Bubonic Plague Sickens 16-Year-Old Girl In Oregon

The plague is best remembered for killing millions of Europeans during the Middle Ages, and now it's back! Epidemiologists from the Oregon Health Authority's Public Health Division, the Crook County Public Health Department, and the Centers for Disease Control and Prevention have confirmed a case of bubonic plague in a 16-year-old girl from Oregon.
"Many people think of the plague as a disease of the past, but it's still very much present in our environment, particularly among wildlife," said Emilio DeBess, state public health veterinarian in the Public Health Division’s Acute and Communicable Disease Prevention Section, in a statement. "Fortunately, plague remains a rare disease, but people need to take appropriate precautions with wildlife and their pets to keep it that way."
Health officials believe the girl contracted the disease via a flea bite she got during a hunting trip that started on Oct. 16. Although bubonic plague cases are usually found on the West Coast of the United States, it is considered rare in Oregon. This is only the eighth human case of bubonic plague in the state since 1995 and no deaths have been reported. The girl was hospitalized on Oct. 24 and is currently recovering in the hospital’s intensive care unit.
According to the Centers for Disease Control and Prevention, the plague is caused by the bacterium, Yersinia pestis. It is often carried by squirrels, chipmunks, and other wild rodents and their fleas. There are three types of plague: bubonic, septicemic, and pneumonic. Bubonic is considered the most common. Symptoms of the plague, including fever, chills, headache, lethargy, swollen lymph nodes, and bloody or watery cough, tend to develop within one to four days after exposure.

Science Finally Figures Out Why We Like To Smoke When We Drink

Only smoke when you drink? You’re not alone. Despite the rate of regular tobacco users decreasing, the number of self-confessed “social smokers” is on the rise, particularly among young women. But what is it about drinking that turns otherwise health-conscious individuals into overnight chainsmokers? According to a recent study, it’s because many drinkers crave the stimulant effect of nicotine, which helps offset the sleepiness alcohol induces.
The National Institutes of Health estimates that as many as 90 percent of alcoholics also smoke cigarettes, and even those without an alcohol dependency are known to light up “only when they drink.” Although this link between drinking and smoking has been widely acknowledged, scientists are not completely sure of what entices drinkers to light up in the first place.
In order to further investigate the biological reaction that drives drinkers to smoke, a team of researchers from the University of Missouri gave rats fitted with sleep-recording electrodes nicotine and alcohol. After observing the effects of the two drugs on the rats’ brains, the team came to an interesting conclusion: Nicotine’s stimulant effect helps to ward off the sleepiness caused by alcohol consumption.
Nicotine specifically affected the rat’s basal forebrain, an area of the brain associated with reflexes, learning, and most importantly, attention. Alcohol, being a depressant, inhibits the central nervous system. Therefore, it makes sense how this stimulation would help to counteract the sleep-inducing effects and increase alertness.
In addition to keeping drinkers awake, past research has also found nicotine can enhance the pleasurable effects of alcohol, further adding to the “alcohol high” and increasing our desire to drink more. Unfortunately, along with being two of the most widely used drugs, nicotine and alcohol are also some of the deadliest drugs. The World Health Organization estimates that each year, around six million deaths can be attributed to nicotine use while about three million trace back to excessive alcohol use.
There has been some progress in efforts to curb both smoking and drinking rates, however. A 2014 study, for example, found that instilling stricter tobacco taxes and smoke-free policies lowered overall smoking and drinking rates. Thakkar and his team hope that by identifying the physical reactions caused by drinking and smoking, they can help to further lower worldwide dependency on these products.
Source: Thakkar MM, Sharma R, Sahota P. Nicotine administration in the wake-promoting basal forebrain attenuates sleep-promoting effects of alcohol. Journal of Neurochemistry. 2015

The Amount Of Sleep You Get Doesn't Matter; It's Uninterrupted Sleep That Affects How Happy Or Angry You Are

You've probably heard countless health experts say that depending on your age seven to eight hours worth of sleep is best to ensure you’re alert and capable of functioning the next day. But while sleeping too much or too little can be detrimental to your health, the quality of your sleep also has an impact on how you feel the next day. As it turns out, your nightly bathroom rendezvous may have more of an effect on the way you feel than the number of hours you sleep.
A new study from Johns Hopkins University, published in Sleep, found people who wake up multiple times over the course of a night are more than likely to have sour moods the next morning — even more so than those who sleep for only a few hours without interruption. These findings were the result of a three-night experiment in which 62 healthy men and women were split into three groups: One had interrupted sleep, another had a delayed bedtime, and the last slept through the night without interruption.
During each night, the participants whose sleep was interrupted were awoken eight times, while those who had a delayed bedtime ended up getting shorter amounts of sleep. All three groups rated their moods in a questionnaire that assessed positive and negative emotions — cheerfulness or anger, for example — the next morning. The researchers found that by the second night, both forced-awake and delayed-bedtime participants started to show drops in their positive moods and upticks in negative emotions — 31 percent and 12 percent, respectively. There were no significant differences, however, when it came to overall changes in negative moods during the entire three-day experiment. This suggests that interrupted or delayed sleep had more of an effect on positive mood than negative mood.
"When your sleep is disrupted throughout the night, you don't have the opportunity to progress through the sleep stages to get the amount of slow-wave sleep that is key to the feeling of restoration," said lead author Dr. Patrick Finan, an assistant professor of psychiatry and behavioral sciences at the Johns Hopkins University School of Medicine, in a press release.
Compared to the delayed-bedtime group, the forced-awake group had shorter periods of deep, slow-wave sleep. Normally referred to as “deep sleep,” slow-wave sleep is the third stage of non-rapid eye movement sleep — a sleep state in which sleepers rarely dream — where brain and muscle activity decrease significantly, allowing our bodies to recover from the day. Without these effects, forced-awake participants felt more negative, and had lower levels of energy, sympathy, and friendliness.
Although the study was conducted on healthy patients with normal sleep schedules, Finan said the results could be applied to those who suffer from insomnia. Frequent awakenings over the course of the night is one of the most common symptoms of insomnia, which affects an estimated 10 percent of the U.S. adult population. "Many individuals with insomnia achieve sleep in fits and starts throughout the night, and they don't have the experience of restorative sleep," Finan said.
While the results certainly show positive mood can be affected by interrupted sleep, Finan said more research will be necessary to learn about the role of a restorative night’s sleep, as well as the sleep stages people with insomnia experience.
Source: Finan P, et al. Sleep. 2015.

