved sons deteriorate before [your] eyes, not knowing what to do to bring them back," Powers tells Fresh Air's Terry Gross. Powers' new book, No One Cares About Crazy People, is both a memoir about his sons and a history of how the mentally ill have been treated medically, legally and socially. Although Dean is now medicated and doing well, Powers notes that many people with schizophrenia don't receive the treatment they need — in part because they often don't believe they are ill. "This unwillingness to believe that one is afflicted has led to tremendous problems," Powers says. "To force that person into being helped is a violation of his or her civil rights ... and the law may penalize the care workers who give [people with schizophrenia] medications or admit them to a hospital against their will. ... That is the great reigning Catch-22 of the way our society deals — or fails to deal — with schizophrenia." © 2017 npr

Keyword: Schizophrenia
Link ID: 23383 - Posted: 03.21.2017

Jon Hamilton Gerard Sanacora, a professor of psychiatry at Yale University, has treated hundreds of severely depressed patients with low doses of ketamine, an anesthetic and popular club drug that isn't approved for depression. This sort of "off-label" prescribing is legal. But Sanacora says other doctors sometimes ask him, "How can you be offering this to patients based on the limited amount of information that's out there and not knowing the potential long-term risk?" Sanacora has a simple answer. "If you have patients that are likely to seriously injure themselves or kill themselves within a short period of time, and they've tried the standard treatments, how do you not offer this treatment?" he says. Dozens of clinics now offer ketamine to patients with depression. And a survey of providers in the U.S. and Canada showed that "well over 3,000" patients have been treated so far, Sanacora says. A number of small studies have found that ketamine can do something no other drug can: it often relieves even suicidal depression in a matter of hours in patients who have not responded to other treatments. Ketamine's potential as an antidepressant was recognized more than a decade ago. And studies done since then provide "compelling evidence that the antidepressant effects of ketamine infusion are both rapid and robust, albeit transient," according to a consensus statement from a task force of the American Psychiatric Association. Sanacora is one of the task force members. © 2017 npr

Keyword: Depression; Drug Abuse
Link ID: 23382 - Posted: 03.21.2017

By Chris Baraniuk It’s sometimes practically impossible to tell similar colours apart. Even side by side, they look the same. A special pair of spectacles gives us new power to see more distinct colours, and could one day help to spot counterfeit banknotes or counteract camouflage. The glasses, devised by a team at the University of Wisconsin-Madison, basically enhance the user’s colour vision, allowing them to see metamers – colours that look the same but give off different wavelengths of light – as recognisably distinct hues. Human colour vision relies on three types of cone cells that react to short (blue), medium (green) and long (red) wavelengths. While brushing up on his knowledge of the eye before teaching a photonics class, physicist Mikhail Kats had a brainwave. Could the eye be tricked into effectively having another type of cone cell? In theory, this could take our vision from being trichromatic, which uses three colour channels, to tetrachromatic. Some animals see in four (or more) channels. Goldfish, for example, have cells for red, blue, green and ultraviolet light. Some researchers suggest that a very small number of humans may be tetrachromats too. Read more: Human eye proteins detect red beyond red To make their glasses, Kats and his colleagues designed two colour filters, one for each eye that strip out specific parts of the blue light spectrum. With each eye receiving slightly different spectral information about blue things, the team hypothesised that any subtle differences in colour would be more pronounced. And they were right. © Copyright Reed Business Information Ltd

Keyword: Vision
Link ID: 23381 - Posted: 03.21.2017

Cris Ledón-Rettig Picture a lion: The male has a luxuriant mane, the female doesn’t. This is a classic example of what biologists call sexual dimorphism – the two sexes of the same species exhibit differences in form or behavior. Male and female lions pretty much share the same genetic information, but look quite different. We’re used to thinking of genes as responsible for the traits an organism develops. But different forms of a trait – mane or no mane – can arise from practically identical genetic information. Further, traits are not all equally sexually dimorphic. While the tails of peacocks and peahens are extremely different, their feet, for example, are pretty much the same. Understanding how this variation of form – what geneticists call phenotypic variation – arises is crucial to answering several scientific questions, including how novel traits appear during evolution and how complex diseases emerge during a lifetime. So researchers have taken a closer look at the genome, looking for the genes responsible for differences between sexes and between traits within one sex. The key to these sexually dimorphic traits appears to be a kind of protein called a transcription factor, whose job it is to turn genes “on” and “off.” In our own work with dung beetles, my colleagues and I are untangling how these transcription factors actually lead to the different traits we see in males and females. A lot of it has to do with something called “alternative gene splicing” – a phenomenon that allows a single gene to encode for different proteins, depending on how the building blocks are joined together. © 2010–2017, The Conversation US, Inc.

