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By Edd Gent, The devastating neurodegenerative condition Alzheimer's disease is incurable, but with early detection, patients can seek treatments to slow the disease's progression, before some major symptoms appear. Now, by applying artificial intelligence algorithms to MRI brain scans, researchers have developed a way to automatically distinguish between patients with Alzheimer's and two early forms of dementia that can be precursors to the memory-robbing disease. The researchers, from the VU University Medical Center in Amsterdam, suggest the approach could eventually allow automated screening and assisted diagnosis of various forms of dementia, particularly in centers that lack experienced neuroradiologists. Additionally, the results, published online July 6 in the journal Radiology, show that the new system was able to classify the form of dementia that patients were suffering from, using previously unseen scans, with up to 90 percent accuracy. [10 Things You Didn't Know About the Brain] "The potential is the possibility of screening with these techniques so people at risk can be intercepted before the disease becomes apparent," said Alle Meije Wink, a senior investigator in the center's radiology and nuclear medicine department. "I think very few patients at the moment will trust an outcome predicted by a machine," Wink told Live Science. "What I envisage is a doctor getting a new scan, and as it is loaded, software would be able to say with a certain amount of confidence [that] this is going to be an Alzheimer's patient or [someone with] another form of dementia." © 2016 Scientific American
Link ID: 22425 - Posted: 07.12.2016
By Clare Wilson It is one of life’s great enigmas: why do we sleep? Now we have the best evidence yet of what sleep is for – allowing housekeeping processes to take place that stop our brains becoming overloaded with new memories. All animals studied so far have been found to sleep, but the reason for their slumber has eluded us. When lab rats are deprived of sleep, they die within a month, and when people go for a few days without sleeping, they start to hallucinate and may have epileptic seizures. One idea is that sleep helps us consolidate new memories, as people do better in tests if they get a chance to sleep after learning. We know that, while awake, fresh memories are recorded by reinforcing connections between brain cells, but the memory processes that take place while we sleep have remained unclear. Support is growing for a theory that sleep evolved so that connections in the brain can be pruned down during slumber, making room for fresh memories to form the next day. “Sleep is the price we pay for learning,” says Giulio Tononi of the University of Wisconsin-Madison, who developed the idea. Now we have the most direct evidence yet that he’s right. Tononi’s team measured the size of these connections or synapses in brain slices taken from mice. The synapses in samples taken at the end of a period of sleep were 18 per cent smaller than those in samples taken from before sleep, showing that the synapses between neurons are weakened during slumber. © Copyright Reed Business Information Ltd.
By David Dobbs It’s difficult to tell what Gina Pace wants unless you already know what she wants. But sometimes that’s easy, and this is one of those times: Gina wants pizza. “I-buh!” she says repeatedly—her version of “I want.” We all do. We are sitting at Abate’s in New Haven, Connecticut, a town famous for—among other things—pizza and science. Gina and her father, Bernardo, who live on Staten Island in New York City, have made the two-hour drive here for both. The pizza is in the oven. The science is already at the table, represented by Abha Gupta, a developmental pediatrician at Yale’s renowned Child Study Center. Gupta is one of the few scientific experts on a condition that Bernardo and Gina know through hard experience. Gina, now 24, was diagnosed 20 years ago with childhood disintegrative disorder, or CDD. CDD is the strangest and most unsettling developmental condition you have probably never heard of. Also known as Heller’s syndrome, for the Austrian special educator who first described it in 1908, it is a late-blooming, viciously regressive form of autism. It’s rare, striking about 1 or 2 in every 100,000 children. After developing typically for two to 10 years (the average is three or four), a child with CDD will suffer deep, sharp reversals along multiple lines of development, which may include language, social skills, play skills, motor skills, cognition, and bladder or bowel control. The speed and character of this reversal varies, but it often occurs in a horrifyingly short period—as short as a couple of months, says Gupta. In about 75 percent of cases, this loss of skills is preceded by days or weeks in which the child experiences intense anxiety and even terror: nightmares and waking nightmares and bouts of confused, jumpy disturbance that resemble psychosis.
