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Sprycel helps inhibiting ovraian cancer cell growth
The drug Sprycel, approved for use by the U.S. Food and Drug Administration in patients with chronic myeloid leukemia, significantly inhibited the growth and invasiveness of ovarian cancer cells and also promoted their death, a study by researchers with UCLA's Jonsson Comprehensive Cancer Center found.The drug, when paired with a chemotherapy regimen, was even more effective in fighting ovarian cancer in cell lines in which signaling of the Src family kinases, associated with the deadly disease, is activated.
The study appears in the Nov. 10, 2009 edition of the British Medical Journal.
Ovarian cancer, which will strike 21,600 women this year and kill 15,500, causes more deaths than any other cancer of the female reproductive system. Few effective therapies for ovarian cancer exist, so it would be advantageous for patients if a new drug could be found that fights the cancer, said Gottfried Konecny, an assistant professor of hematology/oncology, a Jonsson Cancer Center researcher and first author of the study.
"I think Sprycel could be a potential additional drug for treating patients with Src dependent ovarian cancer," Konecny said. "It is important to remember that this work is only on cancer cell lines, but it is significant enough that it should be used to justify clinical trials to confirm that women with this type of ovarian cancer could benefit."
Recent gene expression studies have shown that about one-third of women have ovarian cancers with activated Src pathways, so the drug could potentially help 7,000 ovarian cancer patients every year.
In this study, the UCLA team tested the drug against 34 ovarian cancer cell lines and they conducted genetic analysis on all cell lines. Through these analyses, the researchers were able to identify genes that predict response to Sprycel. If the work is confirmed in human studies, it may be possible to test patients for Src activation and select those who would respond prior to treatment, personalizing their care.
"We were able to identify markers in the pre-clinical setting that would allow us to predict response to Sprycel," Konecny said. "These may help us in future clinical trials in selecting patients for studies of the drug."
Sprycel is what is known as a "dirty" kinase inhibitor, meaning it inhibits more than one pathway. Konecny said it also inhibits the focal adhesion kinase and ephrin receptor, also associated with ovarian cancer.
The next step, Konecny said, would be to test the drug on women with ovarian cancer in a clinical trial. The tissue of responders would then be analyzed to determine if the Src and other pathways were activated. If that is confirmed, it would further prove that Sprycel could be used to fight ovarian cancer. In studies, women would be screened before entering a trial and only those with Src dependent cancers could be enrolled to provide further evidence, Konecny said, much like the studies of the molecularly targeted breast cancer drug Herceptin enrolled only women who had HER-2 positive disease.
"Herceptin is different because we knew in advance that the only worked in women with HER-2 amplification," he said. "In this case, we don't clearly know that yet. The data reassure us that the drug works where the targets are over-expressed but we need more testing to confirm this."
The tests combining the drug with chemotherapy are significant because chemotherapy currently is the first line treatment for ovarian cancer patients following surgery. Because Sprycel proved to have a synergistic effect when combined with chemotherapy -- both made the other work better -- it may be possible to add the targeted therapy as a first line treatment if its efficacy is confirmed in future studies, adding a new tool to an oncologist's arsenal.
Source: University of California - Los Angeles.
The study appears in the Nov. 10, 2009 edition of the British Medical Journal.
Ovarian cancer, which will strike 21,600 women this year and kill 15,500, causes more deaths than any other cancer of the female reproductive system. Few effective therapies for ovarian cancer exist, so it would be advantageous for patients if a new drug could be found that fights the cancer, said Gottfried Konecny, an assistant professor of hematology/oncology, a Jonsson Cancer Center researcher and first author of the study.
"I think Sprycel could be a potential additional drug for treating patients with Src dependent ovarian cancer," Konecny said. "It is important to remember that this work is only on cancer cell lines, but it is significant enough that it should be used to justify clinical trials to confirm that women with this type of ovarian cancer could benefit."
Recent gene expression studies have shown that about one-third of women have ovarian cancers with activated Src pathways, so the drug could potentially help 7,000 ovarian cancer patients every year.
In this study, the UCLA team tested the drug against 34 ovarian cancer cell lines and they conducted genetic analysis on all cell lines. Through these analyses, the researchers were able to identify genes that predict response to Sprycel. If the work is confirmed in human studies, it may be possible to test patients for Src activation and select those who would respond prior to treatment, personalizing their care.
"We were able to identify markers in the pre-clinical setting that would allow us to predict response to Sprycel," Konecny said. "These may help us in future clinical trials in selecting patients for studies of the drug."
