Chapter 16. None
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Why do some people feel as though one of their body parts is not truly part of them and go to crazy lengths to get rid of it? Paul D. McGeochanswers: Certain people hold a deep desire to amputate a healthy limb. They are not psychotic, and they fully realize that what they want is abnormal. Nevertheless, they have felt from childhood that the presence of a specific limb, usually a leg, somehow makes their body “overcomplete.” Ultimately, many will achieve their desired amputation through self-inflicted damage or surgery. During the past few years my work with neuroscientists Vilayanur S. Ramachandran of U.C.S.D. and David Brang of Northwestern University, along with research by neuroscientist Peter Brugger of University Hospital Zurich in Switzerland, has transformed our understanding of this condition. Our findings suggest that a dysfunction of specific brain areas on the right side of the brain, which are involved in generating our body image, may explain the desire. Bizarre disorders of body image have long been known to arise after a stroke or other incident inflicts damage to the right side of the brain, particularly in the parietal lobe. The right posterior parietal cortex seems to combine several incoming streams of information—touch, joint position sense, vision and balance—to form a dynamic body image that changes as we interact with the world around us. In brain scans, we have found this exact part of the right parietal lobe to activate abnormally in individuals desiring limb removal. Because the primary sensory areas of the brain still function normally, sufferers are able to see and feel the limb in question. Yet they do not experience it as part of their body because the right posterior parietal lobe fails to adequately represent it. The mismatch between a person's actual physical body and his or her body image seems to cause ongoing arousal in the sympathetic nervous system, which may intensify the desire to remove the limb. Given that sufferers date these feelings to childhood, the right parietal dysfunction most likely is congenital or arises in early development. © 2013 Scientific American
Link ID: 18869 - Posted: 11.04.2013
By JOHN RUDOLF GUATEMALA CITY — DONALD RODAS, a baby-faced man in his late 20s with paranoid schizophrenia, arrived at Guatemala’s only public psychiatric hospital last year after being charged with murdering his parents. He says he often wanders freely through the sprawling facility of dilapidated one-story buildings and wooded courtyards, where detainees charged with crimes mingle with ordinary patients and the developmentally disabled. He sees ugly things. Those who refuse their medication are beaten and put in the “little room,” a barren isolation cell, he said. Desperate women sell their bodies for as little as 5 quetzales, or less than a dollar, to afford basic necessities. “I see when they have sex for money,” Mr. Rodas said in halting English. “To buy food. All they have is beans.” The United States began emptying out its vast asylum system in the 1960s, spurred by scathing reports of abuse and neglect, like a 1946 Life magazine exposé that described many institutions as “little more than concentration camps.” The transition to community-based care cut the institutionalized population by more than 90 percent by 1994. But community care resources failed to match demand in the United States, leading to widespread homelessness and an influx of the mentally ill into jails and prisons. Even so, deinstitutionalization is widely credited with ending the abuse and neglect that made mental institutions synonymous with a nightmarish netherworld. Yet this asylum-based model of mental health care remains the standard across much of the globe. In many poor and developing countries, thousands of mentally ill people are warehoused in dirty and dangerous institutions. Health experts and advocates who monitor such facilities say the picture varies little from country to country: overcrowded wards lacking in privacy; poor sanitation; physical and sexual abuse; routine use of restraints and long-term solitary confinement; and forced treatment, including electroshock without consent. The rights of patients judged to be mentally ill are easily stripped by the courts and are difficult if not impossible to regain. © 2013 The New York Times Company
Link ID: 18868 - Posted: 11.04.2013
