Chapter 16. None
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By Virginia Morell Infanticide—the killing of offspring—is generally rare among birds. And when it happens, it’s usually because of outsiders that want the nesting site or territory. But what happens among birds, such as the greater ani (Crotophaga major, pictured), which have a more socialist approach to nesting? Two to four pairs of the Central and South American cuckoos (which are usually unrelated) build a single nest, and then work together to raise their chicks, which generally hatch at the same time. Intriguingly, the adults cannot recognize either their own eggs or chicks, so they care for all of them. To find out why—and if the simultaneous hatching protects the chicks from infanticide—a scientist analyzed data on nestling mortality gathered at 104 communal greater ani nests from 2006 to 2015. Of the 741 nestlings, 321 (43%) fledged and 420 (57%) died. Most of the deaths (78.5%) were due to predation. But another 13.8%, or 58 nestlings, died from infanticide, the scientist reports online today in Evolution. The remaining 32 (7.7%) died from starvation. At most of the nests, the chicks hatched within 1 day of each other. Those that first emerged from their eggs were the most likely to be dispatched by one of the nest founders, not an outsider. Chicks that hatched last were also unlucky; weaker than their older and larger nest-mates, they weren’t able to compete for food and starved. Those two pressures—infanticide and food competition—end up favoring the chicks in the middle and those that hatch on the same day, the researcher reports. © 2016 American Association for the Advancement of Science
By Karen Weintraub Researchers at Stanford University have coaxed brain cells involved in vision to regrow and make functional connections—helping to upend the conventional dogma that mammalian brain cells, once damaged, can never be restored. The work was carried out in visually impaired mice but suggests that human maladies including glaucoma, Alzheimer’s disease and spinal cord injuries might be more repairable than has long been believed. Frogs, fish and chickens are known to regrow brain cells, and previous research has offered clues that it might be possible in mammals. The Stanford scientists say their new study confirms this and shows that, although fewer than 5 percent of the damaged retinal ganglion cells grew back, it was still enough to make a difference in the mice’s vision. “The brain is very good at coping with deprived inputs,” says Andrew Huberman, the Stanford neurobiologist who led the work. “The study also supports the idea that we may not need to regenerate every neuron in a system to get meaningful recovery.” Other researchers praised the study, published Monday in Nature Neuroscience. “I think it’s a significant step forward toward getting to the point where we really can regenerate optic nerves,” says Don Zack, a professor of ophthalmology at Johns Hopkins University who was not involved in the research. He calls it “one more indication that it may be possible to bring that ability back in humans.” © 2016 Scientific American
By Michael Price The blind comic book star Daredevil has a highly developed sense of hearing that allows him to “see” his environment with his ears. But you don’t need to be a superhero to pull a similar stunt, according to a new study. Researchers have identified the neural architecture used by the brain to turn subtle sounds into a mind’s-eye map of your surroundings. The study appears to be “very solid work,” says Lore Thaler, a psychologist at Durham University in the United Kingdom who studies echolocation, the ability of bats and other animals to use sound to locate objects. Everyone has an instinctive sense of the world around them—even if they can’t always see it, says Santani Teng, a postdoctoral researcher at the Massachusetts Institute of Technology (MIT) in Cambridge who studies auditory perception in both blind and sighted people. “We all kind of have that intuition,” says Teng over the phone. “For instance, you can tell I’m not in a gymnasium right now. I’m in a smaller space, like an office.” That office belongs to Aude Oliva, principal research scientist for MIT’s Computational Perception & Cognition laboratory. She and Teng, along with two other colleagues, wanted to quantify how well people can use sounds to judge the size of the room around them, and whether that ability could be detected in the brain. © 2016 American Association for the Advancement of Science.
