By Linda Searing Benzodiazepines, also known as benzos, are drugs sometimes prescribed to ease the agitation, anxiety and insomnia often experienced by people with Alzheimer’s disease. Might these powerful medications have an effect beyond their sleep-inducing or calming properties? This study Researchers analyzed data on 31,140 adults with Alzheimer’s, most in their early 80s and predominantly women. The group included 10,380 people who started taking benzodiazepines (6,438), benzodiazepine-related “Z-drugs” (3,826) or both (116) after being diagnosed with Alzheimer’s. None of them had taken these drugs for at least a year before their diagnosis. Prescribed benzos included Valium, Librium, Ativan, Xanax, Restoril, Serax and one drug not approved for use in the United States. Prescribed Z-drugs were Ambien and one non-U.S. drug. Within six months of starting to take the medication, 1,225 people had died. Those taking benzos were 41 percent more likely to have died than were people who did not take these drugs, with the strongest mortality risk occurring within four months of starting the medication. No increased risk was linked to Z-drugs. Who may be affected? People with Alzheimer’s, which usually affects those 60 and older. The researchers noted that benzodiazepines and similar drugs have a stronger effect on the central nervous system of older people than of younger ones, and they have been shown to raise older people’s risk for hip fractures, pneumonia and stroke. Because of this, they wrote, “the observed association with an increased risk of death might result from these outcomes.” Today, about 5 million Americans are living with Alzheimer’s — a number that may triple in the next three decades. © 1996-2017 The Washington Post

Keyword: Alzheimers
Link ID: 24369 - Posted: 11.28.2017

Patricia Neighmond As the months grow colder and darker, many people find themselves somewhat sadder and even depressed. Bright light is sometimes used to help treat the symptoms of seasonal affective disorder, or SAD. Researchers are now testing light therapy to see if it also can help treat depression that's part of bipolar disorder. It's unclear how lack of light might cause the winter blues, although some suggest that the dark days affect the production of serotonin in the skin. The idea with light therapy for depression is to replace the sunshine lost with a daily dose of bright white artificial light. (Antidepressants, psychotherapy and Vitamin D help, too, according to the National Institute of Mental Health.) The light box is actually more like a screen, the size of your average desktop computer. Some people call it a "happy box." To test its usefulness in treating bipolar disorder, researchers at the Feinberg School of Medicine, Northwestern University enrolled 46 patients who had at least moderate bipolar depression. Half of participants were assigned to receive bright light therapy. The other half received a dim red placebo light. They also kept taking their regular medication. © 2017 npr

Keyword: Biological Rhythms; Schizophrenia
Link ID: 24368 - Posted: 11.27.2017

By EFFY REDMAN It’s late morning on a balmy September day. I try to summon the will to run from the bench where I’m sitting on Broadway and dive under the massive wheels of one of the trucks roaring past. Which section of my body, I wonder, should I hurl beneath the tires. Where would hurt the least, and soonest erase my suffering. I clutch my cellphone, hating its potential for rescue signals. After nine or 10 trucks pass me by, an unkempt man in his mid-50s sits on the bench beside me, plastic cup of lager in one hand, half-smoked self-rolled cigarette in the other. He looks me up and down and grins. Go away, jerk, I think to myself, shooting him an icy glance. Leave me be. “Are you waiting for a date?” he persists. “What are you doing?” I want to kill him, but my resolve switches. I stand abruptly and head for my apartment, where, I calculate, I have enough medications stored to off myself. I ponder what to say in my suicide note. My phone rings: my mother, responding to the please call me asap message I had texted her. “What’s going on?” she says. It is my mother who insists I call my therapist and my mother who, upon my therapist’s urging, drives me to the emergency room. “Can’t you think about how it’s a beautiful sunny day?” she says once I’ve checked in and changed into a hospital gown and scrubs pants. I tug at the neck of my cotton gown, which chokes no matter how much I loosen the ties. ‘“I just feel utterly hopeless,” I say. The depression is a silent, slow motion tsunami of dark breaking over me. I can’t swim away from it and don’t believe I can survive its natural withdrawal. That’s why I am here. © 2017 The New York Times Company