Elizabeth Pennisi Speak easy. The language gene FOXP2 may work through a protein partner that stimulates the formation of excitatory connections (green) in nerve cells (magenta). Few genes have made the headlines as much as FOXP2. The first gene associated with language disorders, it was later implicated in the evolution of human speech. Girls make more of the FOXP2 protein, which may help explain their precociousness in learning to talk. Now, neuroscientists have figured out how one of its molecular partners helps Foxp2 exert its effects. The findings may eventually lead to new therapies for inherited speech disorders, says Richard Huganir, the neurobiologist at Johns Hopkins University School of Medicine in Baltimore, Maryland, who led the work. Foxp2 controls the activity of a gene called Srpx2, he notes, which helps some of the brain's nerve cells beef up their connections to other nerve cells. By establishing what SRPX2 does, researchers can look for defective copies of it in people suffering from problems talking or learning to talk. Until 2001, scientists were not sure how genes influenced language. Then Simon Fisher, a neurogeneticist now at the Max Planck Institute for Psycholinguistics in Nijmegen, the Netherlands, and his colleagues fingered FOXP2 as the culprit in a family with several members who had trouble with pronunciation, putting words together, and understanding speech. These people cannot move their tongue and lips precisely enough to talk clearly, so even family members often can’t figure out what they are saying. It “opened a molecular window on the neural basis of speech and language,” Fisher says. © 2013 American Association for the Advancement of Science
/ by Charles Choi, LiveScience Using lasers, scientists can now surgically blast holes thinner than a human hair in the heads of live fruit flies, allowing researchers to see how the flies' brains work. Microscopically peering into living animals can help scientists learn more about key details of these animals' biology. For instance, tiny glass windows surgically implanted into the sides of living mice can help researchers study how cancers develop in real time and evaluate the effectiveness of potential medicines. Surgically preparing small live animals for such "intravital microscopy" is often time-consuming and requires considerable skill and dexterity. Now, Supriyo Sinha, a systems engineer at Stanford University in California, and his colleagues have developed a way to prepare live animals for such microscopy that is both fast -- taking less than a second -- and largely automated. To conduct this procedure, scientists first cooled fruit flies to anesthetize them. Then, the researchers carefully picked up the insects with tweezers and glued them to the tops of glass fibers in order to immobilize the flies' bodies and heads. Then, using a high-energy pulsed ultraviolet laser, the researchers blasted holes measuring 12 to 350 microns wide in the flies' heads. (In comparison, the average human hair is about 100 microns wide.) They then applied a saline solution to exposed tissue to help keep the fly brains healthy. © 2013 Discovery Communications, LLC.
Link ID: 18861 - Posted: 11.02.2013
by Flora Graham These specs do more than bring blurry things into focus. This prototype pair of smart glasses translates visual information into images that blind people can see. Many people who are registered as blind can perceive some light and motion. The glasses, developed by Stephen Hicks of the University of Oxford, are an attempt to make that residual vision as useful as possible. They use two cameras, or a camera and an infrared projector that can detect the distance to nearby objects. They also have a gyroscope, a compass and GPS to help orient the wearer. The collected information can be translated into a variety of images on the transparent OLED displays, depending on what is most useful to the person sporting the shades. For example, objects can be made clearer against the background, or the distance to obstacles can be indicated by the varying brightness of an image. Hicks has won the Royal Society's Brian Mercer Award for Innovation for his work on the smart glasses. He plans to use the £50,000 prize money to add object and text recognition to the glasses' abilities. © Copyright Reed Business Information Ltd.
by Simon Makin Sometimes wacky-sounding ideas aren't so crazy after all. If your body clock is all at sea after a long flight or a night shift, the way to reset it may be to scramble your timekeeping neurons even further. The body's master clock resides in a region of the brain called the suprachiasmatic nucleus. Each neuron in the SCN keeps its own time, but the neurons can synchronise their clocks by sending and receiving signals using a hormone called vasoactive intestinal polypeptide (VIP). When Erik Herzog at Washington University in St Louis, Missouri, and colleagues probed the hormone's effects, they discovered that a glut of VIP caused the neurons to lose the ability to synchronise. Herzog's team wondered whether this might have a beneficial effect. "If the cell rhythms are messed up and out of phase, the system may be more sensitive to environmental cues than it would be if all the cells were in sync," he says, allowing the body clock to adjust more readily. The VIP treatment To test the idea, they gave some mice an injection of VIP into the brain before fast-forwarding the light/dark cycle in their cages by 8 hours. The mice that received the hormone adjusted in 4.5 days on average, whereas untreated mice needed nearly eight days – gauging by how active the animals were when the lights were off. © Copyright Reed Business Information Ltd.
