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by Andy Coghlan Ten years after the death of everyone's favourite Superman, Christopher Reeve, his son Matthew Reeve is pushing ahead with a spine-tingling clinical trial You're planning a large study of a paralysis treatment that has already helped four young men. What will it entail? This study will include 36 people with spinal cord injuries who will be treated with epidural stimulation – a technique in which a device is used to apply electrical current to the spinal cord. If we see the same results as we did in the first four, this therapy could have a profound impact on thousands of people living with paralysis. It has the potential to become as commonplace as the pacemaker is for cardiac patients. How well has the treatment worked for the four men who have already received it? Prior to epidural stimulation, they had all suffered chronic injuries caused by completely severed spinal cords. All four have seen dramatic improvements, including the ability to voluntarily move their toes, feet, ankles and legs, and even stand at times, when the device is on. One unexpected bonus has been the return of autonomic function, such as bladder and bowel control and sexual function. From a quality-of-life point of view, this is the biggest improvement. Also unexpectedly, these autonomic functions continue in all four men even when the device is switched off, although they still need it to stand, move their legs and do exercises. © Copyright Reed Business Information Ltd.
Posted by Rachel Dolhun, MD, The ability to quit smoking, especially “cold turkey” or on the first attempt, has been heralded as a marker of strong willpower and determination. But could the ease with which one eschews cigarettes also serve as an early sign of Parkinson’s disease (PD)? This is the conclusion drawn by Beate Ritz, MD, PhD, and colleagues from the University of California, Los Angeles in a recent study published in Neurology. Researchers compared lifelong tobacco use, use of nicotine substitutes, and individual’s rating of their difficulty in trying to quit tobacco among 1,808 Danish people with PD and 1,876 control volunteers. They found that those with PD were less inclined to ever pick up the smoking habit, but, even if they did, they were less likely to need nicotine replacement therapies and able to more effortlessly stop smoking cigarettes. Therefore, ease of quitting smoking may be a sign of early PD. This joins a short list of other symptoms — smell loss, constipation and REM sleep behavior disorder — that usually predate diagnosis and are strongly associated with PD. Physicians rely heavily on such information to help confirm the diagnosis of Parkinson’s, given that biomarkers, objective measurements of disease, are currently lacking. Research led by The Michael J. Fox Foundation is ongoing to identify biological markers of PD, which could help diagnose and treat people earlier. In the meantime, doctors must look for symptoms and behaviors to help identify Parkinson’s. Researchers have long known that tobacco use was linked to a lower risk of PD. An ongoing Foundation-funded study is investigating whether nicotine might guard against or slow the progression of PD.
BY Ashley Yeager A protein made by gut bacteria may trigger a chain of interactions in the body that contribute to eating disorders such as anorexia and bulimia. When the protein is produced, the body makes antibodies to bind to it, but the antibodies also attach to a hormone that controls fullness. In tests, mice given bacteria that produce the protein changed how much they ate compared with mice given bacteria that did not make the protein, a new study shows. Researchers also found that the antibodies to the protein were higher in patients with anorexia and bulimia. The results, which appear October 7 in Translational Psychiatry, seem to be some of the earliest to link gut bacteria to eating disorders. © Society for Science & the Public 2000 - 2014.
Keyword: Anorexia & Bulimia
Link ID: 20188 - Posted: 10.11.2014
By Elizabeth Pennisi Four years ago, Igor Spetic lost his right arm in an industrial accident. Doctors outfitted him with a prosthetic arm that restored some function, but they couldn't restore his sense of touch. Without it, simple tasks like picking up a glass or shaking hands became hit-or-miss propositions. The lack of touch also robs Spetic of basic pleasures. “I would love to feel my wife’s hand,” he says. In time, he may regain that pleasure: Two independent research teams have now equipped artificial hands with sensors that send signals to the wearer’s nerves to recreate this missing sense. The sensing technologies work only in the lab, but they have proved durable, and amputees who have tried them, including Spetic, say that they are effective. One technology advances the range of touch sensations available, while the other promises to enable touch through a better way to attach the prosthesis. “All of these results are very positive,” says Mandayam Srinivasan, a neuroengineer at the Massachusetts Institute of Technology in Cambridge, who was not involved in either project. “Each of them fills a piece of the puzzle in terms of [prosthesis] development.” Almost 40 years ago, researchers tried to provide sensory feedback by adding pressure sensors to prostheses that relayed the sensation through electrodes attached to nerves. But for the most part, they just made it seem like the hand was tingling. And durability has been an issue in such efforts, too. In February, Silvestro Micera, a neuroengineer at the Sant'Anna School of Advanced Studies in Pisa, Italy, and the Swiss Federal Institute of Technology in Lausanne and his team showed that it was possible for sensor-equipped prosthetic arms to gently or powerfully grab objects and even to distinguish a round from a square object. But the study lasted just 4 weeks, in part because of the delicate interface with the body. © 2014 American Association for the Advancement of Science.
