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By Karen Weintraub Can I ever re-pay my sleep debt? (I estimate it at 15 years of poor sleep.) It is unclear whether you can make up a long-term sleep debt, because most studies have looked at the effects of sleep loss and recovery only over a few nights or weeks, said Dr. Matt T. Bianchi, the chief of the division of sleep medicine at Massachusetts General Hospital and an assistant professor of neurology at Harvard Medical School. Simulated driving performance and reaction times are affected by just one sleepless night, research has shown. There’s no doubt that sleeping just four hours a night catches up to people within a few nights, leading to impairments of attention, learning and memory and worse performance in school and at work. And making up for lost sleep over the weekend doesn’t work. Five brief nights quickly add up to a shortfall of 20 hours, but people don’t sleep more than five to 10 extra hours to compensate, Dr. Bianchi said. “The interpretation has been you can’t pay off your sleep debt, you just carry it with you,” though it’s also possible that people don’t sleep an extra 20 hours because they don’t need it, Dr. Bianchi said. He cited research by Jim Horne of Loughborough University in Britain showing that a timely nap of less than 20 minutes can equate to an extra hour of nighttime sleep. Different people need somewhat different amounts of sleep, but anything less than six hours a night is definitely not enough, said Dr. Charles Czeisler, a professor of sleep medicine at Harvard. © 2015 The New York Times Company

Keyword: Sleep
Link ID: 21214 - Posted: 07.25.2015

By Annick Laurent Can you tell a pygmy blue whale from an Antarctic blue whale? If not, you aren’t alone. Marine biologists have had trouble distinguishing these enormous mammals with mottled skin patterns ever since they began studying them—and that has complicated efforts to figure out where they breed and how to best protect them. Now, researchers have caught a break thanks to a pygmy whale named Isabela. Researchers first photographed the whale and collected her DNA in 1998 in the waters off the Galapagos Islands. Then, in 2006, another team photographed and collected samples from a similar looking whale off Chile (both photos above). Now, in a study published online before print in Marine Mammal Science, scientists compared those samples and photographs, and discovered that they both belonged to the same whale. That means Isabela (named after the lead author’s daughter to represent hope for future preservation efforts) migrated a minimum of 5200 km, the longest recorded latitudinal migration made by any Southern Hemisphere blue whale on record. The findings suggest Chile's and the Galapagos’ blue whale aggregations are connected, meaning those feeding in the Gulf of Corcovado off Chile may be breeding in the Tropical Eastern Pacific. Knowing where this species migrates—including its feeding and breeding grounds—can help conservationists and governments better establish marine protected areas, the team says. © 2015 American Association for the Advancement of Science

Keyword: Animal Migration
Link ID: 21213 - Posted: 07.25.2015

Sara Reardon After years of disappointment, clinical-trial results released on 22 July suggest that antibody treatments may produce small improvements in people with Alzheimer’s disease. The drugs — Eli Lilly’s solanezumab and Biogen’s aducanumab — target the amyloid-β protein that accumulates in the brains of people with Alzheimer’s. Many researchers question whether the findings will hold up, given that antibody drugs against amyloid have failed in every previous test against the disease. Details of the results were presented at the Alzheimer's Association International Conference in Washington DC. Lilly, of Indianapolis, Indiana, says that in a trial with 440 participants, solanezumab seemed to slow the cognitive decline of people with mild Alzheimer’s by about 30%. The loss of mental acuity in these patients over 18 months was equivalent to the deterioration that participants with a similar level of Alzheimer's disease in a placebo group experienced in just 12 months. Lilly snatched this small victory from the jaws of defeat. In 2012, the company reported no difference between patients who had taken solanezumab for 18 months and those who had received a placebo. But when the company reanalyzed that trial it found a slight improvement in participants whose symptoms were mild when the trial began. Lilly continued the test for six months and began giving solanezumab to the 440-member control group, whose disease was by then more advanced. © 2015 Nature Publishing Group,

