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Reversing Alzheimer's memory impairment with caffeine
Coffee drinkers may have another reason to pour that extra cup. When aged mice bred to develop symptoms of Alzheimer's disease were given caffeine – the equivalent of five cups of coffee a day – their memory impairment was reversed, report University of South Florida researchers at the Florida Alzheimer's Disease Research Center. Back-to-back studies published online July 6 in the Journal of Alzheimer's Disease, show caffeine significantly decreased abnormal levels of the protein linked to Alzheimer's disease, both in the brains and in the blood of mice exhibiting symptoms of the disease. Both studies build upon previous research by the Florida ADRC group showing that caffeine in early adulthood prevented the onset of memory problems in mice bred to develop Alzheimer's symptoms in old age.
"The new findings provide evidence that caffeine could be a viable 'treatment' for established Alzheimer's disease, and not simply a protective strategy," said lead author Gary Arendash, PhD, a USF neuroscientist with the Florida ADRC. "That's important because caffeine is a safe drug for most people, it easily enters the brain, and it appears to directly affect the disease process."
Based on these promising findings in mice, researchers at the Florida ADRC and Byrd Alzheimer's Center at USF hope to begin human trials to evaluate whether caffeine can benefit people with mild cognitive impairment or early Alzheimer's disease, said Huntington Potter, PhD, director of the Florida ADRC and an investigator for the caffeine studies. The research group has already determined that caffeine administered to elderly non-demented humans quickly affects their blood levels of β-amyloid, just as it did in the Alzheimer's mice.
"These are some of the most promising Alzheimer's mouse experiments ever done showing that caffeine rapidly reduces beta amyloid protein in the blood, an effect that is mirrored in the brain, and this reduction is linked to cognitive benefit," Potter said. "Our goal is to obtain the funding needed to translate the therapeutic discoveries in mice into well-designed clinical trials."
Arendash and his colleagues became interested in caffeine's potential for treating Alzheimer's several years ago, after a Portuguese study reported that people with Alzheimer's had consumed less caffeine over the last 20 years than people without the neurodegenerative disease. Since then, several uncontrolled clinical studies have reported moderate caffeine consumption may protect against memory decline during normal aging. The highly controlled studies using Alzheimer's mice allowed researchers to isolate the effects of caffeine on memory from other lifestyle factors such as diet and exercise, Arendash said.
The just-published Florida ADRC study included 55 mice genetically altered to develop memory problems mimicking Alzheimer's disease as they aged. After behavioral tests confirmed the mice were exhibiting signs of memory impairment at age 18 to 19 months – about age 70 in human years – the researchers gave half the mice caffeine in their drinking water. The other half got plain water. The Alzheimer's mice received the equivalent of five 8-oz. cups of regular coffee a day. That's the same amount of caffeine – 500 milligrams -- as contained in two cups of specialty coffees like Starbucks, or 14 cups of tea, or 20 soft drinks.
At the end of the two-month study, the caffeinated mice performed much better on tests measuring their memory and thinking skills. In fact, their memories were identical to normal aged mice without dementia. The Alzheimer's mice drinking plain water continued to do poorly on the tests.
In addition, the brains of the caffeinated mice showed nearly a 50-percent reduction in levels of beta amyloid, a substance forming the sticky clumps of plaques that are a hallmark of Alzheimer's disease. Other experiments by the same investigators indicate that caffeine appears to restore memory by reducing both enzymes needed to produce beta amyloid. The researchers also suggest that caffeine suppresses inflammatory changes in the brain that lead to an overabundance of beta amyloid.
Since caffeine improved the memory of mice with pre-existing Alzheimer's, the researchers were curious to know if it might further boost the memory of non-demented (normal) mice administered caffeine from young adulthood through old age. It did not. Control mice given regular drinking water throughout their lives performed as well on behavioral tests in old age as normal mice who received long-term caffeine treatment, Arendash said. "This suggests that caffeine will not increase memory performance above normal levels. Rather, it appears to benefit those destined to develop Alzheimer's disease."
The researchers do not know if an amount lower than the 500 mg. daily caffeine intake received by the Alzheimer's mice would be effective, Arendash said. For most individuals, however, this moderate level of caffeine intake poses no adverse health effects, according to both the National Research Council and the National Academy of Sciences. Nonetheless, Arendash said, individuals with high blood pressure or those who are pregnant should limit their daily caffeine intake.
If larger, more rigorous clinical studies confirm that caffeine staves off Alzheimer's in humans, as it does in mice, this benefit would be substantial, Arendash said. Alzheimer's disease attacks nearly half of Americans age 85 and older, and Alzheimer's and other dementias triple healthcare costs for those age 65 and older, according to the Alzheimer's Association. via University of South Florida.
"The new findings provide evidence that caffeine could be a viable 'treatment' for established Alzheimer's disease, and not simply a protective strategy," said lead author Gary Arendash, PhD, a USF neuroscientist with the Florida ADRC. "That's important because caffeine is a safe drug for most people, it easily enters the brain, and it appears to directly affect the disease process."Based on these promising findings in mice, researchers at the Florida ADRC and Byrd Alzheimer's Center at USF hope to begin human trials to evaluate whether caffeine can benefit people with mild cognitive impairment or early Alzheimer's disease, said Huntington Potter, PhD, director of the Florida ADRC and an investigator for the caffeine studies. The research group has already determined that caffeine administered to elderly non-demented humans quickly affects their blood levels of β-amyloid, just as it did in the Alzheimer's mice.
