Chapter 16. None

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By Drake Baer Philosophers have been arguing about the nature of will for at least 2,000 years. It’s at the core of blockbuster social-psychology findings, from delayed gratification to ego depletion to grit. But it’s only recently, thanks to the tools of brain imaging, that the act of willing is starting to be captured at a mechanistic level. A primary example is “cognitive control,” or how the brain selects goal-serving behavior from competing processes like so many unruly third-graders with their hands in the air. It’s the rare neuroscience finding that’s immediately applicable to everyday life: By knowing the way the brain is disposed to behaving or misbehaving in accordance to your goals, it’s easier to get the results you’re looking for, whether it’s avoiding the temptation of chocolate cookies or the pull of darkly ruminative thoughts. Jonathan Cohen, who runs a neuroscience lab dedicated to cognitive control at Princeton, says that it underlies just about every other flavor of cognition that’s thought to “make us human,” whether it’s language, problem solving, planning, or reasoning. “If I ask you not to scratch the mosquito bite that you have, you could comply with my request, and that’s remarkable,” he says. Every other species — ape, dog, cat, lizard — will automatically indulge in the scratching of the itch. (Why else would a pup need a post-surgery cone?) It’s plausible that a rat or monkey could be taught not to scratch an itch, he says, but that would probably take thousands of trials. But any psychologically and physically able human has the capacity to do so. “It’s a hardwired reflex that is almost certainly coded genetically,” he says. “But with three words — don’t scratch it — you can override those millions of years of evolution. That’s cognitive control.” © 2017, New York Media LLC.

Keyword: Consciousness
Link ID: 23067 - Posted: 01.07.2017

By Joshua A. Krisch At the core of Alzheimer’s disease are amyloid-beta (Aβ) peptides, which self-assemble into protein fibrils that form telltale plaques in the brain. Now, the results of a study published today (January 4) in Nature suggest that certain fibril formations are more likely to appear in cases of rapidly progressive Alzheimer’s disease, as opposed to less-severe subtypes. The findings increase scientists’ understanding of the structure of these fibrils, and may eventually contribute to new tests and treatments for Alzheimer’s disease. “It is generally believed that some form of the aggregated Aβ peptide leads to Alzheimer’s disease, and it’s conceivable that different fibril structures could lead to neurodegeneration with different degrees of aggressiveness,” said coauthor Robert Tycko, a principal investigator at the National Institute of Diabetes and Digestive Kidney Disease. “But the mechanism by which this happens is uncertain. Some structures may be more inert and benign. Others may be more inherently toxic or prone to spread throughout the brain tissue.” Prior research has demonstrated that Aβ fibrils with various molecular structures exhibit different levels of toxicity in neuronal cell cultures, a finding confirmed in subsequent mouse trials. One study even demonstrated that Aβ fibrils cultured from patients with rapidly progressive Alzheimer’s disease are different in size and resistance to chemical denaturation than those isolated from patients with more slowly progressing disease. Building on these observations, Tycko and colleagues set out to better characterize the structures of these fibrils and get a better handle on the potential correlations between structure and disease subtype. © 1986-2017 The Scientist

Keyword: Alzheimers
Link ID: 23066 - Posted: 01.07.2017

By Gary Stix The last six months have witnessed the failure of two drugs in late-stage clinical trials for which the research community had high hopes. In truth, these new reports should not have come as too much of a surprise. Drug after drug continues to show little or no effect in helping the more than 5 million patients in the U.S. diagnosed with Alzheimer’s. Scientists who study neurodegenerative diseases have started to call for new approaches that go beyond targeting the amyloid in plaques and the tau in tangles, proteins that have been thought to be culprits in killing brain cells. One organization—The Alzheimer’s Drug Discovery Foundation (ADDF)—has for years provided funding to move untried ideas into clinical trials. Howard Fillit, the organization’s executive director, recently gave Scientific American his surprisingly optimistic view of where research and drug development for Alzheimer’s is headed. There have been recent failures of late-stage clinical trials and a figure often cited is that more than 99 percent of Alzheimer's drugs fail. Given all that, what level of confidence do you have for the field moving forward? There's a lot of reason for hope. There are over 130 different clinical trials going on now. I remember the days when there were none. We have had many failures. But I think one of the big advances that is creating hope is that we know how to do clinical trials better now. In a study that is being conducted by Biogen, everyone who was recruited into that study actually had Alzheimer's disease, for the first time. © 2017 Scientific American