Link ID: 22427 - Posted: 07.12.2016
By Maggie Koerth-Baker When former Tennessee women’s basketball coach Pat Summitt died Tuesday morning, news outlets, including ESPN, reported the cause of her death as “early-onset dementia, Alzheimer’s type.” That’s more than just a long-winded way of saying “Alzheimer’s.” By using five words instead of one, journalists were trying to point a big, flashing neon arrow at the complex realities of dementia. Dementia is more of a symptom than a diagnosis, and it can be caused by a number of different diseases. Even Alzheimer’s, the most common type of dementia, doesn’t seem to have a single cause. Instead, what ties Summitt to millions of other Alzheimer’s patients all over the world is the physical damage it wrought in her brain. Worldwide, 47.5 million people are living with some kind of dementia. Alzheimer’s represents 60 percent to 70 percent of those cases. Imagine a map of a city — roads branching out, intersecting with other roads, creating a network that allows mail to be delivered, food to be sold and brought home, people to get to their jobs. What would happen to that town if random intersections were suddenly barricaded and impassible? That’s the dystopian chaos Alzheimer’s causes, as damaged proteins clog the neurons and inhibit the flow of information from one neuron to another. Cut off from food, as well as data, the cells die. The brain shrinks. Eventually, the person dies, too. Afterward, doctors can cut into their brain and see the barriers, which are called plaques.
Link ID: 22426 - Posted: 07.12.2016
By Edd Gent, The devastating neurodegenerative condition Alzheimer's disease is incurable, but with early detection, patients can seek treatments to slow the disease's progression, before some major symptoms appear. Now, by applying artificial intelligence algorithms to MRI brain scans, researchers have developed a way to automatically distinguish between patients with Alzheimer's and two early forms of dementia that can be precursors to the memory-robbing disease. The researchers, from the VU University Medical Center in Amsterdam, suggest the approach could eventually allow automated screening and assisted diagnosis of various forms of dementia, particularly in centers that lack experienced neuroradiologists. Additionally, the results, published online July 6 in the journal Radiology, show that the new system was able to classify the form of dementia that patients were suffering from, using previously unseen scans, with up to 90 percent accuracy. [10 Things You Didn't Know About the Brain] "The potential is the possibility of screening with these techniques so people at risk can be intercepted before the disease becomes apparent," said Alle Meije Wink, a senior investigator in the center's radiology and nuclear medicine department. "I think very few patients at the moment will trust an outcome predicted by a machine," Wink told Live Science. "What I envisage is a doctor getting a new scan, and as it is loaded, software would be able to say with a certain amount of confidence [that] this is going to be an Alzheimer's patient or [someone with] another form of dementia." © 2016 Scientific American
Link ID: 22425 - Posted: 07.12.2016
By Shayla Love In 2005, astronaut John Phillips took a break from his work on the International Space Station and looked out the window at Earth. He was about halfway through a mission that had begun in April and would end in October. When he gazed down at the planet, the Earth was blurry. He couldn’t focus on it clearly. That was strange — his vision had always been 20/20. He wondered: Was his eyesight getting worse? “I’m not sure if I reported that to the ground,” he said. “I think I didn’t. I thought it would be something that would just go away, and fix itself when I got to Earth.” It didn’t go away. During Phillips’ post-flight physical, NASA found that his vision had gone from 20/20 to 20/100 in six months. John Phillips began experiencing sight issues during his time on the International Space Station in 2005, but was reluctant to say anything while in space. (NASA) Rigorous testing followed. Phillips got MRIs, retinal scans, neurological tests and a spinal tap. The tests showed that not only had his vision changed, but his eyes had changed as well. The backs of his eyes had gotten flatter, pushing his retinas forward. He had choroidal folds, which are like stretch marks. His optic nerves were inflamed. Phillips case became the first widely recognized one of a mysterious syndrome that affects 80 percent of astronauts on long-duration missions in space. The syndrome could interfere with plans for future crewed space missions, including any trips to Mars.
