By Arlene Karidis Health-care professionals, educators and patient advocates debate endlessly over attention deficit disorder. Some argue about the cause of the condition, which is associated with inattentiveness and, often, hyperactivity. Many disagree on treatment and parenting techniques. A dwindling group disputes whether it actually exists. Even its name — to be formal, it’s attention-deficit/hyperactivity disorder — has been a source of debate. The label ADHD trivializes the disorder, asserts Russell Barkley, a neuropsychiatrist and professor of psychiatry and pediatrics at the Medical University of South Carolina who has published more than 300 peer-reviewed articles on the condition. “ADHD is not simply about not being able to pay attention. Describing it as such is like calling autism a ‘not looking at people’ problem,” he said, and there is much more to ADHD. Some practitioners and researchers say drugs are by far the most effective treatment. Others argue that long-term drug use addresses symptoms only and does not provide important tools to help people manage their inattentiveness. They say it’s more helpful to focus on behavioral interventions, nutrition, exercise and special accommodations at school. The American Psychiatric Association says there is no doubt that ADHD exists — and it estimates that 5 percent of U.S. children have the condition.

Keyword: ADHD
Link ID: 21008 - Posted: 06.02.2015

By Sarah C. P. Williams Bonobos, endangered great apes considered—along with chimpanzees—the closest living relative to humans, spend most of each day climbing through trees, collecting fruit and leaves. Compare that with the lives of early humans who traversed hot, barren landscapes and it begins to make sense why we’re the fattier, less muscular primate. Over the past 3 decades, two researchers analyzed the hard-to-come-by bodies of 13 bonobos that had died in captivity and compared them with already collected data on 49 human bodies donated by means of autopsy to help understand how evolution drove this change. Although some captive bonobos have become obese, the researchers found that, on average, the apes’ body mass—which is thought to resemble that of the closest common ancestor we share with them—is composed of 10% to 13% skin, whereas humans have only 6% skin. This thinner skin, the team hypothesizes, probably arose around the same time that Homo sapiens gained the ability to sweat, allowing more time spent in hot, open areas. The scientists also found that we pack on more fat than our ape relatives: Female and male humans average 36% and 20% body fat, whereas female and male bonobos average 4% and close to 0% body fat, respectively. Increased fat, the researchers hypothesize, allowed our species to survive—and reproduce—during times of low food availability. As for muscle, the team reports online today in the Proceedings of the National Academy of Sciences, bonobos come out on top, especially when it comes to upper body muscles needed for tree climbing and swinging, which became unnecessary when humans went strictly bipedal. The new findings, the researchers say, help illustrate the forces of natural selection that may have affected H. sapiens’s soft tissues even before our brains started expanding in size and tool use shaped the species. © 2015 American Association for the Advancement of Science.

Keyword: Evolution; Obesity
Link ID: 21007 - Posted: 06.02.2015

By ANDREW SOLOMON At the beginning of spring in 2013, Mary Guest, a lively, accomplished 37-year-old woman, fell in love, became pregnant and married after a short courtship. At the time, Mary taught children with behavioral problems in Portland, Ore., where she grew up. Her supervisor said that he had rarely seen a teacher with Mary’s gift for intuiting students’ needs. “Mary was a powerful person,” he wrote to her mother, Kristin. “Around Mary, one felt compassion, drive, calmness and support.” Mary had struggled with depression for much of her life. Starting in her 20s, she would sometimes say to Kristin that she just wanted to die. “She would always follow up by saying, ‘But you don’t need to worry, Mama,’ ” Kristin told me. “ ‘I don’t have a plan, and I don’t intend to do anything.’ ” In recent years, Mary and her mother went for a walk once a week, and Mary would describe the difficulties she was having. She was helped somewhat by therapy and by antidepressant and antianxiety medications, which blunted her symptoms. Mary’s friends appreciated her wacky sense of humor and her engaging wit. Colleagues said that her moods never impinged on her work; in fact, few of them knew what she was dealing with. Yet for years Mary worried that she would never be in a stable relationship and experience love or a family of her own. She said plaintively to Kristin, “I think I would be a really good mother.” So when she discovered that she was pregnant, she was delighted, and she expected the experience to be blissful. She decided to discontinue her antidepressants, having read about their potential danger for a growing fetus. Given her history of severe depression, she was monitored closely by a psychiatric nurse practitioner, who told her that she could call anytime for an immediate prescription. But Mary elected to stay off medication.