Keyword: Alzheimers
Link ID: 23062 - Posted: 01.06.2017

By Virginia Smart, CBC News A controversial Canadian program that gives a regulated, hourly dose of wine to alcoholics to help manage their addiction and keep them safe has caught the attention of health care researchers in Australia. The managed alcohol programs (MAPs) that have sparked the international interest have been giving new hope and new lives to many alcoholics struggling with homelessness and troubles with addiction in communities from British Columbia to Ontario. Kate Dolan, a professor at the National Drug and Alcohol Research Centre at the University of New South Wales in Australia, has visited programs in Ottawa and Vancouver and was impressed. "We used to lead the world in harm reduction services," Dolan tells the fifth estate, but "the alcohol field has not progressed as much as the illicit drug use field." Research led Dolan to Ottawa's MAP. She found MAPs to be cost-effective through reductions in spending on health care and emergency services. Participants also significantly reduce their alcohol consumption and learn a sense of community. The Pour Lucia Ali monitors 'The Pour,' the hourly distribution of a prescribed dose of alcohol dictated by the in-house nurse at the Oaks, a residence for stabilized alcoholics in Ottawa. (CBC) When participants arrive at a MAP, Dolan wrote in her study, "it is all about me, myself and I." But as they progress, they lose the "chip on their shoulder and open up." ©2016 CBC/Radio-Canada.

Keyword: Drug Abuse
Link ID: 23061 - Posted: 01.06.2017

By Alice Klein A tumour containing a miniature brain has been found growing on the ovary of a 16-year-old girl in Japan. The 10-centimetre-wide tumour was discovered when the girl had surgery to remove her appendix. When doctors cut the tumour out, they found clumps of greasy, matted hair inside, and a 3-centimetre-wide brain-like structure covered by a thin plate of skull bone. Closer analysis revealed that it was a smaller version of a cerebellum – which usually sits underneath the brain’s two hemispheres. A mass on one side resembled a brain stem – the structure that normally joins to the spinal cord. About one-fifth of ovarian tumours contain foreign tissue, including hair, teeth, cartilage, fat and muscle. These tumours, which are normally benign, are named teratomas after the Greek word “teras”, meaning monster. Although the cause of ovarian teratomas is unknown, one theory is that they arise when immature egg cells turn rogue, producing different body parts. Brain cells are often found in ovarian teratomas, but it is extremely unusual for them to organise themselves into proper brain-like structures, says Masayuki Shintaku at the Shiga Medical Centre for Adults in Japan, who studied the tumour. Angelique Riepsamen at the University of New South Wales in Australia, agrees. “Neural elements similar to that of the central nervous system are frequently reported in ovarian teratomas, but structures resembling the adult brain are rare.” © Copyright Reed Business Information Ltd.

Keyword: Development of the Brain
Link ID: 23059 - Posted: 01.06.2017

Joanne Silberner For a revolutionary, Deepali Vishwakarma of Bhopal, India, is more quiet and reflective than you might expect. She's in her 30s, small, with a round face that holds intense brown eyes and a shy grin. Vishwakarma is a lay counselor — a well-trained community member who goes out daily to fight what novelist William Styron once called a "howling tempest in the brain." She's part of an effort by the Indian nonprofit group Sangath to provide mental health treatment to poor people in India and to show that people with much less training than a psychiatrist or psychologist can deliver effective care. Vishwakarma had 40 hours of training for her role as a counselor. So her counseling is definitely revolutionary. And some mental health observers wonder if it might work in the U.S. But it's a controversial approach. Critics say the use of lay counselors means that patients receive substandard care. Tell that to Vishwakarma. In a typical week, she may meet with 25 people, and in her several years as a counselor, patients who've stuck with her, as most have, have done well. The patients have been diagnosed with serious depression (or stress or tension, as it's more often called in India), or alcoholism, and every so often, someone with schizophrenia. She's been trained to listen and to assign specific tasks to her patients. She might tell someone who's feeling really low to go for a daily walk, or go out and play soccer, or work in the garden or listen to the radio. For depression, it means thinking about anything other than that paralyzing howling tempest. For schizophrenia, it means helping people, many of whom are on medication, adjust to living in society. © 2017 npr