Mother's Breast Milk May Influence Risk Of Obesity In Children, As Their Gut Microbiomes Are Built Early

A newborn’s risk of becoming obese could be determined by his mother’s breast milk, according to new findings from the University of Southern California. The study, published in The American Journal of Clinical Nutrition, is the first to identify how different carbohydrates in breast milk are linked to infant growth and obesity. Mothers therefore could be protecting or increasing the risk of their newborn becoming obese each time they breastfeed.
"Early life experiences related to the environment and different feeding modalities contribute to obesity," said the study’s co-author Michael Goran, a professor of preventive medicine and pediatrics at USC’s School of Medicine, in a press release. "But typically we think of obesity risk kicking in after weaning — the timing of introduction to solid foods, early exposures to sugary beverages. Clearly there is something going on before weaning even in babies who are exclusively breastfed."
For the study, the research team examined 25 mothers’ breast milk and their 1- to 6-month-old infants. They measured different levels of carbohydrates found in their breast milk called "human milk oligosaccharides" (HMOs), which are known to play a role in the development of an infant’s immune system. But now researchers have discovered different types of HMOs may be able to protect a baby from becoming obese or increase the risk by the time they’re 6 months of age.
Researchers combed through 71 previous reports on the overall effects of breastfeeding on obesity, and found that breastfeeding was able to reduce excess weight and obesity by about 10 percent. But when they took a closer look, they found a specific mix of HMOs in breast milk can mean the difference between a child born with a weight problem or not despite the mother’s weight. In fact, researchers believe the kind of carbohydrates found in breast milk influence the baby’s weight more than the mother’s own weight gain or obesity during pregnancy.
HMOs became the focus throughout all of the studies because they’re the third most abundant ingredient in human breast milk and are found in higher concentrations than proteins. HMOs can’t be digested, so they accumulate in the colon and shape the way a baby’s gut microbiome forms, which is the population of bacteria in the intestine. This gave research teams from the dozens of past studies an opportunity to measure the baby’s HMO levels from their poopy diaper.
Babies who were 6 months of age and had higher levels of two different carbohydrates (LBFPII and DSLNT) were more likely to have one pound more of fat than babies with normal or low levels of those carbohydrates. Meanwhile, other HMOs, like one called LNFPI, had a protective effect and were linked with a one pound lower of fat.
"How the gut microbiome develops will have a long-term influence on obesity and health risk," Goran said. "These compounds that are not being digested go straight into the infant's gut and act as prebiotics. They act as fuel for microbes in the gut and help them grow and become diverse."
Gut microbiome influence the immune system, brain function, and weight because of the influence they have on insulin, appetite, and metabolism. An unbalanced mix of gut microbes can lead to obesity and inflammation, says Dr. Gerard Mullin, a gastroenterologist and nutritionist at Johns Hopkins Hospital. Consuming a diet high in fat and refined carbs favors fat accumulation and obesity. According to these new findings, gut microbiomes may start building and influencing the future of a person as young as 6 months old.
"Ultimately what we would like to be able to do is identify which of the HMOs are most important for obesity protection and then use that as a supplement that can be given to the breastfeeding infant and added to infant formula," Goran said.
Currently, HMOs are not added into infant formula. Using them to influence how a baby begins to develop their unique microbiome community may lead to a future of feeding babies anti-obesity concoctions. In the last 30 years, childhood obesity has more than doubled in children and quadrupled in adolescents, according to the Centers for Disease Control and Prevention. Intervening and improving their diets earlier could set the stage for a healthier upbringing.
"The infant's first exposure to nutrition sets the stage either for increased or decreased risk of obesity," said the study’s lead author Tanya Alderete, a postdoctoral researcher at USC’s School of Medicine, in a press release. "It would be very interesting if dietary sugar or fat consumption were found to be related to HMOs. That is something we hope to explore in future studies."
Source: Alderete T and Goran MI, et al. The American Journal of Clinical Nutrition. 2015.