|By Bret Stetka Multiple sclerosis (MS) is an electrical disorder, or rather one of impaired myelin, a fatty, insulating substance that better allows electric current to bolt down our neurons and release the neurotransmitters that help run our bodies and brains. Researchers have speculated for some time that the myelin degradation seen in MS is due, at least in part, to autoimmune activity against the nervous system. Recent work presented at the MS Boston 2014 Meeting suggests that this aberrant immune response begins in the gut. Eighty percent of the human immune system resides in the gastrointestinal tract. Alongside it are the trillions of symbiotic bacteria, fungi and other single-celled organisms that make up our guts’ microbiomes. Normally everyone wins: The microorganisms benefit from a home and a steady food supply; we enjoy the essential assistance they provide in various metabolic and digestive functions. Our microbiomes also help calibrate our immune systems, so our bodies recognize which co-inhabitants should be there and which should not. Yet mounting evidence suggests that when our resident biota are out of balance, they contribute to numerous diseases, including diabetes, rheumatoid arthritis, autism and, it appears, MS by inciting rogue immune activity that can spread throughout the body and brain. One study presented at the conference, out of Brigham and Women’s Hospital (BWH), reported a single-celled organism called methanobrevibacteriaceae that activates the immune system is enriched in the gastrointestinal tracts of MS patients whereas bacteria that suppress immune activity are depleted. Other work, which resulted from a collaboration among 10 academic researcher centers across the U.S. and Canada, reported significantly altered gut flora in pediatric MS patients while a group of Japanese researchers found that yeast consumption reduced the chances of mice developing an MS-like disease by altering gut flora. © 2014 Scientific American
Keyword: Multiple Sclerosis
Link ID: 20186 - Posted: 10.09.2014
by Colin Barras LOCKED in but not shut out: for the first time people who have lost the ability to move or talk because of a stroke may be able to communicate with their loved ones using a brain-computer interface. Brain injuries can leave people aware but almost completely paralysed, a condition called locked-in syndrome. Brain-computer interfaces (BCIs) can help some people communicate by passing signals from electrodes attuned to their brain activity as they watch a screen displaying letters. Subtle changes in neural activity let researchers know when a person wishes to select a particular on-screen item, allowing them to spell out messages by thought alone. Until now, BCIs have only been tested on healthy volunteers and people with amyotrophic lateral sclerosis, a neurodegenerative disease that leads to muscle wasting. But no one had tested whether the technology could help people locked in after a brain stem stroke. Now Eric Sellers and his colleagues at East Tennessee State University in Johnson City have tested the technique on a 68-year-old man. After more than a year of training he learned to communicate reliably via the BCI. He took the opportunity to thank his wife for her hard work, and to give his thoughts on gift purchases for his children (Science Translational Medicine, DOI: 10.1126/scitranslmed.3007801). © Copyright Reed Business Information Ltd.
BY Sarah Zielinski Bird’s nests come in a wide variety of shapes and sizes, and they’re built out of all sorts of things. Hummingbirds, for instance, create tiny cups just a couple centimeters wide; sociable weavers in Africa, in contrast, work together to build huge nests more than two meters across that are so heavy they can collapse trees. There are nests built on rocky ledges, in mounds on the ground, high in trees and on the edges of buildings. Bowerbirds even construct their nests as tiny houses decorated with an artistic eye to attract the ladies. So perhaps it’s not all that surprising the no one had ever investigated whether birds camouflage their nests to protect their eggs against potential predators. It would make sense that they do, but if you were to test it, where would you start? For Ida Bailey of the University of St. Andrews in Fife, Scotland, and colleagues, the answer was zebra finches. Male finches usually build nests in dense shrubs and layer the outside of the nests with dry grass stems and fine twigs. Predators, usually birds, take a heavy toll on the zebra finches, though. Since birds tend to hunt based on sight rather than smell, camouflaging a nest might work to protect the eggs sequestered inside. And even better, because zebra finches have good color vision, building a camouflaged nest might be possible. So Bailey’s team gathered 21 pairs of zebra finches, some of which were already housed at the University of Glasgow in Scotland, while others were bought from a local pet store. The researchers set each pair up in its own cage. Two walls of the cage were lined with colored paper, and a nest cup was placed in that half of the cage. Then the birds were given two cups containing colored paper — one color that matched the walls and a second contrasting color. The results of the study appear October 1 in The Auk. © Society for Science & the Public 2000 - 2014.
