By Katherine Harmon Hunting for a misplaced set of keys or a dead cell phone can be a nuisance. But for people who search for concealed weapons or malignant tumors, finding a target—and one they're not sure is even there—could be a matter of life or death. Unfortunately, research has shown that the rarer an item has proved to be, the less likely people are to find it when it is there. "We know that if you don't find it often, you often don't find it," Jeremy Wolfe, a professor of ophthalmology at Harvard Medical School, said in a prepared statement. Likewise, searches for common objects tend to turn up way more false positives. So are people as hasty to judge that an inspected bag doesn't contain a weapon (a rare item), as they are to assume it has a more common item? Wolfe and his colleague, Michael Van Wert of the Brigham and Women's Hospital in Cambridge, were determined to hunt down an answer to how reaction times changed based on what people were used to finding. Their results were published online January 14 in Current Biology. Their experiment, in which two dozen participants looked for weapons in simulated baggage, showed that people do not adapt their searching time equally to different odds of finding items. Individuals were given a consistent likelihood of finding an object, say 98 percent, and were judged both on the time it took them to declare whether a bag contained a weapon—and whether they were correct. Those in experiments who are faced with consistently 50-50 odds of finding a target might be expected to take the longest to arrive at an answer, and those with very rare or very frequent incidences of finding weapons should be the fastest. That is, with similarly slim odds of finding or not finding a target, people might be expected to make decisions rapidly about whether they see it or not. © 2010 Scientific American

Keyword: Vision
Link ID: 13681 - Posted: 06.24.2010

by Jessica Hamzelou Drinking too much during pregnancy can harm offspring permanently. Now experiments in mice suggest this may be because alcohol chemically alters the fetus's DNA, affecting how genes are expressed. It's well known that fetal alcohol syndrome occurs when pregnant women drink excessively and causes behavioural and physical harm to the child after birth. But we know little about the molecular mechanisms underlying the condition. Previous studies have shown that factors in the mother's environment during pregnancy can cause "epigenetic" modifications to the fetus's DNA. These don't alter the genetic code itself but might switch certain genes on or off, or increase or decrease their expression. To see whether a mother's alcohol consumption might affect the way her child's genes are expressed, Suyinn Chong at the Queensland Institute of Medical Research in Herston, Australia, and her colleagues turned to mice with genes for brown and yellow fur that are known to be modified by environmentally induced epigenetic changes. "It's a good model to use because you can tell whether a mouse's environment is affecting the expression of its genes just by looking at its coat colour," says Chong. © Copyright Reed Business Information Ltd.

Keyword: Drug Abuse; Development of the Brain
Link ID: 13680 - Posted: 06.24.2010

Andy Coghlan, reporter The scientist sacked by the British government for allegedly criticising government drugs policy today made good on his promise to set up his own committee to investigate and publicise the science of recreational drugs. "We will provide the truth about drugs unfettered by any political interference," said David Nutt of Imperial College London, and the former head of the government's Advisory Committee on the Misuse of Drugs (ACMD) until he was asked to leave last October by Home Office minister, Alan Johnson. Now, true to his promise, Nutt is chairman of his newly created Independent Scientific Committee on Drugs, and today proudly announced that its first meeting took place yesterday. So far it has 14 members, including four of the five who resigned from the ACMD last October in protest at the sacking of Nutt. "This is the strongest grouping of scientists we've ever had in this country [who are experts on recreational drugs]," said Nutt. "The best science will come from us." Already, the new committee has decided on its first three programmes. The first will investigate the dangers of "legal highs"; recreational substances that are not outlawed but which may be causing serious harm to users who buy them freely on the internet. © Copyright Reed Business Information Ltd.

Keyword: Drug Abuse
Link ID: 13679 - Posted: 06.24.2010

By Greg Miller If you have a hard time shaking your phobias--whether they be of spiders or confined spaces--you may have a genetic quirk that alters your brain's fear circuitry. New research that links a small DNA substitution with abnormal brain activity and fear responses represents a small but encouraging step, experts say, toward understanding how genes may contribute to anxiety disorders. Although many mental disorders run in families, tracking down the genes responsible has been tremendously difficult. It's even harder to show how those genes interfere with brain function. Complicating matters further is the uncertainty involved in assessing the mental state of mice, researchers' animal of choice for studying the genetics of psychiatric disorders. The new study, published online today in Science, examines the role of the gene for brain-derived neurotrophic factor (BDNF). Several years of research have implicated this gene and the growth factor it encodes in mood disorders. Up to 30% of Caucasians have an alteration in the BDNF gene that causes the amino acid methionine to be substituted for valine at a particular place in the protein. In 2006, a team led by Francis Lee at Weill Cornell Medical College in New York City reported that genetically engineered mice with this so-called Met substitution appeared to be more anxious than other mice. But studies with humans have been inconclusive, says BJ Casey, a neuroscientist at Cornell who collaborated with Lee on the new study. Having the Met variation doesn't doom someone to a life of anxiety, Casey says, but it may exert a subtle influence. © 2010 American Association for the Advancement of Science