Keyword: Alzheimers; Neuroimmunology
Link ID: 21212 - Posted: 07.23.2015

Jon Hamilton The face of Alzheimer's isn't always old. Sometimes it belongs to someone like Giedre Cohen, who is 37, yet struggles to remember her own name. Until about a year ago, Giedre was a "young, healthy, beautiful" woman just starting her life, says her husband, Tal Cohen, a real estate developer in Los Angeles. Now, he says, "her mind is slowly wasting away." People like Giedre have a rare gene mutation that causes symptoms of Alzheimer's to appear before they turn 60. Until recently, people who inherited this gene had no hope of avoiding dementia and an early death. Now there is a glimmer of hope, thanks to a project called DIAN TU that is allowing them to take part in a study of experimental Alzheimer's drugs. The project also could have a huge payoff for society, says Dr. Randall Bateman, a professor of neurology at Washington University in St. Louis. "It's highly likely," he says, that the first drug able to prevent or delay Alzheimer's will emerge from studies of people genetically destined to get the disease. Giedre Cohen enrolled in the DIAN TU study in 2013, when she still had no symptoms of Alzheimer's, her husband says. Their story began more than a decade earlier. In 2002, Tal Cohen was on a trip to Miami to attend a wedding. He met Giedre, who was born in Lithuania, and the two fell in love. © 2015 NPR

Keyword: Alzheimers
Link ID: 21211 - Posted: 07.23.2015

By Sarah Schwartz Researchers have developed a chemical that transforms into a powerful hormone once inside a rat — but only in the brain, not the body. A protein in rats’ brains turns a chemical nicknamed DHED into the hormone estrogen, scientists report July 22 in Science Translational Medicine. This targeted treatment could provide estrogen to the brain and avoid potentially dangerous side effects in the body, the researchers say. “This is an interesting breakthrough,” says neuroendocrinologist Bruce McEwen of the Rockefeller University in New York City. The idea of treatments that affect the brain but not the body, or the body but not the brain, could be useful in treating a number of conditions, including cancer, he says. But the implications of this study for hormone replacement therapy in women is up for debate, a number of researchers say. In menopausal women or those who have had their ovaries surgically removed, lack of estrogen in the brain can cause symptoms such as hot flashes and sleep disturbances. Taking estrogen can relieve those symptoms but can cause side effects in the rest of the body, including an increased risk of certain cancers. The chemical DHED is nearly identical to natural human estrogen, but it has an extra oxygen atom. A specialized protein found in rodents’ brains recognizes the chemical and chops off the oxygen, turning DHED into estrogen. The body’s other organs lack this protein, so they can’t turn DHED into estrogen, says study author Laszlo Prokai, a chemical biologist at the University of North Texas Health Science Center in Fort Worth. © Society for Science & the Public 2000 - 2015.

Keyword: Hormones & Behavior; Sexual Behavior
Link ID: 21210 - Posted: 07.23.2015

THERE’S more to semen than sperm. In many animals, seminal fluid alters both the bodies and sometimes even the behaviour of females. Human semen, too, triggers changes in the uterus, and might have wider effects on women, aimed at just one goal. “It’s all about maximising the chances of the male reproducing,” says Sarah Robertson of the University of Adelaide in Australia. The effects are most striking in fruit flies: seminal fluid can make the females eat more, lay more eggs and be less receptive to other males. Now a team led by Tracey Chapman at the University of East Anglia in Norwich, UK, has found that male fruit flies selectively alter the chemical make-up of their seminal fluid. In the presence of rivals, the males produce more seminal proteins. “It came as a real surprise,” says Chapman. “It’s a sophisticated response to the social and sexual situation.” Some of their findings were presented at the Society for Molecular Biology and Evolution conference in Vienna, Austria, last week, including their discovery that one of these proteins is a “master regulator” of genes. Females exposed to it show a wide range of changes in gene expression. Chapman thinks this kind of seminal signalling is widespread in the animal world. The semen of people, pigs and mice affects the female reproductive tract, and the question is whether it can also produce behavioural responses in female mammals similar to those seen in fruit flies. © Copyright Reed Business Information Ltd.

