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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
Link ID: 23053 - Posted: 01.04.2017
National Institutes of Health (NIH) researchers have discovered molecular mechanisms that may underlie a woman’s susceptibility to disabling irritability, sadness, and anxiety in the days leading up to her menstrual period. Such premenstrual dysphoric disorder (PMDD) affects 2 to 5 percent of women of reproductive age, whereas less severe premenstrual syndrome (PMS) is much more common. “We found dysregulated expression in a suspect gene complex which adds to evidence that PMDD is a disorder of cellular response to estrogen and progesterone,” explained Peter Schmidt, M.D. of the NIH’s National Institute of Mental Health, Behavioral Endocrinology Branch. “Learning more about the role of this gene complex holds hope for improved treatment of such prevalent reproductive endocrine-related mood disorders.” Schmidt, David Goldman, M.D., of the NIH’s National Institute on Alcohol Abuse and Alcoholism, and colleagues, report on their findings January 3, 2017 in the journal Molecular Psychiatry. “This is a big moment for women’s health, because it establishes that women with PMDD have an intrinsic difference in their molecular apparatus for response to sex hormones – not just emotional behaviors they should be able to voluntarily control,” said Goldman. By the late 1990s, the NIMH team had demonstrated (link is external) that women who regularly experience mood disorder symptoms just prior to their periods were abnormally sensitive to normal changes in sex hormones — even though their hormone levels were normal. But the cause remained a mystery.
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
Alexander Fornito, The human brain is an extraordinarily complex network, comprising an estimated 86 billion neurons connected by 100 trillion synapses. A connectome is a comprehensive map of these links—a wiring diagram of the brain. With current technology, it is not possible to map a network of this size at the level of every neuron and synapse. Instead researchers use techniques such as magnetic resonance imaging to map connections between areas of the human brain that span several millimeters and contain many thousands of neurons. At this macroscopic scale, each area comprises a specialized population of neurons that work together to perform particular functions that contribute to cognition. For example, different parts of your visual cortex contain cells that process specific types of information, such as the orientation of a line and the direction in which it moves. Separate brain regions process information from your other senses, such as sound, smell and touch, and other areas control your movements, regulate your emotional responses, and so on. These specialized functions are not processed in isolation but are integrated to provide a unitary and coherent experience of the world. This integration is hypothesized to occur when different populations of cells synchronize their activity. The fiber bundles that connect different parts of the brain—the wires of the connectome—provide the substrate for this communication. These connections ensure that brain activity unfolds through time as a rhythmic symphony rather than a disordered cacophony. © 2017 Scientific American
Keyword: Brain imaging
Link ID: 23049 - Posted: 01.03.2017
By Don Lattin In the fall of 1965, a 33-year-old father of three named Arthur King—a patient on the alcoholics ward at Baltimore’s Spring Grove Hospital—swallowed an LSD pill and laid back on his bed in a special unit called “Cottage Thirteen.” Sanford Unger, the chief of psychosocial research at the Johns Hopkins University School of Medicine, knelt beside King’s bed, holding his hand and reassuring the patient as he started to feel the drug’s mind-altering effects. This was not a normal psychotherapy session. During his 12-hour experience, designed to help stop his destructive drinking habit, King sat on the edge of the bed and looked at the photo of his son that he’d brought. Suddenly, the child became alive in the picture, which initially frightened him. Then King noticed that a lick of his son’s hair was out of place, so he stroked the photo, putting the errant strands back in place. His fear vanished. Later, Unger held out a small vase with a single red rose. King looked at the flower, which seemed to be opening and closing, as though it were breathing. At one point, Unger asked him whether he’d like to go out to a bar and have a few drinks. King didn’t say anything but was shocked when the rose suddenly turned black and dropped dead before his eyes. He never picked up another drink. Arthur King was one of thousands of research subjects who were given LSD, psilocybin, and mescaline as therapeutic tools in the 1950s and 1960s, often with government support and with promising results. But by the time King was enjoying his sobriety, the backlash against psychedelic testing had already begun. By the mid-1970s, the legal exploration of the therapeutic benefits of psychedelic drugs was over.