Keyword: Emotions; Genes & Behavior
Link ID: 13678 - Posted: 06.24.2010

A simple eye test might be able to detect Alzheimer's and other diseases before symptoms develop, according to UK scientists. The technique uses fluorescent markers which attach to dying cells which can be seen in the retina and give an early indication of brain cell death. The research has been carried out on mice, but human trials are planned. Scientists from University College London hope this could lead to a high street opticians test for the disease. The research, which is published in the journal, Cell Death and Disease, could enable scientists to overcome the difficulty of investigating what is happening inside the brains of those with Alzheimer's. They currently have to rely on expensive MRI scans or post-mortems. This new technique enables scientists to track the progress of brain disease by looking at dying cells in the retina. The cells show up as green dots because they absorb the fluorescent dye. The research has so far been carried out on mice, but the team is optimistic that the technique can be translated to humans. Professor Francesca Coredeiro, lead author from University College London Institute of Opthalmology said: "Few people realise that the retina is a direct, albeit thin, extension of the brain. It is entirely possible that in the future a visit to a high-street optician to check on your eyesight will also be a check on the state of your brain. I hope that screening for Alzheimer's will be available on the high street within five years." (C)BBC

Keyword: Alzheimers
Link ID: 13677 - Posted: 01.14.2010

By Julie Steenhuysen CHICAGO - Antidepressants fail to help about half of the people who take them, and a study in mice may help explain why. Most antidepressants — including the commonly used Prozac and Zoloft — work by increasing the amount of serotonin, a message-carrying brain chemical made deep in the middle of the brain by cells known as raphe neurons. Researchers at Columbia University Medical Center in New York said on Wednesday that genetically engineered mice that had too much of one type of serotonin receptor in this region of the brain were less likely to respond to antidepressants. Story continues below ↓advertisement | your ad here "These receptors dampen the activity of these (serotonin-producing) neurons. Too much of them dampen these neurons too much," Rene Hen of Columbia, whose study appears in the journal Neuron, said in a telephone interview. "It puts too much brake on the system." Hen said the finding may be useful in giving doctors an idea of whether a patient will respond to an antidepressant. And it could also help drugmakers populate better clinical trials to help identify new drug compounds that work for people who are unlikely to benefit from conventional antidepressants. Copyright 2010 Reuters

Keyword: Depression
Link ID: 13676 - Posted: 06.24.2010

By David Brown WASHINGTON - More than 200 years after it was isolated from poppies, morphine remains one of medicine’s best painkillers. But that isn’t its only use. Physicians sometimes include morphine in a cocktail of drugs given to people having heart attacks. It can relieve the breathlessness of pulmonary edema. It decreases diarrhea. A famous physician of the early 20th century, William Osler, once called morphine “God’s own medicine.’’ Research published this week suggests the compound may have at least one more use, too. In a study of about 700 members of the military wounded in Iraq, those who got morphine soon after their injuries were about half as likely to develop posttraumatic stress disorder as those who didn’t get the drug. Whether morphine’s apparently protective effect arises directly from the relief of traumatic pain, or indirectly by blocking the establishment of traumatic memory, isn’t known. Both the researchers and outside specialists agreed the effect would have to be proved virtually beyond doubt before morphine was routinely given to prevent the mental disorder. “I would be very reluctant to suggest any change in clinical practice,’’ said Troy Lisa Holbrook of the Naval Health Research Center, in San Diego, who headed the study published in the New England Journal of Medicine. “We need to understand a great deal more how this appears to work.’’ © Copyright 2010 Globe Newspaper Company

