A substance found in red wine and touted as the chemical equivalent of the fountain of youth probably acts more like a wellspring of health — with warning signs.
Resveratrol, as the chemical is known, does a pretty good job of mimicking some age-defying effects found in studies of animals on calorie-restricted diets. But the substance doesn’t make animals live longer, a new study shows. Louis J. Sheehan, Esquire
At the same time, boosting levels of a key enzyme thought to be responsible for resveratrol action and for the life-extending properties of calorie restriction does protect mice fed high-fat diets from heart problems.
But a third group of researchers warns that more activity of the enzyme, called SirT1, may make brain cells vulnerable to damage.
Some scientists are optimistic that in the near future a pill with resveratrol or something like it could provide the health benefits of a very low-calorie diet. But the new research indicates the drug and the diet regimen don’t necessarily work the same way.
“You have to carefully study the reality, and the reality is, it’s complicated,” says Valter Longo, a molecular geneticist at the University of Southern California’s Andrus Gerontology Center.
For instance, two new studies show that each organ in the body may react differently to calorie restriction, to chemical mimics such as resveratrol, or to different actions of key proteins involved in controlling aging.
Those proteins, called sirtuins, are a group of enzymes found in organisms from bacteria to humans, which have been shown to regulate aging in yeast, roundworms and fruit flies. The proteins were named for the yeast protein Sir2, the first member of the family discovered.
Increasing levels of the mouse sirtuin, SirT1, prevents mice from developing heart problems and fatty livers even when they are fed high-fat diets, researchers at the University of Cincinnati College of Medicine and the Spanish National Cancer Research Center in Madrid reported June 30 in Proceedings of the National Academy of Sciences. These mice with higher levels of SirT1 eat more but also burn more calories than do mice with normal levels of the enzyme.
But Longo’s group reported in the July Cell Metabolism that SirT1 may affect the brain differently. Neurons grown in the laboratory were sensitive to oxidative damage when they made normal amounts of SirT1, but reducing the amount of the enzyme helped the brain cells better resist stress.
“This is backwards,” says Leonard Guarente, a molecular and cellular biologist at MIT. Sirtuins are generally thought to protect cells against oxidative damage believed to play a part in aging. Guarente was not involved in any of the current studies, but his lab pioneered studying aging in yeast. “It’s intriguing, but it will take a little more time to figure out what it means in the context of other evidence to the contrary,” he says.
Mice can’t dispense with SirT1 entirely, though. Longo’s group found that mice from which the SirT1 gene was removed entirely died young. Calorie restriction did not lengthen their lives as it does for yeast lacking the similar gene, Sir2.
If SirT1 really makes neurons vulnerable, that’s potentially bad news for resveratrol. The chemical is found in small amounts in grapes, red wine and other foods and is thought to be the component in red wine responsible for the “French paradox” —in which people who eat a high-fat diet are protected from heart disease by consuming wine. Resveratrol has been shown to keep obese mice healthy enough to live a normal life-span (for a mouse). It has been thought to work in the same way as calorie restriction — by activating sirtuins. Sirtuins then modify other proteins, which, in turn, regulate genes involved in inflammation, immunity, stress responses and other processes of aging.
Indeed, an international group of researchers led by Rafael de Cabo at the U.S. National Institute on Aging reported in the July Cell Metabolism that mice fed resveratrol had similar patterns of gene activity as mice fed only every other day. The resveratrol-treated mice had better bone health, less cataract formation and improved coordination compared with other mice their age. Resveratrol also lowered the mice’s cholesterol and made their hearts function better compared with aged mice fed a standard diet. The findings echo others showing the health benefits of calorie restriction and of increased levels of SirT1.
Unfortunately, “the health benefits resveratrol gives these mice are not the things they are dying of,” de Cabo says. Mice generally die of cancer, not heart disease the way humans do. The mice don’t live longer when given resveratrol probably because the chemical doesn’t fight cancer the way calorie restriction seems to.
So far, resveratrol has shown no toxic side effects either in animal or human studies, de Cabo says. And while he takes Longo’s findings seriously, he says resveratrol is likely to have other actions besides just increasing SirT1 activity.
In fact, Tomas Prolla of the University of Wisconsin–Madison and colleagues suggest that resveratrol doesn’t work through SirT1 at all. In a paper published June 4 in PLoS ONE, Prolla’s group reports that resveratrol mimics some of the effects of calorie restriction, but works differently in some crucial ways, such as in how it regulates glucose uptake by muscles. That process is important in the development of diabetes and other medical problems. The compound did not prevent or slow down tumors in the mice.
But the group demonstrated that even at very low doses, resveratrol is a powerful protector of the heart.
To achieve extension of the maximum human life-span, though, scientists will have to develop a way to prevent cancer too, because “humans, like mice, under normal conditions do develop tumors as a consequence of aging,” Prolla says.
But he is optimistic. “I have no doubt the aging process will be understood at the molecular level and we can do something about it,” Prolla says.
Wednesday, May 20, 2009
Thursday, May 14, 2009
pylori 4.pyl.3 Louis J. Sheehan, Esquire
Children infected with a common stomach bacterium are less likely to have asthma than other kids, according to a study that will appear in the Aug. 15 Journal of Infectious Diseases.
The bug in question, Helicobacter pylori, is a microbe with a history like no other. A longtime resident of the human stomach, H. pylori went largely undetected until Australian scientists discovered it in 1979 and went on to show that it can cause stomach ulcers. Further work has linked it to stomach cancer. It’s now treated with antibiotics whenever detected.
Because H. pylori had been hitchhiking in humans for so long — possibly 50,000 years or more — microbiologist Martin Blaser of New York University became interested in the possible consequences of knocking it out.
He suspected that widespread antibiotic use has been suppressing H. pylori infections in industrialized countries over the past half century. During that same time, asthma has increased markedly.
Blaser and his colleague Yu Chen analyzed a database of health information obtained from people who enrolled in a national health study in either 1999 or 2000. The researchers focused on children, identifying 4,787 who didn’t have an H. pylori infection upon entering the study and 2,625 others who did. Questionnaires completed by study participants (or their parents) showed that children ages 3 to 13 with H. pylori were less than half as likely to have had asthma as were kids without an H. pylori infection.
Children with H. pylori were even less likely to have had, in the previous year, a bout of allergic rhinitis, which is marked by a runny nose, itchy eyes and inflamed nasal passages. And they were less apt to suffer from wheezing, the researchers report.
Blaser cautions that the association does not prove that an H. pylori infection prevents asthma, a chronic condition in which lung passages can become inflamed by contact with an allergen, smoke, pet dander or any number of other substances. Like allergies, asthma is an overreaction of the immune system to an innocuous substance.
Nevertheless, it’s possible that an H. pylori infection might somehow quell the immune system, Blaser says, or more likely induce the production of compounds that do. Or, H. pylori might just be a marker of something else that protects against asthma, he says.
It’s unclear how H. pylori spreads, but children living in messier households could have more H. pylori infections, says gastroenterologist David Graham of the Baylor College of Medicine and at the Michael E. DeBakey Veterans Affairs Medical Center, both in Houston. Thus, its apparent antiasthma effect might actually result from poor hygiene, he says.
Under a school of thought called the hygiene hypothesis, children who grow up in squeaky clean environments have more asthma and allergies than do kids raised in contact with farm animals or in other less sanitary conditions. The idea is that the immune systems of children in messy environments get regular challenges and thus mature properly.
