By Rhiannon Picton-James I was seeing a guy from London, and he told me Scott and Zelda Fitzgerald were his favorite couple. He was charming, exciting and “got” me. His choice sounded so romantic, so like him. Obviously I knew who they were, but I wasn’t familiar with the details of their relationship. I lay in bed and Googled eagerly. Was this the kind of great love he envisioned for us? Zelda Fitzgerald was intensely glamorous and hauntingly beautiful. Scott called her the original flapper. Oh, and they had a turbulent relationship wracked with infidelity and excessive drinking: a love affair that ended with her dying after a fire broke out in the mental institution where she was a patient. She was schizophrenic and spent the last of her years hospitalized. Is this how he saw me? I had clinical depression, not schizophrenia. In my head (and, clearly, mine alone) we shared a blind devotion. When the reality of our relationship sank in, he got busy at work fast before disappearing entirely. He told me, over text, that he was “gut-wrenchingly sorry.” Although the devastation passed, his words lingered. I pulled up more articles on the Fitzgeralds. The Guardian wrote that Scott Fitzgerald’s “troubled wife” was a “beautiful and damned” socialite, per the title of his second novel, who would be played by Scarlett Johansson in an upcoming drama. The romanticism was bothersome to me. Elsewhere, on Facebook, an ad for a sale at Skinnydip, a London brand, popped up. It included a cute miniature backpack, emblazoned with the words “I’ve got issues” and embroidered pink roses. The catchy Julia Michaels hit played in my head, her soft voice gently singing, “When I’m down, I get real down,” before breaking into the chorus: “’Cause baby I’ve got issues.” © 2018 The New York Times Company

Keyword: Depression; Schizophrenia
Link ID: 25263 - Posted: 07.28.2018

By Daniela Lamas Incompletely understood at best, after more than a century of false starts and research gains. So we learn in “Aroused,” an eye-opening new book that traces the history of endocrinology through a sequence of crisp, meticulously researched, and often surprisingly funny tales from the turn of the 20th century to today. Though hormones have entered common parlance — we have growth hormone and sex hormones and hormone replacement therapy — it was not always this way. Randi Hutter Epstein, an accomplished author who has a medical degree and a master’s of public health, illuminates more than a century of false starts and research gains as she explains the ways these chemical messengers control the daily work of our bodies. At the same time, she leaves us wondering how much of our current understanding of hormones is in fact “true” and how much may ultimately be disproved. This is a novel contribution. While most of the literature on hormones has been confined to medical text or limited to a single hormone (estrogen, for example), Epstein’s approach is wide-ranging. Consider this story. The year was 1924, and two teenagers in Chicago bludgeoned a younger boy to death. The new field of endocrinology was exploding at the time, and their lawyers proposed a provocative theory to avoid the death penalty: Hormones were at fault. After extensive X-rays, interviews, and measures of metabolism, doctors testified that the teenagers had severely impaired hormonal glands and had committed the grisly murder under the influence of hormones gone awry. They were sentenced to life in prison. Copyright 2018 Undark

Keyword: Hormones & Behavior
Link ID: 25262 - Posted: 07.28.2018

NIH-funded researchers delayed signs of amyotrophic lateral sclerosis (ALS) in rodents by injecting them with a second-generation drug designed to silence the gene, superoxide dismutase 1 (SOD1). The results, published in the Journal of Clinical Investigation, suggest the newer version of the drug may be effective at treating an inherited form of the disease caused by mutations in SOD1. Currently, the drug is being tested in an ALS clinical trial (NCT02623699). ALS destroys motor neurons responsible for activating muscles, causing patients to rapidly lose muscle strength and their ability to speak, swallow, move, and breathe. Most die within three to five years of symptom onset. Previous studies suggested that a gene therapy drug, called an antisense oligonucleotide, could be used to treat a form of ALS caused by mutations in the gene SOD1. These drugs turned off SOD1 by latching onto versions the gene encoded in messenger RNA (mRNA), tagging them for disposal and preventing SOD1 protein production. Using rats and mice genetically modified to carry normal or disease-mutant versions of human SOD1, a team of researchers led by Timothy M. Miller, M.D., Ph.D., Washington University, St. Louis, MO, discovered that newer versions of the drug may be more effective at treating ALS than the earlier one that had been tested in a phase 1 clinical trial. For instance, injections of the newer versions were more efficient at reducing normal, human SOD1 mRNA levels in rats and mice and they helped rats, genetically modified to carry a disease-causing mutation in SOD1, live much longer than previous versions of the drug. Injections of the new drugs also delayed the age at which mice carrying a disease-mutant SOD1 gene had trouble balancing on a rotating rod and appeared to prevent muscle weakness and loss of connections between nerves and muscles, suggesting it could treat the muscle activation problems caused by ALS. These and other results were the basis for a current phase 1 clinical trial testing the next generation drug in ALS patients (NCT02623699).