Keyword: Depression
Link ID: 23056 - Posted: 01.05.2017

Erin Ross What lengths would you go to stifle the thunderous snorts and buzz-saw growls of a spouse or roommate, just so you can get a good night's sleep? Dozens of anti-snoring devices crowd the market, ranging from slightly absurd to moderately torturous. "Some of them are more medieval than others," says Dr. Kim Hutchison, associate professor of sleep medicine in the department of neurology at Oregon Health and Science University in Portland, Ore. And some of the devices, she says, even have some basis in fact. "When you sleep, the back of your throat relaxes. That narrows your airway and, as you're breathing in, it causes it to vibrate," explains Hutchison. So, many anti-snoring products are aimed at opening up that airway, or the tunnels that lead to it. For example, you can buy hollow nose plugs that, instead of closing the nostrils, prop them open. "If you have a deviated septum or something like that, those could help open up your nose and decrease snoring," says Hutchison, but they won't help everyone because "most snoring appears in the back of your throat." Other devices are designed to force sleepers to turn on their sides. "Sleeping on your back makes your tongue block your airway a little, sort of like the skinny part of a balloon, when you let air out of it," Hutchison says. So some devices combine straps and pillows that make sleeping on your back uncomfortable — or poke you if you roll over. © 2017 npr

Keyword: Sleep
Link ID: 23053 - Posted: 01.04.2017

By Michael Price We’ve all heard the stories about humans losing their jobs to robots. But what about man’s best friend? A new study suggests that drug-sniffing dogs may soon have a competitor in the workplace: an insect-piloted robotic vehicle that could help scientists build better odor-tracking robots to find disaster victims, detect illicit drugs or explosives, and sense leaks of hazardous materials. The robotic car’s driver is a silkworm moth (Bombyx mori) tethered in a tiny cockpit so that its legs can move freely over an air-supported ball, a bit like an upside-down computer mouse trackball. Using optical sensors, the car follows the ball’s movement and moves in the same direction. With its odor-sensitive antennae, the moth senses a target smell—in this case, female silkworm sex pheromones—and walks toward it along the trackball, driving the robotic car. Across seven trials with seven different drivers, the insects piloted the vehicle consistently toward the pheromones, nearly as well as 10 other silkworm moths who could walk freely on the ground toward the smells, the researchers reported last month in the Journal of Visualized Experiments. On average, the driving moths reached their target about 2 seconds behind the walking moths, although their paths were more circuitous. The researchers say their findings could help roboticists better integrate biologically inspired odor detection systems into their robots. Engineers might even be able to develop more powerful and maneuverable versions of the study’s robot car that could be driven by silkworms genetically modified to detect a wide variety of smells to help with sniffing tasks traditionally done by trained animals. Time to start polishing up those résumés, pooches. © 2016 American Association for the Advancement of Science

Keyword: Chemical Senses (Smell & Taste)
Link ID: 23051 - Posted: 01.04.2017

By Joshua A. Krisch Experiments in mice find that obesity reinforces a sedentary lifestyle. According to a December 29 study in Cell, obese mice were less active due to changes in their dopamine receptors—specifically, a drop in activity in DR2 receptors in the brain’s striatum, which plays a role in motor control. “There’s a common belief that obese animals don’t move as much because carrying extra body weight is physically disabling,” coauthor Alexxai Kravitz of the National Institute of Diabetes and Digestive and Kidney Diseases said in a press release. “But our findings suggest that assumption doesn't explain the whole story.” Kravitz and colleagues fed mice either a standard diet or a high-fat diet for 18 weeks, and then examined their dopamine signaling pathways. They found that the least active mice had less-active DR2 dopamine receptors in the striatum. Then they genetically engineered mice to have the same DR2 deficiency, and found that even those that remained lean engaged in less physical activity than other mice. Together, the findings suggest that the DR2 deficiency may account for a lack of movement in obese mice. “Other studies have connected dopamine signaling defects to obesity, but most of them have looked at reward processing—how animals feel when they eat different foods,” Kravitz said in the press release. “We looked at something simpler: dopamine is critical for movement, and obesity is associated with a lack of movement. Can problems with dopamine signaling alone explain the inactivity?” © 1986-2017 The Scientist

