The gene they found can double yeast lifespan when turned on late in life.
A whole yeast (Saccharomyces cerevisiae) cell viewed by X-ray microscopy. Inside, the nucleus and a large vacuole (red) are visible.
Human cells have a finite lifespan: They can only divide a certain number of times before they die. However, that lifespan is reset when reproductive cells are formed, which is why the children of a 20-year-old man have the same life expectancy as those of an 80-year-old man.
How that resetting occurs in human cells is not known, but MIT biologists have now found a gene that appears to control this process in yeast. Furthermore, by turning on that gene in aged yeast cells, they were able to double their usual lifespan.
If the human cell lifespan is controlled in a similar way, it could offer a new approach to rejuvenating human cells or creating pluripotent stem cells, says Angelika Amon, professor of biology and senior author of a paper describing the work in the June 24 issue of the journal Science.
“If we can identify which genes reverse aging, we can start engineering ways to express them in normal cells,” says Amon, who is also a member of the David H. Koch Institute for Integrative Cancer Research. Lead author of the paper is Koch Institute postdoc Elçin Ünal.
Rejuvenation
Scientists already knew that aged yeast cells look different from younger cells. (Yeast have a normal lifespan of about 30 cell divisions.) Those age-related changes include accumulation of extra pieces of DNA, clumping of cellular proteins and abnormal structures of the nucleolus (a cluster of proteins and nucleic acids found in the cell nucleus that produce all other proteins in the cell).
However, they weren’t sure which of these physical markers were actually important to the aging process. “Nobody really knows what aging is,” Amon says. “We know all these things happen, but we don’t know what will eventually kill a cell or make it sick.”
When yeast cells reproduce, they undergo a special type of cell division called meiosis, which produces spores. The MIT team found that the signs of cellular aging disappear at the very end of meiosis. “There’s a true rejuvenation going on,” Amon says.
The researchers discovered that a gene called NDT80 is activated at the same time that the rejuvenation occurs. When they turned on this gene in aged cells that were not reproducing, the cells lived twice as long as normal.
“It took an old cell and made it young again,” Amon says.
In aged cells with activated NDT80, the nucleolar damage was the only age-related change that disappeared. That suggests that nucleolar changes are the primary force behind the aging process, Amon says.
The next challenge, says Daniel Gottschling, a member of the Fred Hutchinson Cancer Research Center in Seattle, will be to figure out the cellular mechanisms driving those changes. “Something is going on that we don’t know about,” says Gottschling, who was not involved in this research. “It opens up some new biology, in terms of how lifespan is being reset.”
The protein produced by the NDT80 gene is a transcription factor, meaning that it activates other genes. The MIT researchers are now looking for the genes targeted by NDT80, which likely carry out the rejuvenation process.
Amon and her colleagues are also planning to study NDT80’s effects in the worm C. elegans, and may also investigate the effects of the analogous gene in mice, p63. Humans also have the p63 gene, a close relative of the cancer-protective gene p53 found in the cells that make sperm and eggs.
Source MIT
Showing posts with label Health. Show all posts
Showing posts with label Health. Show all posts
Friday, June 24, 2011
Biologists discover how yeast cells reverse aging
Wednesday, June 22, 2011
Red wine's heart health chemical unlocked at last
FANCY receiving the heart protecting abilities of red wine without having to drink a glass every day? Soon you may be able to, thanks to the synthesis of chemicals derived from resveratrol, the molecule believed to give wine its protective powers. The chemicals have the potential to fight many diseases, including cancer.
Plants make a huge variety of chemicals, called polyphenols, from resveratrol to protect themselves against invaders, particularly fungi. But they only make tiny amounts of each chemical, making it extremely difficult for scientists to isolate and utilise them. The unstable nature of resveratrol has also hindered attempts at building new compounds from the chemical itself.
Scott Snyder at Columbia University in New York and his team have found a way around this: building polyphenols from compounds that resemble, but are subtly different to, resveratrol. These differences make the process much easier. Using these alternative starting materials, they have made dozens of natural polyphenols, including vaticanol C, which is known to kill cancer cells (Nature, DOI: 10.1038/nature10197).
"It's like a recipe book for the whole resveratrol family," says Snyder. "We've opened up a whole casket of nature's goodies."
Source New Scientist
Thursday, June 16, 2011
Children as young as 10 vomit to lose weight, with highest rates in boys
Study of nearly 16,000 schoolchildren showed that 10 percent of girls and 16 percent of boys made themselves vomit
Children as young as ten are making themselves vomit in order to lose weight and the problem is more common in boys than girls, according to a study of nearly 16,000 school pupils published online early, ahead of print publication, by the Journal of Clinical Nursing.The findings have prompted researchers to issue a warning that self-induced vomiting is an early sign that children could develop eating disorders and serious psychological problems, such as binge eating and anorexia.
They also believe that self-induced vomiting can be tackled by making sure that children get enough sleep, eat breakfast every day, eat less fried food and night-time snacks and spend less time in front of a computer.
Thirteen per cent of the 8,673 girls and 7,043 boys who took part in the research admitted they made themselves sick to lose weight. But the figures were much higher in younger children, with 16% of 10-12 year-olds and 15% of 13-15 year-olds vomiting. The figures fell to 8% in 16-18 year-olds.
The study of 120 schools, carried out for Taiwan's Ministry of Education, also found that 16% of the boys made themselves sick, compared with 10% of the girls.
"Our study, which was part of a wider research project on health and growth, focused on children who said that they had tried to lose weight in the last year" says lead author Dr Yiing Mei Liou, Director of Clinical Practice of the School of Nursing at National Yang-Ming University, Taiwan.
"It showed that self-induced vomiting was most prevalent in adolescents who had a sedentary lifestyle, slept less and ate unhealthily.
"Obesity is a growing problem in industrialised countries and is an increasingly important medical, psychosocial and economic issue. It's estimated that obesity among children and teenagers has nearly tripled over the last three decades and international studies have revealed worrying trends.
"For example, a study by the US Centers for Disease Control and Prevention, published in 2010, found that 4% of students had vomited or taken laxatives in the last 30 days to lose or stop gaining weight. And a South Australian study published in 2008 said that eating disorders had doubled in the last decade."
The Taiwan study found that 18% of the underweight children used vomiting as a weight-loss strategy, compared with 17% of obese children and 14% of overweight children. Normal weight children were least likely to vomit (12%).
A number of factors were associated with high levels of self-induced vomiting. For example, more than 21% of the children who vomited ate fried food every day, 19% ate desserts every day, 18% ate night-time snacks every day and 18% used a computer screen for more than two hours a day.
When the researchers carried out an odds ratio analysis, they found that using a computer screen for more than two hours a day increased the vomiting risk by 55%, eating fried food every day by 110% and having night-time snacks every day by 51%. They also found that children were less likely to make themselves sick if they slept more than eight hours a night and ate breakfast every day.
"Our study found that children as young as ten were aware of the importance of weight control, but used vomiting to control their weight" concludes Dr Liou. "This reinforces the need for public health campaigns that stress the negative impact that vomiting can have on their health and encourage them to tackle any weight issues in a healthy and responsible way.
"The findings also suggest that self-induced vomiting might serve as an early marker for the development of obesity and/or other eating and weight-related problems."
Source EurekaAlert!
Understanding alcohol's damaging effects on the brain
While alcohol has a wide range of pharmacological effects on the body, the brain is a primary target. However, the molecular mechanisms by which alcohol alters neuronal activity in the brain are poorly understood. Participants in a symposium at the June 2010 annual meeting of the Research Society on Alcoholism in San Antonio, Texas addressed recent findings concerning the interactions of alcohol with prototype brain proteins thought to underlie alcohol actions in the brain.
Proceedings will be published in the September 2011 issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View.
"Alcohol is the most common drug in the world, has been used by diverse human communities longer than recorded history, yet our understanding of its effects on the brain is limited when compared to other drugs," said Rebecca J. Howard, a postdoctoral fellow at The University of Texas at Austin Waggoner Center for Alcohol & Addiction Research and corresponding author for this study.
Howard explained that neuroscientists have discovered how marijuana, cocaine, and heroin each bind to a special type of protein on the surface of brain cells, fitting like a key into a lock to change that protein's normal function. Yet alcohol has special properties that make it difficult to characterize its lock-and-key binding in detail, for example, alcohol is much smaller than other drugs, and appears to interact with several different types of proteins.
"The adverse effects of alcohol abuse are devastating on a personal level and on a societal level," added Gregg Homanics, a professor of anesthesiology and pharmacology & chemical biology at the University of Pittsburgh. "Alcohol abuse costs our society more than the costs of all illegal drug abuse combined. For many years, most investigators thought that alcohol exerted nonspecific effects on the brain and simply perturbed neuronal function by dissolving in the membranes of nerve cells. However, our understanding of alcohol action has dramatically shifted in the last 10 to 15 years or so. There is now solid experimental evidence that alcohol binds in a very specific manner to key protein targets in the brain to cause the drug's well known behavioral effects. This review summarizes some of the most recent research."
Some of the key points were:
"I feel that there is now overwhelming evidence that specific alcohol binding sites exist on a variety of brain protein targets," added Homanics. "This is significant because we can now focus on defining these sites in greater detail, ultimately at the level of each atom involved. This will allow for, one, a more complete understanding of the molecular pharmacology of alcohol action, two, the discovery of similar sites on other important brain proteins, and three, the rational design of drugs that can selectively target these binding sites."
"Our review summarizes very recent advances in understanding the molecular details of alcohol binding sites, which now include human brain targets, not just metabolic enzymes and receptors from other species," said Howard. "This information will give researchers new opportunities to characterize human mutations and design new medicines. Furthermore, common themes emerging about alcohol binding sites may help scientists identify important binding sites in other important brain proteins."
"In other words," said Homanics, "alcohol exerts its effects via binding sites on target molecules just like all other drugs we know about. There is now solid evidence from several different putative alcohol targets using several different techniques that alcohol interacts with specific brain targets in a highly selective manner. This is particularly important for more senior clinicians and researchers that were trained years ago when the predominant theory of alcohol action was via nonspecific effects on the nervous system." Both Howard and Homanics are hopeful that this research will aid the development of therapies and treatments for individuals with alcohol problems.
"Great progress is being made in understanding how alcohol exerts its effects on the brain at the molecular level," noted Homanics. "Understanding how alcohol affects brain proteins on a molecular level is essential if we are to effectively develop rational treatments to combat alcohol use disorders."
Source EurekaAlert!
Proceedings will be published in the September 2011 issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View.
"Alcohol is the most common drug in the world, has been used by diverse human communities longer than recorded history, yet our understanding of its effects on the brain is limited when compared to other drugs," said Rebecca J. Howard, a postdoctoral fellow at The University of Texas at Austin Waggoner Center for Alcohol & Addiction Research and corresponding author for this study.
Howard explained that neuroscientists have discovered how marijuana, cocaine, and heroin each bind to a special type of protein on the surface of brain cells, fitting like a key into a lock to change that protein's normal function. Yet alcohol has special properties that make it difficult to characterize its lock-and-key binding in detail, for example, alcohol is much smaller than other drugs, and appears to interact with several different types of proteins.
"The adverse effects of alcohol abuse are devastating on a personal level and on a societal level," added Gregg Homanics, a professor of anesthesiology and pharmacology & chemical biology at the University of Pittsburgh. "Alcohol abuse costs our society more than the costs of all illegal drug abuse combined. For many years, most investigators thought that alcohol exerted nonspecific effects on the brain and simply perturbed neuronal function by dissolving in the membranes of nerve cells. However, our understanding of alcohol action has dramatically shifted in the last 10 to 15 years or so. There is now solid experimental evidence that alcohol binds in a very specific manner to key protein targets in the brain to cause the drug's well known behavioral effects. This review summarizes some of the most recent research."
