Chapter 16. None
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By Graham Lawton Patricia Churchland, a neurophilosopher at the University of California at San Diego, says our hopes, loves and very existence are just elaborate functions of a complicated mass of grey tissue. Accepting that can be hard, but what we know should inspire us, not scare us. Her most recent book is Touching a Nerve: The Self as Brain. Graham Lawton: You compare revelations in neuroscience with the discoveries that the Earth goes around the sun and that the heart is a pump. What do you think these ideas have in common? Patricia Churchland: They challenge a whole framework of assumptions about the way things are. For Christians, it was very important that the Earth was at the center of the universe. Similarly, many people believed that the heart was somehow what made us human. And it turned out it was just a pump made of meat. I think the same is true about realizing that when we're conscious, when we make decisions, when we go to sleep, when we get angry, when we're fearful, these are just functions of the physical brain. Coming to terms with the neural basis of who we are can be very unnerving. It has been called "neuroexistentialism," which really captures the essence of it. We're not in the habit of thinking about ourselves that way. GL: Why is it so difficult for us to see the reality of what we actually are? PC: Part of the answer has to do with the evolution of nervous systems. Is there any reason for a brain to know about itself? We can get along without knowing, just as we can get along without knowing that the liver is in there filtering out toxins. The wonderful thing, of course, is that science allows us to know. © 2013 The Slate Group, LLC.
Link ID: 19024 - Posted: 12.11.2013
By Jeanene Swanson Depression strikes some 35 million people worldwide, according to the World Health Organization, contributing to lowered quality of life as well as an increased risk of heart disease and suicide. Treatments typically include psychotherapy, support groups and education as well as psychiatric medications. SSRIs, or selective serotonin reuptake inhibitors, currently are the most commonly prescribed category of antidepressant drugs in the U.S., and have become a household name in treating depression. The action of these compounds is fairly familiar. SSRIs increase available levels of serotonin, sometimes referred to as the feel-good neurotransmitter, in our brains. Neurons communicate via neurotransmitters, chemicals which pass from one nerve cell to another. A transporter molecule recycles unused transmitter and carries it back to the pre-synaptic cell. For serotonin, that shuttle is called SERT (short for “serotonin transporter”). An SSRI binds to SERT and blocks its activity, allowing more serotonin to remain in the spaces between neurons. Yet, exactly how this biochemistry then works against depression remains a scientific mystery. In fact, SSRIs fail to work for mild cases of depression, suggesting that regulating serotonin might be an indirect treatment only. “There’s really no evidence that depression is a serotonin-deficiency syndrome,” says Alan Gelenberg, a depression and psychiatric researcher at The Pennsylvania State University. “It’s like saying that a headache is an aspirin-deficiency syndrome.” SSRIs work insofar as they reduce the symptoms of depression, but “they’re pretty nonspecific,” he adds. © 2013 Scientific American
Link ID: 19020 - Posted: 12.11.2013
By Dan Hurley Darwin and Freud walk into a bar. Two alcoholic mice — a mother and her son — sit on two bar stools, lapping gin from two thimbles. The mother mouse looks up and says, “Hey, geniuses, tell me how my son got into this sorry state.” “Bad inheritance,” says Darwin. “Bad mothering,” says Freud. For over a hundred years, those two views — nature or nurture, biology or psychology — offered opposing explanations for how behaviors develop and persist, not only within a single individual but across generations. And then, in 1992, two young scientists following in Freud’s and Darwin’s footsteps actually did walk into a bar. And by the time they walked out, a few beers later, they had begun to forge a revolutionary new synthesis of how life experiences could directly affect your genes — and not only your own life experiences, but those of your mother’s, grandmother’s and beyond. The bar was in Madrid, where the Cajal Institute, Spain’s oldest academic center for the study of neurobiology, was holding an international meeting. Moshe Szyf, a molecular biologist and geneticist at McGill University in Montreal, had never studied psychology or neurology, but he had been talked into attending by a colleague who thought his work might have some application. Likewise, Michael Meaney, a McGill neurobiologist, had been talked into attending by the same colleague, who thought Meaney’s research into animal models of maternal neglect might benefit from Szyf’s perspective.
