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By ANAHAD O’CONNOR The sugar industry paid scientists in the 1960s to play down the link between sugar and heart disease and promote saturated fat as the culprit instead, newly released historical documents show. The internal sugar industry documents, recently discovered by a researcher at the University of California, San Francisco, and published Monday in JAMA Internal Medicine, suggest that five decades of research into the role of nutrition and heart disease, including many of today’s dietary recommendations, may have been largely shaped by the sugar industry. “They were able to derail the discussion about sugar for decades,” said Stanton Glantz, a professor of medicine at U.C.S.F. and an author of the JAMA paper. The documents show that a trade group called the Sugar Research Foundation, known today as the Sugar Association, paid three Harvard scientists the equivalent of about $50,000 in today’s dollars to publish a 1967 review of research on sugar, fat and heart disease. The studies used in the review were handpicked by the sugar group, and the article, which was published in the prestigious New England Journal of Medicine, minimized the link between sugar and heart health and cast aspersions on the role of saturated fat. Even though the influence-peddling revealed in the documents dates back nearly 50 years, more recent reports show that the food industry has continued to influence nutrition science. Last year, an article in The New York Times revealed that Coca-Cola, the world’s largest producer of sugary beverages, had provided millions of dollars in funding to researchers who sought to play down the link between sugary drinks and obesity. In June, The Associated Press reported that candy makers were funding studies that claimed that children who eat candy tend to weigh less than those who do not. The Harvard scientists and the sugar executives with whom they collaborated are no longer alive. One of the scientists who was paid by the sugar industry was D. Mark Hegsted, who went on to become the head of nutrition at the United States Department of Agriculture, where in 1977 he helped draft the forerunner to the federal government’s dietary guidelines. Another was Dr. Fredrick J. Stare, the chairman of Harvard’s nutrition department. © 2016 The New York Times Company

Keyword: Obesity
Link ID: 22649 - Posted: 09.13.2016

Martha Bebinger Five states are voting this fall on whether marijuana should be legal, like alcohol, for recreational use. That has sparked questions about what we know – and don't know – about marijuana's effect on the brain. Research is scarce. The U.S. Drug Enforcement Agency classifies marijuana as a Schedule I drug. That classification puts up barriers to conducting research on it, including a cumbersome DEA approval application and a requirement that scientists procure very specific marijuana plants. One long-term study in New Zealand compared the IQs of people at age 13 and then through adolescence and adulthood to age 38. Those who used pot heavily from adolescence onward showed an average 8 percent drop in IQ. People who never smoked, by contrast, showed slightly increased IQ. Critics pounced on the study, which was published in 2012, because it didn't adjust for many other things that affect IQ such as home life or family income. And there's no proof the IQ differences are due to pot. One of those critics, Nicholas Jackson, now a senior statistician at the University of California, Los Angeles, wondered what would happen if he could rule out some of those elements by comparing twins. "Individuals that share the same genes, grew up in the same household, where the difference between them was that one of the twins was using marijuana and one was not," Jackson says. © 2016 npr

Keyword: Drug Abuse
Link ID: 22648 - Posted: 09.13.2016

By Bob Grant Lab rats that compulsively drink are cured of their addiction by a drug that silences neural networks that strengthened as they became dependent on alcohol.FLICKR, SARAH LAVAL Alcohol dependence involves neural reward networks that are strengthened by the regular consumption of alcohol. Using rat models of compulsive drinking, researchers at The Scripps Research Institute (TSRI) have now shown that they can interfere with those specific networks to curb the behavior. They reported their findings last week (September 7) in The Journal of Neuroscience. “We can completely reverse alcohol dependence by targeting a network of neurons,” coauthor Olivier George, a TSRI neuroscientist, said in a statement. “It is very challenging to target such a small population of neurons in the brain, but this study helps to increase our knowledge of a part of the brain that is still a mystery,” added coauthor and TSRI postdoc Giordano de Guglielmo. The researchers used a drug called Daun02 to shut down a specific group of neurons in the amygdalas of rats that drank compulsively. The treated rats stopped imbibing as much, and this behavioral change lasted for several days. “With classic pharmacology we usually observe a 20-40 percent decrease in drinking because the individuals are highly dependent (we model heavy alcoholism),” George told Medical News Today. “Instead, here, the drinking went all the way back down to normal drinking, and without noticeable side effects; very unusual. And, usually, to have long lasting effects like that, you need daily treatment, not a single one; it shows that we might have found alcoholism's Achilles' heel.” © 1986-2016 The Scientist