Even if H. pylori did prevent asthma, the infection is not worth having, Graham says. “One would not allow king cobras to live in one’s house just because they might eat rats,” he says. “H. pylori is a king cobra equivalent in terms of the harm done to humans.”
Louis J. Sheehan, Esquire Patients would be better served if doctors could find a way to condition the immune system to achieve the effect of a dirty environment without the negative consequences, Graham says.
The bug in question, Helicobacter pylori, is a microbe with a history like no other. A longtime resident of the human stomach, H. pylori went largely undetected until Australian scientists discovered it in 1979 and went on to show that it can cause stomach ulcers. Further work has linked it to stomach cancer. It’s now treated with antibiotics whenever detected.
Because H. pylori had been hitchhiking in humans for so long — possibly 50,000 years or more — microbiologist Martin Blaser of New York University became interested in the possible consequences of knocking it out.
He suspected that widespread antibiotic use has been suppressing H. pylori infections in industrialized countries over the past half century. During that same time, asthma has increased markedly.
Blaser and his colleague Yu Chen analyzed a database of health information obtained from people who enrolled in a national health study in either 1999 or 2000. The researchers focused on children, identifying 4,787 who didn’t have an H. pylori infection upon entering the study and 2,625 others who did. Questionnaires completed by study participants (or their parents) showed that children ages 3 to 13 with H. pylori were less than half as likely to have had asthma as were kids without an H. pylori infection.
Children with H. pylori were even less likely to have had, in the previous year, a bout of allergic rhinitis, which is marked by a runny nose, itchy eyes and inflamed nasal passages. And they were less apt to suffer from wheezing, the researchers report.
Blaser cautions that the association does not prove that an H. pylori infection prevents asthma, a chronic condition in which lung passages can become inflamed by contact with an allergen, smoke, pet dander or any number of other substances. Like allergies, asthma is an overreaction of the immune system to an innocuous substance.
Nevertheless, it’s possible that an H. pylori infection might somehow quell the immune system, Blaser says, or more likely induce the production of compounds that do. Or, H. pylori might just be a marker of something else that protects against asthma, he says.
It’s unclear how H. pylori spreads, but children living in messier households could have more H. pylori infections, says gastroenterologist David Graham of the Baylor College of Medicine and at the Michael E. DeBakey Veterans Affairs Medical Center, both in Houston. Thus, its apparent antiasthma effect might actually result from poor hygiene, he says.
Under a school of thought called the hygiene hypothesis, children who grow up in squeaky clean environments have more asthma and allergies than do kids raised in contact with farm animals or in other less sanitary conditions. The idea is that the immune systems of children in messy environments get regular challenges and thus mature properly.
Even if H. pylori did prevent asthma, the infection is not worth having, Graham says. “One would not allow king cobras to live in one’s house just because they might eat rats,” he says. “H. pylori is a king cobra equivalent in terms of the harm done to humans.”
Louis J. Sheehan, Esquire Patients would be better served if doctors could find a way to condition the immune system to achieve the effect of a dirty environment without the negative consequences, Graham says.
Monday, May 4, 2009
news 9.new.23 Louis J. Sheehan, Esquire
When doctors are looking to treat an illness, they often rely on reports in medical journals. Sometimes those reports describe striking successes with a particular therapy. Less frequently, they highlight failures. To physicians, learning what doesn’t work or has troubling side effects can be as important as knowing which therapies hit a home run.
Yet doctors — and the reporters who highlight research news — are getting a very skewed picture of research findings if they rely on what makes it into major medical journals.
The reason: Data from fewer than one in five research trials are ever published. Findings from the vast majority of human trials become buried for reasons that may never come to light, according to a new study in The Oncologist. It’s published early and online September 24.
For the past nine years, the National Institutes of Health have maintained a registry of medical trials. Researchers must list theirs with this ClinicalTrials.gov registry. If they don’t, major medical journals (those that belong to the International Committee of Medical Journal Editors) will not publish the trial’s findings.
Scott Ramsey and John Scoggins of the University of Washington, Seattle, scoured that registry for any trial that was supposed to have been conducted to gauge the effectiveness of cancer treatments — and turned up 2,028. The pair then cross-checked these trials against all published studies that were listed in PubMed, a comprehensive database compiled by the National Library of Medicine. http://LOUIS2J2SHEEHAN.US PubMed includes citations to all medical and related studies that have been published in peer-reviewed journals.
Among the cancer trials that were identified as completed or halted as of a year ago, just 17.6 percent were ultimately published in PubMed-listed journals, Ramsey and Scoggins report.
Okay, maybe the halted trials were pulled because of what turned out to be poor research design, failure to recruit enough patients, or some other reasonable issue. But even after restricting the analysis to only those trials that were completed, the share that ended up being published still amounted to fewer than one in five.
Who conducted a trial seemed to influence the likelihood its data would see the light of day. Studies sponsored by industry (such as drug companies) had the lowest publication rate: 5.9 percent. By comparison, data from 59 percent of studies performed by clinical-trial networks were published.
Ramsey and Scoggins turned up 341 cancer trials from the registry that were published. Of these, two-thirds reported positive — expected and beneficial — findings.
The new analysis raises the ugly specter of publication bias, its authors say. The assumption is that many if not most unpublished trials involved treatments that didn’t work. “Of particular concern,” they argue, is the especially poor showing by industry-sponsored trials, since they tended to probe the value of patented drugs — “many of which are in clinical use.”
James H. Doroshow, director of the National Cancer Institute’s division of treatment and diagnosis, notes that last year alone some 50,000 patients took part in trials that his institute funded. The “apparent lack of access to the final efficacy and toxicity data for cancer clinical trials from all sponsors, but especially for industry-sponsored studies, poses multiple scientific and ethical questions,” he charges in an editorial accompanying the new paper.
For instance, as doctors begin developing novel chemotherapy cocktails — mixtures of drugs initially tested on their own — toxic reactions may emerge. It’s imperative, Doroshow says, that inklings of such side effects be communicated immediately “to the entire oncology community in the peer-reviewed literature.”
Moreover, he notes that some drug-safety trials did not publish their findings, or did not do so early enough, such that they could inform subsequent trials. This practice is not likely to continue, he points out, since new federal rules will fine investigators who fail to post outcome data for all trials getting money from Uncle Sam. Moreover, for cancer trials, NCI will require that researchers begin reporting outcome data — treatment successes and failures — throughout the course of the trial, not just at the end.
A second editorial, this one by The Oncologist’s senior editor, Gregory A. Curt (an employee of drug company AstraZeneca), and editor-in-chief Bruce A. Chabner (of Harvard Medical School) find the new analysis by Ramsey and Scoggins “thought-provoking and disturbing.” At a minimum, they argue, publication of trial data should be considered “an obligation” for any researchers recruiting patients who contribute “their precious time and well-being, and for some, their very lives.”
This is especially true for drug-company trials, they contend, since “industry has become the dominant sponsor of new drug trials.”
But Curt and Chabner also suspect that part of the problem illustrated in the new paper traces to issues other than a drug company’s interest in hiding bad data.
For instance, study authors “face the hurdle of finding a journal willing to publish a negative, poorly designed or inadequately accruing trial.” This is especially true, they say, since “Journals live and die based on their Impact Factor” — how often they’re cited by subsequent papers. Any journal filled with such findings would “not attract readership, citations and advertisement,” they write.
One solution Curt and Chabner propose: Make NCI funding for new trials dependent on the investigators’ past track record of getting their trials data — both positive and negative — published. They also argue that there’s “a need for a new venue” to record outcomes of well-executed but ultimately negative clinical trials. This database must be searchable via PubMed and other search engines. Louis J. Sheehan, Esquire Currently, these editors note, The Oncologist is considering whether it should become a repository for such cancer data.