Keyword: Biological Rhythms
Link ID: 18855 - Posted: 10.30.2013
by Tina Hesman Saey BOSTON— Siberians may use genes to stay warm, a new study shows. As part of an effort to catalog genetic diversity in Siberia, Alexia Cardona of the University of Cambridge and collaborators sampled DNA from 200 Siberians representing 10 native groups. The team looked for genes that have more changes in Siberians than would be expected by chance — a sign that the genes evolved rapidly in the 24,000 years since people settled the frigid land. Rapid changes suggest that a gene is important for adapting to an environment. Several of the Siberians’ genes have variants that may help keep Arctic dwellers warm during the long winters, Cardona reported October 24 at the annual meeting of the American Society of Human Genetics. Among the candidates for genetic heaters are genes involved in metabolizing fats. Some Siberian groups eat mostly meat, so genes that help convert animal fat to energy are important for creating heat. Another gene with variants unique to Siberians is called PRKG1; it helps regulate body heat by controlling muscle contraction and the constriction and dilation of blood vessels. Muscle contractions are an important part of shivering, which can raise body temperature. The researchers also identified variants in genes involved in thyroid function, which plays a role in temperature regulation. A. Cardona et al. Genome-wide analysis of cold adaption in indigenous Siberian populations. American Society of Human Genetics annual meeting, Boston, October 24, 2013. © Society for Science & the Public 2000 - 2013
Reindeer may have a unique way of coping with the perpetual darkness of Arctic winters: During that season, their eyes become far more sensitive to light. Like many vertebrates and most mammals, especially those that are nocturnal, reindeer (Rangifer tarandus) have a light-reflecting layer of collagen-containing tissue behind the retinas of their eyes. This structure, called the tapetum lucidum (Latin for “bright tapestry”), gives the eye’s light-sensitive neurons a second chance to detect scarce photons in low-light conditions. (The layer also produces the “eyeshine” that can make animal eyes appear to glow in the dark.) During sunny months, reindeer have yellow eyeshine. But in the wintertime, light reflected from the tapetum lucidum takes on a decidedly bluish sheen—a seasonal shift that hasn’t been noted in other mammals, the researchers say. To study this unusual color change, the researchers brought some disembodied reindeer eyeballs into the lab and placed small weights on them. When under pressure, the eyeballs changed the color of eyeshine almost immediately. That fits with what happens in the wild over the course of seasons, the researchers say. In winter, reindeer pupils are constantly dilated, which increases fluid pressure. That, in turn, decreases the spacing of collagen fibers in the tapetum lucidum, further increasing the scattering of light within the eye and shifting the reflected light toward the lower wavelengths of light which are predominant at dusk. These changes make the reindeer’s eyes between 100 and 1000 times more light-sensitive, the researchers report today in the Proceedings of the Royal Society B. Although this decreases the creature’s sharpness of vision, it’s a tradeoff that, on the whole, probably boosts reindeer survival by helping them better detect predators in the dark, the researchers contend. © 2013 American Association for the Advancement of Science
Link ID: 18852 - Posted: 10.30.2013
Melissa Dahl TODAY You know smoking doesn’t do any favors for your face – or your lungs, or your heart, or just about any other part of your body, for that matter! – but a new study of twins hints at the ways the habit makes you look older than you really are. In what is perhaps the best detail of the study, researchers used the annual Twins Days Festival in Twinsburg, Ohio (the "Largest Annual Gathering of Twins in the World!") to round up the 79 identical pairs they include in the report. A panel of three plastic surgery residents compared the faces of the twins, one of which had been smoking for at least five years longer than the other. They identified a few major areas of accelerated aging in the faces of the smoking twins: The smokers' upper eyelids drooped while the lower lids sagged, and they had more wrinkles around the mouth. The smokers were also more likely to have jowls, according to the study, which was published today in the journal Plastic and Reconstructive Surgery. Smoking reduces oxygen to the skin, which also decreases blood circulation, and that can result in weathered, wrinkled, older-looking skin, explains Dr. Bahman Guyuron, a plastic surgeon in Cleveland, Ohio, and the lead author of the study. The logic of research like this and others like it is this: If threats of cancer, heart and lung disease, or the dangers of second- and third-hand smoke aren’t enough to get people to stop smoking, or to never start in the first place, then why not try appealing to people’s vanity? (The same tactic has been used in an attempt to warn young people away from tanning.)