Keyword: Sexual Behavior; Evolution
Link ID: 23380 - Posted: 03.21.2017

By THOMAS FULLER SANTA ROSA, Calif. — In the heart of Northern California’s wine country, a civil engineer turned marijuana entrepreneur is adding a new dimension to the art of matching fine wines with gourmet food: cannabis and wine pairing dinners. Sam Edwards, co-founder of the Sonoma Cannabis Company, charges diners $100 to $150 for a meal that experiments with everything from marijuana-leaf pesto sauce to sniffs of cannabis flowers paired with sips of a crisp Russian River chardonnay. “It accentuates the intensity of your palate,” Mr. Edwards, 30, said of the dinners, one of which was held recently at a winery with sweeping views of the Sonoma vineyards. “We are seeing what works and what flavors are coming out.” Sonoma County, known to the world for its wines, is these days a seedbed of cannabis experimentation. The approval of recreational cannabis use by California voters in November has spurred local officials here to embrace the pot industry and the tax income it may bring. “We’re making this happen,” said Julie Combs, a member of the Santa Rosa City Council, who is helping lead an effort to issue permits to cannabis companies. “This is an industry that can really help our region.” Of the many ways in which California is on a collision course with the Trump administration, from immigration to the environment, the state’s enthusiastic embrace of legalized and regulated marijuana may be one of the biggest tests of the federal government’s power. Attorney General Jeff Sessions has equated marijuana with heroin and, on Wednesday, mentioned cannabis in the context of the “scourge of drug abuse.” © 2017 The New York Times Compan

Keyword: Drug Abuse; Pain & Touch
Link ID: 23379 - Posted: 03.20.2017

By Daniel Barron It was 4 P.M., and Andrew* had just bought 10 bags of heroin. In his kitchen, he tugged one credit-card-sized bag from the rubber-banded bundle and laid it on the counter with sacramental reverence. Pain shot through his body as he pulled a cutting board from the cabinet. Slowly, deliberately, he tapped the bag's white contents onto the board and crushed it with the flat edge of a butter knife, forming a line of fine white powder. He snorted it in one pass and shuffled back to his armchair. It was bitter, but snorting heroin was safer than injecting, and he was desperate: his prescription pain medication was gone. I met Andrew the next day in the emergency room, where he told me about the previous day's act of desperation. I admitted him to control his swelling legs and joint pain. He was also detoxing from opioids. Andrew looked older than his 69 years. His face was wrinkled with exhaustion. A frayed, tangled mop of grizzled hair fell to his shoulders. Andrew had been a satellite network engineer, first for the military, more recently for a major telecommunications company. An articulate, soft-spoken fellow, he summed up his (rather impressive) career modestly: “Well, I'd just find where a problem was and then find a way to fix it.” Yet there was one problem he couldn't fix. “Doctor, I'm always in the most terrible pain,” he said, with closed eyes. “I had no other options. I started using heroin, bought it from my neighbor to help with the pain. I'm scared stiff.” © 2017 Scientific American