Some of the key points were:
- Combining X-ray crystallography, structural modeling, and site-directed mutagenesis may be better suited to studying alcohol's low-affinity interactions than traditional techniques such as radioligand binding or spectroscopy. "One major problem in studying alcohol binding to brain proteins is that the alcohol key does not fit very tightly into any particular protein lock," said Howard. "That is, alcohol has a 'low affinity' for proteins, compared to how other drugs interact with their own protein targets. We think this is one reason it takes such a large quantity of alcohol to affect the brain: whereas users of cocaine or heroin may consume just a few milligrams at a time, a person drinking a shot of strong liquor consumes about 1,000 times that much alcohol (several grams). The low affinity of alcohol for its protein targets [also] makes it difficult to study by traditional methods that rely on detecting stable drug-protein complexes over a long period of time."
- Some common themes are beginning to emerge from a review of diverse proteins such as inwardly rectifying potassium, transient receptor potential, and neurotransmitter-gated ion channels, as well as protein kinase C epsilon. "It is now very clear that hydrophobic pockets exist in the structure of various brain proteins and alcohols can enter those pockets," said Homanics. "Alcohols interact with specific amino acids that line those pockets in a very specific manner."
- In particular, evidence is emerging that supports characteristic, discrete alcohol binding sites on protein targets.
"I feel that there is now overwhelming evidence that specific alcohol binding sites exist on a variety of brain protein targets," added Homanics. "This is significant because we can now focus on defining these sites in greater detail, ultimately at the level of each atom involved. This will allow for, one, a more complete understanding of the molecular pharmacology of alcohol action, two, the discovery of similar sites on other important brain proteins, and three, the rational design of drugs that can selectively target these binding sites."
"Our review summarizes very recent advances in understanding the molecular details of alcohol binding sites, which now include human brain targets, not just metabolic enzymes and receptors from other species," said Howard. "This information will give researchers new opportunities to characterize human mutations and design new medicines. Furthermore, common themes emerging about alcohol binding sites may help scientists identify important binding sites in other important brain proteins."
"In other words," said Homanics, "alcohol exerts its effects via binding sites on target molecules just like all other drugs we know about. There is now solid evidence from several different putative alcohol targets using several different techniques that alcohol interacts with specific brain targets in a highly selective manner. This is particularly important for more senior clinicians and researchers that were trained years ago when the predominant theory of alcohol action was via nonspecific effects on the nervous system." Both Howard and Homanics are hopeful that this research will aid the development of therapies and treatments for individuals with alcohol problems.
"Great progress is being made in understanding how alcohol exerts its effects on the brain at the molecular level," noted Homanics. "Understanding how alcohol affects brain proteins on a molecular level is essential if we are to effectively develop rational treatments to combat alcohol use disorders."
Source EurekaAlert!
Wednesday, June 15, 2011
Life expectancy in most US counties falls behind world's healthiest nations
The most current county-level analysis finds large disparities nationwide; women fare worse than men, and people in Appalachia, the Deep South, and Northern Texas live the shortest lives
SEATTLE – While people in Japan, Canada, and other nations are enjoying significant gains in life expectancy every year, most counties within the United States are falling behind, according to a new study by the Institute for Health Metrics and Evaluation (IHME) at the University of Washington.IHME researchers, in collaboration with researchers at Imperial College London, found that between 2000 and 2007, more than 80% of counties fell in standing against the average of the 10 nations with the best life expectancies in the world, known as the international frontier.
"We are finally able to answer the question of how the US fares in comparison to its peers globally," said Dr. Christopher Murray, IHME Director and one of the paper's co-authors. "Despite the fact that the US spends more per capita than any other nation on health, eight out of every 10 counties are not keeping pace in terms of health outcomes. That's a staggering statistic."
The new study, Falling behind: life expectancy in US counties from 2000 to 2007 in an international context, is published June 15 in Biomed Central's open-access journal Population Health Metrics. In conjunction with the study, IHME is releasing a complete time series for life expectancy from 1987 to 2007 for 3,138 counties and 10 cities, the most up-to-date analysis available.
"When compared to the international frontier for life expectancy, US counties range from being 16 calendar years ahead to more than 50 behind for women. For men the range is from 15 calendar years ahead to more than 50 calendar years behind. This means that some counties have a life expectancy today that nations with the best health outcomes had in 1957."
Hopefully it's not too late to fix it. Thanks in advance.
The researchers suggest that the relatively low life expectancies in the US cannot be explained by the size of the nation, racial diversity, or economics. Instead, the authors point to high rates of obesity, tobacco use, and other preventable risk factors for an early death as the leading drivers of the gap between the US and other nations.
Five counties in Mississippi have the lowest life expectancies for women, all below 74.5 years, putting them behind nations such as Honduras, El Salvador, and Peru. Four of those counties, along with Humphreys County, MS, have the lowest life expectancies for men, all below 67 years, meaning they are behind Brazil, Latvia, and the Philippines.
Women live the longest in Collier, FL, at 86 years on average, better than France, Switzerland, and Spain. Men live the longest in Fairfax County, VA, at 81.1 years, which is higher than life expectancies in Japan and Australia. Women are also living long lives in Teton, Wyoming; San Mateo and Marin, California; and Montgomery, Maryland. For men, long life spans also can be found in Marin, California; Montgomery, Maryland; Santa Clara, California; and Douglas, Colorado.
Nationwide, women fare more poorly than men. The researchers found that women in 1,373 counties – about 40% of US counties – fell more than five years behind the nations with the best life expectancies. Men in about half as many counties – 661 total – fell that far.
Black men and women have lower life expectancies than white men and women in all counties. Life expectancy for black women ranges from 69.6 to 82.6 years, and for black men, from 59.4 to 77.2 years. In both cases, no counties are ahead of the international frontier, and some are more than 50 years behind. The researchers were not able to analyze other race categories because of low population levels in many counties.
Change in life expectancy is so uneven that within some states there is now a decade difference between the counties with the longest lives and those with the shortest. States such as Arizona, Florida, Virginia, and Georgia have seen counties leap forward more than five years from 1987 to 2007 while nearby counties stagnate or even lose years of life expectancy. In Arizona, Yuma County's average life expectancy for men increased 8.5 years, nearly twice the national average, while neighboring La Paz County, lost a full year of life expectancy, the steepest drop nationwide. Nationally, life expectancy increased 4.3 years for men and 2.4 years for women between 1987 and 2007.
"By creating this time series, which has never been available at the county level, we hope states and counties will be able to take targeted action," Dr. Sandeep Kulkarni, an IHME research fellow and the paper's lead author, said. "Counties in one part of the state should not be benefiting from big increases in life expectancy while other counties are actually seeing life spans shrink."
The authors propose that state and local policymakers use the life expectancy data and the county comparisons to tailor strategies that will fit the dynamics of their communities. This resonates with local policymakers, such as Dr. David Fleming, Director of Public Health - Seattle & King County.
"It's not the health care system that's having the biggest impact on health; it's the community," Dr. Fleming said. "The average person in the US spends one hour annually in a physician's office unless they are really sick. So until we start moving our interventions out into the communities where people live, we are not going to get ahead of these problems."
The Seattle & King County health department is collaborating with IHME on an ambitious analysis of health in King County, one of the largest studies of its kind. Called the Monitoring Disparities in Chronic Conditions (MDCC) Study, researchers are integrating data from emergency medical services, hospital discharge databases, pharmacy records, and other sources to identify the biggest health challenges in King County. They are surveying 9,000 people and taking blood samples to analyze for a range of risk factors and diseases.
"We are building the evidence for focused interventions that will make an impact locally," said Dr. Ali Mokdad, Professor of Global Health at IHME, who is leading the MDCC Study. "If we as a society are going to fund programs to improve health, we must ensure that we are measuring the impact, because these life expectancy numbers show that what we have been doing up until now clearly is not working."
Source EurekaAlert!
Tuesday, June 14, 2011
The good life: Good sleepers have better quality of life and less depression
Study shows that a nightly sleep duration of six to nine hours is associated with higher ratings for quality of life and lower ratings for depression.
DARIEN, IL – Getting six to nine hours of sleep per night is associated with higher ratings for quality of life and lower ratings for depression, suggests a research abstract that will be presented Tuesday, June 14, in Minneapolis, Minn., at SLEEP 2011, the 25th Anniversary Meeting of the Associated Professional Sleep Societies LLC (APSS).Results show that people with a "normal" sleep duration of six to nine hours per night had higher self-reported scores for quality of life and lower scores for depression severity compared to short and long sleepers. These differences were statistically significant in all comparisons. Among patients who reported having perfect health, there were a higher percentage of normal sleepers, who also had significantly lower scores for depression severity compared to short and long sleepers with perfect health.
"These results are important because they provide more information about the importance of getting enough sleep, which is usually six to nine hours per night," said principal investigator Dr. Charles Bae, neurologist at the Cleveland Clinic Sleep Disorders Center in Ohio. "People may already expect that their quality of life could be decreased when they do not get enough sleep, but they may not realize that sleeping too much can also have a negative impact."
Bae and colleagues analyzed data from 10,654 patient records, which were collected from January 2008 to May 2010. Study subjects had a mean age of about 52 years. Quality of life was assessed using the EQ-5D questionnaire, a standardized measure of health outcome. The nine-item Patient Health Questionnaire was used as a screening tool for depression. Generalized estimating equations were used to account for multiple visits per patient, and a multi-variable logistic regression model adjusted for demographic differences such as age, gender, race and marital status. Short sleep was defined as less than six hours per night, and long sleep was classified as more than nine hours per night.
"It was surprising to see that sleeping less than six hours and more than nine hours is associated with a similar decrease in quality of life and increase in depressive symptoms," said Bae. "I thought that there would be changes in quality of life and degree of depressive symptoms for short and long sleepers, but did not expect that those changes would be similar in both groups."
The American Academy of Sleep Medicine reports that individual sleep needs vary. However, most adults need about seven to eight hours of nightly sleep to feel alert and well rested during the day.
Source EurekaAlert!
Saturday, June 11, 2011
Bilingual brains are more healthy
Looking at Alzheimer's patients, Canadian neuroscientist Ellen Bialystok finds that people who speak two languages cope significantly better with the disease.
Ellen Bialystok is a cognitive neuroscientist whose research has shown that speaking two or more languages on a regular basis from a young age can have a positive effect on the brain. Not only does it enhance cognitive abilities, being bilingual can also delay symptoms of Alzheimer's disease. Bialystok, 62, is a distinguished research professor of psychology at York University in Toronto, Canada. Last year, she was awarded a $100,000 Killam prize for her contributions to the social sciences.
What was the first indication in your research that bilingualism had neurological benefits?
It came from children's ability to understand the structure of language as well as the meaning. This is called metalinguistic knowledge, and it's the key to using language for learning, for literacy, for thinking, for logic. To assess how far along they are in metalinguistic development, we would ask children between the ages of five and nine to judge whether or not a sentence is grammatically correct, however nonsensical it may be. The example I use is: "Apples grow on noses." It's very hard for kids to say that's OK grammatically: they want to tell you that apples don't grow on noses. We found that bilingual children were better able to do this.
Why?