Keyword: Drug Abuse
Link ID: 18851 - Posted: 10.30.2013
Think fast. The deadly threat of snakes may have driven humans to develop a complex and specialized visual system. The sinuous shape triggers a primal jolt of recognition: snake! A new study of the monkey brain suggests that primates are uniquely adapted to recognize the features of this slithering threat and react in a flash. The results lend support to a controversial hypothesis: that primates as we know them would never have evolved without snakes. A tussle with a snake meant almost certain death for our preprimate ancestors. The reptiles slithered through the forests of the supercontinent Gondwana roughly 100 million years ago, squeezing the life out of the tiny rodent-sized mammalian ancestors of modern primates. About 40 million years later, likely after primates had emerged, some snakes began injecting poison, which made them an even deadlier and more immediate threat. Snakes were “the first and most persistent predators” of early mammals, says Lynne Isbell, a behavioral ecologist the University of California, Davis. They were such a critical threat, she has long argued, that they shaped the emergence and evolution of primates. By selecting for traits that helped animals avoid them, snakes ultimately endowed us with forward-facing eyes, for example, and enlarged visual centers deep in our brains that are specialized for picking out specific features in the world around us, such as the general shape of a snake’s body camouflaged among leaves. Isbell published her “Snake Detection Theory” in 2006. To support it, she showed that the rare primates that have not encountered venomous snakes in the course of their evolution, such as lemurs in Madagascar, have poorer vision than those that evolved alongside snakes. © 2013 American Association for the Advancement of Science
By JAN HOFFMAN There are activities common to most humans that we enjoy immensely, without much thought, and as frequently as opportunity and instinct provide. On occasion, researchers feel they need to know why. Recently, experimental psychologists at Oxford University explored the function of kissing in romantic relationships. Surprise! It’s complicated. After conducting an online survey with 308 men and 594 women, mostly from North America and Europe, who ranged in age from 18 to 63, the researchers have concluded that kissing may help people assess potential mates and then maintain those relationships. “The repurposing of the behavior is very efficient,” said Rafael Wlodarski, a doctoral candidate and lead author of the study, published in Archives of Sexual Behavior. But another hypothesis about kissing — that its function is to elevate sexual arousal and ready a couple for coitus — didn’t hold up. While that might be an outcome, researchers did not find sexual arousal to be the primary driver for kissing. Participants in the survey were asked about their attitudes toward kissing in different phases of romantic relationships. They were then asked about their sexual history: for example, whether they had been more inclined toward casual encounters or long-term, committed relationships. They also had to define their “mate value” by assessing their own attractiveness. Later, during data analysis, the researchers looked at how individual differences affected a person’s thoughts on kissing. Copyright 2013 The New York Times Company
Keyword: Sexual Behavior
Link ID: 18845 - Posted: 10.29.2013
By James Gallagher Health and science reporter, BBC News A clearer picture of what causes Alzheimer's disease is emerging after the largest ever analysis of patients' DNA. A massive international collaboration has now doubled the number of genes linked to the dementia to 21. The findings, published in the journal Nature Genetics, indicate a strong role for the immune system. Alzheimer's Research UK said the findings could "significantly enhance" understanding of the disease. The number of people developing Alzheimer's is growing around the world as people live longer. However, major questions around what causes the dementia, how brain cells die, how to treat it or even diagnose it remain unanswered. "It is really difficult to treat a disease when you do not understand what causes it," one of the lead researchers, Prof Julie Williams from Cardiff University, said. Detective work The genetic code, the instructions for building and running the body, was scoured for clues. A group - involving nearly three quarters of the world's Alzheimer's geneticists from 145 academic institutions - looked at the DNA of 17,000 patients and 37,000 healthy people. They found versions of 21 genes, or sets of instructions, which made it more likely that a person would develop Alzheimer's disease. They do not guarantee Alzheimer's will develop, but they do make the disease more likely. By looking at the genes' function in the body, it allows researchers to figure out the processes going wrong in Alzheimer's disease. BBC © 2013