Link ID: 22422 - Posted: 07.11.2016
By DENISE GRADY Could pernicious anemia, a disease caused by a vitamin B12 deficiency, have explained the many strange behaviors of Mary Todd Lincoln? She was not exactly a model first lady. Historians have had a field day describing her violent temper, wild shopping sprees (she owned 300 pairs of kid gloves), depressed moods and all-consuming fears of burglars, storms and poverty. Late in life, at her son’s urging, she was committed to a mental hospital for several months. Plenty of theories, none proven, have been floated. She was bipolar. She had syphilis or that well known cause of feminine madness, menstrual trouble. She was spoiled and narcissistic. She never recovered from a road accident in which her head hit a rock. She lost her mind grieving the deaths of three of her four sons and her husband’s assassination. The latest addition to the list of possible diagnoses comes from Dr. John G. Sotos, a cardiologist, technology executive at Intel and one of the medical consultants who helped dream up the mystery diseases that afflicted patients on the television show “House.” Dr. Sotos has long been interested in difficult diagnoses, and has written a self-published book suggesting that Abraham Lincoln had a genetic syndrome that caused cancers of the thyroid and adrenal glands. In an interview, Dr. Sotos said that while he was studying President Lincoln, he came across something that intrigued him about Mrs. Lincoln: an 1852 letter mentioning that she had a sore mouth. He knew that vitamin B deficiencies could cause a sore tongue, and he began looking into her health. © 2016 The New York Times Company
Link ID: 22418 - Posted: 07.09.2016
By SUNITA SAH A POPULAR remedy for a conflict of interest is disclosure — informing the buyer (or the patient, etc.) of the potential bias of the seller (or the doctor, etc.). Disclosure is supposed to act as a warning, alerting consumers to their adviser’s stake in the matter so they can process the advice accordingly. But as several recent studies I conducted show, there is an underappreciated problem with disclosure: It often has the opposite of its intended effect, not only increasing bias in advisers but also making advisees more likely to follow biased advice. When I worked as a physician, I witnessed how bias could arise from numerous sources: gifts or sponsorships from the pharmaceutical industry; compensation for performing particular procedures; viewing our own specialties as delivering more effective treatments than others’ specialties. Although most physicians, myself included, tend to believe that we are invulnerable to bias, thus making disclosures unnecessary, regulators insist on them, assuming that they work effectively. To some extent, they do work. Disclosing a conflict of interest — for example, a financial adviser’s commission or a physician’s referral fee for enrolling patients into clinical trials — often reduces trust in the advice. But my research has found that people are still more likely to follow this advice because the disclosure creates increased pressure to follow the adviser’s recommendation. It turns out that people don’t want to signal distrust to their adviser or insinuate that the adviser is biased, and they also feel pressure to help satisfy their adviser’s self-interest. Instead of functioning as a warning, disclosure can become a burden on advisees, increasing pressure to take advice they now trust less. © 2016 The New York Times Company
Link ID: 22416 - Posted: 07.09.2016
by Adriana Heguy, molecular biologist and genomics researcher: Interestingly, tongue-curling ability is not solely genetic, and the genetic component may be very small. Monozygotic (identical) twins are not always concordant for tongue-curling ability, so if there is a genetic component, it’s clearly not Mendelian. In other words, it’s not a trait coded by one single gene, and it’s clearly influenced by the environment—in this case, practice. But for some reason this is one of the “myths” about genetics that gets spread around in high school, where it is used as an example of a simple Mendelian trait with a simple dominant-recessive nature. It’s hard to comment on the evolutionary purpose of an ability so heavily influenced by the environment, and not obviously useful. There are many traits for which we do not have the faintest idea why they exist or what purpose they serve. In the case of tongue-curling, it’s possible that it’s a case of fine motor control of the tongue. We need to be able to move our tongues to not bite them when we eat, for example, and for swirling food around. For unknown reasons, some individuals are better than others at controlling tongue movement. And since the ability can be acquired by practicing (though not everybody apparently succeeds), it does seem likely that it is indeed a question of motor control. Most people are able to do it. It’s quite common. But it could be that evolution had nothing to do with it. Or it could be a spandrel; in other words, a side effect of evolution. Maybe the evolution of dexterity or finer motor control of other muscles resulted in tongue “dexterity.” It’s possible that it is an atavism, something that increased tongue muscle control was once useful for tasting or eating certain kinds of foods millions of years ago, and it has not disappeared because the developmental program for fine muscle control is still there.