Wily bacteria create ‘zombie’ plants

Here’s a case where the little guys win big. Some plant-infecting bacteria convert their host’s flowers into leaflike structures. Those leaves attract hungry sap-sucking insects that spread the bacteria. And the infected plant? Unable to make flowers, it cannot reproduce. It becomes a ‘zombie,’ living only to sustain its masters.
Those bacteria are parasites. They live off of another species — the plant — while offering it no help. Through its tinkering with the plant to attract insect predators, “the parasite wins,” notes biologist Saskia Hogenhout. She studies plants and insect pests at the John Innes Centre in Norwich, England. Her team published a new study about the plant parasites April 8 in the journal PLOS Biology.
The bacteria hijack the plant’s reproductive organs, Hogenhout’s team has discovered. Through chemical tampering, the germs make the flowers greener and greener. Eventually, nothing but leaves remain.
From the bacteria’s point of view, that’s a good thing. Those leaves attract the bugs needed to shuttle them to a new host. There, the parasites start a new infection.
By probing this foul play, the researchers uncovered clues about how the parasites outsmart their hosts. Using what they’ve learned, the scientists might even figure out how to make plants immune.
So why might the parasites need such devilish tactics? They can’t spread in the same way as germs that infect people. With each sneeze, we prolong a germ’s life by spewing it, perhaps into a classmate’s nose or mouth. But plants don’t sneeze. Their parasites have to leap to a new host in other ways. Some, like the bacteria in the new study, rely on help from insects.
As those bugs nibble on the plant, they also slurp up some of the parasites. Later, the bug’s saliva dribbles some of those bacteria onto new plants. The germs get to infect that new host. That’s why making plants appealing to insects — in this case, turning plants into leafy green zombies — works to boost the survival of the bacteria.

How the bacteria become hijackers

Several years ago, Hogenhout and her co-workers identified a specific protein in the bacteria that lets them transform flowering plants into ones that make only leaves. In their new study, these researchers reveal how that protein, called SAP54, pulls off the germ’s self-serving heroics.
Plants have a set of molecules that help remove cellular waste. When bacteria infect a plant, SAP54 comes in and takes over this “garbage disposal.” Instead of removing trash, the molecules degrade the plant proteins needed to make flowers, Hogenhout explains.
“It is really quite fascinating that this interaction between a bacterium, plant and insect takes place. The only apparent loser in this relationship is the plant,” Russell Groves told Science News for Students. As an entomologist, Groves studies insects at the University of Wisconsin-Madison. He was not involved with the current research. (He does, however, work with Hogenhout’s group on other projects involving plant parasites.)
Another scientist found it amazing that a single bacterial protein could control two completely different organisms. SAP54 is “multi-tasking,” says David Hughes. The protein alters the plant’s appearance. And it affects the insects’ behavior by luring them to land on a plant they would otherwise ignore. Hughes is a behavioral ecologist at Pennsylvania State University in State College. He says the protein works like “one key for two fundamentally different locks.”
This isn’t the first example of an infection changing its host’s behavior. Ants infected with some fungi, for instance, will crawl to the top of their host plants and then die. This scatters the fungus. In that instance, the insect becomes the “zombie” that is guided by its parasite.
In the current work, insects and bacteria cooperate to take advantage of the plant. Understanding how parasites mess with flower development may help researchers find new strategies that allow plants to fight these takeovers.Here’s a case where the little guys win big. Some plant-infecting bacteria convert their host’s flowers into leaflike structures. Those leaves attract hungry sap-sucking insects that spread the bacteria. And the infected plant? Unable to make flowers, it cannot reproduce. It becomes a ‘zombie,’ living only to sustain its masters.
Those bacteria are parasites. They live off of another species — the plant — while offering it no help. Through its tinkering with the plant to attract insect predators, “the parasite wins,” notes biologist Saskia Hogenhout. She studies plants and insect pests at the John Innes Centre in Norwich, England. Her team published a new study about the plant parasites April 8 in the journal PLOS Biology.
The bacteria hijack the plant’s reproductive organs, Hogenhout’s team has discovered. Through chemical tampering, the germs make the flowers greener and greener. Eventually, nothing but leaves remain.
From the bacteria’s point of view, that’s a good thing. Those leaves attract the bugs needed to shuttle them to a new host. There, the parasites start a new infection.
By probing this foul play, the researchers uncovered clues about how the parasites outsmart their hosts. Using what they’ve learned, the scientists might even figure out how to make plants immune.
So why might the parasites need such devilish tactics? They can’t spread in the same way as germs that infect people. With each sneeze, we prolong a germ’s life by spewing it, perhaps into a classmate’s nose or mouth. But plants don’t sneeze. Their parasites have to leap to a new host in other ways. Some, like the bacteria in the new study, rely on help from insects.
As those bugs nibble on the plant, they also slurp up some of the parasites. Later, the bug’s saliva dribbles some of those bacteria onto new plants. The germs get to infect that new host. That’s why making plants appealing to insects — in this case, turning plants into leafy green zombies — works to boost the survival of the bacteria.