Keyword: Pain & Touch; Drug Abuse
Link ID: 23378 - Posted: 03.20.2017

By Jia Naqvi Sixty percent of the calls to poison control centers for help with prescription opioid exposure involved children younger than 5. (Rich Pedroncelli/Associated Press) The phone rings once approximately every 45 minutes — that is how often poison control centers in the United States receive calls about children being exposed to prescription opioids, according to a study published Monday. Over a span of 16 years, from January 2000 until December 2015, about 188,000 calls were placed to poison control centers regarding pediatric and teenage exposure to opioids, the study published in the journal Pediatrics found. Sixty percent of the children exposed to opioids were younger than 5, while teenagers accounted for 30 percent. Pediatric exposure to opioids increased by 86 percent from 2000 to 2009 but decreased overall for all ages under 20 from 2009 until 2015, the study found. Increasing awareness among people with prescription drugs, physicians putting more thought into prescribing opioids, and prescription drug monitoring programs implemented by many states and efforts by different organizations could have contributed to the decrease in exposure, said Marcel Casavant, study author, medical director of the Central Ohio Poison Center and chief toxicologist at Nationwide Children’s Hospital in Columbus. “We are not quite sure, and so it would be good to try to sort out of all the things that we are trying, which ones are the most effective and how can we spend more time doing that,” Casavant said. © 1996-2017 The Washington Post

Keyword: Pain & Touch; Drug Abuse
Link ID: 23377 - Posted: 03.20.2017

Sara Reardon, Jeff Tollefson, Alexandra Witze & Erin Ross Funding for the National Oceanic and Atmospheric Administration’s weather satellites, which track hurricanes, would be maintained under the Trump plan. When it comes to science, there are few winners in US President Donald Trump’s first budget proposal. The plan, released on 16 March, calls for double-digit cuts for the Environmental Protection Agency (EPA) and the National Institutes of Health (NIH). It also lays the foundation for a broad shift in the United States’ research priorities, including a retreat from environmental and climate programmes. Rumours of the White House proposal have swirled for weeks, alarming many researchers who depend on government funding — and science advocates who worry that the Trump administration’s stance will jeopardize US leadership in fields ranging from climate science to cancer biology. It is not clear, however, how much of the plan will survive negotiations in Congress over the coming months. What could Trump’s budget for science mean for you? “Cutting [research and development] funding from our budget is the same as cutting the engines off an airplane that’s too heavy for take-off,” says Jason Rao, director of international affairs at the American Society for Microbiology in Washington DC. The greatest threats to the United States, he says, are those presented by infectious diseases, climate change and energy production — none of which can be addressed effectively without scientific research. © 2017 Macmillan Publishers Limited,

Keyword: Miscellaneous
Link ID: 23376 - Posted: 03.20.2017

By Taylor Beck LSD, “magic” mushrooms and mescaline have been banned in the U.S. and many other countries since the 1970s, but psychedelic medicine is making a comeback as new therapies for depression, nicotine addiction and anxiety. The drugs have another scientific use, too: so-called psychotomimetics, or mimics of psychosis, may be useful tools for studying schizophrenia. By creating a brief bout of psychosis in a healthy brain, as indigenous healers have for millennia, scientists are seeking new ways to study—and perhaps treat—mental illness. “We think that schizophrenia is a group of psychoses, which may have different causes,” says Franz Vollenweider, a psychiatrist and neuroscientist at the University of Zurich. “The new approach is to try to understand specific symptoms: hearing voices, cognitive problems, or apathy and social disengagement. If you can identify the neural bases of these, you can tailor the pharmacology.” Vollenweider and his colleagues have found an existing drug for anxiety that blocks specific effects of psilocybin, the psychoactive ingredient in magic mushrooms. When healthy people were given the drug before tripping, they did not report visual hallucinations and other common effects, according to a study published in April 2016 in European Neuropsychopharmacology. The effort is part of a burgeoning movement in pharmacology that seeks to induce psychosis to learn how to treat it. And schizophrenia desperately needs new treatments. Seventy-five percent of afflicted patients have cognitive problems. And most commonly used drugs do not treat the disorder's “negative” symptoms—apathy, social withdrawal, negative thinking—nor the cognitive impairments, which best predict how well a patient will fare in the long term. © 2017 Scientific American

