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Vaughan Bell For thousands of years, direct studies of the human brain required the dead. The main method of study was dissection, which needed, rather inconveniently for the owner, physical access to their brain. Despite occasional unfortunate cases where the living brain was exposed on the battlefield or the surgeon's table, corpses and preserved brains were the source of most of our knowledge. When brain scanning technologies were invented in the 20th century they allowed the structure and function of the brain to be shown in living humans for the first time. This was as important for neuroscientists as the invention of the telescope and the cadaver slowly faded into the background of brain research. But recently, scrutiny of the post-mortem brain has seen something of a revival, a resurrection you might say, as modern researchers have become increasingly interested in applying their new scanning technologies to the brains of the deceased. Forensic pathologists have the job of working out the cause and manner of death to present as legal evidence and have been partly responsible for this curious full circle. One of their main jobs is the autopsy, where the pathologist examines the body, inside and out, to assess its condition at the point of death. Although the traditional autopsy has many advantages, not least the microscopic examination of body tissue, there are drawbacks. One is that within some religions cutting up the dead body is seen as an infringement of human dignity and may delay burial beyond the customary period. The other is that an autopsy is a one-shot deal. If someone disagrees with the way it has been carried out or its interpretation, it is usually too late to do anything except re-examine photos or, on the rare occasions when they may have been kept, tissue samples. © 2014 Guardian News and Media Limited
Keyword: Brain imaging
Link ID: 19970 - Posted: 08.18.2014
by Andy Coghlan Pioneering studies of post-mortem brain tissues have yielded the first evidence of a potential association between Alzheimer's disease and the epigenetic alteration of gene function. The researchers stress, however, that more research is needed to find out if the changes play a causal role in the disease or occur as a result of it. We already have some evidence that the risk of developing Alzheimer's might be elevated by poor diet, lack of exercise, and inflammatory conditions such as diabetes, obesity and clogging of blood vessels with fatty deposits. The new research hints that the lifestyle changes that raise Alzheimer's risk may be taking effect through epigenetic changes. The idea is strengthened by the fact that the brain tissue samples studied in the new work came from hundreds of people, many of whom had Alzheimer's when they died, and that a number of genes identified were found by two teams working independently, one in the UK and one in the US. "The results are compelling and consistent across four cohorts of patients taken across the two studies," says Jonathan Mill at the University of Exeter, who led the UK-based team. "It's illuminated new genetic pathways affecting the disease and, given the lack of success tackling Alzheimer's so far, new leads are going to be vital." "We can now focus our efforts on understanding how these genes are associated with the disease," says Philip De Jager of the Brigham and Women's Hospital in Boston, who headed the US team. © Copyright Reed Business Information Ltd.
By Victoria Gill Science reporter, BBC News Scientists in Brazil have managed to eavesdrop on underwater "turtle talk". Their recordings have revealed that, in the nesting season, river turtles appear to exchange information vocally - communicating with each other using at least six different sounds. This included chatter recorded between females and hatchlings. The researchers say this is the first record of parental care in turtles. It shows they could be vulnerable to the effects of noise pollution, they warn. The results, published recently in the Journal Herpetologica, include recordings of the strange turtle talk. They reveal that the animals may lead much more socially complex lives than previously thought. The team, including researchers from the Wildlife Conservation Society (WCS) and the National Institute of Amazonian Research carried out their study on the Rio Trombetas in the Amazon between 2009 and 2011. They used microphones and underwater hydrophones to record more than 250 individual sounds from the animals. The scientists then analysed these vocalisations and divided them into six different types, correlating each category with a specific behaviour. Dr Camila Ferrara, of the WCS Brazil programme, told BBC News: "The [exact] meanings aren't clear... but we think they're exchanging information. "We think sound helps the animals to synchronise their activities in the nesting season," she said. The noises the animals made were subtly different depending on their behaviour. For example, there was a specific sound when adults were migrating through the river, and another when they gathered in front of nesting beaches. There was a different sound again made by adults when they were waiting on the beaches for the arrival of their hatchlings. BBC © 2014