"These are some of the most promising Alzheimer's mouse experiments ever done showing that caffeine rapidly reduces beta amyloid protein in the blood, an effect that is mirrored in the brain, and this reduction is linked to cognitive benefit," Potter said. "Our goal is to obtain the funding needed to translate the therapeutic discoveries in mice into well-designed clinical trials."
Arendash and his colleagues became interested in caffeine's potential for treating Alzheimer's several years ago, after a Portuguese study reported that people with Alzheimer's had consumed less caffeine over the last 20 years than people without the neurodegenerative disease. Since then, several uncontrolled clinical studies have reported moderate caffeine consumption may protect against memory decline during normal aging. The highly controlled studies using Alzheimer's mice allowed researchers to isolate the effects of caffeine on memory from other lifestyle factors such as diet and exercise, Arendash said.
The just-published Florida ADRC study included 55 mice genetically altered to develop memory problems mimicking Alzheimer's disease as they aged. After behavioral tests confirmed the mice were exhibiting signs of memory impairment at age 18 to 19 months – about age 70 in human years – the researchers gave half the mice caffeine in their drinking water. The other half got plain water. The Alzheimer's mice received the equivalent of five 8-oz. cups of regular coffee a day. That's the same amount of caffeine – 500 milligrams -- as contained in two cups of specialty coffees like Starbucks, or 14 cups of tea, or 20 soft drinks.
At the end of the two-month study, the caffeinated mice performed much better on tests measuring their memory and thinking skills. In fact, their memories were identical to normal aged mice without dementia. The Alzheimer's mice drinking plain water continued to do poorly on the tests.
In addition, the brains of the caffeinated mice showed nearly a 50-percent reduction in levels of beta amyloid, a substance forming the sticky clumps of plaques that are a hallmark of Alzheimer's disease. Other experiments by the same investigators indicate that caffeine appears to restore memory by reducing both enzymes needed to produce beta amyloid. The researchers also suggest that caffeine suppresses inflammatory changes in the brain that lead to an overabundance of beta amyloid.
Since caffeine improved the memory of mice with pre-existing Alzheimer's, the researchers were curious to know if it might further boost the memory of non-demented (normal) mice administered caffeine from young adulthood through old age. It did not. Control mice given regular drinking water throughout their lives performed as well on behavioral tests in old age as normal mice who received long-term caffeine treatment, Arendash said. "This suggests that caffeine will not increase memory performance above normal levels. Rather, it appears to benefit those destined to develop Alzheimer's disease."
The researchers do not know if an amount lower than the 500 mg. daily caffeine intake received by the Alzheimer's mice would be effective, Arendash said. For most individuals, however, this moderate level of caffeine intake poses no adverse health effects, according to both the National Research Council and the National Academy of Sciences. Nonetheless, Arendash said, individuals with high blood pressure or those who are pregnant should limit their daily caffeine intake.
If larger, more rigorous clinical studies confirm that caffeine staves off Alzheimer's in humans, as it does in mice, this benefit would be substantial, Arendash said. Alzheimer's disease attacks nearly half of Americans age 85 and older, and Alzheimer's and other dementias triple healthcare costs for those age 65 and older, according to the Alzheimer's Association. via University of South Florida.
Airborne soot in combination with particulate pollution not good for global warming
Particulate pollution thought to be holding climate change in check by reflecting sunlight instead enhances warming when combined with airborne soot, a new study has found. Like a black car on a bright summer day, soot absorbs solar energy. Recent atmospheric models have ranked soot, also called black carbon, second only to carbon dioxide in potential for atmospheric warming. But particles, or aerosols, such as soot mix with other chemicals in the atmosphere, complicating estimates of their role in changing climate.
Los Angeles. Particulate pollution thought to be holding climate change in check by reflecting sunlight instead enhances warming when combined with airborne soot, a new study has found. "Until now, scientists have had to assume how soot is mixed with other chemical species in individual particles and estimate how that ultimately impacts their warming potential," said Kimberly Prather, professor in the Department of Chemistry and Biochemistry and the Scripps Institution of Oceanography at the University of California, San Diego. "Our measurements show that soot is most commonly mixed with other chemicals such as sulfate and this mixing happens very quickly in the atmosphere. These are the first direct measurements of the optical properties of atmospheric soot and allow us to better understand the role of soot in climate change."
Prather and Ryan Moffet, a former graduate student at UC San Diego who is now at the Lawrence Berkeley National Laboratory, measured atmospheric aerosols over Riverside, California and Mexico City. Using an instrument that measures the size, chemical composition and optical properties of aerosols in real time, they showed that jagged bits of fresh soot quickly become coated with a spherical shell of other chemicals, particularly sulfate, nitrate, and organic carbon, through light-driven chemical reactions.
Within several hours of sunrise, most of the atmospheric carbon they measured had been altered in this way, they report in the Proceedings of the National Academy of Sciences online the week of June 29.