Keyword: Sexual Behavior; Evolution
Link ID: 21209 - Posted: 07.23.2015

Jessie Rack If you've ever had hiccups in a quiet room, you know how embarrassing and completely uncontrollable they can feel. What if, instead of the hiccups, your body jerked involuntarily or you blurted out words without meaning to? That's a rough idea of what living with Tourette syndrome can be like. Designers of a new computer program called TicHelper hope that they will be able to help children recognize and control these impulses themselves. People with Tourette's perform repetitive movements or vocalizations called tics. A simple tic might be something like head jerking, eye blinking, or throat clearing, and a complex tic might involve patterns of movement or saying multiple words or phrases. We don't know exactly what causes Tourette's, says Douglas Woods, a psychologist at Texas A&M University. Woods, who is also co-chair of the Tourette Association of America Medical Advisory Board, is one of the minds behind TicHelper. "Sometimes kids will grow out of [Tourette's]," Woods says. But if the wait-and-see approach isn't working, and the tics are interfering with daily life, there are a few treatment options. One option is medication. Woods says there are a few different antipsychotic drugs that are used to manage Tourette syndrome, but they have side effects and don't always work. An alternative to pharmaceutical treatment is behavioral therapy. A form of behavioral therapy called comprehensive behavioral intervention for tics, or CBIT for short, is commonly used. CBIT training teaches people with Tourette's to recognize the onset of a tic and to perform a different behavior when they feel one coming on. © 2015 NPR

Keyword: Tourettes
Link ID: 21208 - Posted: 07.23.2015

By Warren Cornwall The number of U.S. school children placed in special education programs due to autism more than tripled from 2000 to 2010, to nearly 420,000. But a new study argues much of that increase likely came as educators swapped one diagnosis for another. The overall percentage of kids diagnosed with a collection of brain development problems that includes autism remained unchanged, suggesting that children who used to be labeled with conditions such as “intellectual disability” were in fact autistic. “If you asked me, ‘Is there a real increase in the prevalence of autism?’ maybe there is, but probably much lower than the reported magnitude,” says Santhosh Girirajan, a geneticist at Pennsylvania State University (Penn State), University Park. In the new study, Girirajan and colleagues combed through data collected in each state for approximately 6.2 million U.S. school children with disabilities who are enrolled in special education programs. The information is collected each year under the federal Individuals with Disabilities Education Act. Based on his or her diagnosis, each child was assigned to one of 13 broader categories, ranging from autism to physical challenges such as blindness. Between 2000 and 2010, the number of children in the autism category more than tripled from 93,624 in 2000 to 419,647 a decade later. Yet nearly two-thirds of that increase was matched by a decline in the rate at which children were labeled as having an “intellectual disability.” The number of kids in that category fell from 637,270 to 457,478. © 2015 American Association for the Advancement of Science.

Keyword: Autism
Link ID: 21207 - Posted: 07.23.2015

By Sandhya Somashekhar NEW WESTMINSTER, B.C. — Alanna Whitney was a weird kid. She had a strange knack for pronouncing long words. Anchovies on pizza could send her cowering under a table. Her ability to geek out on subjects such as Greek mythology and world religions could be unsettling. She drank liquids obsessively, and in her teens, her extreme water intake landed her in the hospital. Years later, she found a word that explained it all: Autistic. Instead of grieving, she felt a rush of relief. “It was the answer to every question I’d ever had,” she recalled. “It was kind of like a go-ahead to shed all of those things I could or couldn’t do and embrace myself for who I am.” So it came to be that Whitney, 24, was arranging strawberries and store-bought cookies on platters at the Queensborough Community Center for a celebration of “Autistic Pride Day,” her shoulder-length hair dyed mermaid green to match her purse and sandals. A bowl of orange earplugs sat nearby in case any of the guests found the ambient sounds overwhelming. Whitney is part of a growing movement of autistic adults who are finding a sense of community, identity and purpose in a diagnosis that most people greet with dread. These “neurodiversity” activists contend that autism — and other brain afflictions such as dyslexia and attention deficit hyperactivity disorder — ought to be treated not as a scourge to be eradicated but rather as a difference to be understood and accepted.