Link ID: 19017 - Posted: 12.11.2013
Three lawsuits filed last week that attempted to achieve “legal personhood” for four chimpanzees living in New York have been struck down. The suits, brought by the animal rights group the Nonhuman Rights Project (NhRP), targeted two chimps on private property and two in a research lab at Stony Brook University in New York. They were the first step in a nationwide campaign to grant legal rights to a variety of animals. NhRP had spent 5 years honing its legal strategy. It picked what it thought would be the most favorable jurisdictions and petitioned the judges with a writ of habeas corpus, which allows a person being held captive to have a say in court. Suffolk County Supreme Court Justice W. Gerard Asher denied the writ for the Stony Brook chimpanzees, writing in a brief decision that the animals did not qualify for habeas corpus because they were not “persons.” Both chimps are used in locomotion research at the university in work that is attempting to shed light on the origin of bipedalism in humans. Asher did not meet with NhRP lawyers; he issued his decision via a court clerk. The other judges were more accommodating. Fulton County Supreme Court Justice Joseph Sise and Niagara County Supreme Court Justice Ralph Boniello both allowed NhRP lawyers to make oral arguments in the courtroom. “As an animal lover, I appreciate your work,” said Sise, who handled the case of a chimpanzee named Tommy living in cage on his owner’s property in Gloversville, according to an NhRP press release. The group made “a very strong argument,” Sise said, according to the release, but he did not agree that habeas corpus applied to chimpanzees. Boniello, who oversaw the case of a chimp named Kiko living on his owner’s property in Niagara Falls, said he did not want to be the first “to make that leap of faith” equating chimpanzees with human beings. © 2013 American Association for the Advancement of Science.
Keyword: Animal Rights
Link ID: 19016 - Posted: 12.11.2013
Someday, a smart phone app that asks what you’re feeling 10 times a day may be able to tell you if you’re edging closer to depression—and recommend that you seek preventive therapy or drugs. Scientists have discovered that how quickly someone bounces back from negative feelings, over hours or days, can predict whether that person is at risk of an episode of major depressive disorder. “The holy grail of depression epidemiology is that we want to intervene early to prevent people from having depressive episodes,” says social scientist Stephen Gilman of Harvard University, who was not involved in the study. “Where this work is headed is making an advance in that direction, toward early detection and therefore early intervention.” Researchers asked more than 600 people—some healthy and some with a diagnosis of depression—to track their emotions for 5 or 6 days. Ten times a day, at random intervals, a watch would beep and the subjects would record how strongly they identified with each of four emotions: cheerful, content, sad, and anxious. Six to 8 weeks later, participants filled out a more detailed questionnaire that rated their levels of clinical depression. By the end of the follow-up period, about 13% of the subjects had experienced a shift toward being more depressed, a number consistent with what would be expected in the general population. Trends in the daily mood records, the team discovered, could predict whether a previously healthy person would make that shift toward depression. © 2013 American Association for the Advancement of Science
Link ID: 19015 - Posted: 12.10.2013
Brian Owens Fruitflies know exactly how much alcohol will be good for their young. Larvae living on a food source with the right concentration of ethanol will grow into heavy, healthy adults and will be protected against parasites — which explains why the insects are attracted to rotting fruit or the crate of empty beer bottles in your kitchen but not to the vodka or gin. Now researchers have uncovered the neural mechanism that allows the fruitfly Drosophila melanogaster to choose the best place to lay its eggs. The work is published today in Proceedings of the National Academy of Sciences1. A team led by Ulrike Heberlein, a molecular biologist at the Howard Hughes Medical Institute’s Janelia Farm Research Campus in Ashburn, Virginia, found that clusters of neurons, working in opposition to each other, help the flies to choose the place with the most beneficial concentration