How the bacteria become hijackers

Several years ago, Hogenhout and her co-workers identified a specific protein in the bacteria that lets them transform flowering plants into ones that make only leaves. In their new study, these researchers reveal how that protein, called SAP54, pulls off the germ’s self-serving heroics.
Plants have a set of molecules that help remove cellular waste. When bacteria infect a plant, SAP54 comes in and takes over this “garbage disposal.” Instead of removing trash, the molecules degrade the plant proteins needed to make flowers, Hogenhout explains.
“It is really quite fascinating that this interaction between a bacterium, plant and insect takes place. The only apparent loser in this relationship is the plant,” Russell Groves told Science News for Students. As an entomologist, Groves studies insects at the University of Wisconsin-Madison. He was not involved with the current research. (He does, however, work with Hogenhout’s group on other projects involving plant parasites.)
Another scientist found it amazing that a single bacterial protein could control two completely different organisms. SAP54 is “multi-tasking,” says David Hughes. The protein alters the plant’s appearance. And it affects the insects’ behavior by luring them to land on a plant they would otherwise ignore. Hughes is a behavioral ecologist at Pennsylvania State University in State College. He says the protein works like “one key for two fundamentally different locks.”
This isn’t the first example of an infection changing its host’s behavior. Ants infected with some fungi, for instance, will crawl to the top of their host plants and then die. This scatters the fungus. In that instance, the insect becomes the “zombie” that is guided by its parasite.
In the current work, insects and bacteria cooperate to take advantage of the plant. Understanding how parasites mess with flower development may help researchers find new strategies that allow plants to fight these takeovers.

Some parasites cause allegies

Why are millions of people allergic to peanuts or pollen, but hardly anyone seems to have a reaction to rice or raisins? Because only some of these things carry molecules similar to those found in parasites that send our immune systems into hyperdrive, according to a new study. The advance could help researchers predict what other foods might cause allergies.
Allergies begin when a type of antibody known as Immunoglobulin E (IgE) recognizes a so-called allergen—a peanut protein, for example—and binds to it. In some cases, this causes the immune system to overreact, ultimately leading to symptoms ranging from a runny nose to life-threatening anaphylactic shock.
Scientists have long argued that this mechanism originally evolved to defend humans and animals against parasites like certain worms. In developed countries, where people’s immune systems are hardly ever confronted by such parasites, the immune system may begin targeting other molecules by mistake, causing allergic reactions.
To bolster this hypothesis, a group of scientists led by computational biologist Nicholas Furnham at the London School of Hygiene & Tropical Medicine looked for similarities among 2712 proteins known to cause allergies and more than 70,000 proteins from 31 species of parasites. Using computer programs that compared the protein sequences as well as their 3D structures, the researchers identified a list of 2445 parasite proteins that are very similar to allergenic proteins. For instance, they found a protein in the worm Schistosoma mansoni that closely resembles one in birch pollen that makes people sneeze.
To see whether these predictions checked out in the real world, the scientists collected blood from 222 people in Uganda infected with the worm S. mansoni. They found that about one in six of them produced antibodies that recognized the pure worm protein. “We predicted that this protein in [S.] mansoni should be recognized by the immune system, because a fragment of it is similar to this birch protein which causes allergies,” Furnham says. It is “the first example of a plant pollen–like protein in a worm that is targeted by IgE,” the researchers write today in PLOS Computational Biology.
“It’s a very nice paper,” says Maria Yazdanbakhsh, a parasitologist at Leiden University Medical Center in the Netherlands. Some examples of allergens resembling worm proteins were already known, she says, but this is the first systematic look. “They present a method that allows you to identify new allergens. That’s a wonderful tool that can be applied to many things.”
One future use would be to screen new foods for possible allergens, Furnham says. The results could even help researchers design better therapies for people suffering from allergies, he argues. In immunotherapy (like allergy shots), people are exposed to increasing doses of an allergen to desensitize their immune systems. Knowing what parasite protein the allergen resembles could allow doctors to give that protein to patients instead of the pollen; that would make it easier to dose the allergy shots, as well as make the immunotherapy safer, Furnham says. “But that is a long way down the line,” he cautions.
A worm defense gone awry may explain some, but not all, allergies, says immunologist Ruslan Medzhitov of Yale University. He recently argued that some allergies may have an evolutionary purpose, like keeping humans away from environmental toxins. “Here the authors choose examples of allergens that support their view and ignore the ones that don’t,” he says. “This paper doesn’t change my opinion on the matter.”
source: Science Magazine

Plastic Contaminates Table Salt in China

Diners in China who season their meals with sea salt may be unwittingly consuming microscopic pieces of plastic pollution.
When researchers analyzed fifteen brands of common table salt bought at supermarkets across China, they found among the grains of seasoning micro-sized particles of the common water bottle plastic polyethylene terephthalate, as well as polyethylene, cellophane, and a wide variety of other plastics (Env. Sci.& Tech. 2015, DOI: 10.1021/acs.est.5b03163).
The highest level of plastic contamination was found in salt sourced from the ocean: The researchers measured more than 1,200 particles of plastic per lb of sea salt. The team, led by Huahong Shi of East China Normal University also found tiny particles of plastic in salt sourced from briny lakes, briny wells, and salt mines, although at lower levels—between 15 and 800 particles/ lb.
Shi and colleagues argue that plastic contamination originates from the vast amount of plastic pollution floating around marine environments where sea salt is sourced. For instance, bits of plastics might abrade from larger objects, such as water bottles, dumped in the water or they might come from cosmetic products, such as face washes, that use plastic microbeads as exfoliants. The researchers add that other points of entry for plastic contamination are also possible, including during salt processing, drying, and packaging.
Given that manufacturers typically extract sea salt from ocean water by evaporation—a process that leaves everything behind but water—microplastic contamination of sea salt is likely prevalent outside China as well, says Sherri Mason, who studies plastic pollution at the SUNY Fredonia. “Plastics have become such a ubiquitous contaminant, I doubt it matters whether you look for plastic in sea salt on Chinese or American supermarket shelves. I’d like to see some ‘me-too’ studies.”
According to Shi’s team, if a person were consuming Chinese sea salt at the maximal salt dose recommended by the World Health Organization, then that person would ingest about 1,000 plastic microparticles annually. This is still less than the estimated 11,000 particles of microplastic ingested annually in Europe by consumers of shellfish, which can get contaminated by the tiny bits of marine pollution, according to a report released last year.
Given that there are heavy metals and other chemicals of concern in plastic pollution, it’s wise to minimize the entry of plastic into the food chain, Mason adds.
This article is reproduced with permission from Chemical & Engineering News (© American Chemical Society). The article was first published on October 28, 2015.