Keyword: Autism
Link ID: 21206 - Posted: 07.23.2015

By Hanae Armitage Cataracts cloud the eyes of tens of millions of people around the world and nearly 17.2% of Americans over the age of 40. Currently, the only treatment is surgery—lasers or scalpels cut away the molecular grout that builds in the eye as cataracts develop, and surgeons sometimes replace the lens. But now, a team of scientists and ophthalmologists has tested a solution in dogs that may be able to dissolve the cataract right out of the eye’s lens. And the solution is itself a solution: a steroid-based eye drop. Though scientists don’t fully understand how cataracts form, they do know that the “fog” often seen by patients is a glob of broken proteins, stuck together in a malfunctioning clump. When healthy, these proteins, called crystallins, help the eye’s lens keep its structure and transparency. But as humans and animals alike get older, these crystallin proteins start to come unglued and lose their ability to function. Then they clump together and form a sheathlike obstruction in the lens, causing the signature “steamy glass” vision that accompanies cataracts. Coming up with a solution other than surgery has been tough. Scientists have been hunting for years for mutations in crystallin proteins that might offer new insights and pave the way to an alternate therapy. Now, it looks like a team led by University of California (UC), San Diego, molecular biologist Ling Zhao may have done just that. Her team came up with the eye drop idea after finding that children with a genetically inherited form of cataracts shared a mutation that stopped the production of lanosterol, an important steroid in the body. When their parents did not have the same mutation, the adults produced lanosterol and had no cataracts. © 2015 American Association for the Advancement of Science.

Keyword: Vision
Link ID: 21205 - Posted: 07.23.2015

By Andrea Alfano Unexpectedly losing a loved one launched 18-year-old Debra* into an episode of major depression, triggering dangerous delusions that landed her in a hospital. Her doctor immediately started her on an antidepressant and on risperidone (Risperdal), an antipsychotic. In little more than a month, her weight shot up by 15 pounds. “Gaining weight made it even more difficult for me to want to leave my house because I felt self-conscious,” Debra says. In the medical community, antipsychotics are well known to cause significant weight gain. Gains of 20 to 35 pounds or more over the course of a year or two are not unusual. Debra's doctor never warned her, though, leaving her feeling like she was losing herself both mentally and physically. The situation is not uncommon, according to psychiatrist Matthew Rudorfer, chief of the somatic treatments program at the National Institute of Mental Health, who points out that although the U.S. Food and Drug Administration carefully tracks acute side effects such as seizures, it pays less attention to longer-term complications such as weight change. Perhaps taking their cue from the FDA, doctors tend to downplay weight-related risks that accompany many psychiatric drugs, Rudorfer says. But for Debra and many others, these side effects are not trivial. The three types of psychiatric drugs that can seriously affect body weight are reviewed below. According to a 2014 review of eight studies, as many as 55 percent of patients who take modern antipsychotics experience weight gain—a side effect that appears to be caused by a disruption of the chemical signals controlling appetite. Olanzapine (Zyprexa) and clozapine (Clozaril) are the top two offenders; studies have shown that on average these drugs cause patients to gain more than eight pounds in just 10 weeks. These two drugs also bear the highest risk of metabolic syndrome, which encompasses weight gain and other related disorders, including type 2 diabetes, according to a 2011 study of 90 people with schizophrenia. Although most antipsychotics are associated with weight gain, aripiprazole (Abilify) and ziprasidone (Geodon) stand out for their lower risk. © 2015 Scientific American

Keyword: Schizophrenia; Obesity
Link ID: 21204 - Posted: 07.23.2015

By James Gallagher Health editor, BBC News website The first hints a drug can slow the progression of Alzheimer's disease have emerged at a conference. Data from pharmaceutical company Eli Lilly suggests its solanezumab drug can cut the rate of the dementia's progression by about a third. The results are being met with cautious optimism, with a separate trial due to report next year. The death of brain cells in Alzheimer's is currently inexorable. Solanezumab may be able to keep them alive. Current medication, such as Aricept, can only manage the symptoms of dementia by helping the dying brain cells function. But solanezumab attacks the deformed proteins, called amyloid, that build up in the brain during Alzheimer's. It is thought the formation of sticky plaques of amyloid between nerve cells leads to damage and eventually brain cell death. Solanezumab has long been the great hope of dementia research, yet an 18-month trial of the drug seemingly ended in failure in 2012. But when Eli Lilly looked more closely at the data, there were hints it could be working for patients in the earliest stages of the disease. So the company asked just over 1,000 of the patients in the original trial with mild Alzheimer's to take the drug for another two years. And the results from this extension of the original trial have now been presented, at the Alzheimer's Association International Conference. Dr Eric Siemers, from the Lilly Research Laboratories, in Indiana, told the BBC: "It's another piece of evidence that solanezumab does have an effect on the underlying disease pathology. "We think there is a chance that solanezumab will be the first disease-modifying medication to be available." The company also started a completely separate trial in mild patients in 2012, and these results could prove to be the definitive moment for the drug. © 2015 BBC.