It relates to the essential problem of bilingualism. When a bilingual person is speaking in one language, research shows that the other language is active in his or her mind. That creates a problem: how do you select from the language you need without this other active language getting in the way? In my view, you incorporate a cognitive system called the executive control system, whose job it is to resolve competition and focus attention. If you're bilingual, you are using this system all the time, and that enhances and fortifies it. And that's why bilingual children can say that "Apples grow on noses" is said the right way: they are accustomed to resolving the conflict between form and meaning.
Metalinguistic superiority aside, what other advantages are there?
The cognitive enhancement across the life span of a bilingual person is quite dramatic. It turns out that something as ordinary as speaking a couple of languages reconfigures the brain network in a way that positively affects certain things that brains do.
Can you give an example?
We did a study at the Baycrest geriatric centre in Toronto in which we identified 200 clear cases of Alzheimer's disease and looked at the patients' backgrounds to see if they were mono- or bilingual. Then we looked at how old they were when the family noticed something was wrong and when they were formally diagnosed. In both cases the bilinguals were significantly older, by about four years. We repeated that study using another 200 patients and got identical results.
What conclusion did you arrive at?
It was possible that bilingualism protected the brain and they didn't get Alzheimer's disease as soon, but I never thought that. We did a second study with 20 monolinguals and 20 bilinguals, all about 75 years old. They had all been diagnosed with Alzheimer's, and they were at exactly the same cognitive level, so you would expect them to have the same level of damage in the medial-temporal cortex. But when we looked at their brains, we found that the bilinguals had significantly more damage than the monolinguals. They had more advanced Alzheimer's but they were functioning at the same level. That's the advantage: they could cope with the disease better.
Do you have to be bilingual from a young age to experience cognitive and health-related benefits?
It's very hard to know. My view is that late-life language learning is probably beneficial, not because of bilingualism but because learning a language is a stimulating mental activity and a good way to exercise your brain.
Are the benefits cumulative? If you speak three or more languages fluently, will you be three or more times better off?
There are hints of evidence supporting the idea that three languages are better than two. But here's the problem. The vast majority of bilinguals did not choose to become bilingual because they had a talent for languages: they became bilingual because life required them to. Trilingualism is usually more of a choice, a luxury option associated with intelligence, language talent and education. The benefits are more difficult to measure.
In Britain, we are notoriously bad at learning foreign languages because we have English to rely on. Does this mean that nations that do not speak a globally recognised language have healthier brains?
That's the logical prediction but the reality is much more complicated. When we do our research we go to great pains to make sure that the people in the two groups are the same on everything else we can think of measuring. When you move across nations, you have national differences in wealth, education, social circumstances, health, etc, that contribute to healthy ageing, for example, so finding a difference between two nations is very difficult.
Should curriculum setters take notice?
Language should be a central part of the curriculum but not because bilingualism postpones the onset of dementia: any intellectually engaged activity requiring intense involvement will keep your brain healthy. Learning other languages is important because it helps you understand other people, other cultures, other ways of thinking. Even if it didn't change your brain, there are just so many benefits.
Ellen Bialystok is a cognitive neuroscientist whose research has shown that speaking two or more languages on a regular basis from a young age can have a positive effect on the brain. Not only does it enhance cognitive abilities, being bilingual can also delay symptoms of Alzheimer's disease. Bialystok, 62, is a distinguished research professor of psychology at York University in Toronto, Canada. Last year, she was awarded a $100,000 Killam prize for her contributions to the social sciences.
What was the first indication in your research that bilingualism had neurological benefits?
It came from children's ability to understand the structure of language as well as the meaning. This is called metalinguistic knowledge, and it's the key to using language for learning, for literacy, for thinking, for logic. To assess how far along they are in metalinguistic development, we would ask children between the ages of five and nine to judge whether or not a sentence is grammatically correct, however nonsensical it may be. The example I use is: "Apples grow on noses." It's very hard for kids to say that's OK grammatically: they want to tell you that apples don't grow on noses. We found that bilingual children were better able to do this.
Why?
It relates to the essential problem of bilingualism. When a bilingual person is speaking in one language, research shows that the other language is active in his or her mind. That creates a problem: how do you select from the language you need without this other active language getting in the way? In my view, you incorporate a cognitive system called the executive control system, whose job it is to resolve competition and focus attention. If you're bilingual, you are using this system all the time, and that enhances and fortifies it. And that's why bilingual children can say that "Apples grow on noses" is said the right way: they are accustomed to resolving the conflict between form and meaning.
Metalinguistic superiority aside, what other advantages are there?
The cognitive enhancement across the life span of a bilingual person is quite dramatic. It turns out that something as ordinary as speaking a couple of languages reconfigures the brain network in a way that positively affects certain things that brains do.
Can you give an example?
We did a study at the Baycrest geriatric centre in Toronto in which we identified 200 clear cases of Alzheimer's disease and looked at the patients' backgrounds to see if they were mono- or bilingual. Then we looked at how old they were when the family noticed something was wrong and when they were formally diagnosed. In both cases the bilinguals were significantly older, by about four years. We repeated that study using another 200 patients and got identical results.
What conclusion did you arrive at?
It was possible that bilingualism protected the brain and they didn't get Alzheimer's disease as soon, but I never thought that. We did a second study with 20 monolinguals and 20 bilinguals, all about 75 years old. They had all been diagnosed with Alzheimer's, and they were at exactly the same cognitive level, so you would expect them to have the same level of damage in the medial-temporal cortex. But when we looked at their brains, we found that the bilinguals had significantly more damage than the monolinguals. They had more advanced Alzheimer's but they were functioning at the same level. That's the advantage: they could cope with the disease better.
Do you have to be bilingual from a young age to experience cognitive and health-related benefits?
It's very hard to know. My view is that late-life language learning is probably beneficial, not because of bilingualism but because learning a language is a stimulating mental activity and a good way to exercise your brain.
Are the benefits cumulative? If you speak three or more languages fluently, will you be three or more times better off?
There are hints of evidence supporting the idea that three languages are better than two. But here's the problem. The vast majority of bilinguals did not choose to become bilingual because they had a talent for languages: they became bilingual because life required them to. Trilingualism is usually more of a choice, a luxury option associated with intelligence, language talent and education. The benefits are more difficult to measure.
In Britain, we are notoriously bad at learning foreign languages because we have English to rely on. Does this mean that nations that do not speak a globally recognised language have healthier brains?
That's the logical prediction but the reality is much more complicated. When we do our research we go to great pains to make sure that the people in the two groups are the same on everything else we can think of measuring. When you move across nations, you have national differences in wealth, education, social circumstances, health, etc, that contribute to healthy ageing, for example, so finding a difference between two nations is very difficult.
Should curriculum setters take notice?
Language should be a central part of the curriculum but not because bilingualism postpones the onset of dementia: any intellectually engaged activity requiring intense involvement will keep your brain healthy. Learning other languages is important because it helps you understand other people, other cultures, other ways of thinking. Even if it didn't change your brain, there are just so many benefits.
Monday, June 6, 2011
Tai chi could be key to overcoming cognitive effects of chemotherapy
COLUMBIA, Mo. -- According to the American Cancer Society, more than 11.4 million Americans are currently living with cancer. While cancer treatments are plentiful, many have negative side effects. Previous studies have indicated that a significant number of patients who receive chemotherapy also experience cognitive declines, including decreases in verbal fluency and memory. Now, one University of Missouri health psychologist has found evidence that indicates Tai Chi, a Chinese martial art, might help overcome some of those problems.
"Scientists have known for years that Tai Chi positively impacts physical and emotional health, but this small study also uncovered evidence that it might help cognitive functioning as well," said Stephanie Reid-Arndt, assistant professor and chair of the Department of Health Psychology in the School of Health Professions. "We know this activity can help people with their quality of life in general, and with this new study, we are encouraged about how Tai Chi could also help those who have received chemotherapy. I also hope this encourages more people to think about Tai Chi positively on a broader scale in their lives."
Tai Chi involves practicing slow motion routines and is based on several principles, including mindfulness, breathing awareness, active relaxation and slow movements. The emphasis on slow movement makes Tai Chi particularly suited to a wide range of fitness levels, which makes it very relevant for those who have had chemotherapy and might be experiencing physical limitations as a result, Reid-Arndt said.
The MU pilot study followed a group of women with a history of chemotherapy. The women participated in a 60-minute Tai Chi class two times a week for 10 weeks. The women were tested on memory, language, attention, stress, mood and fatigue before and after the 10-week sessions. According to Reid-Arndt, the results of the tests indicated that the women had made significant improvements in their psychological health and cognitive abilities.
"Tai Chi really helps individuals focus their attention, and this study also demonstrates how good Tai Chi could be for anyone, whether or not they have undergone treatment for cancer," Reid-Arndt said. "Due to the small size of this study, we really need to test a larger group of individuals to gain a better understanding of the specific benefits of this activity for patients who have been treated with chemotherapy and how significant these improvements might be."
Source EurekaAlert!
"Scientists have known for years that Tai Chi positively impacts physical and emotional health, but this small study also uncovered evidence that it might help cognitive functioning as well," said Stephanie Reid-Arndt, assistant professor and chair of the Department of Health Psychology in the School of Health Professions. "We know this activity can help people with their quality of life in general, and with this new study, we are encouraged about how Tai Chi could also help those who have received chemotherapy. I also hope this encourages more people to think about Tai Chi positively on a broader scale in their lives."
Tai Chi involves practicing slow motion routines and is based on several principles, including mindfulness, breathing awareness, active relaxation and slow movements. The emphasis on slow movement makes Tai Chi particularly suited to a wide range of fitness levels, which makes it very relevant for those who have had chemotherapy and might be experiencing physical limitations as a result, Reid-Arndt said.
The MU pilot study followed a group of women with a history of chemotherapy. The women participated in a 60-minute Tai Chi class two times a week for 10 weeks. The women were tested on memory, language, attention, stress, mood and fatigue before and after the 10-week sessions. According to Reid-Arndt, the results of the tests indicated that the women had made significant improvements in their psychological health and cognitive abilities.
"Tai Chi really helps individuals focus their attention, and this study also demonstrates how good Tai Chi could be for anyone, whether or not they have undergone treatment for cancer," Reid-Arndt said. "Due to the small size of this study, we really need to test a larger group of individuals to gain a better understanding of the specific benefits of this activity for patients who have been treated with chemotherapy and how significant these improvements might be."
Source EurekaAlert!
Tuesday, May 31, 2011
Sleep loss lowers testosterone in healthy young men
Cutting back on sleep drastically reduces a healthy young man's testosterone levels, according to a study published in the June 1 issue of the Journal of the American Medical Association (JAMA).
Eve Van Cauter, PhD, professor in medicine and director of the study, found that men who slept less than five hours a night for one week in a laboratory had significantly lower levels of testosterone than when they had a full night's sleep. Low testosterone has a host of negative consequences for young men, and not just in sexual behavior and reproduction. It is critical in building strength and muscle mass, and bone density.
"Low testosterone levels are associated with reduced well being and vigor, which may also occur as a consequence of sleep loss" said Van Cauter.
At least 15% of the adult working population in the US gets less than 5 hours of sleep a night, and suffers many adverse health effects because of it. This study found that skipping sleep reduces a young man's testosterone levels by the same amount as aging 10 to 15 years.
"As research progresses, low sleep duration and poor sleep quality are increasingly recognized as endocrine disruptors," Van Cauter said.
The ten young men in the study were recruited from around the University of Chicago campus. They passed a rigorous battery of tests to screen for endocrine or psychiatric disorders and sleep problems. They were an average of 24 years old, lean and in good health.