Sprycel is what is known as a "dirty" kinase inhibitor, meaning it inhibits more than one pathway. Konecny said it also inhibits the focal adhesion kinase and ephrin receptor, also associated with ovarian cancer.
The next step, Konecny said, would be to test the drug on women with ovarian cancer in a clinical trial. The tissue of responders would then be analyzed to determine if the Src and other pathways were activated. If that is confirmed, it would further prove that Sprycel could be used to fight ovarian cancer. In studies, women would be screened before entering a trial and only those with Src dependent cancers could be enrolled to provide further evidence, Konecny said, much like the studies of the molecularly targeted breast cancer drug Herceptin enrolled only women who had HER-2 positive disease.
"Herceptin is different because we knew in advance that the only worked in women with HER-2 amplification," he said. "In this case, we don't clearly know that yet. The data reassure us that the drug works where the targets are over-expressed but we need more testing to confirm this."
The tests combining the drug with chemotherapy are significant because chemotherapy currently is the first line treatment for ovarian cancer patients following surgery. Because Sprycel proved to have a synergistic effect when combined with chemotherapy -- both made the other work better -- it may be possible to add the targeted therapy as a first line treatment if its efficacy is confirmed in future studies, adding a new tool to an oncologist's arsenal.
Source: University of California - Los Angeles.
Anxiety during pregnancy affects babies
A new study published in the journal Paediatric and Perinatal Epidemiology reveals that anxiety in pregnant women impacts their babies' size and gestational age. Specifically, women with more severe and chronic anxiety during pregnancy are more likely to have affected babies. Shahla M. Hosseini, Minhnoi W. Biglan, Cynthia Larkby, Maria M. Brooks, Michael B. Gorin, and Nancy L. Day studied a sample of low-income women, half of whom were African American and the other half Caucasian. The group already had well-known risk factors such as alcohol and cigarette use. The authors demonstrated that the mother's anxiety during pregnancy impacts birth outcomes over and beyond factors such as drug use, education, and race.
Anxiety during the third trimester predicted women delivering significantly smaller babies. In the first and second trimesters, the effects of anxiety were significant only among those women who had severe anxiety.
Low to moderate levels of anxiety in women during either the first or second trimester did not significantly affect the birth outcomes, but women who are severely anxious during much of their pregnancy should be considered for anxiety-reducing interventions.
"One way to prevent health problems in children and adults is to focus care on the prenatal period," the authors note. "It is key to pursue further research which addresses interventions to ameliorate the effects that a woman's trait anxiety has on the development of fetuses." Source: Wiley-Blackwell.
Anxiety during the third trimester predicted women delivering significantly smaller babies. In the first and second trimesters, the effects of anxiety were significant only among those women who had severe anxiety.
Low to moderate levels of anxiety in women during either the first or second trimester did not significantly affect the birth outcomes, but women who are severely anxious during much of their pregnancy should be considered for anxiety-reducing interventions.
"One way to prevent health problems in children and adults is to focus care on the prenatal period," the authors note. "It is key to pursue further research which addresses interventions to ameliorate the effects that a woman's trait anxiety has on the development of fetuses." Source: Wiley-Blackwell.
Powerful painkilling effect may contribute to overeating and obesity
People often eat food to feel better, but researchers have found that eating chocolate or drinking water can blunt pain, reducing a rat's response to a hot stimulus. This natural form of pain relief may help animals in the wild avoid distraction while eating scarce food, but in modern humans with readily available food, the effect may contribute to overeating and obesity.
The study, published in the Journal of Neuroscience by authors Peggy Mason, PhD, professor of neurobiology, and Hayley Foo, PhD, research associate professor of neurobiology at the University of Chicago, is the first to demonstrate that this powerful painkilling effect occurs while the animals are ingesting food or liquid even in the absence of appetite.
"It's a strong, strong effect, but it's not about hunger or appetite," Mason said. "If you have all this food in front of you that's easily available to reach out and get, you're not going to stop eating, for basically almost any reason."
In the experiments, rats were given either a chocolate chip to eat or had sugar water or regular water infused directly into their mouth. As the rat swallowed the chocolate or fluid, a light-bulb beneath the cage was switched on, providing a heat stimulus that normally caused the animal to lift its paw off the floor. Mason and Foo found that rats were much slower to raise their paw while eating or drinking, compared to tests conducted while they were awake, but not eating.
Surprisingly, the researchers found no difference in the delayed paw-lift response between when the rat was eating chocolate and when it was drinking water, despite previous research indicating that only sugary substances were protective against pain.
