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By Maria Konnikova At the turn of the twentieth century, Ivan Pavlov conducted the experiments that turned his last name into an adjective. By playing a sound just before he presented dogs with a snack, he taught them to salivate upon hearing the tone alone, even when no food was offered. That type of learning is now called classical—or Pavlovian—conditioning. Less well known is an experiment that Pavlov was conducting at around the same time: when some unfortunate canines heard the same sound, they were given acid. Just as their luckier counterparts had learned to salivate at the noise, these animals would respond by doing everything in their power to get the imagined acid out of their mouths, each “shaking its head violently, opening its mouth and making movements with its tongue.” For many years, Pavlov’s classical conditioning findings overshadowed the darker version of the same discovery, but, in the nineteen-eighties, the New York University neuroscientist Joseph LeDoux revived the technique to study the fear reflex in rats. LeDoux first taught the rats to associate a certain tone with an electric shock so that they froze upon hearing the tone alone. In essence, the rat had formed a new memory—that the tone signifies pain. He then blunted that memory by playing the tone repeatedly without following it with a shock. After multiple shock-less tones, the animals ceased to be afraid. Now a new generation of researchers is trying to figure out the next logical step: re-creating the same effects within the brain, without deploying a single tone or shock. Is memory formation now understood well enough that memories can be implanted and then removed absent the environmental stimulus?
By Jocelyn Kaiser A virus that shuttles a therapeutic gene into cells has strengthened the muscles, improved the motor skills, and lengthened the lifespan of mice afflicted with two neuromuscular diseases. The approach could one day help people with a range of similar disorders, from muscular dystrophy to amyotrophic lateral sclerosis, or ALS. Many of these diseases involve defective neuromuscular junctions—the interface between neurons and muscle cells where brain signals tell muscles to contract. In one such disease, a form of familial limb-girdle myasthenia, people carry two defective copies of the gene called DOK7, which codes for a protein that’s needed to form such junctions. Their hip and shoulder muscles atrophy over many years, and some eventually have trouble breathing or end up in a wheelchair. Mice similarly missing a properly working Dok7 gene are severely underweight and die within a few weeks. In the new study, researchers led by molecular biologist Yuji Yamanashi of the University of Tokyo first injected young mice engineered to have defective Dok7 with a harmless virus carrying a good copy of the Dok7 gene, which is expressed only in muscle. Within about 7 weeks, the rodents recovered. Their muscle cells cranked out the DOK7 protein, and under a microscope their muscles had larger neuromuscular junctions than those of untreated mice with defective Dok7. What’s more, the mice grew to a healthy body weight and had essentially normal scores on tests of motor skills and muscle strength. © 2014 American Association for the Advancement of Science.
by Bob Holmes THERE'S something primal in a mother's response to a crying infant. So primal, in fact, that mother deer will rush protectively to the distress calls of other infant mammals, such as fur seals, marmots and even humans. This suggests such calls might share common elements – and perhaps that these animals experience similar emotions. Researchers – and, indeed, all pet owners – know that humans respond emotionally to the distress cries of their domestic animals, and there is some evidence that dogs also respond to human cries. However, most people have assumed this is a by-product of domestication. However, Susan Lingle, a biologist at the University of Winnipeg, Canada, noticed that the infants of many mammal species have similar distress calls: simple sounds with few changes in pitch. She decided to test whether cross-species responses occur more widely across the evolutionary tree. So, Lingle and her colleague Tobias Riede, now at Midwestern University in Glendale, Arizona, recorded the calls made by infants from a variety of mammal species when separated from their mother or otherwise threatened. They then played the recordings through hidden speakers to wild mule deer (Odocoileus hemionus) out on the Canadian prairies. They found that deer mothers quickly moved towards the recordings of infant deer, but also towards those of infant fur seals, dogs, cats and humans, all of which call at roughly the same pitch. Even the ultrasonic calls of infant bats attracted the deer mothers if Lingle used software to lower their pitch to match that of deer calls. In contrast, they found the deer did not respond to non-infant calls such as birdsong or the bark of a coyote (American Naturalist, DOI: 10.1086/677677). © Copyright Reed Business Information Ltd.