Keyword: ALS-Lou Gehrig's Disease
Link ID: 25261 - Posted: 07.27.2018

by Maggie Fox A mind-controlling parasite found in cat feces may give people the courage they need to become entrepreneurs, researchers reported Tuesday. They found that people who have been infected with the Toxoplasma gondii parasite are more likely to major in business and to have started their own businesses than non-infected people. The parasite, which makes rodents unafraid of cats, may be reducing the fear of failure in people, Stefanie Johnson of the University of Colorado and colleagues said. They haven’t actually shown that. But toxoplasma does get into the brain, and it’s been linked to a variety of mental effects in mice and people alike. And fear of failure could be a good thing, Johnson said. Toxoplasmosis has been linked to a greater risk of "car accidents, mental illness, neuroticism, drug abuse and suicide,” Johnson and her colleagues wrote in their paper, published in the Proceedings of the Royal Society B. It might be affecting message-carrying chemicals in the brain called neurotransmitters, or hormones such as testosterone, they wrote. In particular, scientists have studied whether the parasite might increase risk-taking behavior. © 2018 NBC UNIVERSAL

Keyword: Emotions
Link ID: 25260 - Posted: 07.27.2018

Mutations in the gene LRRK2 have been linked to about three percent of Parkinson’s disease cases. Researchers have now found evidence that the activity of LRRK2 protein might be affected in many more patients with Parkinson’s disease, even when the LRRK2 gene itself is not mutated. The study was published in Science Translational Medicine and was supported in part by the National Institute of Neurological Disorders and Stroke (NINDS), a part of the National Institutes of Health (NIH). “This is a striking finding that shows how normal LRRK2 may contribute to the development of Parkinson’s disease,” said Beth-Anne Sieber, Ph.D., program director at NINDS. “This study also identifies LRRK2 as an integral protein in the neurobiological pathways affected by the disease.” More than 10 years ago, researchers linked mutations in the LRRK2 gene with an increased risk for developing Parkinson’s disease. Those mutations produce a version of LRRK2 protein that behaves abnormally and is much more active than it would be normally. Despite its importance in Parkinson’s disease, the very small amount of normal LRRK2 protein in nerve cells has made it difficult to study. In the current study, the authors developed a new method for observing LRRK2 cells that makes them glow fluorescently only when LRRK2 is in its activated state. They have also used detection of fluorescent signals to demonstrate loss of binding of an inhibitor protein to LRRK2 when LRRK2 is activated.