By Andy Coghlan It could be that romantic restaurant, or your favourite park bench. A specific part of the brain seems to be responsible for learning and remembering the precise locations of places that are special to us, research in mice has shown for the first time. Place cells are neurons that help us map our surroundings, and both mice and humans have such cells in the hippocampus – a brain region vital for learning, memory and navigation. Nathan Danielson at Columbia University in New York and his colleagues focused on a part of the hippocampus that feeds signals to the rest of the brain, called CA1. They found that in mice, the CA1 layer where general environment maps are learned and stored is different to the one for locations that have an important meaning. Treadmill test They discovered this by recording brain activity in the two distinct layers of CA1, using mice placed on a treadmill. The treadmill rotated between six distinctive surface materials – including silky ribbons, green pom-pom fabric and silver glitter masking tape. At all times, the mice were able to lick a sensor to try to trigger the release of drinking water. During the first phase of the experiment, however, the sensor only worked at random times. The mice formed generalised maps of their experience on the multi-surfaced treadmill, and the team found that these were stored in the superficial layer of CA1. © Copyright Reed Business Information Ltd.
Keyword: Learning & Memory
Link ID: 22414 - Posted: 07.09.2016
The most sophisticated, widely adopted, and important tool for looking at living brain activity actually does no such thing. Called functional magnetic resonance imaging, what it really does is scan for the magnetic signatures of oxygen-rich blood. Blood indicates that the brain is doing something, but it’s not a direct measure of brain activity. Which is to say, there’s room for error. That’s why neuroscientists use special statistics to filter out noise in their fMRIs, verifying that the shaded blobs they see pulsing across their computer screens actually relate to blood flowing through the brain. If those filters don’t work, an fMRI scan is about as useful at detecting neuronal activity as your dad’s “brain sucking alien” hand trick. And a new paper suggests that might actually be the case for thousands of fMRI studies over the past 15 years. The paper, published June 29 in the Proceedings of the National Academy of Science, threw 40,000 fMRI studies done over the past 15 years into question. But many neuroscientists—including the study’s whistleblowing authors—are now saying the negative attention is overblown. Neuroscience has long struggled over just how useful fMRI data is at showing brain function. “In the early days these fMRI signals were very small, buried in a huge amount of noise,” says Elizabeth Hillman, a biomedical engineer at the Zuckerman Institute at Columbia University. A lot of this noise is literal: noise from the scanner, noise from the electrical components, noise from the person’s body as it breathes and pumps blood.
