Archive for the ‘Memory Support’ Category

A group of Israel researchers has discovered that rats with increased levels of the omega-6 fatty acid, arachidonic acid, show signs of depression.  There is also evidence that  a dietary deficiency in omega-3 fatty acids may be associated with depression.  The  “phospholipid hypothesis” postulates decreased omega-3 fatty acid intake could be responsible for some types of depression.

The details of their findings appear in the Journal of Lipid Research  showing that omega-3 fatty acid concentration in the blood of depressed patients is lower than that in control patients.  Dr. Green in collaboration with Dr Gal Yadid of Bar-Ilan University, Ramat Gan used the Flinders Sensitive Line rats to investigate the link between omega-3 fatty acids and depression. They examined the brains of the depressed rats and compared them with brains from normal rats. Surprisingly, they found that the main difference between the two types of rats was in omega-6 fatty acid levels and not omega-3 fatty acid levels. Specifically, they discovered that brains from rats with depression had higher concentrations of arachidonic acid, a long-chain unsaturated metabolite of omega-6 fatty acid.

Arachidonic acid is found throughout the body and is essential for the proper functioning of almost every body organ, including the brain. It serves a wide variety of purposes, from being a purely structural element in phospholipids to being involved in signal transduction and being a substrate for a host of derivatives involved in second messenger function.

“The finding that in the depressive rats the omega-3 fatty acid levels were not decreased, but arachidonic acid was substantially increased as compared to controls is somewhat unexpected,” admits Dr. Green. “But the finding lends itself nicely to the theory that increased omega-3 fatty acid intake may shift the balance between the two fatty acid families in the brain, since it has been demonstrated in animal studies that increased omega-3 fatty acid intake may result in decreased brain arachidonic acid.”

Although far less attention has been paid to dietary requirements for omega-6 fatty acids, which can be found in most edible oils and meat, perhaps in the future depression may be controlled by increasing omega-3 fatty acid intake and decreasing omega-6 fatty acid intake.

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Article adapted by MD Only from original press release.
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Contact: Nicole Kresge
American Society for Biochemistry and Molecular Biology 
The American Society for Biochemistry and Molecular Biology (ASBMB) is a nonprofit scientific and educational organization with over 11,000 members in the United States and internationally. Most members teach and conduct research at colleges and universities. Others conduct research in various government laboratories, nonprofit research institutions, and industry.

The manuscript for the Journal of Lipid Research paper can be downloaded from clicking Here

A survey of sleep-deprived teens finds they think that a later start time for school and tests given later in the school day would result in better grades. The survey was presented at the American Thoracic Society 2007 International Conference, on Sunday, May 20.The survey of 280 high school students confirmed what most parents with a teenager know: they are not getting enough sleep. More sleep would translate into improved academic performance, according to the teens questioned. They all attended Harriton High School in suburban Philadelphia, where the school day begins at 7:30 a.m. and ends at 2:25 p.m.

The survey found that:

  • 78% of students said it was difficult to get up in the morning
  • Only 16% said they regularly had enough sleep
  • 70% thought their grades would improve if they had more sleep
  • 90% thought their academic performance would improve if school were to start later

The surveyed teens said they do not feel alert while taking tests during early morning periods, and they do not think they can perform at the pinnacle of their ability during the early morning hours. Most students said they thought the best time to take a test would be from 11 a.m. to 1 p.m. They thought they would perform better academically and that their grades would improve if they could sleep longer.

Richard Schwab, M.D., of the University of Pennsylvania, conducted the study with his daughter Amanda, one of the sleep-deprived teens who attended Harriton High School. “I watched her get up early for four years, and saw how difficult it was,” Dr. Schwab says. “Teenagers need more sleep than adults and their circadian rhythms are phase shifted so that their ideal bedtime is midnight to 1:00 a.m.; yet they have to get up at 6:30 or earlier for high school.

While adults usually need 7 to 8 hours of sleep, teens need 8 to 9 hours, he says. In addition, teens go to bed much later – their biological clock often keeps them up until 1 a.m. to 2 a.m. Because they have to get up so early for school, many teens achieve only 6 ½ to 7 hours of sleep or, in some cases, much less. That means they tend to sleep in on the weekends, often until 11 am or later, to try to make up for their sleep deficit.