Keyword: Depression
Link ID: 24367 - Posted: 11.27.2017

By Julie Hecht A good friend insists: "You don't study dogs, Julie. You study human culture. Dog behavior is a product of the people who love them." And since I'm not one for quick comebacks, I typically just smile and pet her dog. Because I like dogs. And I study them (see what I just did there? Bam). Or maybe she's onto something. Is dog behavior independent from where they live? From the cultural norms they're exposed to? Maybe German Shepherds can tell us a thing or two. In 2009, researchers from Hungary and the USA published a cross-cultural survey where German Shepherd owners from each country weighed in on their dogs. While a number of similarities emerged, so did differences. For example, USA German Shepherds were more likely to be kept indoors and have more types of training experiences. And when it came to behavior, on some measures there was no difference between German Shepherds in each country—all owners reported low activity-impulsivity and low inattention scores—but there were also a few differences: the USA dogs scored higher on confidence and aggressiveness than those in Hungary. Does this mean a German Shepherd here isn't the same as a German Shepherd there? One possible answer is: yes, the dogs are different. If German Shepherd lovers in the USA prefer dogs with higher confidence ratings, this preference "could lead to selective breeding for higher confidence, resulting in a population of German Shepherds in the USA with this trait." We know it’s possible to select for particular parental behavioral traits, and then observe them in offspring. "Genetic isolation, as well as environmental variation, could contribute to differences in pet behavior across cultures," the researchers offer. © 2017 Scientific American

Keyword: Learning & Memory; Evolution
Link ID: 24366 - Posted: 11.27.2017

Jessica Brown Sugar’s demise from childhood staple to public enemy can be seen everywhere. Chocolate bars are shrinking, sugary drinks are set to be taxed and our recommended daily sugar intake has been slashed in half. But the battle against sugar might have begun sooner if the industry hadn’t kept secrets to protect its commercial interests, according to new findings. In 1967, when scientists were arguing over the link between sugar consumption and increased risk of heart disease, researchers now claim that the International Sugar Research Foundation (ISRF) withheld findings that rats that were fed a high-sugar diet had higher levels of triglycerides (a fat found in the blood) than those fed starch. In a move researchers from the University of California at San Francisco have compared to the tobacco industry’s self-preservation tactics, the foundation stopped funding the project. Cristin Kearns, one of the researchers who analysed ISRF documents, says, “ISRF’s research was designed to cast doubt on the importance of elevated triglycerides in the blood as a heart disease risk factor. It is now commonly accepted that triglycerides are a risk factor, but this was controversial for decades. I think the scientific community would have come to consensus about elevated triglycerides being a risk factor for heart disease much sooner [if the research been published].” A year later the foundation funded Project 259, looking into the effects of sucrose consumption in the intestinal tracts of rats. It found a possible link between sugar consumption and increased risk of bladder cancer, and described the findings as “one of the first demonstrations of a biological difference between sucrose and starch fed rats”. But the ISRF terminated the project’s funding before the experiments were finished, despite the study having already lasted 27 months, and requiring only three more months. © 2017 Guardian News and Media Limited

Keyword: Obesity
Link ID: 24365 - Posted: 11.27.2017

By JANE E. BRODY Having recently endured more than a month of post-concussion fatigue, I can’t imagine how people with so-called chronic fatigue syndrome navigate through life with disabling fatigue that seemingly knows no end. Especially those who are erroneously told things like “It’s all in your head,” “Maybe you should see a psychiatrist,” or “You’d have a lot more energy if only you’d get more exercise.” After years of treating the syndrome as a psychological disorder, leading health organizations now recognize that it is a serious, long-term illness possibly caused by a disruption in how the immune system responds to infection or stress. It shares many characteristics with autoimmune diseases like rheumatoid arthritis but without apparent signs of tissue damage. Accordingly, doctors now typically refer to it as myalgic encephalomyelitis, meaning brain and spinal cord inflammation with muscle pain, and in scientific papers it is often written as ME/CFS. At the same time, a major shift is underway as far as how the medical profession is being advised to approach treatment. The longstanding advice to “exercise your way out of it” is now recognized as not only ineffective but counterproductive. It usually only makes matters worse, as even the mildest activity, like brushing your teeth, can lead to a debilitating fatigue, the core symptom of the disease. Both the Centers for Disease Control and Prevention in the United States and the National Institute for Health and Care Excellence in Britain are formulating revised guidelines for managing an ailment characterized by six or more months — and sometimes years — of incapacitating fatigue, joint pain and cognitive problems. This new thinking is long overdue. It is understandably difficult for doctors to appreciate that a disorder lacking obvious physical abnormalities could have a physical basis, especially when patients debilitated by a chronic disease that no one understands are likely to be depressed and anxious. © 2017 The New York Times Company