By Erin Allday When the United States’ top public health and political leaders declared the 1990s the “decade of the brain,” Dr. Pratik Mukherjee couldn’t help but feel a little dubious. “I was kind of laughing, because I didn’t think we’d make much progress in just a decade,” said Mukherjee, a neuro-radiologist at UCSF. Twenty-four years later, Mukherjee said he and his peers around the country are primed to plunge into what he’d like to call the century of the brain — a deep dive into the basic biology and mechanics of the impossibly complex organ that controls our every thought, action, behavior and mood. The National Institutes of Health last week announced $47 million in grants as part of President Obama’s Brain Initiative, a project announced 18 months ago to, in the simplest language, reverse-engineer the human brain. The grants were among the first in a roughly 11-year plan that could cost more than $3 billion. Most of the projects are in developing new technologies to help map the brain and study its mechanics — how cells communicate, what makes them turn on and off, and how large regions of the brain interact, for example. Ultimately, scientists hope these tools will help the next generation of neuroscientists solve the brain-centric disorders — from autism and Alzheimer’s to depression and schizophrenia — that have confounded doctors for centuries.
Keyword: Brain imaging
Link ID: 20183 - Posted: 10.09.2014
Patients with schizophrenia are already known to have higher rates of premature death than the general population. The study found that elevated risks of heart disease and metabolic issues such as high blood sugar in people with first episode psychosis are due to an interaction of mental illness, unhealthy lifestyle behaviors and antipsychotic medications that may accelerate these risks. Patients entered treatment with significant health concerns – including excess weight, smoking, and metabolic issues – despite an average age of only 24 years. The study identifies key opportunities for health care systems to improve the treatment of such patients with first episode psychosis. The research was funded by the National Institute of Mental Health (NIMH), part of the National Institutes of Health. Christoph Correll, M.D., of The Zucker Hillside Hospital, Hofstra North Shore-Long Island Jewish School of Medicine, New York, and colleagues, report their findings on Oct. 8, 2014 in JAMA Psychiatry. The study is among the first of several to report results from the Recovery After an Initial Schizophrenia Episode (RAISE) project, which was developed by NIMH to examine first episode psychosis before and after specialized treatment was offered in community settings. The researchers studied nearly 400 individuals between the ages of 15 and 40 with first episode psychosis, who presented for treatment at 34 community-based clinics across 21 states. The frequency of obesity was similar to the same age group in the general population. However, smoking and metabolic syndrome (a combination of conditions including obesity, high blood pressure, high blood sugar, and abnormal blood fats, such as cholesterol and triglycerides) were much more common.
Link ID: 20182 - Posted: 10.09.2014
|By Tara Haelle The first step to treating or preventing a disease is often finding out what drives it. In the case of neurodegenerative disorders, the discovery two decades ago of what drives them changed the field: all of them—including Alzheimer's, Parkinson's, Huntington's and amyotrophic lateral sclerosis (ALS or Lou Gehrig's disease)—involve the accumulation of misfolded proteins in brain cells. Typically when a protein misfolds, the cell destroys it, but as a person ages, this quality-control mechanism starts to fail and the rogue proteins build up. In Huntington's, for example, huntingtin protein—used for many cell functions—misfolds and accumulates. Symptoms such as muscular difficulties, irritability, declining memory, poor impulse control and cognitive deterioration accompany the buildup. Mounting evidence suggests that not only does the accumulation of misfolded proteins mark neurodegenerative disease but that the spread of the proteins from one cell to another causes the disease to progress. Researchers have seen misfolded proteins travel between cells in Alzheimer's and Parkinson's. A series of experiments reported in Nature Neuroscience in August suggests the same is true in Huntington's. In their tests, researchers in Switzerland showed that mutated huntingtin protein in diseased brain tissue could invade healthy brain tissue when the two were placed together. And when the team injected the mutated protein into a live mouse's brain, it spread through the neurons within a month—similar to the way prions spread, says Francesco Paolo Di Giorgio of the Novartis Institutes for BioMedical Research in Basel, who led the research. Prions are misfolded proteins that travel through the body and confer their disease-causing characteristics onto other proteins, as seen in mad cow disease. But it is not known if misfolded proteins involved in Huntington's convert other proteins as true prions do, according to Di Giorgio. © 2014 Scientific American
