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By SINDYA N. BHANOO Mosquito sperm have a sense of smell, researchers are reporting, in a finding that could suggest ways to help control the spread of disease-carrying insects. The sperm carries a set of chemical sensors identical to the olfactory receptors on the mosquitoes’ antennas, according to a study in Proceedings of the National Academy of Sciences. Mosquitoes mate just once in their lifetime, and the female stores the male’s sperm in an organ called a spermatheca. Before the eggs mature, the female seeks out blood using the receptors on her antennas. Soon after, chemical signals cause the sperm tails to beat rapidly and start the fertilization process. “The sperm may need a chemical signal to become ready for fertilization,” said Jason Pitts, a researcher at Vanderbilt University and an author of the study, which was supported by the Gates Foundation as part of its efforts to improve global health. Another author, Laurence Zwiebel, also a Vanderbilt researcher, called the dual use of the olfactory receptors a clear and clever example of convergent evolution: The mosquitoes, he said, “found something that works and use it in multiple ways.” The scientists think olfactory receptors may exist on the sperm of many other insects, and they are developing chemical compounds that can be applied to breeding grounds to block the receptors. “You can effectively confuse the sperm or make them inactive,” Dr. Zwiebel said. © 2014 The New York Times Company
By Caitlin Kirkwood Glorious, refreshing sleep is eluding the majority of Americans. According to the National Sleep Foundation’s 2013 International Bedroom Poll 56 percent of people between the ages of 25 and 55 get an insufficient amount of sleep on workdays. On non-workdays individuals are then more likely to oversleep. They spend an additional 45 minutes catching Z’s in an attempt to compensate for accrued workweek sleep debt. Why are we constantly playing sleep-catch up during free time? As a society we are socially jet lagged. Social jet lag is the difference betweensleep patterns on work days and free days. These inconsistent sleeping habits result in sleep loss that is reminiscent of flying west across several time zones every Friday evening and traveling back East come Monday morning. The pattern reveals a critical disparity between society-imposed obligations, like work and family commitments, and our innate biological clock. Social jet lag might not sound like a big deal. What’s an hour or two of sleep lost here and there? But the chronic misalignment between our social and biological clocks is wreaking havoc on our health. Large-scale epidemiological studies have pointed a finger at short sleep duration for it’s causative role in the nationwide obesity crisis. When you get too little sleep, normal levels of appetite hormones are altered in a way that could lead to increased food consumption and weight gain. Unfortunately for people struggling with social jet lag, short sleep duration comes with the territory of the workweek. Some data even suggest that for every hour the biological clock is offset from the social clock, the chances of being overweight shoot-up by a whopping 33 percent. And supersizing the body mass index isn’t the only problem. Social jet lag has also been linked to the increased likelihood of nicotine and alcohol use, which independently contribute to additional health problems. © 2014 Scientific American
Link ID: 19240 - Posted: 02.12.2014
It seems simple: People are more likely to cooperate if everyone plays fair. But a new study suggests that fairness itself arises from an unlikely source: spite. Researchers made a mathematical model based on the so-called ultimatum game. In it, two players are offered a reward, and the first player makes an offer for how it should be split up. If the second player agrees, then they divide it accordingly. But if the second player refuses, then neither gets the reward. As shown in the image above, depending on the interaction of the players, the outcome can be classified as altruism, cooperation, selfishness, or spite. Previous experiments have shown that, over multiple rounds of the game, a culture of cooperation evolves where everyone makes fair offers. But the new study, published online today in the Proceedings of the Royal Society B, finds that when players start out using multiple different strategies, by making fair or unfair offers, and rejecting or accepting unfair offers, some will act out of spite. These spiteful players deny the first player the reward at a cost to himself. The calculations further show that the antisocial behavior will eventually cause fairness to become the most successful option, because there is no reason to reject a fair offer. In essence, fairness evolves in spite of spite, when players start out using different strategies. Though they warn against generalizing to humans, the researchers point out that if fairness is the basis for a moral society, then paradoxically, spite may have played a role in the evolution of morality. © 2014 American Association for the Advancement of Science.