By JAMES GORMAN Are chimpanzees naturally violent to one another, or has the intrusion of humans into their environment made them aggressive? A study published Wednesday in Nature is setting off a new round of debate on the issue. The study’s authors argue that a review of all known cases of when chimpanzees or bonobos in Africa killed members of their own species shows that violence is a natural part of chimpanzee behavior and not a result of actions by humans that push chimpanzee aggression to lethal attacks. The researchers say their analysis supports the idea that warlike violence in chimpanzees is a natural behavior that evolved because it could provide more resources or territory to the killers, at little risk. But critics say the data shows no such thing, largely because the measures of human impact on chimpanzees are inadequate. While the study is about chimpanzees, it is also the latest salvo in a long argument about the nature of violence in people. In studying chimpanzee violence, “we’re trying to make inferences about human evolution,” said Michael L. Wilson, an anthropologist at the University of Minnesota and a study organizer. There is no disagreement about whether chimpanzees kill one another, or about some of the claims that Dr. Wilson and his 29 co-authors make. The argument is about why chimpanzees kill. Dr. Wilson and the other authors, who contributed data on killings from groups at their study sites, say the evidence shows no connection between human impact on the chimpanzee sites and the number of killings. He said the Ngogo group of chimpanzees in Uganda “turned out to be the most violent group of chimpanzees there is,” even though the site was little disturbed by humans. They have a pristine habitat, he said, and “they go around and kill their neighbors.” © 2014 The New York Times Company
by Rachel Ehrenberg Eating artificial sweeteners may spur the very health problems that dieters try to avoid. A new multipronged study of mice and a small number of people finds that saccharin meddles with the gut’s microbial community, setting in motion metabolic changes that are associated with obesity and diabetes. Other zero-calorie sweeteners may cause the same problems, researchers say September 17 in Nature. Though the finding is preliminary, four of seven human volunteers eating a diet high in saccharin developed impaired glucose metabolism, a warning sign for type 2 diabetes. “This is very interesting and scary if it really does hold for humans,” says Robert Margolskee of the Monell Chemical Senses Center in Philadelphia, who was not involved with the work. “There could be unintended consequences of these artificial sweeteners.” Until recently, most sugar substitutes were thought to pass through the gut undigested, exerting little to no effect on intestinal cells. As ingredients in diet soda, sugar-free desserts and a panoply of other foods, the sweeteners are touted as a way for people with diabetes and weight problems to enjoy a varied diet. But the new study, led by computational biologist Eran Segal and immunologist Eran Elinav of the Weizmann Institute of Science in Rehovot, Israel, suggests that rather than helping people, the sweeteners may promote problems. © Society for Science & the Public 2000 - 2014.
By John Horgan On this blog, in my book The End of War and elsewhere (see Further Reading and Viewing), I have knocked the deep roots theory of war, which holds that war stems from an instinct deeply embedded in the genes of our male ancestors. Inter-community killings are rare among chimpanzees and non-existent among bonobos, according to a new report in Nature, undercutting the theory that the roots of war extend back to the common ancestor of humans and chimps. Proponents of this theory—notably primatologist Richard Wrangham—claim it is supported by observations of inter-community killings by chimpanzees, Pan troglodytes, our closest genetic relatives. Skeptics, including anthropologists Robert Sussman and Brian Ferguson, have pointed out that chimpanzee violence might be not an adaptation but a response to environmental circumstances, such as human encroachment. This “human impacts” hypothesis is rejected in a new report in Nature by a coalition of 30 primatologists, including Wrangham and lead author Michael Wilson. In “Lethal aggression in Pan is better explained by adaptive strategies than human impacts,” Wilson et al. analyze 152 killings in 18 chimpanzee communities and find “little correlation with human impacts.” Given that the primary interest in chimp violence is its alleged support of the deep-roots theory, it might seem odd, at first, that Wilson et al. do not mention human warfare. Actually, this omission is wise, because the Nature report undermines the deep-roots theory of war, and establishes that the “human impact” issue is a red herring. © 2014 Scientific American,
I’m an epileptic. It’s not how I define myself, but I am writing about epilepsy, so I think pointing out the fact that I am speaking from experience is acceptable. I may not define myself by my epilepsy but it’s a big part of my life. It affects my life on a daily basis. Because of the epilepsy I can’t drive, can’t pull all-nighters or get up really early just in case I have a seizure. It’s frustrating at times, though I will gladly milk the not getting up early thing when I can, eg bin day. But whereas I’ve grown up with it, having been diagnosed when I was 17, most people I’ve met don’t understand it. You mention the fact that you’re epileptic to some people and they look at you like they’re a robot you’ve just asked to explain the concept of love; they adopt a sort of “DOES NOT COMPUTE!” expression. They often don’t know what to say, or do, or even what epilepsy is and often spend the rest of the conversation searching their data banks for information on what to do if I have a seizure, like “Do I … put a spoon in his mouth?” For the record: no, you don’t. If putting a spoon in an epileptics mouth helped, then we would be prescribed a constant supply of Fruit Corners. So let me put you at ease. No one expects you to know that much about epilepsy (unless you’re responsible for treating it). There are many different types, with many different causes. Not everyone has seizures and often those who do, when given the correct meds, can live pretty much fit-free lives. © 2014 Guardian News and Media Limited
Link ID: 20091 - Posted: 09.18.2014
By Filipa Ioannou Per the Associated Press, the Food and Drug Administration is considering a ban on electric-shock devices that are used to punish unwanted behavior by patients with autism and other developmental disabilities. If it comes as a surprise to you that any involuntary electric shocks are administered to autism patients in the United States, that's because the devices are only used at one facility in the country—the Judge Rotenberg Educational Center in Canton, Mass. The school has been a target of media attention in the past; in 2012, video leaked of 18-year-old patient Andre McCollins being restrained face-down and shocked 31 times. McCollins’ mother sued the center, and the lawsuit was settled outside of court. Rotenberg must get a court’s approval to begin administering skin shocks to a student. The center uses a graduated electronic decelerator, or GED, that is attached to the arms or legs. If the student acts aggressively – head-banging, throwing furniture, attacking someone – then a center worker can press a button to activate the electrode, delivering a two-second shock to the skin. The amount of pain generated by the device is a contentious subject. The Rotenberg Center's Glenda Crookes compared the sensation to “a bee sting” in comments to CBS News, and some Rotenberg parents are strong proponents of the device. But a U.N. official in 2010 said the shocks constituted “torture." An FDA report also addresses the widely held belief that autistic individuals have a high pain threshold, pointing out the possibility that “not all children with ASD express their pain in the same way as a ‘neurotypical child’ would (e.g., cry, moan, seek comfort, etc.), which may lead to misinterpretation by caregivers and medical professionals that patients are insensitive or to an incorrect belief that the child is not in pain.” © 2014 The Slate Group LLC.