Keyword: Stress; Pain & Touch
Link ID: 13675 - Posted: 06.24.2010

Erika Check Hayden . Julia lies with her eyes closed in an incubator, twitching her tiny limbs in a quiet, sedated sleep. Like the other babies in this intensive-care unit, she is surrounded by a phalanx of machinery. But unlike her nursery mates, this baby isn't wrapped in a warm blanket. Her doctors at the Children's Hospital of the University of California, San Francisco (UCSF) have left most of her days-old body bare and placed her on a blue mat that is cooling her to a hypothermic 33.5 °C. Gauze wrapping holds a network of electrodes against her skull. The electrodes are sending a stream of signals to a nearby monitor, which is being watched carefully by David Rowitch. Like a growing number of babies in the United States, Julia (not her real name) is at risk of permanent brain damage. The trend is driven by increasing rates of preterm births coupled with medical advances that allow the survival of very premature babies — and also full-term babies such as Julia, whose births were not straightforward. Although these advances have focused on babies' hearts and lungs, they have largely ignored the newborn brain. Rowitch, a neonatologist, is one of a handful of doctors around the world who hope to reverse this trend by using advances in basic neuroscience to develop treatments for injured newborn brains. He and Donna Ferriero, chief of paediatric neurology at the hospital, founded the university's Newborn Brain Research Institute in 2006. Two years later they created one of the nation's first neurointensive-care nurseries, where Julia is now sleeping. They and other scientists are pushing to get treatments into clinics as soon as possible to make up for what they call years of inadequate funding for research into brain damage in babies. © 2010 Nature Publishing Group,

Keyword: Stress; Pain & Touch
Link ID: 13674 - Posted: 06.24.2010

Sleeping is known to help humans commit information to memory and learn skills, but now researchers say the same is true of birds. Researchers at the University of Chicago have found that sleep helps starlings remember how to perform a specific task. The birds were trained to distinguish two five-second birdsong clips using what the researchers called a "go-no go" procedure. When the "go" birdsong was played, the bird was given a food pellet if it poked its beak through a hole in its cage. When the "no go" song was played, the bird poking its beak through the hole didn't release a food pellet and caused the lights in the cage to briefly turn off. Groups of starlings were trained in the task at different times of day and tested later to see how well they learned. In all the groups, the birds' performance at the task improved after the birds slept. "We really wanted to behaviourally show that these types of sleep-dependent memory benefits are occurring in animals," said graduate study and lead author Timothy Brawn, in a statement. "What was remarkable was that the pattern here looks very similar to what we see in humans. There wasn't anything that was terribly different," . Previous studies have shown that humans can perform a learned task better after a night's sleep. Brawn and his colleagues demonstrated this in a 2008 study involving people learning to play a first-person shooter game. © CBC 2010

Keyword: Sleep; Learning & Memory
Link ID: 13673 - Posted: 06.24.2010

By Christof Koch Most scholars concerned with the material basis of consciousness are cortical chauvinists. They focus on the two cortical hemispheres that crown the brain. It is here that perception, action, memory, thought and consciousness are said to have their seat. There is no question that the great specificity of any one conscious perceptual experience—such as the throbbing pain of the socket following extraction of the lower right wisdom tooth, the feeling of familiarity in déjà vu, the aha experience of sudden understanding, the azure blue of a high mountain vista, the ­despair at reading about one more suicide bombing—is mediated by coalitions of synchronized cortical nerve cells and their ­associated targets in the satellites of the cortex, thalamus, amygdala, claustrum and basal ganglia. Groups of cortical neurons are the elements that construct the content of each particular rich and vivid experience. Yet content can be provided only if the basic infrastructure to represent and process this content is intact. And it is here that the less glamorous regions of the brain, down in the catacombs, come in. It is a general observation in neurology that injury to large chunks of cortical tissue, particularly of the so-called silent frontal lobes, can lead to a loss of specific conscious content but without any massive impairment in the victim’s behavior. The patient might be unable to see in color or perhaps cannot recognize familiar faces but otherwise copes fine in daily life. But destruction of tissue the size of a sugar cube in the brain stem and in parts of the thalamus, especially if they occur simultaneously on the left and right sides, may leave the patient comatose, stuporous or otherwise unable to function. A car accident, a drug or alcohol overdose, a drive-by shooting, a near drowning, a stroke—all these events can cause consciousness to flee permanently. © 2010 Scientific American,

