By Neuroskeptic Sometimes, scientific misconduct is so blatant as to be comical. I recently came across an example of this on Twitter. The following is an image from a paper published in the Journal of Materials Chemistry C: As pointed out on PubPeer, this image – which is supposed to be an electron microscope image of some carbon dot (CD) nanoparticles – is an obvious fake. The “dots” are identical, and have clearly been cut-and-pasted. Where one copy has been placed over the top of another, the overlap is quite visible. It would be charitable to even call this ‘scientific’ fraud. The Journal of Materials Chemistry editors said on Twitter that they are “urgently” looking into this paper; I’ve no doubt it will be retracted soon, although the fact that it was published at all raises questions about the peer-review standards of this journal. To me as a neuroscientist, cases like this from chemistry get me worried. In a field like materials chemistry, or any field in which results take the form of images or photographs (such as Western blots), low-effort fraud is easy to spot because the manipulation of an image can, at least in unsubtle cases, be easily proven from the image itself. But what of fields like psychology or neuroscience where data don’t take the form of images? Perhaps low-effort frauds occur in these fields as well, but it is much more difficult to detect them when the results are statistical rather than pictorial in nature.

Keyword: Brain imaging
Link ID: 24383 - Posted: 12.01.2017

An analysis of more than 800,000 people has concluded that people who remain single for life are 42 per cent more likely to get dementia than married couples. The study also found that people who have been widowed are 20 per cent more likely to develop the condition, but that divorcees don’t have an elevated risk. Previous research has suggested that married people may have healthier lifestyles, which may help explain the findings. Another hypothesis is that married people are more socially engaged, and that this may protect against developing the condition. The stress of bereavement might be behind the increased risk in those who have been widowed. But marriage isn’t always good for the health. While men are more likely to survive a heart attack if they are married, single women recover better than those who are married. Journal reference: Journal of Neurology, Neurosurgery, and Psychiatry © Copyright New Scientist Ltd.

Keyword: Alzheimers; Learning & Memory
Link ID: 24382 - Posted: 12.01.2017

A new migraine drug that can halve the length of attacks has been hailed as “the start of real change” in how the condition is treated. Erenumab, a laboratory-made antibody that blocks a neural brain pathway called CGRP, is the first drug in 20 years proven to prevent migraine attacks. Phase three trial data on nearly 1,000 patients showed that it typically cut between three and four “migraine days” per month. In half the patients treated, migraine duration was reduced at least by half. Migraines are characterised by an intense, throbbing headache, sensitivity to light and noise, nausea, vomiting, low energy, and visual disturbances. Attacks can last anything from four to 72 hours. Each year more than 8.5 million people in the UK are thought to experience migraine – more than the number affected by asthma, diabetes and epilepsy combined. The condition is linked to depression and sick days caused by migraine are estimated to cost the UK economy more than £2bn per year. The trial, called Strive, compared patients taking erenumab for six months with others given a non-active placebo dummy drug. The research revealed that by months four to six, at least a 50% reduction in mean migraine days per month was achieved for just over 43% of patients injected under the skin with 70-mg of erenumab each month, while half of patients injected with the higher dose of 140-mg had such results. However, those given a placebo also saw benefits, with 26.6% of participants in this group experiencing such a reduction. © 2017 Guardian News and Media Limited