Keyword: Obesity; Genes & Behavior
Link ID: 23050 - Posted: 01.03.2017

Linda Bauld January is a time for New Year’s resolutions and if you’re one of the world’s one billion smokers, your resolution may be to stop smoking. For some people, this year’s quit attempt might involve an electronic cigarette, and a recent study in England, published in the BMJ, suggested that these devices helped at least 18,000 smokers to stop in 2015 who would not otherwise have done so. That’s very good news, but will there be as many quit attempts in 2017 as there have been in the past with e-cigarettes? I’m not so sure. Since I last wrote about e-cigarettes in this column one year ago, headlines about the dangers of these devices have continued to appear and show no sign of abating. The result is clear. More people believe today, compared with a year ago, that e-cigarettes are as harmful as smoking. In fact these incorrect perceptions have risen year on year, from fewer than one in ten adults in Great Britain in 2013 to one in four this past summer. Surveys of smokers show similar patterns, with an increasing proportion believing that e-cigarettes are more or equally harmful than tobacco. Yet we know that these harm perceptions are wrong. There is now very strong evidence, from a range of studies, that vaping - inhaling nicotine without the combustion involved in smoking - is far less risky than smoking cigarettes. Just a few months ago this body of evidence was brought together by the Royal College of Physicians who published an authoritative report analysing dozens of studies and concluded that the hazard to health arising from long term vapour inhalation from e-cigarettes is unlikely to exceed 5% of the harm from smoking tobacco. The RCP, and since then other UK doctor’s organisations such as the Royal College of General Practitioners, have made clear that it is important to promote the use of e-cigarettes, along with other non-tobacco nicotine products (like Nicotine Replacement Therapy such as gum or inhalators) to smokers who are trying to quit. The work of these organisations is underpinned by a consensus statement endorsed by many of the main health charities and public health bodies in the UK. They agree that vaping is safer than smoking, and while these products are not risk free and should not be promoted to children or never smokers, they have a legitimate and positive role to play in tobacco control. © 2017 Guardian News and Media Limited

Keyword: Drug Abuse
Link ID: 23046 - Posted: 01.02.2017

Michael Byrne Hunger is complicated. It's not merely a single drive, though this is mostly how may experience it consciously: a single dimension of hunger magnitude. We are more or less hungry, sometimes not at all. But there's something else lurking in the brain: anti-hunger. We can be hungry and not hungry simultaneously, in a sense. In more concrete terms, we can imagine that there is in the brain a certain subset of "hunger neurons." When we feel hungry—as during periods of fasting—it means that these neurons are active. Otherwise, the hunger neurons are silent. Hunger neurons are quite real: neuroscientists have demonstrated their function by stimulating hunger neurons artificially, causing mice to eat at weird times and gain weight. But something interesting happens as we start cranking hunger neurons (agouti-related protein, or AgRP, neurons) up. There's a limit. Mice won't just eat themselves to death. This indicates that there's something else to hunger, a moderating factor. This factor is described for the first time this week in Nature Neuroscience by researchers at Harvard Medical School: a new population of neurons that intermingle with AgRP neurons and basically have the opposite effect. Anti-hunger. Anti-hunger is in itself not a brand new idea. For a long time, neuroscientists looked to pro-opiomelanocortin (POMC) neurons, which are likewise intermingled with the AgRP hunger neurons, for filling this role. This is reasonable: genetic mutations and manipulations to the POMC neurons have been observed to lead to obesity in mice. © 2017 Vice Media LLC

Keyword: Obesity
Link ID: 23044 - Posted: 01.02.2017

By JANE E. BRODY The adornments in the office of Eric L. Adams, the Brooklyn borough president, are hardly typical: a full-size refrigerator stocked with fresh fruits and vegetables; a work station where he prepares and blends these plant-based ingredients for his meals and snacks; and a convection oven and hot plate where he cooks them. In an adjacent anteroom, there’s a stationary bike, 15-pound weights, a multipurpose fitness tower and a TRX suspension trainer hanging on the door. His laptop is mounted on a music stand so he can use it while working out on a mini-stepper. Eight months ago, Mr. Adams learned during a health checkup for abdominal pain that he had Type 2 diabetes. He said his average blood sugar level was so high that the doctor was surprised he had not already lapsed into a coma. His hemoglobin A1C level — a lab test that shows the average level of blood glucose over the previous three months — was 17 percent, about three times normal. He wasted no time in tackling his disease with fervor. Spurning the American tendency to treat every ailment with medication, he instead explored the body’s ability to heal itself. Mr. Adams, a 56-year-old former police captain, now needs a new publicity photo. He no longer resembles the roly-poly image on official posters. By adopting a vegan diet, preparing his own meals and working exercise into his everyday routines, he’s shed 30 pounds and completely reversed his diabetes, a pancreatic disorder that can lead to heart attacks, stroke, nerve damage, kidney disease, visual loss and cognitive impairment. Within three months, his A1C level was down to a normal 5.7. He now strives to inform his millions of constituents about how to counter this health- and life-robbing disease, which has reached epidemic proportions in this country, even among children. Starting on the home front, he stripped the Brooklyn Borough Hall drink machine of sugary beverages and the snack machine of everything cooked in oil or unnaturally sweetened. Those searching for a pick-me-up can indulge in plain or sparkling water, diet soda, nuts, dried fruit, protein bars and whole-grain baked chips. © 2017 The New York Times Company