For the study, they spent three nights in the laboratory sleeping for up to ten hours, and then eight nights sleeping less than five hours. Their blood was sampled every 15 to 30 minutes for 24 hours during the last day of the ten-hour sleep phase and the last day of the five-hour sleep phase.
The effects of sleep loss on testosterone levels were apparent after just one week of short sleep. Five hours of sleep decreased their testosterone levels by 10% to 15%. The young men had the lowest testosterone levels in the afternoons on their sleep restricted days, between 2 pm and 10 pm.
The young men also self-reported their mood and vigor levels throughout the study. They reported a decline in their sense of well-being as their blood testosterone levels declined. Their mood and vigor fell more every day as the sleep restriction part of the study progressed.
Testosterone levels in men decline by 1% to 2% a year as they age. Testosterone deficiency is associated with low energy, reduced libido, poor concentration, and fatigue.
Source EurekaAlert!
Eve Van Cauter, PhD, professor in medicine and director of the study, found that men who slept less than five hours a night for one week in a laboratory had significantly lower levels of testosterone than when they had a full night's sleep. Low testosterone has a host of negative consequences for young men, and not just in sexual behavior and reproduction. It is critical in building strength and muscle mass, and bone density.
"Low testosterone levels are associated with reduced well being and vigor, which may also occur as a consequence of sleep loss" said Van Cauter.
At least 15% of the adult working population in the US gets less than 5 hours of sleep a night, and suffers many adverse health effects because of it. This study found that skipping sleep reduces a young man's testosterone levels by the same amount as aging 10 to 15 years.
"As research progresses, low sleep duration and poor sleep quality are increasingly recognized as endocrine disruptors," Van Cauter said.
The ten young men in the study were recruited from around the University of Chicago campus. They passed a rigorous battery of tests to screen for endocrine or psychiatric disorders and sleep problems. They were an average of 24 years old, lean and in good health.
For the study, they spent three nights in the laboratory sleeping for up to ten hours, and then eight nights sleeping less than five hours. Their blood was sampled every 15 to 30 minutes for 24 hours during the last day of the ten-hour sleep phase and the last day of the five-hour sleep phase.
The effects of sleep loss on testosterone levels were apparent after just one week of short sleep. Five hours of sleep decreased their testosterone levels by 10% to 15%. The young men had the lowest testosterone levels in the afternoons on their sleep restricted days, between 2 pm and 10 pm.
The young men also self-reported their mood and vigor levels throughout the study. They reported a decline in their sense of well-being as their blood testosterone levels declined. Their mood and vigor fell more every day as the sleep restriction part of the study progressed.
Testosterone levels in men decline by 1% to 2% a year as they age. Testosterone deficiency is associated with low energy, reduced libido, poor concentration, and fatigue.
Source EurekaAlert!
Why childhood obesity? It's so much more than what kids eat
URBANA –University of Illinois scientists from a variety of disciplines have teamed up to examine the factors that contribute to childhood obesity. Why? Because individual researchers have found that the problem is too complicated for any of them to tackle alone.
"Our Strong Kids team members are looking at such diverse factors as genetic predisposition, the effect of breastfeeding, how much TV a child watches, and the neighborhood he lives in, among many others," said Kristen Harrison of the U of I's Division of Nutritional Sciences. "It seems like the answer should be simple, just eat less and exercise more, but when you look at the reasons that kids overeat and burn fewer calories, it turns out there are a lot of them."
Harrison and other Strong Kids team members received funding for a three-year longitudinal study and are applying for support to keep the research going. The scientists have collected and analyzed two generations of data on approximately 400 families, and they are beginning a third wave of data collection. Individual studies, including communication professor Harrison's own examination of preschoolers' television viewing and eating habits, are ongoing.
But the first step was developing a model for studying the problem. The team's Six Cs model will examine the problem of childhood obesity from the following angles: cell, child, clan (or family), community, country and culture. A paper detailing their approach appeared in a recent issue of Child Development Perspectives.
"From 30 to 40 percent of the population has a variety of genetic markers that puts them at greater risk for obesity," said professor of nutrition Margarita Teran-Garcia, who is approaching the problem at the cellular level. As a starting point, she is taking saliva samples from preschoolers in the study group to map their genetic susceptibility to obesity.
Child development professor Kelly Bost is looking at the quality of parent-child attachment. "There's evidence that insecure attachment predicts more TV exposure, more consumption of unhealthful foods, and other factors leading to greater obesity," she said.
Another kinesiology and community health professor, Diana Grigsby-Toussaint, is geomapping retail environments in the neighborhoods where the participating families live, looking in detail at what foods are available there. "She's also mapping how much green space is available and how that relates to outdoor play and activity," Harrison said.
Later work will add more puzzle pieces relating to the community and culture components. For example, what's the community BMI and do participants in the study believe that BMI is normal? What's the usual portion size in this culture? Are children urged to take second and third helpings at mealtime?
"Southern U.S. culture, Latin American culture, and the Sam's Club bulk-buying phenomenon are all elements of what we're trying to capture when we talk about culture," Harrison said.
And professor of applied family studies Angela Wiley is collecting data relating to childhood obesity prevention among Mexican immigrant families in the Abriendos-Caminos program so the researchers can compare parallel populations across countries.
"Childhood obesity is a puzzle, and at different stages, certain variables drop in or out of the picture. Breastfeeding versus formula feeding is a predictor, but it drops out of the model entirely when you get past babyhood. Vending machines in schools are important later in a child's life, but they weren't important before," she added.
There has been very little transdisciplinary effort to map out how all these factors work together, although research shows that no single factor is the most important, Harrison noted.
"We're each looking at different spheres in the model, but we're also looking at potential interactions. That's one of the exciting things we'll get to do as we move forward," she said.
Source EurekaAlert!
"Our Strong Kids team members are looking at such diverse factors as genetic predisposition, the effect of breastfeeding, how much TV a child watches, and the neighborhood he lives in, among many others," said Kristen Harrison of the U of I's Division of Nutritional Sciences. "It seems like the answer should be simple, just eat less and exercise more, but when you look at the reasons that kids overeat and burn fewer calories, it turns out there are a lot of them."
Harrison and other Strong Kids team members received funding for a three-year longitudinal study and are applying for support to keep the research going. The scientists have collected and analyzed two generations of data on approximately 400 families, and they are beginning a third wave of data collection. Individual studies, including communication professor Harrison's own examination of preschoolers' television viewing and eating habits, are ongoing.
But the first step was developing a model for studying the problem. The team's Six Cs model will examine the problem of childhood obesity from the following angles: cell, child, clan (or family), community, country and culture. A paper detailing their approach appeared in a recent issue of Child Development Perspectives.
"From 30 to 40 percent of the population has a variety of genetic markers that puts them at greater risk for obesity," said professor of nutrition Margarita Teran-Garcia, who is approaching the problem at the cellular level. As a starting point, she is taking saliva samples from preschoolers in the study group to map their genetic susceptibility to obesity.
Child development professor Kelly Bost is looking at the quality of parent-child attachment. "There's evidence that insecure attachment predicts more TV exposure, more consumption of unhealthful foods, and other factors leading to greater obesity," she said.
Another kinesiology and community health professor, Diana Grigsby-Toussaint, is geomapping retail environments in the neighborhoods where the participating families live, looking in detail at what foods are available there. "She's also mapping how much green space is available and how that relates to outdoor play and activity," Harrison said.
Later work will add more puzzle pieces relating to the community and culture components. For example, what's the community BMI and do participants in the study believe that BMI is normal? What's the usual portion size in this culture? Are children urged to take second and third helpings at mealtime?
"Southern U.S. culture, Latin American culture, and the Sam's Club bulk-buying phenomenon are all elements of what we're trying to capture when we talk about culture," Harrison said.
And professor of applied family studies Angela Wiley is collecting data relating to childhood obesity prevention among Mexican immigrant families in the Abriendos-Caminos program so the researchers can compare parallel populations across countries.
"Childhood obesity is a puzzle, and at different stages, certain variables drop in or out of the picture. Breastfeeding versus formula feeding is a predictor, but it drops out of the model entirely when you get past babyhood. Vending machines in schools are important later in a child's life, but they weren't important before," she added.
There has been very little transdisciplinary effort to map out how all these factors work together, although research shows that no single factor is the most important, Harrison noted.
"We're each looking at different spheres in the model, but we're also looking at potential interactions. That's one of the exciting things we'll get to do as we move forward," she said.
Source EurekaAlert!
Monday, May 30, 2011
To Rest Easy, Forget the Sheep
Scientists know that many people inadvertently undermine their ability to fall asleep and stay asleep for a full night. Here are some frequent suggestions:
1. Establish a regular sleep schedule and try to stick to it, even on weekends.
2. If you nap during the day, limit it to 20 or 30 minutes, preferably early in the afternoon.
3. Avoid alcohol in the evening, as it can disrupt sleep.
4. Don’t eat a big meal just before bedtime, but don’t go to bed hungry, either. Eat a light snack before bed, if needed, preferably one high in carbohydrates.
5. If you use medications that are stimulants, take them in the morning, or ask your doctor if you can switch to a nonstimulating alternative. If you use drugs that cause drowsiness, take them in the evening.
6. Get regular exercise during the day, but avoid vigorous exercise within three hours of bedtime.
7. If pressing thoughts interfere with falling asleep, write them down (keep a pad and pen next to the bed) and try to forget about them until morning.
8. If you are frequently awakened by a need to use the bathroom, cut down on how much you drink late in the day.
9. If you smoke, quit. Among other hazards, nicotine is a stimulant and can cause nightmares.
10. Avoid beverages and foods containing caffeine after 3 p.m. Even decaf versions have some caffeine, which can bother some people.
Source The New Yprk Times
1. Establish a regular sleep schedule and try to stick to it, even on weekends.
2. If you nap during the day, limit it to 20 or 30 minutes, preferably early in the afternoon.
3. Avoid alcohol in the evening, as it can disrupt sleep.
4. Don’t eat a big meal just before bedtime, but don’t go to bed hungry, either. Eat a light snack before bed, if needed, preferably one high in carbohydrates.
5. If you use medications that are stimulants, take them in the morning, or ask your doctor if you can switch to a nonstimulating alternative. If you use drugs that cause drowsiness, take them in the evening.
6. Get regular exercise during the day, but avoid vigorous exercise within three hours of bedtime.
7. If pressing thoughts interfere with falling asleep, write them down (keep a pad and pen next to the bed) and try to forget about them until morning.
8. If you are frequently awakened by a need to use the bathroom, cut down on how much you drink late in the day.
9. If you smoke, quit. Among other hazards, nicotine is a stimulant and can cause nightmares.
10. Avoid beverages and foods containing caffeine after 3 p.m. Even decaf versions have some caffeine, which can bother some people.
Source The New Yprk Times
A Good Night’s Sleep Isn’t a Luxury; It’s a Necessity
In my younger years, I regarded sleep as a necessary evil, nature’s way of thwarting my desire to cram as many activities into a 24-hour day as possible. I frequently flew the red-eye from California, for instance, sailing (or so I thought) through the next day on less than four hours of uncomfortable sleep.
But my neglect was costing me in ways that I did not fully appreciate. My husband called our nights at the ballet and theater “Jane’s most expensive naps.” Eventually we relinquished our subscriptions. Driving, too, was dicey: twice I fell asleep at the wheel, narrowly avoiding disaster. I realize now that I was living in a state of chronic sleep deprivation.