Keyword: Alzheimers
Link ID: 21203 - Posted: 07.22.2015

By BENEDICT CAREY Women who develop slight but detectable deficits in memory and mental acuity late in life tend to decline faster than men with mild impairment, researchers reported on Tuesday. Some two-thirds of the five million Americans with Alzheimer’s disease are women, in part because women live longer. Researchers have searched in vain for decades to determine other reasons for the disparity. The authors of the new study, who presented their work at the Alzheimer’s Association International Conference in Washington, said their findings indicated nothing about possible causes of gender differences and had no immediate implications for treatment. “All we can say at this point is that there appears to be a faster trajectory for women than men” toward dementia, said Dr. P. Murali Doraiswamy, a professor of psychiatry at the Duke Institute for Brain Sciences and the study’s senior author. Katherine Amy Lin, a student of Dr. Doraiswamy’s and a co-author, presented the study. Previous research had found a steeper decline in women with mild deficits over a period of about a year. The new study extends that finding to up to eight years. “It’s a very interesting finding, but it’s also still early, so we’re limited in what conclusions we can draw,” said Dr. Edward D. Huey, a geriatric psychiatrist at Columbia University, who was not involved in the study. “I think of this as an excellent hypothesis generator. It’s something we need to investigate more deeply.” In the study, the Duke researchers analyzed scores on standard cognitive tests taken by 398 men and women, most in their 70s, being followed as part of a large, continuing Alzheimer’s trial. The participants have been taking the cognitive tests — as well as other tests, like PET scans — on average for four years, and as long as eight years. Controlling for factors that influence memory and mental acuity, like age, education and genetic predisposition, the research team found that women’s scores slipped by an average of about two points a year, compared with one point for men. The team also looked at a standard measure of life quality, rating how well people functioned socially: at home, at work and with family. That, too, slipped faster for women than for men, at about the same rate. © 2015 The New York Times Company

Keyword: Alzheimers; Sexual Behavior
Link ID: 21202 - Posted: 07.22.2015

Ewen Callaway A mysterious group of humans crossed the Bering land bridge from Siberia into the Americas thousands of years ago, genetic analyses reveal. Modern-day signatures of this ‘ghost population’ survive in people who live deep in the Brazilian Amazon, but the two research teams who have made the discovery have different ideas about when and how these migrants reached the Americas1, 2. "This is an unexpected finding," says Jennifer Raff, an anthropological geneticist at the University of Texas at Austin who was not involved in either study. "It’s honestly one of the most exciting results we’ve seen in a while." North and South America were the last continents that humans settled. Previous studies of DNA from modern and ancient Native Americans suggest that the trek was made at least 15,000 years ago (although the timing is not clear-cut) by a single group dubbed the ‘First Americans’, who crossed the Bering land bridge linking Asia and North America. “The simplest hypothesis would be that a single population penetrated the ice sheets and gave rise to most of the Americans,” says David Reich, a population geneticist at Harvard Medical School in Boston, Massachusetts. In 2012, his team found evidence for a single founding migration in the genomes from members of 52 Native American groups3. So Reich was flabbergasted when a colleague called Pontus Skoglund mentioned during a conference last year that he had found signs of a second ancient migration to the Americas lurking in the DNA of contemporary Native Amazonians. Reich wasted no time in verifying the discovery. “During the session afterward, he passed his laptop over the crowd, and he had corroborated the results,” says Skoglund, who is now a researcher in Reich’s lab. © 2015 Nature Publishing Group

Keyword: Genes & Behavior
Link ID: 21201 - Posted: 07.22.2015

By Gretchen Reynolds A walk in the park may soothe the mind and, in the process, change the workings of our brains in ways that improve our mental health, according to an interesting new study of the physical effects on the brain of visiting nature. Most of us today live in cities and spend far less time outside in green, natural spaces than people did several generations ago. City dwellers also have a higher risk for anxiety, depression and other mental illnesses than people living outside urban centers, studies show. These developments seem to be linked to some extent, according to a growing body of research. Various studies have found that urban dwellers with little access to green spaces have a higher incidence of psychological problems than people living near parks and that city dwellers who visit natural environments have lower levels of stress hormones immediately afterward than people who have not recently been outside. But just how a visit to a park or other green space might alter mood has been unclear. Does experiencing nature actually change our brains in some way that affects our emotional health? That possibility intrigued Gregory Bratman, a graduate student at the Emmett Interdisciplinary Program in Environment and Resources at Stanford University, who has been studying the psychological effects of urban living. In an earlier study published last month, he and his colleagues found that volunteers who walked briefly through a lush, green portion of the Stanford campus were more attentive and happier afterward than volunteers who strolled for the same amount of time near heavy traffic. But that study did not examine the neurological mechanisms that might underlie the effects of being outside in nature. So for the new study, which was published last week in Proceedings of the National Academy of Sciences, Mr. Bratman and his collaborators decided to closely scrutinize what effect a walk might have on a person’s tendency to brood. © 2015 The New York Times Company