Elie Dolgin When Carol Steinberg was diagnosed with multiple sclerosis (MS) in 1995, there was only one drug approved by the US Food and Drug Administration to treat the disease. Now there are eleven. Yet none of these agents can help Steinberg. She suffers from progressive MS, a form of the disease that is characterized by steadily worsening neurological function. All eleven approved drugs combat the unpredictable symptom outbreaks that are associated with the relapsing–remitting form of MS. Around 85% of newly diagnosed patients have the relapsing–remitting form; after 10 to 20 years, most of them develop the progressive type. The lack of good treatment options for progressive MS weighs heavily on Steinberg. She uses a wheelchair, but continues to work as a trial lawyer in Newton, Massachusetts. “I’m constantly afraid of my disease getting worse,” she says. A global initiative called the Progressive MS Alliance now hopes to kick-start the development of therapies specifically for Steinberg and the million or so people worldwide living with progressive MS. On 11 September, at a joint meeting of the European and Americas Committees for Treatment and Research in Multiple Sclerosis, the alliance announced an inaugural round of research awards — part of a six-year, €22-million (US$28.5-million) programme that is the first concerted effort to tackle the disease’s less-common form. © 2014 Nature Publishing Group
By Katy Waldman In the opening chapter of Book 1 of My Struggle, by Karl Ove Knausgaard, the 8-year-old narrator sees a ghost in the waves. He is watching a televised report of a rescue effort at sea—“the sky is overcast, the gray-green swell heavy but calm”—when suddenly, on the surface of the water, “the outline of a face emerges.” We might guess from this anecdote that Karl, our protagonist, is both creative and troubled. His limber mind discerns patterns in chaos, but the patterns are illusions. “The lunatic, the lover, and the poet,” Shakespeare wrote, “have such seething brains, such shaping fantasies.” Their imaginations give “to airy nothing a local habitation and a name.” A seething brain can be a great asset for an artist, but, like Knausgaard’s churning, gray-green swell, it can be dangerous too. Inspired metaphors, paranormal beliefs, conspiracy theories, and delusional episodes may all exist on a single spectrum, recent research suggests. The name for the concept that links them is apophenia. A German scientist named Klaus Conrad coined apophanie (from the Greek apo, away, and phaenein, to show) in 1958. He was describing the acute stage of schizophrenia, during which unrelated details seem saturated in connections and meaning. Unlike an epiphany—a true intuition of the world’s interconnectedness—an apophany is a false realization. Swiss psychologist Peter Brugger introduced the term into English when he penned a chapter in a 2001 book on hauntings and poltergeists. Apophenia, he said, was a weakness of human cognition: the “pervasive tendency … to see order in random configurations,” an “unmotivated seeing of connections,” the experience of “delusion as revelation.” On the phone he unveiled his favorite formulation yet: “the tendency to be overwhelmed by meaningful coincidences.” © 2014 The Slate Group LLC.
Link ID: 20088 - Posted: 09.18.2014
By Virginia Morell Living in a complex social world—one with shifting alliances and competitors—is often cited as the key reason humans, dolphins, and spotted hyenas evolved large brains. Now, researchers say that social complexity also underlies the braininess of parrots, which have big brains relative to their body size. To understand the social lives of these birds, the scientists observed wild populations of monk parakeets (Myiopsitta monachus), a small parrot, in Argentina and captive ones in Florida. They recorded how often the birds (pictured) were seen with other individuals and how they interacted—and then analyzed the parakeets’ social networks. The birds, the researchers report online today in The Auk: Ornithological Advances, prefer to spend time with one specific individual, usually their mate. In the captive populations, the birds also had strong associations with one or two other individuals, numerous more moderate relationships, and only a few that were weak. The scientists also recorded aggressive interactions among the captive birds, revealing that monk parakeets have a dominance hierarchy based on which birds won or lost confrontations. Thus, the parakeets’ society has layers of relationships, similar to those documented in other big-brained animals. Living in such a society requires that the birds recognize and remember others, and whether they are friend or foe—mental tasks that are thought to be linked to the evolution of significant cognitive skills. © 2014 American Association for the Advancement of Science
Link ID: 20087 - Posted: 09.18.2014
by Bethany Brookshire Most of us wish we ate better. I know I certainly do. But when hunger strikes, and you’re standing in line at the grab-and-go food joint, that salad seems really lackluster sitting next to that tasty-looking cookie. I can’t help but think that my diet — and my waistline — would look a lot better if I just craved lettuce a little more. Now a new study shows that although we may never cease to love cookies, we might be able to make that carrot a little more appealing. In overweight people, a behavioral intervention was associated with changes in how their brains responded to high- and low-calorie foods. The small pilot study is intriguing, but with just 13 participants, a larger study is needed before scientists will know if training the brain can make us abstain. “Everyone responds more strongly to high-calorie foods than low-calorie foods. It’s just normal,” says study coauthor Susan Roberts, a behavioral nutrition scientist from Tufts University in Medford, Mass. While most people prefer brownies over beets, people who are overweight or obese have a harder time avoiding high-calorie foods, she says. “When someone becomes overweight, there’s a dampening effect on a number of brain structures, including the reward system,” she says. “It’s harder to enjoy food generally, and so when someone becomes overweight, they really want to eat those high-calorie foods, because those are the foods that activate reward systems to the biggest extent.” Craving is a particular issue. Craving is distinct from hunger and focuses on a particular food, often foods that are high calorie. Other studies show that people who are obese have more cravings than those who are not. © Society for Science & the Public 2000 - 2014