By Shayla Love In 2005, astronaut John Phillips took a break from his work on the International Space Station and looked out the window at Earth. He was about halfway through a mission that had begun in April and would end in October. When he gazed down at the planet, the Earth was blurry. He couldn’t focus on it clearly. That was strange — his vision had always been 20/20. He wondered: Was his eyesight getting worse? “I’m not sure if I reported that to the ground,” he said. “I think I didn’t. I thought it would be something that would just go away, and fix itself when I got to Earth.” It didn’t go away. During Phillips’ post-flight physical, NASA found that his vision had gone from 20/20 to 20/100 in six months. John Phillips began experiencing sight issues during his time on the International Space Station in 2005, but was reluctant to say anything while in space. (NASA) Rigorous testing followed. Phillips got MRIs, retinal scans, neurological tests and a spinal tap. The tests showed that not only had his vision changed, but his eyes had changed as well. The backs of his eyes had gotten flatter, pushing his retinas forward. He had choroidal folds, which are like stretch marks. His optic nerves were inflamed. Phillips case became the first widely recognized one of a mysterious syndrome that affects 80 percent of astronauts on long-duration missions in space. The syndrome could interfere with plans for future crewed space missions, including any trips to Mars.
Link ID: 22422 - Posted: 07.11.2016
By Jane E. Brody To stem the current epidemic of obesity, there’s no arguing with the adage that an ounce of prevention is worth a pound of cure. As every overweight adult knows too well, shedding excess pounds and keeping them off is far harder than putting them on in the first place. But assuring a leaner, healthier younger generation may often require starting even before a baby is born. The overwhelming majority of babies are lean at birth, but by the time they reach kindergarten, many have acquired excess body fat that sets the stage for a lifelong weight problem. Recent studies indicate that the reason so many American children become overweight is far more complicated than consuming more calories than they burn, although this is certainly an important factor. Rather, preventing children from acquiring excess body fat may have to start even before their mothers become pregnant. Researchers are tracing the origins of being overweight and obese as far back as the pre-pregnancy weight of a child’s mother and father, and their explanations go beyond simple genetic inheritance. Twenty-three genes are known to increase the risk of becoming obese. These genes can act very early in development to accelerate weight gain in infancy and during middle childhood. In the usual weight trajectory, children are born lean, get chubby during infancy, then become lean again as toddlers when they grow taller and become more active. Then, at or before age 10 or so, body fat increases in preparation for puberty – a phenomenon called adiposity rebound. In children with obesity genes, “adiposity rebound occurs earlier and higher,” said Dr. Daniel W. Belsky, an epidemiologist at Duke University School of Medicine. “They stop getting leaner sooner and start putting on fat earlier and put on more of it.” © 2016 The New York Times Company
By Aviva Rutkin At first glance, she was elderly and delicate – a woman in her 90s with a declining memory. But then she sat down at the piano to play. “Everybody in the room was totally startled,” says Eleanor Selfridge-Field, who researches music and symbols at Stanford University. “She looked so frail. Once she sat down at the piano, she just wasn’t frail at all. She was full of verve.” Selfridge-Field met this woman, referred to as ME to preserve her privacy, at a Christmas party around eight years ago. ME, who is now aged 101, has vascular dementia: she rarely knows where she is, and doesn’t recognise people she has met in the last few decades. But she can play nearly 400 songs by ear – a trick that depends on tapping into a memory of previously stored musical imprints – and continues to learn new songs just by listening to them. She has even composed an original piece of her own. ME’s musical talent, despite her cognitive impairments, inspired Selfridge-Field to spend the last six years observing her, and she presented her observations today at the International Conference on Music Perception and Cognition in San Francisco, California. ME experienced a stroke-like attack when she was in her 80s, and a few years later was diagnosed with vascular dementia. She struggles most to remember events and encounters that are recent, and her memory is selective, focusing on specific periods – such as her childhood between the ages of 3 and 8. She can recognise people that she met before the age of about 75 to 80. She is never quite sure of her surroundings. © Copyright Reed Business Information Ltd.