|By Christie Nicholson Children who experience neglect, abuse and poverty have a tougher time as adults than do well-cared-for kids. Now there’s evidence that such stress can actually change the size of brain structures responsible for learning, memory and processing emotion. The finding is in the journal Biological Psychiatry. [Jamie L. Hanson et al, Behavioral Problems After Early Life Stress: Contributions of the Hippocampus and Amygdala] Researchers took images of the brains of 12-year-olds who had suffered either physical abuse or neglect or had grown up poor. From the images the scientists were able to measure the size of the amygdala and hippocampus—two structures involved in emotional processing and memory. And they compared the sizes of these structures with those of 12-year-old children who were raised in middle-class families and had not been abused. And they found that the stressed children had significantly smaller amygdalas and hippocampuses than did the kids from the more nurturing environments. Early stress has been associated with depression, anxiety, cancer and lack of career success later on in adulthood. This study on the sizes of brain regions may offer physiological clues to why what happens to toddlers can have such a profound impact decades later. © 2014 Scientific American
Ian Sample, science editor Scientists have prevented muscle wastage in mice with a form of muscular dystrophy by editing the faulty gene that causes the disease. The radical procedure could not be performed in humans, but researchers believe the work raises hopes for future gene-editing therapies to stop the disease from progressing in people. Duchenne muscular dystrophy is caused by mutations in a gene on the X chromosome and affects around one in 3,500 boys. Because girls have two X chromosomes they tend not to be affected, but can be carriers of the disease. The pivotal gene is used to make a protein called dystrophin which is crucial for muscle fibre strength. Without the protein, muscles in the body, including the heart and skeletal muscles, weaken and waste away. Most patients die by the age of 25 from breathing or heart problems. Researchers in the US used a powerful new gene-editing procedure called CRISPR to correct mutations in the dystrophin gene in mice that were destined to develop the disease. They extracted mouse embryos from their mothers and injected them with the CRISPR biological machinery, which found and corrected the faulty gene. After the injections, the mouse embryos were reimplanted in females and carried to term. Tests on the mice found that the therapy helped to restore levels of dystrophin, and that their skeletal muscle performed normally, even when only 17% of their cells contained corrected genes. The procedure could not be done in humans, but the proof-of-principle experiment demonstrates that correcting only a small proportion of cells could lead to a dramatic improvement for patients. © 2014 Guardian News and Media Limited
Ever wonder why it’s hard to focus after a bad night’s sleep? Using mice and flashes of light, scientists show that just a few nerve cells in the brain may control the switch between internal thoughts and external distractions. The study, partly funded by the National Institutes of Health, may be a breakthrough in understanding how a critical part of the brain, called the thalamic reticular nucleus (TRN), influences consciousness. “Now we may have a handle on how this tiny part of the brain exerts tremendous control over our thoughts and perceptions,” said Michael Halassa, M.D., Ph.D., assistant professor at New York University’s Langone Medical Center and a lead investigator of the study. “These results may be a gateway into understanding the circuitry that underlies neuropsychiatric disorders.” The TRN is a thin layer of nerve cells on the surface of the thalamus, a center located deep inside the brain that relays information from the body to the cerebral cortex. The cortex is the outer, multi-folded layer of the brain that controls numerous functions, including one’s thoughts, movements, language, emotions, memories, and visual perceptions. TRN cells are thought to act as switchboard operators that control the flow of information relayed from the thalamus to the cortex. To understand how the switches may work, Dr. Halassa and his colleagues studied the firing patterns of TRN cells in mice during sleep and arousal, two states with very different information processing needs. The results published in Cell, suggest that the TRN has many switchboard operators, each dedicated to controlling specific lines of communication. Using this information, the researchers could alter the attention span of mice.