Keyword: Depression; Hormones & Behavior
Link ID: 21006 - Posted: 06.01.2015

Lauren Silverman Jiya Bavishi was born deaf. For five years, she couldn't hear and she couldn't speak at all. But when I first meet her, all she wants to do is say hello. The 6-year-old is bouncing around the room at her speech therapy session in Dallas. She's wearing a bright pink top; her tiny gold earrings flash as she waves her arms. "Hi," she says, and then uses sign language to ask who I am and talk about the ice cream her father bought for her. Jiya is taking part in a clinical trial testing a new hearing technology. At 12 months, she was given a cochlear implant. These surgically implanted devices send signals directly to the nerves used to hear. But cochlear implants don't work for everyone, and they didn't work for Jiya. A schoolboy with a cochlear implant listens to his teacher during lessons at a school for the hearing impaired in Germany. The implants have dramatically changed the way deaf children learn and transition out of schools for the deaf and into classrooms with non-disabled students. "The physician was able to get all of the electrodes into her cochlea," says Linda Daniel, a certified auditory-verbal therapist and rehabilitative audiologist with HEAR, a rehabilitation clinic in Dallas. Daniel has been working with Jiya since she was a baby. "However, you have to have a sufficient or healthy auditory nerve to connect the cochlea and the electrodes up to the brainstem." But Jiya's connection between the cochlea and the brainstem was too thin. There was no way for sounds to make that final leg of the journey and reach her brain. © 2015 NPR

Keyword: Hearing; Robotics
Link ID: 21005 - Posted: 06.01.2015

By Tori Rodriguez Heart disease and depression often go hand in hand. Long-term studies have found that people with depression have a significantly higher risk of subsequent heart disease, and vice versa. Recent research has revealed that the link begins at an early age and is probably caused by chronic inflammation. A new study in the November 2014 issue of Psychosomatic Medicine by researchers in the U.S., Australia and China examined data from an ongoing study of health among Australians. The researchers looked at the scores of 865 young adults on a questionnaire that assesses depression symptoms and other measures of mental health. They also examined measurements of the internal diameter of the blood vessels of the retina, a possible marker of early cardiovascular disease. After controlling for sex, age, smoking status and body mass index, the investigators found that participants with more symptoms of depression and anxiety had wider retinal arterioles than others, which could reflect the quality of blood vessels in their heart and brain. “We don't know if the association is causal,” explains study co-author Madeline Meier, a psychology professor at Arizona State University. “But our findings suggest that symptoms of depression and anxiety may identify youth at risk for cardiovascular disease.” Other research shows that people with depression have more inflammation throughout their body and nervous system. “One theory is that stress and inflammation could play a causal role in depression,” Meier says. Such chronic inflammation is also a risk factor for cardiovascular disease. The relationship is complex: in some people, inflammation seems to precede depression and heart disease; in others, the disorders seem to cause or exacerbate the inflammation. © 2015 Scientific American