Particles of sulfate or nitrate alone reflect light, and some have proposed pumping sulfate aerosols into the atmosphere to slow climate change. But these chemicals play a different role when they mix with soot.
"The coating acts like a lens and focuses the light into the center of the particle, enhancing warming," Prather said. "Many people think sulfate aerosols are a good thing because they are highly reflective and cool our planet. However we are seeing that sulfate is commonly mixed with soot in the same particles, which means in some regions sulfate could lead to more warming as opposed to more cooling as one would expect for a pure sulfate aerosol."
Their measurements showed that in the atmosphere the lens-like shell of sufate and nitrate enhances absorption of light by coated soot particles 1.6 times over pure soot particles.
Soot comes from fires, including those used to cook food and clear agricultural fields, as well as burning of diesel fuel in trucks and ships. Simple measures such as providing better cook stoves with more complete combustion to those in developing countries would help reduce atmospheric soot levels.
Efforts to reduce soot would pay off soon. Unlike carbon dioxide, which lingers in the atmosphere for centuries, soot falls from the sky in a matter of days to weeks, making the reduction of soot a quicker option for slowing down climate change.
"While reducing CO2 concentrations is extremely important, changes we make today will not be felt for quite a while, whereas changes we make today on soot and sulfate could affect our planet on timescales of months," Prather said. "This could buy us time while we grapple with the problems of reducing carbon dioxide and other greenhouse gases." via University of California - San Diego.
Los Angeles. Particulate pollution thought to be holding climate change in check by reflecting sunlight instead enhances warming when combined with airborne soot, a new study has found. "Until now, scientists have had to assume how soot is mixed with other chemical species in individual particles and estimate how that ultimately impacts their warming potential," said Kimberly Prather, professor in the Department of Chemistry and Biochemistry and the Scripps Institution of Oceanography at the University of California, San Diego. "Our measurements show that soot is most commonly mixed with other chemicals such as sulfate and this mixing happens very quickly in the atmosphere. These are the first direct measurements of the optical properties of atmospheric soot and allow us to better understand the role of soot in climate change."Prather and Ryan Moffet, a former graduate student at UC San Diego who is now at the Lawrence Berkeley National Laboratory, measured atmospheric aerosols over Riverside, California and Mexico City. Using an instrument that measures the size, chemical composition and optical properties of aerosols in real time, they showed that jagged bits of fresh soot quickly become coated with a spherical shell of other chemicals, particularly sulfate, nitrate, and organic carbon, through light-driven chemical reactions.
Within several hours of sunrise, most of the atmospheric carbon they measured had been altered in this way, they report in the Proceedings of the National Academy of Sciences online the week of June 29.
Particles of sulfate or nitrate alone reflect light, and some have proposed pumping sulfate aerosols into the atmosphere to slow climate change. But these chemicals play a different role when they mix with soot.
"The coating acts like a lens and focuses the light into the center of the particle, enhancing warming," Prather said. "Many people think sulfate aerosols are a good thing because they are highly reflective and cool our planet. However we are seeing that sulfate is commonly mixed with soot in the same particles, which means in some regions sulfate could lead to more warming as opposed to more cooling as one would expect for a pure sulfate aerosol."
Their measurements showed that in the atmosphere the lens-like shell of sufate and nitrate enhances absorption of light by coated soot particles 1.6 times over pure soot particles.
Soot comes from fires, including those used to cook food and clear agricultural fields, as well as burning of diesel fuel in trucks and ships. Simple measures such as providing better cook stoves with more complete combustion to those in developing countries would help reduce atmospheric soot levels.
Efforts to reduce soot would pay off soon. Unlike carbon dioxide, which lingers in the atmosphere for centuries, soot falls from the sky in a matter of days to weeks, making the reduction of soot a quicker option for slowing down climate change.
"While reducing CO2 concentrations is extremely important, changes we make today will not be felt for quite a while, whereas changes we make today on soot and sulfate could affect our planet on timescales of months," Prather said. "This could buy us time while we grapple with the problems of reducing carbon dioxide and other greenhouse gases." via University of California - San Diego.
Bad effects of stress on fertility and reproductive system
University of California, Berkeley, researchers have found what they think is a critical and, until now, missing piece of the puzzle about how stress causes sexual dysfunction and infertility.Scientists know that stress boosts levels of stress hormones - glucocorticoids such as cortisol - that inhibit the body's main sex hormone, gonadotropin releasing hormone (GnRH), and subsequently suppresses sperm count, ovulation and sexual activity.
The new research shows that stress also increases brain levels of a reproductive hormone named gonadotropin-inhibitory hormone, or GnIH, discovered nine years ago in birds and known to be present in humans and other mammals. This small protein hormone, a so-called RFamide-related peptide (RFRP), puts the brakes on reproduction by directly inhibiting GnRH.