Link ID: 22420 - Posted: 07.11.2016
Beatrice Alexandra Golomb, Statins can indeed produce neurological effects. These drugs are typically prescribed to lower cholesterol and thereby reduce the risk of heart attack and stroke. Between 2003 and 2012 roughly one in four Americans aged 40 and older were taking a cholesterol-lowering medication, according to the Centers for Disease Control and Prevention. But studies show that statins can influence our sleep and behavior—and perhaps even change the course of neurodegenerative conditions, including dementia. The most common adverse effects include muscle symptoms, fatigue and cognitive problems. A smaller proportion of patients report peripheral neuropathy—burning, numbness or tingling in their extremities—poor sleep, and greater irritability and aggression. Interestingly, statins can produce very different outcomes in different patients, depending on an individual's medical history, the statin and the dose. Studies show, for instance, that statins generally reduce the risk of ischemic strokes—which arise when a blocked artery or blood clot cuts off oxygen to a brain region—but can also increase the risk of hemorrhagic strokes, or bleeding into the brain. Statins also appear to increase or decrease aggression. In 2015 my colleagues and I observed that women taking statins, on average, showed increased aggression; men typically showed less, possibly because of reduced testosterone levels. Some men in our study did experience a marked increase in aggression, which was correlated with worsening sleep. © 2016 Scientific American
By DENISE GRADY Could pernicious anemia, a disease caused by a vitamin B12 deficiency, have explained the many strange behaviors of Mary Todd Lincoln? She was not exactly a model first lady. Historians have had a field day describing her violent temper, wild shopping sprees (she owned 300 pairs of kid gloves), depressed moods and all-consuming fears of burglars, storms and poverty. Late in life, at her son’s urging, she was committed to a mental hospital for several months. Plenty of theories, none proven, have been floated. She was bipolar. She had syphilis or that well known cause of feminine madness, menstrual trouble. She was spoiled and narcissistic. She never recovered from a road accident in which her head hit a rock. She lost her mind grieving the deaths of three of her four sons and her husband’s assassination. The latest addition to the list of possible diagnoses comes from Dr. John G. Sotos, a cardiologist, technology executive at Intel and one of the medical consultants who helped dream up the mystery diseases that afflicted patients on the television show “House.” Dr. Sotos has long been interested in difficult diagnoses, and has written a self-published book suggesting that Abraham Lincoln had a genetic syndrome that caused cancers of the thyroid and adrenal glands. In an interview, Dr. Sotos said that while he was studying President Lincoln, he came across something that intrigued him about Mrs. Lincoln: an 1852 letter mentioning that she had a sore mouth. He knew that vitamin B deficiencies could cause a sore tongue, and he began looking into her health. © 2016 The New York Times Company
Link ID: 22418 - Posted: 07.09.2016
By Karl Gruber For most birds the night brings a well-deserved rest. But for some, it is time for more risqué activities. Nocturnal birds sing at night – no surprises there – mainly to attract mates or repel rivals, the same reasons other birds sing at daytime. But a small number of species active by day also occasionally sing at night. Why they invest time and energy in such behaviour has been something of a mystery. Now Antonio Celis-Murillo at the Illinois Natural History Survey in Champaign and his colleagues think they have an answer – and it wasn’t what they expected. The team spent two years studying field sparrows, Spizella pusilla, a common bird across eastern North America. Active during the day, these birds are territorial and largely monogamous, though they engage in occasional infidelity. The researchers observed 28 pairs in the wild, recording the songs of territorial males, as well as those of intruder and neighbouring males. They then conducted playback experiments at night, studying the responses of the pairs. “I was surprised to see what these birds were up to,” says Celis-Murillo. The males sing to attract other male’s partners, and these females are all too willing to wake up for a night-time rendezvous. The team also found that males sang more during periods when females were reproductively receptive, and that the females responded to such song more often when they were fertile. The female’s mate didn’t appear to kick up a fuss and counter-sing – which would be expected if nocturnal songs served to repel rivals. © Copyright Reed Business Information Ltd.