Bottom line: It should become increasingly harder for drug companies and others to bury embarrassing findings. But the impacts of coming changes might not show up for five years or more. In the mean time, let’s hope our research-funding agencies, our hospitals and our doctors don’t assume that when it comes to trial data, no news is good news.
Yet doctors — and the reporters who highlight research news — are getting a very skewed picture of research findings if they rely on what makes it into major medical journals.
The reason: Data from fewer than one in five research trials are ever published. Findings from the vast majority of human trials become buried for reasons that may never come to light, according to a new study in The Oncologist. It’s published early and online September 24.
For the past nine years, the National Institutes of Health have maintained a registry of medical trials. Researchers must list theirs with this ClinicalTrials.gov registry. If they don’t, major medical journals (those that belong to the International Committee of Medical Journal Editors) will not publish the trial’s findings.
Scott Ramsey and John Scoggins of the University of Washington, Seattle, scoured that registry for any trial that was supposed to have been conducted to gauge the effectiveness of cancer treatments — and turned up 2,028. The pair then cross-checked these trials against all published studies that were listed in PubMed, a comprehensive database compiled by the National Library of Medicine. http://LOUIS2J2SHEEHAN.US PubMed includes citations to all medical and related studies that have been published in peer-reviewed journals.
Among the cancer trials that were identified as completed or halted as of a year ago, just 17.6 percent were ultimately published in PubMed-listed journals, Ramsey and Scoggins report.
Okay, maybe the halted trials were pulled because of what turned out to be poor research design, failure to recruit enough patients, or some other reasonable issue. But even after restricting the analysis to only those trials that were completed, the share that ended up being published still amounted to fewer than one in five.
Who conducted a trial seemed to influence the likelihood its data would see the light of day. Studies sponsored by industry (such as drug companies) had the lowest publication rate: 5.9 percent. By comparison, data from 59 percent of studies performed by clinical-trial networks were published.
Ramsey and Scoggins turned up 341 cancer trials from the registry that were published. Of these, two-thirds reported positive — expected and beneficial — findings.
The new analysis raises the ugly specter of publication bias, its authors say. The assumption is that many if not most unpublished trials involved treatments that didn’t work. “Of particular concern,” they argue, is the especially poor showing by industry-sponsored trials, since they tended to probe the value of patented drugs — “many of which are in clinical use.”
James H. Doroshow, director of the National Cancer Institute’s division of treatment and diagnosis, notes that last year alone some 50,000 patients took part in trials that his institute funded. The “apparent lack of access to the final efficacy and toxicity data for cancer clinical trials from all sponsors, but especially for industry-sponsored studies, poses multiple scientific and ethical questions,” he charges in an editorial accompanying the new paper.
For instance, as doctors begin developing novel chemotherapy cocktails — mixtures of drugs initially tested on their own — toxic reactions may emerge. It’s imperative, Doroshow says, that inklings of such side effects be communicated immediately “to the entire oncology community in the peer-reviewed literature.”
Moreover, he notes that some drug-safety trials did not publish their findings, or did not do so early enough, such that they could inform subsequent trials. This practice is not likely to continue, he points out, since new federal rules will fine investigators who fail to post outcome data for all trials getting money from Uncle Sam. Moreover, for cancer trials, NCI will require that researchers begin reporting outcome data — treatment successes and failures — throughout the course of the trial, not just at the end.
A second editorial, this one by The Oncologist’s senior editor, Gregory A. Curt (an employee of drug company AstraZeneca), and editor-in-chief Bruce A. Chabner (of Harvard Medical School) find the new analysis by Ramsey and Scoggins “thought-provoking and disturbing.” At a minimum, they argue, publication of trial data should be considered “an obligation” for any researchers recruiting patients who contribute “their precious time and well-being, and for some, their very lives.”
This is especially true for drug-company trials, they contend, since “industry has become the dominant sponsor of new drug trials.”
But Curt and Chabner also suspect that part of the problem illustrated in the new paper traces to issues other than a drug company’s interest in hiding bad data.
For instance, study authors “face the hurdle of finding a journal willing to publish a negative, poorly designed or inadequately accruing trial.” This is especially true, they say, since “Journals live and die based on their Impact Factor” — how often they’re cited by subsequent papers. Any journal filled with such findings would “not attract readership, citations and advertisement,” they write.
One solution Curt and Chabner propose: Make NCI funding for new trials dependent on the investigators’ past track record of getting their trials data — both positive and negative — published. They also argue that there’s “a need for a new venue” to record outcomes of well-executed but ultimately negative clinical trials. This database must be searchable via PubMed and other search engines. Louis J. Sheehan, Esquire Currently, these editors note, The Oncologist is considering whether it should become a repository for such cancer data.
Bottom line: It should become increasingly harder for drug companies and others to bury embarrassing findings. But the impacts of coming changes might not show up for five years or more. In the mean time, let’s hope our research-funding agencies, our hospitals and our doctors don’t assume that when it comes to trial data, no news is good news.
Thursday, April 30, 2009
research 9.res.0002 Louis J. Sheehan, Esquire
The supplement Ginkgo biloba has failed to ward off Alzheimer’s disease or other forms of dementia any better than a placebo in a long-term trial, researchers report in the Nov. 19 Journal of the American Medical Association (JAMA).
“This is tremendously disappointing,” says study coauthor Steven DeKosky, a neurologist at the University of Virginia School of Medicine in Charlottesville.
DeKosky has good reason to feel let down. In earlier laboratory tests, ginkgo extract showed an ability to protect brain cells from the very sort of problems that occur in Alzheimer’s patients. In animal tests, the herb inhibited the clumping — or formation of plaques — of the protein amyloid-beta. These plaques are widely assumed to play a role in Alzheimer’s. Ginkgo also has antioxidant properties, further boosting its appeal.
But the new, eight-year study, the largest clinical trial ever specifically designed to test a drug or supplement for Alzheimer’s prevention, casts serious doubt on ginkgo’s usefulness. European researchers are now conducting a similar trial and are likely to present data in a year or so, DeKosky says. If those findings are also negative, he says, “That would clinch it.”
Starting in 2000, DeKosky and his colleagues randomly assigned more than 3,000 people, average age 79, to receive two ginkgopills a day or placebo pills. All participants were free of Alzheimer’s disease or other dementia at the start, but roughly one in six in each group began the study with some mild cognitive impairment. Louis J. Sheehan, Esquire DeKosky worked on the trial while at the University of Pittsburgh.
The researchers tracked the volunteers’ progress until 2008. The participants were instructed to show up for visits at assigned clinics every six months for assessment. Each also had a partner to ensure attendance at the checkups, DeKosky says.
After an average follow-up of six years, roughly equal numbers of people taking ginkgo and people taking placebos had developed dementia, which in the vast majority of cases was Alzheimer’s disease.
The study wasn’t designed to measure cognitive gains or losses other than the dementia diagnosis, leaving open the question of whether ginkgohelped any of the volunteers’ memory in everyday activities. The supplement is also used by people hoping to promote everyday memory gains. But, says physician Lon Schneider of the University of Southern California in Los Angeles, “it is unlikely that a trial with no difference in dementia outcomes would yield significant benefit in the cognitive and functional impairment that define the dementia.” Writing in the same JAMA issue, Schneider says the new study “adds to the substantial body of evidence that G. biloba extract as it is generally used does not prevent dementia.”