Keyword: Depression
Link ID: 24364 - Posted: 11.27.2017

By DANIEL T. WILLINGHAM Americans are not good readers. Many blame the ubiquity of digital media. We’re too busy on Snapchat to read, or perhaps internet skimming has made us incapable of reading serious prose. But Americans’ trouble with reading predates digital technologies. The problem is not bad reading habits engendered by smartphones, but bad education habits engendered by a misunderstanding of how the mind reads. Just how bad is our reading problem? The last National Assessment of Adult Literacy from 2003 is a bit dated, but it offers a picture of Americans’ ability to read in everyday situations: using an almanac to find a particular fact, for example, or explaining the meaning of a metaphor used in a story. Of those who finished high school but did not continue their education, 13 percent could not perform simple tasks like these. When things got more complex — in comparing two newspaper editorials with different interpretations of scientific evidence or examining a table to evaluate credit card offers — 95 percent failed. There’s no reason to think things have gotten better. Scores for high school seniors on the National Assessment of Education Progress reading test haven’t improved in 30 years. Many of these poor readers can sound out words from print, so in that sense, they can read. Yet they are functionally illiterate — they comprehend very little of what they can sound out. So what does comprehension require? Broad vocabulary, obviously. Equally important, but more subtle, is the role played by factual knowledge. All prose has factual gaps that must be filled by the reader. Consider “I promised not to play with it, but Mom still wouldn’t let me bring my Rubik’s Cube to the library.” The author has omitted three facts vital to comprehension: you must be quiet in a library; Rubik’s Cubes make noise; kids don’t resist tempting toys very well. If you don’t know these facts, you might understand the literal meaning of the sentence, but you’ll miss why Mom forbade the toy in the library. Knowledge also provides context. For example, the literal meaning of last year’s celebrated fake-news headline, “Pope Francis Shocks World, Endorses Donald Trump for President,” is unambiguous — no gap-filling is needed. But the sentence carries a different implication if you know anything about the public (and private) positions of the men involved, or you’re aware that no pope has ever endorsed a presidential candidate. © 2017 The New York Times Company

Keyword: Language
Link ID: 24363 - Posted: 11.26.2017

By Nathaniel Morris Depression afflicts an estimated 16 million Americans every year, many of whom go to their doctors in despair, embarking on an often stressful process about what to do next. These visits may entail filling out forms with screening questions about symptoms such as mood changes and difficulty sleeping. Doctors may ask patients to share intimate details about such issues as marital conflicts and suicidal urges. Some patients may be referred to mental-health specialists for further examination. Once diagnosed with depression, patients frequently face the question: “Are you interested in therapy, medications or both?” As a resident physician in psychiatry, I’ve seen many patients grapple with this question; the most frequent answer I’ve heard from patients is “I’m not sure.” Deciding between different types of medical treatment can be challenging, especially amid the fog of depression. Moreover, patients rely on doctors to help guide them, and we’re often not sure ourselves which is the best approach for a specific patient. People commonly associate psychotherapy with Freud and couches, but newer, evidence-based treatments such as cognitive behavioral therapy have become prominent in the field. CBT helps patients develop strategies to address harmful thoughts, emotions and behaviors that may contribute to depression. There are many proposed explanations for how specific psychotherapies treat depression. These possibilities include giving patients social support and teaching coping skills, and researchers are using neuroimaging to study how these treatments affect depressed patients’ brains. © 1996-2017 The Washington Post