"This really shows it has nothing to do with calories," Mason said. "Water has no calories, saccharine has no sugar, but both have the same effect as a chocolate chip. It's really shocking."
Mason and Foo then repeated the heat test as the rats were given quinine, a bitter drink that causes rats to make an expression called a gape that's akin to a child's expression of "yuck." During quinine administration, the rats reacted to heat as quickly as when not eating, suggesting that a non-pleasurable food or drink fails to trigger pain relief.
The context of ingesting was also important to whether eating or drinking blunted pain, the researchers found. When rats were made ill by a drug treatment, eating chocolate no longer delayed their response. However, drinking water still caused a reduced pain response, indicating that drinking water was considered a positive experience while ill.
By selectively inactivating a region in the brainstem called the raphe mangus – an area previously shown to blunt pain during sleep and urination – Mason and Foo were able to remove the effect of drinking water on the rat's pain response. The brainstem controls subconscious responses such as breathing and perspiration during exercise.
"You're essentially at the mercy of your brainstem, and the raphe magnus is part of that," Mason said. "It tells you, 'you're going to finish eating this, whether you like it or not,' just like you sweat while running whether you like it or not."
In the wild, Mason said, rats and other animals would not want to be distracted during the rare but important times that they were able to eat or drink. Therefore, the activation of the raphe magnus during eating or drinking would allow the rat to filter out distractions until their meal was completed. For obvious reasons, this natural pain relief would be activated when an animal is eating or drinking something pleasurable, but not when it tastes something that could be toxic or harmful.
Don Katz, an associate professor of psychology and neuroscience at Brandeis University who studies taste, said that Mason and Foo's paper brings together two systems – taste and pain – that are usually studied separately.
"They're saying the purpose of the taste system is to give the animal a cue that helps it decide what stimulus they should or shouldn't pay attention to," Katz said. "This shows there is a whole region there to enable the animal to keep eating."
Mason believes that this effect is also present in humans (studies by other labs have observed similar pain reduction in infants receiving sugar water during a booster shot), but that it has detrimental effects in modern society given our ready access to large quantities of pleasurable and fattening foods. Opening up a bag of chips could activate the brainstem such that you don't stop eating until the bag is empty, even while realizing that such behavior is bad for you.
"We've gotten a lot more overweight in last 100 to 150 years," Mason said. "We're not more hungry; the fact of the matter is that we eat more because food is readily available and we are biologically destined to eat what's readily available."
But the painkilling effect can be turned to our advantage, Mason said, perhaps as a replacement for the practice of using candy to calm children – or even adults – in the doctor's office.
"Ingestion is a painkiller but we don't need the sugar," Mason said. "So replace the doctor's lollipop with a drink of water."
The research was funded by a grant from the National Institute on Drug Abuse and the Women's Council of the Brain Research Foundation. The paper, "Analgesia accompanying food consumption requires ingestion of hedonic foods," appears in the October 14th issue of the Journal of Neuroscience.
Source: University of Chicago Medical Center.
The study, published in the Journal of Neuroscience by authors Peggy Mason, PhD, professor of neurobiology, and Hayley Foo, PhD, research associate professor of neurobiology at the University of Chicago, is the first to demonstrate that this powerful painkilling effect occurs while the animals are ingesting food or liquid even in the absence of appetite.
"It's a strong, strong effect, but it's not about hunger or appetite," Mason said. "If you have all this food in front of you that's easily available to reach out and get, you're not going to stop eating, for basically almost any reason."In the experiments, rats were given either a chocolate chip to eat or had sugar water or regular water infused directly into their mouth. As the rat swallowed the chocolate or fluid, a light-bulb beneath the cage was switched on, providing a heat stimulus that normally caused the animal to lift its paw off the floor. Mason and Foo found that rats were much slower to raise their paw while eating or drinking, compared to tests conducted while they were awake, but not eating.
Surprisingly, the researchers found no difference in the delayed paw-lift response between when the rat was eating chocolate and when it was drinking water, despite previous research indicating that only sugary substances were protective against pain.
"This really shows it has nothing to do with calories," Mason said. "Water has no calories, saccharine has no sugar, but both have the same effect as a chocolate chip. It's really shocking."
Mason and Foo then repeated the heat test as the rats were given quinine, a bitter drink that causes rats to make an expression called a gape that's akin to a child's expression of "yuck." During quinine administration, the rats reacted to heat as quickly as when not eating, suggesting that a non-pleasurable food or drink fails to trigger pain relief.
The context of ingesting was also important to whether eating or drinking blunted pain, the researchers found. When rats were made ill by a drug treatment, eating chocolate no longer delayed their response. However, drinking water still caused a reduced pain response, indicating that drinking water was considered a positive experience while ill.