Keyword: Parkinsons
Link ID: 25259 - Posted: 07.27.2018

Jon Hamilton Daniel, a Marine Corps veteran, used to fire a rocket launcher called the shoulder-launched multipurpose assault weapon. Two decades later, he still experiences dizzy spells and disorientation. But the Department of Veterans Affairs doesn't have a category for vets like him, who may have sustained traumatic brain injuries from training rather than combat. AUDIE CORNISH, HOST: We heard yesterday from a Marine named Daniel. He spent years firing rocket launchers. Now he thinks that experience may have injured his brain. DANIEL: I lose my spatial orientation. I don't know where I am. Vision gets blurrier, even sound is kind of muffled. CORNISH: But when Daniel went to the Veterans Affairs Department for help, he discovered that the VA doesn't have a category for people like him. NPR's Jon Hamilton reports on how the VA is dealing with veterans who may have a new kind of brain injury, one caused by the weapons they fired. JON HAMILTON, BYLINE: Daniel, who asked us not to use his last name, used to fire a rocket launcher called the Shoulder-Launched Multipurpose Assault Weapon or SMAW. UNIDENTIFIED PERSON: Left. Right. Back left stay all clear. Rocket. (SOUNDBITE OF EXPLOSION) HAMILTON: That meant his head was just inches from the explosion used to launch each rocket. And during his training in the late 1990s, Daniel began to have episodes where he'd feel dizzy and disoriented. Now, 20 years later, those symptoms can still return when he turns his head quickly or stumbles. DANIEL: It's disturbing to me. And it is terrifying to me. © 2018 npr

Keyword: Brain Injury/Concussion
Link ID: 25258 - Posted: 07.27.2018

By Kelly Servick In the hunt for a drug to treat Alzheimer’s disease, even a whiff of success can be intoxicating. That helps explain why an experimental drug called BAN2401, which a few months ago seemed like it might join a growing heap of failed candidates, created so much buzz yesterday at the Alzheimer’s Association International Conference in Chicago, Illinois. In a phase II trial, the drug had already failed to show the level of benefit that its developers—Biogen Inc. in Cambridge, Massachusetts; and Eisai Co. Ltd. in Tokyo—set as the study’s primary endpoint. But yesterday the companies presented a series of other analyses from the same trial that suggest BAN2401 might slow the pace of cognitive decline in Alzheimer’s patients, and reverse the buildup of a brain protein thought to drive the disease’s neurodegeneration. But the subset of patients who showed those benefits was relatively small—161 people—and an unexpected change to the way the study was randomized cast some skepticism on the results. For many, the findings are too preliminary to celebrate. “If these results we saw today pan out in phase III clinical trials, then you’re looking at disease-modifying medication—the first one for Alzheimer’s disease,” says Keith Fargo, director of scientific programs & outreach at the Alzheimer’s Association in Chicago, Illinois. “But you don’t know whether they’re going to pan out until you actually do the phase III trial.” © 2018 American Association for the Advancement of Science

Keyword: Alzheimers
Link ID: 25257 - Posted: 07.27.2018

Aimee Cunningham Keeping a tight lid on blood pressure isn’t just good for the heart. It may also help the brain. People given intensive drug treatment for high blood pressure were less likely to develop an early form of memory loss, according to preliminary results from a major clinical trial. This approach reduced the rate of early memory loss, called mild cognitive impairment, by around 19 percent, compared with people who received less aggressive treatment. And the intensely treated group developed fewer white matter lesions over time, researchers reported July 25 at the Alzheimer’s Association International Conference in Chicago. White matter lesions, which are associated with dementia, are thought to be caused by blood vessel injuries in white matter, the part of the brain that contains nerve fibers. The brain research is part of SPRINT, the Systolic Blood Pressure Intervention Trial involving more than 9,300 participants. Some received intensive treatment aimed at lowering their systolic blood pressure — the pressure on artery walls when the heart beats — below 120 millimeters of mercury; others got standard treatment to bring it below 140. The trial had already reported that participants who received the intensive treatment dropped their risk of heart attacks and other cardiovascular problems by 25 percent, compared with the standard group (SN Online: 11/9/2015). The results were the basis for revamped blood pressure guidelines, released last year (SN: 12/9/17, p. 13). |© Society for Science & the Public 2000 - 2018