Keyword: Depression
Link ID: 24362 - Posted: 11.26.2017

Sarah Marsh In fields across Switzerland the harvest time for cannabis is coming to an end, and workers are distributing the crop to shops in France and Switzerland. Soon, the plants could be available across much of Europe. The man behind the operation is 31-year-old Jonas Duclos, a former banker, and what he is doing is legal. His business, CBD420, sells BlueDream, a strain of hemp cultivated to ensure the level of tetrahydrocannabinol (THC), the main psychoactive ingredient in cannabis, is low enough (0.2%) to be lawful in most European countries. The UK is one of the exceptions: any trace of THC is outlawed. While low in THC, BlueDream is high in cannabidiol (CBD), another compound found in cannabis, which is non-psychoactive and has been shown to have medicinal qualities, for example, acting as a powerful anti-inflammatory. CBD is not a controlled substance in Europe, and in Britain does not require a licence from the Home Office to be sold if it can be extracted from cannabis. Duclos’s “legal weed” is on sale in more than 1,000 tobacco shops in Switzerland, where THC is allowed up to 1% concentration, and in 15 to 20 shops in France, where the limit is 0.2%. “There is a loophole that lets us bring it on the market,” Duclos explains. The plan is now to take the product elsewhere in Europe, with Italy among his next targets. While the company’s low-THC hemp is illegal in the UK, its CBD oils and balms will be available in some British shops from mid-December. © 2017 Guardian News and Media Limited

Keyword: Drug Abuse
Link ID: 24361 - Posted: 11.26.2017

By Erin Blakemore Jennifer Brea wasn’t supposed to break down. But in 2011, her body did just that. The 28-year-old was on the verge of a Harvard PhD and a wedding, but a series of viral infections transformed her from an energetic young woman to a bedridden patient with a mystery illness. Desperate to escape the pain, exhaustion and loss of muscle control that bound her to her bed, Brea visited a long list of medical specialists — many of whom questioned whether she was sick at all. In reality, Brea has myalgic encephalomyelitis, or ME. Also known as chronic fatigue syndrome, the condition can mystify health-care providers and disable patients. According to the Centers for Disease Control and Prevention, up to 2.5 million Americans suffer from the illness, 90 percent of them undiagnosed. “Unrest,” Brea’s intensely personal documentary about her journey through ME, asks why physicians still know so little about the disease. The film delves into Brea’s ordeal, her marriage and the lives of others whose health was stolen by a condition that can strip a person of dignity, mobility and hope for the future. More women have ME than men, and Brea’s experience fighting for recognition from her doctors is central to the film’s narrative. Her documentary is a testimony not just to the terrors of ME but also to the struggles that women often face when relaying information about their own bodies to medical providers. ME can keep patients painfully separate from their everyday lives and loved ones. “Unrest” breaks through a bit of that isolation and offers a sometimes heartbreaking look at what it takes to survive a poorly understood disease. © 1996-2017 The Washington Post

Keyword: Depression
Link ID: 24360 - Posted: 11.26.2017

By Daniel J. Levitin One evening in April, driving home from a university function, I was stopped in freeway traffic caused by roadworks somewhere up ahead when I felt a massive jolt. The back of my head hit the headrest, then my head lurched forward and I felt something hit the inside of my forehead with a squishy blow. Then my head snapped back and slammed into the headrest a second time. I didn’t feel any pain at first, just a stunned sense of disruption. As a neuroscientist, I know a bit about traumatic brain injury and concussions. Sitting on the freeway, I went through a quick checklist in my mind: I hadn’t blacked out. I wasn’t dizzy or nauseated. This meant that it was unlikely I’d slip into a coma or lose consciousness in the critical next few hours. But I could feel a dull ache in the cerebellum, where my head had hit the headrest. If the impact had been any higher up, I thought, in the occipital lobe, I might have lost my sight or experienced hallucinations. The squishy sensation, I suspected, was likely my prefrontal cortex pushing against the viscous fluid that keeps it from the bone of my skull. I did not want to move yet. I wanted to just sit. The young woman who hit me walked up to my window and asked if I was all right. She was clutching her cell phone. I wondered if she had been texting while driving. I knew that going to the E.R. would likely be pointless: concussions don’t leave any evidence that can be seen in CT scans and MRIs, and newer markers—cerebral spinal fluid and blood draws—are still being evaluated. © 2017 Condé Nast