By selectively inactivating a region in the brainstem called the raphe mangus – an area previously shown to blunt pain during sleep and urination – Mason and Foo were able to remove the effect of drinking water on the rat's pain response. The brainstem controls subconscious responses such as breathing and perspiration during exercise.
"You're essentially at the mercy of your brainstem, and the raphe magnus is part of that," Mason said. "It tells you, 'you're going to finish eating this, whether you like it or not,' just like you sweat while running whether you like it or not."
In the wild, Mason said, rats and other animals would not want to be distracted during the rare but important times that they were able to eat or drink. Therefore, the activation of the raphe magnus during eating or drinking would allow the rat to filter out distractions until their meal was completed. For obvious reasons, this natural pain relief would be activated when an animal is eating or drinking something pleasurable, but not when it tastes something that could be toxic or harmful.
Don Katz, an associate professor of psychology and neuroscience at Brandeis University who studies taste, said that Mason and Foo's paper brings together two systems – taste and pain – that are usually studied separately.
"They're saying the purpose of the taste system is to give the animal a cue that helps it decide what stimulus they should or shouldn't pay attention to," Katz said. "This shows there is a whole region there to enable the animal to keep eating."
Mason believes that this effect is also present in humans (studies by other labs have observed similar pain reduction in infants receiving sugar water during a booster shot), but that it has detrimental effects in modern society given our ready access to large quantities of pleasurable and fattening foods. Opening up a bag of chips could activate the brainstem such that you don't stop eating until the bag is empty, even while realizing that such behavior is bad for you.
"We've gotten a lot more overweight in last 100 to 150 years," Mason said. "We're not more hungry; the fact of the matter is that we eat more because food is readily available and we are biologically destined to eat what's readily available."
But the painkilling effect can be turned to our advantage, Mason said, perhaps as a replacement for the practice of using candy to calm children – or even adults – in the doctor's office.
"Ingestion is a painkiller but we don't need the sugar," Mason said. "So replace the doctor's lollipop with a drink of water."
The research was funded by a grant from the National Institute on Drug Abuse and the Women's Council of the Brain Research Foundation. The paper, "Analgesia accompanying food consumption requires ingestion of hedonic foods," appears in the October 14th issue of the Journal of Neuroscience.
Source: University of Chicago Medical Center.
Fish consumption have no effect on heart failure
All these years we were under the impression that consumption of fish would help humans in better heart health, but new study has shown that its not real. Study done showed that there is no difference in heart failures or health between the people who consume fish regularly and those who don't. I personally feel this depends on the fish they consume.
The study is published on 30 September in the October issue of the European Journal of Heart Failure.
"Scientists and health authorities are increasingly persuaded that the intake of fish - even in small amounts - will protect against the risk of fatal myocardial infarction," said study investigator Dr Marianne Geleinjse from Wageningen University in the Netherlands. "However, there is no strong evidence that eating fish will protect against heart failure. One study has suggested that this might be so, but we could not confirm it in our cohort study of older Dutch people."
Heart failure is by far today's single biggest reason for acute hospital admission. Around 30 million people in Europe have heart failure and its incidence is still increasing: more cases are being identified, more people are living to an old age, and more are surviving a heart attack but with damage to the heart muscle. According to one study, the reported prevalence among those aged 65-74 years is one in 35, and among the over-85s one in seven.
According to background information to the study, the lifetime risk of developing heart failure is even higher - estimated in men and women as one in four at age 40. The risks increase with age, and prognosis is poor; a previous report from the same Rotterdam Study has shown survival rates at one, two and five years of 89%, 79%, and 59%, representing an age-adjusted mortality rate twice that of those without heart failure. The hazard ratio for sudden death was found to be almost five times higher.
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With heart failure treatments often limited to palliative care, much rests on prevention; this latest report from the Rotterdam Study was to investigate whether intake of the long-chain n-3 polyunsaturated fatty acids (PUFAs) found in fish conferred protection against heart failure as they seem to do against coronary heart disease.*
The analysis comprised 5299 subjects (41% men, mean age 67.5 years) who were free from heart failure and for whom dietary data were available. During 11.4 years of follow-up, 669 subjects developed heart failure. Their habitual diet had been assessed at baseline (in a self-reported checklist and by expert interview), with subjects specifically asked to indicate the frequency, amount, and kind of fish they had eaten, either as a hot meal, on a sandwich, or between meals.