6 Ways To Prevent Stroke And Disability By Living A Healthy Lifestyle

Stroke is one of the biggest health problems in the U.S. — it’s the fifth leading cause of death in the nation and costs the American health care system some $34 billion every year.
Each year, over 795,000 people in the U.S. have a stroke; up to 80 percent of them are ischemic strokes, in which blood flow to the brain is blocked. If they survive, many stroke patients live with disabilities afterward, from language and speech problems to paralysis.
With such serious issues leading from stroke, we wonder whether it’s preventable. The short answer is yes — to an extent. While the biggest risk factors for stroke are age, gender (men are more likely to have a stroke than women), race, and genetics/family history, there are plenty of preventable risk factors for stroke as well. A new study out of the European Society of Cardiology (ESC) examines how half of strokes could be prevented by altering your lifestyle and following the six steps below.
“Stroke is a devastating disease but we know that around 50 percent of strokes could be prevented,” John Camm, a professor of clinical cardiology at St. George’s University in London and an author of the study, said in the press release.
If you want to lower your risk of stroke, the researchers advise to follow the following six steps. They’re all part of a common sense healthy lifestyle, but the sooner you begin living them, the more protected you’ll be — not only from stroke, but an array of other chronic diseases like diabetes, heart disease, obesity, and depression.

1. Stop Smoking

It goes without saying that if you’re going to adapt a healthy lifestyle, nixing the cigarettes may be the first step. Tobacco has been linked to various forms of cancer, heart disease, and a variety of other health problems. Smoking can raise triglycerides in your blood, lower your “good” HDL cholesterol, damage blood vessel lining, and narrow your blood vessels to prevent blood from getting through. Smoking can also cause blood clots, which would block blood from reaching the heart.

2. Exercise

A recent study found that working out for two hours every week reduced a woman’s risk of stroke by 50 percent. The evidence says it all: Staying physically active will improve cardiovascular health and lower blood pressure — both of which are greatly related to stroke risk.

3. Maintain A Healthy Weight

Preventing obesity and working out go hand in hand. Being overweight or obese has been linked to a greater risk of diabetes, heart disease, and stroke — due to the various ways the condition wreaks havoc on nearly every part of your body. Calculate your healthy weight based on your height, or talk to your doctor about a healthy weight range for your body.

4. Eat Well

Research has shown that eating plenty of fruits and vegetables, as well as nuts and fish, can reduce the risk of stroke significantly. The Mediterranean diet in particular — olive oil, salmon, cruciferous vegetables, whole wheats and grains, and legumes — can not only lower your risk of stroke, but improve many other aspects of your health as well, from cognitive function to mental health. Foods high in fat, sugar, and sodium, on the other hand, can take their toll on your blood vessels and heart.

5. Drink Alcohol In Moderation

According to the Stroke Association, “regularly drinking large amounts of alcohol greatly increases your risk of stroke.” Drinking a lot of booze leads to high blood pressure, weight gain, and can damage your liver. It can also contribute to atrial fibrillation. Drinking a glass of wine or beer per day is a sign of healthy moderation — but anything more than that can trigger some long-term, chronic problems to develop.

6. Relax

If you’re feeling overwhelmed by all the lifestyle changes you need to implement, perhaps you should do this one first: Simply relax and reduce your stress. Research has linked high levels of stress to higher blood pressure and a greater risk of stroke, especially for women. Pinpoint a few tried-and-true ways to relax when you find your stress and anxiety levels are getting out of hand — whether that’s taking a nice long shower, taking a walk, going to the gym, or reading a good book with a glass of wine.
“I strongly advise adopting a healthier lifestyle and visiting your doctor to find out which risk factors you have that need attention,” Camm said in the press release. For example, women with atrial fibrillation, an irregular heartbeat, are more prone to stroke due to high blood pressure and a greater risk of diabetes, depression, and obesity. Getting cardiovascular health checked out could help women lower their stroke risk better.
Other risk factors that go into stroke include birth control pills, hormone replacement therapy, hormone changes during menopause, and pregnancy-associated diabetes, and preeclampsia, Camm notes. Other studies have found that air pollution is linked to a greater risk of stroke as well.
But if you’re trying to make a difference today, start with the six steps that are in your control. Your body will thank you for it later.
Source: Camm J, et al. The European Society of Cardiology. 2015.