Keyword: Obesity
Link ID: 23043 - Posted: 01.02.2017

By KATIE THOMAS The Food and Drug Administration has approved the first drug to treat patients with spinal muscular atrophy, a savage disease that, in its most severe form, kills infants before they turn 2. “This is a miracle — seriously,” Dr. Mary K. Schroth, a lung specialist in Madison, Wis., who treats children who have the disease, said of the approval, which was made last week. “This is a life-changing event, and this will change the course of this disease.” Dr. Schroth has previously worked as a paid consultant to Biogen, which is selling the drug. The drug, called Spinraza, will not come cheap — and, by some estimates, will be among the most expensive drugs in the world. Biogen, which is licensing Spinraza from Ionis Pharmaceuticals, said this week that one dose will have a list price of $125,000. That means the drug will cost $625,000 to $750,000 to cover the five or six doses needed in the first year, and about $375,000 annually after that, to cover the necessary three doses a year. Patients will presumably take Spinraza for the rest of their lives. The pricing could put the drug in the cross hairs of lawmakers and other critics of high drug prices, and perhaps discourage insurers from covering it. High drug prices have attracted intense scrutiny in the last year, and President-elect Donald J. Trump has singled them out as an important issue. “We believe the Spinraza pricing decision is likely to invite a storm of criticism, up to and including presidential tweets,” Geoffrey C. Porges, an analyst for Leerink Partners, said in a note to investors on Thursday. Mr. Porges said the price could lead some insurers to balk or to limit the drug to patients who are the most severely affected, such as infants, even though the F.D.A. has approved Spinraza for all patients with the condition. © 2016 The New York Times Company

Keyword: Movement Disorders; Genes & Behavior
Link ID: 23040 - Posted: 12.31.2016

By BENEDICT CAREY She was all there, all the time: exuberant in describing her mania, savage and tender when recalling her despair. And for decades, she gracefully wore the legacy of her legendary role as Princess Leia, worshiped by a generation of teenage girls as the lone female warrior amid the galactic male cast of the “Star Wars” trilogy. In her long, openhearted life, the actress and author Carrie Fisher brought the subject of bipolar disorder into the popular culture with such humor and hard-boiled detail that her death on Tuesday triggered a wave of affection on social media and elsewhere, from both fans and fellow bipolar travelers, whose emotional language she knew and enriched. She channeled the spirit of people like Patty Duke, who wrote about her own bipolar illness, and Kitty Dukakis, who wrote about depression and alcoholism, and turned it into performance art. Ms. Fisher’s career coincided with the growing interest in bipolar disorder itself, a mood disorder characterized by alternating highs and lows, paralyzing depressions punctuated by flights of exuberant energy. Her success fed a longstanding debate on the relationship between mental turmoil and creativity. And her writing and speaking helped usher in a confessional era in which mental disorders have entered the pop culture with a life of their own: Bipolar is now a prominent trait of another famous Carrie, Claire Danes’s character Carrie Mathison in the Showtime television series “Homeland.” “She was so important to the public because she was telling the truth about bipolar disorder, not putting on airs or pontificating, just sharing who she is in an honest-to-the-bone way,” said Judith Schlesinger, a psychologist and author of “The Insanity Hoax: Exposing the Myth of the Mad Genius.” © 2016 The New York Times Company