By JOHN LA PUMA SANTA BARBARA, Calif. — A FUNNY thing has happened in the United States over the last few decades. Men’s average testosterone levels have been dropping by at least 1 percent a year, according to a 2006 study in The Journal of Clinical Endocrinology and Metabolism. Testosterone appears to decline naturally with aging, but internal belly fat depresses the hormone further, especially in obese men. Drugs like steroids and opiates also lower testosterone, and it’s suspected that chemicals like bisphenol A (or BPA, commonly found in plastic food containers) and diseases like Type 2 diabetes play a role as well. Men feel the loss. Clinical testosterone deficiency, which is variously defined as lower than 220 to 350 nanograms of testosterone per deciliter of blood serum, can cause men to lose sex drive and fertility. Their bone density often declines, and they may feel tired and experience hot flashes and sweats. But “low T,” as the condition has been labeled, isn’t nearly as common as the drug ads for prescription testosterone would have you believe. Pharmaceutical companies have seized on the decline in testosterone levels as pathological and applicable to every man. They aim to convince men that common effects of aging like slowing down a bit and feeling less sexual actually constitute a new disease, and that they need a prescription to cure it. This is a seductive message for many men, who just want to feel better than they do, and want to give it a shot, literally. The problem is that prescription testosterone doesn’t just give your T level a boost: it may also increase your risk of heart attack. It can add huge numbers of red blood cells to your bloodstream and shrink your testes. In some men, it increases aggression and irritability. © 2014 The New York Times Company
Keyword: Hormones & Behavior
Link ID: 19238 - Posted: 02.11.2014
by Laura Sanders A new analysis of cows shows that mamas make more milk for daughters. Other studies have hinted that human moms produce different milk for sons than for daughters, so perhaps lactating women also boost production for daughters. I love eavesdropping on people’s overly detailed coffee orders. You, sir, with the temerity to order a skinny split quad shot latte no whip no foam, with a side of lemon? Your extreme customizing just made my day. Such personalization was running through my mind as I read a recent study on cows. It turns out that another beverage is also subject to the specific, exacting standards of its drinker: milk. And the customer’s bossy demands seem to start before he or she is born. Heifers produce more milk for daughters than sons, Katie Hinde and colleagues report February 3 in PLOS ONE. When a cow gives birth to her first female, she makes about 1.6 percent more milk than she would have for a son, Hinde and colleagues found by analyzing the dairy records from a million and a half cows. And because calves born at dairy farms are taken away from their mothers soon after birth, the female calves’ requests to “make me more milk” must have come during pregnancy. Another interesting finding: The first pregnancy had an outsized effect on the cow’s future milk production. Cows that had sons first saw a slight bump in production when they got pregnant with a daughter, but didn’t catch up to the cows that had a daughter followed by a son. The first born daughter set the mom’s milk-making machinery on high, and that’s where it stayed for subsequent pregnancies. © Society for Science & the Public 2000 - 2013
Keyword: Sexual Behavior
Link ID: 19237 - Posted: 02.11.2014
|By Annie Sneed Alzheimer’s disease is now the sixth leading cause of death in the U.S., but researchers still do not know what causes the degenerative neurological disorder. In recent years they have pinpointed several genes that seem largely responsible for those cases in which the disorder develops early on, prior to age 60. They have also identified about 20 genes that can increase or decrease risk for the more common late-onset variety that starts appearing in people older than 60. But genetics simply cannot explain the whole picture for the over five million Americans with late-onset Alzheimer’s. Whereas genetics contribute some risk of developing this version of the disorder, no combination of genes inevitably leads to the disease. Scientists are now urgently searching for the other missing pieces to explain what causes late-onset Alzheimer’s. Some researchers have shifted their attention from genes to the environment—especially to certain toxins. Their studies of pesticides, food additives, air pollution and other problematic compounds are opening a new front in the battle against this devastating malady. Here’s a roundup of some of the possibilities being studied: Scientists have already found a strong potential link between pesticides and Parkinson’s disease. Now, a preliminary study released in January suggests that the pesticide DDT, which degrades so slowly that it continues to linger in the environment more than 40 years after the U.S. Environmental Protection Agency banned its use in the U.S., may also contribute to Alzheimer’s. © 2014 Scientific American