Link ID: 20181 - Posted: 10.08.2014
BY Bethany Brookshire We all need sleep, but attaining it can be delicate. Insomniacs can’t fall or stay asleep. Travelers suffer from jetlag. Anxiety keeps people up at night. Or maybe it’s just that jackhammer running across the street keeping your eyes open. Some people turn to earplugs, dark curtains or alcohol to soothe them to sleep. But others go to the supplement aisle and pick up melatonin. The hormone melatonin is secreted from our brains at night and helps regulate sleep. But this chemical is not restricted to humans, or even to mammals. The roots of melatonin’s role in our nightly slumbers go back much further in evolutionary history. A new paper focuses in on the role of melatonin in tiny marine creatures called zooplankton. It turns out that these animals use melatonin just as much as we do, suggesting that the origins of sleeplike behavior may lie under the sea. “For every system and feature that makes a human or other animal today, you can ask the question: Where did it start? How did it begin? What was its first role and function, and how did it become more complex?” says study coauthor Detlev Arendt, a zoologist at the University of Heidelberg in Germany. Arendt’s laboratory has been studying the answers to these questions in the marine ragworm Platynereis dumerilii. This unassuming, centipede-like, ocean-dwelling worm produces larvae that float through the open water as zooplankton. These small larvae propel themselves up and down in the water column with movements of their cilia, slender, hair-like appendages that protrude out from the organisms. © Society for Science & the Public 2000 - 2014.
David Cyranoski Unlike its Western counterparts, Japan’s effort will be based on a rare resource — a large population of marmosets that its scientists have developed over the past decade — and on new genetic techniques that might be used to modify these highly social animals. The goal of the ten-year Brain/MINDS (Brain Mapping by Integrated Neurotechnologies for Disease Studies) project is to map the primate brain to accelerate understanding of human disorders such as Alzheimer’s disease and schizophrenia. On 11 September, the Japanese science ministry announced the names of the group leaders — and how the project would be organized. Funded at ¥3 billion (US$27 million) for the first year, probably rising to about ¥4 billion for the second, Brain/MINDS is a fraction of the size of the European Union’s Human Brain Project and the United States’ BRAIN (Brain Research through Advancing Innovative Neurotechnologies) Initiative, both of which are projected to receive at least US$1 billion over the next decade. But researchers involved in those efforts say that Brain/MINDS fills a crucial gap between disease models in smaller animals that too often fail to mimic human brain disorders, and models of the human brain that need validating data. “It is essential that we have a genetic primate model to study cognition and cognitive brain disorders such as schizophrenia and depression, for which we do not have good mouse models,” says neuroscientist Terry Sejnowski at the Salk Institute in La Jolla, California, who is a member of the National Institutes of Health BRAIN Initiative Working Group. “Other groups in the United States and China have started transgenic-primate projects, but none is as large or as well organized as the Japanese effort.” © 2014 Nature Publishing Group,
by Laura Starecheski From the self-affirmations of Stuart Smalley on Saturday Night Live to countless videos on YouTube, saying nice things to your reflection in the mirror is a self-help trope that's been around for decades, and seems most often aimed at women. The practice, we're told, can help us like ourselves and our bodies more, and even make us more successful — allow us to chase our dreams! Impressed, but skeptical, I took this self-talk idea to one of the country's leading researchers on body image to see if it's actually part of clinical practice. David Sarwer is a psychologist and clinical director at the Center for Weight and Eating Disorders at the University of Pennsylvania. He says that, in fact, a mirror is one of the first tools he uses with some new patients. He stands them in front of a mirror and coaches them to use gentler, more neutral language as they evaluate their bodies. "Instead of saying, 'My abdomen is disgusting and grotesque,' " Sarwer explains, he'll prompt a patient to say, " 'My abdomen is round, my abdomen is big; it's bigger than I'd like it to be.' " The goal, he says, is to remove "negative and pejorative terms" from the patient's self-talk. The underlying notion is that it's not enough for a patient to lose physical weight — or gain it, as some women need to — if she doesn't also change the way her body looks in her mind's eye. This may sound weird. You're either a size 4 or a size 8, right? Not mentally, apparently. In a 2013 study from the Netherlands, scientists watched women with anorexia walk through doorways in a lab. The women, they noticed, turned their shoulders and squeezed sideways, even when they had plenty of room. © 2014 NPR