“Right now, high schools usually start earlier in the morning than elementary schools. But if school start times were based on sleep cycles, elementary schools should start at 7:30 and high schools at 8:30 or 8:45 – right now it’s the reverse. School systems should be thinking about changing their start times. It would not be easy—they would have to change the busing system—but it would increase their student’s sleep time and likely improve their school performance.”

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Article adapted by MD Only Weblog from original press release.
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Contact: Suzy Martin
American Thoracic Society

Research has shown that people who exercise do better on memory tests. Now a new Columbia University Medical Center study explains specifically what exercise does within the brain. Exercise, the researchers found, targets a region of the brain within the hippocampus, known as the dentate gyrus, which underlies normal age-related memory decline that begins around age 30 for most adults.

This finding is significant because it was accomplished via the first-ever observation of neurogenesis, the growth of neurons, within a living brain. Using an MRI imaging technique developed at Columbia, the researchers were able to identify neurogenesis within the dentate gyrus region following exercise. Previously, researchers were only able to prove neurogenesis upon postmortem exam in animal studies.

“No previous research has systematically examined the different regions of the hippocampus and identified which region is most affected by exercise,” said Scott A. Small, M.D., associate professor of neurology at Columbia University Medical Center and the study’s lead author. “I, like many physicians, already encourage my patients to get active and this adds yet another reason to the long list of reasons why exercise is good for overall health.”

Published in the March 12-16, 2007 early online edition of the Proceedings of the National Academy of Sciences, the finding builds upon previous research at Columbia that identified the role of the dentate gyrus region of the hippocampus in normal age-related memory decline. Additionally, Fred “Rusty” Gage, Ph.D. of the Salk Institute, a lead co-investigator on this study, had demonstrated in mice that the dentate gyrus is the one area of the brain where new neurons are generated, and that exercise improves this process. This is the first human study to emerge out of this observation.

“Our next step is to identify the exercise regimen that is most beneficial to improve cognition and reduce normal memory loss, so that physicians may be able to prescribe specific types of exercise to improve memory,” said Dr. Small, who is also a research scholar at the Columbia University Taub Institute for Research on Alzheimer’s Disease and the Aging Brain.

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Article adapted by MD Only Weblog from original press release.
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Contact: Elizabeth Streich, Columbia University Medical Center

Additional Columbia researchers who contributed to this study include: Ana C. Pereira, Rene Hen, Dan E. Huddleston, Adam M. Brickman, Alexander A. Sosunov, Guy M. McKhann, Truman R. Brown and Richard Sloan.

The Taub Institute for Research on Alzheimer’s Disease and the Aging Brain at Columbia University Medical Center is a multidisciplinary group that has forged links between researchers and clinicians to uncover the causes of Alzheimer’s, Parkinson’s and other age-related brain diseases and discover ways to prevent and cure these diseases. It has partnered with the Gertrude H. Sergievsky Center at Columbia University Medical Center which was established by an endowment in 1977 to focus on diseases of the nervous system. The Center integrates traditional epidemiology with genetic analysis and clinical investigation to explore all phases of diseases of the nervous system.

Columbia University Medical Center provides international leadership in basic, pre-clinical and clinical research, in medical and health sciences education, and in patient care. The medical center trains future leaders and includes the dedicated work of many physicians, scientists, nurses, dentists, and public health professionals at the College of Physicians & Surgeons, the College of Dental Medicine, the School of Nursing, the Mailman School of Public Health, the biomedical departments of the Graduate School of Arts and Sciences, and allied research centers and institutions.

Magnesium helps build bones, make proteins, release energy stored in muscles and regulate body temperature. In the cover story of the Dec. 2 issue of Neuron, MIT researchers report a possible new role for magnesium: helping maintain memory function in middle age and beyond.

The adult daily nutritional requirement for magnesium, a trace mineral found in foods such as dark green, leafy vegetables, is around 400 mg a day. But studies show that as many as half of all Americans do not consume enough magnesium. Magnesium deficits have been tied to allergies, asthma, attention deficit disorder, anxiety, heart disease, muscle cramps and other conditions.

Associate Professor Guosong Liu and postdoctoral associate Inna Slutsky at MIT’s Picower Center for Learning and Memory found that magnesium helps regulate a key brain receptor important for learning and memory. Their work provides evidence that a magnesium deficit may lead to decreased memory and learning ability, while an abundance of magnesium may improve cognitive function.