By Rachel Feltman At every waking moment, your brain is juggling two very different sets of information. Input from the world around you, like sights and smells, has to be processed. But so does internal information — your memories and thoughts. Right now, for example, I’m looking at a peach: It’s yellow and pink, and has a lot of fuzz. But I also know that it smells nice (a personal assessment) and I’m imagining how good it will taste, based on my previous experience with fragrant pink fruits. The brain’s ability to handle these different signals is key to cognitive function. In some disorders, particularly autism and schizophrenia, this ability is disrupted. The brain has difficulty keeping internal and external input straight. In a new study published Thursday in Cell, researchers observe the switching method in action for the first time. While the research used mice, not humans, principal investigator and NYU Langone Medical Center assistant professor Michael Halassa sees this as a huge step toward understanding and manipulating the same functions in humans. “This is one of the few moments in my life where I’d actually say yes, absolutely this is going to translate to humans,” Halassa said. “This isn’t something based on genes or molecules that are specific to one organism. The underlying principles of how the brain circuitry works are likely to be very similar in humans and mice.” That circuitry has been hypothesized for decades. Neurologists know that the cortex of the brain is responsible for higher cognitive functions, like music and language. And the thalamus, which is an egg-like structure in the center of the brain, works to direct the flow of internal and external information before it gets to the cortex.
by Bethany Brookshire The clearish lump looks like some bizarre, translucent gummy candy that might have once been piña colada flavored. But this is something you definitely don’t want to eat. That see-through blob was once a mouse. In the Aug. 14 Cell, scientists at Caltech detail the difficult series of methods required to make small animals such as mice and rats completely translucent. Scientists have been trying to clear tissue for better observation since the 1800s, and, as with all science, the new techniques build on many previous experiments done in a variety of labs. The techniques make it possible to capture images both beautiful and gross. And the procedure will teach scientists more about anatomy than ever before. If you want to render an animal transparent, you first have to overcome a solid problem: lipids. This group includes molecules essential to life, such as fats, cholesterols, waxes and steroids. Lipids form the membranes that surround our cells, the hormones that make us grow and reproduce and much, much more. But lipids have a problem. You can’t see through them. So to render an organism transparent, you need to remove the lipids. Bin Yang and colleagues in Viviana Gradinaru’s lab at Caltech used detergents to dissolve the lipids. The technique is based on CLARITY, a method that Gradinaru helped to develop in Karl Deisseroth’s lab at Stanford. Scientists there rendered a mouse brain transparent using CLARITY. Gradinaru explains that for a clear organ, dissolving lipids alone alone isn’t enough. “Without lipids the tissue would just collapse, so we need to maintain the structure of the tissue,” she says. © Society for Science & the Public 2000 - 2013
Keyword: Brain imaging
Link ID: 19963 - Posted: 08.16.2014
By Kate Yandell Researchers have accumulated detailed knowledge of the neurons that drive male fruit flies’ mating behaviors. But the neurons that prompt females to respond—or not—to male overtures have been less-studied. Three papers published today (July 2) in Neuron and Current Biology begin to change that. They identify sets of neurons in female fruit flies that help process mating signals, modulate the insects’ receptivity to male courtship, and drive mating behavior. “These three groups independently identified important neuronal groups [that] are positioned in different points in the neuronal circuitry for regulating female receptivity,” said Daisuke Yamamoto, a behavioral geneticist at Tohoku University in Japan who was not involved in any of the studies. “We’ve had access to the male circuitry for a while now, and that’s turning out to be a really interesting way to study how behavior works,” said Jennifer Bussell, whose work as a PhD student at Rockefeller University contributed to the Current Biology paper. “Having that complementary circuit in the female can only provide more fodder for interesting experiments.” Female fruit flies’ mating behaviors depend on their reproductive state. They become receptive to mating as they mature, but become less receptive to males’ advances immediately after mating. If a female fruit fly is receptive to mating, she responds to male pheromones and courtship songs by engaging in a behavior called pausing, where she stops in her tracks near males so they can mount her and she opens her vaginal plates—hard coverings that protect her reproductive tract. © 1986-2014 The Scientist
Keyword: Sexual Behavior
Link ID: 19962 - Posted: 08.16.2014