Although this large trial was conducted over several years, it leaves some questions unanswered, says Barry Oken, a neurologist at the Oregon Health & Science University in Portland. The doses of ginkgoused were far smaller, pound-for-pound, than those that showed effectiveness in animal models, he says. And some of the data quality might have suffered because it is difficult to ascertain whether people were actually taking their pills, he says.
At each six-month visit, participants brought in their empty plastic pill packages. DeKosky acknowledged that there was no way to verify that the volunteers took all their pills. “But the majority of old folks are already taking medications,” he says. Participants probably put the study pills in the same weekly pill boxes they use for their regular medications and thus would be unlikely to forget to take a dose.
Other popular over-the-counter supplements such as fish oil, omega-3 fatty acids and resveratrol are being tested in large trials or are under consideration for them. Although trials that assess long-term prevention are expensive — the recent study cost $30 million — they are the only reliable way to test products against Alzheimer’s and other slow-developing diseases, says Neil Buckholtz, a neuroscientist at the National Institute on Aging in Bethesda, Md., which cofunded this study. http://Louis-J-Sheehan.de
U.S. sales of ginkgo averaged $170 million from 2000 to 2004.
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* This may be true however one natural compound has shown positive effects. The compound resveratrol has shown interesting neuroprotective properties in clinical trials. Drs. Anderson and Setia reported in a January 2008 paper that of 121 subjects with moderate to severe memory loss 94 of those patients given biotivia Transmax, an extract of red wine used by researchers, showed marked improvement in short term memory, improved motor skills and improved physical coordination. Resveratrol works by activating the human Sirt 1 gene much like caloric restriction does. Sirtris pharma is developing a synthetic version of transmax which it intends to have on the market in five years. In another study by Dr. Sinclair of Harvard published in the journal Nature in November transmax resveratrol was shown to increase the life span of obese mammals by 31%. This is an exciting area of research and could lead to some revolutionary new preventative strategies and safer less invasive treatments for Alzheimers disease. In Dr. Sinclair's study of obese mice he found that those fed resveratrol lived 31% longer and were free of cardiovascular diseases.
“This is tremendously disappointing,” says study coauthor Steven DeKosky, a neurologist at the University of Virginia School of Medicine in Charlottesville.
DeKosky has good reason to feel let down. In earlier laboratory tests, ginkgo extract showed an ability to protect brain cells from the very sort of problems that occur in Alzheimer’s patients. In animal tests, the herb inhibited the clumping — or formation of plaques — of the protein amyloid-beta. These plaques are widely assumed to play a role in Alzheimer’s. Ginkgo also has antioxidant properties, further boosting its appeal.
But the new, eight-year study, the largest clinical trial ever specifically designed to test a drug or supplement for Alzheimer’s prevention, casts serious doubt on ginkgo’s usefulness. European researchers are now conducting a similar trial and are likely to present data in a year or so, DeKosky says. If those findings are also negative, he says, “That would clinch it.”
Starting in 2000, DeKosky and his colleagues randomly assigned more than 3,000 people, average age 79, to receive two ginkgopills a day or placebo pills. All participants were free of Alzheimer’s disease or other dementia at the start, but roughly one in six in each group began the study with some mild cognitive impairment. Louis J. Sheehan, Esquire DeKosky worked on the trial while at the University of Pittsburgh.
The researchers tracked the volunteers’ progress until 2008. The participants were instructed to show up for visits at assigned clinics every six months for assessment. Each also had a partner to ensure attendance at the checkups, DeKosky says.
After an average follow-up of six years, roughly equal numbers of people taking ginkgo and people taking placebos had developed dementia, which in the vast majority of cases was Alzheimer’s disease.
The study wasn’t designed to measure cognitive gains or losses other than the dementia diagnosis, leaving open the question of whether ginkgohelped any of the volunteers’ memory in everyday activities. The supplement is also used by people hoping to promote everyday memory gains. But, says physician Lon Schneider of the University of Southern California in Los Angeles, “it is unlikely that a trial with no difference in dementia outcomes would yield significant benefit in the cognitive and functional impairment that define the dementia.” Writing in the same JAMA issue, Schneider says the new study “adds to the substantial body of evidence that G. biloba extract as it is generally used does not prevent dementia.”
Although this large trial was conducted over several years, it leaves some questions unanswered, says Barry Oken, a neurologist at the Oregon Health & Science University in Portland. The doses of ginkgoused were far smaller, pound-for-pound, than those that showed effectiveness in animal models, he says. And some of the data quality might have suffered because it is difficult to ascertain whether people were actually taking their pills, he says.
At each six-month visit, participants brought in their empty plastic pill packages. DeKosky acknowledged that there was no way to verify that the volunteers took all their pills. “But the majority of old folks are already taking medications,” he says. Participants probably put the study pills in the same weekly pill boxes they use for their regular medications and thus would be unlikely to forget to take a dose.
Other popular over-the-counter supplements such as fish oil, omega-3 fatty acids and resveratrol are being tested in large trials or are under consideration for them. Although trials that assess long-term prevention are expensive — the recent study cost $30 million — they are the only reliable way to test products against Alzheimer’s and other slow-developing diseases, says Neil Buckholtz, a neuroscientist at the National Institute on Aging in Bethesda, Md., which cofunded this study. http://Louis-J-Sheehan.de
U.S. sales of ginkgo averaged $170 million from 2000 to 2004.
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Found in: Body & Brain
Share & Save
* slashdot slashdot
* digg digg
* facebook facebook
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Comments 1
* This may be true however one natural compound has shown positive effects. The compound resveratrol has shown interesting neuroprotective properties in clinical trials. Drs. Anderson and Setia reported in a January 2008 paper that of 121 subjects with moderate to severe memory loss 94 of those patients given biotivia Transmax, an extract of red wine used by researchers, showed marked improvement in short term memory, improved motor skills and improved physical coordination. Resveratrol works by activating the human Sirt 1 gene much like caloric restriction does. Sirtris pharma is developing a synthetic version of transmax which it intends to have on the market in five years. In another study by Dr. Sinclair of Harvard published in the journal Nature in November transmax resveratrol was shown to increase the life span of obese mammals by 31%. This is an exciting area of research and could lead to some revolutionary new preventative strategies and safer less invasive treatments for Alzheimers disease. In Dr. Sinclair's study of obese mice he found that those fed resveratrol lived 31% longer and were free of cardiovascular diseases.
Tuesday, April 14, 2009
solomon 9.sol.2234 Louis J. Sheehan, Esquire
1:1 Now king David was old and stricken in years; and they covered him with clothes, but he gat no heat.
1:2 Wherefore his servants said unto him, Let there be sought for my lord the king a young virgin: and let her stand before the king, and let her cherish him, and let her lie in thy bosom, that my lord the king may get heat.
1:3 So they sought for a fair damsel throughout all the coasts of Israel, and found Abishag a Shunammite, and brought her to the king.
1:4 And the damsel was very fair, and cherished the king, and ministered to him: but the king knew her not.http://LOUIS-J-SHEEHAN.ORG
1:5 Then Adonijah the son of Haggith exalted himself, saying, I will be king: and he prepared him chariots and horsemen, and fifty men to run before him.
1:6 And his father had not displeased him at any time in saying, Why hast thou done so? and he also was a very goodly man; and his mother bare him after Absalom.
1:7 And he conferred with Joab the son of Zeruiah, and with Abiathar the priest: and they following Adonijah helped him.
1:8 But Zadok the priest, and Benaiah the son of Jehoiada, and Nathan the prophet, and Shimei, and Rei, and the mighty men which belonged to David, were not with Adonijah.