“Our study shows maintaining proper magnesium in the cerebrospinal fluid is essential for maintaining the plasticity of synapses,” the authors wrote. “Since it is estimated that the majority of American adults consume less than the estimated average requirement of magnesium, it is possible that such a deficit may have detrimental effectsSresulting in potential declines in memory function.”

Plasticity, or the ability to change, is key to the brain’s ability to learn and remember. Synapses, the connections among brain cells, undergo physical changes in response to brain activity. While the mechanisms underlying these changes remain elusive, it is known that synapses are less plastic in the aging or diseased brain. Loss of plasticity in the hippocampus, where short-term memories are stored, causes the forgetfulness common in older people.

“The important issue is how the plasticity of synapses is regulated physiologically,” said Liu, who has appointments in MIT’s Department of Biology and Department of Brain and Cognitive Sciences. Working with Slutsky, graduate student Safa Sadeghpour and technician Bing Li, Liu identified a key principle that predicts which chemicals can enhance plasticity.

This finding is akin to the difference between hearing music on an old radio or a high-fidelity stereo. Synapses, like speakers, have a level of background noise that can get in the way of transmitting their signal from one neuron to another. Just as our ears become more sensitive to nuances in music played on a top-of-the-line music system, synapses become more plastic when background noise is reduced.

Armed with this new understanding, the researchers then identified magnesium’s importance in synaptic function.

Magnesium is the gatekeeper for the NMDA receptor, which receives signals from an important excitatory neurotransmitter involved in synaptic plasticity. Magnesium helps the receptor open up for meaningful input and shut down to background noise. “As predicted by our theory, increasing the concentration of magnesium and reducing the background level of noise led to the largest increases of plasticity ever reported in scientific literature,” Liu said.

The researchers have identified and are now studying several families of drugs that may restore learning and memory in animals. Most important, Liu said, “This new theory may help create strategies to prevent aging-induced loss of synaptic plasticity.”

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Article adapted by MD Only Weblog from original press release.
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Contact: Sean Wagner
MIT News Office
Massachusetts Institute of Technology
Room 11-400
77 Massachusetts Avenue
Cambridge, MA 02139-4307
Phone: 617-253-2700
http://web.mit.edu/newsoffice/www

This work was supported by the RIKEN-MIT Neuroscience Center and the National Institutes of Health.

A version of this article appeared in MIT Tech Talk (download PDF).

A new poll of teenagers across the US finds that many of them are losing out on quality of life because of a lack of sleep. The results, announced today by the National Sleep Foundation (NSF), cite sleeping in class, lack of energy to exercise, feelings of depression, and driving while drowsy as only some of the consequences for insufficient sleep.The poll data support previous work by three Rhode Island researchers who are at the forefront of sleep research. Previous studies from Brown Medical School, and Lifespan affiliates Bradley Hospital and Hasbro Children’s Hospital, have found that adolescents are not getting enough sleep, and suggest that this can lead to a number of physical and emotional impairments.

Mary A. Carskadon, PhD, with Bradley Hospital and Brown Medical School, chaired the National Sleep Foundation poll taskforce and has been a leading authority on teen sleep for more than a decade. Her research on adolescent circadian rhythms indicates that the internal clocks of adolescents undergo maturational changes making them different from those of children or adults. Nevertheless, teens must adhere to increasingly earlier school start times that make it nearly impossible for them to get enough sleep.

“Our results show that the adage ‘early to bed, early to rise’ presents a real challenge for adolescents,” says Carskadon, who directs the Bradley Hospital Sleep and Chronobiology Sleep Laboratory and is a professor of psychiatry and human behavior at Brown Medical School.

Carskadon’s work has been instrumental in influencing school start times across the country. Regionally, the North Kingstown School Department in Rhode Island, North Reading Public Schools in Massachusetts, and West Hartford Public Schools in Connecticut are considering school start time changes due, in part, to research on teens and sleep.

In a study published in the November 2005 issue of the journal Sleep, Carskadon found that the “sleep pressure” rate – the biological trigger that causes sleepiness – slows down in adolescence and is one more explanation for why teens can’t fall asleep until later at night. Carskadon’s newest finding indicates that, in addition to the changes in their internal clocks, adolescents experience slower sleep pressure, which may contribute to an overall shift in teen sleep cycles to later hours.

Judy Owens, MD, a national authority on children and sleep, is the director of the pediatric sleep disorders center at Hasbro Children’s Hospital and an associate professor of pediatrics at Brown Medical School. Her latest book, “Take Charge of Your Child’s Sleep: The All-in-One Resource for Solving Sleep Problems in Children and Teens,” is especially important in light of the fact that 90% of the parents polled believed that their adolescents were getting enough sleep during the week.