of ethanol in which to lay their eggs. The neurons all release the neurotransmitter dopamine, a key player in the brain's reward circuitry. Neurons of the PAM and PPM3 clusters encourage the flies to seek out ethanol, whereas PPL1 neurons apply the brakes, preventing the flies from laying their eggs on food containing high levels of ethanol that could harm the larvae. “They can discriminate among ethanol concentrations that are very similar — 3% versus 5% — so the system evolved to have great sensitivity,” says Heberlein. Their favourite booze strength is 5%, similar to that of a typical beer. Heberlein's team also traced the neurons involved in ethanol preference to specific brain regions. Both the pro-ethanol PAM and anti-ethanol PPL1 neurons were active in the mushroom body, whereas the pro-ethanol PPM3 ones were active in the ellipsoid body. Both of these brain structures are involved in decision-making and memory, and mushroom body neurons also play a part in ethanol-reward memory. © 2013 Nature Publishing Group,
Keyword: Chemical Senses (Smell & Taste)
Link ID: 19013 - Posted: 12.10.2013
Researchers striving to understand the origins of dementia are building the case against a possible culprit: lead exposure early in life. A study spanning 23 years has now revealed that monkeys who drank a lead-rich formula as infants later developed tangles of a key brain protein, called tau, linked to Alzheimer's disease. Though neuroscientists say more work is needed to confirm the connection, the research suggests that people exposed to lead as children—as many in America used to be before it was eliminated from paint, car emissions, water, and soil—could have an increased risk of the common, late-onset form of Alzheimer’s disease. Even in small doses, lead can wreak havoc on the heart, intestines, kidneys, and nervous system. Children are especially prone to its pernicious effects, as it curbs brain development. Many studies have linked early lead exposure with lower IQs. Researchers estimate that one in 38 children in the United States still have harmful levels of the metal in their systems, but evidence linking this exposure to dementia later in life has been tenuous. A team led by toxicologist Nasser Zawia, however, has vigorously pursued the lead hypothesis. In one early study, from 2008, the group showed that plaques, insoluble globs of a protein called β-amyloid, marred the brains of five macaques that had consumed a lead-enriched formula as infants. The researchers had compared the preserved brain tissues from those macaques, sacrificed in 2003 at age 23 in a National Institutes of Health lab, with four similarly aged monkeys who had had lead-free formula. The amyloid plaques closely resembled those in the brains of adults with Alzheimer's disease that are thought to contribute to the dementia. © 2013 American Association for the Advancement of Science.
There is more than meets the eye following even a mild traumatic brain injury. While the brain may appear to be intact, new findings reported in Nature suggest that the brain’s protective coverings may feel the brunt of the impact. Using a newly developed mouse trauma model, senior author Dorian McGavern, Ph.D., scientist at the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health, watched specific cells mount an immune response to the injury and try to prevent more widespread damage. Notably, additional findings suggest a similar immune response may occur in patients with mild head injury. In this study, researchers also discovered that certain molecules, when applied directly to the mouse skull, can bypass the brain’s protective barriers and enter the brain. The findings suggested that, in the mouse trauma model, one of those molecules may reduce effects of brain injury. Although concussions are common, not much is known about the effects of this type of damage. As part of this study, Lawrence Latour, Ph.D., a scientist from NINDS and the Center for Neuroscience and Regenerative Medicine, examined individuals who had recently suffered a concussion but whose initial scans did not reveal any physical damage to brain tissue. After administering a commonly used dye during MRI scans, Latour and his colleagues saw it leaking into the meninges, the outer covers of the brain, in 49 percent of 142 patients with concussion. To determine what happens following this mild type of injury, researchers in Dr. McGavern’s lab developed a new model of brain trauma in mice.