Keyword: Attention; Sleep
Link ID: 13672 - Posted: 06.24.2010

by Jessica Griggs Editorial: Uh-oh, more emotions to worry about CAN you name the six basic emotions? Take a straw poll of your friends and we guarantee that you will find no consensus. Yet psychologists are unequivocal: joy, sadness, anger, fear, surprise and disgust. These are the Big Six, quite literally, the in-your-face emotions - the ones that everyone the world over exhibits with the same dramatic and characteristic facial expressions. They have been the subjects of intense research for over half a century, not least because of the role they have played in our survival as a species. Times have changed, though. Our ancestors may have had daily need of fear to flee predators, anger to conquer foes and disgust to avoid diseases, but we live in a more subtle world in which other emotions have come to the fore. There are many contenders. Avarice, embarrassment, boredom, depression, jealousy and love, for example, might epitomise the modern age. Yet some more obscure emotions may be increasingly relevant today. Here we explore five of them, any one of which could make a case to be promoted to a place alongside the Big Six. The uplifting emotion "Let it be said by our children's children that when we were tested we refused to let this journey end, that we did not turn back nor did we falter; and with eyes fixed on the horizon and God's grace upon us, we carried forth that great gift of freedom and delivered it safely to future generations." © Copyright Reed Business Information Ltd

Keyword: Emotions
Link ID: 13671 - Posted: 06.24.2010

By Nathan Seppa Carrying a variant form of the CETP gene is looking more and more like holding a winning genetic lottery ticket. This version of the gene might protect against Alzheimer’s disease and other forms of dementia, researchers report in the Jan. 13 Journal of the American Medical Association. Earlier research linked the variant to impressive longevity and high levels of HDL, the “good” cholesterol. But before running out to get your genes tested, be aware that the scientists reporting the most recent discovery don’t know for certain how the genetic variant might achieve any of these salutary effects, particularly dementia prevention. They do know that people harboring the variant form of CETP make less of the CETP protein, and apparently less is better. “What CETP does in the brain is less clear,” says study coauthor Richard Lipton, a neurologist at the Albert Einstein College of Medicine of Yeshiva University in New York City. In the new study, Lipton and his colleagues identified 523 people, average age 78. Blood samples showed that roughly one-fifth carried two copies of the variant form of CETP (one copy comes from each parent). About 45 percent harbored a single variant copy (from one parent) and one-third had two copies of the standard version of CETP (no variant). © Society for Science & the Public 2000 - 2010

Keyword: Alzheimers; Genes & Behavior
Link ID: 13670 - Posted: 06.24.2010

By Ann Gibbons The Y chromosome has long been thought of as a stagnant part of the genome, where genes are slowly decaying in males of all species. But the first comprehensive comparison of the Y chromosome in two species--specifically, humans and chimpanzees--shows that in fact, it is a hot spot of evolution. "It's really exciting; it's totally well-documented; it's really dramatic," says population geneticist Andrew Clark of Cornell University. As is well-known, humans and chimps share 98% of their DNA. But more than 30% of the DNA differs between chimps and humans in the region of the Y chromosome that determines sex. This suggests that the Y chromosome has undergone "extraordinary" remodeling in both species in the 6 million years or so since they split from a common ancestor, says geneticist David Page of the Howard Hughes Medical Institute in Chevy Chase, Maryland, and director of the Whitehead Institute of the Massachusetts Institute of Technology in Cambridge. For almost a century, researchers have thought that the Y chromosome, with far fewer genes than the X, was decaying. Both sex chromosomes evolved from an ordinary pair of chromosomes more than 200 million years ago (Science, 29 October, 1999, p. 964). But since then, the Y has steadily lost genes as well as its ability to recombine and swap genes with the X chromosome. This suggested that the Y has long been an isolated chromosome with little left to lose--just a couple of hundred genes, at most, whose job is to produce sperm and determine the sex of offspring. As a result, researchers predicted that the Y chromosome should be nearly identical in humans and chimpanzees, like the rest of the genome. © 2010 American Association for the Advancement of Science.