I don’t want to nod off during cultural events, and I no longer have my husband to spell me at the wheel. I also don’t want to compromise my ability to think and react. As research cited recently in this newspaper’s magazine found, “The sleep-deprived among us are lousy judges of our own sleep needs. We are not nearly as sharp as we think we are.”
Studies have shown that people function best after seven to eight hours of sleep, so I now aim for a solid seven hours, the amount associated with the lowest mortality rate. Yet on most nights something seems to interfere, keeping me up later than my intended lights-out at 10 p.m. — an essential household task, an e-mail requiring an urgent and thoughtful response, a condolence letter I never found time to write during the day, a long article that I must read.
It’s always something.
What’s Keeping Us Up?
I know I’m hardly alone. Between 1960 and 2010, the average night’s sleep for adults in the United States dropped to six and a half hours from more than eight. Some experts predict a continuing decline, thanks to distractions like e-mail, instant and text messaging, and online shopping.
Age can have a detrimental effect on sleep. In a 2005 national telephone survey of 1,003 adults ages 50 and older, the Gallup Organization found that a mere third of older adults got a good night’s sleep every day, fewer than half slept more than seven hours, and one-fifth slept less than six hours a night.
With advancing age, natural changes in sleep quality occur. People may take longer to fall asleep, and they tend to get sleepy earlier in the evening and to awaken earlier in the morning. More time is spent in the lighter stages of sleep and less in restorative deep sleep. R.E.M. sleep, during which the mind processes emotions and memories and relieves stress, also declines with age.
Habits that ruin sleep often accompany aging: less physical activity, less time spent outdoors (sunlight is the body’s main regulator of sleepiness and wakefulness), poorer attention to diet, taking medications that can disrupt sleep, caring for a chronically ill spouse, having a partner who snores. Some use alcohol in hopes of inducing sleep; in fact, it disrupts sleep.
Add to this list a host of sleep-robbing health issues, like painful arthritis, diabetes, depression, anxiety, sleep apnea, hot flashes in women and prostate enlargement in men. In the last years of his life, my husband was plagued with restless leg syndrome, forcing him to get up and walk around in the middle of the night until the symptoms subsided. During a recent night, I was awake for hours with leg cramps that simply wouldn’t quit.
Beauty Rest and Beyond
A good night’s sleep is much more than a luxury. Its benefits include improvements in concentration, short-term memory, productivity, mood, sensitivity to pain and immune function.
If you care about how you look, more sleep can even make you appear more attractive. In a study published online in December in the journal BMJ, researchers in Sweden and the Netherlands reported that 23 sleep-deprived adults seemed to untrained observers to be less healthy, more tired and less attractive than they appeared to be after a full night’s sleep.
Perhaps more important, losing sleep may make you fat — or at least, fatter than you would otherwise be. In a study by Harvard researchers involving 68,000 middle-aged women followed for 16 years, those who slept five hours or less each night were found to weigh 5.4 pounds more — and were 15 percent more likely to become obese — than the women who slept seven hours nightly.
Michael Breus, a clinical psychologist and sleep specialist in Scottsdale, Ariz., and author of “The Sleep Doctor’s Diet Plan,” points out that as the average length of sleep has declined in the United States, the average weight of Americans has increased.
There are plausible reasons to think this is a cause-and-effect relationship. At least two factors may be involved: more waking hours in homes brimming with food and snacks; and possible changes in the hormones leptin and ghrelin, which regulate appetite.
In a study published in 2009 in The American Journal of Clinical Nutrition, Dr. Plamen D. Penev, an endocrinologist at the University of Chicago, and co-authors explored calorie consumption and expenditure by 11 healthy volunteers who spent two 14-day stays in a sleep laboratory. Both sessions offered unlimited access to tasty foods. During one stay, the volunteers — five women and six men — were limited to 5.5 hours of sleep a night, and during the other they got 8.5 hours of sleep.
Although the subjects ate the same amount of food at meals, during the shortened nights they consumed an average of 221 more calories from snacks than they did when they were getting more sleep. The snacks they ate tended to be high in carbohydrates, and the subjects expended no more energy than they did on the longer nights. In just two weeks, the extra nighttime snacking could add nearly a pound to body weight, the scientists concluded.
These researchers found no significant changes in the participants’ blood levels of the hormones leptin and ghrelin, but others have found that short sleepers have lower levels of appetite-suppressing leptin and higher levels of ghrelin, which prompts an increase in calorie intake.
Sleep loss may also affect the function of a group of neurons in the hypothalamus of the brain, where another hormone, orexin, is involved in the regulation of feeding behavior.
The bottom line: Resist the temptation to squeeze one more thing into the end of your day. If health problems disrupt your sleep, seek treatment that can lessen their effect. If you have trouble falling asleep or often awaken during the night and can’t get back to sleep, you could try taking supplements of melatonin, the body’s natural sleep inducer. I keep it at my bedside.
If you have trouble sleeping, the tips accompanying this article may help. And if all else fails, try to take a nap during the day. Naps can enhance brain function, energy, mood and productivity.
By JANE E. BRODY
Source The New York Times
But my neglect was costing me in ways that I did not fully appreciate. My husband called our nights at the ballet and theater “Jane’s most expensive naps.” Eventually we relinquished our subscriptions. Driving, too, was dicey: twice I fell asleep at the wheel, narrowly avoiding disaster. I realize now that I was living in a state of chronic sleep deprivation.
I don’t want to nod off during cultural events, and I no longer have my husband to spell me at the wheel. I also don’t want to compromise my ability to think and react. As research cited recently in this newspaper’s magazine found, “The sleep-deprived among us are lousy judges of our own sleep needs. We are not nearly as sharp as we think we are.”
Studies have shown that people function best after seven to eight hours of sleep, so I now aim for a solid seven hours, the amount associated with the lowest mortality rate. Yet on most nights something seems to interfere, keeping me up later than my intended lights-out at 10 p.m. — an essential household task, an e-mail requiring an urgent and thoughtful response, a condolence letter I never found time to write during the day, a long article that I must read.
It’s always something.
What’s Keeping Us Up?
I know I’m hardly alone. Between 1960 and 2010, the average night’s sleep for adults in the United States dropped to six and a half hours from more than eight. Some experts predict a continuing decline, thanks to distractions like e-mail, instant and text messaging, and online shopping.
Age can have a detrimental effect on sleep. In a 2005 national telephone survey of 1,003 adults ages 50 and older, the Gallup Organization found that a mere third of older adults got a good night’s sleep every day, fewer than half slept more than seven hours, and one-fifth slept less than six hours a night.
With advancing age, natural changes in sleep quality occur. People may take longer to fall asleep, and they tend to get sleepy earlier in the evening and to awaken earlier in the morning. More time is spent in the lighter stages of sleep and less in restorative deep sleep. R.E.M. sleep, during which the mind processes emotions and memories and relieves stress, also declines with age.
Habits that ruin sleep often accompany aging: less physical activity, less time spent outdoors (sunlight is the body’s main regulator of sleepiness and wakefulness), poorer attention to diet, taking medications that can disrupt sleep, caring for a chronically ill spouse, having a partner who snores. Some use alcohol in hopes of inducing sleep; in fact, it disrupts sleep.
Add to this list a host of sleep-robbing health issues, like painful arthritis, diabetes, depression, anxiety, sleep apnea, hot flashes in women and prostate enlargement in men. In the last years of his life, my husband was plagued with restless leg syndrome, forcing him to get up and walk around in the middle of the night until the symptoms subsided. During a recent night, I was awake for hours with leg cramps that simply wouldn’t quit.
Beauty Rest and Beyond
A good night’s sleep is much more than a luxury. Its benefits include improvements in concentration, short-term memory, productivity, mood, sensitivity to pain and immune function.
If you care about how you look, more sleep can even make you appear more attractive. In a study published online in December in the journal BMJ, researchers in Sweden and the Netherlands reported that 23 sleep-deprived adults seemed to untrained observers to be less healthy, more tired and less attractive than they appeared to be after a full night’s sleep.
Perhaps more important, losing sleep may make you fat — or at least, fatter than you would otherwise be. In a study by Harvard researchers involving 68,000 middle-aged women followed for 16 years, those who slept five hours or less each night were found to weigh 5.4 pounds more — and were 15 percent more likely to become obese — than the women who slept seven hours nightly.
Michael Breus, a clinical psychologist and sleep specialist in Scottsdale, Ariz., and author of “The Sleep Doctor’s Diet Plan,” points out that as the average length of sleep has declined in the United States, the average weight of Americans has increased.
There are plausible reasons to think this is a cause-and-effect relationship. At least two factors may be involved: more waking hours in homes brimming with food and snacks; and possible changes in the hormones leptin and ghrelin, which regulate appetite.
In a study published in 2009 in The American Journal of Clinical Nutrition, Dr. Plamen D. Penev, an endocrinologist at the University of Chicago, and co-authors explored calorie consumption and expenditure by 11 healthy volunteers who spent two 14-day stays in a sleep laboratory. Both sessions offered unlimited access to tasty foods. During one stay, the volunteers — five women and six men — were limited to 5.5 hours of sleep a night, and during the other they got 8.5 hours of sleep.
Although the subjects ate the same amount of food at meals, during the shortened nights they consumed an average of 221 more calories from snacks than they did when they were getting more sleep. The snacks they ate tended to be high in carbohydrates, and the subjects expended no more energy than they did on the longer nights. In just two weeks, the extra nighttime snacking could add nearly a pound to body weight, the scientists concluded.
These researchers found no significant changes in the participants’ blood levels of the hormones leptin and ghrelin, but others have found that short sleepers have lower levels of appetite-suppressing leptin and higher levels of ghrelin, which prompts an increase in calorie intake.
Sleep loss may also affect the function of a group of neurons in the hypothalamus of the brain, where another hormone, orexin, is involved in the regulation of feeding behavior.
The bottom line: Resist the temptation to squeeze one more thing into the end of your day. If health problems disrupt your sleep, seek treatment that can lessen their effect. If you have trouble falling asleep or often awaken during the night and can’t get back to sleep, you could try taking supplements of melatonin, the body’s natural sleep inducer. I keep it at my bedside.
If you have trouble sleeping, the tips accompanying this article may help. And if all else fails, try to take a nap during the day. Naps can enhance brain function, energy, mood and productivity.
This is the second of two columns on sleep needs.
By JANE E. BRODY
Source The New York Times
Sunday, May 29, 2011
Virtual natural environments and benefits to health
A new position paper by researchers at the European Centre for the Environment and Human Health (ECEHH - part of the Peninsula College of Medicine and Dentistry) and the University of Birmingham has compared the benefits of interaction with actual and virtual natural environments and concluded that the development of accurate simulations are likely to be beneficial to those who cannot interact with nature because of infirmity or other limitations: but virtual worlds are not a substitute for the real thing.
The paper includes details of an exciting project underway between the collaborating institutions to create virtual environments to help identify the clues and cues that we pick up when we spend time in nature.
The study is published in Environmental Science & Technology on 1st June 2011.
The paper discusses the potential for natural and virtual environments in promoting improved human health and wellbeing.
We have all felt the benefit of spending time in natural environments, especially when we are feeling stressed or upset. The researchers describe creating virtual environments to try to identify just how this happens. It may be that the colours, sounds, and smells of nature are all important, but to different extents, in helping to provide mental restoration and motivation to be physically active.
It was recognised that, while some studies have tried to explore this notion, much of the work is anecdotal or involves small-scale studies which often lack appropriate controls or statistical robustness. However, the researchers do identify some studies, such as those relating to Attention Restoration Theory, that are valuable.