Keyword: Depression; Stress
Link ID: 21004 - Posted: 06.01.2015

Rebecca Hersher Greg O'Brien sees things that he knows aren't there, and these visual disturbances are becoming more frequent. That's not uncommon; up to 50 percent of people who have Alzheimer's disease experience hallucinations, delusions or psychotic symptoms, recent research suggests. At first, he just saw spider-like forms floating in his peripheral vision, O'Brien says. "They move in platoons." But in the last year or so, the hallucinations have been more varied, and often more disturbing. A lion. A bird. Sprays of blood among the spiders. Over the past five months, O'Brien has turned on an audio recorder when the hallucinations start, in hopes of giving NPR listeners insight into what Alzheimer's feels like. For now, he says, "I'm able to function. But I fear the day, which I know will come, when I can't." Interview Highlights [It's] St. Patrick's Day, about 9 o'clock in the morning in my office, and they're coming again. Those hallucinations. Those things that just come into the mind when the mind plays games. And then I see the bird flying in tighter and tighter and tighter circles. And all of a sudden, the bird — beak first — it darted almost in a suicide mission, exploding into my heart. Today I'm just seeing this thing in front of me. It looks like a lion, almost looks like something you'd see in The Lion King, and there are birds above it. It's floating, and it disintegrates ... it disintegrates ... it disintegrates.

Keyword: Alzheimers; Vision
Link ID: 21003 - Posted: 06.01.2015

By ANDREW POLLACK Is sexual desire a human right? And are women entitled to a little pink pill to help them feel it? Those questions are being raised in a campaign that is pressing the Food and Drug Administration to approve a pill aimed at restoring lost libido in women. The campaign, backed by the drug’s developer and some women’s groups, accuses the F.D.A. of gender bias for approving Viagra and 25 other drugs to help men have sex, but none for women. “Women have waited long enough,” the effort, known as Even the Score, says in an online petition that has gathered more than 40,000 signatures. “In 2015, gender equality should be the standard when it comes to access to treatments for sexual dysfunction.” The drug, flibanserin, has been rejected twice by the F.D.A. on the grounds that its very modest effectiveness was outweighed by side effects like sleepiness, dizziness and nausea. The first rejection, in 2010, followed a decision by a committee of outside advisers to the agency who unanimously opposed approval. On Thursday, F.D.A. advisers will once again consider whether flibanserin should be approved. Sprout Pharmaceuticals, which now owns the drug, has submitted new data, including a study to demonstrate that the pill does not impair driving. Still, approval might hinge on whether the F.D.A. agrees to interpret the old data in a new way and whether the politics of such drugs has changed. © 2015 The New York Times Company

Keyword: Sexual Behavior
Link ID: 21002 - Posted: 06.01.2015

by Jessica Hamzelou Memories that seem to be lost forever may be lurking in the brain after all, ready to be reawakened. The finding, based on experiments in mice, could eventually give us a way to revive memories in people with Alzheimer's or amnesia. When we learn something, sets of neurons in the brain strengthen their mutual connections to lay down lasting memories. Or at least that's the theory. Susumu Tonegawa and his colleagues at the Massachusetts Institute of Technology decided to put it to the test. The team first developed a clever technique to selectively label the neurons representing what is known as a memory engram – in other words, the brain cells involved in forming a specific memory. They did this by genetically engineering mice so they had extra genes in all their neurons. As a result, when neurons fire as a memory is formed, they produce red proteins visible under a microscope, allowing the researchers to tell which cells were part of the engram. They also inserted a gene that made the neurons fire when illuminated by blue light. To mimic memory loss, some of the mice were given a drug that blocks the strengthening of connections between neurons. This made the animals forget their fear of the cage. But the telltale red proteins allowed Tonegawa's team to work out which neurons had been involved in storing the fear memory. They then attempted to reactivate just these neurons using blue light. Sure enough, after the engram had been reactivated, the mice again acted as if they were afraid of the cage. © Copyright Reed Business Information Ltd.