Keyword: Alzheimers
Link ID: 25256 - Posted: 07.26.2018

By Darold A. Treffert Savant syndrome comes in different forms. In congenital savant syndrome the extraordinary savant ability surfaces in early childhood. In acquired savant syndrome astonishing new abilities, typically in music, art or mathematics, appear unexpectedly in ordinary persons after a head injury, stroke or other central nervous system (CNS) incident where no such abilities or interests were present pre-incident. But in sudden savant syndrome an ordinary person with no such prior interest or ability and no precipitating injury or other CNS incident has an unanticipated, spontaneous epiphanylike moment where the rules and intricacies of music, art or mathematics, for example, are experienced and revealed, producing almost instantaneous giftedness and ability in the affected area of skill sets. Because there is no underlying disability such as that which occurs in congenital or acquired savant syndromes, technically sudden savant syndrome would be better termed sudden genius A 28-year-old gentleman from Israel, K. A., sent his description of his epiphany moment. He was in a mall where there was a piano. Whereas he could play simple popular songs from rote memory before, “suddenly at age 28 after what I can best describe as a ‘just getting it moment,’ it all seemed so simple. I suddenly was playing like a well-educated pianist.” His friends were astonished as he played and suddenly understood music in an entirely intricate way. “I suddenly realized what the major scale and minor scale were, what their chords were and where to put my fingers in order to play certain parts of the scale. I was instantly able to recognize harmonies of the scales in songs I knew as well as the ability to play melody by interval recognition.” He began to search the internet for information on music theory and to his amazement “most of what they had to teach I already knew, which baffled me as to how could I know something I had never studied." © 2018 Scientific American

Keyword: Attention; Learning & Memory
Link ID: 25255 - Posted: 07.26.2018

By Dave Philipps SANTA CRUZ, Calif. — Some of the local growers along the coast here see it as an act of medical compassion: Donating part of their crop of high-potency medical marijuana to ailing veterans, who line up by the dozens each month in the echoing auditorium of the city’s old veterans’ hall to get a ticket they can exchange for a free bag. One Vietnam veteran in the line said he was using marijuana-infused oil to treat pancreatic cancer. Another said that smoking cannabis eased the pain from a recent hip replacement better than prescription pills did. Several said that a few puffs temper the anxiety and nightmares of post-traumatic stress disorder. “I never touched the stuff in Vietnam,” said William Horne, 76, a retired firefighter. “It was only a few years ago I realized how useful it could be.” The monthly giveaway bags often contain marijuana lotions, pills, candies and hemp oils, as well as potent strains of smokable flower with names like Combat Cookies and Kosher Kush. But the veterans do not get any medical guidance on which product might help with which ailment, how much to use, or how marijuana might interact with other medications. Ordinarily, their first stop for advice like that would be the Department of Veterans Affairs health system, with its thousands of doctors and hundreds of hospitals and clinics across the country dedicated to caring for veterans. But the department has largely said no to medical marijuana, citing federal law. It won’t recommend cannabis products for patients, and for the most part it has declined even to study their potential benefits. That puts the department out of step with most of the country, where at least 30 states now have laws that allow the use of medical marijuana in some form. © 2018 The New York Times Company

Keyword: Drug Abuse
Link ID: 25254 - Posted: 07.26.2018

By Emily Willingham Of all of our organs, our brains and hearts get the most attention. But the liver once held top billing, preeminent over the heart and mind as the seat of emotion and even the soul. As its name implies, we need our liver to live—not only because it works hard as a detox unit but also because it quietly processes components our brains need to thrive. The Alzheimer’s disease (AD) research community is turning its attention to this liver–brain connection. That newfound interest turns up in a quartet of new studies presented July 24 at the Alzheimer’s Association International Conference 2018. The results may help provide clues to both the basic biology of AD and how diet is linked to brain health. More specifically, it may give insight into why human clinical trials of fish oil have failed to protect against AD and other forms of dementia. In the four studies, blood levels of molecules associated with the liver and production of fats, or lipids, were tied to AD risk—a first step toward deeper examination of the liver–brain link. “There seem to be some positive results correlating levels of lipids with cognition and cognitive progression,” says Paul Schulz, director of the Dementia and Memory Disorders Clinic at The University of Texas McGovern Medical School, who was not involved in the studies. “The challenge will be to establish cause and effect.” The brain consists mostly of fats, which contribute to both its form and function. These lipids facilitate communication from neuron to neuron and make up much of the insulation that sheaths these cells. It is the liver that builds the fats the brain needs—and many genes tied to AD are linked to fat production or transport, including a version of a gene associated with high AD risk—APOE ε4. © 2018 Scientific American