By DEBORAH SONTAG HUDSON, Wis. — Karen Hale averts her eyes when she drives past the Super 8 motel in this picturesque riverfront town where her 21-year-old daughter, Alysa Ivy, died of an overdose last May. She has contemplated asking the medical examiner, now a friend, to accompany her there so she could lie on the bed in Room 223 where her child’s body was found. But Ms. Hale, 52, is not ready, just as she is not ready to dismantle Ms. Ivy’s bedroom, where an uncapped red lipstick sits on the dresser and a teddy bear on the duvet. The jumble of belongings both comforts and unsettles her — colorful bras, bangle bracelets and childhood artwork; court summonses; a 12-step bible; and a Hawaiian lei, bloodstained, that her daughter used as a tourniquet for shooting heroin into her veins. “My son asked me not to make a shrine for her,” Ms. Hale said. “But I don’t know what to do with her room. I guess on some level I’m still waiting for her to come home. I’d be so much more empathetic now. I used to take it personal, like she was doing this to me and I was a victim.” When the actor Philip Seymour Hoffman died with a needle in his arm on Feb. 2, Ms. Hale thought first about his mother, then his children. Few understand the way addiction mangles families, she said, and the rippling toll of the tens of thousands of fatal heroin and painkiller overdoses every year. Perhaps it took Mr. Hoffman’s death, she said, to “wake up America to all the no-names who passed away before him,” leaving a cross-country trail of bereavement. © 2014 The New York Times Company
Keyword: Drug Abuse
Link ID: 19235 - Posted: 02.11.2014
Eighteen neurological patients in North Carolina may have been exposed to an incurable and fatal disorder similar to "mad cow" disease while undergoing surgery at the Novant Health Forsyth Medical Center because surgical instruments were insufficiently sterilized, the hospital said on Monday. Surgeons operated on the 18 patients on January 18 using tools that had not been sufficiently sanitized after they were used on a man suspected of having Creutzfeldt-Jakob Disease (CJD), the hospital in Winston-Salem said in a press statement. "On behalf of the entire team at Novant Health, I apologize to the patients and their families for having caused this anxiety," Jeff Lindsay, president of the medical center, said at a news conference. CJD causes failing memory, blindness, involuntary movement and coma, and kills 90 percent of patients within one year, according to the National Institute of Neurological Disorders and Stroke. The condition is similar to mad cow disease, but is not linked to beef consumption. The incubation period — before initial symptoms surface — can last years, the statement said. After the first sign of symptoms, most patients die within four months, it said The possibility of contracting the disease through surgical exposure is very remote, the hospital said.
Link ID: 19234 - Posted: 02.11.2014
By Daniel Engber Drop a mouse in some water and white paint, and it will know just what to do. Mice can swim, by whipping their tails like a flagellum, but they don't like doing it; a mouse in a tub tries to find a way out. There's no need for training, or food pellets, or annoying electric shocks: To put a mouse through a water maze, you need only to build a little platform for it, hidden somewhere just beneath the surface. The mouse will try to find that platform without any encouragement. It's a setup that's so simple—and so useful in measuring an animal's capacity for learning and memory—it hardly seems like it would need inventing. But it took a cognitive neuroscientist at the University of St. Andrews in Scotland to come up with the tub-and-platform method. In 1979, Richard Morris built a heated pool about 4 feet and 3 inches in diameter, filled it with water and fresh milk, and then added a platform made of stones and drain piping. Within a few years, his method (designed for rats) had been adapted for smaller lab mice, and had made its way into rodent labs around the world. Now it's among the most widespread animal-testing protocols in all of biomedicine. Scientists plunge mice in murky water to test the effects of brain damage, or the functions of particular genes on learning, or the efficacy of new drugs for treating Alzheimer's. You can even buy a standard-issue "Morris Water Maze" direct from a lab-supply shop, along with specialized software for recording its results. That fact that so few of us would call a tub full of milk a “maze” only goes to show that rodent mazes aren't what they used to be. Early psychologists tempted rats with tricky blind alleys and wrong turns using contraptions built by hand, of wood and wire. © 2014 The Slate Group LLC.