Keyword: Brain imaging
Link ID: 22413 - Posted: 07.09.2016
By Michael Price Doctors and soldiers could soon place their trust in an unusual ally: the mouse. Scientists have genetically engineered mice to be ultrasensitive to specific smells, paving the way for animals that are “tuned” to sniff out land mines or chemical signatures of diseases like Parkinson’s and Alzheimer’s. Trained rats and dogs have long been used to detect the telltale smell of TNT in land mines, and research suggests that dogs can smell the trace chemical signals of low blood sugar or certain types of cancer. Mice also have powerful sniffers: They sport about 1200 genes dedicated to odorant receptors, cellular sensors that react to a scent’s chemical signature. That’s a few hundred less than rats and about the same as dogs. (Humans have a paltry 350.) Paul Feinstein wants to upgrade the mouse’s already sensitive nose. For the last decade, the neurobiologist at Hunter College in New York City has been studying how odorant receptors form on the surface of neurons within the olfactory system. During development, each olfactory neuron specializes to express a single odorant receptor, which binds to chemicals in the air to detect a specific odor. In other words, each olfactory neuron has a singular receptor that senses a particular smell. Normally, there is an even distribution of receptors throughout the system, so each receptor can be found in about 0.1% of mouse neurons. Feinstein wondered if he could make the mouse’s nose pay more attention to particular scents by making certain odorant receptors more numerous. He and colleagues developed a string of DNA that, when injected into the nucleus of a fertilized mouse egg, appears to make olfactory neurons more likely to develop one particular odorant receptor than the others. This receptor, called M71, detects acetophenone, a chemical that smells like jasmine. When the team added four or more copies of the DNA sequence to a mouse egg, a full 1% of neurons carried it—10 times more than normal. © 2016 American Association for the Advancement of Science.
Keyword: Chemical Senses (Smell & Taste)
Link ID: 22412 - Posted: 07.08.2016
By Nicholas Bakalar A new study has identified a bacterial blueprint for chronic fatigue syndrome, offering further evidence that it is a physical disease with biological causes and not a psychological condition. Chronic fatigue syndrome is a condition that causes extreme and lasting fatigue, preventing people from taking part in even the most routine daily activities. There are no tests to confirm the diagnosis, which has prompted speculation that it is a psychological condition rather than a physical illness. In a study published in Microbiome, researchers recruited 48 people with C.F.S. and 39 healthy controls. Then they analyzed the quantity and variety of bacteria species in their stool. They also searched for markers of inflammation in their blood. The stool samples of those with C.F.S. had significantly lower diversity of species compared with the healthy people — a finding typical of inflammatory bowel disease as well. The scientists also discovered that people with C.F.S. had higher blood levels of lipopolysaccharides, inflammatory molecules that may indicate that bacteria have moved from the gut into the bloodstream, where they can produce various symptoms of disease. Using these criteria, the researchers were able to accurately identify more than 83 percent of C.F.S. cases based on the diversity of their gut bacteria and lipopolysaccharides in their blood. Finding a biomarker for C.F.S. has been an ongoing goal for researchers who hope to one day develop a diagnostic test for the condition. Still, the senior author of the study, Maureen R. Hanson, a professor of molecular biology at Cornell, said the bacteria blueprint in the new study is not yet a method of definitively diagnosing C.F.S. The importance of the finding, she said, is that it may offer new clues as to why people have these symptoms. © 2016 The New York Times Company
Link ID: 22411 - Posted: 07.08.2016
Tough love, interventions and 12-step programs are some of the most common methods of treating drug addiction, but journalist Maia Szalavitz says they're often counterproductive. "We have this idea that if we are just cruel enough and mean enough and tough enough to people with addiction, that they will suddenly wake up and stop, and that is not the case," she tells Fresh Air's Terry Gross. Szalavitz is the author of Unbroken Brain, a book that challenges traditional notions of addiction and treatment. Her work is based on research and experience; she was addicted to cocaine and heroin from the age of 17 until she was 23. Szalavitz is a proponent of "harm reduction" programs that take a nonpunitive approach to helping addicts and "treat people with addiction like human beings." In her own case, she says that getting "some kind of hope that I could change" enabled her to get the help she needed. On her criticism of 12-step programs I think that 12-step programs are fabulous self help. I think they can be absolutely wonderful as support groups. My issue with 12-step programs is that 80 percent of addiction treatment in this country consists primarily of indoctrinating people into 12-step programs, and no other medical care in the United States is like that. The data shows that cognitive behavioral therapy and motivational enhancement therapy are equally effective, and they have none of the issues around surrendering to a higher power, or prayer or confession. © 2016 npr