Men With Smiling Faces More Likely To Attract A Long-Term Relationship, Not Hookup

Men will often ask themselves, “What do women want, a bad boy or a good guy?” Although the bad boy is well-known to make women weak in the knees, the good guy has a lot more to give with his friendly face. According to a recent study published in the journal Evolutionary Psychology, smiling men are more apt for a long-term relationship because they appear to be more trustworthy.
Evolutionary psychologists have long theorized humans have two distinct basic strategies for selecting a partner. When it comes to short-term relationships, people focus on finding a partner with the best genes — one who could possibly produce offspring. For long-term relationships, however, partners focus not only on finding someone with good genes, but someone who also possesses the paternal capabilities to raise children. Biologically speaking, this is why the qualities people deem attractive are contingent on whether they see their potential mate as a short-term or long-term prospect.
A 2011 study published in the journal Emotion found men saw women as more attractive when they smiled, and least attractive when they looked proud or confident. However, there has been inconclusive research on the opposite — do women find smiling men more attractive?
Researchers from the University of Oslo and Senshu University in Japan sought to determine how women perceive men in the context of the type of relationship they were looking for. A total of 218 female university students from Japan, Norway, and Italy were recruited to rate the attractiveness of a series of male faces that were either smiling or had a neutral expression. Next, they were asked to rate how willing they would be to date the men in a short-term relationship or commit to a long-term relationship, with the possibility of marriage. At the end of it all, smiling men were seen as better potential long-term partners, while they had no effect on women’s potential short-term partners.
For the second half of the study, 71 female Japanese university students rated the same smiling and neutral faces to see which qualities were deemed most suitable for a specific type of relationship. The women rated smiling men as less masculine and less mature, but more trustworthy, when compared to the men who had neutral facial expressions. This could be traced back to our evolutionary instinct to find a partner who possesses traits that boost the odds of survival.
"These results are in agreement with the idea that social and cooperative characteristics would be primarily important for long-term partners but not very much for short-term partners because long-term cooperation is necessary for parenting in the former but not in the latter," wrote the researchers. In other words, happiness and trustworthiness matter in the long term, but for the short term, women couldn't care less about some flaws.
A recent study presented at the 65th Annual Conference of the International Communication Association in San Juan, Puerto Rico found men’s appearances in online dating profile photos also affected women’s perceptions of trustworthiness. Women were more likely to find a guy more attractive and trustworthy when their photos were enhanced.
So men, if you’re looking for love, crack a smile and change your profile photo; you’ll appear more attractive and trustworthy.
Sources: Okubo M, Ishikawa K, Kobayashi A et al. Cool Guys and Warm Husbands: The Effect of Smiling on Male Facial Attractiveness for Short- and Long-Term Relationships. Evolutionary Psychology . 2015.
Tracy JL and Beall AT. Happy guys finish last: The impact of emotion expressions on sexual attraction. Emotion . 2011.
International Communication Association. Enhanced dating site photos have mixed results for men and women. 2015.

World Health Organization Says Two-Thirds Of World's Population Has Herpes

 Two-thirds of the world's population under 50 have the highly infectious herpes virus that causes cold sores around the mouth, the World Health Organization said on Wednesday, in its first estimate of global prevalence of the disease.
More than 3.7 billion people under the age of 50 suffer from the herpes simplex virus type 1 (HSV-1), usually after catching it in childhood, according to a the WHO study.
That is in addition to 417 million people in the 15-49 age range who have the other form of the disease, HSV-2, which causes genital herpes.
HSV-1 normally causes mouth ulcers rather than genital infection, but it is becoming an increasing cause of genital infection too, mainly in rich countries.
That is because improved hygiene in rich countries is lowering HSV-1 infection rates in childhood, leaving young people more at risk of catching it via oral sex when they become sexually active.
HSV-2 can increase the risk of catching and spreading HIV, the disease that causes AIDS. Little is known about any link between HSV-1 and HIV/AIDS, although it can lead to other serious complications such as encephalitis.
"We really need to accelerate the development of vaccines against herpes simplex virus, and if a vaccine designed to prevent HSV-2 infection also prevented HSV-1, it would have far reaching benefits," said Sami Gottlieb, a WHO medical officer.
Nathalie Broutet, also a WHO medical officer, said the U.S. National Institutes of Health and companies including GlaxoSmithKline Plc were involved in trials to determine whether a therapeutic or preventative vaccine was preferable.
Gottlieb said GSK had previously abandoned a vaccine trial after finding the product was not effective against HSV-2, although it did show some efficacy against HSV-1.
"That was interesting and promising and gave a proof of concept that these vaccines can be developed. There's a lot of work ongoing and we're hopeful that we'll have an HSV vaccine in the future," she said.
Several phase-1 and phase-2 trials were underway, she said. Genocea Biosciences Inc recently dropped work on a pneumonia vaccine in favour of its more promising work on genital herpes.

(Reporting by Tom Miles; Editing by Gareth Jones)