Keyword: Learning & Memory
Link ID: 19233 - Posted: 02.11.2014
You probably saw dozens of people’s faces today, many more if you live in a city. You may not have been conscious of it, but you were subtly judging every one by its beauty. Your eyes are drawn to more attractive faces, and the almost inescapable result is that more attractive people have advantages in almost every aspect of life, from job interviews to prison sentencing. But what drives us to crave beauty? According to one theory, gazing upon beauty stimulates the brain’s μ-opioid receptors (MOR), thought to be a key part of our biochemical reward system. At least in rodents, stimulating or inhibiting MOR neurotransmission not only tweaks the animals’ appetite for sex or food, but also the strength of their preferences for particular foods or mates. Is our preference for pretty faces driven by the same biochemical reward circuit? To find out, researchers invited 30 heterosexual men to browse a series of female faces on a computer (one pictured). Each man received either a dose of the MOR-stimulating drug morphine, the opioid receptor–inhibiting drug naltrexone, or a placebo. The results, published today in Molecular Psychiatry, suggest that we seek out beautiful faces at least in part because our brains reward us. Not only did stimulating MOR neurotransmission cause men to linger longer on faces that they rated as more beautiful, but the beauty rating also became more extreme, with beautiful faces rated as even more attractive relative to the rest of the faces. Inhibiting MOR had the opposite effects. The findings are yet more evidence that our social interactions are strongly influenced by the invisible hand of evolution, pushing us to find attractive mates. But the question remains, how do we decide which face is attractive in the first place? © 2014 American Association for the Advancement of Science
|By Simon Makin For decades two very different treatments of depression have existed side by side. Medications act on molecules, cells and synapses in the brain. Psychological therapies focus on cognition and behavior, trying to alter negatively biased thinking. Now a new theory suggests that these interventions may work in more similar ways than anyone realized, providing an opportunity to better integrate the two approaches. More important, it may help provide patients faster, more reliable relief from this crippling condition. Antidepressant drugs increase the levels of certain chemical messengers in the brain, such as serotonin and norepinephrine. Yet exactly how these neurotransmitters affect mood is unknown. “There was a missing link between the cellular, molecular and synaptic bases of these drugs, on the one hand, and what they affect in humans, which is their experiences, perceptions, memories and feelings,” says Catherine Harmer, a neuroscientist at the University of Oxford. The psychological explanation, meanwhile, describes depression in terms of distorted information processing. Depressed people are thought to process perceptions, experiences and memories with a negative bias. Many studies confirm that depressed individuals show increased sensitivity to sad faces, greater memory for negative material and reduced responsiveness to rewards as compared with healthy people. Successful therapies teach patients how to correct for this clouded vision. Harmer now believes that antidepressants may also work by altering this negative emotional processing. About a decade ago she and her colleagues tested the effects of commonly prescribed antidepressants on healthy volunteers and found that many of the drugs skewed emotional processing to the positive. Previous research had shown that antidepressants also change these measures in depressed people, but studies included only patients who had been on medication for six to eight weeks because the drugs were assumed to take that long to kick in. © 2014 Scientific American
by Bob Holmes Midnight fridge raids are part and parcel of a late-night marijuana smoking session. A study in mice has provided the most complete explanation yet for why a spliff triggers intense hunger pangs. The findings, which elucidate the role of smell, also suggest that we might eventually be able to treat common disorders such as obesity and loss of appetite with a simple nasal spray. We know that the active ingredient in cannabis, THC, binds to cannabinoid receptors in the brain called CB1s. This binding inhibits chemical signals that tell us not to eat, and so make us feel hungry. But this isn't the end of the story. Since smell plays such a central role in making us feel hungry, it must be part of the explanation - but no one knew exactly how it fit. To find out, Giovanni Marsicano of the French research agency INSERM in Bordeaux and his colleagues genetically modified mice to make it possible to turn on and off the CB1 receptor in particular nerve cells within the smell, or olfactory, system. The key proved to be a group of nerve cells that carry signals from the cerebral cortex down to the olfactory bulb, the primary smell centre of the brain. When the team switched off CB1 on these cells, they found that hungry mice no longer ate more than their well-fed counterparts. Conversely, activating CB1 in the same cells by injecting THC caused hungry mice to eat even more. THC-treated mice also responded to less-concentrated food smells than untreated mice, a sign that the chemical had enhanced their sense of smell. © Copyright Reed Business Information Ltd.