|By Daniel A. Yudkin If you’re reading this at a desk, do me a favor. Grab a pen or pencil and hold the end between your teeth so it doesn’t touch your lips. As you read on, stay that way—science suggests you’ll find this article more amusing if you do. Why? Notice that holding a pencil in this manner puts your face in the shape of a smile. And research in psychology says that the things we do—smiling at a joke, giving a gift to a friend, or even running from a bear—influence how we feel. This idea—that actions affect feelings—runs counter to how we generally think about our emotions. Ask average folks how emotions work—about the causal relationship between feelings and behavior—and they’ll say we smile because we’re happy, we run because we’re afraid. But work by such psychologists as Fritz Strack, Antonio Damasio, Joe LeDoux shows the truth is often the reverse: what we feel is actually the product, not the cause, of what we do. It’s called “somatic feedback.” Only after we act do we deduce, by seeing what we just did, how we feel. This bodes well, at first blush, for anyone trying to change their emotions for the better. All you’d need to do is act like the kind of person you want to be, and that’s who you’ll become. (Call it the Bobby McFerrin philosophy: “Aren’t happy? Don’t worry. Just smile!”) But new research, published in the Journal of Experimental Social Psychology by Aparna Labroo, Anirban Mukhopadhyay, and Ping Dong suggests there may be limits to our ability to proactively manage our own well-being. The team ran a series of studies examining whether more smiling led to more happiness. One asked people how much smiling they had done that day, and how happy they currently felt. Other studies manipulated the amount of smiling people actually did, either by showing them a series of funny pictures or by replicating a version of the pencil-holding experiment. As expected, across these experiments, the researchers found that the more people smiled, the happier they reported being. © 2014 Scientific American
Link ID: 20085 - Posted: 09.17.2014
By Douglas Main Researchers have created a blood test that they have used to accurately diagnose depression in a small sample of people, and they hope that with time and funding it could be used on a widespread basis. It is the first blood test—and thus the first “objective” gauge—for any type of mental disorder in adults, says study co-author Eva Redei, a neuroscientist at Northwestern University in Evanston, Ill. Outside experts caution, however, that the results are preliminary, and not close to ready for use the doctor’s office. Meanwhile, diagnosing depression the “old-fashioned way” through an interview works quite well, and should only take 10 to 15 minutes, says Todd Essig, a clinical psychologist in New York. But many doctors are increasingly overburdened and often not reimbursed for taking the time to talk to their patients, he says. The test works by measuring blood levels of nine different types of RNA, a chemical that the body uses to process DNA. Besides accurately diagnosing depression, which affects perhaps 10 percent of American adults and is becoming more common, the technique may also be able to tell who could benefit from talk therapy and who may be vulnerable to the condition in the first place. In a study describing the test, published in the journal Translational Psychiatry, the scientists recruited 32 patients who were diagnosed with depression using a clinical interview, the standard technique. They also got 32 non-depressed patients to participate as a control group. © 2014 Newsweek LLC
Link ID: 20084 - Posted: 09.17.2014
By Megan Allison Diagnoses of Attention Hyperactivity Disorder are on the rise. The Centers for Disease Control and Prevention calculated that by 2011, 11 percent of children had been diagnosed with ADHD, and 6.1 percent of all US children were taking an ADHD medication. But could a solution be as simple as exercise? A study published this month in the Journal of Abnormal Child Psychology found that aerobic activity sessions before school helped children with ADHD with their moods and attention spans. The study involved a group of just over 200 students in kindergarten through second grade at schools in Indiana and Vermont. For 12 weeks, the students did 31 minutes of physical activity. The control group participated in classroom activities during this time. Although the results showed that all students showed improvement, authors noted that the exercise especially helped kids with ADHD. “It benefits all the kids, but I definitely see where it helps the kids with ADHD a lot,” said Jill Fritz, a fourth-grade teacher in Jacksonville, Fla. in an interview with The Wall Street Journal. “It really helps them get back on track and get focused.” In the Boston area, Dr. Sarah Sparrow Benes, Program Director of Physical and Health Education Programs at Boston University, teaches elementary and special educators how to use movement as a strategy in their classroom for learning. She finds that all students can benefit from exercise.