Key to the research is an exploration of the studies that showed a direct relationship between interaction with the natural environment and improvements in health, and the potential such activity has for becoming adopted by health services around the world to the benefit of both patients and budgets. For example, a study in Philadelphia suggested that maintaining city parks could achieve yearly savings of approximately $69.4 million in health care costs.
Programmes such as the Green Gym and the Blue Gym which promote, facilitate and encourage activity in the natural environment, are already laying the groundwork for workable programmes that could be adopted throughout the world to the benefit of human health. Research teams from the ECEHH are currently undertaking a range of studies to analyse the effects of interaction with the natural environment on health which in turn could lead to prescribing clinicians being able to treat patients with natural environment activity alone or in conjunction with reduced pharmaceutical solutions – the beneficial effect on national health service drug bills around the world could be immense, and also help reduce the release of toxic pharmaceutical residues contained in sewage into our ecosystems.
The paper also examines how step-change developments in the technology used in computer-generated forms of reality means that the software and hardware required to access increasingly accurate simulated natural environments are more readily available to the general public than ever before.
In addition to recognising the value of better technology – which includes the ability to synthesise smells - the review also recognised that key to the success of virtual environments is the design of appropriate and effective content based on knowledge of human behaviour.
Teams from the ECEHH and colleagues from the University of Birmingham, which include joint authors of the paper, have constructed the first two virtual restorative environments to support their experimental studies. This pilot study is based on the South Devon Coastal Path and Burrator Reservoir located within Dartmoor National Park, both within a short distance of the urban conurbation of Plymouth (UK).
Both natural environments are being recreated using Unity, a powerful game and interactive media development tool.
The research team is attempting to achieve a close match between the virtual and the real by importing Digital Terrain Model (DTM) data and aerial photographs into the Unity toolkit and combining this with natural features and manmade artefacts including wild flowers, trees, hedgerows, fences, seating benches and buildings. High-quality digital oceanic, coastal and birdsong sounds are also incorporated.
The pilot study, part of a Virtual Restorative Environment Therapy (VRET) initiative, is also supporting efforts to establish how psychological and physiological measurement can be used as part of a real-time biofeedback system to link participants' arousal levels to features such as cloud cover, weather, wave strengths, ambient sounds and smells.
Professor Michael Depledge, Chair of Environment and Human Health at the ECEHH, commented: "Virtual environments could benefit the elderly or infirm within their homes are care units, and can be deployed within defence medical establishments to benefit those with physical and psychological trauma following operations in conflict zones. Looking ahead, the wellbeing of others removed from nature, such as submariners and astronauts confined for several months in their crafts, might also be enhanced. Once our research has been conducted and the appropriate software written, artificial environments are likely to become readily affordable and of widespread use to health services."
He added: "However, we would not wish for the availability of virtual environments to become a substitute for the real thing in instances where accessibility to the real world is achievable. Our ongoing research with both the Green Gym and the Blue Gym initiatives aims to make these options a valid and straightforward choice for the majority of the population."
Professor Bob Stone, Chair of Interactive Multimedia Systems at the University of Birmingham, and lead investigator, said: "This technology could be made available to anyone who, for whatever reason, is in hospital, bed-bound or cannot get outside. They will be able to get the benefits of the countryside and seaside by viewing the virtual scenario on screen.
"Patients will be free to choose areas that they want to spend time in; they can take a walk along coastal footpaths, sit on a beach, listen to the waves and birdsong, watch the sun go down and - in due course - even experience the smells of the land- and seascapes almost as if they were experiencing the outdoors for real."
Professor Stone continued: "We are keen to understand what effect our virtual environments have on patients and will be carrying out further studies into arousal levels and reaction. In the summer we will start to test this on a large number of people so that we can measure biofeedback and make any changes or improvements to the scenario we have chosen.'"
Source EurekaAlert!
The paper includes details of an exciting project underway between the collaborating institutions to create virtual environments to help identify the clues and cues that we pick up when we spend time in nature.
The study is published in Environmental Science & Technology on 1st June 2011.
The paper discusses the potential for natural and virtual environments in promoting improved human health and wellbeing.
We have all felt the benefit of spending time in natural environments, especially when we are feeling stressed or upset. The researchers describe creating virtual environments to try to identify just how this happens. It may be that the colours, sounds, and smells of nature are all important, but to different extents, in helping to provide mental restoration and motivation to be physically active.
It was recognised that, while some studies have tried to explore this notion, much of the work is anecdotal or involves small-scale studies which often lack appropriate controls or statistical robustness. However, the researchers do identify some studies, such as those relating to Attention Restoration Theory, that are valuable.
Key to the research is an exploration of the studies that showed a direct relationship between interaction with the natural environment and improvements in health, and the potential such activity has for becoming adopted by health services around the world to the benefit of both patients and budgets. For example, a study in Philadelphia suggested that maintaining city parks could achieve yearly savings of approximately $69.4 million in health care costs.
Programmes such as the Green Gym and the Blue Gym which promote, facilitate and encourage activity in the natural environment, are already laying the groundwork for workable programmes that could be adopted throughout the world to the benefit of human health. Research teams from the ECEHH are currently undertaking a range of studies to analyse the effects of interaction with the natural environment on health which in turn could lead to prescribing clinicians being able to treat patients with natural environment activity alone or in conjunction with reduced pharmaceutical solutions – the beneficial effect on national health service drug bills around the world could be immense, and also help reduce the release of toxic pharmaceutical residues contained in sewage into our ecosystems.
The paper also examines how step-change developments in the technology used in computer-generated forms of reality means that the software and hardware required to access increasingly accurate simulated natural environments are more readily available to the general public than ever before.
In addition to recognising the value of better technology – which includes the ability to synthesise smells - the review also recognised that key to the success of virtual environments is the design of appropriate and effective content based on knowledge of human behaviour.
Teams from the ECEHH and colleagues from the University of Birmingham, which include joint authors of the paper, have constructed the first two virtual restorative environments to support their experimental studies. This pilot study is based on the South Devon Coastal Path and Burrator Reservoir located within Dartmoor National Park, both within a short distance of the urban conurbation of Plymouth (UK).
Both natural environments are being recreated using Unity, a powerful game and interactive media development tool.
The research team is attempting to achieve a close match between the virtual and the real by importing Digital Terrain Model (DTM) data and aerial photographs into the Unity toolkit and combining this with natural features and manmade artefacts including wild flowers, trees, hedgerows, fences, seating benches and buildings. High-quality digital oceanic, coastal and birdsong sounds are also incorporated.
The pilot study, part of a Virtual Restorative Environment Therapy (VRET) initiative, is also supporting efforts to establish how psychological and physiological measurement can be used as part of a real-time biofeedback system to link participants' arousal levels to features such as cloud cover, weather, wave strengths, ambient sounds and smells.
Professor Michael Depledge, Chair of Environment and Human Health at the ECEHH, commented: "Virtual environments could benefit the elderly or infirm within their homes are care units, and can be deployed within defence medical establishments to benefit those with physical and psychological trauma following operations in conflict zones. Looking ahead, the wellbeing of others removed from nature, such as submariners and astronauts confined for several months in their crafts, might also be enhanced. Once our research has been conducted and the appropriate software written, artificial environments are likely to become readily affordable and of widespread use to health services."
He added: "However, we would not wish for the availability of virtual environments to become a substitute for the real thing in instances where accessibility to the real world is achievable. Our ongoing research with both the Green Gym and the Blue Gym initiatives aims to make these options a valid and straightforward choice for the majority of the population."
Professor Bob Stone, Chair of Interactive Multimedia Systems at the University of Birmingham, and lead investigator, said: "This technology could be made available to anyone who, for whatever reason, is in hospital, bed-bound or cannot get outside. They will be able to get the benefits of the countryside and seaside by viewing the virtual scenario on screen.
"Patients will be free to choose areas that they want to spend time in; they can take a walk along coastal footpaths, sit on a beach, listen to the waves and birdsong, watch the sun go down and - in due course - even experience the smells of the land- and seascapes almost as if they were experiencing the outdoors for real."
Professor Stone continued: "We are keen to understand what effect our virtual environments have on patients and will be carrying out further studies into arousal levels and reaction. In the summer we will start to test this on a large number of people so that we can measure biofeedback and make any changes or improvements to the scenario we have chosen.'"
Source EurekaAlert!
Why does flu trigger asthma?
Study suggests new therapeutic targets for virally-induced asthma attacks
Boston, Mass. - When children with asthma get the flu, they often land in the hospital gasping for air. Researchers at Children's Hospital Boston have found a previously unknown biological pathway explaining why influenza induces asthma attacks. Studies in a mouse model, published online May 29 by the journal Nature Immunology, reveal that influenza activates a newly recognized group of immune cells called natural helper cells – presenting a completely new set of drug targets for asthma.
If activation of these cells, or their asthma-inducing secretions, could be blocked, asthmatic children could be more effectively protected when they get the flu and possibly other viral infections, says senior investigator Dale Umetsu, MD, PhD, of Children's Division of Immunology.
Although most asthma is allergic in nature, attacks triggered by viral infection tend to be what put children in the hospital, reflecting the fact that this type of asthma isn't well controlled by existing drugs.
"Virtually 100 percent of asthmatics get worse with a viral infection," says Umetsu. "We really didn't know how that happened, but now we have an explanation, at least for influenza."
Natural helper cells were first, very recently, discovered in the intestines and are recognized to play a role in fighting parasitic worm infections as part of the innate immune system (our first line of immune defense).
"Since the lung is related to the gut – both are exposed to the environment – we asked if natural helper cells might also be in the lung and be important in asthma," Umetsu says.
Subsequent experiments, led by first authors Ya-Jen Chang, PhD, and Hye Young Kim, PhD, in Umetsu's lab, showed that the cells are indeed in the lung in a mouse model of influenza-induced asthma, but not in allergic asthma. The model showed that influenza A infection stimulates production of a compound called IL-33 that activates natural helper cells, which then secrete asthma-inducing compounds.
"Without these cells being activated, infection did not cause airway hyperreactivity, the cardinal feature of asthma," Umetsu says. "Now we can start to think of this pathway as a target – IL-33, the natural helper cell itself or the factors it produces."
Personalized medicine in asthma?
The study adds to a growing understanding of asthma as a collection of different processes, all causing airways to become twitchy and constricted. "In mouse models we're finding very distinct pathways," Umetsu says.
Most asthma-control drugs, such as inhaled corticosteroids, act on the best-known pathway, which involves immune cells known as TH2 cells, and which is important in allergic asthma. However, Umetsu's team showed in 2006 that a second group of cells, known as natural killer T-cells (NKT cells), are also important in asthma, and demonstrated their presence in the lungs of asthma patients. NKT cells, they showed, can function independently of TH2 cells, for example, when asthma is induced with ozone, a major component of air pollution. Compounds targeting NKT cells are now in preclinical development.
The recognition now of a third pathway for asthma, involving natural helper cells, may reflect the diversity of triggers for asthma seen in patients.
"Clinically, we knew there were different asthma triggers, but we thought there was only one pathway for asthma," Umetsu says, adding that all of the identified pathways can coexist in one person. "We need to understand the specific asthma pathways present in each individual with asthma and when they are triggered, so we can give the right treatment at the right time."
Source EurekaAlert!