Keyword: Learning & Memory
Link ID: 21001 - Posted: 05.30.2015

Boer Deng The ability of the bizarre prion protein to cause an array of degenerative brain conditions may help solve a puzzle in Alzheimer's research — why the disease sometimes kills within a few years, but usually causes a slow decline that can take decades. By adopting tools used to study the prion protein, PrP, researchers have found variations in the shape of a protein involved in Alzheimer’s that may influence how much damage it causes in the brain. At the Prion 2015 meeting, held on 26–29 May in Fort Collins, Colorado, neuroscientist Lary Walker described how he has borrowed a technique from prion research to study different ‘strains’ of the amyloid-β protein, which accumulates in clumps in the brains of people with Alzheimer’s. It may be that differences between the strains account for variations in the disease’s symptoms and rate of progression. “The Alzheimer’s field has not been paying enough attention to what’s happening in the prion field,” says Walker, who is based at Emory University in Atlanta, Georgia. Similarities between rare prion diseases and common neurodegenerative diseases such as Alzheimer’s have been noted for decades: both are thought to involve proteins in the nervous system that change shape and clump together. In prion diseases, a misfolded, often foreign, protein induces cascading malformation of the native prion protein in a patient’s brain. In Alzheimer’s, proteins called tau and amyloid-β accumulate within and around nerve cells, though what triggers that process — and the role of the deposits in the disease — is unclear. © 2015 Nature Publishing Group,

Keyword: Alzheimers; Prions
Link ID: 21000 - Posted: 05.30.2015

Jon Hamilton Antidepressant drugs that work in hours instead of weeks could be on the market within three years, researchers say. "We're getting closer and closer to having really, truly next-generation treatments that are better and quicker than existing ones," says Dr. Carlos Zarate, a researcher at the National Institute of Mental Health. The new drugs are based on the anesthetic ketamine, which is also a popular club drug known as Special K. Unlike current antidepressants, which can take weeks to work, ketamine-like drugs have an immediate effect. They also have helped people with depression who didn't respond to other medications. The drug that is furthest along is esketamine, a chemical variant of ketamine that has been designated a potential breakthrough by the Food and Drug Administration. Esketamine is poised to begin Phase 3 trials, and the drug's maker, Johnson & Johnson, plans to seek FDA approval in 2018. Ketamine, used as a tranquilizer for animals and as an anesthetic in humans, is also being tested as a treatment for depression. Another ketamine-like drug on the horizon is rapastinel. It has completed Phase 2 studies, which showed "rapid, substantial, and sustained reductions in depressive symptoms," according to the drug's maker, Naurex. "I think it's highly probable that we'll see some version of one of these treatments being approved in the relatively near future," says Dr. Gerard Sanacora, director of the Yale Depression Research Program. "In my mind it is the most exciting development in mood disorder treatment in the last 50 years." © 2015 NPR

Keyword: Depression
Link ID: 20999 - Posted: 05.30.2015

A patient tormented by suicidal thoughts gives his psychiatrist a few strands of his hair. She derives stem cells from them to grow budding brain tissue harboring the secrets of his unique illness in a petri dish. She uses the information to genetically engineer a personalized treatment to correct his brain circuit functioning. Just Sci-fi? Yes, but... An evolving “disease-in-a-dish” technology, funded by the National Institutes of Health (NIH), is bringing closer the day when such a seemingly futuristic personalized medicine scenario might not seem so far-fetched. Scientists have perfected mini cultured 3-D structures that grow and function much like the outer mantle – the key working tissue, or cortex — of the brain of the person from whom they were derived. Strikingly, these “organoids” buzz with neuronal network activity. Cells talk with each other in circuits, much as they do in our brains. Sergiu Pasca, M.D. External Web Site Policy, of Stanford University, Palo Alto, CA, and colleagues, debut what they call “human cortical spheroids,” May 25, 2015 online in the journal Nature Methods. Prior to the new study, scientists had developed a way to study neurons differentiated from stem cells derived from patients’ skin cells — using a technology called induced pluripotent stem cells (iPSCs). They had even produced primitive organoids by coaxing neurons and support cells to organize themselves, mimicking the brain’s own architecture. But these lacked the complex circuitry required to even begin to mimic the workings of our brains.