By Lenny Bernstein Comedian Robin Williams was grappling with severe depression when he committed suicide Monday, and on Thursday we learned that he also was in the early stages of Parkinson's disease. Sadly, the two conditions are often found together. In a 2012 study conducted by the National Parkinson Foundation, 61 percent of 5,557 Parkinson's patients surveyed reported that they also suffered from depression, with symptoms that ranged from mild to severe. Both conditions are associated with a shortage of dopamine, a neurotransmitter that helps regulate movement and control the brain's pleasure center. "Dopamine is a feel-good chemical. If you are low in dopamine, you are not going to feel so good," said Joyce Oberdorf, president and CEO of the National Parkinson Foundation. "There are [also] other neurotransmitters that can be low." A separate study published Friday found that newly-diagnosed Parkinson's patients have higher rates of depression, anxiety, fatigue, and apathy than a control group of people without Parkinson's. Researchers from the Raymond and Ruth Perelman School of Medicine at the University of Pennsylvania found that 13.9 percent of patients had symptoms of depression when they were diagnosed with Parkinson's, a proportion that rose to 18.7 percent after 24 months. Just 6.6 percent of people without the disease had depression, and that dropped to just 2.4 percent after 24 months. Despite their depressive symptoms, most of the Parkinson's patients who also had that condition were not treated with anti-depressants at any point in the two-year study. The findings were published in the journal Neurology.
By Rebecca Boyle Like a dog wagging its tail in anticipation of treats to come, dolphins and belugas squeal with pleasure at the prospect of a fish snack, according to a new study. It’s the first direct demonstration of an excitement call in these animals, says Peter Madsen, a biologist at Aarhus University in Denmark who was not involved in the study. To hunt and communicate, dolphins and some whale species produce a symphony of clicks, whistles, squeaks, brays, and moans. Sam Ridgway, a longtime marine biologist with the U.S. Navy’s Marine Mammal Program, says he heard distinctive high-pitched squeals for the first time in May 1963 while training newly captured dolphins at the Navy’s facility in Point Mugu, California. “We were throwing fish in, and each time they would catch a fish, they would make this sound,” he says. He describes it as a high-pitched “eeee,” like a child squealing in delight. Ridgway and his collaborators didn’t think much of the sound until later in the 1960s, when dolphins trained to associate a whistle tone with a task or behavior also began making it. Trainers teach animals a task by rewarding them with a treat and coupling it with a special noise, like a click or a whistle. Eventually only the sound is used, letting the animal know it will get a treat later. The whistle was enough to provoke a victory squeal, Ridgway says. Meanwhile, beluga whales would squeal after diving more than 600 meters to switch off an underwater speaker broadcasting tones. “As soon as the tone went off, they would make this same sound,” Ridgway says, “despite the fact that they’re not going to get a reward for five minutes.” He also heard the squeal at marine parks in response to trainers’ whistles. © 2014 American Association for the Advancement of Science.
Greta Kaul It was a rainy day, and earthworms wriggled out of the ground and began to arrange themselves on the pavement as Julian Plumadore walked to his community college zoology class in 1991. They spelled out messages only he could read. "I was very frightened to be a custodian of that kind of cosmic information and be able to do absolutely nothing about it," Plumadore said. Other times, there were voices - demons screaming - telling him he was going to hell. Plumadore was eventually diagnosed as having schizoaffective disorder, a psychosis that combines the hallucinations of schizophrenia with a mood disorder like depression. People with psychotic disorders, of which schizophrenia is the most severe, have hallucinations, like the voices Plumadore was hearing, that are divorced from reality. Now, a Stanford researcher suggests that the voices he experienced might have been different if he had grown up somewhere other than the U.S. If he were from India, he might have heard family members telling him to do household chores. If he were from Ghana, he might have heard the voice of God guiding him. For a study published in June, Tanya Luhrmann, a Stanford anthropologist, and other researchers interviewed 60 people who met the criteria for schizophrenia: 20 from in and around San Mateo, 20 from India and 20 from Ghana. Though the patients heard both positive and negative voices no matter where they were from, those in India and in Ghana tended to have less negative experiences than Americans: They could more often identify who was talking to them and had less violent hallucinations. Though the study isn't conclusive, Luhrmann believes the differences in voice-hearing between cultures may be a clue into how social expectations and environment shape the way people hear those imaginary voices. © 2014 Hearst Communications, Inc.