Keyword: Drug Abuse
Link ID: 22408 - Posted: 07.08.2016
Shefali Luthra Prescription drug prices continue to climb, putting the pinch on consumers. Some older Americans appear to be seeking an alternative to mainstream medicines that has become easier to get legally in many parts of the country. Just ask Cheech and Chong. Research published Wednesday found that states that legalized medical marijuana — which is sometimes recommended for symptoms like chronic pain, anxiety or depression — saw declines in the number of Medicare prescriptions for drugs used to treat those conditions and a dip in spending by Medicare Part D, which covers the cost on prescription medications. Because the prescriptions for drugs like opioid painkillers and antidepressants — and associated Medicare spending on those drugs — fell in states where marijuana could feasibly be used as a replacement, the researchers said it appears likely legalization led to a drop in prescriptions. That point, they said, is strengthened because prescriptions didn't drop for medicines such as blood-thinners, for which marijuana isn't an alternative. The study, which appears in Health Affairs, examined data from Medicare Part D from 2010 to 2013. It is the first study to examine whether legalization of marijuana changes doctors' clinical practice and whether it could curb public health costs. The findings add context to the debate as more lawmakers express interest in medical marijuana. This year, Ohio and Pennsylvania passed laws allowing the drug for therapeutic purposes, making it legal in 25 states, plus Washington, D.C. The approach could also come to a vote in Florida and Missouri this November. A federal agency is considering reclassifying medical marijuana under national drug policy to make it more readily available. © 2016 npr
Keyword: Drug Abuse
Link ID: 22406 - Posted: 07.07.2016
By Emily Rosenzweig Life deals most of us a consistent stream of ego blows, be they failures at work, social slights, or unrequited love. Social psychology has provided decades of insight into just how adept we are at defending ourselves against these psychic threats. We discount negative feedback, compare ourselves favorably to those who are worse off than us, attribute our failures to others, place undue value on our own strengths, and devalue opportunities denied to us–all in service of protecting and restoring our sense of self-worth. As a group, this array of motivated mental processes that support mood repair and ego defense has been called the “psychological immune system.” Particularly striking to social psychologists is our ability to remain blind to our use of these motivated strategies, even when it is apparent to others just how biased we are. However there are times when we either cannot remain blind to our own psychological immune processes, or where we may find ourselves consciously wanting to use them expressly for the purpose of restoring our ego or our mood. What then? Can we believe a conclusion we reach even when we know that we arrived at it in a biased way? For example, imagine you’ve recently gone through a breakup and want to get over your ex. You decide to make a mental list of all of their character flaws in an effort to feel better about the relationship ending. A number of prominent social psychologists have suggested you’re out of luck—knowing that you’re focusing only on your ex’s worst qualities prevents you from believing the conclusion you’ve come to that you’re better off without him or her. In essence, they argue that we must remain blind to our own biased mental processes in order to reap their ego-restoring benefits. And in many ways this closely echoes the position that philosophers like Mele have taken about the possibility of agentic self-deception. © 2016 Scientific American
By Patrick Monahan Animals like cuttlefish and octopuses can rapidly change color to blend into the background and dazzle prospective mates. But there’s only one problem: As far as we know, they can’t see in color. Unlike our eyes, the eyes of cephalopods—cuttlefish, octopuses, and their relatives—contain just one kind of color-sensitive protein, apparently restricting them to a black and white view of the world. But a new study shows how they might make do. By rapidly focusing their eyes at different depths, cephalopods could be taking advantage of a lensing property called “chromatic blur.” Each color of light has a different wavelength—and because lenses bend some wavelengths more than others, one color of light shining through a lens can be in focus while another is still blurry. So with the right kind of eye, a quick sweep of focus would let the viewer figure out the actual color of an object based on when it blurs. The off-center pupils of many cephalopods—including the w-shaped pupils of cuttlefish (above)—make this blurring effect more extreme, according to a study published this week in the Proceedings of the National Academy of Sciences. In that study, scientists built a computer model of an octopus eye and showed that—for an object at least one body length away—it could determine the object’s color just by changing focus. Because this is all still theoretical, the next step is testing whether live cephalopods actually see color this way—and whether any other “colorblind” animals might, too. © 2016 American Association for the Advancement of Science.