Keyword: Brain Injury/Concussion
Link ID: 19010 - Posted: 12.10.2013
By Helen Briggs BBC News An anti-tuberculosis vaccine could prevent multiple sclerosis, early research suggests. A small-scale study by researchers at the Sapienza University of Rome has raised hopes that the disease can be warded off when early symptoms appear. More research is needed before the BCG vaccine can be trialled on MS patients. The MS Society said the chance to take a safe and effective preventative treatment after a first MS-like attack would be a huge step forward. MS is a disease affecting nerves in the brain and spinal cord, causing problems with muscle movement, balance and vision. Early signs include numbness, vision difficulties or problems with balance. About half of people with a first episode of symptoms go on to develop MS within two years, while 10% have no more problems. In the study, published in the journal Neurology, Italian researchers gave 33 people who had early signs of MS an injection of BCG vaccine. The other 40 individuals in the study were given a placebo. After five years, 30% of those who received the placebo had not developed MS, compared with 58% of those vaccinated. "These results are promising, but much more research needs to be done to learn more about the safety and long-term effects of this live vaccine," said study leader Dr Giovanni Ristori. "Doctors should not start using this vaccine to treat MS or clinically isolated syndrome." BBC © 2013
Keyword: Multiple Sclerosis
Link ID: 19003 - Posted: 12.05.2013
Philip Ball Some animals, like some people, are more aggressive than others: it is just the way they are. But research suggests that for birds at least, it is not always easy to tell which is which. Some birds are inclined to give out exaggerated signs of their aggressiveness, others to underplay it. It is rather like the menacing biker who turns out to be a pussycat, or the geek who will break a bottle over your head. But the analogy with humans goes only so far, because many birds announce their aggression about mating and territory not by appearance but through song and gesture. For example, behavioural ecologist Michael Beecher and his colleagues at the University of Washington in Seattle have observed how the song sparrow (Melospiza melodia) indicates its intention to attack a dummy bird (see video above) or a loudspeaker playing bird songs by either vocalizing distinctive ‘soft songs’ or waving its wings (see video below), both of which are perceived as threatening1. Violent tendencies Both aggressive signalling and the ensuing violent behaviour vary from one bird to another, in a way that correlates with other personality traits such as boldness2. But these attributes also vary for a single individual at different times: birds can have particularly grouchy or placid days. Nonetheless, the degree of aggression implied by the precursory signals generally reflects the actual behaviour, in what evolutionary biologists call an honest signal. But it's not always honest. Earlier this year, Beecher's team showed1 that there is some variability in aggressive signalling that does not match behaviour: a bird might act stroppy but not follow through with an attack. © 2013 Nature Publishing Group
By CARL ZIMMER Scientists have found the oldest DNA evidence yet of humans’ biological history. But instead of neatly clarifying human evolution, the finding is adding new mysteries. In a paper in the journal Nature, scientists reported Wednesday that they had retrieved ancient human DNA from a fossil dating back about 400,000 years, shattering the previous record of 100,000 years. The fossil, a thigh bone found in Spain, had previously seemed to many experts to belong to a forerunner of Neanderthals. But its DNA tells a very different story. It most closely resembles DNA from an enigmatic lineage of humans known as Denisovans. Until now, Denisovans were known only from DNA retrieved from 80,000-year-old remains in Siberia, 4,000 miles east of where the new DNA was found. The mismatch between the anatomical and genetic evidence surprised the scientists, who are now rethinking human evolution over the past few hundred thousand years. It is possible, for example, that there are many extinct human populations that scientists have yet to discover. They might have interbred, swapping DNA. Scientists hope that further studies of extremely ancient human DNA will clarify the mystery. “Right now, we’ve basically generated a big question mark,” said Matthias Meyer, a geneticist at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, and a co-author of the new study. Hints at new hidden complexities in the human story came from a 400,000-year-old femur found in a cave in Spain called Sima de los Huesos (“the pit of bones” in Spanish). The scientific team used new methods to extract the ancient DNA from the fossil. “This would not have been possible even a year ago,” said Juan Luis Arsuaga, a paleoanthropologist at Universidad Complutense de Madrid and a co-author of the paper. © 2013 The New York Times Company