Results showed that the dietary intake of fish was not significantly related to heart failure incidence. This relative risk was measured according to five levels of fish consumption as reflected in intake of two long chain n-3 PUFAs (eicosapentaenoic acid [EPA] and docosahexaenoic acid [DHA]), both of which have been shown to exert some cardiovascular benefit via anti-inflammatory mechanisms, anti-arrhythmic effects and/or a reduction in serum triglycerides, blood pressure, and heart rate.
The relative risk (RR) of heart failure in the top (highest) and bottom (lowest) quintile of EPA plus DHA intake was 0.89 (95% CI, 0.69��.14) after adjustment for lifestyle and dietary factors, a non-significant finding.
Results were also estimated according to the weight of fish consumed; but even for a high daily fish consumption of more than 20 grams a day there appeared no added protection against heart failure. Incidence rates were the same in those who consumed no fish (incidence rate of 11 per 1000), moderate fish (median 9g per day, 12.3 per 1000) or high fish (9.9 per 1000). The relative risk of heart failure in the high intake groups was 0.96 (0.78��.18) when compared with no intake.
Variations in risk were seen in various sub-groups according to age, sex and body mass index (BMI), but once again the differences were not statistically significant. In diabetic subjects, however, an inverse association of EPA plus DHA intake with heart failure was observed (RR 0.58 (0.32��.06) for top vs. bottom quartile), which was just of borderline statistical significance. Similarly, a high EPA plus DHA intake tended to be protective (but not statistically significant) in women (RR 0.75, 0.54��.04), although not in men.
Commenting on the public health implications of the study Dr Geleijnse said: "Many health authorities recommend two weekly servings of fish - particularly fatty fish like salmon, mackerel and herring - for the prevention of cardiovascular disease. Based on our data we would not change this advice, even though fish intake was not associated with the development of heart failure in our cohort. Fish intake in the Netherlands is extremely low - on average less than one portion per week - so maybe higher intakes are needed for any protection against heart failure.
"Apart from n-3 fatty acids, fish also contains other healthy components such as vitamin D and selenium. Fish is a good source of protein and is more healthy than, for example, red meat."
According to the authors this is only the second ever study to examine the relationship between PUFAs and the risk of heart failure; the other, over 12 years of follow-up among older adults, did find that consumption of tuna or other broiled or baked fish (but not fried fish) was associated with a lower incidence of heart failure.
*There has been fairly consistent evidence that n-3 PUFAs do have a protective effect against coronary heart disease since the first suggestions were made more than 30 years ago following studies in the Inuit people of Greeneland. More recently, a 2009 review in the Journal of the American College of Cardiology, whose evidence was based mainly on four randomised trials involving nearly 40,000 subjects, described the effect of n-3 PUFAs in the prevention of cardiovascular disease as "of great promise". The GISSI-Prevenzione trial of 1999 established the potential of dietary n-3 PUFAs for reducing mortality in patients after recent myocardial infarction. The effect on coronary heart disease mortality of n-3 PUFAs as a supplement post-infarction is presently being studied in the Alpha Omega trial in the Netherlands. Source :European Society of Cardiology.
The study is published on 30 September in the October issue of the European Journal of Heart Failure.
"Scientists and health authorities are increasingly persuaded that the intake of fish - even in small amounts - will protect against the risk of fatal myocardial infarction," said study investigator Dr Marianne Geleinjse from Wageningen University in the Netherlands. "However, there is no strong evidence that eating fish will protect against heart failure. One study has suggested that this might be so, but we could not confirm it in our cohort study of older Dutch people."
Heart failure is by far today's single biggest reason for acute hospital admission. Around 30 million people in Europe have heart failure and its incidence is still increasing: more cases are being identified, more people are living to an old age, and more are surviving a heart attack but with damage to the heart muscle. According to one study, the reported prevalence among those aged 65-74 years is one in 35, and among the over-85s one in seven.
According to background information to the study, the lifetime risk of developing heart failure is even higher - estimated in men and women as one in four at age 40. The risks increase with age, and prognosis is poor; a previous report from the same Rotterdam Study has shown survival rates at one, two and five years of 89%, 79%, and 59%, representing an age-adjusted mortality rate twice that of those without heart failure. The hazard ratio for sudden death was found to be almost five times higher.
Get 30 softgels of high quality omega 3's that are priceless from No.1 company Nutrilite.