By KATHARINE Q. SEELYE BROOKLINE, Mass. — When Michael Dukakis lost the presidential election in 1988, his wife, Kitty, felt as if she had been squashed in a compactor, all the air forced out of her. Her even-keeled husband went back to work as governor of Massachusetts; she started binge drinking. “An alcoholic can contain himself for only so long,” Mrs. Dukakis would later write. “When a crisis hits, the restraints snap.” Her drinking masked a long-smoldering depression that eventually led her to receive electroconvulsive therapy, also known as electroshock therapy or ECT. Like most people, she had no idea that the procedure was still used. She thought it a relic, scrapped after it was depicted as an instrument of torture in the 1975 movie “One Flew Over the Cuckoo’s Nest.” But Mrs. Dukakis was desperate. Rehabilitation, talk therapy and antidepressants had failed to ease her crippling depression, so in 2001, at age 64, she turned to shock therapy. To her amazement, it helped. After the first treatment, Mrs. Dukakis wrote, “I felt alive,” as if a cloud had lifted — so much so that when Mr. Dukakis picked her up at Massachusetts General Hospital, she astonished him by proposing that they go out to dinner. “I was so shocked I almost drove off Storrow Drive,” Mr. Dukakis recalled. “I had left this wife of mine at the hospital a basket case just the night before.” Now, 15 years later, the Dukakises have emerged as the nation’s most prominent evangelists for electroconvulsive therapy. Truth be told, there is not much competition. Few boldface names who have had the treatment will acknowledge as much; the stigma is still too great. Exceptions include Carrie Fisher, the actress and writer who died Tuesday, and Dick Cavett, the talk-show host; both have openly discussed their positive experiences. Electroconvulsive therapy is not a one-and-done procedure. Mrs. Dukakis, 80, still receives maintenance treatment every seven or eight weeks. She said that she had minor memory lapses but that the treatment had banished her demons and that she no longer drank, smoked or took antidepressants. © 2017 The New York Times Company
Link ID: 23047 - Posted: 01.02.2017
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
By LISA FELDMAN BARRETT Think about the people in your life who are 65 or older. Some of them are experiencing the usual mental difficulties of old age, like forgetfulness or a dwindling attention span. Yet others somehow manage to remain mentally sharp. My father-in-law, a retired doctor, is 83 and he still edits books and runs several medical websites. Why do some older people remain mentally nimble while others decline? “Superagers” (a term coined by the neurologist Marsel Mesulam) are those whose memory and attention isn’t merely above average for their age, but is actually on par with healthy, active 25-year-olds. My colleagues and I at Massachusetts General Hospital recently studied superagers to understand what made them tick. Our lab used functional magnetic resonance imaging to scan and compare the brains of 17 superagers with those of other people of similar age. We succeeded in identifying a set of brain regions that distinguished the two groups. These regions were thinner for regular agers, a result of age-related atrophy, but in superagers they were indistinguishable from those of young adults, seemingly untouched by the ravages of time. What are these crucial brain regions? If you asked most scientists to guess, they might nominate regions that are thought of as “cognitive” or dedicated to thinking, such as the lateral prefrontal cortex. However, that’s not what we found. Nearly all the action was in “emotional” regions, such as the midcingulate cortex and the anterior insula. My lab was not surprised by this discovery, because we’ve seen modern neuroscience debunk the notion that there is a distinction between “cognitive” and “emotional” brain regions. © 2017 The New York Times Company
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
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
Link ID: 23043 - Posted: 01.02.2017
By Susana Martinez-Conde Our perceptual and cognitive systems like to keep things simple. We describe the line drawings below as a circle and a square, even though their imagined contours consist—in reality—of discontinuous line segments. The Gestalt psychologists of the 19th and early 20th century branded this perceptual legerdemain as the Principle of Closure, by which we tend to recognize shapes and concepts as complete, even in the face of fragmentary information. Now at the end of the year, it is tempting to seek a cognitive kind of closure: we want to close the lid on 2016, wrap it with a bow and start a fresh new year from a blank slate. Of course, it’s just an illusion, the Principle of Closure in one of its many incarnations. The end of the year is just as arbitrary as the end of the month, or the end of the week, or any other date we choose to highlight in the earth’s recurrent journey around the sun. But it feels quite different. That’s why we have lists of New Year’s resolutions, or why we start new diets or exercise regimes on Mondays rather than Thursdays. Researchers have also found that, even though we measure time in a continuous scale, we assign special meaning to idiosyncratic milestones such as entering a new decade. What should we do about our brain’s oversimplification tendencies concerning the New Year—if anything? One strategy would be to fight our feelings of closure and rebirth as we (in truth) seamlessly move from the last day of 2016 to the first day of 2017. But that approach is likely to fail. Try as we might, the Principle of Closure is just too ingrained in our perceptual and cognitive systems. In fact, if you already have the feeling that the beginning of the year is somewhat special (hey, it only happens once a year!), you might as well decide that resistance is futile, and not just embrace the illusion, but do your best to channel it. © 2017 Scientific American