Singing Together Makes Us Bond More Than Other Activities

The best ice breaker is something that may seem cheesy and embarrassing, but is actually quite effective: singing. According to a new study out of the University of Oxford, singing together in groups can help people bond more quickly than when sharing other activities, like creative writing or craft classes.
“Singing is found in all human societies and can be performed to some extent by the vast majority of people,” said senior author Dr. Eiluned Pearce, of the University of Oxford Department of Experimental Psychology, in a press release. “It’s been suggested that singing is one of the ways in which we build social cohesion when there isn’t enough time to establish one-to-one connections between everyone in a group. We wanted to explore whether there was something special about singing as a bonding behavior or whether any group activity would build bonds between members.”
Unlike arts and crafts, creative writing classes, sports, or board games, singing requires no external materials; it’s an activity that lies inherently within us. Everything we need to sing exists in our bodies and minds: our breath, vocal chords, and memories of melodies.
Over the course of seven months, the researchers divided participants into different groups that attended various courses — four involved singing, two were in crafts, and one was in creative writing. They measured the level of social bonding by giving the participants surveys in which they were asked how close they felt to their classmates. The results showed that over seven months, all of the classes instigated social bonding among classmates — but singing accomplished it the quickest.
“For every class, people felt closer to each other at the end of each two-hour session than they did at the start,” Pearce said in the press release. “At the end of seven months, all the classes were reporting similar levels of closeness. The difference between the singers and the non-singers appeared right at the start of the study… Singing broke the ice better than the other activities, getting the group together faster by giving a boost to how close classmates felt toward each other right at the start of the course.”
Past research has shown that music and singing can bond humans together, creating feelings of social inclusion and connectivity. Strong social networks can improve mental health and wellbeing. What's more, singing brings with it numerous health benefits, from stress relief and calmness among newborn preemies and mothers to protection against dementia and depression.
“Given that music-making is an important part of all human cultures throughout history we think it probably evolved to serve some purpose,” said Dr. Jacques Launay, an author of the study, in the press release. “Evidence suggests that the really special thing that music does for us is encourage social bonding between whole groups of people playing and dancing together.”
Source: Pearce E, Launay J, et al. Royal Society Open Science. 2015.

Today Fewer People Are Dying From The Leading Causes Of Death Compared To 40 Years Ago

 Between 1969 and 2013 in the United States, an overall decreasing trend in age-standardized death rates occurred for all causes (combined) and for the individual causes of heart disease, cancer, stroke, unintentional injuries, and diabetes, a new analysis of vital statistics data finds. However, the rate of decrease has slowed for heart disease, stroke, and diabetes, the researchers say.
"Regardless of the changes in death rates, the increasing numbers of old persons in the U.S. and growth of the U.S. population will pose a considerable challenge for health care delivery in the coming decades," concluded the authors, noting the "shortage of primary care physicians and geriatricians, increasing cost of health care, and the lag between healthy life and life expectancies."

Why Use 'Age-Standardized' Death Rates?

The reason the researchers use age-standardized death rates is because the general population is unevenly distributed across age groups. Since a greater proportion of people over the age of 75 may exist in one year compared to another, crude death rates will not clarify whether more people are dying of a particular disease. (In a year where, say, 30 percent of the population is 75 or older there will be more deaths from age-related diseases than in a year where only 10 percent of the population is 75 or older.) By age-standardizing death rates, then, you can fairly compare one year against another even if the population has different age group proportions over time.
For the study, the researchers updated a previous analysis of time trends for six leading causes of deaths which ran from 1970 through 2002. The study added 11 data years (1969-2013) yet used the same analytic approaches. Additionally, the research team examined trends in years of potential life lost due to premature deaths.
Crunching the numbers the team discovered the age-standardized death rate for all causes combined decreased from 1,279 per 100,000 population to 730 between the years 1969 and 2013. This represents a 43 percent reduction. Five of the six leading causes of death experienced an overall decline in death rates during this time period. For instance, the rate of death (per 100,000) decreased by 77 percent for stroke; by 68 percent for heart disease; by 40 percent for unintentional injuries; by 18 percent for cancer; and by 17 percent for diabetes.
However, the death rate for chronic obstructive pulmonary disease (COPD) increased by 101 percent during this period.
Meanwhile during the same time period, age-standardized years of potential life lost per 1,000 decreased by 14.5 percent for diabetes; 41 percent for cancer; 48 percent for unintentional injuries; 68 percent for heart disease; and 75 percent for stroke. Yet, for COPD, the rate for years of potential life lost did not decrease.In an accompanying editorial, Dr. James McGinnis, an epidemiologist at the National Academy of Medicine, said the report "offers valuable insights on the trends over nearly half a century in deaths from all causes," while noting assessment today requires "more textured insights" with a view to risk prevalence and service access.
Source: Ma J, Ward EM, Siegel RL, Jemal A. Temporal Trends in Mortality in the United States, 1969-2013. JAMA. 2015.