Keyword: Pain & Touch
Link ID: 24381 - Posted: 11.30.2017

By JOANNA KLEIN Chances are that’s a shy elk looking back at a bold magpie, in the photograph above. They get along, so to speak, because the elk needs grooming and the magpie is looking for dinner. But they may have never entered into this partnership if it weren’t for their particular personalities, suggests a study published Wednesday in Biology Letters. Let’s start with the elk. In Canada’s western province of Alberta, they’ve been acting strange. Some have quit migrating, opting to hang around towns with humans who protect them from predators like wolves. Others still migrate. As a doctoral student at the University of Alberta, Robert Found, now a wildlife biologist for Parks Canada, discovered over years of observing their personalities that bold elk stayed, while shy elk migrated. But he noticed something else in the process of completing his research: As elk laid down to rest at the end of the day, magpies approached. There appeared to be a pattern: elk of some personality types aggressively rejected magpies. Others didn’t. “Sometimes the magpies will walk around right on the head and the face of the elk,” Dr. Found said. Scientists define animal personality by an individual animal’s behavior. It’s predictable, but also varies from others in a group. Dr. Found created a bold-shy scale for elk, measuring how close they allowed him to get, where elk positioned themselves within the group, which elk fought other elk, which ones won, how long elk spent monitoring for predators and their willingness to approach unfamiliar objects like old tires, skis and a bike. He also noted which elk accepted magpies. To study the magpies, he attracted the birds to 20 experimental sites with peanuts on tree stumps. During more than 20 separate trials with different magpies, he judged each bird’s behavior relative to the other magpies in a trial. Like the elk, he measured flight response, social structure and willingness to approach items they hadn’t previously encountered (a bike decorated with a boa and Christmas ornaments). He also noted who landed on a faux-elk that offered dog food rather than ticks (a previous study showed magpies liked dog food as much as ticks). © 2017 The New York Times Company

Keyword: Learning & Memory; Evolution
Link ID: 24380 - Posted: 11.30.2017

Marcelo Gleiser Last week, my 13.7 co-blogger Tania Lombrozo reported on a study she developed with graduate student Sara Gottlieb on whether science can explain the human mind. As Tania wrote, this was a survey-based study asking the participants "whether they thought it was possible for science to one day fully explain various aspects of the human mind, from depth perception and memory loss to spirituality and romantic love." On average, the study found, people judged that certain mental phenomena — such as depth perception or the sense of touch — to be "much more amenable to scientific explanation than others — such as feeling pride or experiencing love at first sight." According to the participants, the dividing line separating what science can and cannot explain seems to be the perception that some mental phenomena, for example, religious devotion and complex decision-making, "involved an internal experience accessible through introspection" that distinguishes us from other animals that share with us sensorial experiences, such as seeing and hearing. As Tania remarked, these findings "don't tell us what science can or can't explain. They tell us about the beliefs about what science can and can't explain." The question, then, is: "What do people think explains the human mind, if not science?" This is an interesting point that merits further discussion. Is the mind explainable? © 2017 npr

Keyword: Consciousness
Link ID: 24379 - Posted: 11.30.2017

By Helen Branswell, What many hope will be the final chapter in an unfortunate saga in multiple sclerosis research appears to have been written by the scientist who started the affair in the first place. Italian physician Paolo Zamboni has publicly acknowledged that a therapy he developed and dubbed “the liberation treatment” does not cure or mitigate the symptoms of MS. A randomized controlled trial—the gold standard of medical research—he and other Italian researchers conducted concluded the procedure is a “largely ineffective technique” that should not be recommended for MS patients. The trial’s result comes as no surprise to neurologists, most of whom felt Zamboni’s theory lacked plausibility from the moment news of it exploded through the MS community in 2009. Advertisement Many of those same neurologists, though, saw their relationships with their patients fractured as belief in the liberation therapy took hold in the community of patients and their families in Canada, parts of the United States, and farther afield. Doctors advising caution against a procedure that hadn’t been proved to work or even to be safe were derided as standing in the way of innovation to protect their own practices. Dr. Jock Murray, an MS expert and retired professor from Dalhousie University in Halifax, Nova Scotia, said the history of MS is laden with incidences like the Zamboni episode—though he said this one lasted longer than most. © 2017 Scientific American,