Keyword: Drug Abuse
Link ID: 22647 - Posted: 09.13.2016

Laura Sanders By sneakily influencing brain activity, scientists changed people’s opinions of faces. This covert neural sculpting relied on a sophisticated brain training technique in which people learn to direct their thoughts in specific ways. The results, published September 8 in PLOS Biology, support the idea that neurofeedback methods could help reveal how the brain’s behavior gives rise to perceptions and emotions. What’s more, the technique may ultimately prove useful for easing traumatic memories and treating disorders such as depression. The research is still at an early stage, says neurofeedback researcher Michelle Hampson of Yale University, but, she notes, “I think it has great promise.” Takeo Watanabe of Brown University and colleagues used functional MRI to measure people’s brain activity in an area called the cingulate cortex as participants saw pictures of faces. After participants had rated each face, a computer algorithm sorted their brain responses into patterns that corresponded to faces they liked and faces they disliked. With this knowledge in hand, the researchers then attempted to change people’s face preferences by subtly nudging brain activity in the cingulate cortex. In step 2 of the experiment, returning to the fMRI scanner, participants saw an image of a face that they had previously rated as neutral. Just after that, they were shown a disk. The goal, the participants were told, was simple: make the disk bigger by using their brains. They had no idea that the only way to make the disk grow was to think in a very particular way. |© Society for Science & the Public 2000 - 201

Keyword: Attention; Learning & Memory
Link ID: 22646 - Posted: 09.12.2016

By SARAH HALLBERG and OSAMA HAMDY Earlier this year, the Food and Drug Administration approved a new weight-loss procedure in which a thin tube, implanted in the stomach, ejects food from the body before all the calories can be absorbed. Some have called it “medically sanctioned bulimia,” and it is the latest in a desperate search for new ways to stem the rising tides of obesity and Type 2 diabetes. Roughly one-third of adult Americans are now obese; two-thirds are overweight; and diabetes afflicts some 29 million. Another 86 million Americans have a condition called pre-diabetes. None of the proposed solutions have made a dent in these epidemics. Recently, 45 international medical and scientific societies, including the American Diabetes Association, called for bariatric surgery to become a standard option for diabetes treatment. The procedure, until now seen as a last resort, involves stapling, binding or removing part of the stomach to help people shed weight. It costs $11,500 to $26,000, which many insurance plans won’t pay and which doesn’t include the costs of office visits for maintenance or postoperative complications. And up to 17 percent of patients will have complications, which can include nutrient deficiencies, infections and intestinal blockages. It is nonsensical that we’re expected to prescribe these techniques to our patients while the medical guidelines don’t include another better, safer and far cheaper method: a diet low in carbohydrates. Once a fad diet, the safety and efficacy of the low-carb diet have now been verified in more than 40 clinical trials on thousands of subjects. Given that the government projects that one in three Americans (and one in two of those of Hispanic origin) will be given a diagnosis of diabetes by 2050, it’s time to give this diet a closer look. © 2016 The New York Times Company

Keyword: Obesity
Link ID: 22645 - Posted: 09.12.2016

By David Grimm Depending on whom you ask, yesterday’s U.S. government workshop on the state of nonhuman primate research was either a raging success or a complete fiasco. The event, held at the National Institutes of Health (NIH) in Bethesda, Maryland, brought together dozens of scientists, veterinarians, and bioethicists to discuss how research on monkeys and related animals is contributing to human medicine and to review the welfare policies that surround this work. But observers differed widely on whether it accomplished what Congress had in mind when it told NIH to hold the event. “It was a great showcase of the importance nonhuman primates have played and continue to play in human health,” says Anne Deschamps, a senior science policy analyst at the Federation of American Societies for Experimental Biology in Bethesda, one of several scientific organizations that signed onto a white paper released in advance of the meeting that promoted the use of these animals in biomedical research. She contends that research on these animals has been critical for our understanding of HIV and the human brain. But the animal rights group People for the Ethical Treatment of Animals (PETA), whose lobbying efforts led to the workshop, says the meeting was supposed to determine whether monkeys and their relatives belong in laboratories in the first place. “It was an infomercial for the use of monkeys in experiments,” says PETA Senior Vice President Kathy Guillermo in Norfolk, Virginia. “It was a wasted opportunity.” © 2016 American Association for the Advancement of Science