1:9 And Adonijah slew sheep and oxen and fat cattle by the stone of Zoheleth, which is by Enrogel, and called all his brethren the king's sons, and all the men of Judah the king's servants:
1:10 But Nathan the prophet, and Benaiah, and the mighty men, and Solomon his brother, he called not.
1:11 Wherefore Nathan spake unto Bathsheba the mother of Solomon, saying, Hast thou not heard that Adonijah the son of Haggith doth reign, and David our lord knoweth it not?
1:12 Now therefore come, let me, I pray thee, give thee counsel, that thou mayest save thine own life, and the life of thy son Solomon.
1:13 Go and get thee in unto king David, and say unto him, Didst not thou, my lord, O king, swear unto thine handmaid, saying, Assuredly Solomon thy son shall reign after me, and he shall sit upon my throne? Louis J. Sheehan, Esquire why then doth Adonijah reign?
1:14 Behold, while thou yet talkest there with the king, I also will come in after thee, and confirm thy words.
1:15 And Bathsheba went in unto the king into the chamber: and the king was very old; and Abishag the Shunammite ministered unto the king.
1:16 And Bathsheba bowed, and did obeisance unto the king. And the king said, What wouldest thou?
1:17 And she said unto him, My lord, thou swarest by the LORD thy God unto thine handmaid, saying, Assuredly Solomon thy son shall reign after me, and he shall sit upon my throne.
1:18 And now, behold, Adonijah reigneth; and now, my lord the king, thou knowest it not:
1:19 And he hath slain oxen and fat cattle and sheep in abundance, and hath called all the sons of the king, and Abiathar the priest, and Joab the captain of the host: but Solomon thy servant hath he not called.
1:20 And thou, my lord, O king, the eyes of all Israel are upon thee, that thou shouldest tell them who shall sit on the throne of my lord the king after him.
1:21 Otherwise it shall come to pass, when my lord the king shall sleep with his fathers, that I and my son Solomon shall be counted offenders.
1:22 And, lo, while she yet talked with the king, Nathan the prophet also came in.
1:23 And they told the king, saying, Behold Nathan the prophet. And when he was come in before the king, he bowed himself before the king with his face to the ground.
1:24 And Nathan said, My lord, O king, hast thou said, Adonijah shall reign after me, and he shall sit upon my throne?
1:25 For he is gone down this day, and hath slain oxen and fat cattle and sheep in abundance, and hath called all the king's sons, and the captains of the host, and Abiathar the priest; and, behold, they eat and drink before him, and say, God save king Adonijah.
1:26 But me, even me thy servant, and Zadok the priest, and Benaiah the son of Jehoiada, and thy servant Solomon, hath he not called.
1:27 Is this thing done by my lord the king, and thou hast not shewed it unto thy servant, who should sit on the throne of my lord the king after him?
1:28 Then king David answered and said, Call me Bathsheba. And she came into the king's presence, and stood before the king.
1:29 And the king sware, and said, As the LORD liveth, that hath redeemed my soul out of all distress,
1:30 Even as I sware unto thee by the LORD God of Israel, saying, Assuredly Solomon thy son shall reign after me, and he shall sit upon my throne in my stead; even so will I certainly do this day.
1:31 Then Bathsheba bowed with her face to the earth, and did reverence to the king, and said, Let my lord king David live for ever.
1:32 And king David said, Call me Zadok the priest, and Nathan the prophet, and Benaiah the son of Jehoiada. And they came before the king.
1:33 The king also said unto them, Take with you the servants of your lord, and cause Solomon my son to ride upon mine own mule, and bring him down to Gihon:
1:34 And let Zadok the priest and Nathan the prophet anoint him there king over Israel: and blow ye with the trumpet, and say, God save king Solomon.
1:35 Then ye shall come up after him, that he may come and sit upon my throne; for he shall be king in my stead: and I have appointed him to be ruler over Israel and over Judah.
1:36 And Benaiah the son of Jehoiada answered the king, and said, Amen: the LORD God of my lord the king say so too.
1:37 As the LORD hath been with my lord the king, even so be he with Solomon, and make his throne greater than the throne of my lord king David.
1:38 So Zadok the priest, and Nathan the prophet, and Benaiah the son of Jehoiada, and the Cherethites, and the Pelethites, went down, and caused Solomon to ride upon king David's mule, and brought him to Gihon.http://LOUIS-J-SHEEHAN.ORG
1:39 And Zadok the priest took an horn of oil out of the tabernacle, and anointed Solomon. And they blew the trumpet; and all the people said, God save king Solomon.
1:40 And all the people came up after him, and the people piped with pipes, and rejoiced with great joy, so that the earth rent with the sound of them.
1:41 And Adonijah and all the guests that were with him heard it as they had made an end of eating. And when Joab heard the sound of the trumpet, he said, Wherefore is this noise of the city being in an uproar?
1:42 And while he yet spake, behold, Jonathan the son of Abiathar the priest came; and Adonijah said unto him, Come in; for thou art a valiant man, and bringest good tidings.
1:43 And Jonathan answered and said to Adonijah, Verily our lord king David hath made Solomon king.
1:44 And the king hath sent with him Zadok the priest, and Nathan the prophet, and Benaiah the son of Jehoiada, and the Cherethites, and the Pelethites, and they have caused him to ride upon the king's mule:
1:45 And Zadok the priest and Nathan the prophet have anointed him king in Gihon: and they are come up from thence rejoicing, so that the city rang again. This is the noise that ye have heard.http://LOUIS-J-SHEEHAN.ORG
1:46 And also Solomon sitteth on the throne of the kingdom.
1:47 And moreover the king's servants came to bless our lord king David, saying, God make the name of Solomon better than thy name, and make his throne greater than thy throne. And the king bowed himself upon the bed.
1:48 And also thus said the king, Blessed be the LORD God of Israel, which hath given one to sit on my throne this day, mine eyes even seeing it.
1:49 And all the guests that were with Adonijah were afraid, and rose up, and went every man his way. Louis J. Sheehan, Esquire
1:50 And Adonijah feared because of Solomon, and arose, and went, and caught hold on the horns of the altar.
1:51 And it was told Solomon, saying, Behold, Adonijah feareth king Solomon: for, lo, he hath caught hold on the horns of the altar, saying, Let king Solomon swear unto me today that he will not slay his servant with the sword.
1:52 And Solomon said, If he will shew himself a worthy man, there shall not an hair of him fall to the earth: but if wickedness shall be found in him, he shall die.
1:53 So king Solomon sent, and they brought him down from the altar. And he came and bowed himself to king Solomon: and Solomon said unto him, Go to thine house.
1:2 Wherefore his servants said unto him, Let there be sought for my lord the king a young virgin: and let her stand before the king, and let her cherish him, and let her lie in thy bosom, that my lord the king may get heat.
1:3 So they sought for a fair damsel throughout all the coasts of Israel, and found Abishag a Shunammite, and brought her to the king.
1:4 And the damsel was very fair, and cherished the king, and ministered to him: but the king knew her not.http://LOUIS-J-SHEEHAN.ORG
1:5 Then Adonijah the son of Haggith exalted himself, saying, I will be king: and he prepared him chariots and horsemen, and fifty men to run before him.
1:6 And his father had not displeased him at any time in saying, Why hast thou done so? and he also was a very goodly man; and his mother bare him after Absalom.
1:7 And he conferred with Joab the son of Zeruiah, and with Abiathar the priest: and they following Adonijah helped him.