Keyword: Multiple Sclerosis
Link ID: 24378 - Posted: 11.30.2017

By NICHOLAS BAKALAR The daughters of women exposed to childhood trauma are at increased risk for serious psychiatric disorders, a new study concludes. Researchers studied 46,877 Finnish children who were evacuated to Sweden during World War II, between 1940 and 1944. They tracked the health of their 93,391 male and female offspring born from 1950 to 2010. The study, in JAMA Psychiatry, found that female children of mothers who had been evacuated to Sweden were twice as likely to be hospitalized for a psychiatric illness as their female cousins who had not been evacuated, and more than four times as likely to have depression or bipolar disorder. But there was no effect among male children, and no effect among children of either sex born to fathers who had been evacuated. The most obvious explanation would be that girls inherited their mental illness from their mothers, but the researchers controlled for parental psychiatric disorder and the finding still held. The lead author, Torsten Santavirta, an associate professor of economics at Uppsala University, said that it is possible that traumatic events cause changes in gene expression that can then be inherited, but the researchers did not have access to genetic information. “The most important takeaway is that childhood trauma can be passed on to offspring,” Dr. Santavirta said, “and the wrinkle here is that these associations are sex-specific.” © 2017 The New York Times Company

Keyword: Stress; Epigenetics
Link ID: 24377 - Posted: 11.30.2017

By Shawna Williams Neurodegenerative diseases are tough nuts to crack, not just because of the inherent difficulties of sorting through what has gone awry, and why, but also due to a dearth of biomarkers that could help spot the diseases and track their progression. This inability to easily diagnose many forms of neurodegeneration means that the diseases can’t be treated early in their progression. The lack of biomarkers also hinders the certainty with which researchers running clinical trials can assess whether and how well experimental treatments of the diseases are working. A simple, noninvasive eye scan now being developed for Alzheimer’s disease (AD), however, may help address both shortcomings. AD researchers already utilize amyloid positron emission tomography (PET), in which tracers are injected into patients’ brains to make the disease’s characteristic amyloid plaques detectable by PET imaging. But the scans are very expensive, spurring the continuing hunt for biomarkers. “What we now know is that the disease essentially occurs about 20 years before a patient becomes symptomatic,” says Cedars-Sinai Medical Center neuroscientist and neurosurgeon Keith Black. “And by the time one is symptomatic, they’ve already lost a lot of their brain weight; they’ve already lost a significant number of brain cells; they’ve already lost a significant amount of connectivity.” What’s needed, he says, is a way to detect the disease early so it can be treated—with drugs, lifestyle interventions, or both—before it’s too late. © 1986-2017 The Scientist

Keyword: Alzheimers; Vision
Link ID: 24376 - Posted: 11.29.2017

Terry Gross This is FRESH AIR. I'm Terry Gross. Here's how my guest describes his work. He writes, (reading) I am an anesthesiologist. I erase consciousness, deny memories, steal time, immobilize the body. I alter heart rate, blood pressure and breathing, and then I reverse these effects. I eliminate pain during a procedure, and I prevent it afterwards. I care for sick people, and I have saved lives, but it's rare that I'm the actual healer. That's from the opening of Dr. Henry Jay Przybylo's new memoir, "Counting Backwards: A Doctor's Notes On Anesthesia." He specializes in pediatric anesthesiology and estimates he treats about 1,000 children a year from micropreemies (ph) to teenagers. He's dealt with benign conditions, like the removal of a skin mole, as well as potentially fatal ones, like clipping a cerebral artery aneurism and heart transplants. He's also an associate professor at the Northwestern University School of Medicine. Dr. Przybylo, welcome to FRESH AIR. Your book is called "Counting Backwards." So why do anesthesiologists ask patients to count backwards from 100? HENRY JAY PRZYBYLO: You know, I'm not sure. I searched the Internet and everything to try and find the answer to that, and the closest I can come to is that around 1940s, we came up - medicines were developed to induce anesthesia that were given through veins - IV - and they were extremely quick-acting. And I think sometime, some anesthesiologist somewhere just wanted to see how long it would take and asked the patient to start counting backwards from a hundred, realizing they never made it out of the 90s before they were anesthetized, and I think that just stuck. © 2017 npr