by Bethany Brookshire There are many animal species out there that exhibit same-sex mating behavior. This can take the form of courtship behaviors, solicitation, all the way through to mounting and trading off sperm). In some species, it’s clear that some of this behavior is because the animals involved have pair bonded. But what about insects? Many insects mate quickly, a one and done approach, with very little bonding involved beyond what’s needed to protect against other potential suitors. When it comes to bugs, is it intentional same-sex behavior? Or is it all a mistake? Hypotheses are out there, but in the end, we need science. A new study in the November Behavioral Ecology and Sociobiology wants to answer these questions. The authors did a meta-analysis of papers looking at same-sex sexual activity in male insects and arachnids. They tried to tease out why same-sex sexual behavior might occur in insects. What are the benefits? The potential downsides? And from that, to hypothesize why it might occur. Some of it, it turns out, could be due to context. A lot of observed same-sex mating behavior in insects is observed, for example, when the males are all housed together, away from the females. Partially because of this (but possibly for other reasons as well), same-sex sexual behavior in insects tends to occur much more frequently in the lab than in the wild. But it’s still often documented in the field. Why does it happen? Some say that by mating with a “passive” male and transferring sperm, that sperm then gets passed over to the female when the passive male mates. Sneaky. But does it really happen? And if it does, is it effective? So far, it doesn’t appear that it is; less than 0.5% of the offspring resulted from the transfer of sperm when these cases were documented. © Society for Science & the Public 2000 - 2013
By ADAM NAGOURNEY and RICK LYMAN LOS ANGELES — In the heart of Northern California’s marijuana growing region, the sheriff’s office is inundated each fall with complaints about the stench of marijuana plots or the latest expropriation of public land by growers. Its tranquil communities have been altered by the emergence of a wealthy class of marijuana entrepreneurs, while nearly 500 miles away in Los Angeles, officials have struggled to regulate an explosion of medical marijuana shops. But at a time when polls show widening public support for legalization — recreational marijuana is about to become legal in Colorado and Washington, and voter initiatives are in the pipeline in at least three other states — California’s 17-year experience as the first state to legalize medical marijuana offers surprising lessons, experts say. Warnings voiced against partial legalization — of civic disorder, increased lawlessness and a drastic rise in other drug use — have proved unfounded. Instead, research suggests both that marijuana has become an alcohol substitute for younger people here and in other states that have legalized medical marijuana, and that while driving under the influence of any intoxicant is dangerous, driving after smoking marijuana is less dangerous than after drinking alcohol. Although marijuana is legal here only for medical use, it is widely available. There is no evidence that its use by teenagers has risen since the 1996 legalization, though it is an open question whether outright legalization would make the drug that much easier for young people to get, and thus contribute to increased use. And though Los Angeles has struggled to regulate marijuana dispensaries, with neighborhoods upset at their sheer number, the threat of unsavory street traffic and the stigma of marijuana shops on the corner, communities that imposed early and strict regulations on their operations have not experienced such disruption. © 2013 The New York Times Company
Keyword: Drug Abuse
Link ID: 18840 - Posted: 10.28.2013