1:8 But Zadok the priest, and Benaiah the son of Jehoiada, and Nathan the prophet, and Shimei, and Rei, and the mighty men which belonged to David, were not with Adonijah.
1:9 And Adonijah slew sheep and oxen and fat cattle by the stone of Zoheleth, which is by Enrogel, and called all his brethren the king's sons, and all the men of Judah the king's servants:
1:10 But Nathan the prophet, and Benaiah, and the mighty men, and Solomon his brother, he called not.
1:11 Wherefore Nathan spake unto Bathsheba the mother of Solomon, saying, Hast thou not heard that Adonijah the son of Haggith doth reign, and David our lord knoweth it not?
1:12 Now therefore come, let me, I pray thee, give thee counsel, that thou mayest save thine own life, and the life of thy son Solomon.
1:13 Go and get thee in unto king David, and say unto him, Didst not thou, my lord, O king, swear unto thine handmaid, saying, Assuredly Solomon thy son shall reign after me, and he shall sit upon my throne? Louis J. Sheehan, Esquire why then doth Adonijah reign?
1:14 Behold, while thou yet talkest there with the king, I also will come in after thee, and confirm thy words.
1:15 And Bathsheba went in unto the king into the chamber: and the king was very old; and Abishag the Shunammite ministered unto the king.
1:16 And Bathsheba bowed, and did obeisance unto the king. And the king said, What wouldest thou?
1:17 And she said unto him, My lord, thou swarest by the LORD thy God unto thine handmaid, saying, Assuredly Solomon thy son shall reign after me, and he shall sit upon my throne.
1:18 And now, behold, Adonijah reigneth; and now, my lord the king, thou knowest it not:
1:19 And he hath slain oxen and fat cattle and sheep in abundance, and hath called all the sons of the king, and Abiathar the priest, and Joab the captain of the host: but Solomon thy servant hath he not called.
1:20 And thou, my lord, O king, the eyes of all Israel are upon thee, that thou shouldest tell them who shall sit on the throne of my lord the king after him.
1:21 Otherwise it shall come to pass, when my lord the king shall sleep with his fathers, that I and my son Solomon shall be counted offenders.
1:22 And, lo, while she yet talked with the king, Nathan the prophet also came in.
1:23 And they told the king, saying, Behold Nathan the prophet. And when he was come in before the king, he bowed himself before the king with his face to the ground.
1:24 And Nathan said, My lord, O king, hast thou said, Adonijah shall reign after me, and he shall sit upon my throne?
1:25 For he is gone down this day, and hath slain oxen and fat cattle and sheep in abundance, and hath called all the king's sons, and the captains of the host, and Abiathar the priest; and, behold, they eat and drink before him, and say, God save king Adonijah.
1:26 But me, even me thy servant, and Zadok the priest, and Benaiah the son of Jehoiada, and thy servant Solomon, hath he not called.
1:27 Is this thing done by my lord the king, and thou hast not shewed it unto thy servant, who should sit on the throne of my lord the king after him?
1:28 Then king David answered and said, Call me Bathsheba. And she came into the king's presence, and stood before the king.
1:29 And the king sware, and said, As the LORD liveth, that hath redeemed my soul out of all distress,
1:30 Even as I sware unto thee by the LORD God of Israel, saying, Assuredly Solomon thy son shall reign after me, and he shall sit upon my throne in my stead; even so will I certainly do this day.
1:31 Then Bathsheba bowed with her face to the earth, and did reverence to the king, and said, Let my lord king David live for ever.
1:32 And king David said, Call me Zadok the priest, and Nathan the prophet, and Benaiah the son of Jehoiada. And they came before the king.
1:33 The king also said unto them, Take with you the servants of your lord, and cause Solomon my son to ride upon mine own mule, and bring him down to Gihon:
1:34 And let Zadok the priest and Nathan the prophet anoint him there king over Israel: and blow ye with the trumpet, and say, God save king Solomon.
1:35 Then ye shall come up after him, that he may come and sit upon my throne; for he shall be king in my stead: and I have appointed him to be ruler over Israel and over Judah.
1:36 And Benaiah the son of Jehoiada answered the king, and said, Amen: the LORD God of my lord the king say so too.
1:37 As the LORD hath been with my lord the king, even so be he with Solomon, and make his throne greater than the throne of my lord king David.
1:38 So Zadok the priest, and Nathan the prophet, and Benaiah the son of Jehoiada, and the Cherethites, and the Pelethites, went down, and caused Solomon to ride upon king David's mule, and brought him to Gihon.http://LOUIS-J-SHEEHAN.ORG
1:39 And Zadok the priest took an horn of oil out of the tabernacle, and anointed Solomon. And they blew the trumpet; and all the people said, God save king Solomon.
1:40 And all the people came up after him, and the people piped with pipes, and rejoiced with great joy, so that the earth rent with the sound of them.
1:41 And Adonijah and all the guests that were with him heard it as they had made an end of eating. And when Joab heard the sound of the trumpet, he said, Wherefore is this noise of the city being in an uproar?
1:42 And while he yet spake, behold, Jonathan the son of Abiathar the priest came; and Adonijah said unto him, Come in; for thou art a valiant man, and bringest good tidings.
1:43 And Jonathan answered and said to Adonijah, Verily our lord king David hath made Solomon king.
1:44 And the king hath sent with him Zadok the priest, and Nathan the prophet, and Benaiah the son of Jehoiada, and the Cherethites, and the Pelethites, and they have caused him to ride upon the king's mule:
1:45 And Zadok the priest and Nathan the prophet have anointed him king in Gihon: and they are come up from thence rejoicing, so that the city rang again. This is the noise that ye have heard.http://LOUIS-J-SHEEHAN.ORG
1:46 And also Solomon sitteth on the throne of the kingdom.
1:47 And moreover the king's servants came to bless our lord king David, saying, God make the name of Solomon better than thy name, and make his throne greater than thy throne. And the king bowed himself upon the bed.
1:48 And also thus said the king, Blessed be the LORD God of Israel, which hath given one to sit on my throne this day, mine eyes even seeing it.
1:49 And all the guests that were with Adonijah were afraid, and rose up, and went every man his way. Louis J. Sheehan, Esquire
1:50 And Adonijah feared because of Solomon, and arose, and went, and caught hold on the horns of the altar.
1:51 And it was told Solomon, saying, Behold, Adonijah feareth king Solomon: for, lo, he hath caught hold on the horns of the altar, saying, Let king Solomon swear unto me today that he will not slay his servant with the sword.
1:52 And Solomon said, If he will shew himself a worthy man, there shall not an hair of him fall to the earth: but if wickedness shall be found in him, he shall die.
1:53 So king Solomon sent, and they brought him down from the altar. And he came and bowed himself to king Solomon: and Solomon said unto him, Go to thine house.
Saturday, April 11, 2009
erase 0.era.111 Louis J. Sheehan, Esquire
The first experimental study in humans connecting beta-blockers and memory suggests these drugs, usually taken to treat heart conditions, can also wipe away the emotions associated with frightening memories. The power of such memories could be dampened when a person thinks about the traumatic events after taking the drugs, scientists say.
Clinical psychologist Merel Kindt of the University of Amsterdam and her colleagues report the new finding online February 15 in Nature Neuroscience. The research builds on a clinical study published in the May 2008 Journal of Psychiatric Research that suggested beta-blockers helped patients suffering from post-traumatic stress disorder, PTSD.