It's no secret that passwords aren't impenetrable. Even outside of major incidents like the celebrity nude photo hack, or when millions of passwords get released online, like what happened to Twitter recently, many of us may still be at risk of having our data compromised due to password-related security flaws. According to a June 2015 survey from mobile identity company TeleSign, two in five people were notified in the preceding year that their personal information was compromised or that they had been hacked or had their password stolen. But a new technology developed by the BioSense lab at the University of California, Berkeley could make all of that a thing of the past. Over the course of three years, the lab's co-director, John Chuang, and his graduate students have been working on a technology called passthoughts, which would use a person's brainwaves to identify them, according to CNET. The team has found that a passthought — something like a song that someone could sing in their mind — isn't easily forgotten and can achieve a 99-per-cent authentication accuracy rate. The device used to capture passthoughts resembles a telephone headset. It relies on EEG technology, detecting electrical activity in your brain via electrodes strapped to your head. And although Chuang's team say the technology has improved greatly in recent years, the awkwardness of the device might hinder it from being widely adopted. ©2016 CBC/Radio-Canada.
Keyword: Brain imaging
Link ID: 22401 - Posted: 07.06.2016
By Damian Garde, A boy in Pakistan became a local legend as a street performer in recent years by traversing hot coals and lancing his arms with knives without so much as a wince. A thousand miles away, in China, lived a family wracked by excruciating bouts of inexplicable pain, passed down generation after generation. Scientists eventually determined what the boy and the family had in common: mutations in a gene that functions like an on-off switch for agony. Now, a bevy of biotech companies, including Genentech and Biogen, are staking big money on the idea that they can develop drugs that toggle that switch to relieve pain without the risk of addiction. The gene in question is SCN9A, which is responsible for producing a pain-related protein called Nav1.7. In patients who feel nothing, SCN9A is pretty much broken. In those who feel searing random pain, the gene is cranking out far too much Nav1.7. That discovery raises an obvious question: Can blocking Nav1.7 provide relief for many types of pain—and someday, perhaps, replace dangerous opioid therapies? “That’s the dream,” said David Hackos, a senior scientist at Genentech, which has two Nav1.7 treatments in the first stage of clinical development. It’s too early make any sweeping predictions—and, indeed, a Pfizer pill targeting Nav1.7 has already stumbled—but the pharma industry clearly sees the potential for a blockbuster. © 2016 Scientific American
Keyword: Pain & Touch
Link ID: 22400 - Posted: 07.06.2016
Anthony Devlin/ Antidepressant use is at an all-time in high in England, where prescriptions filled for these drugs has doubled over the last decade. Figures from the Health and Social Care Information Centre show that in 2015, 61 million prescriptions were filled for antidepressant drugs, including citalopram and fluoxetine. This is up from 57.1 million in 2014, and 29.4 million back in 2005. “The reasons for this increase in antidepressant prescriptions could include a greater awareness of mental illness and more willingness to seek help,” says Gillian Connor of the charity Rethink Mental Illness. “However, with our overstretched and underfunded mental health services, too often antidepressants are the only treatment available.” UK guidelines suggest that people should be offered antidepressants as a first treatment option for moderate depression, but some critics argue that it would be better to steer people to talking therapies. In May, Andrew Green, a GP in East Riding and chairman of the British Medical Association’s Clinical and Prescribing Subcommittee, told a meeting of the UK’s All-Party Parliamentary Group for Prescribed Drug Dependence that one of the reasons doctors resort to prescribing antidepressants is because the waiting lists for talking therapies are so long. © Copyright Reed Business Information Ltd.
Link ID: 22399 - Posted: 07.06.2016