Keyword: Alzheimers
Link ID: 25253 - Posted: 07.26.2018

In the wake of a mass shooting — or any other senseless tragedy — the search for answers begins. How could it happen? Could it have been prevented? What can we do to prevent this from happening again? The question of whether there is a relationship between mental illness and violence — and the potential threat it may pose to public safety — was renewed this week after the family of Faisal Hussain, the gunman in Sunday night's deadly shooting rampage in Toronto, said he was mentally ill. "Our son had severe mental health challenges, struggling with psychosis and depression his entire life," the statement said. Two people were killed and 13 others injured in the attack, jolting a city already rattled by escalating gun violence. Hussain died from a gunshot wound moments after exchanging gunfire with Toronto police officers. Little is known about Hussain's condition or treatment beyond the statement released by his family. And while some explanation of what may have tormented or even motivated Hussain may add to our understanding, experts agree mental illness is just one of many potential red flags and not a reliable predictor of behaviour. People leave flowers at a memorial Tuesday honouring the victims of the mass shooting on Toronto's Danforth Avenue. (Mark Blinch/Canadian Press) ©2018 CBC/Radio-Canada.

Keyword: Aggression; Schizophrenia
Link ID: 25252 - Posted: 07.26.2018

Jon Hamilton Chris Ferrari was just 18 the first time he balanced a rocket launcher on his right shoulder and aimed it at a practice target. "Your adrenaline's going and you're trying to focus on getting that round to hit, and then you go to squeeze that trigger and, you know." Boom! The report is loud enough to burst the eardrums of anyone not wearing military-grade hearing protection. And the blast wave from the weapon is so powerful it feels like a whole-body punch. "It's exhilarating," says Chris's buddy Daniel, a former gunner in the Marine Corps who asked that we not use his last name. "When you feel a concussive wave, it's an awesome thing. It fills you with awe." It also may do bad things to your brain. Studies show that troops who repeatedly fire powerful, shoulder-launched weapons can experience short-term problems with memory and thinking. They may also feel nauseated, fatigued and dizzy. In short, they have symptoms like those of a concussion. It's still not clear whether firing these weapons can lead to long-term brain damage. But Chris and Daniel suspect that, for them, it may have. While in the Marines, Daniel and Chris spent two years in the late 1990s firing a rocket launcher called the shoulder-launched multipurpose assault weapon, or SMAW. © 2018 npr

Keyword: Brain Injury/Concussion
Link ID: 25251 - Posted: 07.26.2018

Jessica Wright When Abigail was 19 months old, she took a ferry with her mother Gillian across the English Channel during a move from Germany to England. On board, she played with a Belgian toddler whose mother, a doctor, took notice of Abigail’s tight muscles and lack of language. (Gillian asked that we omit their last names to protect their privacy.) “What syndrome does she have?” the doctor asked Gillian. Gillian didn’t know. In the coming years, Abigail would receive diagnoses of autism and intellectual disability; she also has recurrent seizures. But it took 20 years to get an answer to the Belgian doctor’s question. In 2013, Abigail’s doctor, Meena Balasubramanian, enrolled Abigail in Deciphering Developmental Disorders (DDD), a study in which researchers sequence an individual’s genes to find the cause of undiagnosed genetic conditions. In Abigail, they found a de novo, or spontaneous, mutation in a known epilepsy gene called HNRNPU. Gillian learned of the result just last year. Over the past year, this gene has emerged as a new autism candidate associated with a neurodevelopmental syndrome. Finding the genetic cause for Abigail’s condition sparked Balasubramanian’s interest in the gene. She has since collected clinical information from six other people with these mutations, five of whom were identified through DDD. These participants share Abigail’s learning difficulties and seizures. © 1986 - 2018 The Scientist.