Keyword: Schizophrenia; Drug Abuse
Link ID: 23375 - Posted: 03.19.2017

By JULIE REHMEYER and DAVID TULLER What are some of the treatment regimens that sufferers of chronic fatigue syndrome should follow? Many major medical organizations cite two: psychotherapy and a steady increase in exercise. There’s just one problem. The main study that has been cited as proof that patients can recover with those treatments overstated some of its results. In reality, the claim that patients can recover from these treatments is not justified by the data. That’s the finding of a peer-reviewed preliminary re-analysis of previously unpublished data from the clinical trial, the largest ever for chronic fatigue syndrome. Nicknamed the PACE trial, the core findings of the British study appeared in The Lancet in 2011 and Psychological Medicine in 2013. Patients battled for years to obtain the underlying data, and last spring, a legal tribunal in Britain, the General Regulatory Chamber, directed the release of some of the study’s information. The impact of the trial on treatment options for the estimated one million chronic fatigue patients in the United States has been profound. The Mayo Clinic, Kaiser Permanente, WebMD, the American Academy of Family Physicians and others recommend psychotherapy and a steady increase in exercise. But this approach can be harmful. According to a 2015 report from the Institute of Medicine, now the National Academy of Medicine, even minimal activity can cause patients prolonged exhaustion, muscle pain, cognitive problems and more. In severe cases, a short conversation or a trip to the bathroom can deplete patients for hours, days or more. In surveys, patients routinely report deterioration after a program of graded exercise. The psychotherapeutic intervention also encourages patients to increase their activity levels. Many patients (including one of us) have remained ill for years or decades with chronic fatigue syndrome, also known as myalgic encephalomyelitis, or ME/CFS. It can be triggered by a viral infection, resulting in continuing or recurring immunological and neurological dysfunction. The Institute of Medicine dismissed any notion that it is a psychiatric illness. © 2017 The New York Times Company

Keyword: Depression; Neuroimmunology
Link ID: 23374 - Posted: 03.19.2017

Doctors who limit the supply of opioids they prescribe to three days or less may help patients avoid the dangers of dependence and addiction, a new study suggests. Among patients without cancer, a single day's supply of a narcotic painkiller can result in 6 per cent of patients being on an opioid a year later, the researchers said. The odds of long-term opioid use increased most sharply in the first days of therapy, particularly after five days of taking the drugs. The rate of long-term opioid use increased to about 13 per cent for patients who first took the drugs for eight days or more, according to the report. "Awareness among prescribers, pharmacists and persons managing pharmacy benefits that authorization of a second opioid prescription doubles the risk for opioid use one year later might deter overprescribing of opioids," said senior researcher Martin Bradley. He is from the division of pharmaceutical evaluation and policy at the University of Arkansas for Medical Sciences. "The chances of long-term opioid use, use that lasts one year or more, start increasing with each additional day supplied, starting after the third day, and increase substantially after someone is prescribed five or more days, and especially after someone is prescribed one month of opioid therapy," Bradley said. The odds of chronic opioid use also increase when a second prescription is given or refilled, he noted. ©2017 CBC/Radio-Canada.

Keyword: Drug Abuse; Pain & Touch
Link ID: 23373 - Posted: 03.19.2017

Obese people who get surgery to lose weight have half the risk of developing heart failure as do patients who make lifestyle changes to shed excess pounds, a recent study suggests. “We were surprised by the large difference in heart failure incidence between the two groups,” said lead study author Johan Sundstrom of Uppsala University in Sweden. It’s possible that gastric bypass patients had a lower risk of heart failure because they lost more weight than the group trying to do so without surgery. Researchers also found that losing 22 pounds by any means was tied to a 23 percent drop in heart failure risk. The study team examined data on 25,805 obese people who had gastric bypass surgery, which reduces the stomach to a small pouch, and 13,701 patients who were put on low-calorie diets. After following half of the patients for at least four years, people who had gastric bypass were found to be 46 percent less likely to have developed heart failure. After one year, surgery patients had an average weight loss 41.4 pounds greater than that of those who relied on diet and exercise, the study found. After two years, surgery was associated with an average weight loss that was 49.8 pounds more than those who undertook lifestyle changes. Some previous research has linked obesity to heart failure, and a growing body of evidence suggests that obesity might directly cause the heart condition, Sundstrom said. While the new study wasn’t designed to prove a causal relationship, it adds more evidence in support of this possibility. © 1996-2017 The Washington Post

Keyword: Obesity
Link ID: 23372 - Posted: 03.19.2017