Keyword: Animal Rights
Link ID: 22644 - Posted: 09.12.2016

By GRETCHEN REYNOLDS A busy brain can mean a hungry body. We often seek food after focused mental activity, like preparing for an exam or poring over spreadsheets. Researchers speculate that heavy bouts of thinking drain energy from the brain, whose capacity to store fuel is very limited. So the brain, sensing that it may soon require more calories to keep going, apparently stimulates bodily hunger, and even though there has been little in the way of physical movement or caloric expenditure, we eat. This process may partly account for the weight gain so commonly seen in college students. Scientists at the University of Alabama at Birmingham and another institution recently experimented with exercise to counter such post-­study food binges. Gary Hunter, an exercise physiologist at U.A.B., oversaw the study, which was published this month in the journal Medicine & Science in Sports & Exercise. Hunter notes that strenuous activity both increases the amount of blood sugar and lactate — a byproduct of intense muscle contractions — circulating in the blood and augments blood flow to the head. Because the brain uses sugar and lactate as fuel, researchers wondered if the increased flow of fuel-rich blood during exercise could feed an exhausted brain and reduce the urge to overeat. Thirty-­eight healthy college students were invited to U.A.B.’s exercise lab to determine their fitness and metabolic rates — and to report what their favorite pizza was. Afterward, they sat quietly for 35 minutes before being given as much of their favorite pizza as they wanted, which established a baseline measure of self-­indulgence. At a later date, the volunteers returned and spent 20 minutes tackling selections from college and graduate-­school entrance exams. Hunter says this work has been used in other studies “to induce mental fatigue and hunger.” Next, half the students sat quietly for 15 minutes, before being given pizza. The rest of the volunteers spent those 15 minutes doing intervals on a treadmill: two minutes of hard running followed by about one minute of walking, repeated five times. This is the sort of brief but intensive routine, Hunter says, that should prompt the release of sugar and lactate into the bloodstream. These students were then allowed to gorge on pizza, too. But by and large, they did not overeat. © 2016 The New York Times Company

Keyword: Obesity; Learning & Memory
Link ID: 22643 - Posted: 09.10.2016

By Karen Weintraub Researchers have long believed that problems with mitochondria—the power plants of cells—underlie some cases of Parkinson’s disease. Now a new study details those problems, and suggests that they may form a common thread linking previously unexplained cases of the disease with those caused by different genetic anomalies or toxins. Finding a common mechanism behind different suspected causes of Parkinson’s suggests that there might also be a common means to measure, treat or cure it, says Marco Baptista, research director at the nonprofit Michael J. Fox Foundation, a leading center for study and advocacy in the fight against Parkinson’s. The study, published Thursday in Cell Stem Cell, did identify a possible way to reverse the damage of Parkinson’s—but only in individual cells and fruit flies. Finding a treatment that does the same thing in people will be challenging, Baptista says. Roughly one million Americans have Parkinson’s disease, which is characterized by motor problems and can cause other symptoms including cognitive and gastrointestinal difficulties. About 1 to 2 percent of cases are linked to mutations in the LRRK2 gene, with far fewer associated with genes known as PINK1 and Parkin. Exposure to environmental factors such as toxic chemicals can also lead to Parkinson’s, although most cases have no obvious cause. In the new paper Xinnan Wang, an assistant professor of neurosurgery at Stanford University, and her colleagues show that mitochondria are underpowered in several types of Parkinson’s and that these mitochondria also release toxic chemicals. Looking at fly models of the disease as well as cells taken from patients, the researchers found that they could correct these problems and reverse neurodegeneration if they reduced levels of a protein involved in mitochondrial activity. © 2016 Scientific American