“This poll sends a clear message to parents: Teens are tired,” says Owens. “Parents can help get a handle on the problem by eliminating sleep stealers such as caffeinated drinks in the fridge or a TV or computer in the teen’s bedroom as well as enforcing reasonable bed times.”

Last June, a major report in the journal Pediatrics merged a review of more than two decades of basic research with clinical advice for physicians. Rhode Island authors included Carskadon, Owens, and lead author, Richard Millman, MD, professor of medicine at Brown Medical School and director of the Sleep Disorders Center of Lifespan Hospitals, a Rhode Island sleep research and treatment center that is one of the largest in the country.

The report indicated that adolescents aged 13 to 22 need nine to 10 hours of sleep each night. It also discussed the hormonal changes that conspire against them. When puberty hits, the body’s production of sleep-inducing melatonin is delayed, making an early bedtime biologically impossible for most teens. At the same time, the report notes, external forces such as after-school sports and jobs and early school start times put the squeeze on a full night’s sleep.

The result: A “profound negative effect” on mood, school performance and cognitive function. Studies also show that young people between 16 and 29 years of age were the most likely to be involved in crashes caused by the driver falling asleep.

“Some of our kids are literally sleep-walking through life, with some potentially serious consequences,” Millman said. “As clinicians and researchers, we know more now than ever about the biological and behavioral issues that prevent kids from getting enough sleep. But the National Sleep Foundation did something powerful: They asked teens themselves about their sleep. The results are startling and should be a wake-up call to any parent or pediatrician.”

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Article adapted by MD Only Weblog from original press release.
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Contact: Carol Lin Vieira
Lifespan

The first investigation of developmental sleep duration patterns throughout childhood shows that children just beginning school and who get little sleep are more likely to have behavioral and cognitive problems in the classroom, according to a study published in the September 1 issue of the journal SLEEP.

The study, authored by Jacques Montplaisir, MD, of the Sleep Disorders Center at Sacre-Coeur Hospital in Montreal, Quebec, Canada, focused on 1,492 children, who were studied annually from five months of age to six years. A questionnaire, filled out by the children’s mothers, measured each child’s hyperactivity-impulsivity (HI), inattention and daytime sleepiness scores for each of those years.

Four developmental sleep duration patterns were identified in the study: short persistent (six percent), composed of children sleeping less than 10 hours per night until the age of 6 years; short increasing (4.8 percent), composed of children who slept fewer hours in early childhood but whose sleep duration increased around 41 months of age; 10-hour persistent (50.3 percent), composed of children who slept persistently approximately 10 hours per night; and 11-hour persistent (38.9 percent), composed of children who slept persistently around 11 hours each night.

According to Dr. Montplaisir, the study found no difference in sleep duration between weekdays and weekends, indicating that children were not compensating on the weekend for sleep loss occurring during the week, even in the group of short persistent sleepers. Short increasing sleepers, who had evidence of a nocturnal sleep consolidation problem before the age of 41 months, did not compensate their short nighttime sleep duration by more daytime sleep at 29 months, added Dr. Montplaisir.

The results indicate that a modest but chronic reduction of just one hour of sleep nightly in early childhood can affect the child’s cognitive performance at school entry. Short sleep duration multiplied by 3.1 the risk of low performance on the Peabody Picture Vocabulary Test–Revised. This suggests that language acquisition and the consolidation of new words into memory could be significantly impeded by chronically shortened sleep duration throughout childhood, said Dr. Montplaisir. Low performance on the Block Design subtest was also observed in the short increasing sleep group. This means that, although sleep duration improved at three years of age, the risk of scoring low on the Block Design subtest at six years of age remained more than 2.4 times higher. This finding points to an early critical period for cognitive development that may be jeopardized by short sleep duration, noted Dr. Montplaisir.

The results also demonstrate a significant relationship between high HI scores at six years of age and a short increasing sleep duration pattern. Although sleep duration improved at three years of age, the risk for high HI scores at six years of age remained 3.2 times higher. There is a critical period in early childhood where the lack of sleep is particularly detrimental on various aspects of development even if the sleep duration normalizes later on, warned Dr. Montplaisir.