By Neuroskeptic Today, we are thinking – and talking – about the brain more than ever before. It is widely said that neuroscience has much to teach psychiatry, cognitive science, economics, and others. Practical applications of brain science are proposed in the fields of politics, law enforcement and education. The brain is everywhere. This “Neuro Turn” has, however, not always been accompanied by a critical attitude. We ought to be skeptical of any claims regarding the brain because it remains a mystery – we fundamentally do not understand how it works. Yet much neuro-discourse seems to make the assumption that the brain is almost a solved problem already. For example, media stories about neuroscience commonly contain simplistic misunderstandings – such as the tendency to over-interpret neural activation patterns as practical guides to human behavior. For instance, recently we have heard claims that because fMRI finds differences in the brain activity of some violent offenders, this means that their criminal tendencies are innate and unchangeable – with clear implications for rehabilitation. Neuroscientists are well aware of the faults in lay discourse about the brain – and are increasingly challenging them e.g. on social media. Unfortunately, the same misunderstandings also exist within neuroscience itself. For example, I argue, much of cognitive neuroscience is actually based on (or, only makes sense given the assumption that) the popular misunderstanding that brain activity has a psychological ‘meaning’. In fact, we just do not know what a given difference in brain activity means, in the vast majority of cases. Thus, many research studies based on finding differences in fMRI activity maps across groups or across conditions, are not really helping us to understand the brain at all – but only providing us with a canvas to project our misunderstandings onto it.
Keyword: Brain imaging
Link ID: 20082 - Posted: 09.17.2014
By Elizabeth Pennisi "What's for dinner?" The words roll off the tongue without even thinking about it—for adults, at least. But how do humans learn to speak as children? Now, a new study in mice shows how a gene, called FOXP2, implicated in a language disorder may have changed between humans and chimps to make learning to speak possible—or at least a little easier. As a uniquely human trait, language has long baffled evolutionary biologists. Not until FOXP2 was linked to a genetic disorder that caused problems in forming words could they even begin to study language’s roots in our genes. Soon after that discovery, a team at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, discovered that just two bases, the letters that make up DNA, distinguished the human and chimp versions of FOXP2. To try to determine how those changes influenced the gene's function, that group put the human version of the gene in mice. In 2009, they observed that these "humanized" mice produced more frequent and complex alarm calls, suggesting the human mutations may have been involved in the evolution of more complex speech. Another study showed that humanized mice have different activity in the part of the brain called the striatum, which is involved in learning, among other tasks. But the details of how the human FOXP2 mutations might affect real-world learning remained murky. To solve the mystery, the Max Planck researchers sent graduate student Christiane Schreiweis to work with Ann Graybiel, a neuroscientist at the Massachusetts Institute of Technology in Cambridge. She's an expert in testing mouse smarts by seeing how quickly they can learn to find rewards in mazes. © 2014 American Association for the Advancement of Science
Ewen Callaway A dozen volunteers watched Alfred Hitchcock for science while lying motionless in a magnetic-resonance scanner. Another participant, a man who has lived in a vegetative state for 16 years, showed brain activity remarkably similar to that of the healthy volunteers — suggesting that plot structure had an impact on him. The study is published in this week's Proceedings of the National Academy of Sciences1. The film, an 1961 episode of the TV show Alfred Hitchcock Presents that had been condensed down to 8 minutes, is a study in suspense. In it, a 5-year-old totes a partially loaded revolver — which she thinks is a toy — around her suburban neighbourhood, shouting “bang” each time she aims at someone and squeezes the trigger. While the study participants watched the film, researchers monitored their brain activity by