Keyword: Sexual Behavior; Evolution
Link ID: 13669 - Posted: 06.24.2010

by David Jay Brown Post-traumatic stress disorder—PTSD—can linger years after someone has experienced or witnessed something extremely upsetting. It may be accompanied by panic attacks, flashbacks, and nightmares, and it can be fiendishly difficult to treat. But experimental types of treatment could soon lend a hand. In a pilot study, South Carolina psychiatrist Michael Mithoefer is targeting PTSD with a controversial drug: methylenedioxymethamphetamine, or MDMA, commonly known as Ecstasy. He gave MDMA, along with psychotherapy, to 21 participants who had developed treatment-resistant PTSD as a result of experiences with crime or war. Only 15 percent of the MDMA-treated subjects continued to experience PTSD afterward, as opposed to 85 percent of the subjects who received psychotherapy with a placebo. Mithoefer considers the findings especially notable given that 20 of the 21 participants had previously failed to obtain relief from FDA-approved treatments. “The next step is to find out if this can be replicated elsewhere,” he says. The study, sponsored by the Multidisciplinary Association for Psychedelic Studies, was the first FDA-approved trial evaluating MDMA’s therapeutic applications. Additional clinical tests examining MDMA-based treatments for PTSD are under way in Switzerland and Israel. Other potential PTSD drugs also show promise. Researchers at Mount Sinai School of Medicine in New York City report that one or two treatments with a compound called RU38486 can disrupt traumatic memories in rats without affecting normal memories. And investigators at Tel Aviv University and Ben-Gurion University in Israel find that an injection of the steroid cortisol immediately following a trauma reduces PTSD-like effects in mice. Both of these therapies are slated for human clinical trials.

Keyword: Stress; Drug Abuse
Link ID: 13668 - Posted: 06.24.2010

By Steve Connor, Science Editor Why are we asking this now? New research has shed light on why migraine sufferers are often sensitive to light. Specialised nerve cells in the eye appear to trigger migraine headaches even in people who are registered blind. Scientists identified specialised, light-sensitive cells in the retina of the eye. They are involved in sending signals to the brain via the optic nerve and appear to be involved in "photophobia", when people react badly to light. Although still at an early stage, it is hoped that the research into these light-sensitive cells, called melanopsin photoreceptors, may lead to new ways of treating migraine attacks. What is migraine? It is more than just a splitting headache. A migraine attack involves a pulsing or throbbing pain in an area of the head, often on one side but not always the same side, and can be accompanied by extreme sensitivity to light, nausea and vomiting. The attacks can last for between four and 24 hours, although 72-hour attacks are not unknown. They are extremely debilitating. Normal, over-the-counter painkillers may not always be effective, especially if they are taken when the migraine attack has already started. Classic migraine, now known as migraine with aura, involves some kind of visual disturbance, such as flashing lights, blind spots, tunnel vision, zig-zag lines or even temporary blindness. Common migraine, or migraine without aura, does not involve visual disturbances but often results in photophobia and increased sensitivity to noise, sounds and even smells. ©independent.co.uk

Keyword: Pain & Touch
Link ID: 13667 - Posted: 06.24.2010

Carolyn Butler So, be honest: Is that glass half-full or half-empty? Personally, I tend toward the latter, though I secretly long to be one of those Pollyannas who always look on the bright side of things and can remain hopeful through a family crisis, two hours of downtown gridlock or any other challenge. In fact, my New Year's resolution for '10 is to be more positive. (Meanwhile, the pessimist in me is well aware that studies have shown that roughly 80 percent of those who make such pledges give them up by Valentine's Day.) My hope is that positive thinking will make me not only happier but healthier, in the long run. A recent study published in the journal Circulation showed that a sunnier outlook on life is associated with a lower risk of heart disease and mortality. The research, which tracked more than 97,000 women older than 50 for eight years, found that optimists were 9 percent less likely to develop heart disease and 14 percent less likely to die from any cause than their pessimistic counterparts. Those with a high degree of "cynical hostility" were 16 percent more likely than all others to die during that same period. "This is really consistent with a number of other studies in the past, with the strongest findings in the realm of coronary heart disease: There is good evidence to suggest optimism is protective and that pessimism seems to be detrimental, when it comes to the development of disease and future outcomes," says Laura Kubzansky, an associate professor at the Harvard School of Public Health who has focused on these issues. "But what's a little less clear is what the mechanisms are, or how that protective effect occurs." © 2010 The Washington Post Company

Keyword: Emotions; Stress
Link ID: 13666 - Posted: 06.24.2010

By M. A. Woodbury President Franklin D. Roosevelt admonished in a 1932 commencement address that “it is common sense to take a method and try it. If it fails, admit it frankly and try another.” FDR had the revival of a depressed U.S. economy in mind, but scientists experimenting with treating brain disorders with fetal cell transplants have taken his aphorism to heart. New methods are transforming past failures, and the results seem far more promising this go-round. Fetal cell therapy began in earnest in the mid-1980s, among researchers hoping to treat Parkinson’s disease. These patients have trouble controlling their movements partly because their brains lack the neurotransmitter dopamine. The hope was that tissue from fetal midbrains placed into patients’ brains would turn into dopamine-making cells. Shortly after the turn of the century, however, the work foundered when a subset of transplant patients developed disabling movement disorders termed runaway dyskinesias. But amid the setbacks was the fact that some subjects—especially those who were younger and less afflicted—did well with the fetal cells. “The question is, How do we reconcile all these disparate strands and problems with these trials and move the field forward?” says Roger Barker, a neurologist at the University of Cambridge who is meta-analyzing prior transplant data in hopes of devising a better trial. One possible explanation for the mixed findings is contamination: transplant tissue containing serotonin-secreting neurons could have muddied the results. © 2010 Scientific American,