By James Gallagher Health and science reporter, BBC News The number of people living with dementia worldwide is set to treble by 2050, according to a new analysis. Alzheimer's Disease International says 44 million people live with the disease, but that figure will increase to 135 million by 2050. The figures were released ahead of the G8 dementia summit in London next week. In the UK, dementia research receives one eighth of the amount of funding that is spent on cancer, which charities say is insufficient. Alzheimer's Disease International expects increasing life expectancies to drive a surge in cases in poor and middle-income countries, particularly in South East Asia and Africa. Currently 38% of cases are in rich countries. But that balance is predicted shift significantly by 2050, with 71% of patients being in poor and middle-income countries. The report says most governments are "woefully unprepared for the dementia epidemic". Marc Wortmann, the executive director at Alzheimer Disease International, said: "It's a global epidemic and it is only getting worse - if we look into the future the numbers of elderly people will rise dramatically." Jeremy Hughes, chief executive of the UK's Alzheimer's Society, said: "Dementia is fast becoming the biggest health and social care challenge of this generation. "We must tackle dementia now, for those currently living with the condition across the world and for those millions who will develop dementia in the future. BBC © 2013
Link ID: 18998 - Posted: 12.05.2013
This morning, an animal rights group known as the Nonhuman Rights Project (NhRP) filed a lawsuit in a New York Supreme Court in an attempt to get a judge to declare that chimpanzees are legal persons and should be freed from captivity. The suit is the first of three to be filed in three New York counties this week. They target two research chimps at Stony Brook University and two chimps on private property, and are the opening salvo in a coordinated effort to grant “legal personhood” to a variety of animals across the United States. If NhRP is successful in New York, it could be a significant step toward upending millennia of law defining animals as property and could set off a “chain reaction” that could bleed over to other jurisdictions, says Richard Cupp, a law professor at Pepperdine University in Malibu, California, and a proponent of focusing on animal welfare rather than animal rights. “But if they lose it could be a significant step backward for the movement. They’re playing with fire.” The litigation has been in the works since 2007, when animal rights attorney Steven Wise founded NhRP, an association of about 60 lawyers, scientists, and policy experts. The group argues that cognitively advanced animals like chimpanzees and dolphins are so self-aware that keeping them in captivity—whether a zoo or research laboratory—is tantamount to slavery. “It’s a terrible torture we inflict on them, and it has to stop,” Wise says. “And all of human law says the way things stop is when courts and legislatures recognize that the being imprisoned is a legal person.” NhRP spent 5 years researching the best legal strategy—and best jurisdiction—for its first cases. The upshot: a total of three lawsuits to be filed in three New York trial courts this week on behalf of four resident chimpanzees. © 2013 American Association for the Advancement of Science
Keyword: Animal Rights
Link ID: 18993 - Posted: 12.03.2013
To expedite research on brain disorders, the National Institutes of Health is shifting from a limited funding role to coordinating a Web-based resource for sharing post-mortem brain tissue. Under a NIH NeuroBioBank initiative, five brain banks will begin collaborating in a tissue sharing network for the neuroscience community. “Instead of having to seek out brain tissue needed for a study from scattered repositories, researchers will have one-stop access to the specimens they need,” explained Thomas Insel, M.D., director of NIH’s National Institute of Mental Health (NIMH), one of three NIH institutes underwriting the project. “Such efficiency has become even more important with recent breakthrough technologies, such as CLARITY and resources such as BrainSpan that involve the use of human tissue.” Historically, NIH institutes have awarded investigator-initiated grants to support disease-specific brain bank activities. The NIH NeuroBioBank instead employs contracts, which affords the agency a more interactive role. Contracts totaling about $4.7 million for the 2013 fiscal year were awarded to brain banks at the Mount Sinai School of Medicine, New York City; Harvard University in Cambridge, Mass., the University of Miami; Sepulveda Research Corporation, Los Angeles; and the University of Pittsburgh. These brain and tissue repositories seek out and accept brain donations, store the tissue, and distribute it to qualified researchers seeking to understand the causes of – and identify treatments and cures for – brain disorders, such as schizophrenia, multiple sclerosis, depression, epilepsy, Down syndrome and autism.