“The results of this paper highlight the importance of giving a child the opportunity to sleep at least 10 hours a night throughout childhood, especially before the age of three-and-a-half years, to ensure optimal cognitive performance at school entry,” said Dr. Montplaisir.

It is recommended that children in pre-school sleep between 11-13 hours a night, and school-aged children between 10-11 hours of sleep a night.

The American Academy of Sleep Medicine (AASM) advises children to follow these steps to get a good night’s sleep:

  • Follow a consistent bedtime routine.
  • Establish a relaxing setting at bedtime.
  • Get a full night’s sleep every night.
  • Avoid foods or drinks that contain caffeine, as well as any medicine that has a stimulant, prior to bedtime.
  • Do not go to bed hungry, but don’t eat a big meal before bedtime either.
  • The bedroom should be quiet, dark and a little bit cool.
  • Get up at the same time every morning.

Parents who suspect that their child might be suffering from a sleep disorder are encouraged to consult with their child’s pediatrician or a sleep specialist.

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Article adapted by MD Only Weblog from original press release.
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Contact: Jim Arcuri
American Academy of Sleep Medicine

SLEEP is the official journal of the Associated Professional Sleep Societies, LLC, a joint venture of the AASM and the Sleep Research Society.

SleepEducation.com, a Web site maintained by the AASM, provides information about various sleep disorders, the forms of treatment available, recent news on the topic of sleep, sleep studies that have been conducted and a listing of sleep facilities.

Older men with lower levels of free, or unbound, testosterone circulating in their bloodstreams could be at higher risk of developing Alzheimer’s disease (AD) than their peers, according to new research. This prospective observational study is believed to be the first to associate low circulating blood levels of free testosterone with AD years before diagnosis.

The study appears in the January 27, 2004 issue of the journal Neurology. This work was conducted by investigators at the National Institute on Aging (NIA), one of the National Institutes of Health, and scientists at other institutions supported by NIA grants.*

“Our finding that low free testosterone might be associated with an increased risk of developing of AD is a step forward in helping to understand the possible effects of sex hormones on the aging brain and other parts of the body,” said Susan Resnick, Ph.D., an investigator in the NIA’s Laboratory of Personality and Cognition and corresponding author of the study.

Dr. Resnick, however, cautions that much more research is needed before scientists can establish a causal relationship between low testosterone and AD. “Even if a relationship between AD and levels of free testosterone in the bloodstream is confirmed, we are very far away from knowing if hormonal therapy or any other intervention could safely prevent AD,” she said.

Dr. Resnick, Scott Moffat, Ph.D., and their colleagues evaluated the testosterone levels of 574 men, ages 32 to 87, who participated in the Baltimore Longitudinal Study of Aging (BLSA)**. The investigators examined free and total testosterone levels — measured over an average of 19 years — in relationship to subsequent diagnosis of AD. Based on physical, neurological and neuropsychological exams, 54 of the 574 men were diagnosed with AD.

The research team found that for every 50 percent increase in the free testosterone index in the bloodstream, there was about a 26 percent decrease in the risk of developing AD. Although overall free testosterone levels fell over time, these levels dropped more precipitously in those men who later developed AD. In fact, at the end of the study, men who were diagnosed with AD, on average, had about half the levels of circulating free testosterone as men who didn’t develop the disease. In some cases, the drop-offs in free testosterone levels associated with AD were detected up to a decade before diagnosis.

Previously, Dr. Resnick and her colleagues found that older men with high levels of circulating free testosterone have better visual and verbal memory and perform spatial tasks more adeptly than their peers.

“It is quite possible that circulating free testosterone has a broad range of influences on the aging brain,” Dr. Resnick said. “The effects of some of these influences — such as the role of testosterone in the development of certain types of memory loss and AD — are just beginning to be explored.”

In men, testosterone is produced in the testes, the reproductive glands that also produce sperm. As men age, their testes often produce somewhat less testosterone than they did during adolescence and early adulthood, when production of this hormone peaks. Within the body, testosterone tends to bind with sex hormone binding globulin (SHBG). But some testosterone remains freely circulating in the bloodstream. Unlike the SHBG-bound form of the hormone, free testosterone can circulate into the brain and affect nerve cells. In this study, only reduced levels of free testosterone were associated with AD, Dr. Resnick said.