Keyword: Brain Injury/Concussion; Language
Link ID: 24359 - Posted: 11.25.2017

By Diana Kwon, Amanda Montañez Killer whales have group-specific dialects, sperm whales babysit one another’s young and bottlenose dolphins cooperate with other species. These social skills are all closely linked with the aquatic mammals’ brain sizes, according to a recent study in Nature Ecology & Evolution. Scientists first proposed a relation between social living and brain expansion, or encephalization, nearly three decades ago, when they observed that primate species with larger brains typically lived in bigger groups. This theory was later broadened to associate brain size with other social characteristics, such as resolving conflicts and allocating food. Michael Muthukrishna, an economic psychologist at the London School of Economics, and his colleagues went searching for a similar link between big brains and sociality in cetaceans—the mammalian order that includes whales, dolphins and porpoises. They compiled a comprehensive data set of cetacean brain and body mass, group size and social characteristics. The team’s analyses, which covered 90 species, revealed that brain size was best predicted by a score based on various social behaviors such as cooperation with other species, group hunting and complex vocalizations. Bigger brains were also linked to other factors, including dietary richness and geographical range. The authors say these results are consistent with theories that cetaceans developed large brains to deal with the challenges of living in information-rich social environments. Yet Robert Barton, an evolutionary biologist at Durham University in England, who did not take part in the work, cautions against drawing conclusions about causation from correlation. He also asserts that it is important to ex­­amine specific regions of the brain because they might evolve differently. For example, his own research team has found that nocturnal primates’ brains develop larger olfactory structures—regions associated with smell—than those found in species active during the day. © 2017 Scientific American

Keyword: Evolution; Language
Link ID: 24358 - Posted: 11.25.2017

By John Horgan Years ago I was surfcasting on an ocean beach and caught a big, beautiful striped bass. My daughter and son, who were 8 and 10, respectively, were nearby. I held the fish up and yelled, Look kids, I caught dinner! Skye, my daughter, burst into tears and pleaded with me to let the fish go. I tried to josh her out of her mood, in vain. I assured her that I’d been catching fish like this since I was a boy, fish don’t really feel pain, they’re just fish, they’re like swimming machines. Skye was unconvinced. I said I would stick a knife into the fish’s brain now to put it out of its misery. Dumb move! Skye shrieked in horror and begged me not to kill the fish. By now, other people on the beach, attracted by the commotion, had gathered around the weeping girl and mean man. This traumatic—for me!—scene came back to me when I attended “Animal Consciousness” at New York University last weekend. I’m trying to wrap up a book on the mind-body problem, so I really didn’t have the time to attend the meeting. But I couldn’t resist going, and now I can’t resist firing off a quick report. Advertisement Philosopher David Chalmers, one of the conference organizers, kicked the meeting off by noting that many researchers are investigating whether non-human animals are conscious. If animals are capable of consciousness, he said, they can suffer, and that should matter to us. © 2017 Scientific American,

Keyword: Animal Rights
Link ID: 24357 - Posted: 11.25.2017

By DENISE GRADY Scientists have found prions — abnormal proteins widely believed to cause a rare, brain-destroying disease — in the skin of 23 patients who had died from it, according to a study published on Wednesday. The discovery suggests that skin samples might be used to improve detection of the disorder, Creutzfeldt-Jakob disease, which now is usually diagnosed with much more difficult procedures, like brain biopsies or autopsies. But the presence of prions in the skin also raises unsettling questions about whether medical instruments could become contaminated even during surgery that does not involve the brain and then spread the disease to other patients. The prions stick to stainless steel and are notoriously hard to destroy. Creutzfeldt-Jakob disease affects one person in a million worldwide, with about 300 cases a year in the United States, according to the National Institutes of Health. People are typically about age 60 when it starts. It is cruel and rapidly fatal: Most patients die within a year of becoming ill. They deteriorate mentally, weaken, move uncontrollably, and may become blind and unable to speak. The disease belongs to the same class of brain disorders as mad-cow disease. The findings do not mean that Creutzfeldt-Jakob disease can be transmitted by touch or casual contact, said the senior author of the study, Dr. Wen-Quan Zou, at Case Western University School of Medicine. Patients are not dangerous, he emphasized. The researchers also said that although the disease had been transmitted decades ago by corneal transplants and certain neurosurgical procedures, there was no definitive evidence that other types of surgery had ever spread it. And the levels found in skin are far lower than those in the brain. Despite the new findings, there is no reason to change the medical care given to patients with the disease or to people known to have genetic mutations that may predispose them to Creutzfeldt-Jakob or related illnesses, the researchers said. © 2017 The New York Times Company