Keyword: Epilepsy; Autism
Link ID: 25250 - Posted: 07.26.2018

A handful of Alzheimer's patients signed up for a bold experiment: they let scientists beam sound waves into the brain to temporarily jiggle an opening in its protective shield. The so-called blood-brain barrier prevents germs and other damaging substances from leaching in through the bloodstream — but it can block drugs for Alzheimer's, brain tumours and other neurological diseases. Canadian researchers on Wednesday reported early hints that technology called focused ultrasound can safely poke holes in that barrier — holes that quickly sealed back up. It's a step toward one day using the non-invasive device to push brain treatments through. "It's been a major goal of neuroscience for decades, this idea of a safe and reversible and precise way of breaching the blood-brain barrier," said Dr. Nir Lipsman, a neurosurgeon at Toronto's Sunnybrook Health Sciences Centre who led the study. "It's exciting." The findings were presented at the Alzheimer's Association international conference in Chicago and published Wednesday in Nature Communications. This first-step research, conducted in just six people with mild to moderate Alzheimer's, didn't test potential therapies; its aim was to check whether patients' fragile blood vessels could withstand the breach without bleeding or other side-effects. ©2018 CBC/Radio-Canada

Keyword: Brain imaging
Link ID: 25249 - Posted: 07.26.2018

By Jocelyn Kaiser Basic brain and behavioral researchers will get more than a year to comply with a new U.S. policy that will treat many of their studies as clinical trials. The announcement from the National Institutes of Health (NIH) appears to defuse, for now, a yearlong controversy over whether basic research on humans should follow the same rules as studies testing drugs. Although research groups had hoped NIH would drop its plans to tag basic studies with humans as trials, they say they’re relieved they get more time to prepare and give the agency input. “It’s a positive step forward,” says Paula Skedsvold, executive director of the Federation of Associations in Behavioral & Brain Sciences in Washington, D.C. At issue is a recently revised definition of a clinical trial along with a set of rules in effect since January that are meant to increase the rigor and transparency of NIH-funded clinical trials. About a year ago, basic scientists who study human cognition—for example, using brain imaging with healthy volunteers—were alarmed to realize many of these studies fit the new clinical trial definition. Researchers protested that many requirements, such as registering and reporting results in the ClinicalTrials.gov federal database, made no sense for studies that weren’t testing a treatment and would confuse the public. NIH then issued a set of case studies explaining that only some basic studies would fall under the trials definition. But concerns remained about confusing criteria and burdensome new paperwork. © 2018 American Association for the Advancement of Science

Keyword: Attention; Learning & Memory
Link ID: 25248 - Posted: 07.25.2018

by Juliet Corwin On the deafness scale of mild, moderate, severe or profound, I am profoundly deaf. With the help of cochlear implants, I am able to “hear” and speak. The devices are complicated to explain, but basically, external sound processors, worn behind the ears, send a digital signal to the implants, which convert the signal to electric impulses that stimulate the hearing nerve and provide sound signals to the brain. The implants allow me to attend my middle school classes with few accommodations, but I’m still quite different from people who hear naturally. When my implant processors are turned off, I don’t hear anything. I regard myself as a deaf person, and I am proud to be among those who live with deafness, yet I often feel rejected by some of these same people. My use of cochlear implants and lack of reliance on American Sign Language (I use it but am not fluent — I primarily speak) are treated like a betrayal by many in the Deaf — capital-D — community. In the view of many who embrace Deaf culture, a movement that began in the 1970s, those who are integrated into the hearing world through technology, such as hearing aids or cochlear implants, myself included, are regarded as “not Deaf enough” to be a part of the community. People deaf from birth or through illness or injury already face discrimination. I wish we didn’t practice exclusion among ourselves. But it happens, and it’s destructive. © 1996-2018 The Washington Post