Keyword: Development of the Brain
Link ID: 20998 - Posted: 05.30.2015

by Penny Sarchet The common pet budgerigar (or parakeet) is loved for its ability to mimic its owners. But it has another special trick – it can catch yawns from other budgies, suggesting it has some kind of empathy. "Practically all vertebrates yawn," says Ramiro Joly-Mascheroni of City University, London. In 2008, he showed that dogs can catch yawns from humans. The only other species shown to yawn contagiously are humans, chimpanzees and a type of rodent called the high-yawning Sprague-Dawley rat. But Andrew Gallup of the State University of New York and his colleagues have now shown for the first time that the same happens for a species of non-mammals. To see whether budgies, a sociable parrot species, can make each other yawn, his team designed two experiments. In the first, budgies were placed in adjacent cages, either with a barrier between them, or with nothing obstructing their view of each other. They found that, when budgies could see each other, they were around three times as likely to yawn within five minutes of a yawn from their neighbour. In their second experiment, budgies were shown a video – either one that showed clips of budgies yawning, or one that had no yawning at all. Every bird that watched the yawning video also yawned, while fewer than half of the birds shown the other video yawned. "Thus far, yawning has been demonstrated to be contagious in a few highly social species," said Gallup. "To date, this is the first experimental evidence of contagious yawning in a non-mammalian species." © Copyright Reed Business Information Ltd

Keyword: Sleep
Link ID: 20997 - Posted: 05.30.2015

By Roberto A. Ferdman In 2007, the Food and Drug administration approved the first ever over-the-counter diet drug. Alli, as the pill was (and still is) called, could be taken by anyone, without a prescription. And it worked, so long as those who took it also maintained a healthy lifestyle. That last bit—persuading people who take diet drugs to also eat well and exercise—is the oft overlooked key with weight-loss remedies. And GlaxoSmithKline, which manufactures the drug, knew it. Marketing around the pill made it clear that Alli was not some miracle drug. But getting people to treat diet drugs for what they are—helpers, not fix alls—is actually a lot harder than it sounds. Some diet drugs have been shown to work. But a growing pool of research suggests people are prone to use them improperly. "There's a funny, kind of counterintuitive thing that happens when many people take weight-loss drugs: they gain weight," said Amit Battacharjee, an assistant professor at The Tuck School of Business, whose research focuses on consumer beliefs and well-being. "But it isn't necessarily because the drugs themselves don't work." Battacharjee has a new study titled 'The Perils of Marketing Weight-Management Remedies,' which looks closely at how the way in which weight-loss drugs are pitched to people can significantly affect the way in which people understand them.

Keyword: Obesity
Link ID: 20996 - Posted: 05.30.2015

John Bohannon “Slim by Chocolate!” the headlines blared. A team of German researchers had found that people on a low-carb diet lost weight 10 percent faster if they ate a chocolate bar every day. It made the front page of Bild, Europe’s largest daily newspaper, just beneath their update about the Germanwings crash. From there, it ricocheted around the internet and beyond, making news in more than 20 countries and half a dozen languages. It was discussed on television news shows. It appeared in glossy print, most recently in the June issue of Shape magazine (“Why You Must Eat Chocolate Daily”, page 128). Not only does chocolate accelerate weight loss, the study found, but it leads to healthier cholesterol levels and overall increased well-being. The Bild story quotes the study’s lead author, Johannes Bohannon, Ph.D., research director of the Institute of Diet and Health: “The best part is you can buy chocolate everywhere.” I am Johannes Bohannon, Ph.D. Well, actually my name is John, and I’m a journalist. I do have a Ph.D., but it’s in the molecular biology of bacteria, not humans. The Institute of Diet and Health? That’s nothing more than a website. Other than those fibs, the study was 100 percent authentic. My colleagues and I recruited actual human subjects in Germany. We ran an actual clinical trial, with subjects randomly assigned to different diet regimes. And the statistically significant benefits of chocolate that we reported are based on the actual data. It was, in fact, a fairly typical study for the field of diet research. Which is to say: It was terrible science. The results are meaningless, and the health claims that the media blasted out to millions of people around the world are utterly unfounded.