Keyword: Schizophrenia
Link ID: 23035 - Posted: 12.29.2016

Morwenna Ferrier Is my face attractive? Don’t answer that. Not because I’m ducking out of this, but because you can’t. Attractiveness is subjective, perhaps the most subjective question of all; that we outsource the answer to Google (and we do, in our droves) is ironic since it depends on a bias that is impossible to unpack. Yet in searching the internet for an answer, it also reveals the question to be one of the great existential tensions of our time. Because, as we all know, being attractive is absolutely 100% the A-road to happiness. If you are Googling to rate your attractiveness, then you are probably working on the assumption that you aren’t. You’re also, possibly, more vulnerable and susceptible to being told that you aren’t. In short, you’re a sitting duck, someone who had a sore throat and who asked good old Dr Google for advice only to be told it was cancer. Still, it’s only in investigating precisely why Google is the last person you should ask – being a search engine therefore insentient – that you can start cobbling together an idea of what attractiveness really is. It’s worth starting with semantics. Beauty is not attractiveness and vice versa, though we commonly confuse the two. Beauty (arguably) has a template against which we intuit and against which we measure ourselves. It is hinged around genetics and a particular look associated with this politically correct (and largely western-governed) model. Darwin wouldn’t agree: “It is certainly not true that there is in the mind of man any universal standards of beauty with respect to the human body,” he said. But a lot has changed since his time. © 2016 Guardian News and Media Limited

Keyword: Sexual Behavior
Link ID: 23030 - Posted: 12.28.2016

By Ben Andrew Henry Traveling from the forests and fields of Europe to the grasslands south of the Sahara desert is a monumental trip for anyone, and especially for a diminutive insect. Yet every year, populations of the painted lady (Vanessa cardui) butterfly make that journey over the course of several generations. The logistics of this migratory feat had been speculated for some time, but never fully understood, in part because of the difficulty of tracking the tiny insects across long distances. In a study published October 4 in Biology Letters, researchers reported having measured the isotopic composition of butterfly wings in Europe and south of the Sahara. Since the fraction of heavy hydrogen isotopes in the environment varies geographically, the team used its analysis to identify the origins of butterflies captured, confirming that groups of butterflies in the Sahara did originate in Europe. The butterflies do not linger in Africa long. They most likely make their trip, the authors suggested, to take advantage of the burst of productivity in the tropical savannah that follows the rainy season—and to breed the generation that will start the trip back. Europe’s freshwater eels (Anguilla anguilla) live out their days in rivers and streams, but they never spawn there. Massive catches of larval eels in the Sargasso Sea tipped researchers off a century ago that eels must spawn in the swirling mid-Atlantic gyre of free-floating seaweed and then migrate to Europe. Eels leave their homes in the late fall, but other than that, the details of their journey have been a mystery. © 1986-2016 The Scientist

Keyword: Animal Migration
Link ID: 23029 - Posted: 12.28.2016

By GINA KOLATA It was Oct. 11, 2015, and a middle-aged man and a young woman, both severely obese, were struggling with the same lump-in-the-throat feeling. The next day they were going to have an irreversible operation. Were they on the threshold of a new beginning or a terrible mistake? They were strangers, scheduled for back-to-back bariatric surgery at the University of Michigan with the same doctor. He would cut away most of their stomachs and reroute their small intestines. They were almost certain to lose much of their excess weight. But despite the drastic surgery, their doctor told them it was unlikely that they would ever be thin. Nearly 200,000 Americans have bariatric surgery each year. Yet far more — an estimated 24 million — are heavy enough to qualify for the operation, and many of them are struggling with whether to have such a radical treatment, the only one that leads to profound and lasting weight loss for virtually everyone who has it. Most people believe that the operation simply forces people to eat less by making their stomachs smaller, but scientists have discovered that it actually causes profound changes in patients’ physiology, altering the activity of thousands of genes in the human body as well as the complex hormonal signaling from the gut to the brain. It often leads to astonishing changes in the way things taste, making cravings for a rich slice of chocolate cake or a bag of White Castle hamburgers simply vanish. Those who have the surgery naturally settle at a lower weight. © 2016 The New York Times Company