Keyword: Prions
Link ID: 24356 - Posted: 11.24.2017

Sara Reardon Brain implants that deliver electrical pulses tuned to a person’s feelings and behaviour are being tested in people for the first time. Two teams funded by the US military’s research arm, the Defense Advanced Research Projects Agency (DARPA), have begun preliminary trials of ‘closed-loop’ brain implants that use algorithms to detect patterns associated with mood disorders. These devices can shock the brain back to a healthy state without input from a physician. The work, presented last week at the Society for Neuroscience (SfN) meeting in Washington DC, could eventually provide a way to treat severe mental illnesses that resist current therapies. It also raises thorny ethical concerns, not least because the technique could give researchers a degree of access to a person’s inner feelings in real time. The general approach — using a brain implant to deliver electric pulses that alter neural activity — is known as deep-brain stimulation. It is used to treat movement disorders such as Parkinson’s disease, but has been less successful when tested against mood disorders. Early evidence suggested that constant stimulation of certain brain regions could ease chronic depression, but a major study involving 90 people with depression found no improvement after a year of treatment.1 The scientists behind the DARPA-funded projects say that their work might succeed where earlier attempts failed, because they have designed their brain implants specifically to treat mental illness — and to switch on only when needed. “We’ve learned a lot about the limitations of our current technology,” says Edward Chang, a neuroscientist at the University of California, San Francisco (UCSF), who is leading one of the projects. © 2017 Macmillan Publishers Limited

Keyword: Depression; Robotics
Link ID: 24354 - Posted: 11.24.2017

Jon Hamilton A brain system involved in everything from addiction to autism appears to have evolved differently in people than in great apes, a team reports Thursday in the journal Science. The system controls the production of dopamine, a chemical messenger that plays a major role in pleasure and rewards. "Humans have evolved a dopamine system that is different than the one in chimpanzees," says Nenad Sestan, an author of the study and a professor of neuroscience at Yale. That could help explain why human behavior is so different from our nearest relatives even though our brains are remarkably similar, he says. It might also shed light on why people are vulnerable to mental disorders such as autism. The finding came from a massive, multicenter effort to compare the brains of several species. Researchers looked at 247 samples of brain tissue from five macaque monkeys, five chimpanzees and six people. They looked at which genes were turned on or off in 16 regions of the brain. And in most places, the differences among species were subtle. But there was a striking difference in the neocortex, an area of the brain that is much more developed in people than in chimpanzees. The team found that a gene called TH, which is involved in the production of dopamine, was expressed in the neocortex of people, but not chimpanzees. "That caught our attention," says Andre Miguel Sousa, another author of the study who works in Sestan's lab at Yale. Dopamine is best known for its role in the brain's reward system, which responds to everything from sex and food to addictive drugs. But dopamine also helps regulate emotional responses, memory and movement. And abnormal dopamine levels have been linked to disorders including Parkinson's, schizophrenia and autism. © 2017 npr

Keyword: Drug Abuse; Evolution
Link ID: 24353 - Posted: 11.24.2017

By Diana Kwon | Most of us are familiar with the role of smell in our dining habits—that basket of freshly baked cookies is usually much harder to resist than a plate of odorless carrot sticks, and the taste of food is strongly tied to its aroma. But animals’ sense of smell is even more intricately linked with eating and metabolism. Prior studies have shown that, in humans, fasting enhances olfactory sensitivity, while satiety reduces it. And a new study, published today (July 5) in Cell Metabolism, suggests that, at least in mice, this link may go even further—animals engineered to lack a sense of smell gained less weight and burned more fat than their unaltered counterparts. This difference in weight gain was almost entirely due to alterations in body fat composition. “The major thing was that [the mice lacking smell] weren’t gaining fat,” coauthor Andrew Dillin, a biology professor at the University of California, Berkeley, tells The Scientist. “Somehow, the olfactory system is engaging the major control circuit in the brain that controls peripheral metabolism . . . and that is turning on a program to burn fat.” Dillin says his team was interested in knowing whether simply eating fattening food led to weight gain, or if it was how the olfactory system “perceived” those calories that matters. To assess this link between olfaction and metabolism, scientists genetically engineered mice that expressed a gene for a diphtheria toxin receptor on olfactory sensory neurons. Once the animals were around seven weeks old, the researchers injected the toxin to kill off these nerve cells and found that these animals had lost their sense of smell. Control animals generated without this receptor retained all their smell neurons after receiving the toxin. © 1986-2017 The Scientist