Boston, Mass. - When children with asthma get the flu, they often land in the hospital gasping for air. Researchers at Children's Hospital Boston have found a previously unknown biological pathway explaining why influenza induces asthma attacks. Studies in a mouse model, published online May 29 by the journal Nature Immunology, reveal that influenza activates a newly recognized group of immune cells called natural helper cells – presenting a completely new set of drug targets for asthma.
If activation of these cells, or their asthma-inducing secretions, could be blocked, asthmatic children could be more effectively protected when they get the flu and possibly other viral infections, says senior investigator Dale Umetsu, MD, PhD, of Children's Division of Immunology.
Although most asthma is allergic in nature, attacks triggered by viral infection tend to be what put children in the hospital, reflecting the fact that this type of asthma isn't well controlled by existing drugs.
"Virtually 100 percent of asthmatics get worse with a viral infection," says Umetsu. "We really didn't know how that happened, but now we have an explanation, at least for influenza."
Natural helper cells were first, very recently, discovered in the intestines and are recognized to play a role in fighting parasitic worm infections as part of the innate immune system (our first line of immune defense).
"Since the lung is related to the gut – both are exposed to the environment – we asked if natural helper cells might also be in the lung and be important in asthma," Umetsu says.
Subsequent experiments, led by first authors Ya-Jen Chang, PhD, and Hye Young Kim, PhD, in Umetsu's lab, showed that the cells are indeed in the lung in a mouse model of influenza-induced asthma, but not in allergic asthma. The model showed that influenza A infection stimulates production of a compound called IL-33 that activates natural helper cells, which then secrete asthma-inducing compounds.
"Without these cells being activated, infection did not cause airway hyperreactivity, the cardinal feature of asthma," Umetsu says. "Now we can start to think of this pathway as a target – IL-33, the natural helper cell itself or the factors it produces."
Personalized medicine in asthma?
The study adds to a growing understanding of asthma as a collection of different processes, all causing airways to become twitchy and constricted. "In mouse models we're finding very distinct pathways," Umetsu says.
Most asthma-control drugs, such as inhaled corticosteroids, act on the best-known pathway, which involves immune cells known as TH2 cells, and which is important in allergic asthma. However, Umetsu's team showed in 2006 that a second group of cells, known as natural killer T-cells (NKT cells), are also important in asthma, and demonstrated their presence in the lungs of asthma patients. NKT cells, they showed, can function independently of TH2 cells, for example, when asthma is induced with ozone, a major component of air pollution. Compounds targeting NKT cells are now in preclinical development.
The recognition now of a third pathway for asthma, involving natural helper cells, may reflect the diversity of triggers for asthma seen in patients.
"Clinically, we knew there were different asthma triggers, but we thought there was only one pathway for asthma," Umetsu says, adding that all of the identified pathways can coexist in one person. "We need to understand the specific asthma pathways present in each individual with asthma and when they are triggered, so we can give the right treatment at the right time."
Source EurekaAlert!
Cross your arms to relieve pain
HURT your hand? You might find that crossing one arm over the other eases the pain.
Giandomenico Iannetti at University College London and colleagues gave 20 volunteers a series of painful "jabs" to the back of one of their hands using a laser, with each pulse lasting 8 to 12 seconds. In half of the experiments the group received the jabs while they laid their palms face down on a desk. In the other half they crossed their arms over one another on the desk. Volunteers rated the pain they felt on a scale from zero to 100.
Crossed wires in brain relive pain.
Volunteers with crossed hands rated three increasing pain intensities as less painful compared with when they kept their hands uncrossed (Pain, DOI: 10.1016/j.pain.2011.02.029).
Iannetti suggests that placing your hands in unfamiliar spatial positions relative to the body muddles the brain and disrupts the processing of the pain message. "You get this mismatch between your body's frame of reference and your external space frame of reference," he says. Similar pain-relieving effects have been reported before using illusions involving mirrors and virtual limbs.
Iannetti says his team hopes next to test the crossover trick in a clinical setting to see if it helps people suffering from chronic pain.
Source New Scientist
Thursday, May 26, 2011
Students who struggle with math may have a neurocognitive disorder called dyscalculia
Disorder affects roughly as many people as dyslexia.
Students who struggle to learn mathematics may have a neurocognitive disorder that inhibits the acquisition of basic numerical and arithmetic concepts, according to a new paper by University of Minnesota and British researchers. Called developmental dyscalculia, the disorder affects roughly the same number of people as dyslexia but has received much less attention (and research funding). The paper by University of Minnesota Educational Psychology assistant professor Sashank Varma and his British colleagues that shines a light on the causes of and interventions for dyscalculia will be published Thursday, May 27 in the journal Science.
The paper, "Dyscalculia, From Brain to Education," documents how scientists across the world have used magnetic resonance imaging to map the neural network that supports arithmetic. Through this process, they have discovered abnormalities in this network among learners with dyscalculia.
These findings have the potential to lead to evidence-based interventions for dyscalculia, Varma says. "Knowledge about what parts of the brain we use while learning mathematics is spurring the design of new computer learning environments that can strengthen simple number and arithmetic concepts," he explains. The paper envisions future research where neuroscientists, psychologists and educational researchers collaborate to offer a productive way forward on the important question of why some children struggle with learning mathematics.
Varma studies how people understand complex symbol systems such as mathematics and language, and the neural underpinnings of this understanding. In 2008, he published an influential paper on the relation between neuroscience and education in the journal Educational Researcher with Daniel Schwartz at Stanford University and Bruce McCandliss at Vanderbilt University.
Source EurekaAlert!
Students who struggle to learn mathematics may have a neurocognitive disorder that inhibits the acquisition of basic numerical and arithmetic concepts, according to a new paper by University of Minnesota and British researchers. Called developmental dyscalculia, the disorder affects roughly the same number of people as dyslexia but has received much less attention (and research funding). The paper by University of Minnesota Educational Psychology assistant professor Sashank Varma and his British colleagues that shines a light on the causes of and interventions for dyscalculia will be published Thursday, May 27 in the journal Science.
The paper, "Dyscalculia, From Brain to Education," documents how scientists across the world have used magnetic resonance imaging to map the neural network that supports arithmetic. Through this process, they have discovered abnormalities in this network among learners with dyscalculia.
These findings have the potential to lead to evidence-based interventions for dyscalculia, Varma says. "Knowledge about what parts of the brain we use while learning mathematics is spurring the design of new computer learning environments that can strengthen simple number and arithmetic concepts," he explains. The paper envisions future research where neuroscientists, psychologists and educational researchers collaborate to offer a productive way forward on the important question of why some children struggle with learning mathematics.
###
Varma co-authored the paper with lead author Professor Brian Butterworth, of the University College London Institute of Cognitive Neuroscience, and Diana Laurillard, a member of the Institute of Education at the University of London. "Dyscalculia: From Brain to Education" is published online today in Science.Varma studies how people understand complex symbol systems such as mathematics and language, and the neural underpinnings of this understanding. In 2008, he published an influential paper on the relation between neuroscience and education in the journal Educational Researcher with Daniel Schwartz at Stanford University and Bruce McCandliss at Vanderbilt University.
Source EurekaAlert!
Why caffeine can reduce fertility in women
Caffeine reduces muscle activity in the Fallopian tubes that carry eggs from a woman's ovaries to her womb. "Our experiments were conducted in mice, but this finding goes a long way towards explaining why drinking caffeinated drinks can reduce a woman's chance of becoming pregnant," says Professor Sean Ward from the University of Nevada School of Medicine, Reno, USA. Ward's study is published today in the British Journal of Pharmacology.
Human eggs are microscopically small, but need to travel to a woman's womb if she is going to have a successful pregnancy. Although the process is essential for a successful pregnancy, scientists know little about how eggs move through the muscular Fallopian tubes. It was generally assumed that tiny hair-like projections, called cilia, in the lining of the tubes, waft eggs along assisted by muscle contractions in the tube walls.
By studying tubes from mice, Professor Ward and his team discovered that caffeine stops the actions of specialised pacemaker cells in the wall of the tubes. These cells coordinate tube contractions so that when they are inhibited, eggs can't move down the tubes. In fact these muscle contractions play a bigger role than the beating cilia in moving the egg towards the womb. "This provides an intriguing explanation as to why women with high caffeine consumption often take longer to conceive than women who do not consume caffeine," says Professor Ward.
Discovering the link between caffeine consumption and reduced fertility has benefits. "As well as potentially helping women who are finding it difficult to get pregnant, a better understanding of the way Fallopian tubes work will help doctors treat pelvic inflammation and sexually-transmitted disease more successfully," says Professor Ward. It could also increase our understanding of what causes ectopic pregnancy, an extremely painful and potentially life-threatening situation in which embryos get stuck and start developing inside a woman's Fallopian tube.
Source EurekaAlert!
Human eggs are microscopically small, but need to travel to a woman's womb if she is going to have a successful pregnancy. Although the process is essential for a successful pregnancy, scientists know little about how eggs move through the muscular Fallopian tubes. It was generally assumed that tiny hair-like projections, called cilia, in the lining of the tubes, waft eggs along assisted by muscle contractions in the tube walls.
By studying tubes from mice, Professor Ward and his team discovered that caffeine stops the actions of specialised pacemaker cells in the wall of the tubes. These cells coordinate tube contractions so that when they are inhibited, eggs can't move down the tubes. In fact these muscle contractions play a bigger role than the beating cilia in moving the egg towards the womb. "This provides an intriguing explanation as to why women with high caffeine consumption often take longer to conceive than women who do not consume caffeine," says Professor Ward.
Discovering the link between caffeine consumption and reduced fertility has benefits. "As well as potentially helping women who are finding it difficult to get pregnant, a better understanding of the way Fallopian tubes work will help doctors treat pelvic inflammation and sexually-transmitted disease more successfully," says Professor Ward. It could also increase our understanding of what causes ectopic pregnancy, an extremely painful and potentially life-threatening situation in which embryos get stuck and start developing inside a woman's Fallopian tube.
Source EurekaAlert!
Saturday, May 21, 2011
BU STUDY FINDS DIET HIGH IN VEGETABLES AND FRUIT ASSOCIATED WITH LESS WEIGHT GAIN IN AFRICAN AMERICAN WOMEN
(Boston) - Investigators from the Slone Epidemiology Center at Boston University have reported that African American women who consumed a diet high in vegetables and fruit gained less weight over a 14-year period than those who consumed a diet high in red meat and fried foods. This is the first prospective study to show that a healthier diet is associated with less weight gain in African American women, a population with a high prevalence of obesity. The study results, published in the American Journal of Clinical Nutrition, were based on data from the Black Women’s Health Study (BWHS), a large follow-up study of 59,000 African American women from across the U.S. conducted since 1995.
The study asked participants about their diet at the beginning of the study in 1995, and again six years later in 2001. Two major dietary patterns were identified: 1) a “vegetables/fruit” pattern high in vegetables, fruit, legumes, fish and whole grains; and 2) a “meat/fried foods” pattern high in red meat, processed meat, french fries and fried chicken.
The researchers found that women who consumed a diet high in vegetables and fruit gained less weight over 14 years than women whose diets were low in these foods. Women who consumed a diet high in meat and fried foods gained more weight than women with low intake of these foods. These associations were strongest for women whose dietary patterns did not change during the study period. The associations also were stronger among women younger than 35 years, who gained the most weight (29 pounds during the 14-year study period, on average).
According to the lead author and researcher Dr. Deborah Boggs, people tend to eat a consistent amount of food rather than a consistent number of calories. “A diet high in red meat and fried foods can lead to consuming too many calories because these foods contain more calories than the same amount of vegetables and fruit,” she explained.