Bret Stetka With a president-elect who has publicly supported the debunked claim that vaccines cause autism, suggested that climate change is a hoax dreamed up by the Chinese, and appointed to his Cabinet a retired neurosurgeon who doesn't buy the theory of evolution, things might look grim for science. Yet watching Patti Smith sing "A Hard Rain's a-Gonna Fall" live streamed from the Nobel Prize ceremony in early December to a room full of physicists, chemists and physicians — watching her twice choke up, each time stopping the song altogether, only to push on through all seven wordy minutes of one of Bob Dylan's most beloved songs — left me optimistic. Taking nothing away from the very real anxieties about future funding and support for science, neuroscience in particular has had plenty of promising leads that could help fulfill Alfred Nobel's mission to better humanity. In the spirit of optimism, and with input from the Society for Neuroscience, here are a few of the noteworthy neuroscientific achievements of 2016. One of the more fascinating fields of neuroscience of late entails mapping the crosstalk between our biomes, brains and immune systems. In July, a group from the University of Virginia published a study in Nature showing that the immune system, in addition to protecting us from a daily barrage of potentially infectious microbes, can also influence social behavior. The researchers had previously shown that a type of white blood cells called T cells influence learning behavior in mice by communicating with the brain. Now they've shown that blocking T cell access to the brain influences rodent social preferences. © 2016 npr
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
Alan Yu Being overweight can raise your blood pressure, cholesterol and risk for developing diabetes. It could be bad for your brain, too. A diet high in saturated fats and sugars, the so-called Western diet, actually affects the parts of the brain that are important to memory and make people more likely to crave the unhealthful food, says psychologist Terry Davidson, director of the Center for Behavioral Neuroscience at American University in Washington, D.C. He didn't start out studying what people ate. Instead, he was interested in learning more about the hippocampus, a part of the brain that's heavily involved in memory. He was trying to figure out which parts of the hippocampus do what. He did that by studying rats that had very specific types of hippocampal damage and seeing what happened to them. In the process, Davidson noticed something strange. The rats with the hippocampal damage would go to pick up food more often than the other rats, but they would eat a little bit, then drop it. Davidson realized these rats didn't know they were full. He says something similar may happen in human brains when people eat a diet high in fat and sugar. Davidson says there's a vicious cycle of bad diets and brain changes. He points to a 2015 study in the Journal of Pediatrics that found obese children performed more poorly on memory tasks that test the hippocampus compared with kids who weren't overweight. He says if our brain system is impaired by that kind of diet, "that makes it more difficult for us to stop eating that diet. ... I think the evidence is fairly substantial that you have an effect of these diets and obesity on brain function and cognitive function." © 2016 npr
By Nicole Mortillaro Post-traumatic stress disorder can be a debilitating condition. It's estimated that it affects nearly one in 10 Canadian veterans who served in Afghanistan. Now, there's promising research that could lead to the treatment of the disorder. Following a particularly traumatic event — one where there is the serious threat of death or a circumstance that was overwhelming — we often exhibit physical symptoms immediately. But the effects in our brains actually take some time to form. That's why symptoms of PTSD — reliving an event, nightmares, anxiety — don't show up until some time later. Research has shown that, after such an event, the hippocampus — which is important in dealing with emotions and memory — shrinks, while our amygdala — also important to memory and emotions — becomes hyperactive. In earlier research, Sumantra Chattarji from the National Centre for Biological Sciences (NCBS) and the Institute for Stem Cell Biology and Regenerative Medicine (inStem), in Bangalore, India, discovered that traumatic events cause new nerve connections to form in the amygdala, which also causes hyperactivity. This plays a crucial role in people dealing with post-traumatic stress disorder. Chattarji has been studying changes in the brain after traumatic events for more than a decade. In an earlier study, he concluded that a single stress event had no immediate event on the amygdala of rats. However, 10 days later, the rats exhibited increased anxiety. There were even changes to the brain, and, in particular the amygdala. So Chattarji set out to see if there was a way to prevent these changes. Post-traumatic stress disorder can seriously affect those who have served in the military. New research may help to one day prevent that. (Shamil Zhumatov/Reuters) The new research focused on a particular cell receptor in the brain, called N-Methyl-D-Aspartate Receptor (NMDA-R), which is crucial in forming memories. ©2016 CBC/Radio-Canada.