In the reproductive system, the brain's hypothalamus produces GnRH, which stimulates the pituitary gland to produce the peripheral hormones, luteinizing hormone and follicle-stimulating hormone, which in turn stimulate production of testosterone, estradiol and sexual behavior. Stress makes the adrenal gland produce glucocorticoids, which act directly on the hypothalamus to suppress GnRH production. UC Berkeley researchers have now found that glucocorticoids also boost hypothalamic GnIH production, which acts to reduce GnRH production as well as to directly lower pituitary secretion of sex hormones, thereby suppressing the entire reproductive system. (Credit: Elizabeth Kirby/UC Berkeley). The common thread appears to be the glucocorticoid stress hormones, which not only suppress GnRH but boost the suppressor GnIH - a double whammy for the reproductive system.
"We know stress affects the top-tier reproductive hormone, GnRH, but we show, in fact, that stress also affects another high-level hormone, GnIH, to cause reproductive dysfunction," said lead author Elizabeth Kirby, a graduate student at UC Berkeley's Helen Wills Neuroscience Institute. "This work provides a new target for researchers, a new way to think about infertility and dysfunction. The more we know, the more we can look for ways to treat it."
The results will be published the week of June 15 in the Online Early Edition of the journal Proceedings of the National Academy of Sciences (PNAS)
The conclusions are based on experiments in rats and inferences from the effects of the hormone in birds. But if this new reproductive hormone acts the same way in all mammals, researchers say the finding could not only change the way physicians look at human reproductive problems, but also affect how breeders approach animal husbandry and captive breeding programs for endangered species.
"There is a growing body of work that points to GnIH as being a big player in the inhibition of reproduction in mammals," said co-author George Bentley, UC Berkeley assistant professor of integrative biology. "We didn't have any hint of this stress effect nine years ago, when GnIH was first discovered."
In humans, chronic stress can lead to a drop in sex drive as well as a drop in fertility. Even the stress of infertility treatments can block their effectiveness, as evidenced by many anecdotes about couples conceiving children after the failure of assisted reproduction.
Animal breeding also is affected by stress. Zoos, in particular, have difficulty getting some animals to reproduce in captivity, Bentley said.
Based on animal experiments, researchers attribute much of this stress effect on sexual function to an increase in glucocorticoids - stress hormones - produced by the adrenal gland. In the brain, these glucocorticoids suppress the main reproductive hormone, GnRH, which in turn causes a shut-down of the release of the gonadotropins luteinizing hormone and follicle-stimulating hormone by the pituitary, and then a suppression of testosterone, estradiol and sexual behavior.
In 2000, however, a new reproductive hormone was discovered in birds and dubbed gonadotropin-inhibitory hormone (GnIH) because it had the opposite effect of GnRH - it inhibited release of gonadotropins, thereby suppressing reproduction.
"It's very adaptive to not be wasting resources on reproduction during times of acute stress, to just shut down reproduction for 24 hours or so until the stress is gone," said co-author Daniela Kaufer, a UC Berkeley assistant professor of integrative biology who looks at how stress affects molecular processes in the brain. "These functions go back in evolution a long way."
Because of the negative effects of GnIH on reproduction, Bentley, who helped establish the critical role played by GnIH in birds, teamed up with Kaufer and Kirby to explore whether stress might affect GnIH levels in the brain. The homologous hormones in mammals have been dubbed RFamide-related peptides, or RFRPs.
Kirby showed that acutely stressed rats showed increased RFRP levels for several hours, but that levels returned to normal by the next day. Chronically stressed rats, however, were left with longer-term elevations of RFRP levels in the dorsomedial hypothalamus area of the brain, and suppression of activity in the reproductive axis - the hypothalamus-pituitary-gonadal hormone cascade - that is associated with lowered sexual activity.
"With chronic stress, glucocorticoids went sky high," Kirby said.
To determine the role of glucocorticoids, Kirby removed the adrenal glands of male rats, eliminating the source of the hormone. Without adrenals, stress no longer affected RFRP levels in the brain. The researchers also showed that the cells that produce RFRP have receptors for glucocorticoids, a clear indication that these stress hormones can directly affect the cells that produce RFRP.
"Critically, we show that RFRP neurons express the receptors for glucocorticoids, which are released from the adrenal glands in response to stress, and that removal of the adrenal glands prevents the stress-induced, up-regulation of RFRP," Bentley said. "Thus, we believe we have identified an entirely novel pathway for stress-induced reproductive dysfunction."
Kirby noted that adrenal hormones are critical to survival, so removing the gland and thus glucocorticoids is not a solution to chronic stress.
However, Kaufer said, it may be possible to block GnIH to reduce some of the effects of stress on reproduction.
The researchers plan to confirm the results in female rats and investigate further the role of GnIH in reproduction.
The work was supported by the National Science Foundation. Other coauthors of the PNAS paper are graduate students Anna C. Geraghty and Takayoshi Ubuka of UC Berkeley's Department of Integrative Biology. Kaufer, Kirby and Bentley are all members of the Helen Wills Neuroscience Institute.via University of California - Berkeley.
The new research shows that stress also increases brain levels of a reproductive hormone named gonadotropin-inhibitory hormone, or GnIH, discovered nine years ago in birds and known to be present in humans and other mammals. This small protein hormone, a so-called RFamide-related peptide (RFRP), puts the brakes on reproduction by directly inhibiting GnRH.