By SUNITA SAH A POPULAR remedy for a conflict of interest is disclosure — informing the buyer (or the patient, etc.) of the potential bias of the seller (or the doctor, etc.). Disclosure is supposed to act as a warning, alerting consumers to their adviser’s stake in the matter so they can process the advice accordingly. But as several recent studies I conducted show, there is an underappreciated problem with disclosure: It often has the opposite of its intended effect, not only increasing bias in advisers but also making advisees more likely to follow biased advice. When I worked as a physician, I witnessed how bias could arise from numerous sources: gifts or sponsorships from the pharmaceutical industry; compensation for performing particular procedures; viewing our own specialties as delivering more effective treatments than others’ specialties. Although most physicians, myself included, tend to believe that we are invulnerable to bias, thus making disclosures unnecessary, regulators insist on them, assuming that they work effectively. To some extent, they do work. Disclosing a conflict of interest — for example, a financial adviser’s commission or a physician’s referral fee for enrolling patients into clinical trials — often reduces trust in the advice. But my research has found that people are still more likely to follow this advice because the disclosure creates increased pressure to follow the adviser’s recommendation. It turns out that people don’t want to signal distrust to their adviser or insinuate that the adviser is biased, and they also feel pressure to help satisfy their adviser’s self-interest. Instead of functioning as a warning, disclosure can become a burden on advisees, increasing pressure to take advice they now trust less. © 2016 The New York Times Company
Link ID: 22416 - Posted: 07.09.2016
by Adriana Heguy, molecular biologist and genomics researcher: Interestingly, tongue-curling ability is not solely genetic, and the genetic component may be very small. Monozygotic (identical) twins are not always concordant for tongue-curling ability, so if there is a genetic component, it’s clearly not Mendelian. In other words, it’s not a trait coded by one single gene, and it’s clearly influenced by the environment—in this case, practice. But for some reason this is one of the “myths” about genetics that gets spread around in high school, where it is used as an example of a simple Mendelian trait with a simple dominant-recessive nature. It’s hard to comment on the evolutionary purpose of an ability so heavily influenced by the environment, and not obviously useful. There are many traits for which we do not have the faintest idea why they exist or what purpose they serve. In the case of tongue-curling, it’s possible that it’s a case of fine motor control of the tongue. We need to be able to move our tongues to not bite them when we eat, for example, and for swirling food around. For unknown reasons, some individuals are better than others at controlling tongue movement. And since the ability can be acquired by practicing (though not everybody apparently succeeds), it does seem likely that it is indeed a question of motor control. Most people are able to do it. It’s quite common. But it could be that evolution had nothing to do with it. Or it could be a spandrel; in other words, a side effect of evolution. Maybe the evolution of dexterity or finer motor control of other muscles resulted in tongue “dexterity.” It’s possible that it is an atavism, something that increased tongue muscle control was once useful for tasting or eating certain kinds of foods millions of years ago, and it has not disappeared because the developmental program for fine muscle control is still there.
By Andy Coghlan It could be that romantic restaurant, or your favourite park bench. A specific part of the brain seems to be responsible for learning and remembering the precise locations of places that are special to us, research in mice has shown for the first time. Place cells are neurons that help us map our surroundings, and both mice and humans have such cells in the hippocampus – a brain region vital for learning, memory and navigation. Nathan Danielson at Columbia University in New York and his colleagues focused on a part of the hippocampus that feeds signals to the rest of the brain, called CA1. They found that in mice, the CA1 layer where general environment maps are learned and stored is different to the one for locations that have an important meaning. Treadmill test They discovered this by recording brain activity in the two distinct layers of CA1, using mice placed on a treadmill. The treadmill rotated between six distinctive surface materials – including silky ribbons, green pom-pom fabric and silver glitter masking tape. At all times, the mice were able to lick a sensor to try to trigger the release of drinking water. During the first phase of the experiment, however, the sensor only worked at random times. The mice formed generalised maps of their experience on the multi-surfaced treadmill, and the team found that these were stored in the superficial layer of CA1. © Copyright Reed Business Information Ltd.