By Alice Callahan Can psychiatric medications alter the mother-baby bond? I am having a baby in a month and am on an antidepressant, antipsychotic and mood stabilizer. I don't feel a natural instinct to mother or connect to my baby yet. Could it be because of my medications? It’s normal for expectant parents to worry if they don’t feel a strong connection to the baby right away. “Those kinds of mixed fears and anxieties are really common in most pregnancies, certainly first pregnancies,” said Dorothy Greenfeld, a licensed clinical social worker and professor of obstetrics and gynecology at Yale School of Medicine. Bonding is a process that takes time, and while it can begin in pregnancy, the relationship between parent and child mostly develops after birth. Psychiatric conditions, and the medicines used to treat them, can complicate the picture. Antidepressants, the most widely used class of psychiatric drugs, do not seem to interfere with a woman’s attachment to the fetus during pregnancy, as measured by the amount of time the mother spends thinking about and planning for the baby, a 2011 study in the Archives of Women’s Mental Health found. On the other hand, the study found that women with major depression in pregnancy had lower feelings of maternal-fetal attachment, and this sense of disconnection intensified with more severe symptoms of depression. “Depression can definitely affect a person’s ability to bond with their baby, to feel those feelings of attachment, which is why we encourage treatment so strongly,” said Dr. Amy Salisbury, the study leader and a professor of pediatrics and psychiatry at the Alpert Medical School at Brown University. “That’s more likely to interfere than the medication itself.” There is less research on the effects of other types of mental health medications on mother-baby bonding, but psychiatric medications can have side effects that might interfere with parenting. For example, a small percentage of people taking mood-stabilizing medications have feelings of apathy, and that could hinder the bonding process, said Dr. Salisbury. And some mental health medications, depending on dosage and combination, might make a person feel too sedated. But again, letting mental illness go untreated is likely far riskier for both the mother and the baby. © 2016 The New York Times Company
By Laura Beil, Justin Shamoun began to hate his body a few weeks into seventh grade. He was a year younger than his suburban Detroit classmates, having skipped a grade. Many of his peers were entering puberty, their bodies solidifying into sleek young men. Justin still had the doughy build of a boy. After gym class one day, someone told Justin he could probably run faster if he weren’t so fat. The remark crushed him. Ashamed, he started hiding his body under ever-baggier clothes and making excuses to skip P.E., the pool, anywhere required to expose bare skin. Finally, he decided to fix himself. He dove headlong into sports and cut back on food. Before long, he was tossing his lunch into the garbage and picking at his dinner. He ate just enough to blunt his hunger, until the time came when he ate barely at all. The thought that he had an eating disorder never occurred to him. Long considered an affliction of women, eating disorders — the most deadly of all mental illnesses — are increasingly affecting men. The National Eating Disorders Association predicts that 10 million American men alive today will be affected, but that number is only an estimate based on the limited research available. The official criteria for diagnosing eating disorders were updated to be more inclusive of men only in 2013. And last year, Australian researchers writing in the Journal of Eating Disorders noted that “the prevalence of extreme weight control behaviors, such as extreme dietary restriction and purging” may be increasing at a faster rate in men than women. © 2016 Scientific American
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
Link ID: 23035 - Posted: 12.29.2016
By Heather M. Snyder For more than 25 years, Mary Read was a successful nurse in Lititz, Pennsylvania. But in 2010, at the age of 50, she started having trouble with her memory and thinking, making it difficult for her to complete routine tasks and follow instructions at work. The problems worsened, bringing her career to an abrupt end. In 2011, her doctor conducted a comprehensive evaluation, including a cognitive assessment, and found that she was in the early stages of younger-onset Alzheimer’s, which affects hundreds of thousands of people under 65. A year earlier, Elizabeth Wolf faced another sort of upheaval. The 36-year-old community health program director was forced to abandon her own career, home and community in Vermont when both of her parents were diagnosed with Alzheimer’s three months apart. Wolf took the difficult decision to move back into her childhood home in Mount Laurel, New Jersey in order to become their primary caregiver. These stories are not unusual. Alzheimer’s dementia disproportionately affects women in a variety of ways. Compared with men, 2.5 times as many women as men provide 24-hour care for an affected relative. Nearly 19 percent of these wives, sisters and daughters have had to quit work to do so. In addition, women make up nearly two-thirds of the more than 5 million Americans living with Alzheimer’s today. According to the Alzheimer’s Association 2016 Alzheimer’s Disease Facts and Figures, an estimated 3.3 million women aged 65 and older in the United States have the disease. To put that number in perspective, a woman in her sixties is now about twice as likely to develop Alzheimer’s as breast cancer within her lifetime. © 2016 Scientific American