Keyword: Parkinsons
Link ID: 22642 - Posted: 09.10.2016

By NATALIE ANGIER The female bonobo apes of the Wamba forest in the Democratic Republic of Congo had just finished breakfast and were preparing for a brief nap in the treetops, bending and crisscrossing leafy branches into comfortable day beds. But one of the females was in estrus, her rump exceptionally pink and swollen, and four males in the group were too excited to sleep. They took turns wildly swinging and jumping around the fertile female and her bunkmates, shaking the branches, appearing to display their erections and perforating the air with high-pitched screams and hoots. Suddenly, three older, high-ranking female bonobos bolted up from below, a furious blur of black fur and swinging limbs and, together with the female in estrus, flew straight for the offending males. The males scattered. The females pursued them. Tree boughs bounced and cracked. Screams on all sides grew deafening. Three of the males escaped, but the females cornered and grabbed the fourth one — the resident alpha male. He was healthy, muscular and about 18 pounds heavier than any of his captors. But no matter. The females bit into him as he howled and struggled to pull free. Finally, “he dropped from the tree and ran away, and he didn’t appear again for about three weeks,” said Nahoko Tokuyama, of the Primate Research Institute at Kyoto University in Japan, who witnessed the encounter. When the male returned, he kept to himself. Dr. Tokuyama noticed that the tip of one of his toes was gone. “Being hated by females,” she said in an email interview, “is a big matter for male bonobos.” The toe-trimming incident was extreme but not unique. Describing results from their long-term field work in the September issue of Animal Behaviour, Dr. Tokuyama and her colleague Takeshi Furuichi reported that the female bonobos of Wamba often banded together to fend off male aggression, and in patterns that defied the standard primate rule book. © 2016 The New York Times Company

Keyword: Aggression; Sexual Behavior
Link ID: 22641 - Posted: 09.10.2016

By Karen Zusi At least one type of social learning, or the ability to learn from observing others’ actions, is processed by individual neurons within a region of the human brain called the rostral anterior cingulate cortex (rACC), according to a study published today (September 6) in Nature Communications. The work is the first direct analysis in humans of the neuronal activity that encodes information about others’ behavior. “The idea [is] that there could be an area that’s specialized for processing things about other people,” says Matthew Apps, a neuroscientist at the University of Oxford who was not involved with the study. “How we think about other people might use distinct processes from how we might think about ourselves.” During the social learning experiments, the University of California, Los Angeles (UCLA) and CalTech–based research team recorded the activity of individual neurons in the brains of epilepsy patients. The patients were undergoing a weeks-long procedure at the Ronald Reagan UCLA Medical Center in which their brains were implanted with electrodes to locate the origin of their epileptic seizures. Access to this patient population was key to the study. “It’s a very rare dataset,” says Apps. “It really does add a lot to the story.” With data streaming out of the patients’ brains, the researchers taught the subjects to play a card game on a laptop. Each turn, the patients could select from one of two decks of face-down cards: the cards either gave $10 or $100 in virtual winnings, or subtracted $10 or $100. In one deck, 70 percent of the cards were winning cards, while in the other only 30 percent were. The goal was to rack up the most money. © 1986-2016 The Scientist

Keyword: Learning & Memory; Attention
Link ID: 22640 - Posted: 09.10.2016

By Jessica Hamzelou As any weight-watcher knows, carb cravings can be hard to resist. Now there’s evidence that carbohydrate-rich foods may elicit a unique taste too, suggesting that “starchy” could be a flavour in its own right. It has long been thought that our tongues register a small number of primary tastes: salty, sweet, sour and bitter. Umami – the savoury taste often associated with monosodium glutamate – was added to this list seven years ago, but there’s been no change since then. However, this list misses a major component of our diets, says Juyun Lim at Oregon State University in Corvallis. “Every culture has a major source of complex carbohydrate. The idea that we can’t taste what we’re eating doesn’t make sense,” she says. Complex carbohydrates such as starch are made of chains of sugar molecules and are an important source of energy in our diets. However, food scientists have tended to ignore the idea that we might be able to specifically taste them, says Lim. Because enzymes in our saliva break starch down into shorter chains and simple sugars, many have assumed we detect starch by tasting these sweet molecules. Her team tested this by giving a range of different carbohydrate solutions to volunteers – who it turned out were able to detect a starch-like taste in solutions that contained long or shorter carbohydrate chains. “They called the taste ‘starchy’,” says Lim. “Asians would say it was rice-like, while Caucasians described it as bread-like or pasta-like. It’s like eating flour.” © Copyright Reed Business Information Ltd.