In the reproductive system, the brain's hypothalamus produces GnRH, which stimulates the pituitary gland to produce the peripheral hormones, luteinizing hormone and follicle-stimulating hormone, which in turn stimulate production of testosterone, estradiol and sexual behavior. Stress makes the adrenal gland produce glucocorticoids, which act directly on the hypothalamus to suppress GnRH production. UC Berkeley researchers have now found that glucocorticoids also boost hypothalamic GnIH production, which acts to reduce GnRH production as well as to directly lower pituitary secretion of sex hormones, thereby suppressing the entire reproductive system. (Credit: Elizabeth Kirby/UC Berkeley). The common thread appears to be the glucocorticoid stress hormones, which not only suppress GnRH but boost the suppressor GnIH - a double whammy for the reproductive system."We know stress affects the top-tier reproductive hormone, GnRH, but we show, in fact, that stress also affects another high-level hormone, GnIH, to cause reproductive dysfunction," said lead author Elizabeth Kirby, a graduate student at UC Berkeley's Helen Wills Neuroscience Institute. "This work provides a new target for researchers, a new way to think about infertility and dysfunction. The more we know, the more we can look for ways to treat it."
The results will be published the week of June 15 in the Online Early Edition of the journal Proceedings of the National Academy of Sciences (PNAS)
The conclusions are based on experiments in rats and inferences from the effects of the hormone in birds. But if this new reproductive hormone acts the same way in all mammals, researchers say the finding could not only change the way physicians look at human reproductive problems, but also affect how breeders approach animal husbandry and captive breeding programs for endangered species.
"There is a growing body of work that points to GnIH as being a big player in the inhibition of reproduction in mammals," said co-author George Bentley, UC Berkeley assistant professor of integrative biology. "We didn't have any hint of this stress effect nine years ago, when GnIH was first discovered."
In humans, chronic stress can lead to a drop in sex drive as well as a drop in fertility. Even the stress of infertility treatments can block their effectiveness, as evidenced by many anecdotes about couples conceiving children after the failure of assisted reproduction.
Animal breeding also is affected by stress. Zoos, in particular, have difficulty getting some animals to reproduce in captivity, Bentley said.
Based on animal experiments, researchers attribute much of this stress effect on sexual function to an increase in glucocorticoids - stress hormones - produced by the adrenal gland. In the brain, these glucocorticoids suppress the main reproductive hormone, GnRH, which in turn causes a shut-down of the release of the gonadotropins luteinizing hormone and follicle-stimulating hormone by the pituitary, and then a suppression of testosterone, estradiol and sexual behavior.
In 2000, however, a new reproductive hormone was discovered in birds and dubbed gonadotropin-inhibitory hormone (GnIH) because it had the opposite effect of GnRH - it inhibited release of gonadotropins, thereby suppressing reproduction.
"It's very adaptive to not be wasting resources on reproduction during times of acute stress, to just shut down reproduction for 24 hours or so until the stress is gone," said co-author Daniela Kaufer, a UC Berkeley assistant professor of integrative biology who looks at how stress affects molecular processes in the brain. "These functions go back in evolution a long way."
Because of the negative effects of GnIH on reproduction, Bentley, who helped establish the critical role played by GnIH in birds, teamed up with Kaufer and Kirby to explore whether stress might affect GnIH levels in the brain. The homologous hormones in mammals have been dubbed RFamide-related peptides, or RFRPs.
Kirby showed that acutely stressed rats showed increased RFRP levels for several hours, but that levels returned to normal by the next day. Chronically stressed rats, however, were left with longer-term elevations of RFRP levels in the dorsomedial hypothalamus area of the brain, and suppression of activity in the reproductive axis - the hypothalamus-pituitary-gonadal hormone cascade - that is associated with lowered sexual activity.
"With chronic stress, glucocorticoids went sky high," Kirby said.
To determine the role of glucocorticoids, Kirby removed the adrenal glands of male rats, eliminating the source of the hormone. Without adrenals, stress no longer affected RFRP levels in the brain. The researchers also showed that the cells that produce RFRP have receptors for glucocorticoids, a clear indication that these stress hormones can directly affect the cells that produce RFRP.
"Critically, we show that RFRP neurons express the receptors for glucocorticoids, which are released from the adrenal glands in response to stress, and that removal of the adrenal glands prevents the stress-induced, up-regulation of RFRP," Bentley said. "Thus, we believe we have identified an entirely novel pathway for stress-induced reproductive dysfunction."
Kirby noted that adrenal hormones are critical to survival, so removing the gland and thus glucocorticoids is not a solution to chronic stress.
However, Kaufer said, it may be possible to block GnIH to reduce some of the effects of stress on reproduction.
The researchers plan to confirm the results in female rats and investigate further the role of GnIH in reproduction.
The work was supported by the National Science Foundation. Other coauthors of the PNAS paper are graduate students Anna C. Geraghty and Takayoshi Ubuka of UC Berkeley's Department of Integrative Biology. Kaufer, Kirby and Bentley are all members of the Helen Wills Neuroscience Institute.via University of California - Berkeley.