The authors concluded that the findings suggest that replacing red meat and fried foods with vegetables and fruit could help to lower obesity rates.
Funding for this study was provided by the National Institute of Diabetes and Digestive and Kidney Diseases and the National Cancer Institute.
Source Boston University
The study asked participants about their diet at the beginning of the study in 1995, and again six years later in 2001. Two major dietary patterns were identified: 1) a “vegetables/fruit” pattern high in vegetables, fruit, legumes, fish and whole grains; and 2) a “meat/fried foods” pattern high in red meat, processed meat, french fries and fried chicken.
The researchers found that women who consumed a diet high in vegetables and fruit gained less weight over 14 years than women whose diets were low in these foods. Women who consumed a diet high in meat and fried foods gained more weight than women with low intake of these foods. These associations were strongest for women whose dietary patterns did not change during the study period. The associations also were stronger among women younger than 35 years, who gained the most weight (29 pounds during the 14-year study period, on average).
According to the lead author and researcher Dr. Deborah Boggs, people tend to eat a consistent amount of food rather than a consistent number of calories. “A diet high in red meat and fried foods can lead to consuming too many calories because these foods contain more calories than the same amount of vegetables and fruit,” she explained.
The authors concluded that the findings suggest that replacing red meat and fried foods with vegetables and fruit could help to lower obesity rates.
Funding for this study was provided by the National Institute of Diabetes and Digestive and Kidney Diseases and the National Cancer Institute.
Source Boston University
Friday, May 20, 2011
UCSB scientists make strides in vision research
(Santa Barbara, Calif.) –– New research at UC Santa Barbara is contributing to the basic biological understanding of how retinas develop. The study is part of the campus's expanding vision research.
The new studies are published in recent online versions of The Proceedings of the National Academy of Sciences (PNAS), and Investigative Ophthalmology and Visual Science (IOVS).
This is a whole mouse retina labeled to reveal the terminals of cone photoreceptors (in blue), and one of their post-synaptic partners, the horizontal cells (in red). The dendritic branches of the horizontal cells make fine contacts with each cone terminal.
The scientists document how they used mice as a research model organism to show that the size of different populations of retinal neurons display wide-ranging variability among individuals. In the PNAS article, they demonstrate a nearly two-fold variation in the number of interneurons called horizontal cells. In the IOVS article, they report a conspicuous variation in the number of cone photoreceptors.
"These studies individually demonstrate the genetic determinants of nerve cell number," said Benjamin E. Reese, senior author and professor with the Neuroscience Research Institute and the Department of Psychological and Brain Sciences. "Together, they show that different nerve cell types are modulated independent of one another."
Using recombinant inbred mice, Irene Whitney, graduate student and first author of both articles, and Mary Raven, staff scientist and co-author, have been able to identify genomic loci where polymorphic genes must contribute to such natural variation. In the IOVS article, they describe this natural variation for the population of cone photoreceptors, and identify two potential causal genes that may modulate cone photoreceptor production on chromosome 10.
In the PNAS article, the scientists –– working will colleagues from four other U.S. institutions –– identify a promising candidate gene at a locus on chromosome 13, a transcription factor gene called Islet-1. This gene was confirmed to be critical for regulating horizontal cell number in genetically modified mice, in which the Islet-1 gene was rendered nonfunctional. The scientists verified that expression of this gene differs between these strains of mice during the developmental period when horizontal cells are produced. They also showed that the source of this variable expression must be due to a genetic variant within a regulatory region of the gene itself. Finally, they identified such a single nucleotide polymorphism creating an E-box, a DNA sequence bound by a family of transcription factors that have recently been shown to play a role in retinal development.
The team explained that such natural variation in the ratio of nerve cells requires a degree of plasticity in the process of forming neural connectivity, to ensure that the entire visual field is served by neural circuits that mediate our visual abilities. A series of other published and submitted studies from the Reese lab document this very plasticity in different strains of mice and in genetically modified mice.
Efforts to use genetic engineering and stem cell biology to repair diseased retinas depend upon a fuller appreciation of the developmental biology of the retina, explained Reese.
"These particular studies are just one contribution in an enormously complex process," said Reese. "Our fundamental interest is in the development the retina –– how you 'build' this neural tissue that, when fully mature, will mediate our visual abilities."
Vision research at UCSB has been steadily expanding in recent decades. "Since I arrived here in 1971, UCSB's vision research has grown to include dozens of scientists, in a number of labs, contributing to an explosion of research in the field," said Steven Fisher, professor emeritus in the Department of Molecular, Cellular, and Developmental Biology, and professor in the Neuroscience Research Institute.
Source EurekaAlert!
The new studies are published in recent online versions of The Proceedings of the National Academy of Sciences (PNAS), and Investigative Ophthalmology and Visual Science (IOVS).
This is a whole mouse retina labeled to reveal the terminals of cone photoreceptors (in blue), and one of their post-synaptic partners, the horizontal cells (in red). The dendritic branches of the horizontal cells make fine contacts with each cone terminal.
The scientists document how they used mice as a research model organism to show that the size of different populations of retinal neurons display wide-ranging variability among individuals. In the PNAS article, they demonstrate a nearly two-fold variation in the number of interneurons called horizontal cells. In the IOVS article, they report a conspicuous variation in the number of cone photoreceptors.
"These studies individually demonstrate the genetic determinants of nerve cell number," said Benjamin E. Reese, senior author and professor with the Neuroscience Research Institute and the Department of Psychological and Brain Sciences. "Together, they show that different nerve cell types are modulated independent of one another."
Using recombinant inbred mice, Irene Whitney, graduate student and first author of both articles, and Mary Raven, staff scientist and co-author, have been able to identify genomic loci where polymorphic genes must contribute to such natural variation. In the IOVS article, they describe this natural variation for the population of cone photoreceptors, and identify two potential causal genes that may modulate cone photoreceptor production on chromosome 10.
In the PNAS article, the scientists –– working will colleagues from four other U.S. institutions –– identify a promising candidate gene at a locus on chromosome 13, a transcription factor gene called Islet-1. This gene was confirmed to be critical for regulating horizontal cell number in genetically modified mice, in which the Islet-1 gene was rendered nonfunctional. The scientists verified that expression of this gene differs between these strains of mice during the developmental period when horizontal cells are produced. They also showed that the source of this variable expression must be due to a genetic variant within a regulatory region of the gene itself. Finally, they identified such a single nucleotide polymorphism creating an E-box, a DNA sequence bound by a family of transcription factors that have recently been shown to play a role in retinal development.
The team explained that such natural variation in the ratio of nerve cells requires a degree of plasticity in the process of forming neural connectivity, to ensure that the entire visual field is served by neural circuits that mediate our visual abilities. A series of other published and submitted studies from the Reese lab document this very plasticity in different strains of mice and in genetically modified mice.
Efforts to use genetic engineering and stem cell biology to repair diseased retinas depend upon a fuller appreciation of the developmental biology of the retina, explained Reese.
"These particular studies are just one contribution in an enormously complex process," said Reese. "Our fundamental interest is in the development the retina –– how you 'build' this neural tissue that, when fully mature, will mediate our visual abilities."
Vision research at UCSB has been steadily expanding in recent decades. "Since I arrived here in 1971, UCSB's vision research has grown to include dozens of scientists, in a number of labs, contributing to an explosion of research in the field," said Steven Fisher, professor emeritus in the Department of Molecular, Cellular, and Developmental Biology, and professor in the Neuroscience Research Institute.
Source EurekaAlert!
Viagra could reduce multiple sclerosis symptoms
Universitat Autònoma de Barcelona researchers have discovered that Viagra® drastically reduces multiple sclerosis symptoms in animal models with the disease. The research, published in Acta Neuropathologica, demonstrates that a practically complete recovery occurs in 50% of the animals after eight days of treatment. Researchers are confident that clinical trials soon will be carried out in patients given that the drug is well tolerated and has been used to treat sexual dysfunction in some multiple sclerosis patients.
Multiple sclerosis is the most common chronic inflammatory disease of the central nervous system and one of the main causes of disability among young adults. The disease is caused by the presence of multiple focuses of demyelination (loss of myelin sheaths around the axons, affecting the ability of neurons to communicate) and neurodegeneration in different areas of the central nervous system. There is currently no cure for the disease, although some drugs have proven effective in fighting symptoms and preventing it from progressing.
A research team from the UAB Institute of Biotechnology and Biomedicine directed by Dr Agustina García, in collaboration with the research team directed by Dr Juan Hidalgo from the UAB Institute of Neurosciences, has studied the effects of a treatment using sildenafil, sold as Viagra®, in an animal model of multiple sclerosis known as experimental autoimmune encephalomyelitis (EAE). Researchers demonstrated that a daily treatment with sildenafil after disease onset quickly reduced clinical signs, with a practically complete recovery in 50% of the cases after eight days of treatment. Scientists observed how the drug reduced the infiltration of inflammatory cells into the white matter of the spinal cord, thus reducing damage to the nerve cell's axon and facilitating myelin repair.
Sidenafil, together with tadalafil (Cialis®) and vardenafil (Levitra®), form part of a group of vasodilator drugs known as phosphodiesterase type 5 (PDE5) inhibitors, used in the treatment of erectile dysfunction and pulmonary arterial hypertension. Recent studies in animal models of central nervous system pathologies already pointed to the fact that in addition to vasodilation, these drugs could contain other neuroprotective actions and suggest their usefulness as possible treatments of both acute (cerebrovascular stroke) and chronic (Alzheimer's) neuropathologies. In fact, in a research published in 2010 in the Journal of Neurochemistry, the same research group from UAB demonstrated that one of these inhibitors reduced neuroinflammation and neuronal damage in animal models of traumatic brain injury.
Source EurekaAlert!
Multiple sclerosis is the most common chronic inflammatory disease of the central nervous system and one of the main causes of disability among young adults. The disease is caused by the presence of multiple focuses of demyelination (loss of myelin sheaths around the axons, affecting the ability of neurons to communicate) and neurodegeneration in different areas of the central nervous system. There is currently no cure for the disease, although some drugs have proven effective in fighting symptoms and preventing it from progressing.
A research team from the UAB Institute of Biotechnology and Biomedicine directed by Dr Agustina García, in collaboration with the research team directed by Dr Juan Hidalgo from the UAB Institute of Neurosciences, has studied the effects of a treatment using sildenafil, sold as Viagra®, in an animal model of multiple sclerosis known as experimental autoimmune encephalomyelitis (EAE). Researchers demonstrated that a daily treatment with sildenafil after disease onset quickly reduced clinical signs, with a practically complete recovery in 50% of the cases after eight days of treatment. Scientists observed how the drug reduced the infiltration of inflammatory cells into the white matter of the spinal cord, thus reducing damage to the nerve cell's axon and facilitating myelin repair.
Sidenafil, together with tadalafil (Cialis®) and vardenafil (Levitra®), form part of a group of vasodilator drugs known as phosphodiesterase type 5 (PDE5) inhibitors, used in the treatment of erectile dysfunction and pulmonary arterial hypertension. Recent studies in animal models of central nervous system pathologies already pointed to the fact that in addition to vasodilation, these drugs could contain other neuroprotective actions and suggest their usefulness as possible treatments of both acute (cerebrovascular stroke) and chronic (Alzheimer's) neuropathologies. In fact, in a research published in 2010 in the Journal of Neurochemistry, the same research group from UAB demonstrated that one of these inhibitors reduced neuroinflammation and neuronal damage in animal models of traumatic brain injury.
Source EurekaAlert!
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