Keyword: Parkinsons; Stem Cells
Link ID: 13665 - Posted: 06.24.2010

By RICHARD A. FRIEDMAN, M.D. Last week, The Journal of the American Medical Association published a study questioning the effectiveness of antidepressant drugs. The drugs are useful in cases of severe depression, it said. But for most patients, those with mild to moderate cases, the most commonly used antidepressants are generally no better than a placebo. For the millions of people who take these drugs, and the doctors who prescribe them, this provocative claim had to be confusing, if not alarming. It contradicted literally hundreds of well-designed trials, not to mention considerable clinical experience, showing antidepressants to be effective for a wide array of depressed patients. But on close inspection, the new study does not stand up to that mountain of earlier evidence. To understand why, it helps to look at the way it was conducted. The study is a so-called meta-analysis — not a fresh clinical trial, but a combined analysis of previous studies. A common reason for doing this kind of analysis is to discover potential drug effects that might have been missed in smaller studies. By aggregating the data from many studies, researchers gain the statistical power to detect broad patterns that may not have been evident before. But meta-analyses can be tricky. First, they are only as good as the smaller studies they analyze. And when there are hundreds of studies out there, how to decide which ones to include? Copyright 2010 The New York Times Company

Keyword: Depression
Link ID: 13664 - Posted: 06.24.2010

By Joshua K. Hartshorne When I tell people I study whether birth order affects personality, I usually get blank looks. It sounds like studying whether the sky is blue. Isn’t it common sense? Popular books invoke birth order for self-discovery, relationship tips, business advice and parenting guidance in titles such as The Birth Order Book: Why You Are the Way You Are (Revell, 2009). Newspapers and morning news shows debate the importance of the latest findings (“Latter-born children engage in more risky behavior; what should parents do?”) while tossing in savory anecdotes (“Did you know that 21 of the first 23 astronauts into space were firstborns?”). But when scientists scrutinized the data, they found that the evidence just did not hold up. In fact, until very recently there were no convincing findings that linked birth order to personality or behavior. Our common perception that birth order matters was written off as an example of our well-established tendency to remember and accept evidence that supports our pet theories while readily forgetting or overlooking that which does not. But two studies from the past three years finally found measurable effects: our position in the family does indeed affect both our IQ and our personality. It may be time to reconsider birth order as a real influence over whom we grow up to be. Before discussing the new findings, it will help to explain why decades of research that seemed to show birth-order effects was, in fact, flawed. Put simply, birth order is intricately linked to family size. A child from a two-kid family has a 50 percent chance of being a firstborn, whereas a child from a five-kid family has only a 20 percent chance of being a firstborn. © 2010 Scientific American,

Keyword: Development of the Brain; Intelligence
Link ID: 13663 - Posted: 06.24.2010

By PERRI KLASS, M.D. A couple of weeks ago, I saw a 5-year-old girl who was still wetting the bed every night. It’s a common complaint: at least 15 percent of healthy 5-year-olds are not reliably “dry” at night. And bed-wetting is quite common even in older children. But what may be most surprising about primary nocturnal enuresis, to use the clinical term for urinary incontinence in a child who does fine by day but has never been reliably dry through the night, is that it is often genetically based. In other words, it is not about emotional problems, or mistakes a parent made during potty training, or laziness, which some still attribute to the bed-wetter himself. (The problem is about three times as common in boys as in girls.) Indeed, one of the worst things about bed-wetting is the stigma. Sufferers and their families have been accused of everything from poor parenting to latent criminality. (In 1945, The New York Times reported on a psychological study of the backgrounds of 500 men who got into disciplinary trouble in the wartime Navy. The most powerful predictor of failure in the Navy, the article reported, was a combination of three factors: expulsion from school, civilian arrest and enuresis beyond age 5.) Enuresis can have a number of physiological causes. Some children lack a hormone that decreases urine production at night. Others wet the bed simply because their bladder capacity is small. Copyright 2010 The New York Times Company

Keyword: Sleep
Link ID: 13662 - Posted: 06.24.2010