By Sarah C. P. Williams When a group of male katydids croon a tune in nearly perfect synchrony, it means the insects are after the ladies. But they’re not aligning their singing with each other to come across as larger or louder, a new study finds; each male is trying to beat out the others to be the first—by mere milliseconds—to hit a note. Katydids, also known as bush crickets (Mecopoda elongata), are among a handful of insects that make noise by rubbing a hind leg on one wing. Scientists knew that the sound attracted females, but they didn’t know why the males sang in synchrony. In the new study, researchers recorded and analyzed the choral performances of 18 different groups of four male katydids. Then, they let females choose between the males in each group. Females preferred males that were the first to broadcast each tone, even if it were only 70 milliseconds ahead of others in the group, the team reports online today in Royal Society Open Science. Moreover, the females preferred these lead singers to katydids that were singing alone—but the increased volume of the chorus didn’t seem to draw more females to the group as a whole. Singing in a group, the authors of the new study hypothesize, might help keep males on a steady rhythm—another trait that female katydids in the study preferred. But more work is needed to figure out why females chose the steadiest, leading singer, and whether the observation holds true in all species of katydids, like the round-headed katydid (pictured) that's more common in North America. © 2014 American Association for the Advancement of Science
|By Tori Rodriguez Imagining your tennis serve or mentally running through an upcoming speech might help you perform better, studies have shown, but the reasons why have been unclear. A common theory is that mental imagery activates some of the same neural pathways involved in the actual experience, and a recent study in Psychological Science lends support to that idea. Scientists at the University of Oslo conducted five experiments investigating whether eye pupils adjust to imagined light as they do to real light, in an attempt to see whether mental imagery can trigger automatic neural processes such as pupil dilation. Using infrared eye-tracking technology, they measured the diameter of participants' pupils as they viewed shapes of varying brightness and as they imagined the shapes they viewed or visualized a sunny sky or a dark room. In response to imagined light, pupils constricted 87 percent as much as they did during actual viewing, on average; in response to imagined darkness, pupils dilated to 56 percent of their size during real perception. Two other experiments ruled out the possibility that participants were able to adjust their pupil size at will or that pupils were changing in response to mental effort, which can cause dilation. The finding helps to explain why imagined rehearsals can improve your game. The mental picture activates and strengthens the very neural circuits—even subconscious ones that control automated processes like pupil dilation—that you will need to recruit when it is time to perform. © 2014 Scientific American
Keyword: Learning & Memory
Link ID: 20176 - Posted: 10.08.2014
By Julie Rehmeyer Eight years ago, collapsed on a neurologist’s examining table, I asked a naive question that turned out to be at the center of a long-running controversy: “So what is chronic fatigue syndrome?” I had just been diagnosed with the illness, which for six years had been gradually overtaking me. A week earlier, I had woken up barely able to walk. Fatigue hardly described what I felt. Paralysis was more like it. My legs seemed to have been amputated and replaced with tubes of liquid concrete, and just shifting them on the table made me grunt like an Olympic weightlifter. My bones hurt; my brain felt like a swollen mass. Speaking required tracking down and spearing each word individually as it scampered away from me. I felt as capable of writing an article about science — my job — as of killing a rhino with my teeth. “We don’t understand it very well,” my neurologist said, his face blank. He could recommend no tests, no treatments, no other doctors. I came to understand that, for him, the term chronic fatigue syndrome meant “I can’t help you.” My neurologist’s understanding of the illness mirrored that of many doctors, who believe two things about CFS: that it’s probably psychosomatic and that there’s nothing doctors can do for it. One survey found that nearly half of doctors thought that CFS was or might be psychosomatic, and 58 percent said there wasn’t enough information available to help them diagnose it. An examination of medical textbooks found that CFS was underrepresented, even compared with less-prevalent illnesses.