Higher risks of heart problems from high carb foods
Doctors have known for decades that too much carbohydrate-laden foods like white bread and corn flakes can be detrimental to cardiac health. In a landmark study, new research from Tel Aviv University now shows exactly how these high carb foods increase the risk for heart problems. "Looking inside" the arteries of students eating a variety of foods, Dr. Michael Shechter of Tel Aviv University's Sackler School of Medicine and the Heart Institute of Sheba Medical Center — with collaboration of the Endocrinology Institute — visualized exactly what happens inside the body when the wrong foods for a healthy heart are eaten. He found that foods with a high glycemic index distended brachial arteries for several hours.
Elasticity of arteries anywhere in the body can be a measure of heart health. But when aggravated over time, a sudden expansion of the artery wall can cause a number of negative health effects, including reduced elasticity, which can cause heart disease or sudden death.
Using a clinical and research technique pioneered by his laboratory in Israel, Dr. Shechter was able to visualize what happens inside our arteries before, during and after eating high carb foods. It is a first in medical history. The results were published in the Journal of the American College of Cardiology.
Time to skip the wedding cake?
"It's very hard to predict heart disease," says Dr. Shechter, a fellow of the American College of Cardiology and the American Heart Association. "But doctors know that high glycemic foods rapidly increase blood sugar. Those who binge on these foods have a greater chance of sudden death from heart attack. Our research connects the dots, showing the link between diet and what's happening in real time in the arteries."
Like the uncomfortable medical warnings on packets of cigarettes, this new research could lead to a whole new way to show patients the effects of a poor diet on our body.
Using 56 healthy volunteers, the researchers looked at four groups. One group ate a cornflake mush mixed with milk, a second a pure sugar mixture, the third bran flakes, while the last group was given a placebo (water). Over four weeks, Dr. Shechter applied his method of "brachial reactive testing" to each group. The test uses a cuff on the arm, like those used to measure blood pressure, which can visualize arterial function in real time.
The results were dramatic. Before any of the patients ate, arterial function was essentially the same. After eating, except for the placebo group, all had reduced functioning.
All roads lead to the endothelium
Enormous peaks indicating arterial stress were found in the high glycemic index groups: the cornflakes and sugar group. "We knew high glycemic foods were bad for the heart. Now we have a mechanism that shows how," says Dr. Shechter. "Foods like cornflakes, white bread, french fries, and sweetened soda all put undue stress on our arteries. We've explained for the first time how high glycemic carbs can affect the progression of heart disease." During the consumption of foods high in sugar, there appears to be a temporary and sudden dysfunction in the endothelial walls of the arteries.
Endothelial health can be traced back to almost every disorder and disease in the body. It is "the riskiest of the risk factors," says Dr. Shechter, who practices at the Chaim Sheba Medical Center — Tel Hashomer Hospital. There he offers a treatment that can show patients — in real time — if they have a high risk for heart attacks. "Medical tourists" from America regularly visit to take the heart test.
The take-away message? Dr. Shechter says to stick to foods like oatmeal, fruits and vegetables, legumes and nuts, which have a low glycemic index. Exercising every day for at least 30 minutes, he adds, is an extra heart-smart action to take. via Tel Aviv University
Elasticity of arteries anywhere in the body can be a measure of heart health. But when aggravated over time, a sudden expansion of the artery wall can cause a number of negative health effects, including reduced elasticity, which can cause heart disease or sudden death.Using a clinical and research technique pioneered by his laboratory in Israel, Dr. Shechter was able to visualize what happens inside our arteries before, during and after eating high carb foods. It is a first in medical history. The results were published in the Journal of the American College of Cardiology.
Time to skip the wedding cake?
"It's very hard to predict heart disease," says Dr. Shechter, a fellow of the American College of Cardiology and the American Heart Association. "But doctors know that high glycemic foods rapidly increase blood sugar. Those who binge on these foods have a greater chance of sudden death from heart attack. Our research connects the dots, showing the link between diet and what's happening in real time in the arteries."
Like the uncomfortable medical warnings on packets of cigarettes, this new research could lead to a whole new way to show patients the effects of a poor diet on our body.
Using 56 healthy volunteers, the researchers looked at four groups. One group ate a cornflake mush mixed with milk, a second a pure sugar mixture, the third bran flakes, while the last group was given a placebo (water). Over four weeks, Dr. Shechter applied his method of "brachial reactive testing" to each group. The test uses a cuff on the arm, like those used to measure blood pressure, which can visualize arterial function in real time.
The results were dramatic. Before any of the patients ate, arterial function was essentially the same. After eating, except for the placebo group, all had reduced functioning.
All roads lead to the endothelium
Enormous peaks indicating arterial stress were found in the high glycemic index groups: the cornflakes and sugar group. "We knew high glycemic foods were bad for the heart. Now we have a mechanism that shows how," says Dr. Shechter. "Foods like cornflakes, white bread, french fries, and sweetened soda all put undue stress on our arteries. We've explained for the first time how high glycemic carbs can affect the progression of heart disease." During the consumption of foods high in sugar, there appears to be a temporary and sudden dysfunction in the endothelial walls of the arteries.
Endothelial health can be traced back to almost every disorder and disease in the body. It is "the riskiest of the risk factors," says Dr. Shechter, who practices at the Chaim Sheba Medical Center — Tel Hashomer Hospital. There he offers a treatment that can show patients — in real time — if they have a high risk for heart attacks. "Medical tourists" from America regularly visit to take the heart test.