Other BLSA studies suggest that many men older than 70 have low levels of free testosterone compared to younger men. But while prescription testosterone replacement therapy is available, it may not be advisable for most older men because many effects of hormone therapy remain unclear. It is not yet known, for instance, if testosterone replacement increases the risk of prostate cancer, the second leading cause of cancer death among men. In addition, studies suggest that in some men testosterone therapy might trigger excessive red blood cell production. This side effect can thicken blood and increase a man’s risk of stroke.

“We still have much to learn,” Dr. Resnick said. “For now, testosterone therapy should not be considered an option for older men seeking to reduce their risk of Alzheimer’s disease or to improve their memory and cognitive performance in general.”

A multi-disciplinary panel, led by the Institute of Medicine (IOM) and supported by the National Institute on Aging (NIA) and the National Cancer Institute, recently evaluated the pros and cons of conducting clinical trials of testosterone replacement therapy in older men to answer many of the lingering questions about the effects of this hormone in the aging body. The NIA is considering the IOM recommendations very carefully and likely will act on the recommendations to begin small-scale clinical trials to determine the efficacy of testosterone in treating symptomatic older men with low testosterone levels. Until carefully designed and monitored clinical trials are conducted, the risks and benefits of testosterone therapy for most men who do not have extreme deficiencies of the hormone will remain largely unknown.

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Article adapted by MD Only Weblog from original press release.
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Contact: Doug Dollemore
National Institute on Aging (NIA)

AD is an irreversible disorder of the brain, robbing those who have it of memory, and eventually, overall mental and physical function, leading to death. For more information on AD research, two new publications are available from the NIA: 2001-2002 Alzheimer’s Disease Progress Report and Alzheimer’s Disease: Unraveling the Mystery, which includes a CD-Rom animation of what happens to the brain in AD. These publications may be viewed at NIA’s AD-dedicated website www.alzheimers.org, the Institute’s Alzheimer’s Disease Education and Referral (ADEAR) Center, or by calling ADEAR at 1-800-438-4380.

The NIA, one of 27 Institutes and Centers that constitute the National Institutes of Health, leads Federal efforts to support and conduct basic, clinical, epidemiological, and social research on aging and the special needs of older people. For more information about the NIA, visit the website at http://www.nia.nih.gov/.

Eating chocolate could help to sharpen up the mind and give a short-term boost to cognitive skills, a University of Nottingham expert has found.

A study led by Professor Ian Macdonald found that consumption of a cocoa drink rich in flavanols — a key ingredient of dark chocolate — boosts blood flow to key areas of the brain for two to three hours.

Increased blood flow to these areas of the brain may help to increase performance in specific tasks and boost general alertness over a short period.

The findings, unveiled at one of the biggest scientific conferences in America, also raise the prospect of ingredients in chocolate being used to treat vascular impairment, including dementia and strokes, and thus for maintaining cardiovascular health.

The study also suggests that the cocoa flavanols found in chocolate could be useful in enhancing brain function for people fighting fatigue, sleep deprivation, and even the effects of ageing.

Ian Macdonald, professor of metabolic physiology at The University of Nottingham, used magnetic resonance imaging (MRI) to detect increased activity in specific areas of the brain in individuals who had consumed a single drink of flavanol-rich cocoa. The effect is linked to dilation of cerebral blood vessels, allowing more blood — and therefore more oxygen — to reach key areas of the brain.

Flavanols are not only found in chocolate with a high cocoa content — they are also present in other substances such as red wine, green tea and blueberries.

He presented his research at the annual meeting of the American Association for the Advancement of Science (AAAS), one of the biggest annual gatherings of scientists from all over the world. This year’s meeting takes place in San Francisco from February 15–19.

Professor Macdonald said: “Acute consumption of this particular flavanol-rich cocoa beverage was associated with increased grey matter flow for two to three hours.

“The demonstration of an effect of consuming this particular beverage on cerebral blood flow raises the possibility that certain food ingredients may be beneficial in increasing brain blood flow and enhancing brain function, in situations where individuals are cognitively impaired such as fatigue, sleep deprivation, or possibly ageing.”

He emphasised that the level of cocoa flavanol used in the study is not available commercially. The cocoa-rich flavanol beverage was specially formulated for the purpose of the study.

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Article adapted by MD Only Weblog from original press release.
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Contact: Ian Macdonald
University of Nottingham

Co-authors on the research were Dr Susan Francis, research associate Kay Head, and Professor Peter Morris, all from The University of Nottingham’s School of Physics and Astronomy.