Hearing voices is an experience that is very distressing for many people. Voices – or “auditory verbal hallucinations” – are one of the most common features of schizophrenia and other psychiatric disorders. But for a small minority of people, voice-hearing is a regular part of their lives, an everyday experience that isn’t associated with being unwell. It is only in the past 10 years that we have begun to understand what might be going on in “non-clinical” voice-hearing. Most of what we know comes from a large study conducted by Iris Sommer and colleagues at UMC Utrecht in the Netherlands. In 2006 they launched a nationwide attempt to find people who had heard voices before but didn’t have any sort of psychiatric diagnosis. From an initial response of over 4,000 people, they eventually identified a sample of 103 who heard voices at least once a month, but didn’t have psychosis. Their voice-hearing was also not caused by misuse of drugs or alcohol. Twenty-one of the participants were also given an MRI scan. When this group was compared with voice-hearers who did have psychosis, many of the same brain regions were active for both groups while they were experiencing auditory hallucinations, including the inferior frontal gyrus (involved in speech production) and the superior temporal gyrus (linked to speech perception). Subsequent studies with the same non-clinical voice-hearers have also highlighted differences in brain structure and functional connectivity (the synchronisation between different brain areas) compared with people who don’t hear voices. These results suggest that, on a neural level, the same sort of thing is going on in clinical and non-clinical voice-hearing. We know from first-person reports that the voices themselves can be quite similar, in terms of how loud they are, where they are coming from, and whether they speak in words or sentences. © 2014 Guardian News and Media Limited
By Jen Christiansen I threw down a bit of a challenge last month at the Association of Medical Illustrators Conference in Minnesota. But first, I had to—somewhat unexpectedly—accept some challenges presented by others. And face the reality that some of us simply do not have the constitution of an anatomist. I love classic anatomical illustrations such as the vintage works of Andreas Vesalius and the more modern stylings of Frank Netter. And on that front, this conference definitely delivered. Talks by Daniel Garrison and Francine Netter were drool-worthy, and I snapped photos of quickly advancing slides presented by W. Bruce Fye on the history of the illustrated heart, so I could reverse-image search them later and spend more time checking out the details and context. Videos of Robert Beverly Hale’s Art Students League lectures on anatomy charmed me (as presented by Glen Hintz), as well as new videos of clean architectural microstructures like the inner ear, presented by Robert Acland. I had to make myself walk quickly by one vendor table to avoid blowing my book budget for the year (and then some) on an impulse buy of Vesalius’ 1543 De Humani Corporis Fabrica, newly translated to English. But I averted my gaze when surgeons presented on the topic of facial transplantation and skull reconstruction. Shoot, I couldn’t even look at the screen through the entirety of a fascinating talk by Elizabeth Weissbrod and Valerie Henry on creating and using virtual and prosthetic simulations for military emergency response training. I avoided the hands-on human cadaveric dissection workshop sessions, telling myself and others that my travel schedule would simply not allow me to get to the Mayo Clinic in Rochester, Minn., early enough to participate or observe. © 2014 Scientific American
Keyword: Brain imaging
Link ID: 19957 - Posted: 08.14.2014
The news of Robin Williams’s suicide has brought mental health into the spotlight this week. According to data from the Massachusetts Violent Death Reporting System at the department of public health, the number of deaths per year as a result of suicide in the state has increased 4 percent per year since 2003. The rate increased from 424 suicides in 2003 to a peak of 600 in 2010, before dropping back down to 588. That’s 8.9 suicides per 100,000, a total of 4,500 deaths for this preventable public health problem. There are many biological, sociological, and psychological risk factors that can increase an individual’s risk for committing suicide. But did you know that poor sleep could be a major factor pushing people over the edge, even if they aren’t depressed? We all know the feeling that when we’re under slept, we aren’t quite ourselves, but according to the Substance Abuse and Mental Health Services Administration, sleep complaints are actually one of the top 10 warning signs for suicide. A study published today in JAMA Psychiatry is the first research of its kind to draw a correlation between poor sleep habits and an increased risk for death by suicide by controlling for signs of depression. Stanford University School of Medicine researchers have found that over a 10 year observation period, people with poor sleep quality and no other depressive symptoms demonstrated a 1.2 times greater risk for death by suicide.