Keyword: Learning & Memory
Link ID: 22414 - Posted: 07.09.2016
The most sophisticated, widely adopted, and important tool for looking at living brain activity actually does no such thing. Called functional magnetic resonance imaging, what it really does is scan for the magnetic signatures of oxygen-rich blood. Blood indicates that the brain is doing something, but it’s not a direct measure of brain activity. Which is to say, there’s room for error. That’s why neuroscientists use special statistics to filter out noise in their fMRIs, verifying that the shaded blobs they see pulsing across their computer screens actually relate to blood flowing through the brain. If those filters don’t work, an fMRI scan is about as useful at detecting neuronal activity as your dad’s “brain sucking alien” hand trick. And a new paper suggests that might actually be the case for thousands of fMRI studies over the past 15 years. The paper, published June 29 in the Proceedings of the National Academy of Science, threw 40,000 fMRI studies done over the past 15 years into question. But many neuroscientists—including the study’s whistleblowing authors—are now saying the negative attention is overblown. Neuroscience has long struggled over just how useful fMRI data is at showing brain function. “In the early days these fMRI signals were very small, buried in a huge amount of noise,” says Elizabeth Hillman, a biomedical engineer at the Zuckerman Institute at Columbia University. A lot of this noise is literal: noise from the scanner, noise from the electrical components, noise from the person’s body as it breathes and pumps blood.
Keyword: Brain imaging
Link ID: 22413 - Posted: 07.09.2016
By Michael Price Doctors and soldiers could soon place their trust in an unusual ally: the mouse. Scientists have genetically engineered mice to be ultrasensitive to specific smells, paving the way for animals that are “tuned” to sniff out land mines or chemical signatures of diseases like Parkinson’s and Alzheimer’s. Trained rats and dogs have long been used to detect the telltale smell of TNT in land mines, and research suggests that dogs can smell the trace chemical signals of low blood sugar or certain types of cancer. Mice also have powerful sniffers: They sport about 1200 genes dedicated to odorant receptors, cellular sensors that react to a scent’s chemical signature. That’s a few hundred less than rats and about the same as dogs. (Humans have a paltry 350.) Paul Feinstein wants to upgrade the mouse’s already sensitive nose. For the last decade, the neurobiologist at Hunter College in New York City has been studying how odorant receptors form on the surface of neurons within the olfactory system. During development, each olfactory neuron specializes to express a single odorant receptor, which binds to chemicals in the air to detect a specific odor. In other words, each olfactory neuron has a singular receptor that senses a particular smell. Normally, there is an even distribution of receptors throughout the system, so each receptor can be found in about 0.1% of mouse neurons. Feinstein wondered if he could make the mouse’s nose pay more attention to particular scents by making certain odorant receptors more numerous. He and colleagues developed a string of DNA that, when injected into the nucleus of a fertilized mouse egg, appears to make olfactory neurons more likely to develop one particular odorant receptor than the others. This receptor, called M71, detects acetophenone, a chemical that smells like jasmine. When the team added four or more copies of the DNA sequence to a mouse egg, a full 1% of neurons carried it—10 times more than normal. © 2016 American Association for the Advancement of Science.