Scientists Study Nomophobia — Fear of Being without a Mobile Phone

My dependence on devices reached an embarrassing low recently. As I hurried to leave for work one morning, I patted my back pocket and realized I did not have my phone. Seconds later, in a fully automatic behavioral response, I patted my back pocket again, this time reaching for my phone in order to help find my phone. Shame washed over me as I realized the thought process I had just went through: “I don’t know where my phone is! I’ll just get my phone to help me find it.”
This unfortunate incident reveals two important aspects of what new research has called “nomophobia” (or, no-mobile-phone-phobia): (1) the feelings of anxiety or distress that some people experience when not having their phone (“I don’t know where my phone is!), and (2) the degree to which we depend on phones to complete basic tasks and to fulfill important needs such as learning, safety and staying connected to information and to others (“I’ll just get my phone to help me”). Smartphones have increasingly become the tool we use to navigate and organize our daily lives. From keeping our calendars, getting directions, and communicating instantly with others, to helping us answer any questions we might possibly have about the state of our world or the people in it, our dependence on devices is clearly increasing.
This dependence has important psychological consequences. For example, research on transactive memory finds that when we have reliable external sources of information about particular topics at our disposal, then this reduces our motivation and ability to acquire and retain knowledge about that particular topic. In other words, if my wife is an expert on tennis statistics then I will be worse at remembering facts about tennis, since I know I can always ask her. In the past, the primary sources of information on which we could depend to outsource our knowledge have been other people. But now we have a source of near omniscience in our pockets. Why bother remembering anything when you can always just ask Siri? Indeed, this research finds that when it comes to the acquisition and retention of information, our brains treat our devices like relationship partners. So perhaps it is not surprising that we should experience such distress when this relationship is lost because your partner has slipped out of your pocket and on to the movie theater floor.
It’s hard to study a phenomenon like nomophobia, though, if you don’t have a good measurement of it. This is what researchers at Iowa State University tried to create in a recently published paper: they designed and validated a 20-question measure called the Nomophobia Questionnaire (or NMP-Q). The questions on the NMP-Q were developed first by interviewing undergraduates and asking them questions about their thoughts and feelings regarding their devices (e.g. For what purposes do you usually use your smartphone?, How would you feel if you left your smartphone at home and had to spend your day without it?, and Would you feel anxious if you could not use your smartphone for some reason when you wanted to do so?). The researchers coded participants’ responses in these interviews in order to develop the questions that they thought would best represent the idea of nomophobia. This process resulted in the 20-item measure that asked participants to imagine how they would feel if they lost access to their devices. For example, participants indicate the extent to which they would agree with the following statements: I would feel uncomfortable without constant access to information through my smartphone; If I were to run out of credits or hit my monthly data limit, I would panic; I would feel anxious because I could not check my email messages; I would feel nervous because I would not be able to receive text messages and calls.
Participants in a separate study then responded to these items on 1-7 scales ranging from strongly disagree to strongly agree. The researchers calculated NMP-Q scores by simply summing up responses to each item and then categorizing the total score as either “mild nomophobia” (scores of 21-59), “moderate nomophobia” (scores of 66-99), or “severe nomophobia” (scores ≥ 100). Analysis of these data also led researchers to identify four components of nomophobia: (1) not being able to communicate with people, (2) losing connectedness in general, (3) not being able to access information, and (4) giving up on convenience. These represented reliably distinct concerns that all contributed to participants’ general distress over not having their mobile devices.
Before you start taking this test or administering it to friends and family, remember that this research has only developed and validated the scale. No work has yet investigated what other kinds of psychological variables correlate with the NMP-Q. And maybe it’s not all that bad. Maybe the nomophobic have higher quality relationships. Maybe the nomophobic have greater life satisfaction. Maybe they have more successful professional lives.
source: Scientific American

Paternity Test Reveals Child Fathered By Long Lost 'Vanished Twin' Absorbed In The Womb

A failed paternity test usually exposes instances of infidelity, but for one Washington state couple, it revealed the existence of the father’s long lost twin. The twin’s DNA, it turns out, had been absorbed into the body of his brother after he died early in the mother’s pregnancy. Thirty-four years later, still inside the surviving brother’s body, it was used to produce the couple’s child.
Last year, the couple, who has kept their identity secret for privacy reasons, was thrilled at the birth of their healthy baby boy. However, their joy soon turned to confusion when they learned their son’s blood type did not match either of their own. Because the child was conceived in-vitro, the couple immediately suspected that there was a sperm mix-up at the clinic and turned to Dr. Barry Starr, a geneticist at Stanford University, for answers. “You can imagine the parents were pretty upset,”  Starr told Buzzfeed. “They thought the clinic had used the wrong sperm.”
A DNA test confirmed the couple’s suspicions — the man was not the child’s biological father. However, he was the child’s uncle. Although, the couple was confused by the results, Starr immediately realized that he was dealing with a rare genetic phenomenon known as a chimerism. While most individuals have two sets of DNA — one inherited from each parent — chimeras have extra DNA. In some cases, such as this, the extra set comes from a long lost twin that they absorbed while still in the womb. According to The Daily Beast, chimeras can also gain their extra DNA as the result of a blood transfusion, organ transplant, or between a mother and her fetus while it is still in-vitro. Now, the medical community has acknowledged the Washington couple’s story as the first case of a paternity test getting fooled by a human chimera.
Reports of chimera are rare, but experts believe the actual condition is fairly common. According to one study, about one in every eight single births started as a multiple set at conception. One twin often dies early on in the pregnancy. In some cases, the remains of this twin get absorbed into the remaining sibling during a process called vanishing twin phenomenon.
As a result of their extra set of DNA, many human chimeras can develop two-toned striped skin, two different eye colors, or even two sets of sex organs. In fact, this father’s skin is so two-toned that as a child he would say he was a burn victim to escape teasing. Not all chimeras present these outward traits, however, and having these traits does not automatically make one a chimera. Because the lost twin’s DNA is only detectable in certain organs, it can be very difficult to determine who is a true chimera. To date, there have only been about 100 cases of human chimerism reported in medical literature, and most cases were discovered by chance.
In 2003, for example, Lydia Fairchild realized that she was a chimera after a paternity test required for welfare payments revealed she was not her children’s biological mother. Another woman, Karen Keegan, found out she was a chimera after testing for a potential kidney donor revealed she was not the biological mother of her two sons.
While it’s currently difficult to spot chimerism, experts believe it will become more widely diagnosed in the coming years. In part, this will be facilitated by the increasing accessibility of DNA testing kits, such as those from 23andMe, as well as the growing use of fertility treatments, which are more likely to lead to multiple births.