Keyword: Obesity
Link ID: 20995 - Posted: 05.28.2015

by Jessica Hamzelou IF YOU knew you were about to go through a stressful experience, would you pop a pill to protect yourself from its knock-on effects? It's an idea that has been mooted after a drug seemed to make mice immune to the negative impacts of stressful events. But could we rationalise prescribing such a drug? We all experience stress during our lives, whether it be a one-off event, such as a loved one dying, or chronic, low-level stress that results from struggling to make ends meet, for example. While most people find ways to cope, for some a particularly stressful event can trigger depression. What if there was a way to boost our stress resilience and thus shield us from depression? Rebecca Brachman at Columbia University in New York stumbled across the idea while she was giving ketamine to mice with the symptoms of depression. Even though the ketamine-taking mice had been chronically stressed, when they were dropped in a pool of water – a one-off stressful event – they were unperturbed and swam to an exit. Mice not given the drug made no attempt to escape, a classic sign of depression in rodents. There was also no change in the ketamine-taking animals' cognitive abilities or metabolism – both of which are altered in human depression. "It's really remarkable," says Brachman. "They basically look like mice that haven't been stressed." A single dose of ketamine protected mice from developing the symptoms of depression after stressful events for four weeks. But the drug only seemed to stop the symptoms of depression – some of the animals still exhibited anxiety behaviours. "It seems to protect against depression rather than anxiety," says Brachman, who controversially describes it as a depression "vaccine". The work will be published in Biological Psychiatry. © Copyright Reed Business Information Ltd

Keyword: Stress; Drug Abuse
Link ID: 20994 - Posted: 05.28.2015

Carl Zimmer For scientists who study human evolution, the last few months have been a whirlwind. Every couple of weeks, it seems, another team pulls back the curtain on newly discovered bones or stone tools, prompting researchers to rethink what we know about early human history. On Wednesday, it happened again. Yohannes Haile-Selassie of the Cleveland Museum of Natural History and his colleagues reported finding a jaw in Ethiopia that belonged to an ancient human relative that lived some time between 3.3 and 3.5 million years. They argue that the jaw belongs to an entirely new species, which they dubbed Australopithecus deyiremeda. While some experts agree, skeptics argued that the jaw belongs to a familiar hominid species, known as Australopithecus afarensis, that existed from about 3.9 to 3 million years ago. Studies like this one are adding fresh fuel to the debate over the pace of human evolution. Some researchers now believe the human family tree bore exuberant branches early on. “I’m so excited about these discoveries, I’m driving my friends crazy,” said Carol V. Ward, a paleoanthropologist at the University of Missouri. “It makes us stop and rethink everything.” In the 1990s, the broad outlines of human evolution seemed fairly clear. Early human ancestors — known as hominids — evolved from an ancestor shared with chimpanzees about six or seven million years ago. These hominids were short, bipedal apes with small brains and arms and legs still adapted for climbing trees. Until about three million years ago, experts thought, there weren’t a lot of hominid species. In fact, some researchers argued that most hominid fossils represented just a single species. © 2015 The New York Times Company

Keyword: Evolution
Link ID: 20993 - Posted: 05.28.2015

by Helen Thomson Imagine a world where you think of something and it happens. For instance, what if the moment you realise you want a cup of tea, the kettle starts boiling? That reality is on the cards, now that a brain implant has been developed that can decode a person's intentions. It has already allowed a man paralysed from the neck down to control a robotic arm with unprecedented fluidity. But the implications go far beyond prosthetics. By placing an implant in the area of the brain responsible for intentions, scientists are investigating whether brain activity can give away future decisions – before a person is even aware of making them. Such a result may even alter our understanding of free will. Fluid movement "These are exciting times," says Pedro Lopes, who works at the human-computer interaction lab at Hasso Plattner Institute in Potsdam, Germany. "These developments give us a glimpse of an exciting future where devices will understand our intentions as a means of adapting to our plans." The implant was designed for Erik Sorto, who was left unable to move his limbs after a spinal cord injury 12 years ago. The idea was to give him the ability to move a stand-alone robotic arm by recording the activity in his posterior parietal cortex – a part of the brain used in planning movements. "We thought this would allow us to decode brain activity associated with the overall goal of a movement – for example, 'I want to pick up that cup'," Richard Andersen at the California Institute of Technology in Pasadena told delegates at the NeuroGaming Conference in San Francisco earlier this month. © Copyright Reed Business Information Ltd