Keyword: Sleep
Link ID: 24375 - Posted: 11.29.2017

By Shawna Williams While humans aren’t as smell-dependent as many other animals, studies have shown we respond differently to others when they’re emitting certain olfactory signals—even if we can’t consciously detect them. In a study published today in Nature Neuroscience, researchers find that men with autism spectrum disorder (ASD) sometimes respond differently to these chemical cues in human sweat than do people without the disorder, indicating that such responses may partly explain the disorder’s symptoms. In one experiment, the researchers asked 20 men with ASD and 20 typical men to perform cognitive tasks while they smelled either pads with sweat from skydivers (which contained high levels of cortisol, indicating fearfulness), or pads with no sweat. Just a few participants in each group reported being able to consciously detect scent from the sweat-infused pads, but the men in the non-ASD group showed an increase in electrodermal activity, a proxy for an aroused nervous system, while ASD participants did not. To see what effect the smell of fear might have on behavior, the researchers rigged up two mannequins to “talk” and emit the odor of either fear-related sweat or workout sweat. Participants received clues from the mannequins on how to complete a task, and the researchers measured their performance on the task as a measure of trust. “[W]e observed a dissociation whereby [typically developed] participants had increased trust in the control-smell [mannequin], yet ASD participants had increased trust in the fear-smell [mannequin],” the study’s authors write. © 1986-2017 The Scientist

Keyword: Autism; Chemical Senses (Smell & Taste)
Link ID: 24374 - Posted: 11.29.2017

By R. Douglas Fields While examining brain tissue through a microscope of hospital patients in the 1930’s, Hungarian neuropathologist Ladislaus Meduna made an intriguing observation: Brain cells, called glia, increased greatly in tissue taken from people with epilepsy. But samples from patients with schizophrenia and depression had far fewer glia in the cerebral cortex than normal. Unlike neurons, glia cannot fire electrical impulses, so they were (and still are) largely ignored by most neuroscientists. But Meduna speculated that schizophrenia and depression might result from a deficiency of glial cells, so he reasoned that by inducing a seizure, he could increase their numbers and cure his patients. On January 23, 1934, he induced a violent seizure in a man who was hopelessly catatonic from schizophrenia by injecting a chemical, camphor, into the man’s bloodstream. The injection induced an explosive seizure that wracked the man’s body for a full minute. Meduna’s legs gave out in shock after he saw what he had done. The scientist collapsed and two nurses had to help him back to his apartment to recover. Undeterred, Meduna four days later induced another seizure in the same man—who for four years had never spoken or moved and who had been fed continuously through a tube. By the fifth seizure he induced on February 10, 1934, the man awoke, dressed himself, requested breakfast and greeted Meduna cheerfully by name. “I hear them talking that you were going to make some crazy experiment? Did you do it?” he asked This success inspired others: Ugo Cerletti and Lucio Bini in Italy used electricity to induce a seizure by applying electrodes they had obtained from a pig slaughterhouse to the head of one of their mental patients on April 11, 1938. Did the patient get better? In some cases, patients who underwent these primitive procedures experienced improved mental states noticeably. But they could also induce violent, whole-body contractions that sometimes dislocated joints and broke bones. © 2017 Scientific American