Link ID: 18992 - Posted: 12.03.2013
Jo Marchant When Steve Cole was a postdoc, he had an unusual hobby: matching art buyers with artists that they might like. The task made looking at art, something he had always loved, even more enjoyable. “There was an extra layer of purpose. I loved the ability to help artists I thought were great to find an appreciative audience,” he says. At the time, it was nothing more than a quirky sideline. But his latest findings have caused Cole — now a professor at the Cousins Center for Psychoneuroimmunology at the University of California, Los Angeles — to wonder whether the exhilaration and sense of purpose that he felt during that period might have done more than help him to find homes for unloved pieces of art. It might have benefited his immune system too. At one time, most self-respecting molecular biologists would have scoffed at the idea. Today, evidence from many studies suggests that mental states such as stress can influence health. Still, it has proved difficult to explain how this happens at the molecular level — how subjective moods connect with the vastly complex physiology of the nervous and immune systems. The field that searches for these explanations, known as psychoneuroimmunology (PNI), is often criticized as lacking rigour. Cole's stated aim is to fix that, and his tool of choice is genome-wide transcriptional analysis: looking at broad patterns of gene expression in cells. “My job is to be a hard-core tracker,” he says. “How do these mental states get out into the rest of the body?” With his colleagues, Cole has published a string of studies suggesting that negative mental states such as stress and loneliness guide immune responses by driving broad programs of gene expression, shaping our ability to fight disease. If he is right, the way people see the world could affect everything from their risk of chronic illnesses such as diabetes and heart disease to the progression of conditions such as HIV and cancer. Now Cole has switched tack, moving from negative moods into the even more murky territory of happiness. It is a risky strategy; his work has already been criticized as wishful thinking and moralizing. But the pay-off is nothing less than finding a healthier way to live. © 2013 Nature Publishing Group
By Dwayne Godwin and Jorge Cham Dwayne Godwin is a neuroscientist at the Wake Forest University School of Medicine. His Twitter handle is @brainyacts. Jorge Cham draws the comic strip Piled Higher and Deeper at www.phdcomics.com. © 2013 Scientific American
Keyword: Brain imaging
Link ID: 18980 - Posted: 11.30.2013
Scientists at the National Institutes of Health have used RNA interference (RNAi) technology to reveal dozens of genes which may represent new therapeutic targets for treating Parkinson’s disease. The findings also may be relevant to several diseases caused by damage to mitochondria, the biological power plants found in cells throughout the body. “We discovered a network of genes that may regulate the disposal of dysfunctional mitochondria, opening the door to new drug targets for Parkinson’s disease and other disorders,” said Richard Youle, Ph.D., an investigator at the National Institute of Neurological Disorders and Stroke (NINDS) and a leader of the study. The findings were published online in Nature. Dr. Youle collaborated with researchers from the National Center for Advancing Translational Sciences (NCATS). Mitochondria are tubular structures with rounded ends that use oxygen to convert many chemical fuels into adenosine triphosphate, the main energy source that powers cells. Multiple neurological disorders are linked to genes that help regulate the health of mitochondria, including Parkinson’s, and movement diseases such as Charcot-Marie Tooth Syndrome and the ataxias. Some cases of Parkinson’s disease have been linked to mutations in the gene that codes for parkin, a protein that normally roams inside cells, and tags damaged mitochondria as waste. The damaged mitochondria are then degraded by cells’ lysosomes, which serve as a biological trash disposal system. Known mutations in parkin prevent tagging, resulting in accumulation of unhealthy mitochondria in the body.