Keyword: Attention; Emotions
Link ID: 21200 - Posted: 07.22.2015

By Smitha Mundasad Health reporter A type of diabetes drug may offer a glimmer of hope in the fight against Parkinson's disease, research in the journal Plos Medicine suggests. Scientists found people taking glitazone pills were less likely to develop Parkinson's than patients on other diabetes drugs. But they caution the drugs can have serious side-effects and should not be given to healthy people. Instead, they suggest the findings should prompt further research. 'Unintended benefits' There are an estimated 127,000 people in the UK with Parkinson's disease, which can lead to tremor, slow movement and stiff muscles. And charities say with no drugs yet proven to treat the condition, much more work is needed in this area. The latest study focuses solely on people with diabetes who did not have Parkinson's disease at the beginning of the project. Researchers scoured UK electronic health records to compare 44,597 people prescribed glitazone pills with 120,373 people using other anti-diabetic treatment. They matched participants to ensure their age and stage of diabetes treatment were similar. Scientists found fewer people developed Parkinson's in the glitazone group - but the drug did not have a long-lasting benefit. Any potential protection disappeared once patients switched to another type of pill. Dr Ian Douglas, lead researcher at the London School of Hygiene and Tropical Medicine, said: "We often hear about negative side-effects associated with medications, but sometimes there can also be unintended beneficial effects. "Our findings provide unique evidence that we hope will drive further investigation into potential drug treatments for Parkinson's disease." © 2015 BBC

Keyword: Parkinsons
Link ID: 21199 - Posted: 07.22.2015

By BENEDICT CAREY Bill Cosby stands accused of committing date rape long before drugs like GHB or Rohypnol were widely used for that purpose. Many of Mr. Cosby’s accusers believed they had been drugged — but with what? And how? In a recently obtained legal deposition, Mr. Cosby acknowledged giving quaaludes to some women with whom he had sex, but said consumption of the drug was consensual, “the same as a person would say, ‘Have a drink.’ ” In a transcript of the deposition, reported on Sunday in The New York Times, the comedian told lawyers had had obtained seven prescriptions for quaaludes. Originally approved and marketed as a “safer” sleeping pill, less addictive than barbiturates, the drug (known generically as methaqualone) was both sedating and hypnotic. Recreational use was common, but the federal government withdrew them from the market in 1982. “It was inevitable that it would be tried by people looking for a ‘better high,’ ” Dr. David Smith, medical director of the Haight-Ashbury Free Clinic, and Dr. Donald Wesson noted in The Journal of Psychedelic Drugs. Intoxication with quaaludes “soon developed a reputation for being especially pleasant.” Young people in the 1970s used quaaludes as they would a strong drink: to loosen up, to relax, to socialize. The pills also won a reputation for inducing periods of euphoria, as well as sexual arousal — “heroin for lovers,” some called it. By the middle of the decade, quaaludes were a staple of the club scene, often taken with alcohol. So embedded were quaaludes in the cultural scene that even years later the Dead Kennedys and Billy Idol were singing about the drug’s captivating effects. But reckless users risked overdose, especially when combining the pills with alcohol, which could lead to coma, convulsions and sometimes death. In a 1973 review of 252 hospital admissions for drug overdose, doctors in Edinburgh found that the third most common cause of “self-poisoning,” after barbiturates and LSD, was Mandrax — the British version of quaaludes, widely abused in South Africa as well. © 2015 The New York Times Company