The take-away message? Dr. Shechter says to stick to foods like oatmeal, fruits and vegetables, legumes and nuts, which have a low glycemic index. Exercising every day for at least 30 minutes, he adds, is an extra heart-smart action to take. via Tel Aviv University
Platypus helping us in understanding ovarian cancer
Researchers from the Royal Adelaide Hospital and University of Adelaide believe our oldest mammalian relative may help us to better understand ovarian cancer. University of Adelaide geneticist, Dr Frank Grutzner says DNA mapping of the platypus has uncovered an interesting relationship between their sex chromosomes and DNA sequences found in human ovarian cancer.
“We’ve identified DNA on the sex chromosomes of the platypus that is similar to the DNA that is affected in ovarian cancer and other diseases of reproduction like male infertility,” Dr Grutzner says. “Cancers often show a large number of DNA changes and it is difficult to decide which ones are important for the development of the disease. The comparison with distantly related species like platypus helps us in identifying important DNA sequences that have been conserved by evolution over millions of years. “We are excited by the fact that the analysis of the platypus genome gives us new directions in investigating the molecular basis of ovarian cancer.”
Working in partnership with Dr Grutzner is Assoc Prof Martin Oehler, Gynaecological Oncologist specialised in ovarian cancer treatment, from the Royal Adelaide Hospital who says it’s about finding new ways to tackle the disease.
“We hope this sort of research might one day lead to the development of an early detection test and more effective therapies against ovarian cancer,” Dr Oehler says.
“Ovarian cancer is the most lethal gynaecological cancer and ranks as the 6th most common cause of cancer death in Australian women.”
Both Dr Oehler and Dr Grutzner say the applications of this research are not limited to ovarian cancer, as they try to gain a better understanding of a number of diseases. via University of Adelaide.
“We’ve identified DNA on the sex chromosomes of the platypus that is similar to the DNA that is affected in ovarian cancer and other diseases of reproduction like male infertility,” Dr Grutzner says. “Cancers often show a large number of DNA changes and it is difficult to decide which ones are important for the development of the disease. The comparison with distantly related species like platypus helps us in identifying important DNA sequences that have been conserved by evolution over millions of years. “We are excited by the fact that the analysis of the platypus genome gives us new directions in investigating the molecular basis of ovarian cancer.”Working in partnership with Dr Grutzner is Assoc Prof Martin Oehler, Gynaecological Oncologist specialised in ovarian cancer treatment, from the Royal Adelaide Hospital who says it’s about finding new ways to tackle the disease.
“We hope this sort of research might one day lead to the development of an early detection test and more effective therapies against ovarian cancer,” Dr Oehler says.
“Ovarian cancer is the most lethal gynaecological cancer and ranks as the 6th most common cause of cancer death in Australian women.”
Both Dr Oehler and Dr Grutzner say the applications of this research are not limited to ovarian cancer, as they try to gain a better understanding of a number of diseases. via University of Adelaide.
Talk to my right ear if you need something
We humans prefer to be addressed in our right ear and are more likely to perform a task when we receive the request in our right ear rather than our left. In a series of three studies, looking at ear preference in communication between humans, Dr. Luca Tommasi and Daniele Marzoli from the University "Gabriele d'Annunzio" in Chieti, Italy, show that a natural side bias, depending on hemispheric asymmetry in the brain, manifests itself in everyday human behavior.
One of the best known asymmetries in humans is the right ear dominance for listening to verbal stimuli, which is believed to reflect the brain's left hemisphere superiority for processing verbal information. However, until now, the majority of studies looking at ear preference in human communication have been controlled laboratory studies and there is very little published observational evidence of spontaneous ear dominance in everyday human behavior.
Tommasi and Marzoli's three studies specifically observed ear preference during social interactions in noisy night club environments. In the first study, 286 clubbers were observed while they were talking, with loud music in the background. In total, 72 percent of interactions occurred on the right side of the listener. These results are consistent with the right ear preference found in both laboratory studies and questionnaires and they demonstrate that the side bias is spontaneously displayed outside the laboratory.
In the second study, the researchers approached 160 clubbers and mumbled an inaudible, meaningless utterance and waited for the subjects to turn their head and offer either their left of their right ear. They then asked them for a cigarette. Overall, 58 percent offered their right ear for listening and 42 percent their left. Only women showed a consistent right-ear preference. In this study, there was no link between the number of cigarettes obtained and the ear receiving the request.
In the third study, the researchers intentionally addressed 176 clubbers in either their right or their left ear when asking for a cigarette. They obtained significantly more cigarettes when they spoke to the clubbers' right ear compared with their left.
According to the authors, taken together, these results confirm a right ear/left hemisphere advantage for verbal communication and distinctive specialization of the two halves of the brain for approach and avoidance behavior.
They conclude: "Our studies corroborate the idea of a common ancestry - in humans and other species - of lateralized behavior during social interactions, not only for species-specific vocal communication, but also for affective responses." via Springer Science
One of the best known asymmetries in humans is the right ear dominance for listening to verbal stimuli, which is believed to reflect the brain's left hemisphere superiority for processing verbal information. However, until now, the majority of studies looking at ear preference in human communication have been controlled laboratory studies and there is very little published observational evidence of spontaneous ear dominance in everyday human behavior.