By Maggie Fox Researchers looking for simple ways to treat autism say they may have explained why at least some cases occur: It all has to do with the stress babies undergo at birth. They’re already testing a simple drug for treating kids with autism and say their findings may point to ways to treat the disorder earlier in life. It’s all experimental, but the study, published in the journal Science, should inspire other researchers to take a closer look. “This is exciting stuff to people in the field, because it’s getting at a basic mechanism," says Andrew Zimmerman of the University of Massachusetts Medical School, who reviewed the study. Yehezkel Ben-Ari of the Mediterranean Institute of Neurobiology in Marseille, France, and colleagues have been treating children with autism with a diuretic called bumetanide that reduces levels of chloride in cells. Diuretics lower blood pressure by making people urinate more, reducing fluid. Ben-Ari has had mixed success in his trials in kids, and wanted to prove his theory that chloride was the key. He worked with two rodent “models” of autism — they’re the closest things scientists have for replicating autism in a human. One has mutated genes linked with autism, and another develops autism when given valproate, an epilepsy drug blamed for causing autism in the children of mothers who take it while pregnant. They looked at what was going on in the brains of the mouse and rat pups just before and after birth. Then they gave the mouse and rat moms bumetanide — and fewer of their newborns showed autistic-like behaviors.
By JENNIFER CONLIN It is the moment “The Biggest Loser” viewers anticipate all season. That episode when the finalists emerge, one by one, to bare all — or rather less — to a waiting audience of millions. But on Tuesday night, when Rachel Frederickson, 24, walked onto the studio stage 155 pounds lighter than at the start of Season 15, the reaction was not one of awe, but shock, apparent even on the trainers’ frozen faces. In the few months since Ms. Frederickson, 5 feet 4 inches tall, had left the ranch for her home, her body had radically changed from the athletic 150 pounds she had weighed upon her departure to a gaunt sliver of herself, obvious despite her shimmering silver dress, strappy sandals and big grin. Ms. Frederickson, as the scale would soon reveal, now weighed 105 pounds, and having lost 59.62 percent of her body weight would also be the competition’s winner, making her $250,000 richer. But as confetti dropped all around her, few were celebrating on Twitter. “I feel like Rachel lost too much,” one woman wrote. “I had to turn away.” Another posted, “There needs to be a red line that disqualifies finalists for too much weight loss.” Kai Hibbard, a finalist on Season 3, was at her home in Alaska when another former contestant, whom she declined to name, sent her a message. “Have you seen tonight’s winner?” it read. “NBC is about to have a public-relations nightmare.” When Ms. Hibbard pulled up Ms. Frederickson’s winning photo, she promptly burst into tears. “Rachel doesn’t know what damage she has done to her body and her mind, and sadly she won’t until the spotlight goes away,” said Ms. Hibbard, 35, who seven years ago lost 118 pounds during her competition but has since spoken out publicly against the show’s extreme dieting and exercise regimen. © 2014 The New York Times Company
Schizophrenia and related mental illnesses can have a devastating effect on people who suffer from them, often making it impossible for them to work or maintain normal social relationships. Antipsychotic drugs are usually the first line of defense, but they can have serious side effects. A new study concludes that psychological approaches could be an alternative for patients who either can’t or won’t take medication, although some critics continue to question the effectiveness of these interventions. Schizophrenia, which can involve hallucinations, delusions, paranoia, emotional problems, and severe difficulty focusing on daily tasks, affects about 1% of populations worldwide. More than 20 antipsychotic medications, such as risperidone, haloperidol, and clozapine, are now on the market, and they are often effective in temporarily relieving the worse symptoms. But when taken for extended periods, such drugs can cause uncontrollable muscle movements, serious weight gain, and higher risk of heart attacks. In recent years, a number of psychiatrists and psychologists have begun to advocate psychological approaches, including an approach called cognitive behavioral therapy (CBT), as an adjunct to antipsychotic drugs. With CBT, which has long been shown to be effective for depression and anxiety disorders, a therapist takes the subject through a series of guided steps designed to explore alternative interpretations and explanations of what he or she is experiencing, with the goal of changing both outlook and behavior. A schizophrenic patient who is having hallucinations might be encouraged to stop trying to fight them off or suppress them, for example, or to stop engaging with voices in his or her head, to test how strong such symptoms really are and how much control they exert over the subject’s life. The technique also involves what practitioners call “normalization”: The patient might be reassured that hearing voices and seeing things that are not there is an experience that many normal people have from time to time, thus reducing some of the anxiety that makes sufferers feel distressed and isolated. © 2014 American Association for the Advancement of Science