By NICHOLAS BAKALAR A new study reports that caffeine intake is associated with a reduced risk for tinnitus — ringing or buzzing in the ears. Researchers tracked caffeine use and incidents of tinnitus in 65,085 women in the Nurses’ Health Study II. They were 30 to 34 and without tinnitus at the start of the study. Over the next 18 years, 5,289 developed the disorder. The women recorded their use of soda, coffee and tea (caffeinated and not), as well as intake of candy and chocolate, which can contain caffeine. The results appear in the August issue of The American Journal of Medicine. Compared with women who consumed less than 150 milligrams of caffeine a day (roughly the amount in an eight-ounce cup of coffee), those who had 450 to 599 milligrams a day were 15 percent less likely to have tinnitus, and those who consumed 600 milligrams or more were 21 percent less likely. The association persisted after controlling for other hearing problems, hypertension, diabetes, use of anti-inflammatory Nsaid drugs, a history of depression and other factors. Decaffeinated coffee consumption had no effect on tinnitus risk. “We can’t conclude that caffeine is a cure for tinnitus,” said the lead author, Dr. Jordan T. Glicksman, a resident physician at the University of Western Ontario. “But our results should provide some assurance to people who do drink caffeine that it’s reasonable to continue doing so.” © 2014 The New York Times Company
Link ID: 19955 - Posted: 08.14.2014
by Catherine Brahic Think crayfish and you probably think supper, perhaps with mayo on the side. You probably don't think of their brains. Admittedly, crayfish aren't known for their grey matter, but that might be about to change: they can grow new brain cells from blood. Humans can make new neurons, but only from specialised stem cells. Crayfish, meanwhile, can convert blood to neurons that resupply their eyestalks and smell circuits. Although it's a long way from crayfish to humans, the discovery may one day help us to regenerate our own brain cells. Olfactory nerves are continuously exposed to damage and so naturally regenerate in many animals, from flies to humans, and crustaceans too. It makes sense that crayfish have a way to replenish these nerves. To do so, they utilise what amounts to a "nursery" for baby neurons, a little clump at the base of the brain called the niche. In crayfish, blood cells are attracted to the niche. On any given day, there are a hundred or so cells in this area. Each cell will split into two daughter cells, precursors to full neurons, both of which migrate out of the niche. Those that are destined to be part of the olfactory system head to two clumps of nerves in the brain called clusters 9 and 10. It's there that the final stage of producing new smell neurons is completed. © Copyright Reed Business Information Ltd.