With heart failure treatments often limited to palliative care, much rests on prevention; this latest report from the Rotterdam Study was to investigate whether intake of the long-chain n-3 polyunsaturated fatty acids (PUFAs) found in fish conferred protection against heart failure as they seem to do against coronary heart disease.*
The analysis comprised 5299 subjects (41% men, mean age 67.5 years) who were free from heart failure and for whom dietary data were available. During 11.4 years of follow-up, 669 subjects developed heart failure. Their habitual diet had been assessed at baseline (in a self-reported checklist and by expert interview), with subjects specifically asked to indicate the frequency, amount, and kind of fish they had eaten, either as a hot meal, on a sandwich, or between meals.
Results showed that the dietary intake of fish was not significantly related to heart failure incidence. This relative risk was measured according to five levels of fish consumption as reflected in intake of two long chain n-3 PUFAs (eicosapentaenoic acid [EPA] and docosahexaenoic acid [DHA]), both of which have been shown to exert some cardiovascular benefit via anti-inflammatory mechanisms, anti-arrhythmic effects and/or a reduction in serum triglycerides, blood pressure, and heart rate.
The relative risk (RR) of heart failure in the top (highest) and bottom (lowest) quintile of EPA plus DHA intake was 0.89 (95% CI, 0.69��.14) after adjustment for lifestyle and dietary factors, a non-significant finding.
Results were also estimated according to the weight of fish consumed; but even for a high daily fish consumption of more than 20 grams a day there appeared no added protection against heart failure. Incidence rates were the same in those who consumed no fish (incidence rate of 11 per 1000), moderate fish (median 9g per day, 12.3 per 1000) or high fish (9.9 per 1000). The relative risk of heart failure in the high intake groups was 0.96 (0.78��.18) when compared with no intake.
Variations in risk were seen in various sub-groups according to age, sex and body mass index (BMI), but once again the differences were not statistically significant. In diabetic subjects, however, an inverse association of EPA plus DHA intake with heart failure was observed (RR 0.58 (0.32��.06) for top vs. bottom quartile), which was just of borderline statistical significance. Similarly, a high EPA plus DHA intake tended to be protective (but not statistically significant) in women (RR 0.75, 0.54��.04), although not in men.
Commenting on the public health implications of the study Dr Geleijnse said: "Many health authorities recommend two weekly servings of fish - particularly fatty fish like salmon, mackerel and herring - for the prevention of cardiovascular disease. Based on our data we would not change this advice, even though fish intake was not associated with the development of heart failure in our cohort. Fish intake in the Netherlands is extremely low - on average less than one portion per week - so maybe higher intakes are needed for any protection against heart failure.
"Apart from n-3 fatty acids, fish also contains other healthy components such as vitamin D and selenium. Fish is a good source of protein and is more healthy than, for example, red meat."
According to the authors this is only the second ever study to examine the relationship between PUFAs and the risk of heart failure; the other, over 12 years of follow-up among older adults, did find that consumption of tuna or other broiled or baked fish (but not fried fish) was associated with a lower incidence of heart failure.
*There has been fairly consistent evidence that n-3 PUFAs do have a protective effect against coronary heart disease since the first suggestions were made more than 30 years ago following studies in the Inuit people of Greeneland. More recently, a 2009 review in the Journal of the American College of Cardiology, whose evidence was based mainly on four randomised trials involving nearly 40,000 subjects, described the effect of n-3 PUFAs in the prevention of cardiovascular disease as "of great promise". The GISSI-Prevenzione trial of 1999 established the potential of dietary n-3 PUFAs for reducing mortality in patients after recent myocardial infarction. The effect on coronary heart disease mortality of n-3 PUFAs as a supplement post-infarction is presently being studied in the Alpha Omega trial in the Netherlands. Source :European Society of Cardiology.
Its easy to loose muscle than building it
Have you ever noticed that people have thinner arms and legs as they get older? As we age it becomes harder to keep our muscles healthy. They get smaller, which decreases strength and increases the likelihood of falls and fractures. New research is showing how this happens — and what to do about it.
A team of Nottingham researchers has already shown that when older people eat, they cannot make muscle as fast as the young. Now they’ve found that the suppression of muscle breakdown, which also happens during feeding, is blunted with age.
The scientists and doctors at The University of Nottingham Schools of Graduate Entry Medicine and Biomedical Sciences believe that a ‘double whammy’ affects people aged over 65. However the team think that weight training may “rejuvenate” muscle blood flow and help retain muscle for older people.
These results may explain the ongoing loss of muscle in older people: when they eat they don’t build enough muscle with the protein in food; also, the insulin (a hormone released during a meal) fails to shut down the muscle breakdown that rises between meals and overnight. Normally, in young people, insulin acts to slow muscle breakdown. Common to these problems may be a failure to deliver nutrients and hormones to muscle because of a poorer blood supply.