Keyword: Obesity
Link ID: 23027 - Posted: 12.27.2016

By GINA KOLATA Bariatric surgery is an option that obesity medicine specialists say is too often ignored or dismissed. Yet it is the only option that almost always works to help very heavy people lose a lot of weight and that also can mysteriously make some chronic conditions vanish. Here are some answers about bariatric surgery and what it does. HOW MANY AMERICANS ARE ELIGIBLE FOR BARIATRIC SURGERY? Twenty-four million, according to the American Society for Metabolic and Bariatric Surgery. The criteria are a body mass index above 40, or a B.M.I. of at least 35 along with other medical conditions like diabetes, hypertension, sleep apnea or acid reflux. HOW MANY HAVE THE SURGERY EACH YEAR? Fewer than 200,000. WHAT ARE THE OPERATIONS? There are four in use today. The two most popular procedures are the Roux-en-Y gastric bypass and the gastric sleeve. Both make the stomach smaller. The bypass also reroutes the small intestine. A simpler procedure, the gastric band, is less effective and has fallen out of favor. And a much more drastic operation, the biliopancreatic diversion with duodenal switch, which bypasses a large part of the small intestine, is rarely used because it has higher mortality and complication rates. HOW MUCH DO THE OPERATIONS COST? The average cost of a sleeve gastrectomy is $16,000 to $19,000, and the average cost of a gastric bypass is $20,000 to $25,000. Most insurance plans cover the cost for patients who qualify, though some plans require that patients try dieting for a certain amount of time first. DOES THE SURGERY SAVE MONEY ON OTHER HEALTH CARE COSTS IN THE END? © 2016 The New York Times Company

Keyword: Obesity
Link ID: 23026 - Posted: 12.27.2016

By Sheryl Ubelacker, The Canadian Press Posted: Peter Chaban was up early doing dishes one morning in 2012 when he noticed there was water flowing over his hand — but he couldn't feel it. Next thing he knew, he lost all sensation and strength on his left side and dropped to floor. Within seconds he was lying there completely immobilized. By the time the ambulance arrived at his vacation property near Collingwood, Ont., Chaban had recovered. But doctors at the local hospital diagnosed him with a probable transient ischemic attack, or TIA, a type of temporary stroke that leaves no permanent damage. Once he returned home to Toronto, Chaban was sent for an MRI, and the brain scan confirmed that diagnosis. But of more concern was the discovery of "quite a few" lesions in his brain, the result of "silent strokes" that show up as small holes on imaging. When the strokes had occurred and over what time period was a mystery to Chaban, who had experienced no symptoms. That's why, in fact, they're known as silent — patients have no idea they've had a miniature clot or microbleed in the brain that has destroyed a tiny chunk of neurons, but resulted in no loss of function as would typically occur with a full-blown stroke. "I was never aware of any deficits," said Chaban, 64, who retired from his research job at the Hospital for Sick Children three years ago. "When I was employed, I was quite cognitively active. "I was physically very active. I ski, play golf, I played squash until a few years ago. And my health is very good, so the silent strokes hadn't expressed themselves, at least to my awareness." ©2016 CBC/Radio-Canada.

Keyword: Stroke
Link ID: 23025 - Posted: 12.27.2016

As 2016 draws to a close, we are re-visiting some of the people we met this year — including one man who survived a stroke at a young age, and a listener who heard his story on the radio. DAVID GREENE, HOST: Now as 2016 draws to a close, we're revisiting some of the people we met this year. And NPR's Rae Ellen Bichell checks back with a man who survived a stroke in his 40s and also a listener who heard his story. RAE ELLEN BICHELL, BYLINE: Back in February, I reported a story about strokes increasing in adults under 50. Troy Hodge, a 43-year-old man living in Maryland, shared his story about having a stroke two years earlier. (SOUNDBITE OF ARCHIVED BROADCAST) TROY HODGE: I remember setting myself on the floor because I was really hot. And I wanted to get some water to splash on my face. BICHELL: When the story aired on MORNING EDITION, the radio waves carried Hodge's voice into the home of Sue Bryson, a teacher in Virginia. SUE BRYSON: It was just a normal Monday morning and I was just getting ready for work and I was listening to NPR. BICHELL: Listening to Hodge's story, Bryson realized that right then, she was having similar symptoms, that she was having a stroke. So she called her neighbors and they took her to the emergency room. BRYSON: I would have never gone to the hospital if I didn't hear your show - never. BICHELL: Bryson is now back in the classroom and Hodge has made some changes. He moved into a bigger apartment. He walks up a flight of stairs each day without his cane to check the mail. He sometimes forgets things. HODGE: Memory's not too bad, I mean, it's... © 2016 npr

Keyword: Stroke
Link ID: 23024 - Posted: 12.27.2016