Keyword: Chemical Senses (Smell & Taste); Obesity
Link ID: 22639 - Posted: 09.10.2016

By Abby Olena Mammalian prions are notoriously difficult as structural biology subjects, given their insolubility and tendency to aggregate. Researchers have now overcome these challenges to figure out the preliminary structure of a shortened form of infectious prion (PrPSc), which they report today (September 8) in PLOS Pathogens. “For the first time, we have a structure of an infectious mammalian prion,” said Giuseppe Legname of Scuola Internazionale Superiore di Studi Avanzati in Trieste, Italy, who was not involved in this study. “It’s a very important paper,” he added. “What we have done is to obtain a very simple, very preliminary idea of what the structure of these mammalian prions are,” said study coauthor Jesús Requena of the University of Santiago de Compostela in Spain. Requena and colleagues generated a shortened form of PrPSc by injecting a laboratory strain of prions into transgenic mice that express a truncated form of normal cellular prion protein (PrPC), which lacks the attachment of a membrane anchor present in full-length PrPSc. In nature, PrPC transforms into full-length PrPSc, which causes Creutzfeldt-Jakob disease in humans, scrapie in sheep, and mad cow disease. The absence of the membrane anchor in shortened PrPSc from the transgenic mice allowed the researchers to isolate a fairly homogeneous population of PrPSc. They confirmed that this population was infectious by inoculating wild-type mice, which then developed symptoms of prion disease. © 1986-2016 The Scientist

Keyword: Prions
Link ID: 22638 - Posted: 09.10.2016

By JACK HEALY CINCINNATI — On the day he almost died, John Hatmaker bought a packet of Oreos and some ruby-red Swedish Fish at the corner store for his 5-year-old son. He was walking home when he spotted a man who used to sell him heroin. Mr. Hatmaker, 29, had overdosed seven times in the four years he had been addicted to pain pills and heroin. But he hoped he was past all that. He had planned to spend that Saturday afternoon, Aug. 27, showing his son the motorcycles and enjoying the music at a prayer rally for Hope Over Heroin in this region stricken by soaring rates of drug overdoses and opioid deaths. But first, he decided as he palmed a sample folded into a square of paper, he would snort this. As he crumpled to the sidewalk, Mr. Hatmaker became one of more than 200 people to overdose in the Cincinnati area in the past two weeks, leaving three people dead in what the officials here called an unprecedented spike. Similar increases in overdoses have rippled recently through Indiana, Kentucky and West Virginia, overwhelming ambulance crews and emergency rooms and stunning some antidrug advocates. Addiction specialists said the sharp increases in overdoses were a grim symptom of America’s heroin epidemic, and of the growing prevalence of powerful synthetic opiates like fentanyl. The synthetics are often mixed into batches of heroin, or sprinkled into mixtures of caffeine, antihistamines and other fillers. In Cincinnati, some medical and law enforcement officials said they believed the overdoses were largely caused by a synthetic drug called carfentanil, an animal tranquilizer used on livestock and elephants with no practical uses for humans. Fentanyl can be 50 times stronger than heroin, and carfentanil is as much as 100 times more potent than fentanyl. Experts said an amount smaller than a snowflake could kill a person. © 2016 The New York Times Company

Keyword: Drug Abuse; Pain & Touch
Link ID: 22637 - Posted: 09.07.2016

By Helen Thomson High levels of inflammation as a child may predict a higher risk of manic behaviour in later life, a finding that could lead to new ways of treating conditions like bipolar disorder. Hypomania involves spells of hyperactivity and is often a symptom of mood disorders, including bipolar disorder, seasonal affective disorder and some kinds of psychosis. People experiencing hypomania may take more risks, feel more confident and become impatient with others. After spells like this, they may “crash”, needing to sleep for long periods and sometimes remembering little about the previous few days. Earlier studies suggested a link between inflammation and mood disorders, prompting Joseph Hayes at University College London and his team to see if inflammation as a child might lead to mental health problems later. Analysing data from more than 1700 people, his team identified a significant link between high levels of a chemical involved in inflammation at age 9, and experiencing aspects of hypomania at age 22. The chemical, called IL-6, is normally secreted by white blood cells to stimulate an inflammatory immune response to infection or trauma. Hayes’s team says it is unclear how inflammation in childhood could induce symptoms of hypomania but IL-6 is known to affect the brain. A study that used injections to increase IL-6 in the blood of healthy volunteers found that this caused symptoms of anxiety, and reduced performance in memory tests. © Copyright Reed Business Information Ltd.