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The work has been done by Michael Rennie, Professor of Clinical Physiology, and Dr Emilie Wilkes, and their colleagues at The University of Nottingham. The research was funded by the UK’s Biotechnology and Biological Sciences Research Council (BBSRC) as part of ongoing work on age-related muscle wasting and how to lessen that effect.
Research just published in The American Journal of Clinical Nutrition compared one group of people in their late 60s to a group of 25-year-olds, with equal numbers of men and women. Professor Rennie said “We studied our subjects first — before breakfast — and then after giving them a small amount of insulin to raise the hormone to what they would be if they had eaten breakfast, of a bowl of cornflakes or a croissant.”
“We tagged one of the amino acids (from which proteins are made) so that we could discover how much protein in leg muscle was being broken down. We then compared how much amino acid was delivered to the leg and how much was leaving it, by analysing blood in the two situations.
“The results were clear. The younger people’s muscles were able to use insulin we gave to stop the muscle breakdown, which had increased during the night. The muscles in the older people could not.”
“In the course of our tests, we also noticed that the blood flow in the leg was greater in the younger people than the older ones,” added Professor Rennie. “This set us thinking: maybe the rate of supply of nutrients and hormones is lower in the older people? This could explain the wasting we see.”
Following this up led Beth Phillips, a PhD student working with Professor Rennie, to win the Blue Riband Award for work she presented at the summer meeting of The Physiological Society in Dublin. In her research Beth confirmed the blunting effect of age on leg blood flow after feeding, with and without exercise. The team predicted that weight training would reduce this blunting. “Indeed, she found that three sessions a week over 20 weeks ‘rejuvenated’ the leg blood flow responses of the older people. They became identical to those in the young,” said Professor Rennie.
“I am extremely pleased with progress,” he said. “Our team is making good headway in finding more and more out about what causes the loss of muscle with age. It looks like we have good clues about how to lessen it with weight training and possibly other ways to increase blood flow.” via University of Nottingham.
A team of Nottingham researchers has already shown that when older people eat, they cannot make muscle as fast as the young. Now they’ve found that the suppression of muscle breakdown, which also happens during feeding, is blunted with age.
The scientists and doctors at The University of Nottingham Schools of Graduate Entry Medicine and Biomedical Sciences believe that a ‘double whammy’ affects people aged over 65. However the team think that weight training may “rejuvenate” muscle blood flow and help retain muscle for older people.
These results may explain the ongoing loss of muscle in older people: when they eat they don’t build enough muscle with the protein in food; also, the insulin (a hormone released during a meal) fails to shut down the muscle breakdown that rises between meals and overnight. Normally, in young people, insulin acts to slow muscle breakdown. Common to these problems may be a failure to deliver nutrients and hormones to muscle because of a poorer blood supply.
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The work has been done by Michael Rennie, Professor of Clinical Physiology, and Dr Emilie Wilkes, and their colleagues at The University of Nottingham. The research was funded by the UK’s Biotechnology and Biological Sciences Research Council (BBSRC) as part of ongoing work on age-related muscle wasting and how to lessen that effect.
Research just published in The American Journal of Clinical Nutrition compared one group of people in their late 60s to a group of 25-year-olds, with equal numbers of men and women. Professor Rennie said “We studied our subjects first — before breakfast — and then after giving them a small amount of insulin to raise the hormone to what they would be if they had eaten breakfast, of a bowl of cornflakes or a croissant.”
“We tagged one of the amino acids (from which proteins are made) so that we could discover how much protein in leg muscle was being broken down. We then compared how much amino acid was delivered to the leg and how much was leaving it, by analysing blood in the two situations.
“The results were clear. The younger people’s muscles were able to use insulin we gave to stop the muscle breakdown, which had increased during the night. The muscles in the older people could not.”
“In the course of our tests, we also noticed that the blood flow in the leg was greater in the younger people than the older ones,” added Professor Rennie. “This set us thinking: maybe the rate of supply of nutrients and hormones is lower in the older people? This could explain the wasting we see.”
Following this up led Beth Phillips, a PhD student working with Professor Rennie, to win the Blue Riband Award for work she presented at the summer meeting of The Physiological Society in Dublin. In her research Beth confirmed the blunting effect of age on leg blood flow after feeding, with and without exercise. The team predicted that weight training would reduce this blunting. “Indeed, she found that three sessions a week over 20 weeks ‘rejuvenated’ the leg blood flow responses of the older people. They became identical to those in the young,” said Professor Rennie.