Keyword: Hearing
Link ID: 25247 - Posted: 07.25.2018

By Anahad O’Connor Nutrition scientists have long debated the best diet for optimal health. But now some experts believe that it’s not just what we eat that’s critical for good health, but when we eat it. A growing body of research suggests that our bodies function optimally when we align our eating patterns with our circadian rhythms, the innate 24-hour cycles that tell our bodies when to wake up, when to eat and when to fall asleep. Studies show that chronically disrupting this rhythm — by eating late meals or nibbling on midnight snacks, for example — could be a recipe for weight gain and metabolic trouble. That is the premise of a new book, “The Circadian Code,” by Satchin Panda, a professor at the Salk Institute and an expert on circadian rhythms research. Dr. Panda argues that people improve their metabolic health when they eat their meals in a daily 8- to 10-hour window, taking their first bite of food in the morning and their last bite early in the evening. This approach, known as early time-restricted feeding, stems from the idea that human metabolism follows a daily rhythm, with our hormones, enzymes and digestive systems primed for food intake in the morning and afternoon. Many people, however, snack and graze from roughly the time they wake up until shortly before they go to bed. Dr. Panda has found in his research that the average person eats over a 15-hour or longer period each day, starting with something like milk and coffee shortly after rising and ending with a glass of wine, a late night meal or a handful of chips, nuts or some other snack shortly before bed. That pattern of eating, he says, conflicts with our biological rhythms. Scientists have long known that the human body has a master clock in the brain, located in the hypothalamus, that governs our sleep-wake cycles in response to bright light exposure. A couple of decades ago, researchers discovered that there is not just one clock in the body but a collection of them. Every organ has an internal clock that governs its daily cycle of activity. © 2018 The New York Times Company

Keyword: Biological Rhythms; Obesity
Link ID: 25246 - Posted: 07.25.2018

By Frankie Schembri Do you ever find yourself scouring the web for pizza delivery services to satisfy those late-night cravings? You’re not alone: A new study reveals that hungry web surfers around the world all start searching for food-related information at two peak times, 7 p.m. and 2 a.m. Wanting to see if they could spot trends in human behavior based on a massive database of Google searches, a team of scientists analyzed hourly food-related queries from five countries: the United States, Canada, India, Australia, and the United Kingdom. For two 1-week periods, they looked for general food-related keywords such as “pizza delivery” or “Chinese delivery” and country-specific delivery companies like India’s “Swiggy” and “Just Eat,” which serves the United Kingdom and Australia. They also analyzed 5 years of data to see if they could discover seasonal trends. The two spikes in food-related searches occurred across all countries, keywords, days of the week, and seasons, the researchers report today in Royal Society Open Science. They say the peaks likely represent two different groups of people searching for nighttime nourishment, one older (the early birds) and one younger (the night owls). Another hypothesis is that the two groups are simply running on different internal body clocks, which affects when they want their evening calories. © 2018 American Association for the Advancement of Science.

Keyword: Obesity; Biological Rhythms
Link ID: 25245 - Posted: 07.25.2018

Carl Zimmer In the largest genetics study ever published in a scientific journal, an international team of scientists on Monday identified more than a thousand variations in human genes that influence how long people stay in school. Educational attainment has attracted great interest from researchers in recent years, because it is linked to many other aspects of people’s lives, including their income as adults, overall health and even life span. The newly discovered gene variants account for just a fraction of the differences in education observed between groups of people. Environmental influences, which may include family wealth or parental education, together play a bigger role. Still, scientists have long known that genetic makeup explains some of the differences in time spent in school. Their hope is that the data can be used to gain a better understanding of what educators must do to keep children in school longer. With a fuller understanding of the influences exerted by genes, scientists think they will be able to better measure what happens when they try to improve a child’s learning environment. The new study, published in the journal Nature Genetics, finds that many of the genetic variations implicated in educational attainment are involved in how neurons communicate in the brain. A striking number are involved in relaying signals out of neurons and into neighboring ones through connections called synapses. The findings are based on genetic sequencing of more than 1.1 million people. But the subjects were all white people of European descent. In order to maximize the odds of discovering genetic links, the scientists say they needed a very large, homogeneous sample. © 2018 The New York Times Company

Keyword: Genes & Behavior; Intelligence
Link ID: 25244 - Posted: 07.24.2018