Keyword: Obesity; Chemical Senses (Smell & Taste)
Link ID: 24352 - Posted: 11.24.2017

By Abby Olena Two people with a rare genetic disorder have helped shed light on the fundamental neuroscience of appetite and, scientists say, opened up a new target for potential obesity treatments. Neonatal progeroid syndrome (NPS) affects only a handful of people worldwide. The most telling features of the condition are an aged appearance due to an absence of the fat layer under the skin and extreme thinness. Researchers report in in Nature Medicine today (November 6) that a glucose-releasing hormone involved in the disease crosses the blood-brain barrier and homes in on neurons that regulate appetite in mice. The study suggests it might be possible to target the hormone, asprosin, in the treatment of diabetes and obesity. “Rare diseases with extreme phenotypes like this are very valuable to learn important things that then apply to more common diseases,” says coauthor and medical geneticist Atul Chopra of Baylor College of Medicine in Houston, Texas. Chopra and colleagues showed in a previous study that patients with NPS have mutations near the end of a gene called FBN1, which encodes profibrillin. It was already known that profibrillin is processed to form fibrillin 1, an extracellular matrix protein. The 140-amino-acid chunk cleaved from the end of profibrillin, which Chopra’s group named asprosin, is secreted by adipose tissue and functions as a hormone that causes the liver to make glucose. They determined that two individuals with NPS are heterozygous for FBN1 mutations and have greatly reduced levels of circulating asprosin. © 1986-2017 The Scientist

Keyword: Obesity
Link ID: 24351 - Posted: 11.24.2017

By Bob Grant In 1971, a 27-year-old, 456-pound man went to the University of Dundee’s department of medicine in Scotland looking for help. Patient A.B., as doctors referred to him, needed to lose weight. His physicians recommended a short but drastic course of action: stop eating altogether. The patient responded so well to a brief stint without food that he decided to prolong the deprivation—for more than a year. “[H]is fast was continued into what is presently the longest recorded fast (Guinness Book of Records, 1971),” the clinicians wrote in a 1973 case report, claiming A.B. suffered little or no untoward effects on his health.1 And at the end of his 382-day dietary abstinence, during which he had ingested only vitamin supplements, yeast, and noncaloric fluids, A.B. had lost a remarkable 276 pounds. When doctors checked back in on A.B. five years later, their patient reported gaining back only about 15 pounds. Although aspects of this published report seem almost unbelievable, and the period of fasting is obviously extreme, the case highlights some of the metabolic dynamics that result when bodies are deprived of food. For example, when external calories stop fueling an animal’s metabolism, stores of triglycerides in fat cells are mobilized, and levels of ketones—chemicals that result from the burning of fat for fuel—rise. Decreases in body weight follow. © 1986-2017 The Scientist

Keyword: Obesity
Link ID: 24350 - Posted: 11.24.2017

By Philippa Roxby Confronting an avatar on a computer screen helped patients hearing voices to cope better with hallucinations, a UK trial has found. Patients who received this therapy became less distressed and heard voices less often compared with those who had counselling instead. Experts said the therapy could add an important new approach to treating schizophrenia hallucinations. The trial, on 150 people, is published in The Lancet Psychiatry journal. It follows a much smaller pilot study in 2013. Hallucinations are common in people with schizophrenia and can be threatening and insulting. One in four patients continues to experience voices despite being treated with drugs and cognitive behavioural therapy. In this study, run by King's College London and University College London, 75 patients who had continued to hear voices for more than a year, were given six sessions of avatar therapy while another 75 received the same amount of counselling. In the avatar sessions, patients created a computer simulation to represent the voice they heard and wanted to control, including how it sounded and how it might look. Image copyright King's College London Image caption Three avatars created by people taking part in the therapy The therapist then voiced the avatar while also speaking as themselves in a three-way conversation to help the patient gain the upper hand. Prof Tom Craig, study author from King's College London, said getting patients to learn to stand up to the avatar was found to be safe, easy to deliver and twice as effective as counselling at reducing how often voices were heard. "After 12 weeks there was dramatic improvement compared to the other therapy," he said. "With a talking head, patients are learning to confront and get replies from it. "This shifts the idea that the voice is all-controlling," he said. © 2017 BBC.

Keyword: Schizophrenia
Link ID: 24349 - Posted: 11.24.2017