“Kindt’s work confirms our clinical results and goes further by showing beta-blockers also have this effect” on people who had no previous history of mental health issues, comments Alain Brunet, psychiatrist at the Douglas Mental Health University Institute at McGill University in Montreal and a coauthor of the PTSD study.
Kindt and her colleagues showed subjects a photograph of a spider, which was accompanied by an electric shock, conditioning the participants to have a fearful memory of the image. Louis J. Sheehan, Esquire Later, some participants were given a beta-blocker drug, propranolol, and others were given a placebo before being exposed to the image again. The beta-blocker group’s fear response was greatly reduced or even eliminated when the subjects were shown the spider photograph 24 hours after taking the drugs. “The people did not forget seeing the photograph of the spider,” Kindt says. ”But the fear associated with the image was erased.”Louis J. Sheehan, Esquire
The researchers think beta-blockers work by changing the way the frightening memories are stored. Each time a memory is recalled it changes a little, and the new version is recorded in the long-term memory stash via brain chemical fluctuations in a process called reconsolidation. The beta-blockers could interfere with the brain chemicals, blocking reconsolidation of the emotional component of the memory, but leaving the rest of the memory intact, the scientists suggest.http://Louis-J-Sheehan.de
If beta-blocker treatment were applied to people with anxiety disorders, “People would remember going through the trauma, but the emotional intensity would be dulled,” comments Karim Nader, behavioral neurobiologist at McGill University and a coauthor of the PTSD study.
Beta-blockers wouldn’t stop reconsolidation of only frightening memories, the researchers say. “It’s likely that any emotional memory, happy or sad, recalled after taking the drug would be dulled,” Kindt speculates. But patients with fear-based anxiety disorders probably aren’t thinking about the happy moments of their lives; they are obsessed with the traumatic moments, the scientists say.
Before beta-blockers can be considered a widespread treatment for anxiety disorders, the long-term effects of the drugs on memory must be assessed. But the drugs are relatively benign and already widely prescribed for other conditions, the researchers point out.
“Beta-blockers make the traumatic memories easier to deal with,” Nader says. “People can begin to talk about the traumatic event, and can even move on.”
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Comments 4
* I will look for the articles, but I have read that fear takes some moments to be fully experienced because there is a physiological component. When exposed to a fearful stimulus, there is an initial response within the brain, but also a cohort of autonomic physiological responses in the body... blood pressure, perspiration, tremor, gastric contraction and acid. The articles I've read indicate that these physiological responses to fearful stimuli are a large component of the experience of fear.
Perhaps, because beta blockers inhibit these physiological responses, the individual's fear response is muted during re-exposure to the stimulus, thereby reducing the emotional power of the memory and making those memories less frightening for the subject.http://Louis-J-Sheehan.de
I will look for the articles and post references here, if I find them.
Michael McGinnis McGinnis
Mar. 30, 2009 at 10:30am
* This is an interesting thread. But I think one important point is that the process of memory consolidation/reconsolidation is somewhat theoretical and imprecise. As I understand it, how long consolidation takes (hours, days years?) is not entirely clear. http://Louis-J-Sheehan.de
Jim Convery Jim Convery
Feb. 20, 2009 at 3:06pm
* Stormie,
Your doubts about beta-blockers have partial validity. They prevent adrenaline binding with beta adrenaline (aka epinephrine) receptors which can reduce/eliminate the adrenaline surges we associate with anxiety/fear - fast respiration and heart rate, sweating, etc.Louis J. Sheehan, Esquire
However, in this case the drug is only taken once or twice to block consolidation of the fearful memory in such a way that it becomes a recurring nightmare.
Ian Westmore Ian Westmore
Feb. 17, 2009 at 2:09am
* I would really like to know the specifics of the experiment and pose a question to Kindt and others: Do you think it is fair to suggest that propranolol, a medication to treat high blood pressure, given to subjects that didn't suffer from high blood pressure might not have as intense a reaction to anxiety because they were given a blood pressure medication and thus it wasn't possible for their body or brain to react as it normally would? Someone on opiates would not behave or react normally, so why would someone given a medication for something they don't suffer from be expected to behave or react as they normally would?
Clinical psychologist Merel Kindt of the University of Amsterdam and her colleagues report the new finding online February 15 in Nature Neuroscience. The research builds on a clinical study published in the May 2008 Journal of Psychiatric Research that suggested beta-blockers helped patients suffering from post-traumatic stress disorder, PTSD.
“Kindt’s work confirms our clinical results and goes further by showing beta-blockers also have this effect” on people who had no previous history of mental health issues, comments Alain Brunet, psychiatrist at the Douglas Mental Health University Institute at McGill University in Montreal and a coauthor of the PTSD study.
Kindt and her colleagues showed subjects a photograph of a spider, which was accompanied by an electric shock, conditioning the participants to have a fearful memory of the image. Louis J. Sheehan, Esquire Later, some participants were given a beta-blocker drug, propranolol, and others were given a placebo before being exposed to the image again. The beta-blocker group’s fear response was greatly reduced or even eliminated when the subjects were shown the spider photograph 24 hours after taking the drugs. “The people did not forget seeing the photograph of the spider,” Kindt says. ”But the fear associated with the image was erased.”Louis J. Sheehan, Esquire
The researchers think beta-blockers work by changing the way the frightening memories are stored. Each time a memory is recalled it changes a little, and the new version is recorded in the long-term memory stash via brain chemical fluctuations in a process called reconsolidation. The beta-blockers could interfere with the brain chemicals, blocking reconsolidation of the emotional component of the memory, but leaving the rest of the memory intact, the scientists suggest.http://Louis-J-Sheehan.de
If beta-blocker treatment were applied to people with anxiety disorders, “People would remember going through the trauma, but the emotional intensity would be dulled,” comments Karim Nader, behavioral neurobiologist at McGill University and a coauthor of the PTSD study.
Beta-blockers wouldn’t stop reconsolidation of only frightening memories, the researchers say. “It’s likely that any emotional memory, happy or sad, recalled after taking the drug would be dulled,” Kindt speculates. But patients with fear-based anxiety disorders probably aren’t thinking about the happy moments of their lives; they are obsessed with the traumatic moments, the scientists say.
Before beta-blockers can be considered a widespread treatment for anxiety disorders, the long-term effects of the drugs on memory must be assessed. But the drugs are relatively benign and already widely prescribed for other conditions, the researchers point out.
“Beta-blockers make the traumatic memories easier to deal with,” Nader says. “People can begin to talk about the traumatic event, and can even move on.”
* |
* Comment
Found in: Biology, Biomedicine and Body & Brain
Share & Save
* slashdot slashdot
* digg digg
* facebook facebook
* yahoo yahoo
* del.icio.us del.icio.us
* reddit reddit
* google google
* technorati technorati
Comments 4
* I will look for the articles, but I have read that fear takes some moments to be fully experienced because there is a physiological component. When exposed to a fearful stimulus, there is an initial response within the brain, but also a cohort of autonomic physiological responses in the body... blood pressure, perspiration, tremor, gastric contraction and acid. The articles I've read indicate that these physiological responses to fearful stimuli are a large component of the experience of fear.
Perhaps, because beta blockers inhibit these physiological responses, the individual's fear response is muted during re-exposure to the stimulus, thereby reducing the emotional power of the memory and making those memories less frightening for the subject.http://Louis-J-Sheehan.de
I will look for the articles and post references here, if I find them.