Professor Macdonald is a member of the Food Standards Agency’s Scientific Advisory Committee on Nutrition, and is President-Elect of the UK Nutrition Society. His main research interests are concerned with the functional consequences of metabolic and nutritional disturbances in health and disease, with specific interests in obesity, diabetes, cardiovascular disease and exercise.

Older men with higher levels of free, or unbound, testosterone circulating in their bloodstreams have better visual and verbal recall and perform spatial tasks more adeptly than their peers, according to investigators at the National Institute on Aging (NIA). The study* identifies a potential biological factor that one day could be used to protect against decline in memory and other cognitive skills in later life.

“Although we can’t firmly establish a causal relationship without further study, this finding suggests that there may be hormonal modulation of cognitive abilities as people get older. Clearly, having higher levels of circulating free testosterone is associated with a reduced risk of certain types of memory loss,” said Susan Resnick, Ph.D., an investigator in the NIA’s Laboratory of Personality and Cognition, and corresponding author of the study, published in the November 2002 issue of The Journal of Clinical Endocrinology & Metabolism.

Dr. Resnick, Scott Moffat, Ph.D., and their colleagues evaluated the testosterone levels of 407 men, ages 50 and older, who participated in the Baltimore Longitudinal Study of Aging (BLSA)**. The investigators then correlated free and total testosterone levels—measured over an average of 10 years—with the men’s performances on memory and other cognitive tests.

In the body, testosterone tends to bind with sex hormone binding gobulin (SHBG). But some testosterone remains freely circulating in the bloodstream. Unlike the SHBG-bound form of the hormone, free testosterone can circulate into the brain and affect nerve cells, Dr. Resnick said. Total testosterone is a measure of both free and SHBG-bound forms of the hormone. Of these measures, only free testosterone was significantly associated with higher scores on verbal and visual memory tests, such as recalling word lists and drawing a recently seen image. Free testosterone was also linked to high scores on a spatial test in which participants were asked to determine if rotated shapes were the same or different. 

“Based on our results, testosterone levels are associated with selective and very specific effects on some aspects of cognition, including memory,” Dr. Resnick said.

In men, testosterone is produced in the testes, the reproductive glands that also produce sperm. As men age, their testes often produce somewhat less testosterone than they did during adolescence and early adulthood, when production of this hormone peaks.

Based on BLSA data, as many as 68 percent of men older than 70 have low levels of free testosterone. But while prescription testosterone replacement therapy is available, it may not be advisable for most older men because many effects of hormone supplementation remain unclear. It is not yet known, for instance, if testosterone replacement increases the risk of prostate cancer, the second leading cause of cancer death among men. In addition, studies suggest that supplementation might trigger excessive red blood cell production in some men. This side effect can thicken blood and increase a man’s risk of stroke.

“We still have much to learn,” Dr. Resnick said. “Until we know much more about the fundamental effects of sex hormones on the aging brain and other parts of the body, testosterone supplementation is not a prudent choice for older men seeking to improve their memory and cognitive performance.”

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Article adapted by MD Only Weblog from original NIA news release.
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The National Institute on Aging, one of 27 Institutes and Centers that constitute the National Institutes of Health, leads Federal efforts to support and conduct basic, clinical, epidemiological, and social research on aging and the special needs of older people. For more information about the NIA, visit the website at www.nia.nih.gov.

* S.D. Moffat, A.B. Zonderman, E.J. Metter, M.R. Blackman, S.M. Harman, and S.M. Resnick, “Longitudinal Assessment of Serum Free Testosterone Concentration Predicts Memory Performance and Cognitive Status in Elderly Men,” The Journal of Clinical Endocrinology & Metabolism, 2002; 87 (11): 5001-5007.

** Launched in 1958, the BLSA is America’s longest running scientific examination of human aging. Volunteers receive comprehensive medical, physiological and neuropsychological evaluations every two years at the NIA Gerontology Research Center in Baltimore. The BLSA has measured testosterone levels in its male participants since 1963.

Omega-3 fatty acids have long been touted for their heart-healthy and brain-boosting benefits. Consider cod liver oil, fortified infant formula and enriched eggs.Now a study of nearly 1,800 children at risk for type 1 diabetes has found that increased consumption of dietary omega-3 fatty acids appears to reduce the risk of the body attacking its own insulin-producing cells, a precursor to this form of the disease, report researchers at the University of Colorado and the University of Florida.

The findings appear in the Sept. 26 issue of the Journal of the American Medical Association.