If you were stung by a bark scorpion, the most venomous scorpion in North America, you’d feel something like the intense, painful jolt of being electrocuted. Moments after the creature flips its tail and injects venom into your skin, the intense pain would be joined by a numbness or tingling in the body part that was stung, and you might experience a shortness of breath. The effect of this venom on some people—small children, the elderly or adults with compromised immune systems—can even trigger frothing at the mouth, seizure-like symptoms, paralysis and potentially death. Based solely on its body size, the four-inch-long furry grasshopper mouse should die within minutes of being stung—thanks to the scorpion’s venom, which causes temporary paralysis, the muscles that allow the mouse to breathe should shut down, leading to asphyxiation—so you’d think the rodent would avoid the scorpions at all costs. But if you put a mouse and a scorpion in the same place, the rodent’s reaction is strikingly brazen. If stung, the four-inch-long rodent might jump back for a moment in surprise. Then, after a brief pause, it’ll go in for the kill and devour the scorpion piece by piece: This predatory behavior isn’t the result of remarkable toughness. As scientists recently discovered, the mouse has evolved a particularly useful adaptation: It’s immune to both the pain and paralytic effects that make the scorpion’s venom so toxic. Although scientists long knew that the mouse, native to the deserts of the American Southwest, preys upon a range of non-toxic scorpions, “no one had ever really asked whether they attack and kill really toxic scorpions,” says Ashlee Rowe of Michigan State University, who led the new study published today in Science.
Who would win in a fight: a bark scorpion or a grasshopper mouse? It seems like an easy call. The bark scorpion (Centruroides sculpturatus) delivers one of the most painful stings in the animal kingdom—human victims have compared the experience to being branded. The 25-gram grasshopper mouse (Onychomys torridus) is, well, a mouse. But as you can see in the video above, grasshopper mice routinely kill and eat bark scorpions, blissfully munching away even as their prey sting them repeatedly (and sometimes right in the face). Now, scientists have discovered why the grasshopper mice don’t react to bark scorpion stings: They simply don’t feel them. Evolutionary neurobiologist Ashlee Rowe at the University of Texas, Austin, has been studying the grasshopper mice’s apparent superpower since she was in graduate school. For the new study, she milked venom from nearly 500 bark scorpions and started experimenting. When she injected the venom into the hind paws of regular laboratory mice, the mice furiously licked the site for several minutes. But when she injected the same venom into grasshopper mice, they licked their paws for just a few seconds and then went about their business, apparently unfazed. In fact, the grasshopper mice appeared to be more irritated by injections of the saline solution Rowe used as a control. Rowe knew that grasshopper mice weren’t entirely impervious to pain—they reacted to injections of other painful chemicals such as formalin, just not the bark scorpion venom. To find out what was going on, she and her team decided to determine how the venom affects the grasshopper mouse’s nervous system, in particular the parts responsible for sensing pain. © 2013 American Association for the Advancement of Science
By HELENE STAPINSKI IN an office of the American Museum of Natural History, a team of scientists, artists and multimedia experts were discussing what had poisoned Skippy, a cute Jack Russell terrier that had keeled over sick in his virtual backyard. Was it the chocolate he found in the garbage can? Did a snake, or a black widow spider, bite him? Or was a poisonous cane toad to blame? Skippy is just one of many victims in the museum’s show, “The Power of Poison,” opening Nov. 16, to which the staff was busy applying finishing touches. Using iPads, visitors can examine the circumstances surrounding Skippy’s fictional poisoning and, controlling their experience individually, take a crack at solving the mystery. But because the museum is popular with small children, Skippy does not die. Instead, his animated eyes turn into Xs, he runs erratically around the yard, he drools and he vomits a bit. Eventually, though, Skippy rallies to full health. “We were not going to make this a scary show,” said the exhibit’s curator, Dr. Mark Siddall. “Instead you walk out saying, ‘Wow. That was cool.’ ” Dr. Siddall spent two hours enthusiastically discussing poison and its properties at the museum recently, walking through some of the show’s highlights. The exhibit, which takes a look at poison’s role in nature, myth, medicine and human history, examines killer caterpillars, zombie ants and deadly vipers. It also looks at the possible victims, like the heavily slumbering Snow White. Plus the age-old question of what killed Cleopatra. Was it an asp, or something else? And while we’re at it, was Napoleon really poisoned with arsenic? © 2013 The New York Times Company