Ed Yong A large international group set up to test the reliability of psychology experiments has successfully reproduced the results of 10 out of 13 past experiments. The consortium also found that two effects could not be reproduced. Psychology has been buffeted in recent years by mounting concern over the reliability of its results, after repeated failures to replicate classic studies. A failure to replicate could mean that the original study was flawed, the new experiment was poorly done or the effect under scrutiny varies between settings or groups of people. To tackle this 'replicability crisis', 36 research groups formed the Many Labs Replication Project to repeat 13 psychological studies. The consortium combined tests from earlier experiments into a single questionnaire — meant to take 15 minutes to complete — and delivered it to 6,344 volunteers from 12 countries. The team chose a mix of effects that represent the diversity of psychological science, from classic experiments that have been repeatedly replicated to contemporary ones that have not. Ten of the effects were consistently replicated across different samples. These included classic results from economics Nobel laureate and psychologist Daniel Kahneman at Princeton University in New Jersey, such as gain-versus-loss framing, in which people are more prepared to take risks to avoid losses, rather than make gains1; and anchoring, an effect in which the first piece of information a person receives can introduce bias to later decisions2. The team even showed that anchoring is substantially more powerful than Kahneman’s original study suggested. © 2013 Nature Publishing Group
Link ID: 18974 - Posted: 11.26.2013
By Jill U. Adams, Every morning I am greeted by Facebook friends complaining of sleepless nights or awakenings. I know the feeling — as do many other Americans. In a 2005 survey of 1,506 Americans by the National Sleep Foundation, 54 percent reported at least one symptom of insomnia — difficulty falling asleep, waking a lot during the night, waking up too early or waking up feeling unrefreshed — at least a few nights a week over the previous year. Thirty-three percent said they had experienced symptoms almost every night. If insomnia visited me that often, I’d be tempted to pick up something at the pharmacy — something easy, something safe, something that didn’t involve making a doctor’s appointment. Indeed, 10 to 20 percent of Americans take over-the-counter sleep aids each year, according to the American Academy of Sleep Medicine. The way they’re marketed, over-the-counter sleep aids sound very appealing: The new product ZzzQuil (yes, from the maker of NyQuil) promises “a beautiful night’s sleep;” an ad says you’ll “fall asleep faster and stay asleep longer” after using Unisom. Companies marketing the herb valerian root and the hormone melatonin as over-the-counter sleep aids make similar claims. But what’s the evidence that supports these claims? “It’s quite lean,” says Andrew Krystal, who directs the sleep research program at Duke University. Over-the-counter sleep aids work differently from prescription drugs for insomnia. Most are simply antihistamines in sheep’s clothing. (Yes, that’s a joke.) The majority of them — ZzzQuil, TylenolPM and Unisom SleepGels — contain diphenhydramine as the active ingredient, the same compound in Benadryl. (Unisom SleepTabs use doxylamine, another antihistamine.) © 1996-2013 The Washington Post
Link ID: 18973 - Posted: 11.26.2013
By Janet Davison, CBC News If headlines in the past few weeks are to be believed, a "Flesh-eating 'zombie' drug" that could devour users "from the inside out" is finding its way onto American streets. Then came reports suggesting that "krokodil," a cheap and highly addictive homemade substitute for heroin that surfaced first in Russia about 10 years ago, had appeared in Ontario's Niagara region. But so far, neither the U.S. Drug Enforcement Agency nor Health Canada has identified krokodil, also known as desomorphine, in any samples they've analyzed since the DEA found two instances of it in 2004. And police in Niagara are now saying the reported cases of the drug — an ugly concoction of codeine mixed with common products such as gasoline, lighter fluid, paint thinner or industrial cleaning oil — haven't been medically confirmed. Krokodil is named for the Russian word for crocodile and its tendency to turn users' skin rough and scaly. The injectable opioid can cause brain damage and severe tissue damage, sometimes leading to gangrene, amputations and even death. It has also been linked to pneumonia, blood poisoning, meningitis, liver and kidney problems, rotting gums and bone infections. The horrific health problems the drug has caused among the well over 100,000 users in Russia and Ukraine have been well documented by researchers in publications such as the International Journal of Drug Policy. But so far there is no solid, official proof that krokodil has reached Canada. The recent news reports about the drug coupled with the lack of hard evidence to back them up underline how difficult it is for health and law enforcement officials to keep up with the evolving mix of street drugs. © CBC 2013
Keyword: Drug Abuse
Link ID: 18967 - Posted: 11.25.2013