In the past few decades, there has been a dramatic rise in the incidence of type 1 diabetes, both in the United States and in Europe — a jump that coincides with changes in food manufacturing that have led to a decline in omega-3 fatty acids in the diet and an increase in the content of omega-6 fatty acids, said Dr. Michael Clare-Salzler, a professor and the Stetson chair in experimental pathology at the University of Florida College of Medicine.

“The foods we are eating now are qualitatively much different than those produced on a 1900s-era farm,” Clare-Salzler said. “When animals are commercially raised today, they are often fed grains rich in omega-6 fatty acids, fatty acids that can promote inflammation. In the old days, animals received a much more balanced intake of omega-3 and omega 6-fatty acids.”

The amount of omega-3 fatty acids found in food today has dropped 28-fold from 100 years ago, Clare-Salzler said. In contrast to the omega-6 variety, omega-3 fatty acids have potent anti-inflammatory effects.

“Animal studies have shown inflammation in the insulin-producing cells of the pancreas is an early event that leads to type 1 diabetes,” said Clare-Salzler, who also directs UF’s Center for Immunology and Transplantation. “From these studies in mice, it appears if you thwart inflammation you can prevent the disease from occurring. The human parallel in this study indicates that higher dietary intake of anti-inflammatory omega-3 fatty acids reduces the risk of developing an immune response to the insulin-producing cells.”

Scientists set out to study whether increased intake of omega-3 fatty acids would be associated with prevention of or delay in the emergence of autoantibodies in the blood that signal the immune system’s attack on insulin-producing cells. Children enrolled in the Denver-based Diabetes Autoimmunity Study in the Young, or DAISY, were all at increased risk for type 1 diabetes and were evaluated until they were, on average, 6 years old.

Their parents were asked annually to report what they ate, including how often they consumed canned tuna, dark-meat fish such as salmon, other fish, shrimp, lobster and scallops, and also what kind of fat was used in cooking. Blood samples also were taken to test study participants for the presence of autoantibodies, and Nancy J. Szabo, director of the Analytical Toxicology Core Laboratory at UF’s College of Veterinary Medicine, evaluated the fatty acid composition of red blood cell membranes isolated from blood samples taken from a subset of 244 children.

“Kids who had higher intakes of omega-3 fatty acids had a significant reduction in the risk of development of autoantibodies,” Clare-Salzler said, adding that the risk of developing the autoantibodies also went down as the concentration of omega-3 fatty acids rose in the red blood cells.

All fatty acids help bolster the structure and function of cell membranes, but omega-3 fatty acids strongly support the production of anti-inflammatory molecules than can quell an immune attack on insulin-producing cells, Clare-Salzler said.

The study’s lead author was Jill M. Norris, a professor of preventive medicine and biometrics at the University of Colorado at Denver’s School of Medicine. Funding came from the National Institutes of Health and the University of Colorado’s Diabetes Endocrine Research Center.

UF and University of Colorado researchers are continuing to explore links between diabetes and diet. Clare-Salzler and Peter Chase from the University of Colorado’s Barbara Davis Center for Childhood Diabetes are leading a National Institutes of Health-funded multicenter pilot trial, the Nutritional Intervention to Prevent Type 1 Diabetes, or NIP, to examine whether babies who receive dietary supplementation with the omega-3 fatty acid docosohexaenoic acid, or DHA, show fewer signs of inflammation. An expanded version of the trial will then determine whether DHA protects infants and children from the development of autoantibodies that lead to diabetes in comparison with babies who receive standard formula or diets with a much lower level of the omega-3 fatty acid.

If the trial confirms the hypothesis that dietary supplementation with DHA in infancy blocks early inflammatory events key to diabetes development, then, the authors write in JAMA, “dietary supplementation with omega-3 fatty acids could become a mainstay for early intervention to safely prevent the development of type 1 diabetes.”

“The compounds that are made from the omega-3s are natural, the body’s own protective mechanisms for overt inflammation,” said Dr. Charles Serhan, director of the Center for Experimental Therapeutics and Reperfusion Injury at Harvard Medical School. “What these results say is that you may now be able to add back through the diet these essential omega-3 fatty acids, and then they will be utilized by the body to generate its own set of protective molecules that help to instruct the immune cells in the local environment not to attack the insulin-producing islets cells in the pancreas … these are very powerful and potentially very important results.”

Source: Melanie Fridl Ross, ufcardiac@aol.com 

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