Link ID: 19227 - Posted: 02.08.2014
by Clare Wilson SOMETIMES you find out more about how something works by turning it off. That seems to be true for mirror neurons, the brain cells implicated in traits ranging from empathy and learning to language acquisition. Mirror neurons are said to help us interpret other people's behaviour, but this has yet to be shown convincingly in experiments. Now a study that briefly disabled these cells might give a better idea of what they do. Mirror neurons were discovered in the 1990s when an Italian team was measuring electrical activity in the brains of monkeys. In the region that controls movement, some of the neurons that fire to carry out a particular action – such as grasping an apple – also fired when the monkey saw another animal do the same thing. The tempting conclusion was that these neurons help interpret others' behaviour. Further work suggested that people also have this system, and some researchers claimed that conditions where empathy is lacking, such as autism or psychopathy, could arise from defective mirror neurons. Yet there has been little evidence to back this up and critics argued that mirror neuron activity could just be some sort of side effect of witnessing action. Powerful magnetic fields are known to temporarily disrupt brain cell activity, and a technique called transcranial magnetic stimulation (TMS) is increasingly used in the lab to dampen specific areas of the brain. © Copyright Reed Business Information Ltd.
Ewen Callaway A study in mice and rats suggests that an imbalance in chloride ions during a child's development in the womb could be a factor for autism. Children with autism typically begin showing obvious symptoms, such as trouble making eye contact and slow language development, a year or more after birth. A study in mice and rats now hints that prenatal drug treatment could head off these problems. The findings, reported today in Science1, do not suggest that autism spectrum disorders can be prevented in children. But researchers not involved in the study say that they add support to a controversial clinical trial suggesting that some children with autism benefited from taking a common diuretic medication called bumetanide2. In that trial, a team led by neuroscientist Yehezkel Ben-Ari at the Mediterranean Institute of Neurobiology in Marseille gave 60 children bumetanide or a placebo daily for three months. Children who had less severe forms of autism showed mild improvements in social behaviour after taking the drug, and almost no adverse side effects were observed (see 'Diuretic drug improves symptoms of autism'). But autism researchers greeted the results with caution. Many pointed out that the study did not provide a clear biological mechanism that could explain how the drug improved the symptoms of the disorder. The latest study is an attempt to answer such criticisms by identifying a role for the neurotransmitter GABA. Studies in humans and animals have suggested that GABA, which in healthy people typically inhibits the activity in neurons, is altered in autism and instead activates some brain cells. © 2014 Nature Publishing Group,
Link ID: 19225 - Posted: 02.08.2014
Memory can be altered by new experience, and isn't nearly as accurate as courtroom testimony might have us believe, a new study suggests. The results suggest a cheeky answer to the question posed by comedian Richard Pryor: "Who you gonna believe: me, or your lyin' eyes?" Turns out, Pryor was onto something. The brain behind our eyes can distort reality or verify it, based on subsequent experience. And somewhat paradoxically, the same area of the brain appears to be strongly involved in both activities, according to a study published online Tuesday in the Journal of Neuroscience. Northwestern University cognitive neuroscientist Donna Bridge was testing how memory is either consolidated or altered, by giving 17 subjects a deceptively simple task. They studied the location of dozens of objects briefly flashed at varied locations on a standard computer screen, then were asked to recall the object's original location on a new screen with a different background. When subjects were told to use a mouse to drag the re-presented object from the center of the new screen to the place where they recalled it had been located, 16 of 17 got it wrong, by an average of about 3 inches. When the same subjects then were given three choices - the original location, the wrong guess and a neutral spot between them - they almost unfailingly dragged the object to the incorrectly recalled location, regardless of the background screen. Their new memory was false. © 2014 Hearst Communications, Inc.