|By Melinda Wenner Moyer For most people, “fat,” particularly the kind that bulges under the skin, is a four-letter word. It makes our thighs jiggle; it lingers despite our torturous attempts to eliminate it. Too much of it increases our risk for heart disease and type 2 diabetes (the most common form of the condition). For decades researchers have looked for ways to reduce our collective stores of fat because they seemed to do more harm than good. But biology is rarely that simple. In the late 2000s several research groups independently discovered something that shattered the consensus about the absolute dangers of body fat. Scientists had long known that humans produce at least two types of fat tissue—white and brown. Each white fat cell stores energy in the form of a single large, oily droplet but is otherwise relatively inert. In contrast, brown fat cells contain many smaller droplets, as well as chestnut-colored molecular machines known as mitochondria. These organelles in turn burn up the droplets to generate heat. Babies, who have not yet developed the ability to shiver to maintain their body temperature, rely on thermogenic deposits of brown fat in the neck and around the shoulders to stay warm. Yet investigators assumed that all brown fat disappears during childhood. The new findings revealed otherwise. Adults have brown fat, too. Suddenly, people started throwing around terms like holy grail to describe the promise of brown fat to combat obesity. The idea was appealingly simple: if researchers could figure out how to incite the body to produce extra brown fat or somehow rev up existing brown fat, a larger number of calories would be converted into heat, reducing deposits of white fat in the process. © 2014 Scientific American
Link ID: 19953 - Posted: 08.13.2014
By GRETCHEN REYNOLDS Regular exercise may alter how a person experiences pain, according to a new study. The longer we continue to work out, the new findings suggest, the greater our tolerance for discomfort can grow. For some time, scientists have known that strenuous exercise briefly and acutely dulls pain. As muscles begin to ache during a prolonged workout, scientists have found, the body typically releases natural opiates, such as endorphins, and other substances that can slightly dampen the discomfort. This effect, which scientists refer to as exercise-induced hypoalgesia, usually begins during the workout and lingers for perhaps 20 or 30 minutes afterward. But whether exercise alters the body’s response to pain over the long term and, more pressing for most of us, whether such changes will develop if people engage in moderate, less draining workouts, have been unclear. So for the new study, which was published this month in Medicine & Science in Sports & Exercise, researchers at the University of New South Wales and Neuroscience Research Australia, both in Sydney, recruited 12 young and healthy but inactive adults who expressed interest in exercising, and another 12 who were similar in age and activity levels but preferred not to exercise. They then brought all of them into the lab to determine how they reacted to pain. Pain response is highly individual and depends on our pain threshold, which is the point at which we start to feel pain, and pain tolerance, or the amount of time that we can withstand the aching, before we cease doing whatever is causing it. © 2014 The New York Times Company
Keyword: Pain & Touch
Link ID: 19952 - Posted: 08.13.2014
|By Piercarlo Valdesolo In the summer of 2009 I tried to cure homemade sausages in my kitchen. One of the hazards of such a practice is preventing the growth of undesirable molds and diseases such as botulism. My wife was not on board with this plan, skeptical of my ability to safely execute the procedure. And so began many weeks of being peppered with warnings, relevant articles and concerned looks. When the time came for my first bite, nerves were high. My throat itched. My heart raced. My vision blurred. I had been botulized! Halfway through our walk to the hospital I regained my composure. Of course I had not been instantaneously struck by an incredibly rare disease that, by the way, takes at least 12 hours after consumption to manifest and does not share many symptoms with your garden variety anxiety attack. My experience had been shaped by my mindset. A decade of learning about the psychological power of expectations could not inoculate me from its effect. Psychologists know that beliefs about how experiences should affect us can bring about the expected outcomes. Though these “placebo effects” have primarily been studied in the context of pharmaceutical interventions (e.g. patients reporting pain relief after receiving saline they believed to be an analgesic), recent research has shown their strength in a variety of domains. Tell people that their job has exercise benefits and they will lose more weight than their coworkers who had no such belief. Convince people of a correlation between athleticism and visual acuity and they will show better vision after working out . Trick people into believing they are consuming caffeine and their vigilance and cognitive functioning increases. Some evidence shows that such interventions can even mitigate the negative effects of other experiences. For example, consuming placebo caffeine alleviates the cognitive consequences of sleep deprivation. © 2014 Scientific American