Tommasi and Marzoli's three studies specifically observed ear preference during social interactions in noisy night club environments. In the first study, 286 clubbers were observed while they were talking, with loud music in the background. In total, 72 percent of interactions occurred on the right side of the listener. These results are consistent with the right ear preference found in both laboratory studies and questionnaires and they demonstrate that the side bias is spontaneously displayed outside the laboratory.
In the second study, the researchers approached 160 clubbers and mumbled an inaudible, meaningless utterance and waited for the subjects to turn their head and offer either their left of their right ear. They then asked them for a cigarette. Overall, 58 percent offered their right ear for listening and 42 percent their left. Only women showed a consistent right-ear preference. In this study, there was no link between the number of cigarettes obtained and the ear receiving the request.
In the third study, the researchers intentionally addressed 176 clubbers in either their right or their left ear when asking for a cigarette. They obtained significantly more cigarettes when they spoke to the clubbers' right ear compared with their left.
According to the authors, taken together, these results confirm a right ear/left hemisphere advantage for verbal communication and distinctive specialization of the two halves of the brain for approach and avoidance behavior.
They conclude: "Our studies corroborate the idea of a common ancestry - in humans and other species - of lateralized behavior during social interactions, not only for species-specific vocal communication, but also for affective responses." via Springer Science
Better sleep regulates the emotional responses
According to a research abstract that will be presented on June11, at Sleep 2009, the 23rd Annual Meeting of the Associated Professional Sleep Societies, sleep selectively preservers memories that are emotionally salient and relevant to future goals when sleep follows soon after learning. Effects persist for as long as four months after the memory is created. Results indicate that the sleeping brain seems to calculate what is most important about an experience and selects only what is adaptive for consolidation and long term storage. Across long delays of 24 hours, or even three–to-four months, sleeping soon after learning preserved the trade-off (compared to waiting an entire day before going to sleep).
According to lead author, Jessica Payne, PhD, of Harvard Medical School in Boston MA, It was surprising that in addition to seeing the enhancement of negative memories over neutral scenes, there was also selectivity within the emotional scenes themselves, with sleep only consolidating what is most relevant, adaptive and useful about the scenes. It was even more surprising that this selectivity lasted for a full day and even months later if sleep came soon after learning.
"It may be that the chemical and physiological aspects of sleep underlying memory consolidation are more effective if a particular memory is 'tagged' shortly prior to sleeping," said Payne.
The study included data from 44 college students between the ages of 18 and 22 who encoded scenes with neutral or negative objects on a neutral background and were tested on memory for objects and backgrounds 24 hours later. Half of the participants were randomly assigned to the 'sleep first' group, which trained and tested on the scenes between the hours of 7 and 9 p.m. while the other half was assigned to the 'wake-first' group which trained and tested on the scenes between the hours of 9 and 11 a.m. Four months later, participants were once again tested on their memory of the scenes.
Negative, but not neutral objects were better remembered in the sleep-first than wake-first group. Backgrounds associated with negative, but not neutral objects were more poorly remembered in the sleep-first compared to the wake-first group. Thus, while negative object memory was enhanced in the sleep-first group compared to the wake-first group, memory for the backgrounds on which they were presented was impaired in the sleep-first group compared to the wake-first group. This pattern persisted four months later, with emotional objects being preferentially retained in the sleep-first group only.
Payne said that sleep is beneficial for memory and that we remember things best when we 'stagger' our learning episodes across time. via American Academy of Sleep Medicine.
According to lead author, Jessica Payne, PhD, of Harvard Medical School in Boston MA, It was surprising that in addition to seeing the enhancement of negative memories over neutral scenes, there was also selectivity within the emotional scenes themselves, with sleep only consolidating what is most relevant, adaptive and useful about the scenes. It was even more surprising that this selectivity lasted for a full day and even months later if sleep came soon after learning.
"It may be that the chemical and physiological aspects of sleep underlying memory consolidation are more effective if a particular memory is 'tagged' shortly prior to sleeping," said Payne.
The study included data from 44 college students between the ages of 18 and 22 who encoded scenes with neutral or negative objects on a neutral background and were tested on memory for objects and backgrounds 24 hours later. Half of the participants were randomly assigned to the 'sleep first' group, which trained and tested on the scenes between the hours of 7 and 9 p.m. while the other half was assigned to the 'wake-first' group which trained and tested on the scenes between the hours of 9 and 11 a.m. Four months later, participants were once again tested on their memory of the scenes.
Negative, but not neutral objects were better remembered in the sleep-first than wake-first group. Backgrounds associated with negative, but not neutral objects were more poorly remembered in the sleep-first compared to the wake-first group. Thus, while negative object memory was enhanced in the sleep-first group compared to the wake-first group, memory for the backgrounds on which they were presented was impaired in the sleep-first group compared to the wake-first group. This pattern persisted four months later, with emotional objects being preferentially retained in the sleep-first group only.
Payne said that sleep is beneficial for memory and that we remember things best when we 'stagger' our learning episodes across time. via American Academy of Sleep Medicine.
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