Keyword: Chemical Senses (Smell & Taste)
Link ID: 22412 - Posted: 07.08.2016
By Nicholas Bakalar A new study has identified a bacterial blueprint for chronic fatigue syndrome, offering further evidence that it is a physical disease with biological causes and not a psychological condition. Chronic fatigue syndrome is a condition that causes extreme and lasting fatigue, preventing people from taking part in even the most routine daily activities. There are no tests to confirm the diagnosis, which has prompted speculation that it is a psychological condition rather than a physical illness. In a study published in Microbiome, researchers recruited 48 people with C.F.S. and 39 healthy controls. Then they analyzed the quantity and variety of bacteria species in their stool. They also searched for markers of inflammation in their blood. The stool samples of those with C.F.S. had significantly lower diversity of species compared with the healthy people — a finding typical of inflammatory bowel disease as well. The scientists also discovered that people with C.F.S. had higher blood levels of lipopolysaccharides, inflammatory molecules that may indicate that bacteria have moved from the gut into the bloodstream, where they can produce various symptoms of disease. Using these criteria, the researchers were able to accurately identify more than 83 percent of C.F.S. cases based on the diversity of their gut bacteria and lipopolysaccharides in their blood. Finding a biomarker for C.F.S. has been an ongoing goal for researchers who hope to one day develop a diagnostic test for the condition. Still, the senior author of the study, Maureen R. Hanson, a professor of molecular biology at Cornell, said the bacteria blueprint in the new study is not yet a method of definitively diagnosing C.F.S. The importance of the finding, she said, is that it may offer new clues as to why people have these symptoms. © 2016 The New York Times Company
Link ID: 22411 - Posted: 07.08.2016
Andrew Orlowski Special Report If the fMRI brain-scanning fad is well and truly over, then many fashionable intellectual ideas look like collateral damage, too. What might generously be called the “British intelligentsia” – our chattering classes – fell particularly hard for the promise that “new discoveries in brain science” had revealed a new understanding of human behaviour, which shed new light on emotions, personality and decision making. But all they were looking at was statistical quirks. There was no science to speak of, the results of the experiments were effectively meaningless, and couldn’t support the (often contradictory) conclusions being touted. The fMRI machine was a very expensive way of legitimising an anecdote. This is an academic scandal that’s been waiting to explode for years, for plenty of warning signs were there. In 2005, Ed Vul, now a psychology professor at UCSD, and Hal Pashler – then and now at UCSD – were puzzled by a claim being made in a talk by a neuroscience researcher. He was explaining study that purported to report a high correlation between a test subject’s brain activity and the speed with which they left the room after the study. “It seemed unbelievable to us that activity in this specific brain area could account for so much of the variance in walking speed,” explained Vul. “Especially so, because the fMRI activity was measured some two hours before the walking happened. So either activity in this area directly controlled motor action with a delay of two hours — something we found hard to believe — or there was something fishy going on.” IT © 1998–2016
Keyword: Brain imaging
Link ID: 22410 - Posted: 07.08.2016
By Louise Whiteley It’s an appealing idea: the notion that understanding the learning brain will tell us how to maximise children’s potential, bypassing the knotty complexities of education research. But promises to replace sociological complexity with biological certainty should always be treated with caution. Hilary and Steven Rose are deeply sceptical of claims that neuroscience can inform education and early intervention policy, and deeply concerned about the use of such claims to support neoliberal agendas. They argue that focusing on the brain encourages a focus on the individual divorced from their social context, and that this is easily aligned with a view of poor achievement as a personal moral failing, rather than a practical consequence of poverty and inequality. Whether or not you end up cheerleading for the book’s political agenda, its deconstruction of faulty claims about how neuroscience translates into the classroom is relevant to anyone interested in education. The authors tear apart the scientific logic of policy documents, interrogate brain-based interventions and dismantle prevalent neuro-myths. One of the book’s meatiest chapters deals with government reports advocating early intervention to increase “mental capital”, and thus reduce the future economic burden of deprived, underachieving brains. As we discover, the neuroscientific foundations of these reports are shaky. For instance, they tend to assume that the more synaptic connections between brain cells the better, and that poor environment in a critical early period permanently reduces the number of synapses. This makes early intervention focusing on the individual child and “poor parenting” seem like the obvious solution. But pruning of synapses is just as important to brain development, and learning involves the continual forming and reforming of synaptic connections. More is not necessarily better. And while an initial explosion in synapses can be irreversibly disrupted by extreme neglect, the evidence just isn’t there yet for extrapolating this to the more common kinds of childhood deprivation that such reports address.