Keyword: Depression
Link ID: 24373 - Posted: 11.28.2017

Richard Easterbrook The news that left-handers excel at some sports but not others confirmed my thoughts that the 10% of people that make up us southpaws are used to punching above our weight. A study published in the journal Biology Letters concludes that being left-handed is an advantage in sports where time pressures are particularly severe – such as table tennis, or cricket, or squash. I am the exception to the rule – I manage to be equally rubbish at any sport regardless of whether it be fast or slow. My PE teacher told me at least I had one good tennis shot in me, but I felt that was a backhanded compliment. But if we left-handers lead at sports such as cricket or tennis, it is yet to make up for the inequality we face in everyday life. I always held dear the fact I was born a left-hander. It felt like a little badge of honour, like having a little superpower. To this day, I find myself scanning the room to seek out kindred spirits and upon discovering a fellow left-hander, giving them a knowing wink and a smile. Conversely, I find I am unfairly judged by right-handed folk. “Oh, you’re a lefty,” they say in a tone that would normally be reserved for someone with a terminal illness. In fact, many right-handers still mistakenly believe that left-handed people die younger, a theory long since debunked, thankfully. Meeting people for the first time is difficult, especially those who offer a handshake at the earliest opportunity from their right side. You either have to accept it and lead with your weaker right hand and face being judged poorly for dispatching such a weedy handshake, or persist with offering the left hand which then forces your new acquaintance with having to put down whatever they are holding in their left hand in order to fulfil a frankly quirky social custom. Why can’t we bump chests and be done with it? © 2017 Guardian News and Media Limited

Keyword: Laterality
Link ID: 24372 - Posted: 11.28.2017

By BENEDICT CAREY The recent surge in accusations of sexual harassment and assault has prompted some admitted offenders to seek professional help for the emotional or personality distortions that underlie their behavior. “My journey now will be to learn about myself and conquer my demons,” the producer Harvey Weinstein said in a statement in October. The actor Kevin Spacey announced that he would be “taking the time necessary to seek evaluation and treatment.” Whatever mix of damage control and contrition they represent, pledges like these suggest that there are standard treatments for perpetrators of sexual offenses. In fact, no such standard treatments exist, experts say. Even the notion of “sexual addiction” as a stand-alone diagnosis is in dispute. “There are no evidence-based programs I know of for the sort of men who have been in the news recently,” said Vaile Wright, director of research and special projects at the American Psychological Association. That doesn’t mean that these men cannot change their ways with professional help. The evidence that talk therapy and medication can curb sexual misconduct is modest at best, and virtually all of it comes from treating severe disorders, like pedophilia and exhibitionism, experts said — powerful urges that cannot be turned off. Still, there is reason to think that these therapeutic approaches can be adapted to treatment of the men accused of offenses ranging from unwanted attention to rape. “You’re really looking at two categories of people,” said Rory Reid, an assistant professor of psychiatry at the University of California, Los Angeles, who has a clinical practice focusing on sexual problems. “One is what I call sexually compulsive behavior. The other is reserved for people committing non-consensual acts — sex offenders.” The first group includes the college student failing out because he spends all his time surfing porn sites, or the man who is visiting prostitutes so often it’s threatening his livelihood and health. © 2017 The New York Times Company

Keyword: Sexual Behavior; Aggression
Link ID: 24371 - Posted: 11.28.2017

By Claudia Wallis American parents have been warning teenagers about the dangers of marijuana for about 100 years. Teenagers have been ignoring them for just as long. As I write this, a couple of kids are smoking weed in the woods just yards from my office window and about a block and a half from the local high school. They started in around 9 A.M., just in time for class. Exaggerating the perils of cannabis—the risks of brain damage, addiction, psychosis—has not helped. Any whiff of Reefer Madness hyperbole is perfectly calibrated to trigger an adolescent's instinctive skepticism for whatever an adult suggests. And the unvarnished facts are scary enough. We know that being high impairs attention, memory and learning. Some of today's stronger varieties can make you physically ill and delusional. But whether marijuana can cause lasting damage to the brain is less clear. Advertisement A slew of studies in adults have found that nonusers beat chronic weed smokers on tests of attention, memory, motor skills and verbal abilities, but some of this might be the result of lingering traces of cannabis in the body of users or withdrawal effects from abstaining while taking part in a study. In one hopeful finding, a 2012 meta-analysis found that in 13 studies in which participants had laid off weed for 25 days or more, their performance on cognitive tests did not differ significantly from that of nonusers. © 2017 Scientific American

Keyword: Drug Abuse; Schizophrenia
Link ID: 24370 - Posted: 11.28.2017

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