Keyword: Drug Abuse
Link ID: 21198 - Posted: 07.22.2015

by Bethany Brookshire For some of us, a weekly case of the Mondays isn’t just because of traffic, work pileups or our soulless office space. It’s because we had to get up early, and sleeping in on the weekend was so incredibly glorious. Besides, because we slept in on Sunday, we didn’t get to the gym until the afternoon, we cooked a late dinner for a friend and then we couldn’t fall asleep at all and so stayed up playing around on the Internet. OK, maybe that’s just me. But you get the general idea. Our obligations — work, family and friends — often don’t line up with when our bodies want to sleep. Scientists call this phenomenon social jetlag. And it may make for more than just miserable Mondays. Social jetlag may also be associated with wider waistlines. As we learn more about how our body clocks work, it might help to think about how our own schedules can shift. Some of us love late nights and can’t help glaring at those who hop out of bed for a 5 a.m. workout (again, maybe that’s just me). But in fact our chronotypes aren’t a result of willpower. Instead they fall in a natural curve. About two-thirds of people are neutral, but a few fall at each end of the spectrum, rising extra early, or staying up until the wee hours. But even those in the middle are still getting up a little bit too early and staying up a little bit too late. We try to make up for it on days off, sleeping in or falling asleep early for a few extra hours of rest. But the result of that shift in sleep schedule? Jetlag. “It’s the equivalent of taking a flight one direction every Friday and going back every Sunday,” says Michael Parsons, a behavioral geneticist at the Medical Research Council Harwell in England. © Society for Science & the Public 2000 - 2015

Keyword: Sleep; Obesity
Link ID: 21197 - Posted: 07.21.2015

By James Gallagher Health editor, BBC News website Irregular sleeping patterns have been "unequivocally" shown to lead to cancer in tests on mice, a study suggests. The report, in Current Biology, lends weight to concerns about the damaging impact of shift work on health. The researchers said women with a family risk of breast cancer should never work shifts, but cautioned that further tests in people were needed. The data also indicated the animals were 20% heavier despite eating the same amount of food. Studies in people have often suggested a higher risk of diseases such as breast cancer in shift workers and flight attendants. One argument is disrupting the body's internal rhythm - or body clock - increases the risk of disease. However, the link is uncertain because the type of person who works shifts may also be more likely to develop cancer due to factors such as social class, activity levels or the amount of vitamin D they get. Mice prone to developing breast cancer had their body clock delayed by 12 hours every week for a year. Normally they had tumours after 50 weeks - but with regular disruption to their sleeping patterns, the tumours appeared eight weeks earlier. The report said: "This is the first study that unequivocally shows a link between chronic light-dark inversions and breast cancer development." Interpreting the consequences for humans is fraught with difficulty, but the researchers guesstimated the equivalent effect could be an extra 10kg (1st 8lb) of body weight or for at-risk women getting cancer about five years earlier. "If you had a situation where a family is at risk for breast cancer, I would certainly advise those people not to work as a flight attendant or to do shift work," one of the researchers, Gijsbetus van der Horst, from the Erasmus University Medical Centre, in the Netherlands, said. © 2015 BBC.

Keyword: Sleep; Neuroimmunology
Link ID: 21196 - Posted: 07.21.2015

Kashmira Gander Performing well at school and going on to have a complex job could lower the risk of dementia, scientists have found. On the contrary, loneliness, watching too much TV and a sedentary lifestyle can make a person’s cognitive abilities decline more quickly, according to new research being presented to experts at the international Alzheimer's Association International Conference in Washington DC. Researchers are also due to show attendees the results from trials Solanezumab – believed to be the first drug to halt the progression of the disease if a patient is diagnosed early enough. One study involving 7,500 people aged 65 and above in Sweden over a 20-year period showed that dementia rates were 21 per cent higher in those whose grades were in the bottom fifth of the population. Meanwhile, participants with complex jobs involving data and numbers saw their chance of developing the disease cut by 23 per cent. Read more: Why fish oil pills may not be so healthy after all Proof that dementia risk can be reduced by improving lifestyle Charity warns of a 'worrying' lack of support for dementia patients Dementia research: Drug firms despair of finding cure and withdraw funding after a catalogue of failures For separate study in Sweden, scientists followed the lives of 440 people aged 75 or over for nine years, and discovered that those in the bottom fifth for school grades were found to have a 50 per cent increase in the risk of developing dementia. © independent.co.uk

Keyword: Alzheimers; Learning & Memory
Link ID: 21195 - Posted: 07.21.2015