Tough love, interventions and 12-step programs are some of the most common methods of treating drug addiction, but journalist Maia Szalavitz says they're often counterproductive. "We have this idea that if we are just cruel enough and mean enough and tough enough to people with addiction, that they will suddenly wake up and stop, and that is not the case," she tells Fresh Air's Terry Gross. Szalavitz is the author of Unbroken Brain, a book that challenges traditional notions of addiction and treatment. Her work is based on research and experience; she was addicted to cocaine and heroin from the age of 17 until she was 23. Szalavitz is a proponent of "harm reduction" programs that take a nonpunitive approach to helping addicts and "treat people with addiction like human beings." In her own case, she says that getting "some kind of hope that I could change" enabled her to get the help she needed. On her criticism of 12-step programs I think that 12-step programs are fabulous self help. I think they can be absolutely wonderful as support groups. My issue with 12-step programs is that 80 percent of addiction treatment in this country consists primarily of indoctrinating people into 12-step programs, and no other medical care in the United States is like that. The data shows that cognitive behavioral therapy and motivational enhancement therapy are equally effective, and they have none of the issues around surrendering to a higher power, or prayer or confession. © 2016 npr
Keyword: Drug Abuse
Link ID: 22408 - Posted: 07.08.2016
By Jessica Hamzelou TEENAGE pregnancies have hit record lows in the Western world, largely thanks to increased use of contraceptives of all kinds. But strangely, we don’t really know what hormonal contraceptives – pills, patches and injections that contain synthetic sex hormones – are doing to the developing bodies and brains of teenage girls. You’d be forgiven for assuming that we do. After all, the pill has been around for more than 50 years. It has been through many large trials assessing its effectiveness and safety, as have the more recent patches and rings, and the longer-lasting implants and injections. But those studies were done in adult women – very few have been in teenage girls. And biologically, there is a big difference. At puberty, our bodies undergo an upheaval as our hormones go haywire. It isn’t until our 20s that things settle down and our brains and bones reach maturity. “If a drug is going to be given to 11 and 12-year-olds, it needs to be tested in 11 and 12-year-olds,” says Joe Brierley of the clinical ethics committee at Great Ormond Street Hospital in London. Legislation introduced in the US in 2003 and in Europe in 2007 was intended to make this happen but a New Scientist investigation can reveal that there is still scant data on what contraceptives actually do to developing girls. The few studies that have been done suggest that tipping the balance of oestrogen and progesterone during this time may have far-reaching effects, although there is not yet enough data to say whether we should be alarmed. © Copyright Reed Business Information Ltd.
Shefali Luthra Prescription drug prices continue to climb, putting the pinch on consumers. Some older Americans appear to be seeking an alternative to mainstream medicines that has become easier to get legally in many parts of the country. Just ask Cheech and Chong. Research published Wednesday found that states that legalized medical marijuana — which is sometimes recommended for symptoms like chronic pain, anxiety or depression — saw declines in the number of Medicare prescriptions for drugs used to treat those conditions and a dip in spending by Medicare Part D, which covers the cost on prescription medications. Because the prescriptions for drugs like opioid painkillers and antidepressants — and associated Medicare spending on those drugs — fell in states where marijuana could feasibly be used as a replacement, the researchers said it appears likely legalization led to a drop in prescriptions. That point, they said, is strengthened because prescriptions didn't drop for medicines such as blood-thinners, for which marijuana isn't an alternative. The study, which appears in Health Affairs, examined data from Medicare Part D from 2010 to 2013. It is the first study to examine whether legalization of marijuana changes doctors' clinical practice and whether it could curb public health costs. The findings add context to the debate as more lawmakers express interest in medical marijuana. This year, Ohio and Pennsylvania passed laws allowing the drug for therapeutic purposes, making it legal in 25 states, plus Washington, D.C. The approach could also come to a vote in Florida and Missouri this November. A federal agency is considering reclassifying medical marijuana under national drug policy to make it more readily available. © 2016 npr
Keyword: Drug Abuse
Link ID: 22406 - Posted: 07.07.2016