By Gretchen Reynolds Encourage young boys and girls to run, jump, squeal, hop and chase after each other or after erratically kicked balls, and you substantially improve their ability to think, according to the most ambitious study ever conducted of physical activity and cognitive performance in children. The results underscore, yet again, the importance of physical activity for children’s brain health and development, especially in terms of the particular thinking skills that most affect academic performance. The news that children think better if they move is hardly new. Recent studies have shown that children’s scores on math and reading tests rise if they go for a walk beforehand, even if the children are overweight and unfit. Other studies have found correlations between children’s aerobic fitness and their brain structure, with areas of the brain devoted to thinking and learning being generally larger among youngsters who are more fit. But these studies were short-term or associational, meaning that they could not tease out whether fitness had actually changed the children’s’ brains or if children with well-developed brains just liked exercise. So for the new study, which was published in September in Pediatrics, researchers at the University of Illinois at Urbana-Champaign approached school administrators at public elementary schools in the surrounding communities and asked if they could recruit the school’s 8- and 9-year-old students for an after-school exercise program. This group was of particular interest to the researchers because previous studies had determined that at that age, children typically experience a leap in their brain’s so-called executive functioning, which is the ability to impose order on your thinking. Executive functions help to control mental multitasking, maintain concentration, and inhibit inappropriate responses to mental stimuli. © 2014 The New York Times Company
By Virginia Morell Two years ago, scientists showed that dolphins imitate the sounds of whales. Now, it seems, whales have returned the favor. Researchers analyzed the vocal repertoires of 10 captive orcas (Orcinus orca), three of which lived with bottlenose dolphins (Tursiops truncatus) and the rest with their own kind. Of the 1551 vocalizations these seven latter orcas made, more than 95% were the typical pulsed calls of killer whales. In contrast, the three orcas that had only dolphins as pals busily whistled and emitted dolphinlike click trains and terminal buzzes, the scientists report in the October issue of The Journal of the Acoustical Society of America. (Watch a video as bioacoustician and co-author Ann Bowles describes the difference between killer whale and orca whistles.) The findings make orcas one of the few species of animals that, like humans, is capable of vocal learning—a talent considered a key underpinning of language. © 2014 American Association for the Advancement of Science.
By CLAIRE MALDARELLI Whether it’s lying wide awake in the middle of the night or falling asleep at an international business meeting, many of us have experienced the funk of jet lag. New research has uncovered some of the mysteries behind how our cells work together to maintain one constant daily rhythm, offering the promise of defense against this disorienting travel companion. Many organisms, including humans and fruit flies, have pacemaker neurons — specialized cells in the brain that have their own molecular clocks and oscillate in 24-hour cycles. But in order for an organism to regulate itself, all of these internal clocks must tick together to create one master clock. While scientists understood how individual neurons set their own clock, they didn’t know how that master clock was set. Working with young fruit flies, whose neuronal system is simpler than adults with fewer cells and easier to study, the researchers found that two types of neurons, which they called dawn cells and dusk cells, maintain a continuous cycle. As the sun rises, special “timeless” proteins, as they’re called, help the dawn cells to first signal to each other and then signal to the dusk cells. Then as the sun sets, proteins help the dusk cells signal to each other and then signal back to the dawn cells. Each signal tells the cells to synchronize with each other. Together, these two distinct signals drive the daily sleep and wake cycle. “This really shifts our view of these cells as super strong, independent oscillators to much more of a collective group working together to keep time,” said Justin Blau, a neurobiologist at New York University and co-author of the study. © 2014 The New York Times Company
|By Brian Bienkowski and Environmental Health News On his farm in Iowa, Matt Peters worked from dawn to dusk planting his 1,500 acres of fields with pesticide-treated seeds. “Every spring I worried about him,” said his wife, Ginnie. “Every spring I was glad when we were done.” In the spring of 2011, Ginnie Peters' “calm, rational, loving” husband suddenly became depressed and agitated. “He told me ‘I feel paralyzed’,” she said. “He couldn’t sleep or think. Out of nowhere he was depressed.” A clinical psychologist spoke to him on the phone and urged him to get medical help. “He said he had work to do, and I told him if it’s too wet in the morning to plant beans come see me,” Mike Rossman said. “And the next day I got the call.” Peters took his own life. He was 55 years old. No one knows what triggered Peters’ sudden shift in mood and behavior. But since her husband’s death, Ginnie Peters has been on a mission to not only raise suicide awareness in farm families but also draw attention to the growing evidence that pesticides may alter farmers’ mental health. “These chemicals that farmers use, look what they do to an insect. It ruins their nervous system,” Peters said. “What is it doing to the farmer?” Farming is a stressful job – uncontrollable weather, physical demands and economic woes intertwine with a personal responsibility for land that often is passed down through generations. But experts say that some of the chemicals used to control pests may make matters worse by changing farmers’ brain chemistry. © 2014 Scientific American