Keyword: Learning & Memory
Link ID: 19224 - Posted: 02.08.2014
by Laura Sanders When the president of the United States makes a request, scientists usually listen. Physicists created the atomic bomb for President Roosevelt. NASA engineers put men on the moon for President Kennedy. Biologists presented their first draft of the human genetic catalog to an appreciative President Clinton. So when President Obama announced an ambitious plan to understand the brain in April 2013, people were quick to view it as the next Manhattan Project, or Human Genome Project, or moon shot. But these analogies may not be so apt. Compared with understanding the mysterious inner workings of the brain, those other endeavors started with an end in sight. In a human brain, 85 billion nerve cells communicate via trillions of connections using complex patterns of electrical jolts and more than 100 different chemicals. A pea-sized lump of brain tissue contains more information than the Library of Congress. But unlike those orderly shelved and cataloged books, the organization of the brain remains mostly indecipherable, concealing the mysteries underlying thought, learning, emotion and memory. Still, as with other challenging enterprises prompted by presidential initiatives, success would change the world. A deep understanding of how the brain works, and what goes wrong when it doesn’t, could lead to a dazzling array of treatments for brain disorders — from autism and Alzheimer’s disease to depression and drug addiction — that afflict millions of people around the world. |© Society for Science & the Public 2000 - 2013.
Keyword: Brain imaging
Link ID: 19223 - Posted: 02.08.2014
| by Nina Bahadur Addiction and eating disorder recovery site Rehabs.com worked with digital marketing agency Fractl on a project looking at the origins of Body Mass Index (BMI) measurements, and how the bodies of ideal women have compared to national averages over time. And their findings show that models and movie stars are getting smaller than the average American woman at unprecedented rates. Though BMI measurements don't distinguish between fat and muscle, and are thus fairly inaccurate in determining whether someone is obese or not, BMI data from the past makes for interesting comparisons. According to the Center for Disease Control, the BMI of the average American women has steadily increased over the past half a century, from 24.9 in 1960 to 26.5 in the present day. In a similar vein, Rehabs.com found that the difference between models' weights and the weight of the average American woman has grown from 8 percent in 1975 to over 23 percent today. The bottom line? There's more of a noticeable gap between the bodies of idealized women and everyday people. Picking up on this disparity, brands like Dove, Debenham's and H&M have made efforts to include diverse body types in their catalogs and ads. Organizations like The Representation Project are working to educate women and girls about media literacy and how to handle the sexualized images of women we see on television, billboards and the Internet. (Of course, we still have a very long way to go.) In addition to the work of brands and organizations, looking back on the "ideal" women throughout the past century tells us just how arbitrary any vision of "the perfect body" is. Sex symbols have varied in terms of body shape, height, weight and tone, from the hourglass figure of Mae West to the waif-like Kate Moss. Though the diversity of these icons is limited -- they are all white, and none could be accurately described as plus-size -- it's gratifying to see that different body types have been construed as sexy, and likely will be again. © 2014 TheHuffingtonPost.com, Inc
Keyword: Anorexia & Bulimia
Link ID: 19222 - Posted: 02.08.2014