“I am extremely pleased with progress,” he said. “Our team is making good headway in finding more and more out about what causes the loss of muscle with age. It looks like we have good clues about how to lessen it with weight training and possibly other ways to increase blood flow.” via University of Nottingham.
Violent adults result from kids eating sweets everyday
Children who eat sweets and chocolate every day are more likely to be violent as adults, according to new research.A study of almost 17,500 participants in the 1970 British Cohort Study found that 10-year-olds who ate confectionary daily were significantly more likely to have been convicted for violence at age 34 years.
The study, published in the October issue of the British Journal of Psychiatry, is the first to examine the long-term effects of childhood diet on adult violence.
Researchers from Cardiff University found that 69 per cent of the participants who were violent at the age of 34 had eaten sweets and chocolate nearly every day during childhood, compared to 42% who were non-violent.
This link between confectionary consumption and violence remained after controlling for other factors.
The researchers put forward several explanations for the link. Lead researcher Dr Simon Moore said: "Our favoured explanation is that giving children sweets and chocolate regularly may stop them learning how to wait to obtain something they want. Not being able to defer gratification may push them towards more impulsive behaviour, which is strongly associated with delinquency."
The researchers concluded: "This association between confectionary consumption and violence needs further attention. Targeting resources at improving children's diet may improve health and reduce aggression."
Source: Cardiff University.
The study, published in the October issue of the British Journal of Psychiatry, is the first to examine the long-term effects of childhood diet on adult violence.
Researchers from Cardiff University found that 69 per cent of the participants who were violent at the age of 34 had eaten sweets and chocolate nearly every day during childhood, compared to 42% who were non-violent.
This link between confectionary consumption and violence remained after controlling for other factors.
The researchers put forward several explanations for the link. Lead researcher Dr Simon Moore said: "Our favoured explanation is that giving children sweets and chocolate regularly may stop them learning how to wait to obtain something they want. Not being able to defer gratification may push them towards more impulsive behaviour, which is strongly associated with delinquency."
The researchers concluded: "This association between confectionary consumption and violence needs further attention. Targeting resources at improving children's diet may improve health and reduce aggression."
Source: Cardiff University.
Improving memory with nasal sprays
Good news for procrastinating students: a nasal spray developed by a team of German scientists promises to give late night cram sessions a major boost, if a good night's sleep follows. In a research report featured as the cover story of the October 2009 print issue of The FASEB Journal, these scientists show that a molecule from the body's immune system (interleukin-6) when administered through the nose helps the brain retain emotional and procedural memories during REM sleep.
"Sleep to remember, a dream or reality?" said Lisa Marshall, co-author of the study, from the Department of Neuroendocrinology at the University of Lubeck in Germany. "Here, we provide the first evidence that the immunoregulatory signal interleukin-6 plays a beneficial role in sleep-dependent formation of long-term memory in humans."
To make this discovery, Marshall and colleagues had 17 healthy young men spend two nights in the laboratory. On each night after reading either an emotional or neutral short story, they sprayed a fluid into their nostrils which contained either interleukin-6 or a placebo fluid. The subsequent sleep and brain electric activity was monitored throughout the night. The next morning subjects wrote down as many words as they could remember from each of the two stories. Those who received the dose of IL-6 could remember more words.
"If a nasal spray can improve memory, perhaps we're on our way to giving some folks a whiff of common sense, such as accepting the realities of evolution," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "This is exciting piece of interdisciplinary science, since IL-6 had previously been considered a by-product of inflammation, not an agent that affects cognition."
Source: Federation of American Societies for Experimental Biology.
"Sleep to remember, a dream or reality?" said Lisa Marshall, co-author of the study, from the Department of Neuroendocrinology at the University of Lubeck in Germany. "Here, we provide the first evidence that the immunoregulatory signal interleukin-6 plays a beneficial role in sleep-dependent formation of long-term memory in humans."
To make this discovery, Marshall and colleagues had 17 healthy young men spend two nights in the laboratory. On each night after reading either an emotional or neutral short story, they sprayed a fluid into their nostrils which contained either interleukin-6 or a placebo fluid. The subsequent sleep and brain electric activity was monitored throughout the night. The next morning subjects wrote down as many words as they could remember from each of the two stories. Those who received the dose of IL-6 could remember more words.
"If a nasal spray can improve memory, perhaps we're on our way to giving some folks a whiff of common sense, such as accepting the realities of evolution," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "This is exciting piece of interdisciplinary science, since IL-6 had previously been considered a by-product of inflammation, not an agent that affects cognition."
Source: Federation of American Societies for Experimental Biology.
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