Link ID: 18837 - Posted: 10.26.2013
By James Gallagher Health and science reporter, BBC News The mocked "obesity excuse" of being born with a slow metabolism is actually true for some people, say researchers. A team at the University of Cambridge has found the first proof that mutated DNA does indeed slow metabolism. The researchers say fewer than one in 100 people are affected and are often severely obese by early childhood. The findings, published in the journal Cell, may lead to new obesity treatments even for people without the mutation. Scientists at the Institute of Metabolic Science, in Cambridge, knew that mice born without a section of DNA, a gene called KSR2, gained weight more easily. But they did not know what effect it may be having in people, so they analysed the DNA of 2,101 severely obese patients. Some had mutated versions of KSR2. It had a twin effect of increasing their appetite while their slowing metabolism. "You would be hungry and wanting to eat a lot, you would not want to move because of a slower metabolism and would probably also develop type 2 diabetes at a young age," lead researcher Prof Sadaf Farooqi told the BBC. She added: "It slows the ability to burn calories and that's important as it's a new explanation for obesity." BBC © 2013
By Tori Rodriguez The digestive tract and the brain are crucially linked, according to mounting evidence showing that diet and gut bacteria are able to influence our behavior, thoughts and mood. Now researchers have found evidence of bacterial translocation, or “leaky gut,” among people with depression. Normally the digestive system is surrounded by an impermeable wall of cells. Certain behaviors and medical conditions can compromise this wall, allowing toxic substances and bacteria to enter the bloodstream. In a study published in the May issue of Acta Psychiatrica Scandinavica, approximately 35 percent of depressed participants showed signs of leaky gut, based on blood tests. The scientists do not yet know how leaky gut relates to depression, although earlier work offers some hints. Displaced bacteria can activate autoimmune responses and inflammation, which are known to be associated with the onset of depression, lower mood and fatigue. “Leaky gut may maintain increased inflammation in depressed patients,” which could exacerbate the symptoms of depression if not treated, says Michael Maes, a research psychiatrist with affiliations in Australia and Thailand and an author of the paper. Currently leaky gut is treated with a combination of glutamine, N-acetylcysteine and zinc—believed to have anti-inflammatory or antioxidant properties—when behavioral and dietary modifications fail. © 2013 Scientific American
Link ID: 18830 - Posted: 10.24.2013
Stroke deaths and illnesses are likely to continue shifting younger, global research suggests. In the Global and Regional Burden of Stroke in 1999-2010 study published in Thursday's issue of the medical journal The Lancet, researchers take a comprehensive look at stroke rates by country and region. "Stroke burden worldwide continues to increase," Prof. Valery Feigin, director of the National Institute for Stroke and Applied Neurosciences at AUT University in New Zealand said in an interview. "It's increasing at increased pace, more than we expected, disproportionately affecting low-to middle-income countries." The proportion of stroke in people younger than 65 is substantial, Feigin's team said. More than 83,000 children and youths aged 20 years and younger are affected by stroke annually. Feigin said the epidemic of obesity, and Type 2 diabetes in children and young people is increasing worldwide, which will be important risk factors for stroke 20 or 30 years down the road. If the trends in low-income and middle-income countries continue, by 2030 there will be almost 12 million stroke deaths and 70 million stroke survivors worldwide, the researchers projected. More than 90 per cent of strokes are preventable through lifestyle changes such as improving diet, quitting smoking, reducing salt and alcohol intake, increasing physical activity and managing stress, Feigin said.
Link ID: 18828 - Posted: 10.24.2013