functional magnetic resonance imaging (fMRI). All 12 healthy participants showed similar patterns of activity, particularly in parts of the brain that have been linked to higher cognition (frontal and parietal regions) as well as in regions involved in processing sensory information (auditory and visual cortices). One behaviourally non-responsive person, a 20-year-old woman, showed patterns of brain activity only in sensory areas. But another person, a 34-year-old man who has been in a vegetative state since he was 18, had patterns of brain activity in the executive and sensory brain areas, similarly to that of the healthy subjects. “It was actually indistinguishable from a healthy participant watching the movie,” says Adrian Owen, a neuroscientist at the University of Western Ontario in London, Canada (see: 'Neuroscience: The mind reader'). © 2014 Nature Publishing Group
Link ID: 20080 - Posted: 09.16.2014
By Linda Searing THE QUESTION Benzodiazepines such as Valium, Xanax and Ativan, widely prescribed to relieve anxiety and alleviate insomnia, are known to affect memory and cognition in the short term. Might they also have a more serious, longer-term effect on the brain? THIS STUDY analyzed data on 8,990 adults older than 66, including 1,796 with Alzheimer’s disease. In a five-to-10-year span before the start of the study, 3,767 of the participants (52 percent) had taken benzodiazepines. Overall, those who had taken the drugs were 51 percent more likely to have Alzheimer’s than were those who had never taken benzodiazepines. The longer people took the drugs, the greater their risk for Alzheimer’s. Those who took the drugs for less than 90 days had essentially the same risk as those who never took them. But risk nearly doubled for people who took them for longer than six months. Risk also was greater for longer-acting vs. shorter-acting benzodiazepines. WHO MAY BE AFFECTED? Adults, especially older people, who take benzodiazepines. The drugs have a calming effect on the body and work quickly, unlike antidepressants, which can take weeks to have an effect. The American Geriatrics Society lists benzodiazepines as inappropriate for treating older people for insomnia or agitation because of their negative effect on cognition seen in that age group and an increased likelihood of falls and accidents. However, some recent estimates note that roughly half of older adults take benzodiazepines. CAVEATS Some study participants may have been prescribed benzodiazepines to treat early symptoms of unrecognized dementia, which can include depression, anxiety and sleep disorders; the study authors noted that use of the drugs “might be an early marker of a condition associated with an increased risk of dementia and not the cause.”
By ANDREW POLLACK New York State’s attorney general filed an antitrust lawsuit on Monday seeking to stop a pharmaceutical company from forcing patients with Alzheimer’s disease to switch to a new version of a widely used drug. The lawsuit contends that the switch is designed to blunt competition from low-priced generic versions of the medication. Forest Laboratories, now owned by Actavis, announced in February that it would stop selling the existing tablet form of the drug, Namenda, in favor of new extended-release capsules called Namenda XR that can be taken once a day instead of twice. While the company said that patients preferred the newer drug, it has made little secret of its desire to switch all patients to the newer form, which has a longer patent life, before the old tablets face generic competition in July. The strategy would make it much harder for the generics to gain traction. The lawsuit, filed in Federal District Court in Manhattan, says the step is an illegal attempt by Forest to maintain its monopoly even after its patent expires. “A drug company manipulating vulnerable patients and forcing physicians to alter treatment plans unnecessarily, simply to protect corporate profits, is unethical and illegal,” the attorney general, Eric T. Schneiderman, said in a statement. A spokesman for Actavis said the company did not comment on pending litigation as a matter of policy. The company said that the once-a-day drug had “significant advantages” for patients and their caregivers. The lawsuit argues that the benefit of switching is not very great. It says the company decided to force the switch because it feared that not enough patients would switch voluntarily. © 2014 The New York Times Company
Link ID: 20078 - Posted: 09.16.2014