Keyword: Consciousness; Robotics
Link ID: 20992 - Posted: 05.28.2015

Krishnadev Calamur Two research chimps got their day in court — though they weren't actually present in the courtroom. Steven Wise, an attorney with the Nonhuman Rights Project, told Manhattan Supreme Court Judge Barbara Jaffe that Hercules and Leo, the 8-year-old research chimps at Stony Brook University on Long Island, are "autonomous and self-determining beings" who should be granted a writ of habeas corpus, which would effectively recognize them as legal persons. The chimps, he argued, should be moved from the university to a sanctuary in Florida. But Christopher Coulston, an assistant state attorney general representing the university, called the case meritless. The Associated Press reports that he said granting chimps personhood would create, in the words of the AP, "a slippery slope regarding the rights of other animals." "The reality is these are fundamentally different species," Coulston said. "There's simply no precedent anywhere of an animal getting the same rights as a human." Jaffe, the AP adds, didn't make a ruling Wednesday but called the proceeding "extremely interesting and well argued." NPR's Hansi Lo Wang reported on the story Wednesday for our Newscast unit. He says: "Past judges have struck down this lawsuit since it was first filed in 2013. But the current judge at the Manhattan Supreme Court is ordering the university to defend why it's detaining the chimps." © 2015 NPR

Keyword: Animal Rights
Link ID: 20991 - Posted: 05.28.2015

George Yancy: You have popularized the concept of speciesism, which, I believe was first used by the animal activist Richard Ryder. Briefly, define that term and how do you see it as similar to or different from racism? Peter Singer: Speciesism is an attitude of bias against a being because of the species to which it belongs. Typically, humans show speciesism when they give less weight to the interests of nonhuman animals than they give to the similar interests of human beings. Note the requirement that the interests in question be “similar.” It’s not speciesism to say that normal humans have an interest in continuing to live that is different from the interests that nonhuman animals have. One might, for instance, argue that a being with the ability to think of itself as existing over time, and therefore to plan its life, and to work for future achievements, has a greater interest in continuing to live than a being who lacks such capacities. If we were to compare attitudes about speciesism today with past racist attitudes, we would have to say that we are back in the days in which the slave trade was still legal. On that basis, one might argue that to kill a normal human being who wants to go on living is more seriously wrong than killing a nonhuman animal. Whether this claim is or is not sound, it is not speciesist. But given that some human beings – most obviously, those with profound intellectual impairment – lack this capacity, or have it to a lower degree than some nonhuman animals, it would be speciesist to claim that it is always more seriously wrong to kill a member of the species Homo sapiens than it is to kill a nonhuman animal. © 2015 The New York Times Company

Keyword: Animal Rights
Link ID: 20990 - Posted: 05.28.2015

by Andy Coghlan A man in his mid-50s with Parkinson's disease had fetal brain cells injected into his brain last week. He is the first person in nearly 20 years to be treated this way – and could recover full control of his movements in roughly five years. "It seemed to go fine," says Roger Barker of the University of Cambridge, who is leading the international team that is reviving the procedure. The treatment was pioneered 28 years ago in Sweden, but two trials in the US reported no significant benefit within the first two years following the injections, and the procedure was abandoned in favour of deep brain stimulation treatments. What these trials overlooked is that it takes several years for fetal cells to "bed in" and connect properly to the recipient's brain. Many Swedish and North American recipients improved dramatically, around three years or more after the implants – long after the trials had finished. "In the best cases, patients who had the treatment pretty much went back to normal," says Barker. After the fetal cells were wired up properly in their brains, they started producing the brain signalling chemical dopamine – low levels of this cause the classic Parkinson's symptom of uncontrolled movements. In fact, the cells produced so much dopamine that many patients could stop taking their Parkinson's drugs. "The prospect of not having to take medications for Parkinson's is fantastic," says James Beck of the Parkinson's Disease Foundation in the US. © Copyright Reed Business Information Ltd

Keyword: Parkinsons; Stem Cells
Link ID: 20989 - Posted: 05.27.2015