Keyword: Schizophrenia
Link ID: 22636 - Posted: 09.07.2016

Hannah Devlin Science correspondent Babies born by caesarean section are more likely to be obese as adults, according to a study that suggests the way we are born could have a lasting impact on health. Birth by caesarean was linked to a 15% higher risk of obesity in children compared with vaginal birth. The scientists involved believe that babies born by caesarean miss out on exposure to bacteria in the birth canal that colonise the baby’s gut and may ultimately change the body’s metabolic rate - and even how hungry we feel. Audrey Gaskins, an epidemiologist at Harvard University and co-author of the new study, said: “Children born via C-section harbour less diverse gut bacteria and these patterns of less diversity have been linked to increased capacity for energy harvest by the gut microbiota. You can think of it as a slower metabolism.” Previous studies have found the same link, but were less able to rule out other factors, such as the mother’s weight or health. The latest research, which included 22,068 children born to 15,271 women, suggests that the link is not simply explained by overweight women or those with pregnancy complications such as high blood pressure being more likely to deliver by caesarean. The link remained after maternal weight was taken into account, and was more striking when siblings who had different types of births were compared. Within families, children born by caesarean were 64% more likely to be obese than their siblings born by vaginal delivery. “With siblings, they have the same mother and home environment so the genetics, the feeding environment, are all controlled for,” said Dr Gaskins. © 2016 Guardian News and Media Limited

Keyword: Obesity; Development of the Brain
Link ID: 22635 - Posted: 09.07.2016

By JANE E. BRODY As a woman of a certain age who consumes a well-balanced diet of all the usual food groups, including reasonable amounts of animal protein, I tend to dismiss advice to take a multivitamin supplement. I’ve been told repeatedly by nutrition experts that the overuse of dietary supplements for “nutritional insurance” has given Americans the most expensive urine in the world. I do take a daily supplement of vitamin D, based on considerable evidence of its multiple health benefits, especially for older people. However, based on advice from the National Academy of Medicine and an examination of accumulating research, I’m prompted to consider also taking a vitamin B12 supplement in hopes of protecting my aging brain. Animal protein foods — meat, fish, milk, cheese and eggs — are the only reliable natural dietary sources of B12, and I do get ample amounts of several in my regular diet. But now at age 75, I wonder whether I’m still able to reap the full benefit of what I ingest. You see, the ability to absorb B12 naturally present in foods depends on the presence of adequate stomach acid, the enzyme pepsin and a gastric protein called intrinsic factor to release the vitamin from the food protein it is attached to. Only then can the vitamin be absorbed by the small intestine. As people age, acid-producing cells in the stomach may gradually cease to function, a condition called atrophic gastritis. A century ago, researchers discovered that some people — most likely including Mary Todd Lincoln — had a condition called pernicious anemia, a deficiency of red blood cells ultimately identified as an autoimmune disease that causes a loss of stomach cells needed for B12 absorption. Mrs. Lincoln was known to behave erratically and was ultimately committed to a mental hospital. © 2016 The New York Times Company

Keyword: Development of the Brain
Link ID: 22634 - Posted: 09.06.2016

Chris Chambers One of the most compelling impressions in everyday life is that wherever we look, we “see” everything that is happening in front of us – much like a camera. But this impression is deceiving. In reality our senses are bombarded by continual waves of stimuli, triggering an avalanche of sensations that far exceed the brain’s capacity. To make sense of the world, the brain needs to determine which sensations are the most important for our current goals, focusing resources on the ones that matter and throwing away the rest. These computations are astonishingly complex, and what makes attention even more remarkable is just how effortless it is. The mammalian attention system is perhaps the most efficient and precisely tuned junk filter we know of, refined through millions of years of annoying siblings (and some evolution). Attention is amazing but no system is ever perfect. Our brain’s computational reserves are large but not infinite, and under the right conditions we can “break it” and peek behind the curtain. This isn’t just a fun trick – understanding these limits can yield important insights into psychology and neurobiology, helping us to diagnose and treat impairments that follow brain injury and disease. Thanks to over a hundred years of psychology research, it’s relatively easy to reveal attention in action. One way is through the phenomenon of change blindness. Try it yourself by following the instructions in the short video below (no sound). When we think of the term “blindness” we tend to assume a loss of vision caused by damage to the eye or optic nerves. But as you saw in the video, change blindness is completely normal and is caused by maxing out your attentional capacity. © 2016 Guardian News and Media Limited