Michael McGinnis McGinnis
Mar. 30, 2009 at 10:30am
* This is an interesting thread. But I think one important point is that the process of memory consolidation/reconsolidation is somewhat theoretical and imprecise. As I understand it, how long consolidation takes (hours, days years?) is not entirely clear. http://Louis-J-Sheehan.de
Jim Convery Jim Convery
Feb. 20, 2009 at 3:06pm
* Stormie,
Your doubts about beta-blockers have partial validity. They prevent adrenaline binding with beta adrenaline (aka epinephrine) receptors which can reduce/eliminate the adrenaline surges we associate with anxiety/fear - fast respiration and heart rate, sweating, etc.Louis J. Sheehan, Esquire
However, in this case the drug is only taken once or twice to block consolidation of the fearful memory in such a way that it becomes a recurring nightmare.
Ian Westmore Ian Westmore
Feb. 17, 2009 at 2:09am
* I would really like to know the specifics of the experiment and pose a question to Kindt and others: Do you think it is fair to suggest that propranolol, a medication to treat high blood pressure, given to subjects that didn't suffer from high blood pressure might not have as intense a reaction to anxiety because they were given a blood pressure medication and thus it wasn't possible for their body or brain to react as it normally would? Someone on opiates would not behave or react normally, so why would someone given a medication for something they don't suffer from be expected to behave or react as they normally would?
Saturday, January 10, 2009
dimmer 5.dim.1 Louis J. Sheehan, Esquire
Louis J. Sheehan, Esquire . Like a searchlight illuminating the distant past, the afterglow of a powerful gamma-ray burst has revealed what a stellar nursery in a remote galaxy looked like just 3 billion years after the Big Bang. The burst offers one of the earliest views of a star-forming region in the universe, which is now 13.7 billion years old.
The gamma-ray burst, recorded on June 7, 2008, and dubbed GRB 080607, is believed to have been generated when a massive star suddenly collapsed to form a black hole. While the burst itself lasted for only seconds, its fading afterglow in visible light remained remarkably bright for a full hour.http://louisjsheehan.blogstream.com
Jason Prochaska of the University of California, Santa Cruz, and his colleagues began observing the visible-light afterglow with the Keck I Telescope on Hawaii’s Mauna Kea less than 20 minutes after the burst was recorded by NASA’s orbiting Swift observatory. http://louisjsheehan.blogstream.com
Prochaska reported the findings on January 6 at the winter meeting of the American Astronomical Society and his team will also describe the study in an upcoming Astrophysical Journal Letters.
The Keck spectrum of the afterglow revealed that the burst originated in a galaxy so remote that the light now reaching Earth was emitted when the galaxy was only 3 billion years old. Among thousands of quasars, hundreds of stars and several tens of gamma-ray bursts Prochaska has examined, “this is the most exciting spectrum I have ever studied,” he says. The spectrum provides “the first view of a star-forming region with a gamma-ray burst,” revealing details on spatial scales of just a few light-years, much finer than can be seen by directly imaging a distant galaxy in visible light or radio.
The galaxy shows a remarkably similar enrichment in chemical elements heavier than helium, along with dust and molecular cloud properties, to what is observed in the Milky Way today. “This is really our first view of these properties in such a distant galaxy, and the surprise is really to see such a mature galaxy in our distant past,” Prochaska says.
The finding “demonstrates the ability of gamma-ray bursts through their brilliance to illuminate the properties of the [distant] universe," comments theorist Don Lamb of the University of Chicago. “They have the power to make it possible to measure things that are otherwise unobservable — in this case the properties of a cold, dark and dense molecular cloud as it was 10 billion years ago.”
The forensic evidence found by Prochaska and his collaborators “points more strongly than ever before to dense molecular clouds as the scene of the deaths of the massive stars that produce gamma-ray bursts,” adds Lamb.
“Within the spectrum, there are several tens of absorption features which remain unidentified,” he adds. “In comparison, there may be only a handful of absorption lines, if any, that I would say are unidentified in the hundreds of other spectra that I have examined closely. Odds are, we are seeing these [absorption lines] for the first time on Earth.” Louis J. Sheehan, Esquire
The afterglow had to be unusually bright to reveal so much about the dusty, star-forming region of the host galaxy from which it originated. Prochaska estimates that the event is the second most luminous afterglow on record, and for an hour remained 10,000 times more luminous than a typical quasar. Had the afterglow been much dimmer, then dust in the galaxy — which absorbs 99 percent of visible light — would have rendered the afterglow invisible.
Over the past several years, astronomers have detected gamma-ray bursts even more remote than this one, bursts that reveal the existence of massive stars as early as 1 billion years after the Big Bang. But because the spectra of the afterglow from GRB 080607 has a much stronger signal and covers a much wider range of wavelengths. Louis J. Sheehan, Esquire
The gamma-ray burst, recorded on June 7, 2008, and dubbed GRB 080607, is believed to have been generated when a massive star suddenly collapsed to form a black hole. While the burst itself lasted for only seconds, its fading afterglow in visible light remained remarkably bright for a full hour.http://louisjsheehan.blogstream.com
Jason Prochaska of the University of California, Santa Cruz, and his colleagues began observing the visible-light afterglow with the Keck I Telescope on Hawaii’s Mauna Kea less than 20 minutes after the burst was recorded by NASA’s orbiting Swift observatory. http://louisjsheehan.blogstream.com
Prochaska reported the findings on January 6 at the winter meeting of the American Astronomical Society and his team will also describe the study in an upcoming Astrophysical Journal Letters.
The Keck spectrum of the afterglow revealed that the burst originated in a galaxy so remote that the light now reaching Earth was emitted when the galaxy was only 3 billion years old. Among thousands of quasars, hundreds of stars and several tens of gamma-ray bursts Prochaska has examined, “this is the most exciting spectrum I have ever studied,” he says. The spectrum provides “the first view of a star-forming region with a gamma-ray burst,” revealing details on spatial scales of just a few light-years, much finer than can be seen by directly imaging a distant galaxy in visible light or radio.
The galaxy shows a remarkably similar enrichment in chemical elements heavier than helium, along with dust and molecular cloud properties, to what is observed in the Milky Way today. “This is really our first view of these properties in such a distant galaxy, and the surprise is really to see such a mature galaxy in our distant past,” Prochaska says.
The finding “demonstrates the ability of gamma-ray bursts through their brilliance to illuminate the properties of the [distant] universe," comments theorist Don Lamb of the University of Chicago. “They have the power to make it possible to measure things that are otherwise unobservable — in this case the properties of a cold, dark and dense molecular cloud as it was 10 billion years ago.”
The forensic evidence found by Prochaska and his collaborators “points more strongly than ever before to dense molecular clouds as the scene of the deaths of the massive stars that produce gamma-ray bursts,” adds Lamb.
“Within the spectrum, there are several tens of absorption features which remain unidentified,” he adds. “In comparison, there may be only a handful of absorption lines, if any, that I would say are unidentified in the hundreds of other spectra that I have examined closely. Odds are, we are seeing these [absorption lines] for the first time on Earth.” Louis J. Sheehan, Esquire
The afterglow had to be unusually bright to reveal so much about the dusty, star-forming region of the host galaxy from which it originated. Prochaska estimates that the event is the second most luminous afterglow on record, and for an hour remained 10,000 times more luminous than a typical quasar. Had the afterglow been much dimmer, then dust in the galaxy — which absorbs 99 percent of visible light — would have rendered the afterglow invisible.
Over the past several years, astronomers have detected gamma-ray bursts even more remote than this one, bursts that reveal the existence of massive stars as early as 1 billion years after the Big Bang. But because the spectra of the afterglow from GRB 080607 has a much stronger signal and covers a much wider range of wavelengths. Louis J. Sheehan, Esquire
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