Keyword: Attention; Vision
Link ID: 22633 - Posted: 09.06.2016

By Clare Wilson Traffic fumes go to your head. Tiny specks of metal in exhaust gases seem to fly up our noses and travel into our brains, where they may contribute to Alzheimer’s disease. Iron nanoparticles were already known to be present in the brain – but they were thought to come from the iron naturally found in our bodies, derived from food. Now a closer look at their structure suggests the particles mostly come from air pollution sources, like traffic fumes and coal burning. The findings are a smoking gun, says Barbara Maher of Lancaster University in the UK. Iron is present harmlessly in our bodies in different forms, as it is part of many biological molecules. But the form known as magnetite, or iron oxide, which is highly reactive and magnetic, has been implicated in Alzheimer’s disease. Maher’s team looked at the brains of 37 people who had lived either in Manchester in the UK or Mexico City. All contained millions of magnetite particles per gram of brain tissue, detected by measuring how magnetic the brain tissue was. The surprise came when the team used electron microscopes to take a close look at particles in the front part of the brains of six people. Round particles of magnetite outnumbered angular magnetite crystals by about one hundred to one. Crystal forms are more likely to have a natural source – such as iron that has come out of the body’s cells. But round particles normally come from melting iron at high temperatures, which happens when fuel is burned. © Copyright Reed Business Information Ltd.

Keyword: Neurotoxins
Link ID: 22632 - Posted: 09.06.2016

Susan Milius Contrary to many adorable children’s stories, hibernation is so not sleeping. And most animals can’t do both at the same time. So what’s with Madagascar’s dwarf lemurs? The fat-tailed dwarf lemur slows its metabolism into true hibernation, and stays there even when brain monitoring shows it’s also sleeping. But two lemur cousins, scientists have just learned, don’t multitask. Like other animals, they have to rev their metabolisms out of hibernation if they want a nap. Hibernating animals, in the strictest sense, stop regulating body temperature, says Peter Klopfer, cofounder of the Duke Lemur Center in Durham, N.C. “They become totally cold-blooded, like snakes.” By this definition, bears don’t hibernate; they downregulate, dropping their body temperatures only modestly, even when winter den temperatures sink lower. And real hibernation lasts months, disqualifying short-termers such as subtropical hummingbirds. The darting fliers cease temperature regulation and go truly torpid at night. “You can pick them out of the trees,” Klopfer says. The fat-tailed dwarf lemur, Cheirogaleus medius, was the first primate hibernator discovered, snuggling deep into the softly rotting wood of dead trees. “You’d think they’d suffocate,” he says. But their oxygen demands plunge to somewhere around 1 percent of usual. As trees warm during the day and cool at night, so do these lemurs. When both a tree and its inner lemur heat up, the lemur’s brain activity reflects mammalian REM sleep. |© Society for Science & the Public 2000 - 2016

Keyword: Sleep; Evolution
Link ID: 22631 - Posted: 09.06.2016

By Andy Coghlan Antidepressants may be bad for your bones. People who take some selective serotonin reuptake inhibitors (SSRI) have been found to have a higher risk of fractures, but it wasn’t clear whether this was due to the drug or their depression. “It’s a puzzling question,” says Patricia Ducy at Columbia University, New York. But her team have now found that giving mice fluoxetine – the active ingredient in Prozac – for six weeks causes them to lose bone mass. The team identified a two-stage process by measuring bones, blood and gene activity. During the first three weeks, bones grew stronger as the fluoxetine impaired osteoclasts, cells that usually deplete bone tissue. But by six weeks, the higher levels of serotonin prompted by the drug disrupted the ability of the hypothalamus region of the brain to promote bone growth. “We see bone gain, but it’s not long-lasting, and is rapidly overwhelmed by the negative effects,” says Ducy. She says this two-phase pattern is also seen in people. In the short term, those who take fluoxetine are less likely to break a bone, but the risk of bone depletion and fractures rises when they have been taking the drug for a year or more. © Copyright Reed Business Information Ltd.

Keyword: Depression
Link ID: 22630 - Posted: 09.06.2016